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    <title>American Journal of Physiology-Gastrointestinal and Liver Physiology Podcast</title>
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    <description>Podcasts of the American Journal of Physiology-Gastrointestinal and Liver Physiology</description>
    <pubDate>Mon, 08 Sep 2025 16:56:41 -0300</pubDate>
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        <copyright>Copyright 2026 American Physiological Society</copyright>
    <category>Science</category>
    <ttl>1440</ttl>
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        <title>American Journal of Physiology-Gastrointestinal and Liver Physiology Podcast</title>
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        <title>Cinnabarinic acid protects against metabolic dysfunction-associated steatohepatitis by activating Aryl hydrocarbon Receptor-dependent AMPK signaling</title>
        <itunes:title>Cinnabarinic acid protects against metabolic dysfunction-associated steatohepatitis by activating Aryl hydrocarbon Receptor-dependent AMPK signaling</itunes:title>
        <link>https://ajpgi.podbean.com/e/cinnabarinic-acid-protects-against-metabolic-dysfunction-associated-steatohepatitis-by-activating-aryl-hydrocarbon-receptor-dependent-ampk-signaling/</link>
                    <comments>https://ajpgi.podbean.com/e/cinnabarinic-acid-protects-against-metabolic-dysfunction-associated-steatohepatitis-by-activating-aryl-hydrocarbon-receptor-dependent-ampk-signaling/#comments</comments>        <pubDate>Mon, 08 Sep 2025 16:56:41 -0300</pubDate>
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                                    <description><![CDATA[<p>In this episode, Dr. Aditya Joshi and coauthors discuss their team’s recently published study, “Cinnabarinic acid protects against metabolic dysfunction-associated steatohepatitis by activating Aryl hydrocarbon Receptor-dependent AMPK signaling." The study showed that absence of AhR in hepatocytes results in exacerbated metabolic dysfunction-associated steatohepatitis (MASH) in mice subjected to Western-style high-fat high-fructose high-cholesterol diet. Moreover, treatment with a tryptophan catabolite, cinnabarinic acid (CA) mitigated hallmarks of MASH in an AhR-dependent manner. In conclusion, the study delineates the significance of hepatic AhR-dependent AMPK signaling in CA-mediated protection against MASH.</p>
<p> </p>
<p><a href='https://journals.physiology.org/doi/prev/20250310-aop/abs/10.1152/ajpgi.00337.2024'>Cinnabarinic acid protects against metabolic dysfunction-associated steatohepatitis by activating Aryl hydrocarbon Receptor-dependent AMPK signaling.</a></p>
<p>Nikhil Y. Patil, Iulia Rus, Felix Ampadu, Hassan M. Abu Shukair, Sarah Bonvicino, Richard S. Brush, Elena Eaton, Martin-Paul Agbaga, Tae Gyu Oh, Jacob E. Friedman, and Aditya D. Joshi</p>
<p>2025 329:4, G433-G447</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode, Dr. Aditya Joshi and coauthors discuss their team’s recently published study, “Cinnabarinic acid protects against metabolic dysfunction-associated steatohepatitis by activating Aryl hydrocarbon Receptor-dependent AMPK signaling." The study showed that absence of AhR in hepatocytes results in exacerbated metabolic dysfunction-associated steatohepatitis (MASH) in mice subjected to Western-style high-fat high-fructose high-cholesterol diet. Moreover, treatment with a tryptophan catabolite, cinnabarinic acid (CA) mitigated hallmarks of MASH in an AhR-dependent manner. In conclusion, the study delineates the significance of hepatic AhR-dependent AMPK signaling in CA-mediated protection against MASH.</p>
<p> </p>
<p><a href='https://journals.physiology.org/doi/prev/20250310-aop/abs/10.1152/ajpgi.00337.2024'>Cinnabarinic acid protects against metabolic dysfunction-associated steatohepatitis by activating Aryl hydrocarbon Receptor-dependent AMPK signaling.</a></p>
<p>Nikhil Y. Patil, Iulia Rus, Felix Ampadu, Hassan M. Abu Shukair, Sarah Bonvicino, Richard S. Brush, Elena Eaton, Martin-Paul Agbaga, Tae Gyu Oh, Jacob E. Friedman, and Aditya D. Joshi</p>
<p>2025 329:4, G433-G447</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/hrfxhy2cjgxxmfrn/GI-00337-2024R1.mp3" length="9294890" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode, Dr. Aditya Joshi and coauthors discuss their team’s recently published study, “Cinnabarinic acid protects against metabolic dysfunction-associated steatohepatitis by activating Aryl hydrocarbon Receptor-dependent AMPK signaling." The study showed that absence of AhR in hepatocytes results in exacerbated metabolic dysfunction-associated steatohepatitis (MASH) in mice subjected to Western-style high-fat high-fructose high-cholesterol diet. Moreover, treatment with a tryptophan catabolite, cinnabarinic acid (CA) mitigated hallmarks of MASH in an AhR-dependent manner. In conclusion, the study delineates the significance of hepatic AhR-dependent AMPK signaling in CA-mediated protection against MASH.
 
Cinnabarinic acid protects against metabolic dysfunction-associated steatohepatitis by activating Aryl hydrocarbon Receptor-dependent AMPK signaling.
Nikhil Y. Patil, Iulia Rus, Felix Ampadu, Hassan M. Abu Shukair, Sarah Bonvicino, Richard S. Brush, Elena Eaton, Martin-Paul Agbaga, Tae Gyu Oh, Jacob E. Friedman, and Aditya D. Joshi
2025 329:4, G433-G447]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>519</itunes:duration>
                <itunes:episode>50</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Uncovering the Gut-Adipose-Liver Axis: Microbiota Encroachment and Metabolic Dysfunction in MASLD</title>
        <itunes:title>Uncovering the Gut-Adipose-Liver Axis: Microbiota Encroachment and Metabolic Dysfunction in MASLD</itunes:title>
        <link>https://ajpgi.podbean.com/e/uncovering-the-gut-adipose-liver-axis-microbiota-encroachment-and-metabolic-dysfunction-in-masld/</link>
                    <comments>https://ajpgi.podbean.com/e/uncovering-the-gut-adipose-liver-axis-microbiota-encroachment-and-metabolic-dysfunction-in-masld/#comments</comments>        <pubDate>Thu, 24 Jul 2025 12:00:43 -0300</pubDate>
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                                    <description><![CDATA[<p>In this episode, coauthors Daria Igudesman and Karen D. Corbin discuss their team’s recently published study, "Microbiota encroachment and a gut-adipose-liver axis in metabolic dysfunction-associated steatotic liver disease." This first-in-human study explores how changes in the gut microbiota may contribute to metabolic dysfunction through a gut-adipose-liver axis. The researchers found that colonic expression of insulin and lipid-related genes may link microbial encroachment in the colon with adipose tissue insulin resistance and the development of metabolic dysfunction-associated steatotic liver disease (MASLD). Tune in to learn how these findings offer new insights into the complex interplay between the gut microbiome and metabolic health.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00381.2024'>Microbiota encroachment and a gut-adipose-liver axis in metabolic dysfunction-associated steatotic liver disease</a>
Daria Igudesman, GongXin Yu, Charlene Dauriat, Torfay Roman, Maryam R. Kashi, Elizabeth Blakley, Benoit Chassaing, and Karen D. Corbin
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 329:1, G201-G214</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode, coauthors Daria Igudesman and Karen D. Corbin discuss their team’s recently published study, <em>"Microbiota encroachment and a gut-adipose-liver axis in metabolic dysfunction-associated steatotic liver disease."</em> This first-in-human study explores how changes in the gut microbiota may contribute to metabolic dysfunction through a gut-adipose-liver axis. The researchers found that colonic expression of insulin and lipid-related genes may link microbial encroachment in the colon with adipose tissue insulin resistance and the development of metabolic dysfunction-associated steatotic liver disease (MASLD). Tune in to learn how these findings offer new insights into the complex interplay between the gut microbiome and metabolic health.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00381.2024'>Microbiota encroachment and a gut-adipose-liver axis in metabolic dysfunction-associated steatotic liver disease</a>
Daria Igudesman, GongXin Yu, Charlene Dauriat, Torfay Roman, Maryam R. Kashi, Elizabeth Blakley, Benoit Chassaing, and Karen D. Corbin
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 329:1, G201-G214</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/3be2qk8rzipftwuz/GI_00381_2024_Finalaft9u.mp3" length="13292372" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode, coauthors Daria Igudesman and Karen D. Corbin discuss their team’s recently published study, "Microbiota encroachment and a gut-adipose-liver axis in metabolic dysfunction-associated steatotic liver disease." This first-in-human study explores how changes in the gut microbiota may contribute to metabolic dysfunction through a gut-adipose-liver axis. The researchers found that colonic expression of insulin and lipid-related genes may link microbial encroachment in the colon with adipose tissue insulin resistance and the development of metabolic dysfunction-associated steatotic liver disease (MASLD). Tune in to learn how these findings offer new insights into the complex interplay between the gut microbiome and metabolic health.
 
Microbiota encroachment and a gut-adipose-liver axis in metabolic dysfunction-associated steatotic liver disease
Daria Igudesman, GongXin Yu, Charlene Dauriat, Torfay Roman, Maryam R. Kashi, Elizabeth Blakley, Benoit Chassaing, and Karen D. Corbin
American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 329:1, G201-G214]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>577</itunes:duration>
                <itunes:episode>49</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
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    <item>
        <title>Modeling Eosinophilic Esophagitis: Insights from Mouse Models into Mechanisms and Therapies</title>
        <itunes:title>Modeling Eosinophilic Esophagitis: Insights from Mouse Models into Mechanisms and Therapies</itunes:title>
        <link>https://ajpgi.podbean.com/e/modeling-eosinophilic-esophagitis-insights-from-mouse-models-into-mechanisms-and-therapies/</link>
                    <comments>https://ajpgi.podbean.com/e/modeling-eosinophilic-esophagitis-insights-from-mouse-models-into-mechanisms-and-therapies/#comments</comments>        <pubDate>Thu, 24 Jul 2025 11:02:12 -0300</pubDate>
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                                    <description><![CDATA[<p>In this episode, coauthors Jazmyne L. Jackson, Abigail J. Staub, Annie D. Fuller, and Kelly A. Whelan join us to discuss their recently published review, "Mouse models of eosinophilic esophagitis: molecular and translational insights." Eosinophilic esophagitis (EoE) is a chronic allergic inflammatory disease of the esophagus with growing prevalence and clinical impact, yet many of its underlying mechanisms remain poorly understood. The authors explore how murine models have advanced our knowledge of EoE pathogenesis, highlighting key molecular and translational findings uncovered through in vivo research. This episode delves into the strengths and limitations of existing models, current challenges, and future opportunities for leveraging mouse models to guide diagnosis, monitoring, and therapy development in EoE.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00396.2024'>Mouse models of eosinophilic esophagitis: molecular and translational insights</a>
Jazmyne L. Jackson, Abigail J. Staub, Annie D. Fuller, John M. Crespo, Travis H. Bordner, Courtney Worrell, No’ad Shanas, Danielle Waheed, Tatiana A. Karakasheva, Melanie Ruffner, Amanda B. Muir, and Kelly A. Whelan
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 329:1, G215-G231</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode, coauthors Jazmyne L. Jackson, Abigail J. Staub, Annie D. Fuller, and Kelly A. Whelan join us to discuss their recently published review, <em>"Mouse models of eosinophilic esophagitis: molecular and translational insights."</em> Eosinophilic esophagitis (EoE) is a chronic allergic inflammatory disease of the esophagus with growing prevalence and clinical impact, yet many of its underlying mechanisms remain poorly understood. The authors explore how murine models have advanced our knowledge of EoE pathogenesis, highlighting key molecular and translational findings uncovered through in vivo research. This episode delves into the strengths and limitations of existing models, current challenges, and future opportunities for leveraging mouse models to guide diagnosis, monitoring, and therapy development in EoE.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00396.2024'>Mouse models of eosinophilic esophagitis: molecular and translational insights</a>
Jazmyne L. Jackson, Abigail J. Staub, Annie D. Fuller, John M. Crespo, Travis H. Bordner, Courtney Worrell, No’ad Shanas, Danielle Waheed, Tatiana A. Karakasheva, Melanie Ruffner, Amanda B. Muir, and Kelly A. Whelan
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 329:1, G215-G231</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/rvsqxnm4wsnvurfs/GI_00396_2024_Final8vqmd.mp3" length="13855546" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode, coauthors Jazmyne L. Jackson, Abigail J. Staub, Annie D. Fuller, and Kelly A. Whelan join us to discuss their recently published review, "Mouse models of eosinophilic esophagitis: molecular and translational insights." Eosinophilic esophagitis (EoE) is a chronic allergic inflammatory disease of the esophagus with growing prevalence and clinical impact, yet many of its underlying mechanisms remain poorly understood. The authors explore how murine models have advanced our knowledge of EoE pathogenesis, highlighting key molecular and translational findings uncovered through in vivo research. This episode delves into the strengths and limitations of existing models, current challenges, and future opportunities for leveraging mouse models to guide diagnosis, monitoring, and therapy development in EoE.
 
Mouse models of eosinophilic esophagitis: molecular and translational insights
Jazmyne L. Jackson, Abigail J. Staub, Annie D. Fuller, John M. Crespo, Travis H. Bordner, Courtney Worrell, No’ad Shanas, Danielle Waheed, Tatiana A. Karakasheva, Melanie Ruffner, Amanda B. Muir, and Kelly A. Whelan
American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 329:1, G215-G231]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>647</itunes:duration>
                <itunes:episode>48</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Probiotics, Tryptophan, and Gut Health: How L. rhamnosus GG Remodels Arginine Metabolism to Protect the Barrier</title>
        <itunes:title>Probiotics, Tryptophan, and Gut Health: How L. rhamnosus GG Remodels Arginine Metabolism to Protect the Barrier</itunes:title>
        <link>https://ajpgi.podbean.com/e/probiotics-tryptophan-and-gut-health-how-l-rhamnosus-gg-remodels-arginine-metabolism-to-protect-the-barrier/</link>
                    <comments>https://ajpgi.podbean.com/e/probiotics-tryptophan-and-gut-health-how-l-rhamnosus-gg-remodels-arginine-metabolism-to-protect-the-barrier/#comments</comments>        <pubDate>Thu, 24 Jul 2025 10:41:52 -0300</pubDate>
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                                    <description><![CDATA[<p>In this episode, Jayson M. Antonio and Ronaldo P. Ferraris discuss their team’s recently published study, "Lacticaseibacillus rhamnosus GG-driven remodeling of arginine metabolism mitigates gut barrier dysfunction." The research reveals a novel probiotic-driven mechanism that links dietary tryptophan with host arginine metabolism. The probiotic Lacticaseibacillus rhamnosus GG, when combined with tryptophan, enhances gut barrier integrity by upregulating argininosuccinate lyase (ASL), a key enzyme in arginine biosynthesis. The study also identifies ASL downregulation and increased serum argininosuccinate levels in a mouse model of colitis, pointing to a promising target for precision probiotic therapies.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00366.2024'>Lacticaseibacillus rhamnosus GG-driven remodeling of arginine metabolism mitigates gut barrier dysfunction</a>
Jayson M. Antonio, Yue Liu, Panan Suntornsaratoon, Abigail Jones, Jayanth Ambat, Ajitha Bala, Joshua Joby Kanattu, Juan Flores, Sheila Bandyopadhyay, Ravij Upadhyay, Jagannatham Naidu Bhupana, Xiaoyang Su, Wei Vivian Li, Nan Gao, and Ronaldo P. Ferraris
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 329:1, G162-G185</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode, Jayson M. Antonio and Ronaldo P. Ferraris discuss their team’s recently published study, <em>"Lacticaseibacillus rhamnosus GG-driven remodeling of arginine metabolism mitigates gut barrier dysfunction."</em> The research reveals a novel probiotic-driven mechanism that links dietary tryptophan with host arginine metabolism. The probiotic Lacticaseibacillus rhamnosus GG, when combined with tryptophan, enhances gut barrier integrity by upregulating argininosuccinate lyase (ASL), a key enzyme in arginine biosynthesis. The study also identifies ASL downregulation and increased serum argininosuccinate levels in a mouse model of colitis, pointing to a promising target for precision probiotic therapies.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00366.2024'><em>Lacticaseibacillus rhamnosus GG</em>-driven remodeling of arginine metabolism mitigates gut barrier dysfunction</a>
Jayson M. Antonio, Yue Liu, Panan Suntornsaratoon, Abigail Jones, Jayanth Ambat, Ajitha Bala, Joshua Joby Kanattu, Juan Flores, Sheila Bandyopadhyay, Ravij Upadhyay, Jagannatham Naidu Bhupana, Xiaoyang Su, Wei Vivian Li, Nan Gao, and Ronaldo P. Ferraris
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 329:1, G162-G185</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/jdtiz3iwdndexfpq/GI_00366_2024_Final8aajx.mp3" length="8975497" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode, Jayson M. Antonio and Ronaldo P. Ferraris discuss their team’s recently published study, "Lacticaseibacillus rhamnosus GG-driven remodeling of arginine metabolism mitigates gut barrier dysfunction." The research reveals a novel probiotic-driven mechanism that links dietary tryptophan with host arginine metabolism. The probiotic Lacticaseibacillus rhamnosus GG, when combined with tryptophan, enhances gut barrier integrity by upregulating argininosuccinate lyase (ASL), a key enzyme in arginine biosynthesis. The study also identifies ASL downregulation and increased serum argininosuccinate levels in a mouse model of colitis, pointing to a promising target for precision probiotic therapies.
 
Lacticaseibacillus rhamnosus GG-driven remodeling of arginine metabolism mitigates gut barrier dysfunction
Jayson M. Antonio, Yue Liu, Panan Suntornsaratoon, Abigail Jones, Jayanth Ambat, Ajitha Bala, Joshua Joby Kanattu, Juan Flores, Sheila Bandyopadhyay, Ravij Upadhyay, Jagannatham Naidu Bhupana, Xiaoyang Su, Wei Vivian Li, Nan Gao, and Ronaldo P. Ferraris
American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 329:1, G162-G185]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>551</itunes:duration>
                <itunes:episode>47</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Dietary Fibers and Gut Signals: How Fructooligosaccharides Modulate Colonic Motility via Calcium and 5-HT3 Receptors</title>
        <itunes:title>Dietary Fibers and Gut Signals: How Fructooligosaccharides Modulate Colonic Motility via Calcium and 5-HT3 Receptors</itunes:title>
        <link>https://ajpgi.podbean.com/e/dietary-fibers-and-gut-signals-how-fructooligosaccharides-modulate-colonic-motility-via-calcium-and-5-ht3-receptors/</link>
                    <comments>https://ajpgi.podbean.com/e/dietary-fibers-and-gut-signals-how-fructooligosaccharides-modulate-colonic-motility-via-calcium-and-5-ht3-receptors/#comments</comments>        <pubDate>Thu, 24 Jul 2025 10:06:42 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/69f2076d-3fd9-3486-9858-6c681f1a9b4a</guid>
                                    <description><![CDATA[<p>In this episode, we’re joined by coauthors Preedajit Wongkrasant and Keith A. Sharkey to discuss their recent publication, "Fructooligosaccharides slow colonic motility and activate myenteric neurons via calcium sensing and 5-HT3 receptors in the proximal colon." Calcium-sensing receptors are known to play an important role in gastrointestinal physiology. This study reveals a new function of fructooligosaccharides, a type of dietary fiber, in regulating colonic motility and activating the enteric nervous system. The effects are mediated through calcium-sensing and 5-HT3 receptors, providing new insights into gut–brain communication and potential therapeutic targets for gastrointestinal disorders.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00039.2025'>Fructooligosaccharides slow colonic motility and activate myenteric neurons via calcium sensing and 5-HT3 receptors in the proximal colon</a>
Preedajit Wongkrasant, Laurie E. Wallace, Wallace K. MacNaughton, and Keith A. Sharkey
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 328:6, G734-G745</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode, we’re joined by coauthors Preedajit Wongkrasant and Keith A. Sharkey to discuss their recent publication, <em>"Fructooligosaccharides slow colonic motility and activate myenteric neurons via calcium sensing and 5-HT3 receptors in the proximal colon."</em> Calcium-sensing receptors are known to play an important role in gastrointestinal physiology. This study reveals a new function of fructooligosaccharides, a type of dietary fiber, in regulating colonic motility and activating the enteric nervous system. The effects are mediated through calcium-sensing and 5-HT3 receptors, providing new insights into gut–brain communication and potential therapeutic targets for gastrointestinal disorders.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00039.2025'>Fructooligosaccharides slow colonic motility and activate myenteric neurons via calcium sensing and 5-HT3 receptors in the proximal colon</a>
Preedajit Wongkrasant, Laurie E. Wallace, Wallace K. MacNaughton, and Keith A. Sharkey
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 328:6, G734-G745</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/8a9ej6t52f5krhit/GI_00039_2025_Final6ew8r.mp3" length="8790263" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode, we’re joined by coauthors Preedajit Wongkrasant and Keith A. Sharkey to discuss their recent publication, "Fructooligosaccharides slow colonic motility and activate myenteric neurons via calcium sensing and 5-HT3 receptors in the proximal colon." Calcium-sensing receptors are known to play an important role in gastrointestinal physiology. This study reveals a new function of fructooligosaccharides, a type of dietary fiber, in regulating colonic motility and activating the enteric nervous system. The effects are mediated through calcium-sensing and 5-HT3 receptors, providing new insights into gut–brain communication and potential therapeutic targets for gastrointestinal disorders.
 
Fructooligosaccharides slow colonic motility and activate myenteric neurons via calcium sensing and 5-HT3 receptors in the proximal colon
Preedajit Wongkrasant, Laurie E. Wallace, Wallace K. MacNaughton, and Keith A. Sharkey
American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 328:6, G734-G745]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>599</itunes:duration>
                <itunes:episode>46</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Unraveling Appetite: The Microbiota-Brain Connection Across the Lifespan</title>
        <itunes:title>Unraveling Appetite: The Microbiota-Brain Connection Across the Lifespan</itunes:title>
        <link>https://ajpgi.podbean.com/e/unraveling-appetite-the-microbiota-brain-connection-across-the-lifespan/</link>
                    <comments>https://ajpgi.podbean.com/e/unraveling-appetite-the-microbiota-brain-connection-across-the-lifespan/#comments</comments>        <pubDate>Thu, 22 May 2025 12:25:53 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/9e21384b-4eaa-37fe-8ddc-6335a15ae135</guid>
                                    <description><![CDATA[In this episode, coauthors Gabriela Ribeiro, Marta P. Silvestre, Harriët Schellekens, and Cristina Cuesta-Marti discuss their recent review published in AJP-Gastrointestinal and Liver Physiology, titled "A menu for microbes: unraveling appetite regulation and weight dynamics through the microbiota-brain connection across the lifespan."
 
