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        <title>Am J Physiol Gastroi... via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Am J Physiol Gastroi...' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Am+J+Physiol+Gastroi...&t=Am+J+Physiol+Gastroi...&s=Search&f=source]]></link>
        <lastBuildDate>Fri, 19 Mar 2010 15:26:55 +0100</lastBuildDate>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +18 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3375024&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%29%2520AND%2520%25222010%252F03%252F14%252011.02%2522%255BMHDA%255D%253A%25222010%252F03%252F18%252004.54%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222010%252F03%252F14%252011.02%2522%255BEDAT%255D%29%29</link>
            <description>18 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These pubmed results were generated on 2010/03/18PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3375024</comments>
            <pubDate>Thu, 18 Mar 2010 08:54:02 +0100</pubDate>
            <guid isPermaLink="false">3375024</guid>        </item>
        <item>
            <title>Sox9-Expression Marks a Subset of CD24-expressing Small Intestine Epithelial Stem Cells that Form Organoids in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=3313828&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20185687%26dopt%3DAbstract</link>
            <description>Authors: Gracz AD, Ramalingam S, Magness ST
    The inability to identify, isolate, and culture intestinal epithelial stem cells (IESCs) has been prohibitive to the study and therapeutic utilization of these cells. Using a Sox9(EGFP) mouse model, we demonstrate that Sox9(EGFP) fluorescence signatures can be used to differentiate between and enrich for progenitors (Sox9(EGFPsubLo)) and multipotent IESCs (Sox9(EGFPlo)). Sox9(EGFPlo) cells generate 'organoids' in a recently defined culture system that mimics the native IESC niche. These organoids possess all four differentiated cell types of the small intestine epithelium demonstrating the multipotent capacity of Sox9(EGFPlo) cells. Our results are consistent with the previously reported observation that single IESCs generate crypt-like units...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3313828</comments>
            <pubDate>Thu, 25 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3313828</guid>        </item>
        <item>
            <title>Advances of Endomicroscopy for Gastrointestinal Physiology and Diseases.</title>
            <link>http://www.medworm.com/index.php?rid=3313826&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20185688%26dopt%3DAbstract</link>
            <description>Authors: Goetz M, Kiesslich R
    Confocal endomicroscopy is a novel technique that permits in vivo microscopy of the human gastrointestinal mucosa during ongoing endoscopy, thereby providing optical virtual biopsies. Endomicroscopy has been demonstrated to reveal histologic information in a multitude of diseases in the upper and lower gastrointestinal tract in vivo. Most studies have focused on inflammation and neoplasia, such as Barrett's esophagus, gastric cancer, celiac disease, Crohn's disease and ulcerative colitis, or colorectal neoplasias. Endomicroscopy allows obtaining &quot;smart&quot;, targeted biopsies from regions with microscopic alterations rather than having to rely on random untargeted tissue sampling. This reduces the number of biopsies while increasing the diagnostic yield. In ad...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3313826</comments>
            <pubDate>Thu, 25 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3313826</guid>        </item>
        <item>
            <title>Presynaptic inhibition of neural vasodilator pathways to submucosal arterioles by release of purines from sympathetic nerves.</title>
            <link>http://www.medworm.com/index.php?rid=3313825&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20185689%26dopt%3DAbstract</link>
            <description>This study examined whether release of sympathetic purines can modulate dilator nerves. In vitro submucosal preparations from guinea-pig ileum were modified to leave the parent mesenteric artery intact so that perivascular sympathetic and extrinsic afferent nerves could be activated by a bipolar stimulating electrode placed on the parent artery, and submucosal vasodilator neurons were activated using focal electrodes placed on submucosal ganglia. The outside diameter of submucosal arterioles was monitored using videomicroscopy and dilator responses were examined after preconstricting vessels 80-95 % with prostaglandin F2alpha (400 nM). Mesenteric nerve stimulation evoked a frequency-dependent dilation, with suramin (100 muM) present throughout to inhibit P2X receptor-mediated vasoconstrict...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3313825</comments>
            <pubDate>Thu, 25 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3313825</guid>        </item>
        <item>
            <title>Tetrahydrobiopterin (BH4), a cofactor for nNOS, restores gastric emptying and nNOS expression in female diabetic rats.</title>
            <link>http://www.medworm.com/index.php?rid=3313824&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20185690%26dopt%3DAbstract</link>
            <description>In this study, we have explored the role of tetrahydrobiopterin (BH4), a major co-factor for nNOSalpha activity and NO synthesis in diabetic gastroparesis. Diabetes was induced with single injection of streptozotocin (55 mg/Kg b.w, i.p.) in female rats, with experiments performed on week 3 or 9 following induction, with or without three week BH4 supplementation. Gastric pyloric BH4 levels were significantly decreased in diabetic female rats compared to control (18.6+/-1.45 vs. 31.0+/-2.31pmol/mg protein). In vitro studies on pyloric strips showed that 2, 4-diamino-6-hydroxypyrimidine (DAHP), an inhibitor of BH4 synthesis, significantly decreased NO release and nitrergic relaxation. Three week dietary supplementation of BH4 either from day 1 or 6 wk significantly attenuated diabetes-induced...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3313824</comments>
            <pubDate>Thu, 25 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3313824</guid>        </item>
        <item>
            <title>Differential Processing of Pro Glucose-Dependent Insulinotropic Polypeptide (ProGIP) in Gut.</title>
            <link>http://www.medworm.com/index.php?rid=3313823&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20185691%26dopt%3DAbstract</link>
            <description>Authors: Fujita Y, Asadi A, Yang GK, Kwok YN, Kieffer TJ
    Glucose-dependent insulinotropic polypeptide (GIP) is a hormone released from enteroendocrine K-cells in response to meals. Post-translational processing of the precursor protein proGIP at residue 65 by proprotein convertase subtilisin/kexin type 1 (PC1/3) in gut K-cells gives rise to the established 42 amino acid form of GIP (GIP(1-42)). However, the proGIP peptide sequence contains a consensus cleavage site for PC2 at residues 52-55 and we identified PC2 immunoreactivity in a subset of K-cells, suggesting the potential existence of a C-terminal truncated GIP isoform, GIP(1-30). Indeed a subset of mouse and human K-cells display GIP immunoreactivity with GIP antibodies directed to the mid portion of the peptide, but not with a C...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3313823</comments>
            <pubDate>Thu, 25 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3313823</guid>        </item>
        <item>
            <title>Amplification loop of the inflammatory process is induced by P2X7R activation in intestinal epithelial cells in response to neutrophil transepithelial migration.</title>
            <link>http://www.medworm.com/index.php?rid=3313820&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20185692%26dopt%3DAbstract</link>
            <description>Authors: Cesaro A, Brest P, Hofman V, H&amp;#xE9;buterne X, Wildman S, Ferrua B, Marchetti S, Doglio A, Vouret-Craviari V, Galland F, Naquet P, Mograbi B, Unwin RJ, Hofman PM
    Inflammatory bowel diseases (IBD) are characterized during their active phase by polymorphonuclear leukocyte (PMNL) transepithelial migration. The efflux of PMNL into the mucosa is associated with the production of pro-inflammatory cytokines and the release of ATP from damaged and necrotic cells. The expression and function of purinergic P2X(7) receptors (P2X(7)R) in intestinal epithelial cells (IEC), and its potential role in the 'cross-talk' between IEC and PMNL, have not been explored. The aims of the present study were: i) to examine P2X(7)R expression in IEC (T84 cells) and in human intestinal biopsies; ii) to de...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3313820</comments>
            <pubDate>Thu, 25 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3313820</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +25 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3292243&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%29%2520AND%2520%25222010%252F02%252F16%252004.56%2522%255BMHDA%255D%253A%25222010%252F02%252F21%252019.58%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222010%252F02%252F16%252004.56%2522%255BEDAT%255D%29%29</link>
            <description>25 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These pubmed results were generated on 2010/02/21PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3292243</comments>
            <pubDate>Mon, 22 Feb 2010 00:58:03 +0100</pubDate>
            <guid isPermaLink="false">3292243</guid>        </item>
        <item>
            <title>Impaired Cardiovascular Function in Primary Biliary Cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=3247466&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20133949%26dopt%3DAbstract</link>
            <description>Conclusion: Our findings suggest the presence of altered myocardial function in PBC. Autonomic &quot;dysfunction&quot; may, rather than being an abnormal process, represent a compensatory mechanism to increase cardiac return to mitigate these effects.