Appetite regulation is a complex and dynamic process influenced by behavioral, metabolic, and neurological factors — and increasingly, the gut microbiota. Our guests explore how the microbiota-gut-brain axis impacts appetite and obesity, highlighting how emerging omics tools and microbiota-targeted interventions may pave the way for precision treatments in nutrition and weight management. Tune in to hear how these researchers are bridging microbiology, neuroscience, and metabolism to better understand appetite across the lifespan.
 

<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00227.2024'>A menu for microbes: unraveling appetite regulation and weight dynamics through the microbiota-brain connection across the lifespan</a>
Gabriela Ribeiro, Harriët Schellekens, Cristina Cuesta-Marti, Ivie Maneschy, Shámila Ismael, Amanda Cuevas-Sierra, J. Alfredo Martínez, Marta P. Silvestre, Cláudia Marques, André Moreira-Rosário, Ana Faria, Luis A. Moreno, and Conceição Calhau
American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 328:3, G206-G228]]></description>
                                                            <content:encoded><![CDATA[In this episode, coauthors Gabriela Ribeiro, Marta P. Silvestre, Harriët Schellekens, and Cristina Cuesta-Marti discuss their recent review published in <em>AJP-Gastrointestinal and Liver Physiology</em>, titled <em>"A menu for microbes: unraveling appetite regulation and weight dynamics through the microbiota-brain connection across the lifespan."</em>
 
Appetite regulation is a complex and dynamic process influenced by behavioral, metabolic, and neurological factors — and increasingly, the gut microbiota. Our guests explore how the microbiota-gut-brain axis impacts appetite and obesity, highlighting how emerging omics tools and microbiota-targeted interventions may pave the way for precision treatments in nutrition and weight management. Tune in to hear how these researchers are bridging microbiology, neuroscience, and metabolism to better understand appetite across the lifespan.
 

<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00227.2024'>A menu for microbes: unraveling appetite regulation and weight dynamics through the microbiota-brain connection across the lifespan</a>
Gabriela Ribeiro, Harriët Schellekens, Cristina Cuesta-Marti, Ivie Maneschy, Shámila Ismael, Amanda Cuevas-Sierra, J. Alfredo Martínez, Marta P. Silvestre, Cláudia Marques, André Moreira-Rosário, Ana Faria, Luis A. Moreno, and Conceição Calhau
American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 328:3, G206-G228]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/squ683nx8d9d5dq7/AJPGI_-_GI-00227-2024R2_Finalbfs3k.mp3" length="6871200" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode, coauthors Gabriela Ribeiro, Marta P. Silvestre, Harriët Schellekens, and Cristina Cuesta-Marti discuss their recent review published in AJP-Gastrointestinal and Liver Physiology, titled "A menu for microbes: unraveling appetite regulation and weight dynamics through the microbiota-brain connection across the lifespan."
 
Appetite regulation is a complex and dynamic process influenced by behavioral, metabolic, and neurological factors — and increasingly, the gut microbiota. Our guests explore how the microbiota-gut-brain axis impacts appetite and obesity, highlighting how emerging omics tools and microbiota-targeted interventions may pave the way for precision treatments in nutrition and weight management. Tune in to hear how these researchers are bridging microbiology, neuroscience, and metabolism to better understand appetite across the lifespan.
 

A menu for microbes: unraveling appetite regulation and weight dynamics through the microbiota-brain connection across the lifespan
Gabriela Ribeiro, Harriët Schellekens, Cristina Cuesta-Marti, Ivie Maneschy, Shámila Ismael, Amanda Cuevas-Sierra, J. Alfredo Martínez, Marta P. Silvestre, Cláudia Marques, André Moreira-Rosário, Ana Faria, Luis A. Moreno, and Conceição Calhau
American Journal of Physiology-Gastrointestinal and Liver Physiology 2025 328:3, G206-G228]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>616</itunes:duration>
                <itunes:episode>45</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Unraveling Fabry Disease: Lyso-Gb3’s Role in Gut Physiology</title>
        <itunes:title>Unraveling Fabry Disease: Lyso-Gb3’s Role in Gut Physiology</itunes:title>
        <link>https://ajpgi.podbean.com/e/unraveling-fabry-disease-lyso-gb3-s-role-in-gut-physiology/</link>
                    <comments>https://ajpgi.podbean.com/e/unraveling-fabry-disease-lyso-gb3-s-role-in-gut-physiology/#comments</comments>        <pubDate>Mon, 14 Apr 2025 15:22:13 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/8d6bac7f-4258-307a-acab-4c3676b1463d</guid>
                                    <description><![CDATA[
<p class="x_MsoNormal"> In this episode, coauthors Cecilia Delprete, Friederike Uhlig, Marco Caprini, and Niall P. Hyland dive into their latest research titled "Characterization of Fabry disease-associated lyso-Gb3 on mouse colonic ion transport and motility."</p>


<p class="x_MsoNormal">Fabry disease (FD) is a rare genetic disorder with wide-ranging effects across the body, including the gastrointestinal (GI) system—often one of the first to show symptoms. The team explores how the lipid molecule lyso-Gb3, known to accumulate in FD, affects colonic function using ex vivo techniques like Ussing chambers and organ baths.</p>


<p class="x_MsoNormal">The conversation covers key findings: lyso-Gb3 significantly alters ion transport in the colon but doesn't affect motility or nerve responses, suggesting a complex mechanism behind GI symptoms in FD patients. Could this bring us closer to understanding—and eventually treating—the GI discomfort that burdens so many with Fabry disease? Tune in today!</p>
<p class="x_MsoNormal"> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00220.2024'>Characterization of Fabry disease-associated lyso-Gb3 on mouse colonic ion transport and motility</a>
Cecilia Delprete, Friederike Uhlig, Marco Caprini, and Niall P. Hyland
<p class="x_MsoNormal">American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:6, G810-G817</p>
]]></description>
                                                            <content:encoded><![CDATA[
<p class="x_MsoNormal"> In this episode, coauthors Cecilia Delprete, Friederike Uhlig, Marco Caprini, and Niall P. Hyland dive into their latest research titled <em>"Characterization of Fabry disease-associated lyso-Gb3 on mouse colonic ion transport and motility."</em></p>


<p class="x_MsoNormal">Fabry disease (FD) is a rare genetic disorder with wide-ranging effects across the body, including the gastrointestinal (GI) system—often one of the first to show symptoms. The team explores how the lipid molecule lyso-Gb3, known to accumulate in FD, affects colonic function using ex vivo techniques like Ussing chambers and organ baths.</p>


<p class="x_MsoNormal">The conversation covers key findings: lyso-Gb3 significantly alters ion transport in the colon but doesn't affect motility or nerve responses, suggesting a complex mechanism behind GI symptoms in FD patients. Could this bring us closer to understanding—and eventually treating—the GI discomfort that burdens so many with Fabry disease? Tune in today!</p>
<p class="x_MsoNormal"> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00220.2024'>Characterization of Fabry disease-associated lyso-Gb3 on mouse colonic ion transport and motility</a>
Cecilia Delprete, Friederike Uhlig, Marco Caprini, and Niall P. Hyland
<p class="x_MsoNormal">American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:6, G810-G817</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/n5dnzyqzui5qdrvs/GI_00220_2024_Final9nxn0.mp3" length="11582201" type="audio/mpeg"/>
        <itunes:summary><![CDATA[
 In this episode, coauthors Cecilia Delprete, Friederike Uhlig, Marco Caprini, and Niall P. Hyland dive into their latest research titled "Characterization of Fabry disease-associated lyso-Gb3 on mouse colonic ion transport and motility."


Fabry disease (FD) is a rare genetic disorder with wide-ranging effects across the body, including the gastrointestinal (GI) system—often one of the first to show symptoms. The team explores how the lipid molecule lyso-Gb3, known to accumulate in FD, affects colonic function using ex vivo techniques like Ussing chambers and organ baths.


The conversation covers key findings: lyso-Gb3 significantly alters ion transport in the colon but doesn't affect motility or nerve responses, suggesting a complex mechanism behind GI symptoms in FD patients. Could this bring us closer to understanding—and eventually treating—the GI discomfort that burdens so many with Fabry disease? Tune in today!
 
Characterization of Fabry disease-associated lyso-Gb3 on mouse colonic ion transport and motility
Cecilia Delprete, Friederike Uhlig, Marco Caprini, and Niall P. Hyland
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:6, G810-G817
]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>742</itunes:duration>
                <itunes:episode>44</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: A Chance to Put Liver Biopsy Back to Its Former Glory?</title>
        <itunes:title>Got Guts: A Chance to Put Liver Biopsy Back to Its Former Glory?</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-a-chance-to-put-liver-biopsy-back-to-its-former-glory/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-a-chance-to-put-liver-biopsy-back-to-its-former-glory/#comments</comments>        <pubDate>Thu, 13 Mar 2025 16:05:35 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/415d2fb6-9298-3238-ab62-a474c1b08c96</guid>
                                    <description><![CDATA[<p>In this episode, coauthors Camilla Venturin and Luca Fabris delve into their editorial titled "Machine Learning Application to Histology for the Study of Cholangiopathies (BiliQML): A Chance to Put Liver Biopsy Back to Its Former Glory?" The episode explores groundbreaking research by Dominick Hellen and colleagues on the limitations of current histological techniques in studying cholangiocytes and the biliary tree.</p>
<p>Historically, the study of these cells has been constrained by outdated and error-prone methodologies, like two-dimensional cell counting or complex three-dimensional imaging that fails to provide reliable quantification. Enter BiliQML, a novel machine learning model that promises to revolutionize this field. This episode breaks down how BiliQML quantifies biliary forms using anti-Keratin 19 antibody-stained whole slide images, providing a far more accurate and scalable approach.</p>
<p>With an impressive F-score of 0.87, the model's application across a variety of cholangiopathy models, including genetic, surgical, toxicological, and therapeutic, showcases its sensitivity and robustness. The episode reveals how this cutting-edge technology opens new doors for both clinical and basic-science researchers in the field of cholangiopathies. Tune in to discover how machine learning is bringing liver biopsy back to the forefront of research.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00173.2024'>Machine learning application to histology for the study of cholangiopathies (BiliQML): A chance to put liver biopsy back to its former glory?</a>
Camilla Venturin and Luca Fabris
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:6, G733-G736</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode, coauthors Camilla Venturin and Luca Fabris delve into their editorial titled <em>"Machine Learning Application to Histology for the Study of Cholangiopathies (BiliQML): A Chance to Put Liver Biopsy Back to Its Former Glory?"</em> The episode explores groundbreaking research by Dominick Hellen and colleagues on the limitations of current histological techniques in studying cholangiocytes and the biliary tree.</p>
<p>Historically, the study of these cells has been constrained by outdated and error-prone methodologies, like two-dimensional cell counting or complex three-dimensional imaging that fails to provide reliable quantification. Enter <em>BiliQML</em>, a novel machine learning model that promises to revolutionize this field. This episode breaks down how <em>BiliQML</em> quantifies biliary forms using anti-Keratin 19 antibody-stained whole slide images, providing a far more accurate and scalable approach.</p>
<p>With an impressive F-score of 0.87, the model's application across a variety of cholangiopathy models, including genetic, surgical, toxicological, and therapeutic, showcases its sensitivity and robustness. The episode reveals how this cutting-edge technology opens new doors for both clinical and basic-science researchers in the field of cholangiopathies. Tune in to discover how machine learning is bringing liver biopsy back to the forefront of research.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00173.2024'>Machine learning application to histology for the study of cholangiopathies (BiliQML): A chance to put liver biopsy back to its former glory?</a>
Camilla Venturin and Luca Fabris
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:6, G733-G736</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/a4e6kfnkiwcpccmc/GI_000173_2024_Final73fxh.mp3" length="5967665" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode, coauthors Camilla Venturin and Luca Fabris delve into their editorial titled "Machine Learning Application to Histology for the Study of Cholangiopathies (BiliQML): A Chance to Put Liver Biopsy Back to Its Former Glory?" The episode explores groundbreaking research by Dominick Hellen and colleagues on the limitations of current histological techniques in studying cholangiocytes and the biliary tree.
Historically, the study of these cells has been constrained by outdated and error-prone methodologies, like two-dimensional cell counting or complex three-dimensional imaging that fails to provide reliable quantification. Enter BiliQML, a novel machine learning model that promises to revolutionize this field. This episode breaks down how BiliQML quantifies biliary forms using anti-Keratin 19 antibody-stained whole slide images, providing a far more accurate and scalable approach.
With an impressive F-score of 0.87, the model's application across a variety of cholangiopathy models, including genetic, surgical, toxicological, and therapeutic, showcases its sensitivity and robustness. The episode reveals how this cutting-edge technology opens new doors for both clinical and basic-science researchers in the field of cholangiopathies. Tune in to discover how machine learning is bringing liver biopsy back to the forefront of research.
 
Machine learning application to histology for the study of cholangiopathies (BiliQML): A chance to put liver biopsy back to its former glory?
Camilla Venturin and Luca Fabris
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:6, G733-G736]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>397</itunes:duration>
                <itunes:episode>43</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" The Micro Version: Pacing Inhibits Slow Wave Dysrhythmias in the Intestine</title>
        <itunes:title>"Got Guts" The Micro Version: Pacing Inhibits Slow Wave Dysrhythmias in the Intestine</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-pacing-inhibits-slow-wave-dysrhythmias-in-the-intestine/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-pacing-inhibits-slow-wave-dysrhythmias-in-the-intestine/#comments</comments>        <pubDate>Fri, 21 Feb 2025 11:54:06 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/577a765f-e6ce-3026-9dbb-991f9a62b76a</guid>
                                    <description><![CDATA[<p>In this podcast coauthors <a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00254.2023?journalCode=ajpgi'>Nipuni D. Nagahawatte</a> and <a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00254.2023?journalCode=ajpgi'>Leo K. Cheng</a> discuss their research titled "High-energy pacing inhibits slow-wave dysrhythmias in the small intestine." Glucagon was infused in pigs to induce hyperglycemia and the resulting slow-wave response in the intact jejunum was defined in high resolution for the first time. Subsequently, with pacing, the glucagon-induced dysrhythmias were suppressed and spatially entrained for the first time with a success rate of 85%. The ability to suppress slow-wave dysrhythmias through pacing is promising in treating motility disorders that are associated with intestinal dysrhythmias.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00254.2023'>High-energy pacing inhibits slow-wave dysrhythmias in the small intestine</a>
Nipuni D. Nagahawatte, Recep Avci, Niranchan Paskaranandavadivel, and Leo K. Cheng
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:6, G676-G686</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this podcast coauthors <a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00254.2023?journalCode=ajpgi'>Nipuni D. Nagahawatte</a> and <a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00254.2023?journalCode=ajpgi'>Leo K. Cheng</a> discuss their research titled "High-energy pacing inhibits slow-wave dysrhythmias in the small intestine." Glucagon was infused in pigs to induce hyperglycemia and the resulting slow-wave response in the intact jejunum was defined in high resolution for the first time. Subsequently, with pacing, the glucagon-induced dysrhythmias were suppressed and spatially entrained for the first time with a success rate of 85%. The ability to suppress slow-wave dysrhythmias through pacing is promising in treating motility disorders that are associated with intestinal dysrhythmias.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00254.2023'>High-energy pacing inhibits slow-wave dysrhythmias in the small intestine</a>
Nipuni D. Nagahawatte, Recep Avci, Niranchan Paskaranandavadivel, and Leo K. Cheng
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:6, G676-G686</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/5ztbwkb626pqraui/GI_00254_2023_Final7oegs.mp3" length="7153632" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this podcast coauthors Nipuni D. Nagahawatte and Leo K. Cheng discuss their research titled "High-energy pacing inhibits slow-wave dysrhythmias in the small intestine." Glucagon was infused in pigs to induce hyperglycemia and the resulting slow-wave response in the intact jejunum was defined in high resolution for the first time. Subsequently, with pacing, the glucagon-induced dysrhythmias were suppressed and spatially entrained for the first time with a success rate of 85%. The ability to suppress slow-wave dysrhythmias through pacing is promising in treating motility disorders that are associated with intestinal dysrhythmias.
 
High-energy pacing inhibits slow-wave dysrhythmias in the small intestine
Nipuni D. Nagahawatte, Recep Avci, Niranchan Paskaranandavadivel, and Leo K. Cheng
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:6, G676-G686]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>445</itunes:duration>
                <itunes:episode>42</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" Special Episode: The GI and Liver Section at the 2025 American Physiology Summit</title>
        <itunes:title>"Got Guts" Special Episode: The GI and Liver Section at the 2025 American Physiology Summit</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-special-episode-the-gi-and-liver-section-at-the-2025-american-physiology-summit/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-special-episode-the-gi-and-liver-section-at-the-2025-american-physiology-summit/#comments</comments>        <pubDate>Thu, 23 Jan 2025 16:24:37 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/11c24c8b-ddc5-3921-8005-24b998c4f8dc</guid>
                                    <description><![CDATA[In this episode, AJP GI and Liver Physiology's Editor-in-Chief Mark Frey and Nicholas Zachos representative of the Gastrointestinal and Liver Physiology Section provide an exclusive preview of the GI programming at the upcoming APS Summit. They walk listeners through the exciting lineup of sessions, symposia, and featured topics designed to ignite new insights and collaborations within the GI community. From cutting-edge discussions on obesity, metabolic disease, and diet's role in health, to the highly anticipated Game Changer sessions, there's something for everyone to explore.
 
In addition, they highlight some can't-miss events like the John Forte Distinguished Abstract Session, the Trainee Symposium, and the prestigious Davenport Lecture. For those traveling to Baltimore, they also share some insider tips on the best local attractions and places to eat. Whether you're a seasoned professional or a new trainee, this episode gives you everything you need to know to make the most of the APS Summit experience.
 
Tune in for a lively conversation filled with insights, practical advice, and a touch of local flavor!]]></description>
                                                            <content:encoded><![CDATA[In this episode, AJP GI and Liver Physiology's Editor-in-Chief Mark Frey and Nicholas Zachos representative of the Gastrointestinal and Liver Physiology Section provide an exclusive preview of the GI programming at the upcoming APS Summit. They walk listeners through the exciting lineup of sessions, symposia, and featured topics designed to ignite new insights and collaborations within the GI community. From cutting-edge discussions on obesity, metabolic disease, and diet's role in health, to the highly anticipated Game Changer sessions, there's something for everyone to explore.
 
In addition, they highlight some can't-miss events like the John Forte Distinguished Abstract Session, the Trainee Symposium, and the prestigious Davenport Lecture. For those traveling to Baltimore, they also share some insider tips on the best local attractions and places to eat. Whether you're a seasoned professional or a new trainee, this episode gives you everything you need to know to make the most of the APS Summit experience.
 
Tune in for a lively conversation filled with insights, practical advice, and a touch of local flavor!]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/c8t46y3rzidsckpr/GI_Section_Podcast_2025a9rm4.mp3" length="16282107" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode, AJP GI and Liver Physiology's Editor-in-Chief Mark Frey and Nicholas Zachos representative of the Gastrointestinal and Liver Physiology Section provide an exclusive preview of the GI programming at the upcoming APS Summit. They walk listeners through the exciting lineup of sessions, symposia, and featured topics designed to ignite new insights and collaborations within the GI community. From cutting-edge discussions on obesity, metabolic disease, and diet's role in health, to the highly anticipated Game Changer sessions, there's something for everyone to explore.
 
In addition, they highlight some can't-miss events like the John Forte Distinguished Abstract Session, the Trainee Symposium, and the prestigious Davenport Lecture. For those traveling to Baltimore, they also share some insider tips on the best local attractions and places to eat. Whether you're a seasoned professional or a new trainee, this episode gives you everything you need to know to make the most of the APS Summit experience.
 
Tune in for a lively conversation filled with insights, practical advice, and a touch of local flavor!]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1209</itunes:duration>
                <itunes:episode>41</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" The Micro Version: Electromechanical Coupling of the In-Vivo Pylorus</title>
        <itunes:title>"Got Guts" The Micro Version: Electromechanical Coupling of the In-Vivo Pylorus</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-electromechanical-coupling-of-the-in-vivo-pylorus/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-electromechanical-coupling-of-the-in-vivo-pylorus/#comments</comments>        <pubDate>Fri, 01 Nov 2024 12:33:56 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/98d3e9c2-519f-3623-a6d2-eac4052c447a</guid>
                                    <description><![CDATA[<p>Join coauthors Sam Simmonds, Ashton Matthee, and Timothy R. Angeli-Gordon as they delve into their recently published research, "<a href='https://doi.org/10.1152/ajpgi.00018.2024'>Electromechanical Coupling and Anatomy of the In Vivo Gastroduodenal Junction</a>." In this episode, they explore cutting-edge techniques like electrical mapping, impedance planimetry, and histological analysis to investigate the complex dynamics of the gastroduodenal junction. Discover how contractions in the terminal antrum and pyloric sphincter correlate with gastric slow waves, while the duodenum experiences bursts of spike activity that trigger oscillating contractions. The team discusses their intriguing hypothesis regarding the relative scarcity of myenteric interstitial cells of Cajal in the pylorus, which may hinder coupling between antral and duodenal slow waves. </p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00018.2024'>Electromechanical coupling and anatomy of the in vivo gastroduodenal junction</a>
Sam Simmonds, Ashton Matthee, Jarrah M. Dowrick, Andrew J. Taberner, Peng Du, and Timothy R. Angeli-Gordon
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:1, G93-G104</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Join coauthors Sam Simmonds, Ashton Matthee, and Timothy R. Angeli-Gordon as they delve into their recently published research, "<a href='https://doi.org/10.1152/ajpgi.00018.2024'>Electromechanical Coupling and Anatomy of the In Vivo Gastroduodenal Junction</a>." In this episode, they explore cutting-edge techniques like electrical mapping, impedance planimetry, and histological analysis to investigate the complex dynamics of the gastroduodenal junction. Discover how contractions in the terminal antrum and pyloric sphincter correlate with gastric slow waves, while the duodenum experiences bursts of spike activity that trigger oscillating contractions. The team discusses their intriguing hypothesis regarding the relative scarcity of myenteric interstitial cells of Cajal in the pylorus, which may hinder coupling between antral and duodenal slow waves. </p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00018.2024'>Electromechanical coupling and anatomy of the in vivo gastroduodenal junction</a>
Sam Simmonds, Ashton Matthee, Jarrah M. Dowrick, Andrew J. Taberner, Peng Du, and Timothy R. Angeli-Gordon
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:1, G93-G104</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/7yd8hqfyymvkvm8t/GI_00018_2024_Final7rg60.mp3" length="16853221" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Join coauthors Sam Simmonds, Ashton Matthee, and Timothy R. Angeli-Gordon as they delve into their recently published research, "Electromechanical Coupling and Anatomy of the In Vivo Gastroduodenal Junction." In this episode, they explore cutting-edge techniques like electrical mapping, impedance planimetry, and histological analysis to investigate the complex dynamics of the gastroduodenal junction. Discover how contractions in the terminal antrum and pyloric sphincter correlate with gastric slow waves, while the duodenum experiences bursts of spike activity that trigger oscillating contractions. The team discusses their intriguing hypothesis regarding the relative scarcity of myenteric interstitial cells of Cajal in the pylorus, which may hinder coupling between antral and duodenal slow waves. 
 