    PMID: 20133949 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247466</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247466</guid>        </item>
        <item>
            <title>Comparison of Human and Porcine Gastric Clasp and Sling Fiber Contraction by M2 and M3 Muscarinic Receptors.</title>
            <link>http://www.medworm.com/index.php?rid=3247465&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20133950%26dopt%3DAbstract</link>
            <description>Authors: Vegesna AK, Braverman AS, Miller LS, Tallarida RJ, Tiwana MI, Khayyam U, Ruggieri MR
    To compare the gastroesophageal junction of the human with the pig, M(2) and M(3) receptor densities and the potencies of M(2) and M(3) muscarinic receptor subtype selective antagonists were determined in gastric clasp and sling smooth muscle fibers. Total muscarinic and M(2) receptors are higher in pig than human clasp and sling fibers. M(3) receptors are higher in human compared to pig sling fibers but lower in human compared to pig clasp fibers. Clasp fibers have fewer M(3) receptors than sling fibers in both humans and pigs. Similar to human clasp fibers, pig clasp fibers contract significantly less than pig sling fibers. Analysis of the methoctramine Schild plot suggests that M(2) recepto...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247465</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247465</guid>        </item>
        <item>
            <title>Insulin-like growth factors are more effective than progastrin in reversing pro-apoptotic effects of curcumin: Critical role of p38MAPK.</title>
            <link>http://www.medworm.com/index.php?rid=3247464&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20133951%26dopt%3DAbstract</link>
            <description>Authors: Singh P, Sarkar S, Umar S, Rengifo-Cam W, Singh AP, Wood TG
    Progastrin and insulin-like-growth-factors (IGFs) stimulate hyperproliferation of intestinal epithelial cells (IECs) via endocrine/paracrine routes; hyperproliferation is a known risk factor for colon carcinogenesis. In the current study, inhibitory potency of curcumin in the presence or absence of progastrin/IGF-II was examined. Progastrin and IGF-II significantly increased proliferation of an immortalized IEC cell line, IEC-18, while Curcumin decreased the proliferation in a dose-dependent manner. IGF-II was significantly more effective than progastrin in reversing anti-proliferative effects of curcumin, and reversed pro-apoptotic effects of curcumin by &amp;gt;80%; progastrin was relatively ineffective towards reversin...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247464</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247464</guid>        </item>
        <item>
            <title>Cooperation between HNF-1{alpha}, Cdx2 and GATA-4 in initiating an enterocytic differentiation program in a normal, human intestinal progenitor cell line.</title>
            <link>http://www.medworm.com/index.php?rid=3247463&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20133952%26dopt%3DAbstract</link>
            <description>Authors: Benoit YD, Par&amp;#xE9; F, Francoeur C, Jean D, Tremblay E, Boudreau F, Escaffit F, Beaulieu JF
    In the intestinal epithelium, the Cdx, GATA and HNF transcription factor families are responsible for the expression of differentiation markers such as sucrase-isomaltase. Although previous studies have shown that Cdx2 can induce differentiation in rat intestinal IEC-6 cells, no data are available concerning the direct implication of transcription factors on differentiation in human normal intestinal epithelial cell types. We investigated the role of Cdx2, GATA-4 and HNF-1alpha using the undifferentiated human intestinal epithelial crypt cell line HIEC. These transcription factors were tested on proliferation and expression of polarization and differentiation markers. Ectopic expressio...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247463</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247463</guid>        </item>
        <item>
            <title>Stress granule formation mediates the inhibition of colonic Hsp70 translation by interferon gamma and tumor necrosis factor alpha.</title>
            <link>http://www.medworm.com/index.php?rid=3221711&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20110459%26dopt%3DAbstract</link>
            <description>Authors: Hu S, Claud EC, Musch MW, Chang EB
    Mucosal inflammation, through cytokines like interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha), has many effects on the intestinal epithelium, including selective translational inhibition of the cytoprotective protein heat shock protein 70 (Hsp70). To further elucidate the mechanisms underlying this effect, we examined the role of stress granules in mediating the actions of these pro-inflammatory cytokines. Using conditionally-immortalized young adult mouse colonic epithelial cells, we demonstrate that IFN-gamma and TNF-alpha, which up-regulate eukaryotic initiation factor-alpha (eIF-2alpha) phosphorylation and reduce Hsp70 translation, significantly enhance stress granule formation in heat-shocked intestinal epithelial...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3221711</comments>
            <pubDate>Thu, 28 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3221711</guid>        </item>
        <item>
            <title>Hemochromatosis and pregnancy: Iron stores in the Hfe-/- mouse are not reduced by multiple pregnancies.</title>
            <link>http://www.medworm.com/index.php?rid=3221710&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20110460%26dopt%3DAbstract</link>
            <description>In conclusion, multiple pregnancies do not reduce body iron stores in Hfe-/- mice.
    PMID: 20110460 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3221710</comments>
            <pubDate>Thu, 28 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3221710</guid>        </item>
        <item>
            <title>AE2 Cl-/HCO3- Exchanger is Required for Normal cAMP-stimulated Anion Secretion in Murine Proximal Colon.</title>
            <link>http://www.medworm.com/index.php?rid=3221703&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20110461%26dopt%3DAbstract</link>
            <description>Authors: Gawenis LR, Bradford EM, Alper SL, Prasad V, Shull GE
    Anion secretion by colonic epithelium is dependent on apical CFTR-mediated anion conductance and basolateral ion transport. In many tissues, the NKCC1 Na(+)-K(+)-2Cl(-) cotransporter mediates basolateral Cl(-) uptake. However, additional evidence suggests that the AE2 Cl(-)/HCO(3)(-) exchanger, when coupled with the NHE1 Na(+)/H(+) exchanger or a Na(+)-HCO(3)(-) cotransporter (NBC), contributes to HCO(3)(-) and/or Cl(-) uptake. To analyze the secretory functions of AE2 in proximal colon, short-circuit current (I(sc)) responses to cAMP and inhibitors of basolateral anion transporters were measured in muscle-stripped wild-type (WT) and AE2-null (AE2(-/-)) proximal colon. In physiologic Ringers, the magnitude of cAMP-stimulate...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3221703</comments>
            <pubDate>Thu, 28 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3221703</guid>        </item>
        <item>
            <title>Transgenic expression of pancreatic secretory trypsin inhibitor-1 rescues SPINK3 deficient mice and restores a normal pancreatic phenotype.</title>
            <link>http://www.medworm.com/index.php?rid=3221702&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20110462%26dopt%3DAbstract</link>
            <description>Authors: Romac JM, Ohmuraya M, Bittner C, Majeed MF, Vigna SR, Que J, Fee BE, Wartmann T, Yamamura KI, Liddle RA
    Endogenous trypsin inhibitors are synthesized, stored and secreted by pancreatic acinar cells. It is believed that they play a protective role in the pancreas by inhibiting trypsin within the cell should trypsinogen become prematurely activated. Rodent trypsin inhibitors are highly homologous to human serine protease inhibitor Kazal-type 1 (SPINK1). The mouse has one pancreatic trypsin inhibitor known as SPINK3 while the rat has two trypsin inhibitors commonly known as pancreatic secretory trypsin inhibitors I and II (PSTI-I and -II). Rat PSTI-I is a 61 amino acid protein that shares 65% sequence identity with mouse SPINK3. It was recently demonstrated that mice with genetic...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3221702</comments>
            <pubDate>Thu, 28 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3221702</guid>        </item>
        <item>
            <title>miR-221 suppresses ICAM-1 translation and regulates interferon-gamma-induced ICAM-1 expression in human cholangiocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3221701&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20110463%26dopt%3DAbstract</link>
            <description>In this study, we tested the involvement of miRNA-mediated posttranscriptional regulation in IFN-gamma-induced ICAM-1 expression in cholangiocytes. Using both immortalized and non-immortalized human cholangiocyte cell lines, we found that IFN-gamma activated ICAM-1 transcription and increased ICAM-1 protein expression. Inhibition of ICAM-1 transcription could only partially block IFN-gamma-induced ICAM-1 expression at the protein level. In silico target prediction analysis revealed complementarity of miR-221 to the 3'-untranslated region of ICAM-1 mRNA. Targeting of ICAM-1 3'-untranslated region by miR-221 resulted in translational repression in cholangiocytes, but not ICAM-1 mRNA degradation. Functional inhibition of miR-221 with anti-miR-221 induced ICAM-1 protein expression. Moreover, I...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3221701</comments>
            <pubDate>Thu, 28 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3221701</guid>        </item>
        <item>
            <title>Green Tea Catechin (-)-Epigallocatechin-3-Gallate (EGCG) Inhibits Ileal Apical Sodium Bile Acid Transporter ASBT.</title>
            <link>http://www.medworm.com/index.php?rid=3156886&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056894%26dopt%3DAbstract</link>
            <description>In conclusion, our data demonstrate a novel role of lipid rafts in the modulation of ASBT function by the dietary component EGCG, which may underlie the hypocholesterolemic of green tea.