Electromechanical coupling and anatomy of the in vivo gastroduodenal junction
Sam Simmonds, Ashton Matthee, Jarrah M. Dowrick, Andrew J. Taberner, Peng Du, and Timothy R. Angeli-Gordon
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:1, G93-G104]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>782</itunes:duration>
                <itunes:episode>39</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" The Micro Version: Effect of amniotic fluid on the esophageal epithelium</title>
        <itunes:title>"Got Guts" The Micro Version: Effect of amniotic fluid on the esophageal epithelium</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-effect-of-amniotic-fluid-on-the-esophageal-epithelium/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-effect-of-amniotic-fluid-on-the-esophageal-epithelium/#comments</comments>        <pubDate>Tue, 15 Oct 2024 12:10:32 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/a951ac99-0f22-3bbb-adef-3dcf86a274b1</guid>
                                    <description><![CDATA[<p>Join coauthors Mark Rochman and Marc E. Rothenberg as they explore their recently published paper, "<a href='https://doi.org/10.1152/ajpgi.00197.2024'>Amniotic Fluid Modifies Esophageal Epithelium Differentiation and Inflammatory Responses</a>." In this engaging episode, they discuss how the interaction between amniotic fluid and the esophageal epithelium during pregnancy impacts epithelial differentiation and influences the tissue's response to inflammatory stimuli, particularly interleukin 13 (IL-13). Discover the potential implications of these findings, including how they may predispose individuals to inflammatory conditions like eosinophilic esophagitis (EoE) later in life. This episode is a must-listen for anyone interested in developmental biology, immunology, and the long-term effects of prenatal exposures on health.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00197.2024'>Amniotic fluid modifies esophageal epithelium differentiation and inflammatory responses</a>
Mark Rochman, Andrea M. Klinger, Julie M. Caldwell, Yoel Sadovsky, and Marc E. Rothenberg
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:5, G629-G639</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Join coauthors Mark Rochman and Marc E. Rothenberg as they explore their recently published paper, "<a href='https://doi.org/10.1152/ajpgi.00197.2024'>Amniotic Fluid Modifies Esophageal Epithelium Differentiation and Inflammatory Responses</a>." In this engaging episode, they discuss how the interaction between amniotic fluid and the esophageal epithelium during pregnancy impacts epithelial differentiation and influences the tissue's response to inflammatory stimuli, particularly interleukin 13 (IL-13). Discover the potential implications of these findings, including how they may predispose individuals to inflammatory conditions like eosinophilic esophagitis (EoE) later in life. This episode is a must-listen for anyone interested in developmental biology, immunology, and the long-term effects of prenatal exposures on health.</p>
<p> </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00197.2024'>Amniotic fluid modifies esophageal epithelium differentiation and inflammatory responses</a>
Mark Rochman, Andrea M. Klinger, Julie M. Caldwell, Yoel Sadovsky, and Marc E. Rothenberg
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:5, G629-G639</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/x4uith6g7zc6akpk/GI_00197_2024_Final8rnl3.mp3" length="6730836" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Join coauthors Mark Rochman and Marc E. Rothenberg as they explore their recently published paper, "Amniotic Fluid Modifies Esophageal Epithelium Differentiation and Inflammatory Responses." In this engaging episode, they discuss how the interaction between amniotic fluid and the esophageal epithelium during pregnancy impacts epithelial differentiation and influences the tissue's response to inflammatory stimuli, particularly interleukin 13 (IL-13). Discover the potential implications of these findings, including how they may predispose individuals to inflammatory conditions like eosinophilic esophagitis (EoE) later in life. This episode is a must-listen for anyone interested in developmental biology, immunology, and the long-term effects of prenatal exposures on health.
 
Amniotic fluid modifies esophageal epithelium differentiation and inflammatory responses
Mark Rochman, Andrea M. Klinger, Julie M. Caldwell, Yoel Sadovsky, and Marc E. Rothenberg
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:5, G629-G639]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>470</itunes:duration>
                <itunes:episode>40</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" The Micro Version: The Effects of Simulated Gastroesophageal Reflux on Infant Pig Oropharyngeal Feeding Physiology</title>
        <itunes:title>"Got Guts" The Micro Version: The Effects of Simulated Gastroesophageal Reflux on Infant Pig Oropharyngeal Feeding Physiology</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-the-effects-of-simulated-gastroesophageal-reflux-on-infant-pig-oropharyngeal-feeding-physiology/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-the-effects-of-simulated-gastroesophageal-reflux-on-infant-pig-oropharyngeal-feeding-physiology/#comments</comments>        <pubDate>Mon, 14 Oct 2024 10:23:03 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/b2b36a72-4471-3403-bac6-fdf3514d87e0</guid>
                                    <description><![CDATA[<p>Join coauthor Chloe Edmonds in this insightful episode as she delves into her recently published paper, "<a href='https://doi.org/10.1152/ajpgi.00027.2024'>The Effects of Simulated Gastroesophageal Reflux on Infant Pig Oropharyngeal Feeding Physiology</a>." Chloe explores how simulating gastroesophageal reflux in an infant pig model reveals significant alterations in pharyngeal swallowing dynamics. Discover how the integration of esophageal afferents impacts motor outputs to the pharynx, leading to decreased swallow frequency and increased bolus sizes. This research not only sheds light on the mechanisms behind esophageal pathologies and oropharyngeal dysphagia but also highlights the potential for developing intervention strategies grounded in neurophysiology. Tune in for a deep dive into the implications of this work for both animal models and clinical practice!</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00027.2024'>The effects of simulated gastroesophageal reflux on infant pig oropharyngeal feeding physiology</a>
Chloe E. Edmonds, Kaitlyn N. Robbins, Elizabeth G. Dvorak, Stephen P. Howe, Sarah A. Sheldon, Christopher J. Mayerl, Brianna A. Owairu, Brady M. Young, and Rebecca Z. German
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:1, G105-G116</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Join coauthor Chloe Edmonds in this insightful episode as she delves into her recently published paper, "<a href='https://doi.org/10.1152/ajpgi.00027.2024'>The Effects of Simulated Gastroesophageal Reflux on Infant Pig Oropharyngeal Feeding Physiology</a>." Chloe explores how simulating gastroesophageal reflux in an infant pig model reveals significant alterations in pharyngeal swallowing dynamics. Discover how the integration of esophageal afferents impacts motor outputs to the pharynx, leading to decreased swallow frequency and increased bolus sizes. This research not only sheds light on the mechanisms behind esophageal pathologies and oropharyngeal dysphagia but also highlights the potential for developing intervention strategies grounded in neurophysiology. Tune in for a deep dive into the implications of this work for both animal models and clinical practice!</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00027.2024'>The effects of simulated gastroesophageal reflux on infant pig oropharyngeal feeding physiology</a>
Chloe E. Edmonds, Kaitlyn N. Robbins, Elizabeth G. Dvorak, Stephen P. Howe, Sarah A. Sheldon, Christopher J. Mayerl, Brianna A. Owairu, Brady M. Young, and Rebecca Z. German
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:1, G105-G116</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/z5qdynh2h4mmkktr/GI-00027-2024R2_Finaladj9u.mp3" length="6635076" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Join coauthor Chloe Edmonds in this insightful episode as she delves into her recently published paper, "The Effects of Simulated Gastroesophageal Reflux on Infant Pig Oropharyngeal Feeding Physiology." Chloe explores how simulating gastroesophageal reflux in an infant pig model reveals significant alterations in pharyngeal swallowing dynamics. Discover how the integration of esophageal afferents impacts motor outputs to the pharynx, leading to decreased swallow frequency and increased bolus sizes. This research not only sheds light on the mechanisms behind esophageal pathologies and oropharyngeal dysphagia but also highlights the potential for developing intervention strategies grounded in neurophysiology. Tune in for a deep dive into the implications of this work for both animal models and clinical practice!
 
Article Citation: 
The effects of simulated gastroesophageal reflux on infant pig oropharyngeal feeding physiology
Chloe E. Edmonds, Kaitlyn N. Robbins, Elizabeth G. Dvorak, Stephen P. Howe, Sarah A. Sheldon, Christopher J. Mayerl, Brianna A. Owairu, Brady M. Young, and Rebecca Z. German
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:1, G105-G116]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>440</itunes:duration>
                <itunes:episode>38</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" The Micro Version: Autoimmune liver disease and hormonal responses</title>
        <itunes:title>"Got Guts" The Micro Version: Autoimmune liver disease and hormonal responses</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-autoimmune-liver-disease-and-hormonal-responses/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-autoimmune-liver-disease-and-hormonal-responses/#comments</comments>        <pubDate>Fri, 27 Sep 2024 10:48:35 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/2e5573d4-29cf-3d47-b903-62041672372a</guid>
                                    <description><![CDATA[<p>In this episode, coauthors Anne-Sofie H. Jensen and Nicolai J. Wewer Albrechtsen discuss the recently published research titled "Patients with autoimmune liver disease have glucose disturbances that mechanistically differ from steatotic liver disease." The authors reveal that patients with autoimmune liver disease, even in the absence of overt diabetes, experience early glucose disturbances.</p>
<p>Jensen and Albrechtsen highlight key pathophysiological traits specific to these patients, including altered incretin responses. This distinction is crucial because it suggests that the mechanisms underlying glucose metabolism issues in autoimmune liver disease differ significantly from those seen in steatotic liver disease. The authors findings could have important implications for diagnosing and managing glucose dysregulation in patients with autoimmune liver conditions.</p>
<p> </p>
<p>Article Citation</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00047.2024'>Patients with autoimmune liver disease have glucose disturbances that mechanistically differ from steatotic liver disease</a>
Anne-Sofie H. Jensen, Henriette Ytting, Mikkel P. Werge, Elias B. Rashu, Liv E. Hetland, Mira Thing, Puria Nabilou, Johan Burisch, Kirstine N. Bojsen-Møller, Anders E. Junker, Lise Hobolth, Christian Mortensen, Flemming Tofteng, Flemming Bendtsen, Søren Møller, Mogens Vyberg, Reza R. Serizawa, Lise L. Gluud, and Nicolai J. Wewer Albrechtsen
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:6, G736-G746</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode, coauthors Anne-Sofie H. Jensen and Nicolai J. Wewer Albrechtsen discuss the recently published research titled "Patients with autoimmune liver disease have glucose disturbances that mechanistically differ from steatotic liver disease." The authors reveal that patients with autoimmune liver disease, even in the absence of overt diabetes, experience early glucose disturbances.</p>
<p>Jensen and Albrechtsen highlight key pathophysiological traits specific to these patients, including altered incretin responses. This distinction is crucial because it suggests that the mechanisms underlying glucose metabolism issues in autoimmune liver disease differ significantly from those seen in steatotic liver disease. The authors findings could have important implications for diagnosing and managing glucose dysregulation in patients with autoimmune liver conditions.</p>
<p> </p>
<p>Article Citation</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00047.2024'>Patients with autoimmune liver disease have glucose disturbances that mechanistically differ from steatotic liver disease</a>
Anne-Sofie H. Jensen, Henriette Ytting, Mikkel P. Werge, Elias B. Rashu, Liv E. Hetland, Mira Thing, Puria Nabilou, Johan Burisch, Kirstine N. Bojsen-Møller, Anders E. Junker, Lise Hobolth, Christian Mortensen, Flemming Tofteng, Flemming Bendtsen, Søren Møller, Mogens Vyberg, Reza R. Serizawa, Lise L. Gluud, and Nicolai J. Wewer Albrechtsen
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:6, G736-G746</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/77cbh2tdun2qif79/GI_00047_2024_Finalbvvev.mp3" length="5314595" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode, coauthors Anne-Sofie H. Jensen and Nicolai J. Wewer Albrechtsen discuss the recently published research titled "Patients with autoimmune liver disease have glucose disturbances that mechanistically differ from steatotic liver disease." The authors reveal that patients with autoimmune liver disease, even in the absence of overt diabetes, experience early glucose disturbances.
Jensen and Albrechtsen highlight key pathophysiological traits specific to these patients, including altered incretin responses. This distinction is crucial because it suggests that the mechanisms underlying glucose metabolism issues in autoimmune liver disease differ significantly from those seen in steatotic liver disease. The authors findings could have important implications for diagnosing and managing glucose dysregulation in patients with autoimmune liver conditions.
 
Article Citation
Patients with autoimmune liver disease have glucose disturbances that mechanistically differ from steatotic liver disease
Anne-Sofie H. Jensen, Henriette Ytting, Mikkel P. Werge, Elias B. Rashu, Liv E. Hetland, Mira Thing, Puria Nabilou, Johan Burisch, Kirstine N. Bojsen-Møller, Anders E. Junker, Lise Hobolth, Christian Mortensen, Flemming Tofteng, Flemming Bendtsen, Søren Møller, Mogens Vyberg, Reza R. Serizawa, Lise L. Gluud, and Nicolai J. Wewer Albrechtsen
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:6, G736-G746]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>356</itunes:duration>
                <itunes:episode>37</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" The Micro Version: Inhibitory neurotransmission in the internal anal sphincter</title>
        <itunes:title>"Got Guts" The Micro Version: Inhibitory neurotransmission in the internal anal sphincter</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-inhibitory-neurotransmission-in-the-internal-anal-sphincter/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-inhibitory-neurotransmission-in-the-internal-anal-sphincter/#comments</comments>        <pubDate>Fri, 06 Sep 2024 11:47:15 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/f91b180e-2f73-317a-bdf7-f366ce72a59e</guid>
                                    <description><![CDATA[<p>Coauthor Caroline A. Cobine dives into the fascinating world of internal anal sphincter biology in the latest episode of "Gut Guts." The research uncovers direct and indirect neural pathways that modulate intracellular calcium activity in interstitial cells of Cajal, shedding light on their role in smooth muscle cell function.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00309.2023'>Modulation of intracellular calcium activity in interstitial cells of Cajal by inhibitory neural pathways within the internal anal sphincter</a>
Karen I. Hannigan, Emer P. Ni Bhraonain, Thomas W. Gould, Kathleen D. Keef, and Caroline A. Cobine
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:3, G382-G404</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Coauthor Caroline A. Cobine dives into the fascinating world of internal anal sphincter biology in the latest episode of "Gut Guts." The research uncovers direct and indirect neural pathways that modulate intracellular calcium activity in interstitial cells of Cajal, shedding light on their role in smooth muscle cell function.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00309.2023'>Modulation of intracellular calcium activity in interstitial cells of Cajal by inhibitory neural pathways within the internal anal sphincter</a>
Karen I. Hannigan, Emer P. Ni Bhraonain, Thomas W. Gould, Kathleen D. Keef, and Caroline A. Cobine
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:3, G382-G404</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/5f64fd38gcyxvkeh/GI-00309-2023_Final792yq.mp3" length="8472420" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Coauthor Caroline A. Cobine dives into the fascinating world of internal anal sphincter biology in the latest episode of "Gut Guts." The research uncovers direct and indirect neural pathways that modulate intracellular calcium activity in interstitial cells of Cajal, shedding light on their role in smooth muscle cell function.
 
Article Citation:
Modulation of intracellular calcium activity in interstitial cells of Cajal by inhibitory neural pathways within the internal anal sphincter
Karen I. Hannigan, Emer P. Ni Bhraonain, Thomas W. Gould, Kathleen D. Keef, and Caroline A. Cobine
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:3, G382-G404]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>523</itunes:duration>
                <itunes:episode>36</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" The Micro Version: Mechanical Stress-induced Connective Tissue Growth Factor  and Intestinal Fibrosis</title>
        <itunes:title>"Got Guts" The Micro Version: Mechanical Stress-induced Connective Tissue Growth Factor  and Intestinal Fibrosis</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-mechanical-stress-induced-connective-tissue-growth-factor-and-intestinal-fibrosis/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-mechanical-stress-induced-connective-tissue-growth-factor-and-intestinal-fibrosis/#comments</comments>        <pubDate>Fri, 23 Aug 2024 13:01:23 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/d2265890-c76d-3e32-a640-5c758d881282</guid>
                                    <description><![CDATA[<p>In this episode of "Gut Guts" coauthor Xuan-Zheng Shi discusses new research on intestinal fibrosis in Crohn’s-like colitis. The study found that mechanical stress causes a protein called CTGF to increase, leading to fibrosis. In a rat model, easing the mechanical stress reduced connective tissue growth factor (CTGF) and lessened fibrosis. This suggests that mechanical stress may be important in causing fibrosis in Crohn’s disease.</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00123.2024'>Mechanical stress-induced connective tissue growth factor plays a critical role in intestinal fibrosis in Crohn’s-like colitis</a>
You-Min Lin, Ke Zhang, Ramasatyaveni Geesala, Kenneth E. Lipson, Suimin Qiu, Don W. Powell, Steven Cohn, and Xuan-Zheng Shi
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:2, G295-G305</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode of "Gut Guts" coauthor Xuan-Zheng Shi discusses new research on intestinal fibrosis in Crohn’s-like colitis. The study found that mechanical stress causes a protein called CTGF to increase, leading to fibrosis. In a rat model, easing the mechanical stress reduced connective tissue growth factor (CTGF) and lessened fibrosis. This suggests that mechanical stress may be important in causing fibrosis in Crohn’s disease.</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00123.2024'>Mechanical stress-induced connective tissue growth factor plays a critical role in intestinal fibrosis in Crohn’s-like colitis</a>
You-Min Lin, Ke Zhang, Ramasatyaveni Geesala, Kenneth E. Lipson, Suimin Qiu, Don W. Powell, Steven Cohn, and Xuan-Zheng Shi
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:2, G295-G305</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/s4f5k26zci4pdhgi/Podcast_GI-00123-2024_Final9s60s.mp3" length="7458180" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode of "Gut Guts" coauthor Xuan-Zheng Shi discusses new research on intestinal fibrosis in Crohn’s-like colitis. The study found that mechanical stress causes a protein called CTGF to increase, leading to fibrosis. In a rat model, easing the mechanical stress reduced connective tissue growth factor (CTGF) and lessened fibrosis. This suggests that mechanical stress may be important in causing fibrosis in Crohn’s disease.
 
Article Citation: 
Mechanical stress-induced connective tissue growth factor plays a critical role in intestinal fibrosis in Crohn’s-like colitis
You-Min Lin, Ke Zhang, Ramasatyaveni Geesala, Kenneth E. Lipson, Suimin Qiu, Don W. Powell, Steven Cohn, and Xuan-Zheng Shi
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:2, G295-G305]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>505</itunes:duration>
                <itunes:episode>35</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" The Micro Version: Characterization of Rat Gastric Slow Wave Activity</title>
        <itunes:title>"Got Guts" The Micro Version: Characterization of Rat Gastric Slow Wave Activity</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-characterization-of-rat-gastric-slow-wave-activity/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-characterization-of-rat-gastric-slow-wave-activity/#comments</comments>        <pubDate>Wed, 14 Aug 2024 17:59:34 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/b765076c-daf4-3da1-9b96-012b7a7132b7</guid>
                                    <description><![CDATA[<p>Tune in to our latest podcast episode where Peng Du, Omkar N. Athavale, and Madeleine R. Di Natale dive into the fascinating world of gastric slow-wave conduction. They discuss their recent article titled "Mapping the rat gastric slow-wave conduction pathway: bridging in vitro and in vivo methods, revealing a loosely coupled region in the distal stomach" revealing regional variations in the organization of rat gastric slow waves. Don't miss this intriguing discussion bridging in vitro and in vivo methods!</p>
<p> </p>
<p>Mapping of rat gastric slow waves showed regional variations in their organization. In some subjects, separate wavefronts propagated near the lesser and greater curvatures with a loosely coupled region near the midline, between the wavefronts, having a varying slow-wave origin. Furthermore, simultaneous intracellular and extracellular recordings were concordant and independent of movement artifacts, indicating that extracellular recordings can be interpreted in terms of their intracellular counterparts when intracellular recording is not possible.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00069.2024'>Mapping the rat gastric slow-wave conduction pathway: bridging in vitro and in vivo methods, revealing a loosely coupled region in the distal stomach</a>
Omkar N. Athavale, Madeleine R. Di Natale, Recep Avci, Alys R. Clark, John B. Furness, Leo K. Cheng, and Peng Du
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:2, G254-G266</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Tune in to our latest podcast episode where Peng Du, Omkar N. Athavale, and Madeleine R. Di Natale dive into the fascinating world of gastric slow-wave conduction. They discuss their recent article titled "Mapping the rat gastric slow-wave conduction pathway: bridging in vitro and in vivo methods, revealing a loosely coupled region in the distal stomach" revealing regional variations in the organization of rat gastric slow waves. Don't miss this intriguing discussion bridging in vitro and in vivo methods!</p>
<p> </p>
<p>Mapping of rat gastric slow waves showed regional variations in their organization. In some subjects, separate wavefronts propagated near the lesser and greater curvatures with a loosely coupled region near the midline, between the wavefronts, having a varying slow-wave origin. Furthermore, simultaneous intracellular and extracellular recordings were concordant and independent of movement artifacts, indicating that extracellular recordings can be interpreted in terms of their intracellular counterparts when intracellular recording is not possible.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00069.2024'>Mapping the rat gastric slow-wave conduction pathway: bridging in vitro and in vivo methods, revealing a loosely coupled region in the distal stomach</a>
Omkar N. Athavale, Madeleine R. Di Natale, Recep Avci, Alys R. Clark, John B. Furness, Leo K. Cheng, and Peng Du
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:2, G254-G266</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/rgpc4uwqes954rct/GI_00069_2024_Finalar96t.mp3" length="8799932" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Tune in to our latest podcast episode where Peng Du, Omkar N. Athavale, and Madeleine R. Di Natale dive into the fascinating world of gastric slow-wave conduction. They discuss their recent article titled "Mapping the rat gastric slow-wave conduction pathway: bridging in vitro and in vivo methods, revealing a loosely coupled region in the distal stomach" revealing regional variations in the organization of rat gastric slow waves. Don't miss this intriguing discussion bridging in vitro and in vivo methods!
 
Mapping of rat gastric slow waves showed regional variations in their organization. In some subjects, separate wavefronts propagated near the lesser and greater curvatures with a loosely coupled region near the midline, between the wavefronts, having a varying slow-wave origin. Furthermore, simultaneous intracellular and extracellular recordings were concordant and independent of movement artifacts, indicating that extracellular recordings can be interpreted in terms of their intracellular counterparts when intracellular recording is not possible.
 