    PMID: 20056894 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3156886</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3156886</guid>        </item>
        <item>
            <title>The impact of elevation of total bilirubin level and etiology of the liver disease on serum N-glycosylation patterns in mice and men.</title>
            <link>http://www.medworm.com/index.php?rid=3156885&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056895%26dopt%3DAbstract</link>
            <description>Authors: Blomme BA, Van Steenkiste C, Vanhuysse J, Colle I, Callewaert N, Van Vlierberghe H
    The GlycoFibroTest and GlycoCirrhoTest are non-invasive alternatives for liver biopsy that can be used as a follow-up tool for fibrosis patients and to diagnose cirrhotic patients, respectively. These tests are based on the altered N-glycosylation of total serum protein. Our aim was to investigate the impact of etiology on the alteration of N-glycosylation and if other characteristics of liver patients could have an influence on N-glycosylation. In human liver patients, no specific alteration could be found to make a distinction according to etiological factor, although alcoholic patients had a significant higher mean value for the GlycoCirrhioTest. Undergalactosylation did not show a significan...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3156885</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3156885</guid>        </item>
        <item>
            <title>Macrophage-mediated phagocytosis of apoptotic cholangiocytes contributes to reversal of experimental biliary fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=3156884&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056896%26dopt%3DAbstract</link>
            <description>Conclusions: Reconstruction of bile flow after BDL leads to an orchestrated fibrolytic program that results in near complete reversal of advanced fibrosis. The peak of connective tissue remodeling and fibrolytic activity is associated with massive apoptosis of cholangiocytes and their phagocytic clearance by macrophages in vivo. Macrophages upregulate MMPs and become fibrolytic effector cells upon apoptotic cholangiocyte engulfment in vitro, suggesting that phagocytosis-associated MMP induction in macrophages significantly contributes to biliary fibrosis reversal.
    PMID: 20056896 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3156884</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3156884</guid>        </item>
        <item>
            <title>15-Deoxy-{Delta}12,14-Prostaglandin J2 prevents inflammatory response and endothelial cell damage in rats with acute obstructive cholangitis.</title>
            <link>http://www.medworm.com/index.php?rid=3156883&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056897%26dopt%3DAbstract</link>
            <description>Conclusion: These results clearly demonstrate that 15D-PGJ(2) inhibits the inflammatory response and endothelial cell damage seen in acute obstructive cholangitis, and could contribute to improve the outcome of this pathology.
    PMID: 20056897 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3156883</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3156883</guid>        </item>
        <item>
            <title>Transient Outward Potassium Current In ICC.</title>
            <link>http://www.medworm.com/index.php?rid=3156882&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056898%26dopt%3DAbstract</link>
            <description>Authors: Parsons SP, Huizinga JD
    Interstitial cells of Cajal are the pacemakers of the gut, initiating slow wave activity. Several ion channels have been identified that contribute to the depolarization phase of the slow wave. Our aim was to contribute to knowledge about the identity and role of ICC potassium channels in pacemaking. Here we describe a transient outward potassium current in cell-attached patches of ICC. This current was activated almost instantaneously at potentials positive of the resting membrane potential and inactivated as a single- or bi-exponential with time constants that varied widely from patch to patch. Averaged traces gave a bi-exponential inactivation with time constants of ~40 ms and ~500 ms, with no clear voltage dependence. Analysis of single-channel open...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3156882</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3156882</guid>        </item>
        <item>
            <title>Neurophysiological evaluation of convergent afferents innervating the human esophagus and area of referred pain on the anterior chest wall.</title>
            <link>http://www.medworm.com/index.php?rid=3108896&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20023227%26dopt%3DAbstract</link>
            <description>Authors: Hobson AR, Chizh B, Hicks K, Aziz Q, Worthen S, Lawrence P, Dewit O, Boyle Y, Dukes G
    Noxious stimuli in the esophagus cause pain that is referred to the anterior chest wall because of convergence of visceral and somatic afferents within the spinal cord. We sought to characterize the neurophysiological responses of these convergent spinal pain pathways in humans by studying 12 healthy subjects over three visits (V1, V2, and V3). Esophageal pain thresholds (Eso-PT) were assessed by electrical stimulation and anterior chest wall pain thresholds (ACW-PT) by use of a contact heat thermode. Esophageal evoked potentials (EEP) were recorded from the vertex following 200 electrical stimuli, and anterior chest wall evoked potentials (ACWEP) were recorded following 40 heat pulses. The f...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3108896</comments>
            <pubDate>Tue, 22 Dec 2009 13:26:05 +0100</pubDate>
            <guid isPermaLink="false">3108896</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +29 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3101507&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%29%2520AND%2520%25222009%252F12%252F05%252015.56%2522%255BMHDA%255D%253A%25222009%252F12%252F18%252015.22%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F12%252F05%252015.56%2522%255BEDAT%255D%29%29</link>
            <description>29 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These pubmed results were generated on 2009/12/18PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101507</comments>
            <pubDate>Fri, 18 Dec 2009 20:22:02 +0100</pubDate>
            <guid isPermaLink="false">3101507</guid>        </item>
        <item>
            <title>Signaling in TRPV1 induced platelet activating factor (PAF) in human esophageal epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=3060067&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19959817%26dopt%3DAbstract</link>
            <description>Authors: Ma J, Harnett KM, Behar J, Biancani P, Cao W
    TRPV1 receptors were identified in HET-1A cells by RT-PCR, and by Western blot. In Fura-2AM loaded cells, the TRPV1 agonist capsaicin caused a 4-fold cytosolic calcium increase, supporting a role of TRPV1 as a capsaicin-activated cation channel. Capsaicin increased production of PAF, an important inflammatory mediator that acts as a chemoattractant and activator of immune cells. The increase was reduced by the p38 MAP kinase (p38) inhibitor SB203580, by the cytosolic phospholipase A2 (cPLA2) inhibitor AACOCF3 and by the lyso-PAF acetyltransferase inhibitor sanguinarin, indicating that capsaicin-induced PAF production may be mediated by activation of cPLA2, p38 and lyso-PAF acetyltransferase. To establish a sequential signaling pathw...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3060067</comments>
            <pubDate>Thu, 03 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3060067</guid>        </item>
        <item>
            <title>The mechanisms underlying the generation of the colonic migrating motor complex in both wild-type and nNOS knockout mice.</title>
            <link>http://www.medworm.com/index.php?rid=3060066&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19959818%26dopt%3DAbstract</link>
            <description>Authors: Dickson EJ, Heredia DJ, McCann CJ, Hennig GW, Smith TK
    Colonic migrating motor complexes (CMMCs) propel fecal contents and are altered in diseased states, including slow transit constipation. However, the mechanisms underlying the CMMC are controversial, since it has been proposed that 'disinhibition' (turning off of inhibitory neurotransmission) or excitatory nerve activity generate the CMMC. Therefore our aims were to reexamine the mechanisms underlying the CMMC in the colon of wild-type and nNOS (-/-) mice. CMMCs were recorded from the isolated murine large bowel using intracellular recordings of electrical activity from circular muscle (CM) combined with tension recording. Spontaneous CMMCs occurred in both wild type (frequency: 0.3 c/min) and nNOS(-/-) mice (frequency: 0....</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3060066</comments>
            <pubDate>Thu, 03 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3060066</guid>        </item>
        <item>
            <title>Expression of Transient Receptor Potential Channels and Two-pore Potassium Channels in Subtypes of Vagal Afferent Neurons in Rat.</title>
            <link>http://www.medworm.com/index.php?rid=3060065&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19959819%26dopt%3DAbstract</link>
            <description>In this study we explored the distribution of these channels in vagal afferents by quantitative PCR after a capsaicin treatment to eliminate capsaicin-sensitive neurons, and by single-cell PCR measurements in vagal afferent neurons cultured after retrograde labeling from the stomach or duodenum. We found that TRPC1/3/5/6, TRPV1-4, TRPM8, TRPA1, TWIK2, TRAAK, TREK1, and TASK1/2 were all present in rat nodose ganglia. Both lesion results and single-cell PCR results suggested that TRPA1 and TRPC1 were preferentially expressed in neurons that were either capsaicin-sensitive or TRPV1-positive. Expression of TRPM8 varied dynamically after various manipulations, which perhaps explains the disparate results obtained by different investigators. Last, we also examined ion channel distribution with t...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3060065</comments>
            <pubDate>Thu, 03 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3060065</guid>        </item>
        <item>
            <title>Mechanisms of Lysophosphatidic acid (LPA) Mediated Stimulation of Intestinal Apical Cl-/OH- Exchange.</title>
            <link>http://www.medworm.com/index.php?rid=3004814&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19910524%26dopt%3DAbstract</link>
            <description>Authors: Singla A, Dwivedi A, Saksena S, Gill RK, Alrefai WA, Ramaswamy K, Dudeja PK
    Lysophosphatidic acid (LPA), a potent bioactive phospholipid, is a natural component of food products like soy and egg yolk. LPA modulates a number of epithelial functions and has been shown to inhibit cholera toxin induced diarrhea. Anti-diarrheal effects of LPA are known to be mediated by inhibiting chloride secretion. However, the effects of LPA on chloride absorption in the mammalian intestine are not known. The present studies examined the effects of LPA on apical Cl(-)/OH(-) exchangers known to be involved in chloride absorption in intestinal epithelial cells. Caco-2 cells were treated with LPA and Cl(-)/OH(-) exchange activity was measured as DIDS-sensitive (36)Cl(-) uptake. Cell surface biotiny...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3004814</comments>
            <pubDate>Thu, 12 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3004814</guid>        </item>
        <item>
            <title>A Model of the Isolated Perfused Rat Small Intestine.</title>
            <link>http://www.medworm.com/index.php?rid=3004813&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19910525%26dopt%3DAbstract</link>
            <description>Authors: Lautenschl&amp;#xE4;ger I, Dombrowsky H, Frerichs I, Kuchenbecker SC, Bade S, Schultz H, Zabel P, Scholz J, Weiler N, Uhlig S
    Intestinal edema remains a serious clinical problem and novel approaches to study its pathophysiology are needed. It was our aim to develop a long term stable isolated perfused rat small bowel preparation permitting analysis of vascular, luminal, interstitial and lymphatic compartments and to demonstrate the utility of this model by studying the effects of the pro-inflammatory mediator platelet-activating factor (PAF). A temperature-controlled chamber with an integrated balance was designed to perfuse isolated intestines through the mesenteric artery and the gut lumen. Steroids or oxygen carriers were not needed. Functional and morphological integrity of th...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3004813</comments>
            <pubDate>Thu, 12 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3004813</guid>        </item>
        <item>
            <title>Synergistic Anti-Fibrotic Efficacy of Statin and Protein Kinase C Inhibitor in Hepatic Fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=3004812&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19910526%26dopt%3DAbstract</link>
            <description>In conclusion, simultaneous treatment with statin and PKC inhibitor synergistically enhanced the anti-fibrotic efficacy in both in vitro and in vivo models of hepatic fibrosis and may therefore have therapeutic implication for reducing hepatic fibrosis.