Article Citation:
Mapping the rat gastric slow-wave conduction pathway: bridging in vitro and in vivo methods, revealing a loosely coupled region in the distal stomach
Omkar N. Athavale, Madeleine R. Di Natale, Recep Avci, Alys R. Clark, John B. Furness, Leo K. Cheng, and Peng Du
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 327:2, G254-G266]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>509</itunes:duration>
                <itunes:episode>34</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" The Micro Version: Implicating the Cholecystokinin B Receptor in Liver Stem Cell Oncogenesis</title>
        <itunes:title>"Got Guts" The Micro Version: Implicating the Cholecystokinin B Receptor in Liver Stem Cell Oncogenesis</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-implicating-the-cholecystokinin-b-receptor-in-liver-stem-cell-oncogenesis/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-implicating-the-cholecystokinin-b-receptor-in-liver-stem-cell-oncogenesis/#comments</comments>        <pubDate>Fri, 21 Jun 2024 10:50:20 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/1e6a7c09-e52b-33bd-8219-d6ace6aa8fbb</guid>
                                    <description><![CDATA[<p>In this episode of "Got Guts" The Micro Version, Jill P. Smith highlights the recently published research titled "Implicating the cholecystokinin B receptor in liver stem cell oncogenesis." This investigation identified a novel pathway involving the activation of hepatic stem cells and liver oncogenesis. Receptor blockade or genetic disruption of the cholecystokinin-B receptor (CCK-BR) signaling pathway decreased the activation and proliferation of hepatic stem cells after liver injury without eliminating the regenerative capacity of healthy hepatocytes.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00208.2023'>Implicating the cholecystokinin B receptor in liver stem cell oncogenesis</a>
Martha D. Gay, Jack C. Drda, Wenqiang Chen, Yimeng Huang, Amal A. Yassin, Tetyana Duka, Hongbin Fang, Narayan Shivapurkar, and Jill P. Smith
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:3, G291-G309</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode of "Got Guts" The Micro Version, Jill P. Smith highlights the recently published research titled "Implicating the cholecystokinin B receptor in liver stem cell oncogenesis." This investigation identified a novel pathway involving the activation of hepatic stem cells and liver oncogenesis. Receptor blockade or genetic disruption of the cholecystokinin-B receptor (CCK-BR) signaling pathway decreased the activation and proliferation of hepatic stem cells after liver injury without eliminating the regenerative capacity of healthy hepatocytes.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00208.2023'>Implicating the cholecystokinin B receptor in liver stem cell oncogenesis</a>
Martha D. Gay, Jack C. Drda, Wenqiang Chen, Yimeng Huang, Amal A. Yassin, Tetyana Duka, Hongbin Fang, Narayan Shivapurkar, and Jill P. Smith
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:3, G291-G309</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/98crfam9ts5vi2qw/GI_00208_2023_Finalbl262.mp3" length="3585220" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode of "Got Guts" The Micro Version, Jill P. Smith highlights the recently published research titled "Implicating the cholecystokinin B receptor in liver stem cell oncogenesis." This investigation identified a novel pathway involving the activation of hepatic stem cells and liver oncogenesis. Receptor blockade or genetic disruption of the cholecystokinin-B receptor (CCK-BR) signaling pathway decreased the activation and proliferation of hepatic stem cells after liver injury without eliminating the regenerative capacity of healthy hepatocytes.
 
Article Citation:
Implicating the cholecystokinin B receptor in liver stem cell oncogenesis
Martha D. Gay, Jack C. Drda, Wenqiang Chen, Yimeng Huang, Amal A. Yassin, Tetyana Duka, Hongbin Fang, Narayan Shivapurkar, and Jill P. Smith
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:3, G291-G309]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>279</itunes:duration>
                <itunes:episode>33</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" The Micro Version: Corticotropin-Releasing Hormone Effects on Gastric Function</title>
        <itunes:title>"Got Guts" The Micro Version: Corticotropin-Releasing Hormone Effects on Gastric Function</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-corticotropin-releasing-hormone-effects-on-gastric-function/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-corticotropin-releasing-hormone-effects-on-gastric-function/#comments</comments>        <pubDate>Fri, 07 Jun 2024 12:01:15 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/787a4422-53a9-3e1e-a385-0c3cefb9d848</guid>
                                    <description><![CDATA[<p>In this podcast, I-Hsuan Huang highlights the recently published paper titled "<a href='https://doi.org/10.1152/ajpgi.00298.2023'>Effects of corticotropin-releasing hormone on gastric electrical activity and sensorimotor function in healthy volunteers: a double-blinded crossover study.</a>" The aim of this research was to investigate the effects of peripheral corticotropin-releasing hormone infusion on meal-related gastrointestinal symptoms, gastric electrical activity, and gastric sensorimotor function in healthy volunteers (HVs).</p>
<p> </p>
<p>NEW &amp; NOTEWORTHY In healthy volunteers, peripheral corticotropin-releasing hormone (CRH) infusion accelerates gastric-emptying rate and increases postprandial gastric response, accompanied by a rise in symptoms, but does not alter gastric sensitivity or meal-induced accommodation. These findings underscore a significant link between stress and dyspeptic symptoms, with CRH playing a pivotal role in mediating these effects.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00298.2023'>Effects of corticotropin-releasing hormone on gastric electrical activity and sensorimotor function in healthy volunteers: a double-blinded crossover study</a>
I-Hsuan Huang, Jolien Schol, Stefan Calder, Armen A. Gharibans, Karen Van den Houte, Annelies Verheyden, Bert Broeders, Florencia Carbone, Greg O'Grady, and Jan Tack
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:5, G622-G630</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this podcast, I-Hsuan Huang highlights the recently published paper titled "<a href='https://doi.org/10.1152/ajpgi.00298.2023'>Effects of corticotropin-releasing hormone on gastric electrical activity and sensorimotor function in healthy volunteers: a double-blinded crossover study.</a>" The aim of this research was to investigate the effects of peripheral corticotropin-releasing hormone infusion on meal-related gastrointestinal symptoms, gastric electrical activity, and gastric sensorimotor function in healthy volunteers (HVs).</p>
<p> </p>
<p>NEW &amp; NOTEWORTHY In healthy volunteers, peripheral corticotropin-releasing hormone (CRH) infusion accelerates gastric-emptying rate and increases postprandial gastric response, accompanied by a rise in symptoms, but does not alter gastric sensitivity or meal-induced accommodation. These findings underscore a significant link between stress and dyspeptic symptoms, with CRH playing a pivotal role in mediating these effects.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00298.2023'>Effects of corticotropin-releasing hormone on gastric electrical activity and sensorimotor function in healthy volunteers: a double-blinded crossover study</a>
I-Hsuan Huang, Jolien Schol, Stefan Calder, Armen A. Gharibans, Karen Van den Houte, Annelies Verheyden, Bert Broeders, Florencia Carbone, Greg O'Grady, and Jan Tack
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:5, G622-G630</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/4i2k5akc95aqmnse/GI-00298-2023_Final6ubjy.mp3" length="3239545" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this podcast, I-Hsuan Huang highlights the recently published paper titled "Effects of corticotropin-releasing hormone on gastric electrical activity and sensorimotor function in healthy volunteers: a double-blinded crossover study." The aim of this research was to investigate the effects of peripheral corticotropin-releasing hormone infusion on meal-related gastrointestinal symptoms, gastric electrical activity, and gastric sensorimotor function in healthy volunteers (HVs).
 
NEW &amp; NOTEWORTHY In healthy volunteers, peripheral corticotropin-releasing hormone (CRH) infusion accelerates gastric-emptying rate and increases postprandial gastric response, accompanied by a rise in symptoms, but does not alter gastric sensitivity or meal-induced accommodation. These findings underscore a significant link between stress and dyspeptic symptoms, with CRH playing a pivotal role in mediating these effects.
 
Article Citation:
Effects of corticotropin-releasing hormone on gastric electrical activity and sensorimotor function in healthy volunteers: a double-blinded crossover study
I-Hsuan Huang, Jolien Schol, Stefan Calder, Armen A. Gharibans, Karen Van den Houte, Annelies Verheyden, Bert Broeders, Florencia Carbone, Greg O'Grady, and Jan Tack
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:5, G622-G630]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>386</itunes:duration>
                <itunes:episode>32</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" The Micro Version: Effects of L. Casei-Fermented Milk on Mice with DSS Colitis</title>
        <itunes:title>"Got Guts" The Micro Version: Effects of L. Casei-Fermented Milk on Mice with DSS Colitis</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-effects-of-l-casei-fermented-milk-on-mice-with-dss-colitis/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-effects-of-l-casei-fermented-milk-on-mice-with-dss-colitis/#comments</comments>        <pubDate>Fri, 24 May 2024 12:00:58 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/5626c06a-c66c-36c2-89ff-5734d8359873</guid>
                                    <description><![CDATA[<p>Coauthors Mélanie G. Gareau and Maria L. Marco delve into the findings of their latest research titled "<a href='https://doi.org/10.1152/ajpgi.00259.2023'>Milk and Lacticaseibacillus paracasei BL23 effects on intestinal responses in a murine model of colitis</a>." This study marked the first exploration into sex-dependent responses to probiotic Lacticaseibacillus paracasei and milk, as well as the potential of the dairy matrix to enhance probiotic protection against colitis. Surprisingly, female mice exhibited greater sensitivity to colonic injury compared to their male counterparts, and neither treatment effectively mitigated inflammation in both sexes. These sex-specific reactions may be attributed to variances in the baseline proportions of Akkermansia in the gut microbiome of female mice, shedding light on the intricate interplay between sex, diet, probiotics, and colitis outcomes.</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00259.2023'>Milk and Lacticaseibacillus paracasei BL23 effects on intestinal responses in a murine model of colitis</a>
Glory Bui, Cristina Torres-Fuentes, Matteo M. Pusceddu, Mélanie G. Gareau, and Maria L. Marco
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:6, G659-G675</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Coauthors Mélanie G. Gareau and Maria L. Marco delve into the findings of their latest research titled "<a href='https://doi.org/10.1152/ajpgi.00259.2023'>Milk and Lacticaseibacillus paracasei BL23 effects on intestinal responses in a murine model of colitis</a>." This study marked the first exploration into sex-dependent responses to probiotic Lacticaseibacillus paracasei and milk, as well as the potential of the dairy matrix to enhance probiotic protection against colitis. Surprisingly, female mice exhibited greater sensitivity to colonic injury compared to their male counterparts, and neither treatment effectively mitigated inflammation in both sexes. These sex-specific reactions may be attributed to variances in the baseline proportions of Akkermansia in the gut microbiome of female mice, shedding light on the intricate interplay between sex, diet, probiotics, and colitis outcomes.</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00259.2023'>Milk and <em>Lacticaseibacillus paracasei</em> BL23 effects on intestinal responses in a murine model of colitis</a>
Glory Bui, Cristina Torres-Fuentes, Matteo M. Pusceddu, Mélanie G. Gareau, and Maria L. Marco
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:6, G659-G675</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/6nqdhuvvaxyi52db/GI_00259_2023_Finalaqtvo.mp3" length="5774933" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Coauthors Mélanie G. Gareau and Maria L. Marco delve into the findings of their latest research titled "Milk and Lacticaseibacillus paracasei BL23 effects on intestinal responses in a murine model of colitis." This study marked the first exploration into sex-dependent responses to probiotic Lacticaseibacillus paracasei and milk, as well as the potential of the dairy matrix to enhance probiotic protection against colitis. Surprisingly, female mice exhibited greater sensitivity to colonic injury compared to their male counterparts, and neither treatment effectively mitigated inflammation in both sexes. These sex-specific reactions may be attributed to variances in the baseline proportions of Akkermansia in the gut microbiome of female mice, shedding light on the intricate interplay between sex, diet, probiotics, and colitis outcomes.
 
Article Citation: 
Milk and Lacticaseibacillus paracasei BL23 effects on intestinal responses in a murine model of colitis
Glory Bui, Cristina Torres-Fuentes, Matteo M. Pusceddu, Mélanie G. Gareau, and Maria L. Marco
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:6, G659-G675]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>427</itunes:duration>
                <itunes:episode>31</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" The Micro Version: Characterize Mouse Glutamatergic Myenteric Neurons</title>
        <itunes:title>"Got Guts" The Micro Version: Characterize Mouse Glutamatergic Myenteric Neurons</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-characterize-mouse-glutamatergic-myenteric-neurons/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-characterize-mouse-glutamatergic-myenteric-neurons/#comments</comments>        <pubDate>Mon, 13 May 2024 12:00:19 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/d1523003-bd0a-35f9-84f5-61a22cef5a81</guid>
                                    <description><![CDATA[<p>In this episode, Jia Liu and Bin Feng highlight the recently published research titled "Morphological, molecular, and functional characterization of mouse glutamatergic myenteric neurons." In this research, the authors reveal that VGLUT2-positive enteric neurons (EN), although constituting a small fraction of total EN, are homogeneously expressed in the myenteric ganglia, with a slight concentration at the intermediate region between the colon and rectum. Through anatomic, molecular, and functional analyses, we demonstrated that VGLUT2-ENs are activated indirectly by noxious circumferential colorectal stretch via nicotinic cholinergic transmission, suggesting their participation in mechanical visceral nociception.</p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00200.2023'>Morphological, molecular, and functional characterization of mouse glutamatergic myenteric neurons</a>
Jia Liu, Shaopeng Zhang, Sharareh Emadi, Tiantian Guo, Longtu Chen, and Bin Feng
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:3, G279-G290</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode, Jia Liu and Bin Feng highlight the recently published research titled "Morphological, molecular, and functional characterization of mouse glutamatergic myenteric neurons." In this research, the authors reveal that VGLUT2-positive enteric neurons (EN), although constituting a small fraction of total EN, are homogeneously expressed in the myenteric ganglia, with a slight concentration at the intermediate region between the colon and rectum. Through anatomic, molecular, and functional analyses, we demonstrated that VGLUT2-ENs are activated indirectly by noxious circumferential colorectal stretch via nicotinic cholinergic transmission, suggesting their participation in mechanical visceral nociception.</p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00200.2023'>Morphological, molecular, and functional characterization of mouse glutamatergic myenteric neurons</a>
Jia Liu, Shaopeng Zhang, Sharareh Emadi, Tiantian Guo, Longtu Chen, and Bin Feng
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:3, G279-G290</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/zpz7rsm67jgu9ss9/GI_00200_2024_Final_Version98iei.mp3" length="5195400" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode, Jia Liu and Bin Feng highlight the recently published research titled "Morphological, molecular, and functional characterization of mouse glutamatergic myenteric neurons." In this research, the authors reveal that VGLUT2-positive enteric neurons (EN), although constituting a small fraction of total EN, are homogeneously expressed in the myenteric ganglia, with a slight concentration at the intermediate region between the colon and rectum. Through anatomic, molecular, and functional analyses, we demonstrated that VGLUT2-ENs are activated indirectly by noxious circumferential colorectal stretch via nicotinic cholinergic transmission, suggesting their participation in mechanical visceral nociception.
Article Citation:
Morphological, molecular, and functional characterization of mouse glutamatergic myenteric neurons
Jia Liu, Shaopeng Zhang, Sharareh Emadi, Tiantian Guo, Longtu Chen, and Bin Feng
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:3, G279-G290]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>382</itunes:duration>
                <itunes:episode>30</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” The Micro Version: Gastric Neuromuscular Transmission</title>
        <itunes:title>”Got Guts” The Micro Version: Gastric Neuromuscular Transmission</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-gastric-neuromuscular-transmission/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-gastric-neuromuscular-transmission/#comments</comments>        <pubDate>Mon, 04 Mar 2024 16:07:34 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/aa81b052-c9ae-3cf4-adaa-4ebfe0f10232</guid>
                                    <description><![CDATA[<p>In this episode of the Got Guts podcast series Madeleine R. Di Natale of the University of Melbourne discusses the recently published manuscript titled "Characterization of neuromuscular transmission and projections of muscle motor neurons in the rat stomach."  This study provides a detailed mapping of nerve transmission to the circular muscle of the different anatomical regions of rat stomach. It shows that excitatory and inhibitory influences extend around the gastric circumference and that there is a summation of neural influence that allows for finely graded control of muscle tension and length. Nerve-mediated electrical events are qualitatively and quantitatively different between regions, for example, excitatory neurons have direct effects on fundus but not antral muscle.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00194.2023'>Characterization of neuromuscular transmission and projections of muscle motor neurons in the rat stomach</a>
Madeleine R. Di Natale, Billie Hunne, Martin J. Stebbing, Xiaokai Wang, Zhongming Liu, and John B. Furness
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:1, G78-G93</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode of the Got Guts podcast series Madeleine R. Di Natale of the University of Melbourne discusses the recently published manuscript titled "Characterization of neuromuscular transmission and projections of muscle motor neurons in the rat stomach."  This study provides a detailed mapping of nerve transmission to the circular muscle of the different anatomical regions of rat stomach. It shows that excitatory and inhibitory influences extend around the gastric circumference and that there is a summation of neural influence that allows for finely graded control of muscle tension and length. Nerve-mediated electrical events are qualitatively and quantitatively different between regions, for example, excitatory neurons have direct effects on fundus but not antral muscle.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00194.2023'>Characterization of neuromuscular transmission and projections of muscle motor neurons in the rat stomach</a>
Madeleine R. Di Natale, Billie Hunne, Martin J. Stebbing, Xiaokai Wang, Zhongming Liu, and John B. Furness
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:1, G78-G93</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/wewwcb/GI_00194_2023_Final7ca13.mp3" length="4947460" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode of the Got Guts podcast series Madeleine R. Di Natale of the University of Melbourne discusses the recently published manuscript titled "Characterization of neuromuscular transmission and projections of muscle motor neurons in the rat stomach."  This study provides a detailed mapping of nerve transmission to the circular muscle of the different anatomical regions of rat stomach. It shows that excitatory and inhibitory influences extend around the gastric circumference and that there is a summation of neural influence that allows for finely graded control of muscle tension and length. Nerve-mediated electrical events are qualitatively and quantitatively different between regions, for example, excitatory neurons have direct effects on fundus but not antral muscle.
 
Article Citation:
Characterization of neuromuscular transmission and projections of muscle motor neurons in the rat stomach
Madeleine R. Di Natale, Billie Hunne, Martin J. Stebbing, Xiaokai Wang, Zhongming Liu, and John B. Furness
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:1, G78-G93]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>329</itunes:duration>
                <itunes:episode>29</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” The Micro Version: Gene expression and microbiome composition in EsoCaSR-/-mice</title>
        <itunes:title>”Got Guts” The Micro Version: Gene expression and microbiome composition in EsoCaSR-/-mice</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-gene-expression-and-microbiome-composition-in-esocasr-mice/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-gene-expression-and-microbiome-composition-in-esocasr-mice/#comments</comments>        <pubDate>Fri, 23 Feb 2024 11:05:27 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/965af029-9219-3b2f-bf74-ca362fb849f6</guid>
                                    <description><![CDATA[<p>In this episode of the Got Guts Podcast series, Solange M. Abdulnour-Nakhoul of Tulane University, discusses the recently published manuscript titled "Alterations in gene expression and microbiome composition upon calcium sensing receptor deletion in the mouse esophagus." In this research  Abdulnour-Nakhoul et al. highlight why calcium sensing receptor plays a significant role in maintaining the barrier function of esophageal epithelium.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00066.2023'>Alterations in gene expression and microbiome composition upon calcium sensing receptor deletion in the mouse esophagus</a>
Solange M. Abdulnour-Nakhoul, Jay K. Kolls, Eric K. Flemington, Nathan A. Ungerleider, Hani N. Nakhoul, Kejing Song, and Nazih L. Nakhoul
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 0 0:0</p>
<p> </p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode of the Got Guts Podcast series, Solange M. Abdulnour-Nakhoul of Tulane University, discusses the recently published manuscript titled "Alterations in gene expression and microbiome composition upon calcium sensing receptor deletion in the mouse esophagus." In this research  Abdulnour-Nakhoul et al. highlight why calcium sensing receptor plays a significant role in maintaining the barrier function of esophageal epithelium.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00066.2023'>Alterations in gene expression and microbiome composition upon calcium sensing receptor deletion in the mouse esophagus</a>
Solange M. Abdulnour-Nakhoul, Jay K. Kolls, Eric K. Flemington, Nathan A. Ungerleider, Hani N. Nakhoul, Kejing Song, and Nazih L. Nakhoul
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 0 0:0</p>
<p> </p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/e3pzjc/GI_00066_2023_Final9fank.mp3" length="6731923" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode of the Got Guts Podcast series, Solange M. Abdulnour-Nakhoul of Tulane University, discusses the recently published manuscript titled "Alterations in gene expression and microbiome composition upon calcium sensing receptor deletion in the mouse esophagus." In this research  Abdulnour-Nakhoul et al. highlight why calcium sensing receptor plays a significant role in maintaining the barrier function of esophageal epithelium.
 
Article Citation:
Alterations in gene expression and microbiome composition upon calcium sensing receptor deletion in the mouse esophagus
Solange M. Abdulnour-Nakhoul, Jay K. Kolls, Eric K. Flemington, Nathan A. Ungerleider, Hani N. Nakhoul, Kejing Song, and Nazih L. Nakhoul
American Journal of Physiology-Gastrointestinal and Liver Physiology 0 0:0
 
 ]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>448</itunes:duration>
                <itunes:episode>28</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>"Got Guts" Special Episode: The GI and Liver Section at the 2024 American Physiology Summit</title>
        <itunes:title>"Got Guts" Special Episode: The GI and Liver Section at the 2024 American Physiology Summit</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-special-episode-the-gi-and-liver-section-at-the-2024-american-physiology-summit/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-special-episode-the-gi-and-liver-section-at-the-2024-american-physiology-summit/#comments</comments>        <pubDate>Fri, 16 Feb 2024 15:45:35 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/864e43fd-0b6e-3d9d-985a-0f74bc6770fa</guid>
                                    <description><![CDATA[<p>Listen as Editor in Chief of <a href='https://journals.physiology.org/journal/ajpgi'>AJPGI and Liver Physiology,</a> Mark Frey and the Chair of the <a href='https://www.physiology.org/community/aps-communities/sections/Gastrointestinal-Liver?SSO=Y'>Gastrointestinal &amp; Liver Section</a>, Pradeep Dudeja discuss what they are looking forward at the 2024 American Physiology Summit, April 4-7th. </p>
<p> </p>
<p>Registration Deadline for <a href='https://www.physiology.org/professional-development/meetings-events/american-physiology-summit-2023?SSO=Y'>American Physiology Summit</a> is March 11, 2024.</p>
<p> </p>
<p>Click <a href='https://journals.physiology.org/ajpgi/about'>here</a> for more info on the American Journal of Physiology Gastrointestinal and Liver Physiology</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Listen as Editor in Chief of <a href='https://journals.physiology.org/journal/ajpgi'>AJPGI and Liver Physiology,</a> Mark Frey and the Chair of the <a href='https://www.physiology.org/community/aps-communities/sections/Gastrointestinal-Liver?SSO=Y'>Gastrointestinal &amp; Liver Section</a>, Pradeep Dudeja discuss what they are looking forward at the 2024 American Physiology Summit, April 4-7th. </p>
<p> </p>
<p>Registration Deadline for <a href='https://www.physiology.org/professional-development/meetings-events/american-physiology-summit-2023?SSO=Y'>American Physiology Summit</a> is March 11, 2024.</p>
<p> </p>
<p>Click <a href='https://journals.physiology.org/ajpgi/about'>here</a> for more info on the American Journal of Physiology Gastrointestinal and Liver Physiology</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/8btjsu/GI_Section_2024_Podcast_Final8kja5.mp3" length="8784555" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Listen as Editor in Chief of AJPGI and Liver Physiology, Mark Frey and the Chair of the Gastrointestinal &amp; Liver Section, Pradeep Dudeja discuss what they are looking forward at the 2024 American Physiology Summit, April 4-7th. 
 