    PMID: 19910526 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3004812</comments>
            <pubDate>Thu, 12 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3004812</guid>        </item>
        <item>
            <title>Relationship between gene expression of duodenal iron transporters and iron stores in hemochromatosis subjects.</title>
            <link>http://www.medworm.com/index.php?rid=2970890&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19892936%26dopt%3DAbstract</link>
            <description>RELATIONSHIP BETWEEN GENE EXPRESSION OF DUODENAL IRON TRANSPORTERS AND IRON STORES IN HEMOCHROMATOSIS SUBJECTS.
    Am J Physiol Gastrointest Liver Physiol. 2009 Nov 5;
    Authors: Nelson JE, Mugford VR, Kilcourse E, Wang R, Kowdley KV
    To test the hypothesis that differences in duodenal iron absorption may explain the variable phenotypic expression among HFE C282Y homozygotes, we have compared relative gene expression of duodenal iron transporters among C282Y homozygotes (HH) with and without iron overload. Duodenal biopsy samples were analyzed using real time PCR for expression of DMT1, FPN1, DCYTB and HEPH relative to GAPDH from 23 C282Y homozygotes, including 5 &quot;non-expressors&quot; (serum ferritin&amp;lt;ULN and absence of phenotypic features of hemochromatosis) and 18 &quot;expressors&quot;. Four s...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970890</comments>
            <pubDate>Thu, 05 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2970890</guid>        </item>
        <item>
            <title>Mounting evidence against the role of ICC in neurotransmission to smooth muscle in the gut.</title>
            <link>http://www.medworm.com/index.php?rid=2970889&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19892937%26dopt%3DAbstract</link>
            <description>Authors: Goyal RK, Chaudhury A
    How nerves transmit their signals to regulate activity of smooth muscle is of fundamental importance to autonomic and enteric physiology, clinical medicine and therapeutics. A traditional view of neurotransmission to smooth muscles has been that motor nerve varicosities release neurotransmitters that act on receptors on smooth muscles to cause their contraction or relaxation via electromechanical and phamacomechanical signaling pathways in the smooth muscle. In recent years, an old hypothesis that certain interstitial cells of Cajal (ICC) may transduce neural signals to smooth muscle cells has been resurrected. This later hypothesis is based on indirect evidence of closer proximity and presence of synapses between the nerve varicosities and ICC, gap junct...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970889</comments>
            <pubDate>Thu, 05 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2970889</guid>        </item>
        <item>
            <title>Peripheral peptide YY inhibits propulsive colonic motor function through Y2 receptor in conscious mice.</title>
            <link>http://www.medworm.com/index.php?rid=2970888&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19892938%26dopt%3DAbstract</link>
            <description>Authors: Wang L, Gourcerol G, Yuan PQ, Wu SV, Million M, Larauche M, Tach&amp;#xE9; Y
    Peptide YY (PYY) antisecretory effect on intestinal epithelia is well established while less is known about its actions to influence colonic motility in conscious animals. We characterized changes in basal and stimulated colonic motor function induced by PYY-related peptides in conscious mice. PYY(3-36), PYY and neuropeptipde Y (NPY) (8 nmol/kg) injected intraperitoneally (ip) inhibited fecal pellet output (FPO)/h during novel environment stress by 90%, 63% and 57% respectively while the Y(1) preferring agonists, [Pro(34)]PYY and [Leu(31),Pro(34)]NPY had no effect. Corticotrophin-releasing factor 2 receptor antagonist did not alter PYY(3-36) inhibitory action. PYY and PYY(3-36) significantly reduced restr...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970888</comments>
            <pubDate>Thu, 05 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2970888</guid>        </item>
        <item>
            <title>Food restriction, refeeding, and gastric fill fail to affect emesis in musk shrews.</title>
            <link>http://www.medworm.com/index.php?rid=2970887&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19892939%26dopt%3DAbstract</link>
            <description>Authors: Horn CC, Still L, Fitzgerald C, Friedman MI
    Nausea and emesis are common side effects of gastrointestinal disease. Reports indicate that ghrelin and endocannabinoids, agents that stimulate appetite, also reduce emesis evoked by chemotherapy treatment, which suggests that stimulation of feeding inhibits the emetic system. In the following study we conducted a more direct test of this hypothesis by determining the impact of manipulating the motivation to eat on emesis, using food restriction and refeeding. Emesis was induced in musk shrews, a commonly used animal model for emesis research, using the cancer chemotherapy agent cisplatin (20 mg/kg, ip), nicotine (2 mg/kg, sc), or motion (1 Hz, horizontal, 4 cm displacement), because these treatments are known to target separate eme...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970887</comments>
            <pubDate>Thu, 05 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2970887</guid>        </item>
        <item>
            <title>Liver fibrosis causes down-regulation of miRNA-150 and miRNA-194 in hepatic stellate cells and their over-expression causes decreased stellate cell activation.</title>
            <link>http://www.medworm.com/index.php?rid=2970886&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19892940%26dopt%3DAbstract</link>
            <description>Authors: Venugopal SK, Jiang J, Kim TH, Li Y, Wang SS, Torok NJ, Wu J, Zern MA
    Activation of hepatic stellate cells (HSC) results in their proliferation and in the secretion of extracellular matrix (ECM) proteins, which leads to hepatic fibrosis. microRNAs (miRNAs) have been shown to regulate various cell functions, such as proliferation, differentiation and apoptosis. Hence, we have analyzed the miRNAs that were differentially expressed in HSC isolated from sham-operated and bile duct-ligated rats. Expression of two miRNAs, miRNA-150 and miRNA-194, was reduced in HSC isolated from fibrotic rats compared with sham-operated animals. These two miRNAs were over-expressed in LX-2 cells and their ability to inhibit cell proliferation, the expression of smooth muscle alpha-actin (SMA), a mar...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970886</comments>
            <pubDate>Thu, 05 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2970886</guid>        </item>
        <item>
            <title>Divergent Effects of Amygdala Glucocorticoid and Mineralocorticoid Receptors in the Regulation of Visceral and Somatic Pain.</title>
            <link>http://www.medworm.com/index.php?rid=2947126&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19875699%26dopt%3DAbstract</link>
            <description>Authors: Myers B, Greenwood-Van Meerveld B
    Elevated amygdala activity and increased responsiveness of the hypothalamic-pituitary-adrenal axis have been observed in irritable bowel syndrome (IBS) patients. Recently, we demonstrated that corticosterone (CORT) placed on the amygdala induced anxiety-like behavior coupled with decreased thresholds for visceral and somatic pain in rats. Moreover, these studies suggested that the effects of CORT were dependent on both the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR); however, the specific contributions of these receptors to the interaction between corticosteroids and the amygdala are still unclear. In the current study, we sought to define the distinct roles of amygdaloid GR and MR in anxiety-like behavior, visceral sensit...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2947126</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2947126</guid>        </item>
        <item>
            <title>Roles of Stem Cell Factor on the Depletion of Interstitial Cells of Cajal in the Colon of Diabetic Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2947125&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19875700%26dopt%3DAbstract</link>
            <description>Authors: Lin L, Xu LM, Zhang W, Ge YB, Tang YR, Zhang HJ, Li XL, Chen JD
    The aim of this study was to investigate the effects of stem cell factor (SCF) on ICC depletion in the colon of diabetic mice. Male C57/BL6 mice were treated by a single dose intraperitoneal injection of Streptozotocin (STZ), and those displayed sustained high blood glucose were selected as diabetes mellitus (DM) models. Six groups of mice were used: three groups of normal non-diabetic mice (untreated and treated with IgG or SCF antibody), and three gourps of diabetic mice (untreated and treated with vehicle or SCF. Changes of the ICC quantities were analyzed by immunohistochemistry. ICC morphologies were observed with transmission electron microscopy. The SCF levels in sera and colon tissues were detected by ELIS...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2947125</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2947125</guid>        </item>
        <item>
            <title>JNK mitogen-activated protein kinase limits calcium-dependent chloride secretion across colonic epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=2947122&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19875701%26dopt%3DAbstract</link>
            <description>Authors: Donnellan F, Keating N, Geoghegan P, Murray FE, Harvey BJ, Keely SJ
    Neuroimmune agonists induce epithelial Cl(-) secretion through elevations in intracellular Ca(2+) or cAMP. Previously, we demonstrated that epidermal growth factor receptor (EGFR) transactivation and subsequent ERK MAPK activation limits secretory responses to Ca(2+)-, but not cAMP-dependent agonists. Although c-Jun N-terminal kinase (JNK) MAPKs are also expressed in epithelial cells, their role in regulating transport function is unknown. Here, we investigated the potential role for JNK in regulating Cl(-) secretion in T(84) colonic epithelial cells. Western blot analysis revealed that a prototypical Ca(2+)-dependent secretagogue, carbachol (CCh; 100 microM), induced phosphorylation of both the 46kDa and 54kD...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2947122</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2947122</guid>        </item>
        <item>
            <title>A role for Campylobacter jejuni-induced enteritis in inflammatory bowel disease?</title>