Registration Deadline for American Physiology Summit is March 11, 2024.
 
Click here for more info on the American Journal of Physiology Gastrointestinal and Liver Physiology]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>686</itunes:duration>
                <itunes:episode>27</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” The Micro Version: Pf Inhibits Inflammation-Induced Epithelial Break-Down</title>
        <itunes:title>”Got Guts” The Micro Version: Pf Inhibits Inflammation-Induced Epithelial Break-Down</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-pf-inhibits-inflammation-induced-epithelial-break-down/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-pf-inhibits-inflammation-induced-epithelial-break-down/#comments</comments>        <pubDate>Thu, 08 Feb 2024 11:19:16 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/3b315b93-3793-3c2b-ab1e-2d4edce9aec5</guid>
                                    <description><![CDATA[<p>In this episode Marine Mantel of Nantes Université discusses the recently published research in AJP-GI and Liver Physiology titled <a href='https://doi.org/10.1152/ajpgi.00198.2023'>"Propionibacterium freudenreichii CIRM-BIA 129 mitigates colitis through S layer protein B-dependent epithelial strengthening</a>." </p>
<p> </p>
<p>NEW &amp; NOTEWORTHY Propionibacterium freudenreichii reduces dextran sodium sulfate (DSS)-induced intestinal permeability in vivo. P. freudenreichii does not inhibit inflammation but damages linked to inflammation. P. freudenreichii inhibits intestinal epithelial breakdown through S-layer protein B. The protective effects of P. freudenreichii depend on S-layer protein B. Extracellular vesicles from P. freudenreichii CB 129 mimic the protective effect of the probiotic.</p>
<p> </p>
<p>Article Citation:</p>
<p><a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00198.2023'>Propionibacterium freudenreichii CIRM-BIA 129 mitigates colitis through S layer protein B-dependent epithelial strengthening</a></p>
<p>Marine Mantel, Tony Durand, Anne Bessard, Ségolène Pernet, Julie Beaudeau, Juliana Guimaraes-Laguna, Marie-Bernadette Maillard, Eric Guédon, Michel Neunlist, Yves Le Loir, Gwénaël Jan, and Malvyne Rolli-Derkinderen</p>
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:2, G163-G175</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode Marine Mantel of Nantes Université discusses the recently published research in AJP-GI and Liver Physiology titled <a href='https://doi.org/10.1152/ajpgi.00198.2023'>"Propionibacterium freudenreichii CIRM-BIA 129 mitigates colitis through S layer protein B-dependent epithelial strengthening</a>." </p>
<p> </p>
<p>NEW &amp; NOTEWORTHY <em>Propionibacterium freudenreichii</em> reduces dextran sodium sulfate (DSS)-induced intestinal permeability in vivo<em>. P. freudenreichii</em> does not inhibit inflammation but damages linked to inflammation. <em>P. freudenreichii</em> inhibits intestinal epithelial breakdown through S-layer protein B. The protective effects of <em>P. freudenreichii</em> depend on S-layer protein B. Extracellular vesicles from <em>P. freudenreichii</em> CB 129 mimic the protective effect of the probiotic.</p>
<p> </p>
<p>Article Citation:</p>
<p><a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00198.2023'><em>Propionibacterium freudenreichii</em> CIRM-BIA 129 mitigates colitis through S layer protein B-dependent epithelial strengthening</a></p>
<p>Marine Mantel, Tony Durand, Anne Bessard, Ségolène Pernet, Julie Beaudeau, Juliana Guimaraes-Laguna, Marie-Bernadette Maillard, Eric Guédon, Michel Neunlist, Yves Le Loir, Gwénaël Jan, and Malvyne Rolli-Derkinderen</p>
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:2, G163-G175</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/vjjmbk/GI-00198-2023R1_Final.mp3" length="4533756" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode Marine Mantel of Nantes Université discusses the recently published research in AJP-GI and Liver Physiology titled "Propionibacterium freudenreichii CIRM-BIA 129 mitigates colitis through S layer protein B-dependent epithelial strengthening." 
 
NEW &amp; NOTEWORTHY Propionibacterium freudenreichii reduces dextran sodium sulfate (DSS)-induced intestinal permeability in vivo. P. freudenreichii does not inhibit inflammation but damages linked to inflammation. P. freudenreichii inhibits intestinal epithelial breakdown through S-layer protein B. The protective effects of P. freudenreichii depend on S-layer protein B. Extracellular vesicles from P. freudenreichii CB 129 mimic the protective effect of the probiotic.
 
Article Citation:
Propionibacterium freudenreichii CIRM-BIA 129 mitigates colitis through S layer protein B-dependent epithelial strengthening
Marine Mantel, Tony Durand, Anne Bessard, Ségolène Pernet, Julie Beaudeau, Juliana Guimaraes-Laguna, Marie-Bernadette Maillard, Eric Guédon, Michel Neunlist, Yves Le Loir, Gwénaël Jan, and Malvyne Rolli-Derkinderen
American Journal of Physiology-Gastrointestinal and Liver Physiology 2024 326:2, G163-G175]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>316</itunes:duration>
                <itunes:episode>26</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” The Micro Version:  IL-4Rα Signaling in Esophageal Smooth Muscle</title>
        <itunes:title>”Got Guts” The Micro Version:  IL-4Rα Signaling in Esophageal Smooth Muscle</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-il-4r%ce%b1-signaling-in-esophageal-smooth-muscle/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-il-4r%ce%b1-signaling-in-esophageal-smooth-muscle/#comments</comments>        <pubDate>Mon, 18 Dec 2023 16:42:53 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/c27b3a2b-95cf-31cb-b690-4a3cf427919c</guid>
                                    <description><![CDATA[<p>In this episode author, Melissa Nelson of Baylor University Medical Center, discusses the recently published manuscript titled "Th2 Cytokine Signaling through IL-4Rα Increases Eotaxin-3 Secretion and Tension in Human Esophageal Smooth Muscle."</p>
<p> </p>
<p>New and Noteworthy:</p>
<p>Nelson et al. have found that Th2 cytokines increase eotaxin-3 secretion and tension in esophageal smooth muscle (ESM) cells via IL-4Rα signaling. Unlike esophageal epithelial cells, ESM cells do not express H+,K+ATPase, and omeprazole does not inhibit their cytokine-stimulated eotaxin-3 secretion or tension. An IL-4Rα blocking antibody reduces both eotaxin-3 secretion and tension induced by Th2 cytokines in ESM cells, suggesting that an agent such as dupilumab might be preferred for EoE patients with esophageal muscle involvement.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00155.2023'>Th2 Cytokine Signaling through IL-4Rα Increases Eotaxin-3 Secretion and Tension in Human Esophageal Smooth Muscle</a>
Melissa R. Nelson, Xi Zhang, Eitan Podgaetz, Xuan Wang, Qiuyang Zhang, Zui Pan, Stuart Jon Spechler, and Rhonda F. Souza
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 0 0:0</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode author, Melissa Nelson of Baylor University Medical Center, discusses the recently published manuscript titled "Th2 Cytokine Signaling through IL-4Rα Increases Eotaxin-3 Secretion and Tension in Human Esophageal Smooth Muscle."</p>
<p> </p>
<p>New and Noteworthy:</p>
<p>Nelson et al. have found that Th2 cytokines increase eotaxin-3 secretion and tension in esophageal smooth muscle (ESM) cells via IL-4Rα signaling. Unlike esophageal epithelial cells, ESM cells do not express H+,K+ATPase, and omeprazole does not inhibit their cytokine-stimulated eotaxin-3 secretion or tension. An IL-4Rα blocking antibody reduces both eotaxin-3 secretion and tension induced by Th2 cytokines in ESM cells, suggesting that an agent such as dupilumab might be preferred for EoE patients with esophageal muscle involvement.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00155.2023'>Th2 Cytokine Signaling through IL-4Rα Increases Eotaxin-3 Secretion and Tension in Human Esophageal Smooth Muscle</a>
Melissa R. Nelson, Xi Zhang, Eitan Podgaetz, Xuan Wang, Qiuyang Zhang, Zui Pan, Stuart Jon Spechler, and Rhonda F. Souza
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 0 0:0</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/jww56j/GI-00155-2023R1_Finalaoj47.mp3" length="5894886" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode author, Melissa Nelson of Baylor University Medical Center, discusses the recently published manuscript titled "Th2 Cytokine Signaling through IL-4Rα Increases Eotaxin-3 Secretion and Tension in Human Esophageal Smooth Muscle."
 
New and Noteworthy:
Nelson et al. have found that Th2 cytokines increase eotaxin-3 secretion and tension in esophageal smooth muscle (ESM) cells via IL-4Rα signaling. Unlike esophageal epithelial cells, ESM cells do not express H+,K+ATPase, and omeprazole does not inhibit their cytokine-stimulated eotaxin-3 secretion or tension. An IL-4Rα blocking antibody reduces both eotaxin-3 secretion and tension induced by Th2 cytokines in ESM cells, suggesting that an agent such as dupilumab might be preferred for EoE patients with esophageal muscle involvement.
 
Article Citation:
Th2 Cytokine Signaling through IL-4Rα Increases Eotaxin-3 Secretion and Tension in Human Esophageal Smooth Muscle
Melissa R. Nelson, Xi Zhang, Eitan Podgaetz, Xuan Wang, Qiuyang Zhang, Zui Pan, Stuart Jon Spechler, and Rhonda F. Souza
American Journal of Physiology-Gastrointestinal and Liver Physiology 0 0:0]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>382</itunes:duration>
                <itunes:episode>25</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” The Micro Version: Order of Events after Keratin 8 Sequential Downregulation</title>
        <itunes:title>”Got Guts” The Micro Version: Order of Events after Keratin 8 Sequential Downregulation</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-order-of-events-after-keratin-8-sequential-downregulation/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-order-of-events-after-keratin-8-sequential-downregulation/#comments</comments>        <pubDate>Wed, 13 Dec 2023 09:06:14 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/b7921e18-e770-323c-b201-e05e97b421fc</guid>
                                    <description><![CDATA[<p>In this podcast, authors Maria A. Ilomäki and Lauri Polari (both at Åbo Akademi University) discuss their recently published research titled “Defining a timeline of colon pathologies after keratin 8 loss: Rapid crypt elongation and diarrhea are followed by epithelial erosion and cell exfoliation.”</p>
<p> </p>
<p>New and Noteworthy:</p>
<p>Understanding the order in which physiological and molecular events occur helps to recognize the onset of diseases and improve their preclinical models. We utilized Cre-Lox-based inducible keratin 8 deletion in mouse intestinal epithelium to characterize the earliest events after keratin 8 loss leading to colitis. These include diarrhea and crypt elongation, followed by erosion and neutrophil activity. The authors results also support noninvasive methodology for monitoring colon diseases in preclinical models.</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00140.2023'>Defining a timeline of colon pathologies after keratin 8 loss: Rapid crypt elongation and diarrhea are followed by epithelial erosion and cell exfoliation</a>
Maria A. Ilomäki, Lauri Polari, Carl-Gustaf A. Stenvall, Mina Tayyab, Kirah Kähärä, Karen M. Ridge, and Diana M. Toivola
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 0 0:0</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this podcast, authors Maria A. Ilomäki and Lauri Polari (both at Åbo Akademi University) discuss their recently published research titled “Defining a timeline of colon pathologies after keratin 8 loss: Rapid crypt elongation and diarrhea are followed by epithelial erosion and cell exfoliation.”</p>
<p> </p>
<p>New and Noteworthy:</p>
<p>Understanding the order in which physiological and molecular events occur helps to recognize the onset of diseases and improve their preclinical models. We utilized Cre-Lox-based inducible keratin 8 deletion in mouse intestinal epithelium to characterize the earliest events after keratin 8 loss leading to colitis. These include diarrhea and crypt elongation, followed by erosion and neutrophil activity. The authors results also support noninvasive methodology for monitoring colon diseases in preclinical models.</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00140.2023'>Defining a timeline of colon pathologies after keratin 8 loss: Rapid crypt elongation and diarrhea are followed by epithelial erosion and cell exfoliation</a>
Maria A. Ilomäki, Lauri Polari, Carl-Gustaf A. Stenvall, Mina Tayyab, Kirah Kähärä, Karen M. Ridge, and Diana M. Toivola
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 0 0:0</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/jgx6vn/GI-00140-2023_Final8qg07.mp3" length="5544543" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this podcast, authors Maria A. Ilomäki and Lauri Polari (both at Åbo Akademi University) discuss their recently published research titled “Defining a timeline of colon pathologies after keratin 8 loss: Rapid crypt elongation and diarrhea are followed by epithelial erosion and cell exfoliation.”
 
New and Noteworthy:
Understanding the order in which physiological and molecular events occur helps to recognize the onset of diseases and improve their preclinical models. We utilized Cre-Lox-based inducible keratin 8 deletion in mouse intestinal epithelium to characterize the earliest events after keratin 8 loss leading to colitis. These include diarrhea and crypt elongation, followed by erosion and neutrophil activity. The authors results also support noninvasive methodology for monitoring colon diseases in preclinical models.
 
Article Citation: 
Defining a timeline of colon pathologies after keratin 8 loss: Rapid crypt elongation and diarrhea are followed by epithelial erosion and cell exfoliation
Maria A. Ilomäki, Lauri Polari, Carl-Gustaf A. Stenvall, Mina Tayyab, Kirah Kähärä, Karen M. Ridge, and Diana M. Toivola
American Journal of Physiology-Gastrointestinal and Liver Physiology 0 0:0]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>386</itunes:duration>
                <itunes:episode>24</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” The Micro Version: Effects of in utero fluoxetine exposure on the GI tract</title>
        <itunes:title>”Got Guts” The Micro Version: Effects of in utero fluoxetine exposure on the GI tract</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-effects-of-in-utero-fluoxetine-exposure-on-the-gi-tract/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-effects-of-in-utero-fluoxetine-exposure-on-the-gi-tract/#comments</comments>        <pubDate>Fri, 01 Dec 2023 16:07:13 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/255a2e5a-de99-3c6e-9774-ee0354ed433d</guid>
                                    <description><![CDATA[<p>In this episode authors Katherine L. Prowse,, and Elyanne M. Ratcliffe of McMaster University, discuss their recently published article titled “Effects of in utero exposure to fluoxetine on the gastrointestinal tract of rat offspring.”</p>
<p> </p>
<p>NEW &amp; NOTEWORTHY There is increasing recognition of the relevance of in utero and early postnatal exposures in the developmental programming of the gastrointestinal tract. Perinatal exposure to selective serotonin reuptake inhibitors and antidepressant medications is of particular relevance as they are commonly prescribed during pregnancy, and serotonergic pathways play key roles during gastrointestinal development and in postnatal homeostasis. Here, we provide a comprehensive evaluation of clinically relevant outcomes of gastrointestinal motility and susceptibility to colitis in fluoxetine-exposed offspring and highlight changes in colonic serotonergic neurons at the peak of perinatal fluoxetine exposure with sex-dependent changes in serotonin signaling and colonic motility in adulthood.</p>
<p> </p>
<p>Article Citation:</p>
<p><a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00223.2022'>Effects of in utero exposure to fluoxetine on the gastrointestinal tract of rat offspring</a></p>
<p>Katherine L. Prowse, Harriet Law, Sergio Raez-Villanueva, Filip Markovic, Megan Wang, Rajka Borojevic, Sean P. Parsons, Alexander D. Vincent, Alison C. Holloway, and Elyanne M. Ratcliffe</p>
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology</p>
<p> 2023 325:6, G528-G538</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode authors Katherine L. Prowse,, and Elyanne M. Ratcliffe of McMaster University, discuss their recently published article titled “Effects of in utero exposure to fluoxetine on the gastrointestinal tract of rat offspring.”</p>
<p> </p>
<p>NEW &amp; NOTEWORTHY There is increasing recognition of the relevance of in utero and early postnatal exposures in the developmental programming of the gastrointestinal tract. Perinatal exposure to selective serotonin reuptake inhibitors and antidepressant medications is of particular relevance as they are commonly prescribed during pregnancy, and serotonergic pathways play key roles during gastrointestinal development and in postnatal homeostasis. Here, we provide a comprehensive evaluation of clinically relevant outcomes of gastrointestinal motility and susceptibility to colitis in fluoxetine-exposed offspring and highlight changes in colonic serotonergic neurons at the peak of perinatal fluoxetine exposure with sex-dependent changes in serotonin signaling and colonic motility in adulthood.</p>
<p> </p>
<p>Article Citation:</p>
<p><a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00223.2022'>Effects of in utero exposure to fluoxetine on the gastrointestinal tract of rat offspring</a></p>
<p>Katherine L. Prowse, Harriet Law, Sergio Raez-Villanueva, Filip Markovic, Megan Wang, Rajka Borojevic, Sean P. Parsons, Alexander D. Vincent, Alison C. Holloway, and Elyanne M. Ratcliffe</p>
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology</p>
<p> 2023 325:6, G528-G538</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/5h2irg/AJPGI_00223-2022_Final9ifo3.mp3" length="3557686" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode authors Katherine L. Prowse,, and Elyanne M. Ratcliffe of McMaster University, discuss their recently published article titled “Effects of in utero exposure to fluoxetine on the gastrointestinal tract of rat offspring.”
 
NEW &amp; NOTEWORTHY There is increasing recognition of the relevance of in utero and early postnatal exposures in the developmental programming of the gastrointestinal tract. Perinatal exposure to selective serotonin reuptake inhibitors and antidepressant medications is of particular relevance as they are commonly prescribed during pregnancy, and serotonergic pathways play key roles during gastrointestinal development and in postnatal homeostasis. Here, we provide a comprehensive evaluation of clinically relevant outcomes of gastrointestinal motility and susceptibility to colitis in fluoxetine-exposed offspring and highlight changes in colonic serotonergic neurons at the peak of perinatal fluoxetine exposure with sex-dependent changes in serotonin signaling and colonic motility in adulthood.
 
Article Citation:
Effects of in utero exposure to fluoxetine on the gastrointestinal tract of rat offspring
Katherine L. Prowse, Harriet Law, Sergio Raez-Villanueva, Filip Markovic, Megan Wang, Rajka Borojevic, Sean P. Parsons, Alexander D. Vincent, Alison C. Holloway, and Elyanne M. Ratcliffe
American Journal of Physiology-Gastrointestinal and Liver Physiology
 2023 325:6, G528-G538]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>250</itunes:duration>
                <itunes:episode>23</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” The Micro Version:  Colon ion transporter gene expression during cirrhosis</title>
        <itunes:title>”Got Guts” The Micro Version:  Colon ion transporter gene expression during cirrhosis</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-colon-ion-transporter-gene-expression-during-cirrhosis/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-colon-ion-transporter-gene-expression-during-cirrhosis/#comments</comments>        <pubDate>Fri, 17 Nov 2023 11:40:47 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/991fb540-a7ec-3e6b-9fb7-ad72949f0521</guid>
                                    <description><![CDATA[<p><a href='https://journals.physiology.org/doi/full/10.1152/ajpgi.00073.2023'>Diego Alvarez de la Rosa</a> of the University of La Laguna discusses the recently published manuscript titled “Decaying kidney function during cirrhosis correlates with remodeling of distal colon aldosterone target gene expression.”</p>
<p> </p>
<p>NEW &amp; NOTEWORTHY Liver cirrhosis progression significantly alters ion transporter subunit expression in the rat distal colon, a change that correlated well with declining kidney function and the severity of the disease. Natalia Serrano-Morillas et al. data suggests that the steroid hormone aldosterone participates in this homeostatic response to maintain electrolyte balance.</p>
<p> </p>
<p>Article Citation:</p>
<p><a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00073.2023'>Decaying kidney function during cirrhosis correlates with remodeling of distal colon aldosterone target gene expression</a></p>
<p>Natalia Serrano-Morillas, Carlos González-Alayón, Arianna Vastola-Mascolo, Ana E. Rodríguez-Rodríguez, Guadalberto Hernández, Esteban Porrini, Manuel Hernández-Guerra, and Diego Alvarez de la Rosa</p>
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:4, G306-G317</p>
]]></description>
                                                            <content:encoded><![CDATA[<p><a href='https://journals.physiology.org/doi/full/10.1152/ajpgi.00073.2023'>Diego Alvarez de la Rosa</a> of the University of La Laguna discusses the recently published manuscript titled “Decaying kidney function during cirrhosis correlates with remodeling of distal colon aldosterone target gene expression.”</p>
<p> </p>
<p>NEW &amp; NOTEWORTHY Liver cirrhosis progression significantly alters ion transporter subunit expression in the rat distal colon, a change that correlated well with declining kidney function and the severity of the disease. Natalia Serrano-Morillas et al. data suggests that the steroid hormone aldosterone participates in this homeostatic response to maintain electrolyte balance.</p>
<p> </p>
<p>Article Citation:</p>
<p><a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00073.2023'>Decaying kidney function during cirrhosis correlates with remodeling of distal colon aldosterone target gene expression</a></p>
<p>Natalia Serrano-Morillas, Carlos González-Alayón, Arianna Vastola-Mascolo, Ana E. Rodríguez-Rodríguez, Guadalberto Hernández, Esteban Porrini, Manuel Hernández-Guerra, and Diego Alvarez de la Rosa</p>
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:4, G306-G317</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/cp5f4k/GI-00073-2023_Finalacgaf.mp3" length="4919890" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Diego Alvarez de la Rosa of the University of La Laguna discusses the recently published manuscript titled “Decaying kidney function during cirrhosis correlates with remodeling of distal colon aldosterone target gene expression.”
 
NEW &amp; NOTEWORTHY Liver cirrhosis progression significantly alters ion transporter subunit expression in the rat distal colon, a change that correlated well with declining kidney function and the severity of the disease. Natalia Serrano-Morillas et al. data suggests that the steroid hormone aldosterone participates in this homeostatic response to maintain electrolyte balance.
 
Article Citation:
Decaying kidney function during cirrhosis correlates with remodeling of distal colon aldosterone target gene expression
Natalia Serrano-Morillas, Carlos González-Alayón, Arianna Vastola-Mascolo, Ana E. Rodríguez-Rodríguez, Guadalberto Hernández, Esteban Porrini, Manuel Hernández-Guerra, and Diego Alvarez de la Rosa
American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:4, G306-G317]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>509</itunes:duration>
                <itunes:episode>22</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” The Micro Version:  Maternal influenza infection and offspring gut immunity</title>
        <itunes:title>”Got Guts” The Micro Version:  Maternal influenza infection and offspring gut immunity</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-maternal-influenza-infection-and-offspring-gut-immunity/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-maternal-influenza-infection-and-offspring-gut-immunity/#comments</comments>        <pubDate>Tue, 17 Oct 2023 16:37:05 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/fc76bea4-dc40-3bb2-92ad-4a38c55319d9</guid>
                                    <description><![CDATA[<p>In this podcast lead author Dr. Stella Liong of RMIT University, discusses the recently published manuscript titled “Influenza A virus infection during pregnancy causes immunological changes in gut-associated lymphoid tissues of offspring mice.”</p>
<p> </p>
<p>NEW &amp; NOTEWORTHY Influenza A virus (IAV) infection during pregnancy is associated with changes in gut-associated lymphoid tissue (GALT) in the offspring in a region-dependent manner. Neutrophils and monocytes/macrophages were elevated in the cecal patch of offspring from infected dams. This increase in innate immune cell infiltration was not observed in the Peyer’s patches. T cells were also elevated in the cecal patch but not in the Peyer’s patches.</p>
<p> </p>
<p>Article Citation:</p>
<p><a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00062.2023'>Influenza A virus infection during pregnancy causes immunological changes in gut-associated lymphoid tissues of offspring mice</a></p>
<p>Stella Liong, Mark A. Miles, Mitra Mohsenipour, Felicia Liong, Elisa L. Hill-Yardin, and Stavros Selemidis</p>
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:3, G230-G238</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this podcast lead author Dr. Stella Liong of RMIT University, discusses the recently published manuscript titled “Influenza A virus infection during pregnancy causes immunological changes in gut-associated lymphoid tissues of offspring mice.”</p>
<p> </p>
<p>NEW &amp; NOTEWORTHY Influenza A virus (IAV) infection during pregnancy is associated with changes in gut-associated lymphoid tissue (GALT) in the offspring in a region-dependent manner. Neutrophils and monocytes/macrophages were elevated in the cecal patch of offspring from infected dams. This increase in innate immune cell infiltration was not observed in the Peyer’s patches. T cells were also elevated in the cecal patch but not in the Peyer’s patches.</p>
<p> </p>
<p>Article Citation:</p>
<p><a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00062.2023'>Influenza A virus infection during pregnancy causes immunological changes in gut-associated lymphoid tissues of offspring mice</a></p>
<p>Stella Liong, Mark A. Miles, Mitra Mohsenipour, Felicia Liong, Elisa L. Hill-Yardin, and Stavros Selemidis</p>
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:3, G230-G238</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/kktga7/GI_00062_2023_Final705jw.mp3" length="7884835" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this podcast lead author Dr. Stella Liong of RMIT University, discusses the recently published manuscript titled “Influenza A virus infection during pregnancy causes immunological changes in gut-associated lymphoid tissues of offspring mice.”
 
NEW &amp; NOTEWORTHY Influenza A virus (IAV) infection during pregnancy is associated with changes in gut-associated lymphoid tissue (GALT) in the offspring in a region-dependent manner. Neutrophils and monocytes/macrophages were elevated in the cecal patch of offspring from infected dams. This increase in innate immune cell infiltration was not observed in the Peyer’s patches. T cells were also elevated in the cecal patch but not in the Peyer’s patches.
 
Article Citation:
Influenza A virus infection during pregnancy causes immunological changes in gut-associated lymphoid tissues of offspring mice
Stella Liong, Mark A. Miles, Mitra Mohsenipour, Felicia Liong, Elisa L. Hill-Yardin, and Stavros Selemidis
American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:3, G230-G238]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>460</itunes:duration>
                <itunes:episode>21</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” the Micro Version with Kalidas Ramamoorthy</title>
        <itunes:title>”Got Guts” the Micro Version with Kalidas Ramamoorthy</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-kalidas-ramamoorthy/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-kalidas-ramamoorthy/#comments</comments>        <pubDate>Mon, 09 Oct 2023 17:50:42 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/9d5f0caa-8671-362f-a909-674ce30dea4c</guid>
                                    <description><![CDATA[<p>First author, Dr. <a href='https://journals.physiology.org/doi/full/10.1152/ajpgi.00106.2023'>Kalidas Ramamoorthy</a> of the University of California, Irvine discusses the recently published paper titled “miR-122-5p is involved in posttranscriptional regulation of the mitochondrial thiamin pyrophosphate transporter (SLC25A19) in pancreatic acinar cells.”</p>
<p> </p>
<p>NEW &amp; NOTEWORTHY This study shows that the expression and function of mitochondrial TPP transporter (MTPPT) are subject to posttranscriptional regulation by miRNA-122-5p in pancreatic acinar cells.</p>
<p> </p>
<p>Article Citation:</p>
<p><a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00106.2023'>miR-122-5p is involved in posttranscriptional regulation of the mitochondrial thiamin pyrophosphate transporter (SLC25A19) in pancreatic acinar cells</a></p>
<p>Kalidas Ramamoorthy, Subrata Sabui, Kameron I. Manzon, Appakalai N. Balamurugan, and Hamid M. Said</p>
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:4, G347-G355</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>First author, Dr. <a href='https://journals.physiology.org/doi/full/10.1152/ajpgi.00106.2023'>Kalidas Ramamoorthy</a> of the University of California, Irvine discusses the recently published paper titled “miR-122-5p is involved in posttranscriptional regulation of the mitochondrial thiamin pyrophosphate transporter (SLC25A19) in pancreatic acinar cells.”</p>
<p> </p>
<p>NEW &amp; NOTEWORTHY This study shows that the expression and function of mitochondrial TPP transporter (MTPPT) are subject to posttranscriptional regulation by miRNA-122-5p in pancreatic acinar cells.</p>
<p> </p>
<p>Article Citation:</p>
<p><a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00106.2023'>miR-122-5p is involved in posttranscriptional regulation of the mitochondrial thiamin pyrophosphate transporter (<em>SLC25A19</em>) in pancreatic acinar cells</a></p>
<p>Kalidas Ramamoorthy, Subrata Sabui, Kameron I. Manzon, Appakalai N. Balamurugan, and Hamid M. Said</p>
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:4, G347-G355</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/um6dwk/GI-00106-2023_Finala50yj.mp3" length="4613010" type="audio/mpeg"/>
        <itunes:summary><![CDATA[First author, Dr. Kalidas Ramamoorthy of the University of California, Irvine discusses the recently published paper titled “miR-122-5p is involved in posttranscriptional regulation of the mitochondrial thiamin pyrophosphate transporter (SLC25A19) in pancreatic acinar cells.”
 
NEW &amp; NOTEWORTHY This study shows that the expression and function of mitochondrial TPP transporter (MTPPT) are subject to posttranscriptional regulation by miRNA-122-5p in pancreatic acinar cells.
 
Article Citation:
miR-122-5p is involved in posttranscriptional regulation of the mitochondrial thiamin pyrophosphate transporter (SLC25A19) in pancreatic acinar cells
Kalidas Ramamoorthy, Subrata Sabui, Kameron I. Manzon, Appakalai N. Balamurugan, and Hamid M. Said
American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:4, G347-G355]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>309</itunes:duration>
                <itunes:episode>20</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” the Micro Version with Steven Hutchens and Somshuvra Mukhopadhyay</title>
        <itunes:title>”Got Guts” the Micro Version with Steven Hutchens and Somshuvra Mukhopadhyay</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-steven-hutchens-and-somshuvra-mukhopadhyay/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-steven-hutchens-and-somshuvra-mukhopadhyay/#comments</comments>        <pubDate>Wed, 27 Sep 2023 17:36:33 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/7fc3bc68-1904-3709-b646-d5fbdec884df</guid>
                                    <description><![CDATA[<p>In this podcast  Steven Hutchens and Dr. Somshuvra Mukhopadhyay of the University of Texas at Austin discuss the recently published research titled "Hepatic and intestinal manganese excretion are both required to regulate brain manganese during elevated manganese exposure." </p>
<p> </p>
<p>NEW &amp; NOTEWORTHY This article shows that, in contrast with expectations from prior studies and physiological conditions, excretion of manganese by the intestines and liver is equally important in controlling brain manganese during human-relevant manganese exposure. The results provide foundational insights about the interorgan mechanisms that control brain manganese homeostasis at the organism level and have important implications for the development of therapeutics to treat manganese-induced neurological disease.</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00047.2023'>Hepatic and intestinal manganese excretion are both required to regulate brain manganese during elevated manganese exposure</a>
Steven Hutchens, Thomas P. Jursa, Ashvini Melkote, Stephanie M. Grant, Donald R. Smith, and Somshuvra Mukhopadhyay
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:3, G251-G264</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this podcast  Steven Hutchens and Dr. Somshuvra Mukhopadhyay of the University of Texas at Austin discuss the recently published research titled "Hepatic and intestinal manganese excretion are both required to regulate brain manganese during elevated manganese exposure." </p>
<p> </p>
<p>NEW &amp; NOTEWORTHY This article shows that, in contrast with expectations from prior studies and physiological conditions, excretion of manganese by the intestines and liver is equally important in controlling brain manganese during human-relevant manganese exposure. The results provide foundational insights about the interorgan mechanisms that control brain manganese homeostasis at the organism level and have important implications for the development of therapeutics to treat manganese-induced neurological disease.</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00047.2023'>Hepatic and intestinal manganese excretion are both required to regulate brain manganese during elevated manganese exposure</a>
Steven Hutchens, Thomas P. Jursa, Ashvini Melkote, Stephanie M. Grant, Donald R. Smith, and Somshuvra Mukhopadhyay
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:3, G251-G264</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/99vdr7/GI_00047_2023_Final9wl0q.mp3" length="4431922" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this podcast  Steven Hutchens and Dr. Somshuvra Mukhopadhyay of the University of Texas at Austin discuss the recently published research titled "Hepatic and intestinal manganese excretion are both required to regulate brain manganese during elevated manganese exposure." 
 
NEW &amp; NOTEWORTHY This article shows that, in contrast with expectations from prior studies and physiological conditions, excretion of manganese by the intestines and liver is equally important in controlling brain manganese during human-relevant manganese exposure. The results provide foundational insights about the interorgan mechanisms that control brain manganese homeostasis at the organism level and have important implications for the development of therapeutics to treat manganese-induced neurological disease.
 
Article Citation: 
Hepatic and intestinal manganese excretion are both required to regulate brain manganese during elevated manganese exposure
Steven Hutchens, Thomas P. Jursa, Ashvini Melkote, Stephanie M. Grant, Donald R. Smith, and Somshuvra Mukhopadhyay
American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:3, G251-G264]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>390</itunes:duration>
                <itunes:episode>19</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” the Micro Version with Jihane N. Benhammou</title>
        <itunes:title>”Got Guts” the Micro Version with Jihane N. Benhammou</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-jihane-n-benhammou/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-jihane-n-benhammou/#comments</comments>        <pubDate>Fri, 22 Sep 2023 15:26:11 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/6f3f338a-c613-36e6-a327-8681327c05be</guid>
                                    <description><![CDATA[<p>In this episode, Dr. Jihane N. Benhammou of UCLA discusses the recently published article titled "Lipophilic statins inhibit YAP coactivator transcriptional activity in HCC cells through Rho-mediated modulation of actin cytoskeleton."</p>
<p> </p>
<p>NEW &amp; NOTEWORTHY Statins are widely used for the treatment of cardiovascular diseases. Recently, their use has been associated with a decrease in the incidence of hepatocellular carcinoma (HCC); however, their mechanism(s) has remained elusive. In this study, we delineate the mechanism by which statins affect the Yes-associated protein (YAP), which has emerged as a key oncogenic pathway in HCC. We investigate each step of the mevalonate pathway and demonstrate that statins regulate YAP via Rho GTPases.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00089.2023'>Lipophilic statins inhibit YAP coactivator transcriptional activity in HCC cells through Rho-mediated modulation of actin cytoskeleton</a>
Jihane N. Benhammou, Bo Qiao, Arthur Ko, James Sinnett-Smith, Joseph R. Pisegna, and Enrique Rozengurt
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:3, G239-G250</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this episode, Dr. Jihane N. Benhammou of UCLA discusses the recently published article titled "Lipophilic statins inhibit YAP coactivator transcriptional activity in HCC cells through Rho-mediated modulation of actin cytoskeleton."</p>
<p> </p>
<p>NEW &amp; NOTEWORTHY Statins are widely used for the treatment of cardiovascular diseases. Recently, their use has been associated with a decrease in the incidence of hepatocellular carcinoma (HCC); however, their mechanism(s) has remained elusive. In this study, we delineate the mechanism by which statins affect the Yes-associated protein (YAP), which has emerged as a key oncogenic pathway in HCC. We investigate each step of the mevalonate pathway and demonstrate that statins regulate YAP via Rho GTPases.</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00089.2023'>Lipophilic statins inhibit YAP coactivator transcriptional activity in HCC cells through Rho-mediated modulation of actin cytoskeleton</a>
Jihane N. Benhammou, Bo Qiao, Arthur Ko, James Sinnett-Smith, Joseph R. Pisegna, and Enrique Rozengurt
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:3, G239-G250</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/f3i38i/GI_00089_2023_Final6rn8d.mp3" length="7490146" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this episode, Dr. Jihane N. Benhammou of UCLA discusses the recently published article titled "Lipophilic statins inhibit YAP coactivator transcriptional activity in HCC cells through Rho-mediated modulation of actin cytoskeleton."
 
NEW &amp; NOTEWORTHY Statins are widely used for the treatment of cardiovascular diseases. Recently, their use has been associated with a decrease in the incidence of hepatocellular carcinoma (HCC); however, their mechanism(s) has remained elusive. In this study, we delineate the mechanism by which statins affect the Yes-associated protein (YAP), which has emerged as a key oncogenic pathway in HCC. We investigate each step of the mevalonate pathway and demonstrate that statins regulate YAP via Rho GTPases.
 
Article Citation:
Lipophilic statins inhibit YAP coactivator transcriptional activity in HCC cells through Rho-mediated modulation of actin cytoskeleton
Jihane N. Benhammou, Bo Qiao, Arthur Ko, James Sinnett-Smith, Joseph R. Pisegna, and Enrique Rozengurt
American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 325:3, G239-G250]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>522</itunes:duration>
                <itunes:episode>18</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” the Micro Version with Francisco Pascual and Samuel Camilli</title>
        <itunes:title>”Got Guts” the Micro Version with Francisco Pascual and Samuel Camilli</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-francisco-pascual-and-samuel-camilli/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-francisco-pascual-and-samuel-camilli/#comments</comments>        <pubDate>Tue, 05 Sep 2023 16:56:41 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/925d4208-bce1-3666-8455-a2beb97d929c</guid>
                                    <description><![CDATA[<p>In this podcast coauthors Francisco Pascual, and Samuel Camilli of Morsani College of Medicine, University of South Florida discuss the recently published Perspectives titled "Mind-body connection: metabolite 4-ethylphenyl linked to anxiety behavior and oligodendrocyte modification in autism spectrum disorder."</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00221.2022'>Mind-body connection: metabolite 4-ethylphenyl linked to anxiety behavior and oligodendrocyte modification in autism spectrum disorder</a>
Francisco Pascual, Samuel Camilli, Richard F. Lockey, and Narasaiah Kolliputi
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 324:6, G422-G425</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this podcast coauthors Francisco Pascual, and Samuel Camilli of Morsani College of Medicine, University of South Florida discuss the recently published Perspectives titled "Mind-body connection: metabolite 4-ethylphenyl linked to anxiety behavior and oligodendrocyte modification in autism spectrum disorder."</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00221.2022'>Mind-body connection: metabolite 4-ethylphenyl linked to anxiety behavior and oligodendrocyte modification in autism spectrum disorder</a>
Francisco Pascual, Samuel Camilli, Richard F. Lockey, and Narasaiah Kolliputi
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 324:6, G422-G425</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/3bm2w6/GI_00221_2022_Final86rac.mp3" length="4450768" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this podcast coauthors Francisco Pascual, and Samuel Camilli of Morsani College of Medicine, University of South Florida discuss the recently published Perspectives titled "Mind-body connection: metabolite 4-ethylphenyl linked to anxiety behavior and oligodendrocyte modification in autism spectrum disorder."
 
Article Citation:
Mind-body connection: metabolite 4-ethylphenyl linked to anxiety behavior and oligodendrocyte modification in autism spectrum disorder
Francisco Pascual, Samuel Camilli, Richard F. Lockey, and Narasaiah Kolliputi
American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 324:6, G422-G425
 ]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>319</itunes:duration>
                <itunes:episode>17</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” the Micro Version with Theo A.T.G. van Kempen and Gavin M. Boerboom</title>
        <itunes:title>”Got Guts” the Micro Version with Theo A.T.G. van Kempen and Gavin M. Boerboom</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-theo-atg-van-kempen-and-gavin-m-boerboom/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-theo-atg-van-kempen-and-gavin-m-boerboom/#comments</comments>        <pubDate>Tue, 29 Aug 2023 16:32:36 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/c762070f-55cf-3dee-ab0c-28159c6f916f</guid>
                                    <description><![CDATA[<p>In this podcast Prof. Theo A.T.G. van Kempen of North Carolina State University and Dr. Gavin M. Boerboom of Trouw Nutrition discuss their recently published perspectives paper titled "Is the intestinal mucous layer a natural deep eutectic solvent-based digestion matrix?"</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00006.2023'>Is the intestinal mucous layer a natural deep eutectic solvent-based digestion matrix?</a>
Theo A.T.G. van Kempen and Gavin M. Boerboom
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 324:6, G438-G441</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this podcast Prof. Theo A.T.G. van Kempen of North Carolina State University and Dr. Gavin M. Boerboom of Trouw Nutrition discuss their recently published perspectives paper titled "Is the intestinal mucous layer a natural deep eutectic solvent-based digestion matrix?"</p>
<p> </p>
<p>Article Citation:</p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00006.2023'>Is the intestinal mucous layer a natural deep eutectic solvent-based digestion matrix?</a>
Theo A.T.G. van Kempen and Gavin M. Boerboom
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 324:6, G438-G441</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/e764nn/GI_0006_2023_Finalamuwk.mp3" length="5694987" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this podcast Prof. Theo A.T.G. van Kempen of North Carolina State University and Dr. Gavin M. Boerboom of Trouw Nutrition discuss their recently published perspectives paper titled "Is the intestinal mucous layer a natural deep eutectic solvent-based digestion matrix?"
 
Article Citation:
Is the intestinal mucous layer a natural deep eutectic solvent-based digestion matrix?
Theo A.T.G. van Kempen and Gavin M. Boerboom
American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 324:6, G438-G441]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>465</itunes:duration>
                <itunes:episode>16</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” the Micro Version with Jessica A. Breznik</title>
        <itunes:title>”Got Guts” the Micro Version with Jessica A. Breznik</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-jessica-a-breznik/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-jessica-a-breznik/#comments</comments>        <pubDate>Mon, 21 Aug 2023 11:13:45 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/8daaa29b-8a1d-3f0d-9fd2-984545fb9324</guid>
                                    <description><![CDATA[<p>In this podcast first author Dr. Jessica A. Breznik of McMaster University, discusses the recently published manuscript titled "Diet-induced obesity alters intestinal monocyte-derived and tissue-resident macrophages and increases intestinal permeability in female mice independent of tumor necrosis factor." </p>
<p> </p>
<p>NEW &amp; NOTEWORTHY We found that diet-induced obesity in female mice has tissue- and time-dependent effects on intestinal paracellular permeability as well as monocyte-derived and tissue-resident macrophage numbers, surface marker phenotype, and intracellular production of the cytokines IL-10 and TNF. These changes were not mediated by TNF.</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00231.2022'>Diet-induced obesity alters intestinal monocyte-derived and tissue-resident macrophages and increases intestinal permeability in female mice independent of tumor necrosis factor</a>
Jessica A. Breznik, Jennifer Jury, Elena F. Verdú, Deborah M. Sloboda, and Dawn M. E. Bowdish
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 324:4, G305-G321
</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this podcast first author Dr. Jessica A. Breznik of McMaster University, discusses the recently published manuscript titled "Diet-induced obesity alters intestinal monocyte-derived and tissue-resident macrophages and increases intestinal permeability in female mice independent of tumor necrosis factor." </p>
<p> </p>
<p>NEW &amp; NOTEWORTHY We found that diet-induced obesity in female mice has tissue- and time-dependent effects on intestinal paracellular permeability as well as monocyte-derived and tissue-resident macrophage numbers, surface marker phenotype, and intracellular production of the cytokines IL-10 and TNF. These changes were not mediated by TNF.</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00231.2022'>Diet-induced obesity alters intestinal monocyte-derived and tissue-resident macrophages and increases intestinal permeability in female mice independent of tumor necrosis factor</a>
Jessica A. Breznik, Jennifer Jury, Elena F. Verdú, Deborah M. Sloboda, and Dawn M. E. Bowdish
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 324:4, G305-G321<br>
</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/v7atv4/GI_00231_2022_Final7m9u9.mp3" length="6914590" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this podcast first author Dr. Jessica A. Breznik of McMaster University, discusses the recently published manuscript titled "Diet-induced obesity alters intestinal monocyte-derived and tissue-resident macrophages and increases intestinal permeability in female mice independent of tumor necrosis factor." 
 
NEW &amp; NOTEWORTHY We found that diet-induced obesity in female mice has tissue- and time-dependent effects on intestinal paracellular permeability as well as monocyte-derived and tissue-resident macrophage numbers, surface marker phenotype, and intracellular production of the cytokines IL-10 and TNF. These changes were not mediated by TNF.
 