            <link>http://www.medworm.com/index.php?rid=2947120&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19875702%26dopt%3DAbstract</link>
            <description>Authors: Kalischuk LD, Buret AG
    The inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis, are T cell-mediated diseases that are characterized by chronic, relapsing inflammation of the intestinal tract. The pathogenesis of IBD involves the complex interaction between the intestinal microflora, host genetic and immune factors, and environmental stimuli. Epidemiological analyses have implicated acute bacterial enteritis as one of the factors that may incite or exacerbate IBD in susceptible individuals. In this review, we examine how interactions between the common enteric pathogen Campylobacter jejuni, the host intestinal epithelium, and resident intestinal microflora may contribute to the pathogenesis of IBD. Recent experimental evidence indicates that C. jejuni may ...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2947120</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2947120</guid>        </item>
        <item>
            <title>Kupffer cell activation is a causal factor for hepatic insulin resistance.</title>
            <link>http://www.medworm.com/index.php?rid=2947114&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19875703%26dopt%3DAbstract</link>
            <description>Conclusion: Our study clearly shows that hepatic macrophage response participates to the onset of high fat diet-induced hepatic insulin resistance and may therefore represent an attractive target for prevention and treatment of diet- and obesity-induced insulin resistance.
    PMID: 19875703 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2947114</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2947114</guid>        </item>
        <item>
            <title>IL-22 is involved in liver regeneration after hepatectomy.</title>
            <link>http://www.medworm.com/index.php?rid=2947112&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19875704%26dopt%3DAbstract</link>
            <description>Conclusions: These data suggest that IL-22 is involved in liver regeneration and this may be due to interaction with IL-6- and TGF-alpha cascades.
    PMID: 19875704 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2947112</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2947112</guid>        </item>
        <item>
            <title>Transient Receptor Potential Ankyrin-1 has a Major Role in Mediating Visceral Pain in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2947111&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19875705%26dopt%3DAbstract</link>
            <description>Authors: Cattaruzza F, Spreadbury I, Miranda-Morales M, Grady EF, Vanner SJ, Bunnett NW
    The excitatory ion channel transient receptor potential ankyrin-1 (TRPA1) is prominently expressed by primary afferent neurons and is a mediator of inflammatory pain. Inflammatory agents can directly activate (e.g. hydroxynonenal [HNE], prostaglandin metabolites) or indirectly sensitize (e.g. agonists of protease-activated receptor [PAR(2)]) TRPA1 to induce somatic pain and hyperalgesia. However, the contribution of TRPA1 to visceral pain is unknown. We investigated the role of TRPA1 in visceral hyperalgesia by measuring abdominal visceromotor responses (VMR) to colorectal distention (CRD) after intracolonic administration of TRPA1 agonists (mustard oil [MO], HNE), sensitizing agents (PAR(2) activat...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2947111</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2947111</guid>        </item>
        <item>
            <title>Neurotransmission in Lower Esophageal Sphincter of W/Wv Mutant Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2925202&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19850967%26dopt%3DAbstract</link>
            <description>Authors: Zhang Y, Carmichael SA, Wang XY, Huizinga JD, Paterson WG
    To address the controversy surrounding the role of interstitial Cells of Cajal (ICC) in nitrergic neurotransmission to gastrointestinal smooth muscle, circular smooth muscle from the lower esophageal sphincter (LES) of W/W(v) wild-type and mutant (ICC-deficient) mice were studied using intracellular and tension recordings in vitro. Resting membrane potential (MP) was more negative and the spontaneous unitary potentials diminished in mutant mice. In wild-type mice, nerve stimulation induced a biphasic inhibitory junction potential (IJP) consisting of a fast initial IJP followed by a long-lasting slow IJP (LSIJP). The IJP was markedly impaired in a significant proportion of mutant mice, whereas in others it was normal. Ph...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2925202</comments>
            <pubDate>Thu, 22 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2925202</guid>        </item>
        <item>
            <title>Inflammatory cells regulate p53 and caspases in acute pancreatitis.</title>
            <link>http://www.medworm.com/index.php?rid=2925201&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19850968%26dopt%3DAbstract</link>
            <description>Authors: Nakamura Y, Do JH, Yuan J, Odinokova IV, Mareninova OA, Gukovskaya AS, Pandol SJ
    The inflammatory response during pancreatitis regulates necrotic and apoptotic rates of parenchymal cells. Neutrophil depletion using anti-polymorphonuclear serum (anti-PMN) increases apoptosis in experimental pancreatitis but the mechanism has not been determined. Our study was designed to investigate signaling mechanisms in pancreatic parenchymal cells regulating death responses with neutrophil depletion. Rats were neutrophil depleted with anti-PMN treatment. Then cerulein pancreatitis was induced, followed by measurements of apoptosis signaling pathways. There was greater activation of executioner caspases-3 in the pancreas with anti-PMN treatment compared to control. There were no differences ...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2925201</comments>
            <pubDate>Thu, 22 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2925201</guid>        </item>
        <item>
            <title>Neurophysiologic evaluation of convergent afferents innervating the human esophagus and area of referred pain on the anterior chest wall.</title>
            <link>http://www.medworm.com/index.php?rid=2925200&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19850969%26dopt%3DAbstract</link>
            <description>Authors: Hobson AR, Chizh B, Hicks K, Aziz Q, Worthen S, Lawerence P, Dewit O, Boyle Y, Dukes G
    Noxious stimuli in the esophagus cause pain that is referred to the anterior chest wall due to convergence of visceral and somatic afferents within the spinal cord. We sought to characterize the neurophysiologic responses of these convergent spinal pain pathways in man studying 12-healthy subjects over 3-visits (V1, V2 and V3). Esophageal pain thresholds (Eso-PT) were assessed using electrical stimulation and anterior chest wall pain thresholds (ACW-PT) using a contact heat thermode. Esophageal evoked potentials (EEP) were recorded from the vertex following 200-electrical stimuli and anterior chest wall evoked potentials (ACWEP) were recorded following 40-heat pulses. The fear of pain questi...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2925200</comments>
            <pubDate>Thu, 22 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2925200</guid>        </item>
        <item>
            <title>Urotensin II modulates hepatic fibrosis and portal hemodynamic alterations in rats.</title>
            <link>http://www.medworm.com/index.php?rid=2857634&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19797237%26dopt%3DAbstract</link>
            <description>Authors: Kemp W, Kompa A, Phrommintikul A, Herath C, Zhiyuan J, Angus P, McLean C, Roberts S, Krum H
    The influence of circulating urotensin II (UII) on liver disease and portal hypertension is unknown. We aimed to evaluate whether UII executes a pathogenetic role in the development of hepatic fibrosis and portal hypertension. UII was administered by continuous infusion over 4 wk in 20 healthy rats divided into three treatment groups, controls (saline, n = 7), low dose (UII, 1 nmol.kg(-1).h(-1), n = 8), and high dose (UII, 3 nmol.kg(-1).h(-1), n = 5). Hemodynamic parameters and morphometric quantification of fibrosis were assessed, and profibrotic cytokines and fibrosis markers were assayed in hepatic tissue. UII induced a significant dose-dependent increase in portal venous pressure (5...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2857634</comments>
            <pubDate>Wed, 30 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2857634</guid>        </item>
        <item>
            <title>Shedding gloomy light into the black box of the Ussing chamber.</title>
            <link>http://www.medworm.com/index.php?rid=2857633&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19797238%26dopt%3DAbstract</link>
            <description>Authors: Lucas ML
    
    PMID: 19797238 [PubMed - in process] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2857633</comments>
            <pubDate>Wed, 30 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2857633</guid>        </item>
        <item>
            <title>Retraction.</title>
            <link>http://www.medworm.com/index.php?rid=2857632&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19797239%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 19797239 [PubMed - in process] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2857632</comments>
            <pubDate>Wed, 30 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2857632</guid>        </item>
        <item>
            <title>Effect of meal volume and caloric load on postprandial gastric function: Studies under physiological conditions by fiber optic pressure measurement and MRI.</title>
            <link>http://www.medworm.com/index.php?rid=2832885&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19779010%26dopt%3DAbstract</link>
            <description>Conclusion: These findings indicate that gastric wall stress (passive strain and active tone) provides the driving force for gastric emptying, but distal resistance to gastric outflow regulates further passage of nutrients. The distinct 'early phase' of gastric emptying with relatively rapid passage of nutrients into the small bowel, regulated by meal volume but not its nutrient composition, ensures that the delivery of nutrients is related to calorie load.
    PMID: 19779010 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832885</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832885</guid>        </item>
        <item>
            <title>Secretagogue stimulation enhances NBCe1 (electrogenic Na+/HCO3- cotransporter) surface expression in murine colonic crypts.</title>
            <link>http://www.medworm.com/index.php?rid=2832884&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19779011%26dopt%3DAbstract</link>
            <description>Authors: Yu H, Riederer B, Stieger N, Boron W, Shull G, Manns M, Seidler U, Bachmann O
    A Na(+)/HCO(3)(-) cotransporter (NBC) is located in the basolateral membrane of the gastrointestinal epithelium, where it imports HCO(3)(-) during stimulated anion secretion. Having previously demonstrated secretagogue activation of NBC in murine colonic crypts, we now asked whether vesicle traffic and exocytosis are involved in this process. Electrogenic NBCe1-B was expressed at significantly higher levels than electroneutral NBCn1 in colonic crypts as determined by QRT-PCR. In cell surface biotinylation experiments, a time-dependent increase in biotinylated NBCe1 was observed, which occured with a peak of +54.8 % after 20 minutes with forskolin (p&amp;lt;0.05), and more rapidly with a peak of +59.8 % a...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832884</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832884</guid>        </item>
        <item>
            <title>Cystitis increases colorectal afferent sensitivity in the mouse.</title>
            <link>http://www.medworm.com/index.php?rid=2832883&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19779012%26dopt%3DAbstract</link>
            <description>In conclusion, CYP treatment increased mechanical sensitivity of colorectal muscular afferents and increased the proportion of chemosensitive colorectal afferents. These data support a peripheral contribution to cross-organ sensitization of pelvic organs.
    PMID: 19779012 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832883</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832883</guid>        </item>
        <item>
            <title>Human duodenum responses to vitamin D metabolites of TRPV6 and other genes involved in calcium absorption.</title>
            <link>http://www.medworm.com/index.php?rid=2832882&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19779013%26dopt%3DAbstract</link>
            <description>This study has shown that human duodenal TRPV6, PMCA1 and CYP24 transcripts respond rapidly to 1,25(OH)(2)D(3) and provides evidence suggesting that local duodenal production of 1,25(OH)(2)D(3) by 25OHD-1alpha-hydroxylase may have a role in human calcium absorption.
    PMID: 19779013 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832882</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832882</guid>        </item>
        <item>
            <title>Alternative Promoter and GATA5 Transcripts in Mouse.</title>
            <link>http://www.medworm.com/index.php?rid=2832881&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19779014%26dopt%3DAbstract</link>
            <description>Authors: Chen B, Yates E, Huang Y, Kogut P, Ma L, Turner JR, Tao Y, Camoretti-Mercado B, Lang D, Svensson E, Garcia J, Gruber P, Morrisey E, Solway J
    GATA5 is a member of the GATA zinc finger transcription factor family involved in tissue-specific transcriptional regulation during cell differentiation and embryogenesis. Previous reports indicate that null mutation of the zebrafish GATA5 gene results in embryonic lethality, while deletion of exon 1 from the mouse GATA5 gene causes only derangement of female urogenital development. Here, we have identified an alternate promoter within intron 1 of the mouse GATA5 gene that transcribes a 2.5 kb mRNA that lacks exon 1 entirely, but includes 82 bp from intron 1 and all of exons 2-6. The alternative promoter was active during transient transf...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832881</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832881</guid>        </item>
        <item>
            <title>Stimulation of stellate cells by injured acinar cells: A model of acute pancreatitis induced by alcohol and fat (VLDL).</title>
            <link>http://www.medworm.com/index.php?rid=2832880&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19779015%26dopt%3DAbstract</link>
            <description>Conclusion: In the presence of lipoproteins alcohol induces acinar cell injury. Our results provide a biochemical pathway for the clinical observation, that a fat-enriched meal combined with excess alcohol consumption can induce acinar cell injury (acute pancreatitis) followed by repair mechanisms (proliferation and increased matrix synthesis in PSC).
    PMID: 19779015 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832880</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832880</guid>        </item>
        <item>
            <title>Angiotensin II receptors are expressed and functional in the human esophageal mucosa.</title>
            <link>http://www.medworm.com/index.php?rid=2832879&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19779016%26dopt%3DAbstract</link>
            <description>Conclusion: AngII receptors and ACE are expressed in the human esophageal epithelium. The results suggest that AT(2)-receptor stimulation increases epithelial ion transport, whereas the AT(1)-receptor inhibits ion transport and increases epithelial resistance.