Article Citation: 
Diet-induced obesity alters intestinal monocyte-derived and tissue-resident macrophages and increases intestinal permeability in female mice independent of tumor necrosis factor
Jessica A. Breznik, Jennifer Jury, Elena F. Verdú, Deborah M. Sloboda, and Dawn M. E. Bowdish
American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 324:4, G305-G321]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>535</itunes:duration>
                <itunes:episode>15</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>”Got Guts” the Micro Version with Gene Lamanilao</title>
        <itunes:title>”Got Guts” the Micro Version with Gene Lamanilao</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-gene-lamanilao/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-micro-version-with-gene-lamanilao/#comments</comments>        <pubDate>Mon, 14 Aug 2023 17:10:06 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/cda5b269-108a-35e7-9d3e-0172263f365f</guid>
                                    <description><![CDATA[<p>In this micro podcast Dr. Gene G. Lamanilao The University of Tennessee Health Science Center, College of Medicine gives the listeners an overview the recently published manuscript titled "Key hepatoprotective roles of mitochondria in liver regeneration." </p>
<p> </p>
<p>Treatment of advanced liver disease using surgical modalities is possible due to the liver’s innate ability to regenerate following resection. Several key cellular events in the regenerative process converge at the mitochondria, implicating their crucial roles in liver regeneration. Mitochondria enable the regenerating liver to meet massive metabolic demands by coordinating energy production to drive cellular proliferative processes and vital homeostatic functions. Mitochondria are also involved in terminating the regenerative process by mediating apoptosis. Studies have shown that attenuation of mitochondrial activity results in delayed liver regeneration, and liver failure following resection is associated with mitochondrial dysfunction. Emerging mitochondria therapy (i.e., mitotherapy) strategies involve isolating healthy donor mitochondria for transplantation into diseased organs to promote regeneration. This review highlights mitochondria’s inherent role in liver regeneration.</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00220.2022'>Key hepatoprotective roles of mitochondria in liver regeneration</a>
Gene G. Lamanilao, Murat Dogan, Prisha S. Patel, Shafquat Azim, Disha S. Patel, Syamal K. Bhattacharya, James D. Eason, Canan Kuscu, Cem Kuscu, and Amandeep Bajwa
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 324:3, G207-G218</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this micro podcast Dr. Gene G. Lamanilao The University of Tennessee Health Science Center, College of Medicine gives the listeners an overview the recently published manuscript titled "Key hepatoprotective roles of mitochondria in liver regeneration." </p>
<p> </p>
<p>Treatment of advanced liver disease using surgical modalities is possible due to the liver’s innate ability to regenerate following resection. Several key cellular events in the regenerative process converge at the mitochondria, implicating their crucial roles in liver regeneration. Mitochondria enable the regenerating liver to meet massive metabolic demands by coordinating energy production to drive cellular proliferative processes and vital homeostatic functions. Mitochondria are also involved in terminating the regenerative process by mediating apoptosis. Studies have shown that attenuation of mitochondrial activity results in delayed liver regeneration, and liver failure following resection is associated with mitochondrial dysfunction. Emerging mitochondria therapy (i.e., mitotherapy) strategies involve isolating healthy donor mitochondria for transplantation into diseased organs to promote regeneration. This review highlights mitochondria’s inherent role in liver regeneration.</p>
<p> </p>
<p>Article Citation: </p>
<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00220.2022'>Key hepatoprotective roles of mitochondria in liver regeneration</a>
Gene G. Lamanilao, Murat Dogan, Prisha S. Patel, Shafquat Azim, Disha S. Patel, Syamal K. Bhattacharya, James D. Eason, Canan Kuscu, Cem Kuscu, and Amandeep Bajwa
<p>American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 324:3, G207-G218</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/vibvfn/ajpgi002202022_Final9csfo.mp3" length="4764283" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this micro podcast Dr. Gene G. Lamanilao The University of Tennessee Health Science Center, College of Medicine gives the listeners an overview the recently published manuscript titled "Key hepatoprotective roles of mitochondria in liver regeneration." 
 
Treatment of advanced liver disease using surgical modalities is possible due to the liver’s innate ability to regenerate following resection. Several key cellular events in the regenerative process converge at the mitochondria, implicating their crucial roles in liver regeneration. Mitochondria enable the regenerating liver to meet massive metabolic demands by coordinating energy production to drive cellular proliferative processes and vital homeostatic functions. Mitochondria are also involved in terminating the regenerative process by mediating apoptosis. Studies have shown that attenuation of mitochondrial activity results in delayed liver regeneration, and liver failure following resection is associated with mitochondrial dysfunction. Emerging mitochondria therapy (i.e., mitotherapy) strategies involve isolating healthy donor mitochondria for transplantation into diseased organs to promote regeneration. This review highlights mitochondria’s inherent role in liver regeneration.
 
Article Citation: 
Key hepatoprotective roles of mitochondria in liver regeneration
Gene G. Lamanilao, Murat Dogan, Prisha S. Patel, Shafquat Azim, Disha S. Patel, Syamal K. Bhattacharya, James D. Eason, Canan Kuscu, Cem Kuscu, and Amandeep Bajwa
American Journal of Physiology-Gastrointestinal and Liver Physiology 2023 324:3, G207-G218]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>297</itunes:duration>
                <itunes:episode>14</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: Small Intestine Neuroendocrine Tumor: Its cell-of-origin has a curious fate of tumorigenesis</title>
        <itunes:title>Got Guts: Small Intestine Neuroendocrine Tumor: Its cell-of-origin has a curious fate of tumorigenesis</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-small-intestine-neuroendocrine-tumor-its-cell-of-origin-has-a-curious-fate-of-tumorigenesis/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-small-intestine-neuroendocrine-tumor-its-cell-of-origin-has-a-curious-fate-of-tumorigenesis/#comments</comments>        <pubDate>Tue, 18 Apr 2023 15:41:56 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/e3e4c65e-acf4-3256-a19e-5bdad8b0c280</guid>
                                    <description><![CDATA[<p>Take a listen to our latest podcast with coauthor Dr. Yoshi Sei as he discusses the recently published manuscript "<a href='https://doi.org/10.1152/ajpgi.00205.2022'>Tissue- and cell-specific properties of enterochromaffin cells affect the fate of tumorigenesis toward nonendocrine adenocarcinoma of the small intestine</a>" with Editor in Chief Professor Mark Frey. Small intestinal neuroendocrine tumors are of putative enterochromaffin (EC) cell origin and are the most common malignancy in the small intestine, followed by adenocarcinoma. Dr Sei, explains how tissue- and cell-specific properties of EC cells such as cell turnover, migration, and dedifferentiation, affect their fate of tumorigenesis.</p>
<p>Follow us on <a href='https://twitter.com/ajpgi'>Twitter</a>, <a href='https://www.facebook.com/AJPGIandLiver'>Facebook </a>and <a href='https://www.instagram.com/ajpgi_liver/'>Instagram</a></p>
<p>Click <a href='https://journals.physiology.org/ajpgi/about'>here</a> for more info on American Physiology Gastrointestinal and Liver Physiology</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Take a listen to our latest podcast with coauthor Dr. Yoshi Sei as he discusses the recently published manuscript "<a href='https://doi.org/10.1152/ajpgi.00205.2022'>Tissue- and cell-specific properties of enterochromaffin cells affect the fate of tumorigenesis toward nonendocrine adenocarcinoma of the small intestine</a>" with Editor in Chief Professor Mark Frey. Small intestinal neuroendocrine tumors are of putative enterochromaffin (EC) cell origin and are the most common malignancy in the small intestine, followed by adenocarcinoma. Dr Sei, explains how tissue- and cell-specific properties of EC cells such as cell turnover, migration, and dedifferentiation, affect their fate of tumorigenesis.</p>
<p>Follow us on <a href='https://twitter.com/ajpgi'>Twitter</a>, <a href='https://www.facebook.com/AJPGIandLiver'>Facebook </a>and <a href='https://www.instagram.com/ajpgi_liver/'>Instagram</a></p>
<p>Click <a href='https://journals.physiology.org/ajpgi/about'>here</a> for more info on American Physiology Gastrointestinal and Liver Physiology</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/xfmazg/GI_00205_2022a98nk.mp3" length="27215530" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Take a listen to our latest podcast with coauthor Dr. Yoshi Sei as he discusses the recently published manuscript "Tissue- and cell-specific properties of enterochromaffin cells affect the fate of tumorigenesis toward nonendocrine adenocarcinoma of the small intestine" with Editor in Chief Professor Mark Frey. Small intestinal neuroendocrine tumors are of putative enterochromaffin (EC) cell origin and are the most common malignancy in the small intestine, followed by adenocarcinoma. Dr Sei, explains how tissue- and cell-specific properties of EC cells such as cell turnover, migration, and dedifferentiation, affect their fate of tumorigenesis.
Follow us on Twitter, Facebook and Instagram
Click here for more info on American Physiology Gastrointestinal and Liver Physiology]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>2021</itunes:duration>
                <itunes:episode>13</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: The 411 of GI and Liver Section at American Physiology Summit 2023</title>
        <itunes:title>Got Guts: The 411 of GI and Liver Section at American Physiology Summit 2023</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-the-411-of-gi-and-liver-section-at-american-physiology-summit-2023/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-the-411-of-gi-and-liver-section-at-american-physiology-summit-2023/#comments</comments>        <pubDate>Mon, 13 Mar 2023 16:08:14 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/adbb68ce-12bf-3d61-9166-0625aadbea49</guid>
                                    <description><![CDATA[<p>Take a listen to our latest podcast where the magnificent Dr. Karen Edelblum, chair of the <a href='https://www.physiology.org/community/aps-communities/sections/Gastrointestinal-Liver?SSO=Y'>GI and Liver Section</a> discusses what's happening at our first ever American Physiology Summit, April 20-23rd in Long Beach California.</p>
<p>Registration Deadline for <a href='https://www.physiology.org/professional-development/meetings-events/american-physiology-summit-2023?SSO=Y'>American Physiology Summit</a> is March 31, 2023</p>
<p>Click <a href='https://journals.physiology.org/ajpgi/about'>here</a> for more info on American Physiology Gastrointestinal and Liver Physiology</p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Take a listen to our latest podcast where the magnificent Dr. Karen Edelblum, chair of the <a href='https://www.physiology.org/community/aps-communities/sections/Gastrointestinal-Liver?SSO=Y'>GI and Liver Section</a> discusses what's happening at our first ever American Physiology Summit, April 20-23rd in Long Beach California.</p>
<p>Registration Deadline for <a href='https://www.physiology.org/professional-development/meetings-events/american-physiology-summit-2023?SSO=Y'>American Physiology Summit</a> is March 31, 2023</p>
<p>Click <a href='https://journals.physiology.org/ajpgi/about'>here</a> for more info on American Physiology Gastrointestinal and Liver Physiology</p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/paaddm/GI_Section_Podcast_20238twem.mp3" length="16671212" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Take a listen to our latest podcast where the magnificent Dr. Karen Edelblum, chair of the GI and Liver Section discusses what's happening at our first ever American Physiology Summit, April 20-23rd in Long Beach California.
Registration Deadline for American Physiology Summit is March 31, 2023
Click here for more info on American Physiology Gastrointestinal and Liver Physiology]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1269</itunes:duration>
                <itunes:episode>12</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: Initiation and severity of experimental pancreatitis are modified by phosphate</title>
        <itunes:title>Got Guts: Initiation and severity of experimental pancreatitis are modified by phosphate</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-initiation-and-severity-of-experimental-pancreatitis-are-modified-by-phosphate/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-initiation-and-severity-of-experimental-pancreatitis-are-modified-by-phosphate/#comments</comments>        <pubDate>Fri, 27 Jan 2023 12:26:51 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/827f7708-4b30-32b4-a6c1-fbdbfab3c389</guid>
                                    <description><![CDATA[<p>Get to know author Dr. Rodger Liddle (Duke University) in this latest podcast as he goes over his recently published manuscript "<a href='https://doi.org/10.1152/ajpgi.00022.2022'>Initiation and severity of experimental pancreatitis are modified by phosphate</a>" with Editor in Chief Professor Mark Frey. </p>
<p> </p>
<p>New and Noteworthy-Impaired ATP synthesis disrupts acinar cell homeostasis and is an early step in pancreatitis. We report that reduced phosphate availability impairs mitochondrial function and worsens pancreatic injury. Phosphate supplementation improves mitochondrial function and protects against experimental pancreatitis, raising the possibility that phosphate supplementation may be useful in treating pancreatitis.</p>
<p> </p>
<p>Take a look at our recent <a href='https://journals.physiology.org/journal/ajpgi'>articles</a></p>
<p>Follow us on <a href='https://twitter.com/ajpgi'>Twitter</a>, <a href='https://www.facebook.com/AJPGIandLiver'>Facebook </a>and <a href='https://www.instagram.com/ajpgi_liver/'>Instagram</a></p>
<p><a href='https://journals.physiology.org/podcasts'>Listen to other podcasts </a>produced by the American Physiological Society </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Get to know author Dr. Rodger Liddle (Duke University) in this latest podcast as he goes over his recently published manuscript "<a href='https://doi.org/10.1152/ajpgi.00022.2022'>Initiation and severity of experimental pancreatitis are modified by phosphate</a>" with Editor in Chief Professor Mark Frey. </p>
<p> </p>
<p>New and Noteworthy-Impaired ATP synthesis disrupts acinar cell homeostasis and is an early step in pancreatitis. We report that reduced phosphate availability impairs mitochondrial function and worsens pancreatic injury. Phosphate supplementation improves mitochondrial function and protects against experimental pancreatitis, raising the possibility that phosphate supplementation may be useful in treating pancreatitis.</p>
<p> </p>
<p>Take a look at our recent <a href='https://journals.physiology.org/journal/ajpgi'>articles</a></p>
<p>Follow us on <a href='https://twitter.com/ajpgi'>Twitter</a>, <a href='https://www.facebook.com/AJPGIandLiver'>Facebook </a>and <a href='https://www.instagram.com/ajpgi_liver/'>Instagram</a></p>
<p><a href='https://journals.physiology.org/podcasts'>Listen to other podcasts </a>produced by the American Physiological Society </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/m6tkuu/GI_00022_2022_Podcasta4zuh.mp3" length="20701410" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Get to know author Dr. Rodger Liddle (Duke University) in this latest podcast as he goes over his recently published manuscript "Initiation and severity of experimental pancreatitis are modified by phosphate" with Editor in Chief Professor Mark Frey. 
 
New and Noteworthy-Impaired ATP synthesis disrupts acinar cell homeostasis and is an early step in pancreatitis. We report that reduced phosphate availability impairs mitochondrial function and worsens pancreatic injury. Phosphate supplementation improves mitochondrial function and protects against experimental pancreatitis, raising the possibility that phosphate supplementation may be useful in treating pancreatitis.
 
Take a look at our recent articles
Follow us on Twitter, Facebook and Instagram
Listen to other podcasts produced by the American Physiological Society ]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1710</itunes:duration>
                <itunes:episode>11</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: Unravelling the NF-kappa B enigma in the gut</title>
        <itunes:title>Got Guts: Unravelling the NF-kappa B enigma in the gut</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-unravelling-the-nf-kappa-b-enigma-in-the-gut/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-unravelling-the-nf-kappa-b-enigma-in-the-gut/#comments</comments>        <pubDate>Wed, 14 Dec 2022 14:16:40 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/857215e9-4bdb-3a95-a8f7-b8481a882e82</guid>
                                    <description><![CDATA[<p>In this podcast authors Prof D. Mark Pritchard and Dr. Carrie Duckworth of the University of Liverpool, discuss their recently published manuscript “<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00037.2022'>Nfkb2 deficiency and its impact on plasma cells and immunoglobulin expression in murine small intestinal mucosa</a>” with Editor-in-Chief Prof. Mark Frey. Novel transcriptomic analysis of murine proximal intestinal mucosa revealed an unexpected B cell signature in Nfkb2-/- mice. In depth analysis revealed a defect in the CD38+ B cell population and a gut-specific dysregulation of immunoglobulin levels. Take a listen to this latest podcast today!</p>
<p>Take a look at our recent <a href='https://journals.physiology.org/journal/ajpgi'>articles</a></p>
<p>Follow us on <a href='https://twitter.com/ajpgi'>Twitter</a>, <a href='https://www.facebook.com/AJPGIandLiver'>Facebook </a>and <a href='https://www.instagram.com/ajpgi_liver/'>Instagram</a></p>
<p><a href='https://journals.physiology.org/podcasts'>Listen to other podcasts </a>produced by the American Physiological Society </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this podcast authors Prof D. Mark Pritchard and Dr. Carrie Duckworth of the University of Liverpool, discuss their recently published manuscript “<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00037.2022'>Nfkb2 deficiency and its impact on plasma cells and immunoglobulin expression in murine small intestinal mucosa</a>” with Editor-in-Chief Prof. Mark Frey. Novel transcriptomic analysis of murine proximal intestinal mucosa revealed an unexpected B cell signature in Nfkb2-/- mice. In depth analysis revealed a defect in the CD38+ B cell population and a gut-specific dysregulation of immunoglobulin levels. Take a listen to this latest podcast today!</p>
<p>Take a look at our recent <a href='https://journals.physiology.org/journal/ajpgi'>articles</a></p>
<p>Follow us on <a href='https://twitter.com/ajpgi'>Twitter</a>, <a href='https://www.facebook.com/AJPGIandLiver'>Facebook </a>and <a href='https://www.instagram.com/ajpgi_liver/'>Instagram</a></p>
<p><a href='https://journals.physiology.org/podcasts'>Listen to other podcasts </a>produced by the American Physiological Society </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/g5i74u/GI_00037_2022_Podcast7jler.mp3" length="27362661" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this podcast authors Prof D. Mark Pritchard and Dr. Carrie Duckworth of the University of Liverpool, discuss their recently published manuscript “Nfkb2 deficiency and its impact on plasma cells and immunoglobulin expression in murine small intestinal mucosa” with Editor-in-Chief Prof. Mark Frey. Novel transcriptomic analysis of murine proximal intestinal mucosa revealed an unexpected B cell signature in Nfkb2-/- mice. In depth analysis revealed a defect in the CD38+ B cell population and a gut-specific dysregulation of immunoglobulin levels. Take a listen to this latest podcast today!
Take a look at our recent articles
Follow us on Twitter, Facebook and Instagram
Listen to other podcasts produced by the American Physiological Society ]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>2131</itunes:duration>
                <itunes:episode>10</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: Plasticity of Human Barrett’s Organoids</title>
        <itunes:title>Got Guts: Plasticity of Human Barrett’s Organoids</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-plasticity-of-human-barrett-s-organoids/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-plasticity-of-human-barrett-s-organoids/#comments</comments>        <pubDate>Fri, 09 Dec 2022 11:21:13 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/a3f460cd-b1f8-3ffd-9fe9-0be1399bb975</guid>
                                    <description><![CDATA[<p>In our latest podcast senior author Dr. Rhonda Souza discusses her latest published research “<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00017.2022'>A Human Barrett's Esophagus Organoid System Reveals Epithelial-Mesenchymal Plasticity Induced by Acid and Bile Salts</a>” with Editor-in-Chief Prof. Mark Frey. Using Barrett's esophagus (BE) biopsies, the authors established organoids recapitulating key BE features. During early stages of organoid development, a GERD-like wound environment induced features of epithelial-mesenchymal plasticity (EMP) in Barrett's progenitor cells, suggesting that reflux-induced EMP can enable Barrett's cells to migrate underneath squamous epithelium to form subsquamous intestinal metaplasia, a condition that may underlie Barrett's cancers that escape detection by endoscopic surveillance, and recurrences of Barrett's metaplasia following endoscopic eradication therapy.</p>
<p>Take a look at our recent <a href='https://journals.physiology.org/journal/ajpgi'>articles</a></p>
<p>Follow us on <a href='http://ajpgi'>Twitter</a>, <a href='https://www.facebook.com/AJPGIandLiver'>Facebook </a>and <a href='https://www.instagram.com/ajpgi_liver/'>Instagram</a></p>
<p><a href='https://journals.physiology.org/podcasts'>Listen to other podcasts </a>produced by the American Physi8ological Society </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In our latest podcast senior author Dr. Rhonda Souza discusses her latest published research “<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00017.2022'>A Human Barrett's Esophagus Organoid System Reveals Epithelial-Mesenchymal Plasticity Induced by Acid and Bile Salts</a>” with Editor-in-Chief Prof. Mark Frey. Using Barrett's esophagus (BE) biopsies, the authors established organoids recapitulating key BE features. During early stages of organoid development, a GERD-like wound environment induced features of epithelial-mesenchymal plasticity (EMP) in Barrett's progenitor cells, suggesting that reflux-induced EMP can enable Barrett's cells to migrate underneath squamous epithelium to form subsquamous intestinal metaplasia, a condition that may underlie Barrett's cancers that escape detection by endoscopic surveillance, and recurrences of Barrett's metaplasia following endoscopic eradication therapy.</p>
<p>Take a look at our recent <a href='https://journals.physiology.org/journal/ajpgi'>articles</a></p>
<p>Follow us on <a href='http://ajpgi'>Twitter</a>, <a href='https://www.facebook.com/AJPGIandLiver'>Facebook </a>and <a href='https://www.instagram.com/ajpgi_liver/'>Instagram</a></p>
<p><a href='https://journals.physiology.org/podcasts'>Listen to other podcasts </a>produced by the American Physi8ological Society </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/qpfdyh/GI_00017_2022_Podcast7b1qy.mp3" length="22178194" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In our latest podcast senior author Dr. Rhonda Souza discusses her latest published research “A Human Barrett's Esophagus Organoid System Reveals Epithelial-Mesenchymal Plasticity Induced by Acid and Bile Salts” with Editor-in-Chief Prof. Mark Frey. Using Barrett's esophagus (BE) biopsies, the authors established organoids recapitulating key BE features. During early stages of organoid development, a GERD-like wound environment induced features of epithelial-mesenchymal plasticity (EMP) in Barrett's progenitor cells, suggesting that reflux-induced EMP can enable Barrett's cells to migrate underneath squamous epithelium to form subsquamous intestinal metaplasia, a condition that may underlie Barrett's cancers that escape detection by endoscopic surveillance, and recurrences of Barrett's metaplasia following endoscopic eradication therapy.
Take a look at our recent articles
Follow us on Twitter, Facebook and Instagram
Listen to other podcasts produced by the American Physi8ological Society ]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1678</itunes:duration>
                <itunes:episode>9</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: Aryl hydrocarbon receptor (AhR) function is required for optimal interleukin-22 signaling in colonic epithelial stem cells</title>
        <itunes:title>Got Guts: Aryl hydrocarbon receptor (AhR) function is required for optimal interleukin-22 signaling in colonic epithelial stem cells</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-aryl-hydrocarbon-receptor-ahr-function-is-required-for-optimal-interleukin-22-signaling-in-colonic-epithelial-stem-cells/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-aryl-hydrocarbon-receptor-ahr-function-is-required-for-optimal-interleukin-22-signaling-in-colonic-epithelial-stem-cells/#comments</comments>        <pubDate>Mon, 21 Nov 2022 15:14:12 -0400</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/d367db98-2d21-3245-a218-6ae724160199</guid>
                                    <description><![CDATA[<p>In this podcast, coauthors Dr. Huajun Han, and Prof. Robert S. Chapkin of Texas A&M University, discuss their recently published research "<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00074.2021'>Loss of aryl hydrocarbon receptor suppresses the response of colonic epithelial cells to IL22 signaling by upregulating SOCS3</a>" with Editor-in-Chief Prof. Mark Frey. Data from their preclinical orthogonal models indicate that AhR signaling modulates the response of colonic epithelial cells to IL22, resulting in the suppression of carcinogen-associated colon tumorigenesis. These findings provide rationale for targeting AhR as a means of ameliorating IBD and reducing colon cancer risk. Take a listen today! </p>
<p>Be sure to follow us on <a href='https://twitter.com/ajpgi'>Twitter</a></p>
<p><a href='https://journals.physiology.org/podcasts'>Listen</a> to other American Physiological Podcasts </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In this podcast, coauthors Dr. Huajun Han, and Prof. Robert S. Chapkin of Texas A&M University, discuss their recently published research "<a href='https://journals.physiology.org/doi/abs/10.1152/ajpgi.00074.2021'>Loss of aryl hydrocarbon receptor suppresses the response of colonic epithelial cells to IL22 signaling by upregulating SOCS3</a>" with Editor-in-Chief Prof. Mark Frey. Data from their preclinical orthogonal models indicate that AhR signaling modulates the response of colonic epithelial cells to IL22, resulting in the suppression of carcinogen-associated colon tumorigenesis. These findings provide rationale for targeting AhR as a means of ameliorating IBD and reducing colon cancer risk. Take a listen today! </p>
<p>Be sure to follow us on <a href='https://twitter.com/ajpgi'>Twitter</a></p>
<p><a href='https://journals.physiology.org/podcasts'>Listen</a> to other American Physiological Podcasts </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/9p2w9a/GI_0074_2021blgwc.mp3" length="21053086" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In this podcast, coauthors Dr. Huajun Han, and Prof. Robert S. Chapkin of Texas A&M University, discuss their recently published research "Loss of aryl hydrocarbon receptor suppresses the response of colonic epithelial cells to IL22 signaling by upregulating SOCS3" with Editor-in-Chief Prof. Mark Frey. Data from their preclinical orthogonal models indicate that AhR signaling modulates the response of colonic epithelial cells to IL22, resulting in the suppression of carcinogen-associated colon tumorigenesis. These findings provide rationale for targeting AhR as a means of ameliorating IBD and reducing colon cancer risk. Take a listen today! 
Be sure to follow us on Twitter
Listen to other American Physiological Podcasts ]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1659</itunes:duration>
                <itunes:episode>8</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: Lifting the Lid on Diarrheal Diseases</title>
        <itunes:title>Got Guts: Lifting the Lid on Diarrheal Diseases</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-lifting-the-lid-on-diarrheal-diseases/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-lifting-the-lid-on-diarrheal-diseases/#comments</comments>        <pubDate>Tue, 04 Oct 2022 16:12:32 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/cec467b1-ad06-39e1-aa24-bc1f55c54990</guid>
                                    <description><![CDATA[<p>In today’s episode Dr. Stephen Keely from the Royal College of Surgeons in Ireland and Prof Kim Barrett of the University of California, Davis talk about their recent review article “<a href='https://doi.org/10.1152/ajpgi.00316.2021'>Mechanisms of Secretory Diarrhea</a>” with Prof Mark Frey. They discuss why it is we need to talk more about diarrheal diseases, lift the lid on the complex cellular and molecular mechanisms involved, and look to where new therapeutics are likely to arise in the future.</p>
<p> </p>
<p>Be sure to follow us on <a href='https://twitter.com/ajpgi'>Twitter</a></p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In today’s episode Dr. Stephen Keely from the Royal College of Surgeons in Ireland and Prof Kim Barrett of the University of California, Davis talk about their recent review article “<a href='https://doi.org/10.1152/ajpgi.00316.2021'>Mechanisms of Secretory Diarrhea</a>” with Prof Mark Frey. They discuss why it is we need to talk more about diarrheal diseases, lift the lid on the complex cellular and molecular mechanisms involved, and look to where new therapeutics are likely to arise in the future.</p>
<p> </p>
<p>Be sure to follow us on <a href='https://twitter.com/ajpgi'>Twitter</a></p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/k7y533/GI_00316_2021_Podcast7oi5l.mp3" length="20695534" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In today’s episode Dr. Stephen Keely from the Royal College of Surgeons in Ireland and Prof Kim Barrett of the University of California, Davis talk about their recent review article “Mechanisms of Secretory Diarrhea” with Prof Mark Frey. They discuss why it is we need to talk more about diarrheal diseases, lift the lid on the complex cellular and molecular mechanisms involved, and look to where new therapeutics are likely to arise in the future.
 