    PMID: 19779016 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832879</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832879</guid>        </item>
        <item>
            <title>Polysome trafficking of transcripts and microRNAs in regenerating liver after partial hepatectomy.</title>
            <link>http://www.medworm.com/index.php?rid=2832878&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19779017%26dopt%3DAbstract</link>
            <description>Authors: Kren B, Wong P, Shiota A, Zhang X, Zeng Y, Steer C
    Liver regeneration following 70% partial hepatectomy (PH) in rats induces &amp;gt; 95% of hepatocytes to undergo two rounds of semi-synchronous cell replication. Gene expression is controlled primarily by posttranscriptional processing, including changes in mRNA stability. However, the translational activity of a specific mRNA can also be modulated post-PH resulting in significant uncoupling of protein and transcript levels relative to quiescent liver for many genes including c-myc and p53. Although the precise mechanism by which this uncoupling occurs is unknown, the polysomal association of mRNA and microRNA (miRNA) can significantly modulate rate of decay as well as translational activity. Thus, we characterized the association...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832878</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832878</guid>        </item>
        <item>
            <title>Galanin potentiates supramaximal caerulein-stimulated pancreatic amylase secretion via its action on somatostatin secretion.</title>
            <link>http://www.medworm.com/index.php?rid=2832877&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19779018%26dopt%3DAbstract</link>
            <description>Authors: Barreto S, Carati C, Schloithe A, Toouli J, Saccone G
    Galanin inhibits pancreatic amylase secretion from mouse lobules induced by physiological concentrations of caerulein via an insulin-dependent mechanism. We aimed to determine the effect and elucidate the mechanism of action of exogenous galanin on pancreatic amylase secretion induced by supramaximal concentrations of caerulein. Amylase secretion from isolated murine pancreatic lobules was measured. Lobules were co-incubated with galanin (10(-12)M-10(-7)M) and caerulein (10(-7)M). Lobules were pre-incubated with atropine (10(-5)M), tetrodotoxin (10(-5)M), diazoxide (10(-7)M), or the galanin antagonist galantide (10(-12)M-10(-7)M) for 30mins followed by incubation with caerulein alone, or combined with galanin (10(-12)M). Lo...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832877</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832877</guid>        </item>
        <item>
            <title>Spontaneous oscillations in intracellular Ca2+ concentration via purinergic receptors elicit transient cell swelling in rat parotid ducts.</title>
            <link>http://www.medworm.com/index.php?rid=2832876&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19779019%26dopt%3DAbstract</link>
            <description>Authors: Shitara A, Tanimura A, Sato A, Tojyo Y
    Using multiphoton microscopy, we established that rat parotid ductal cells exhibit spontaneous oscillations in intracellular Ca(2+) concentration ([Ca(2+)](i)). These oscillatory Ca(2+) responses were observed during continuous perfusion with a physiological salt solutions at 37 masculineC in the absence of calcium mobilizing agonist stimulation. The timing and patterns of these spontaneous Ca(2+) oscillations varied between individual ductal cells, and the average number of Ca(2+) responses in a single responding ductal cells was 2.1 in a 10-min recording period. High-speed scanning (0.6 s/image) revealed that most spontaneous elevations in [Ca(2+)](i) were initiated at the luminal side of ductal cells, and spread toward the basal side w...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832876</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832876</guid>        </item>
        <item>
            <title>Immunoglobulins (IgGs) from Scleroderma Patients Inhibit Muscarinic Receptor in Internal Anal Sphincter (IAS) Smooth Muscle Cells.</title>
            <link>http://www.medworm.com/index.php?rid=2832875&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19779020%26dopt%3DAbstract</link>
            <description>Authors: Singh J, Mehendiratta V, Del Galdo F, Jimenez S, Cohen S, Dimarino A, Rattan S
    Systemic Sclerosis (SSc) IgGs affecting M(3)-muscarinic receptor (M(3)-R) have been proposed to be responsible for the GI dysmotility. However, the effect of SSc IgGs on smooth muscle cell (SMC) function has not been studied. We determined the effect of SSc IgGs on the muscarinic receptor activation by bethanechol (BeCh; methyl derivate of carbachol) in SMC and smooth muscle strips from rat IAS. IgGs were purified from GI symptomatic SSc patients and normal volunteers, using protein G-sepharose columns. SMC lengths were determined via computerized digital micrometry. The presence of M(3)-R and IgG-M(3)-R complex was determined by Western blot using LI-COR Odyssey(R) Imaging System. IgGs from SSc pat...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832875</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832875</guid>        </item>
        <item>
            <title>TLR3-mediated NF-{kappa}B signaling in human esophageal epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=2832874&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19779021%26dopt%3DAbstract</link>
            <description>Conclusions: Our findings demonstrate for the first time that TLR3 is highly functional in the human esophageal epithelium, and that TLR3-mediated NF-kappaB-signaling may play an important regulatory role in esophageal epithelial homeostasis.
    PMID: 19779021 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832874</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832874</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +21 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2785452&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%29%2520AND%2520%25222009%252F09%252F06%252001.44%2522%255BMHDA%255D%253A%25222009%252F09%252F11%252013.56%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F09%252F06%252001.44%2522%255BEDAT%255D%29%29</link>
            <description>21 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These pubmed results were generated on 2009/09/11PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2785452</comments>
            <pubDate>Fri, 11 Sep 2009 17:56:02 +0100</pubDate>
            <guid isPermaLink="false">2785452</guid>        </item>
        <item>
            <title>Role of thin-filament regulatory proteins in relaxation of colonic smooth muscle contraction.</title>
            <link>http://www.medworm.com/index.php?rid=2769185&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19729493%26dopt%3DAbstract</link>
            <description>Authors: Somara S, Gilmont RR, Bitar KN
    Coordinated regulation of smooth muscle contraction and relaxation is required for colonic motility. Contraction is associated with phosphorylation of myosin light chain (MLC20) and interaction of actin with myosin. Thin-filament regulation of actomyosin interaction is modulated by two actin binding regulatory proteins tropomyosin (TM) and caldesmon (CaD). TM and CaD are known to play crucial role in actomyosin interaction promoting contraction. Contraction is associated with phosphorylation of small heat shock protein, HSP27 concomitant with the phosphorylation of TM and CaD. Phosphorylation of HSP27 is attributed as being the prime modulator of thin filament regulation of contraction. Preincubation of colonic smooth muscle cells (CSMC) with rel...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2769185</comments>
            <pubDate>Wed, 02 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2769185</guid>        </item>
        <item>
            <title>New method of manometric measurement of gastroduodenal motility in conscious mice: Effects of ghrelin and Y2 depletion.</title>
            <link>http://www.medworm.com/index.php?rid=2769184&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19729494%26dopt%3DAbstract</link>
            <description>Authors: Tanaka R, Inui A, Asakawa A, Atsuchi K, Ataka K, Fujimiya M
    Since no previous studies have reported dual measurements of stomach and duodenal motility in conscious mice, we developed a manometric method to measure the gastroduodenal motility in the physiological fed and fasted states of conscious mice. By this method we measured, for the first time, the gastroduodenal motility in Y2 knockout mice and analyzed the effects of ghrelin on the gastroduodenal motility in conscious mice. To evaluate this new method, we provide the comparison on the effects of CCK-8 examined by present and previous methods. In the fasted state of mice, phase III-like contractions with frequencies of 7.8 +/- 0.5/h in the antrum and 6.6 +/- 0.7/h in the duodenum were observed. This fasted pattern was di...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2769184</comments>
            <pubDate>Wed, 02 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2769184</guid>        </item>
        <item>
            <title>Impact of Roux-en-Y gastric bypass surgery on rat intestinal glucose transport.</title>
            <link>http://www.medworm.com/index.php?rid=2769183&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19729495%26dopt%3DAbstract</link>
            <description>Conclusions: We have shown duodenal exclusion significantly influences both intestinal structure and glucose transport function, with glucose absorptive capacity reduced after RYGB. This provides a novel mechanistic explanation for some of the antidiabetic effects of RYGB. Key words: glucose transport, sglt1, bariatric surgery, diabetes.
    PMID: 19729495 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2769183</comments>
            <pubDate>Wed, 02 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2769183</guid>        </item>
        <item>
            <title>The angiogenic effect of probiotic Bacillus polyfermenticus on human intestinal microvascular endothelial cells is mediated by IL-8.</title>
            <link>http://www.medworm.com/index.php?rid=2769182&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19729496%26dopt%3DAbstract</link>
            <description>Authors: Im E, Choi YJ, Kim CH, Fiocchi C, Pothoulakis C, Rhee SH
    Angiogenesis is required for wound healing and repair, but dysregulated angiogenesis is involved in gastrointestinal inflammation. Bacillus polyfermenticus (B.P.) is a probiotic bacterium clinically used for a variety of intestinal disorders in East Asia. Here we investigated the effect of B.P. on angiogenesis of human intestinal microvascular endothelial cells (HIMECs) and wound healing in intestinal mucosa. Exposure of HIMECs to the conditioned medium of B.P. cultures (B.P. CM) increased cell migration, permeability and tube formation. Production of the pro-angiogenic cytokine IL-8 was increased by B.P. CM, and neutralizing antibodies against IL-8 or IL-8 receptor CXCR2 reduced tube formation as well as actin stress fi...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2769182</comments>
            <pubDate>Wed, 02 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2769182</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +19 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2738521&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%29%2520AND%2520%25222009%252F08%252F22%252009.10%2522%255BMHDA%255D%253A%25222009%252F08%252F27%252021.22%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F08%252F22%252009.10%2522%255BEDAT%255D%29%29</link>
            <description>19 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These pubmed results were generated on 2009/08/27PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2738521</comments>
            <pubDate>Fri, 28 Aug 2009 01:22:03 +0100</pubDate>
            <guid isPermaLink="false">2738521</guid>        </item>
        <item>
            <title>Regulation of Hsp60 and the role of MK2 in a new model of severe experimental pancreatitis.</title>
            <link>http://www.medworm.com/index.php?rid=2723053&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19696141%26dopt%3DAbstract</link>
            <description>The objective of this study was to investigate the role of (MK2) and HSP60 in the pathogenesis of a new model of severe acute pancreatitis (AP). MK2 plays a significant role in the regulation of cytokines. It has been shown that induction and expression of several Heat shock proteins (HSPs) can protect against experimental pancreatitis. Interplay between both systems seems of high interest. Mice with a homozygous deletion of the MK2 gene were used. Severe AP was induced by combined i.p. injections of cerulein with LPS. AP was assessed by biochemical markers and histology. The IL-6- and lung MPO-levels were determined for assessing the extent of systemic inflammatory response. Expression of HSP25, HSP60, HSP70 and HSP90 was analyzed by Western blotting. Repeated injections of cerulein alone...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2723053</comments>
            <pubDate>Wed, 19 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2723053</guid>        </item>
        <item>
            <title>Alterations in mechanical properties of mesenteric resistance arteries in experimental portal hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=2723052&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19696142%26dopt%3DAbstract</link>
            <description>Conclusion: In long-standing severe portal hypertension such as ascitic LC but not in short-term conditions such as PVL, mesenteric resistance arteries exhibit vascular remodeling and markedly less resistant mechanical properties leading to decreased vessel stiffness accompanied by structural changes in the IEL. This may well contribute to the maintenance and severity of splanchnic arterial vasodilation in liver cirrhosis. Key words: vasodilation, portal hypertension, myogenic tone, mesenteric arteries.