Be sure to follow us on Twitter]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1605</itunes:duration>
                <itunes:episode>7</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: Embracing our heterogeneity</title>
        <itunes:title>Got Guts: Embracing our heterogeneity</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-embracing-our-heterogeneity/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-embracing-our-heterogeneity/#comments</comments>        <pubDate>Wed, 20 Jul 2022 09:52:15 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/90cb2036-0f91-35d6-9df2-fbec73d2f188</guid>
                                    <description><![CDATA[<p>In a rapidly evolving era of single cell technologies, the authors of "<a href='https://doi.org/10.1152/ajpgi.00254.2021'>Stiffness is associated with hepatic stellate cell heterogeneity during liver fibrosis</a>" explain the mechanism of an amplification loop during liver fibrosis. By deciphering how stiffness macro and microscopic heterogeneity promote differential gene expression in hepatic stellate cell sub-populations, the authors find a novel stiffness-promoted molecule involved in liver fibrosis progression. Get to know authors Dr. Enis Kostallari and Dr. Vijay Shah of the Mayo Clinic as they discuss their recently published manuscript and what life is like as a researcher with Editor-in-Chief Professor Mark Frey. </p>
<p> </p>
<p><a href='https://journals.physiology.org/journal/ajpgi'>https://journals.physiology.org/journal/ajpgi</a> </p>
<p>Be sure to follow us on  <a href='https://twitter.com/ajpgi'>Twitter </a></p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>In a rapidly evolving era of single cell technologies, the authors of "<a href='https://doi.org/10.1152/ajpgi.00254.2021'>Stiffness is associated with hepatic stellate cell heterogeneity during liver fibrosis</a>" explain the mechanism of an amplification loop during liver fibrosis. By deciphering how stiffness macro and microscopic heterogeneity promote differential gene expression in hepatic stellate cell sub-populations, the authors find a novel stiffness-promoted molecule involved in liver fibrosis progression. Get to know authors Dr. Enis Kostallari and Dr. Vijay Shah of the Mayo Clinic as they discuss their recently published manuscript and what life is like as a researcher with Editor-in-Chief Professor Mark Frey. </p>
<p> </p>
<p><a href='https://journals.physiology.org/journal/ajpgi'>https://journals.physiology.org/journal/ajpgi</a> </p>
<p>Be sure to follow us on  <a href='https://twitter.com/ajpgi'>Twitter </a></p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/kpr2xj/GI_00254_202195ccs.mp3" length="14973550" type="audio/mpeg"/>
        <itunes:summary><![CDATA[In a rapidly evolving era of single cell technologies, the authors of "Stiffness is associated with hepatic stellate cell heterogeneity during liver fibrosis" explain the mechanism of an amplification loop during liver fibrosis. By deciphering how stiffness macro and microscopic heterogeneity promote differential gene expression in hepatic stellate cell sub-populations, the authors find a novel stiffness-promoted molecule involved in liver fibrosis progression. Get to know authors Dr. Enis Kostallari and Dr. Vijay Shah of the Mayo Clinic as they discuss their recently published manuscript and what life is like as a researcher with Editor-in-Chief Professor Mark Frey. 
 
https://journals.physiology.org/journal/ajpgi 
Be sure to follow us on  Twitter 
 ]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1181</itunes:duration>
                <itunes:episode>6</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: HOPX+ injury-resistant intestinal stem cells drive epithelial recovery after severe intestinal ischemia</title>
        <itunes:title>Got Guts: HOPX+ injury-resistant intestinal stem cells drive epithelial recovery after severe intestinal ischemia</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-hopx-injury-resistant-intestinal-stem-cells-drive-epithelial-recovery-after-severe-intestinal-ischemia/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-hopx-injury-resistant-intestinal-stem-cells-drive-epithelial-recovery-after-severe-intestinal-ischemia/#comments</comments>        <pubDate>Fri, 24 Jun 2022 18:22:05 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/c76856e7-a0c2-3baa-b5d0-0fc75c6616c9</guid>
                                    <description><![CDATA[<p>Get to know senior author Dr. Liara M. Gonzalez of North Carolina State University as she discusses the recently published paper entitled "HOPX+ injury-resistant intestinal stem cells drive epithelial recovery after severe intestinal ischemia" with EIC Prof. Mark Frey.  This paper supports that rISCs are resistant to ischemic injury and likely an important source of cellular renewal following near-complete epithelial loss. Furthermore, the authors have evidence that HOPX controls ISC activity state and may be a critical signaling pathway during ISC-mediated repair. Finally, they use multiple novel methods to evaluate ISCs in a translationally relevant large animal model of severe intestinal injury and provide evidence for the potential role of rISCs as therapeutic targets. </p>
<p>Amy Stieler Stewart, Cecilia Renee Schaaf, Jennifer A. Luff, John M. Freund, Thomas C. Becker, Sara R. Tufts, James B. Robertson, and Liara M. Gonzalez</p>
<p><a href='https://doi.org/10.1152/ajpgi.00165.2021'>https://doi.org/10.1152/ajpgi.00165.2021</a></p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Get to know senior author Dr. Liara M. Gonzalez of North Carolina State University as she discusses the recently published paper entitled "HOPX+ injury-resistant intestinal stem cells drive epithelial recovery after severe intestinal ischemia" with EIC Prof. Mark Frey.  This paper supports that rISCs are resistant to ischemic injury and likely an important source of cellular renewal following near-complete epithelial loss. Furthermore, the authors have evidence that <em>HOPX</em> controls ISC activity state and may be a critical signaling pathway during ISC-mediated repair. Finally, they use multiple novel methods to evaluate ISCs in a translationally relevant large animal model of severe intestinal injury and provide evidence for the potential role of rISCs as therapeutic targets. </p>
<p>Amy Stieler Stewart, Cecilia Renee Schaaf, Jennifer A. Luff, John M. Freund, Thomas C. Becker, Sara R. Tufts, James B. Robertson, and Liara M. Gonzalez</p>
<p><a href='https://doi.org/10.1152/ajpgi.00165.2021'>https://doi.org/10.1152/ajpgi.00165.2021</a></p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/ybie8s/GI_00165_2021_audiob6oe3.mp3" length="19265398" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Get to know senior author Dr. Liara M. Gonzalez of North Carolina State University as she discusses the recently published paper entitled "HOPX+ injury-resistant intestinal stem cells drive epithelial recovery after severe intestinal ischemia" with EIC Prof. Mark Frey.  This paper supports that rISCs are resistant to ischemic injury and likely an important source of cellular renewal following near-complete epithelial loss. Furthermore, the authors have evidence that HOPX controls ISC activity state and may be a critical signaling pathway during ISC-mediated repair. Finally, they use multiple novel methods to evaluate ISCs in a translationally relevant large animal model of severe intestinal injury and provide evidence for the potential role of rISCs as therapeutic targets. 
Amy Stieler Stewart, Cecilia Renee Schaaf, Jennifer A. Luff, John M. Freund, Thomas C. Becker, Sara R. Tufts, James B. Robertson, and Liara M. Gonzalez
https://doi.org/10.1152/ajpgi.00165.2021]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1534</itunes:duration>
                <itunes:episode>5</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: A new approach to treat gastrointestinal motility disorders</title>
        <itunes:title>Got Guts: A new approach to treat gastrointestinal motility disorders</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-a-new-approach-to-treat-gastrointestinal-motility-disorders/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-a-new-approach-to-treat-gastrointestinal-motility-disorders/#comments</comments>        <pubDate>Fri, 13 May 2022 14:48:20 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/a4bf2412-63ef-3889-9f15-676a4ea1b3df</guid>
                                    <description><![CDATA[<p class="reader-text-block__paragraph">Looking for a new pharmacological approach to treat gastrointestinal motility disorders?</p>
<p class="reader-text-block__paragraph">In this podcast authors Dr. Daniel Poole and Dr. Simona Carbone of Monash University discuss their recent paper, where they investigated the therapeutic potential of a positive allosteric modulator to enhance endogenous delta-opioid receptor signaling in the gut. Take a listen today! </p>
<p class="reader-text-block__paragraph">Jesse J. DiCello, Simona E. Carbone, Ayame Saito, Vi Pham, Agata Szymaszkiewicz, Arisbel B. Gondin, Sadia Alvi, Kiliana Marique, Priyank Shenoy, Nicholas A. Veldhuis, Jakub Fichna, Meritxell Canals, Arthur Christopoulos, Celine Valant, and Daniel P. Poole </p>
<p class="reader-text-block__paragraph"><a href='https://doi.org/10.1152/ajpgi.00297.2021'>https://doi.org/10.1152/ajpgi.00297.2021</a></p>
]]></description>
                                                            <content:encoded><![CDATA[<p class="reader-text-block__paragraph">Looking for a new pharmacological approach to treat gastrointestinal motility disorders?</p>
<p class="reader-text-block__paragraph">In this podcast authors Dr. Daniel Poole and Dr. Simona Carbone of Monash University discuss their recent paper, where they investigated the therapeutic potential of a positive allosteric modulator to enhance endogenous delta-opioid receptor signaling in the gut. Take a listen today! </p>
<p class="reader-text-block__paragraph">Jesse J. DiCello, Simona E. Carbone, Ayame Saito, Vi Pham, Agata Szymaszkiewicz, Arisbel B. Gondin, Sadia Alvi, Kiliana Marique, Priyank Shenoy, Nicholas A. Veldhuis, Jakub Fichna, Meritxell Canals, Arthur Christopoulos, Celine Valant, and Daniel P. Poole </p>
<p class="reader-text-block__paragraph"><a href='https://doi.org/10.1152/ajpgi.00297.2021'>https://doi.org/10.1152/ajpgi.00297.2021</a></p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/quywfh/GI_00297_2021_Audiobuq6k.mp3" length="19525642" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Looking for a new pharmacological approach to treat gastrointestinal motility disorders?
In this podcast authors Dr. Daniel Poole and Dr. Simona Carbone of Monash University discuss their recent paper, where they investigated the therapeutic potential of a positive allosteric modulator to enhance endogenous delta-opioid receptor signaling in the gut. Take a listen today! 
Jesse J. DiCello, Simona E. Carbone, Ayame Saito, Vi Pham, Agata Szymaszkiewicz, Arisbel B. Gondin, Sadia Alvi, Kiliana Marique, Priyank Shenoy, Nicholas A. Veldhuis, Jakub Fichna, Meritxell Canals, Arthur Christopoulos, Celine Valant, and Daniel P. Poole 
https://doi.org/10.1152/ajpgi.00297.2021]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1511</itunes:duration>
                <itunes:episode>4</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Unraveling the mysteries of stem cells in inflammatory bowel disease</title>
        <itunes:title>Unraveling the mysteries of stem cells in inflammatory bowel disease</itunes:title>
        <link>https://ajpgi.podbean.com/e/unraveling-the-mysteries-of-stem-cells-in-inflammatory-bowel-disease/</link>
                    <comments>https://ajpgi.podbean.com/e/unraveling-the-mysteries-of-stem-cells-in-inflammatory-bowel-disease/#comments</comments>        <pubDate>Thu, 28 Apr 2022 16:41:27 -0300</pubDate>
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                                    <description><![CDATA[<p>Three investigators at Children's Hospital Los Angeles, Nandini Girish, Dr. Cambrian Liu, and Dr. Brent Polk, talk about their recent work to visualize the fates and functions of epithelial stem cells in models of inflammatory bowel disease with Editor-in-Chief Professor Mark Frey. The investigators discuss their diverse backgrounds, reveal how they started the work, and begin a spirited debate on the relative values of minivans and dogs and cats.</p>
<p>Check out the manuscript associated with this podcast here:</p>
<p><a href='https://doi.org/10.1152/ajpgi.00248.2020'>https://doi.org/10.1152/ajpgi.00248.2020</a></p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Three investigators at Children's Hospital Los Angeles, Nandini Girish, Dr. Cambrian Liu, and Dr. Brent Polk, talk about their recent work to visualize the fates and functions of epithelial stem cells in models of inflammatory bowel disease with Editor-in-Chief Professor Mark Frey. The investigators discuss their diverse backgrounds, reveal how they started the work, and begin a spirited debate on the relative values of minivans and dogs and cats.</p>
<p>Check out the manuscript associated with this podcast here:</p>
<p><a href='https://doi.org/10.1152/ajpgi.00248.2020'>https://doi.org/10.1152/ajpgi.00248.2020</a></p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/nebza7/GI_00248_2020_Corrected_Intro7xl8m.mp3" length="20060278" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Three investigators at Children's Hospital Los Angeles, Nandini Girish, Dr. Cambrian Liu, and Dr. Brent Polk, talk about their recent work to visualize the fates and functions of epithelial stem cells in models of inflammatory bowel disease with Editor-in-Chief Professor Mark Frey. The investigators discuss their diverse backgrounds, reveal how they started the work, and begin a spirited debate on the relative values of minivans and dogs and cats.
Check out the manuscript associated with this podcast here:
https://doi.org/10.1152/ajpgi.00248.2020]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1596</itunes:duration>
                <itunes:episode>3</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: Behind the science with an Organoid Diva</title>
        <itunes:title>Got Guts: Behind the science with an Organoid Diva</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-behind-the-science-with-an-organoid-diva/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-behind-the-science-with-an-organoid-diva/#comments</comments>        <pubDate>Fri, 15 Apr 2022 14:09:13 -0300</pubDate>
        <guid isPermaLink="false">ajpgi.podbean.com/b34906e3-fd85-3156-ad0d-490ddf6b1bc2</guid>
                                    <description><![CDATA[<p>Many times we read a manuscript but don’t really get to know the amazing author behind the great science.  Behind those black typewritten letters that spell a scientists name lies a person that is usually creative, intelligent, quirky, and fun.  This is certainly the case with the author of “Use of human tissue stem cell-derived organoid cultures to model enterohepatic circulation”, Dr. Sarah Blutt.  Please listen in as we learn a little bit about one of the fields Organoid Divas and what makes her tick as we discuss organoids as a biological toll booth and other topics.</p>
<p>Check out the manuscript associated with this podcast here: https://doi.org/10.1152/ajpgi.00177.2021 </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Many times we read a manuscript but don’t really get to know the amazing author behind the great science.  Behind those black typewritten letters that spell a scientists name lies a person that is usually creative, intelligent, quirky, and fun.  This is certainly the case with the author of “Use of human tissue stem cell-derived organoid cultures to model enterohepatic circulation”, Dr. Sarah Blutt.  Please listen in as we learn a little bit about one of the fields Organoid Divas and what makes her tick as we discuss organoids as a biological toll booth and other topics.</p>
<p>Check out the manuscript associated with this podcast here: https://doi.org/10.1152/ajpgi.00177.2021 </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/f6umj6/GI_001772021893a7.mp3" length="11702206" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Many times we read a manuscript but don’t really get to know the amazing author behind the great science.  Behind those black typewritten letters that spell a scientists name lies a person that is usually creative, intelligent, quirky, and fun.  This is certainly the case with the author of “Use of human tissue stem cell-derived organoid cultures to model enterohepatic circulation”, Dr. Sarah Blutt.  Please listen in as we learn a little bit about one of the fields Organoid Divas and what makes her tick as we discuss organoids as a biological toll booth and other topics.
Check out the manuscript associated with this podcast here: https://doi.org/10.1152/ajpgi.00177.2021 ]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>902</itunes:duration>
                <itunes:episode>2</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>Got Guts: What’s Cooking at EB 2022</title>
        <itunes:title>Got Guts: What’s Cooking at EB 2022</itunes:title>
        <link>https://ajpgi.podbean.com/e/got-guts-what-s-cooking-at-eb-2022/</link>
                    <comments>https://ajpgi.podbean.com/e/got-guts-what-s-cooking-at-eb-2022/#comments</comments>        <pubDate>Mon, 28 Mar 2022 15:23:39 -0300</pubDate>
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                                    <description><![CDATA[<p>Welcome to AJP- Gastrointestinal Liver’s Physiology’s Podcast series, Got Guts? Our first episode is a  joint effort with Dr. Pradeep Dudeja, Chair of the GI and Liver Section and Dr. Karen Edelblum, Chair of GI and Liver Program Committee with host Editor-In-Chief, Professor Mark Frey. In this podcast we will be talking about all things Experimental Biology 2022. For more information on Experimental Biology 2022 please go to <a href='http://www.experimentalbiology.org'>www.experimentalbiology.org</a> . To learn more about the journal and section please go to <a href='http://www.physiology.org'>www.physiology.org</a>. If you are interested in submitting a manuscript and have questions, please email Jami Jones at <a href='mailto:jjones@physiology.org'>jjones@physiology.org</a> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>Welcome to AJP- Gastrointestinal Liver’s Physiology’s Podcast series, Got Guts? Our first episode is a  joint effort with Dr. Pradeep Dudeja, Chair of the GI and Liver Section and Dr. Karen Edelblum, Chair of GI and Liver Program Committee with host Editor-In-Chief, Professor Mark Frey. In this podcast we will be talking about all things Experimental Biology 2022. For more information on Experimental Biology 2022 please go to <a href='http://www.experimentalbiology.org'>www.experimentalbiology.org</a> . To learn more about the journal and section please go to <a href='http://www.physiology.org'>www.physiology.org</a>. If you are interested in submitting a manuscript and have questions, please email Jami Jones at <a href='mailto:jjones@physiology.org'>jjones@physiology.org</a> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/rvk8ps/GISection_Joint_Podcastb39l7.mp3" length="12203858" type="audio/mpeg"/>
        <itunes:summary><![CDATA[Welcome to AJP- Gastrointestinal Liver’s Physiology’s Podcast series, Got Guts? Our first episode is a  joint effort with Dr. Pradeep Dudeja, Chair of the GI and Liver Section and Dr. Karen Edelblum, Chair of GI and Liver Program Committee with host Editor-In-Chief, Professor Mark Frey. In this podcast we will be talking about all things Experimental Biology 2022. For more information on Experimental Biology 2022 please go to www.experimentalbiology.org . To learn more about the journal and section please go to www.physiology.org. If you are interested in submitting a manuscript and have questions, please email Jami Jones at jjones@physiology.org ]]></itunes:summary>
        <itunes:author>ajpgi</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>894</itunes:duration>
                <itunes:episode>1</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
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