    PMID: 19696142 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2723052</comments>
            <pubDate>Wed, 19 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2723052</guid>        </item>
        <item>
            <title>Localization of acyl ghrelin- and des-acyl ghrelin-immunoreactive cells in the rat stomach and their responses to intragastric pH.</title>
            <link>http://www.medworm.com/index.php?rid=2723051&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19696143%26dopt%3DAbstract</link>
            <description>Authors: Mizutani M, Atsuchi K, Asakawa A, Matsuda N, Fujimura M, Inui A, Kato I, Fujimiya M
    Acyl ghrelin has a 28 amino acid sequence with O-n-octanoyl acid modification at the serine 3 position, while des-acyl ghrelin has no octanoyl acid modification. Although these peptides exert different physiological functions, no previous studies have shown the different localization of acyl ghrelin and des-acyl ghrelin in the stomach. Here we have developed an antibody specific for des-acyl ghrelin that does not crossreact with acyl ghrelin. Both acyl ghrelin- and des-acyl ghrelin-immunoreative cells were distributed in the oxyntic and antral mucosa of the rat stomach, with higher density in the antral mucosa than oxyntic mucosa. Immunofluorescence double staining showed that acyl ghrelin- and...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2723051</comments>
            <pubDate>Wed, 19 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2723051</guid>        </item>
        <item>
            <title>Intestinal Cell Kinase, a MAP Kinase-Related Kinase, Regulates Proliferation and G1 Cell Cycle Progression of Intestinal Epithelial Cells.</title>
            <link>http://www.medworm.com/index.php?rid=2723050&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19696144%26dopt%3DAbstract</link>
            <description>In this study, we report that suppression of ICK expression in cultured intestinal epithelial cells by short hairpin RNA (shRNA) interference significantly impaired cellular proliferation and induced features of gene expression characteristic of colonic or enterocytic differentiation. Down-regulation of ICK altered expression of cell cycle regulators (cyclin D1, c-myc and p21(Cip1/WAF1)) of G1-S transition, consistent with the G1 cell cycle delay induced by ICK shRNA. ICK deficiency also led to a significant decrease in the expression and/or activity of p70 ribosomal protein S6 Kinase (S6K1) and eukaryotic initiation factor 4E (eIF4E), concomitant with reduced expression of their upstream regulators, the mammalian target of rapamycin (mTOR) and the regulatory associated protein of mTOR (Ra...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2723050</comments>
            <pubDate>Wed, 19 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2723050</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +26 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2679162&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%29%2520AND%2520%25222009%252F08%252F02%252002.20%2522%255BMHDA%255D%253A%25222009%252F08%252F07%252015.06%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F08%252F02%252002.20%2522%255BEDAT%255D%29%29</link>
            <description>26 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These pubmed results were generated on 2009/08/07PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2679162</comments>
            <pubDate>Fri, 07 Aug 2009 19:06:02 +0100</pubDate>
            <guid isPermaLink="false">2679162</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +27 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2661296&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%29%2520AND%2520%25222009%252F07%252F25%252017.10%2522%255BMHDA%255D%253A%25222009%252F08%252F02%252002.20%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F07%252F25%252017.10%2522%255BEDAT%255D%29%29</link>
            <description>27 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These pubmed results were generated on 2009/08/02PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2661296</comments>
            <pubDate>Sun, 02 Aug 2009 06:20:03 +0100</pubDate>
            <guid isPermaLink="false">2661296</guid>        </item>
        <item>
            <title>Calcium-dependent and Calcium-independent inhibition of contraction by cGMP/cGKI in intestinal smooth muscle.</title>
            <link>http://www.medworm.com/index.php?rid=2638342&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19628652%26dopt%3DAbstract</link>
            <description>Authors: Frei E, Huster M, Smital P, Schlossmann J, Hofmann F, Wegener JW
    cGMP dependent protein kinase I (cGKI) induces relaxation of smooth muscle via several pathways that include inhibition of intracellular Ca(2+) signalling and/or involve activation of myosin phosphatase. In the present study, we investigated these mechanisms comparatively in colon and jejunum longitudinal smooth muscle from mice. In simultaneous recordings from colon muscle, 8-Br-cGMP reduced both carbachol-induced tension and carbachol-induced increase in intracellular calcium ([Ca(2+)]i). These effects of 8-Br-cGMP were absent in colon from mice carrying a mutated IRAG gene or lacking cGKI. However, in jejunum, 8-Br-cGMP reduced carbachol-induced tension but did not change corresponding [Ca2+]i signals. This se...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2638342</comments>
            <pubDate>Wed, 22 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2638342</guid>        </item>
        <item>
            <title>Enteropathogenic Escherichia coli inhibits intestinal vitamin B1 (thiamin) uptake: Studies with human-derived intestinal epithelial Caco-2 cells.</title>
            <link>http://www.medworm.com/index.php?rid=2638341&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19628653%26dopt%3DAbstract</link>
            <description>Authors: Ashokkumar B, Kumar JS, Hecht GA, Said HM
    Infection with the gram-negative enteropathogenic Escherichia coli (EPEC), a food-borne pathogen, represents a significant risk to human health. While diarrhea is a major consequence of this infection, mal-nutrition also occurs especially in severe and prolonged cases, which may aggravate the health status of the infected hosts. Here we examined the effect of EPEC infection on the intestinal uptake of the water-soluble vitamin B1 (thiamin) using an established human intestinal epithelial Caco-2 cell model. The results showed that infecting Caco-2 cells with wild-type EPEC (but not with non-pathogenic E. coli, killed EPEC or filtered supernatant) leads to a significant (P &amp;lt; 0.01) inhibition in thiamin uptake. Kinetic parameters of bo...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2638341</comments>
            <pubDate>Wed, 22 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2638341</guid>        </item>
        <item>
            <title>Role of endothelial nitric oxide synthase in the development of portal hypertension in the carbon tetrachloride induced liver fibrosis model.</title>
            <link>http://www.medworm.com/index.php?rid=2638340&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19628654%26dopt%3DAbstract</link>
            <description>Conclusion: The systemic hyperemia component of hyperdynamic circulation is eNOS dependant and precedes increased changes in hepatic resistance. Alternative mechanisms, possibly involving cyclooxygenase, may contribute. eNOS maintains normal hepatic resistance following CCl4 induced fibrosis. Consequently, increased portal pressure following chronic CCl4 exposure is linked to hyperdynamic circulation in wild type mice and increased hepatic resistance in eNOS(-/-) mice. Key words: portal hypertension, eNOS, mice, CCl4.
    PMID: 19628654 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2638340</comments>
            <pubDate>Wed, 22 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2638340</guid>        </item>
        <item>
            <title>Glucagon-Like Peptide-2 Modulates Neurally-Evoked Mucosal Chloride Secretion In Guinea Pig Small Intestine In Vitro.</title>
            <link>http://www.medworm.com/index.php?rid=2638339&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19628655%26dopt%3DAbstract</link>
            <description>Authors: Baldassano S, Liu S, Qu MH, Mule F, Wood JD
    Glucagon-like peptide-2 (GLP-2) is an important messenger protein in intestinal physiology. It influences digestion, absorption, epithelial growth, motility and blood flow. We studied involvement of GLP-2 in intestinal mucosal secretory behavior. Submucosal/mucosal preparations from guinea pig ileum were mounted in Ussing chambers for measurement of short-circuit current (Isc) as a surrogate for chloride secretion. GLP-2 action on neuronal release of acetylcholine was determined with ELISA. Enteric neuronal expression of the GLP-2 receptor (GLP-2R) was studied with immunohistochemical methods. Application of GLP-2 (0.1-100nM) to the serosal or mucosal side of the preparations evoked no change in baseline Isc and did not alter transep...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2638339</comments>
            <pubDate>Wed, 22 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2638339</guid>        </item>
        <item>
            <title>Effects of Losartan on Hepatic Expression of Non-phagocytic NADPH Oxidase and Fibrogenic Genes in Patients with Chronic Hepatitis C.</title>
            <link>http://www.medworm.com/index.php?rid=2638338&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19628656%26dopt%3DAbstract</link>
            <description>Authors: Colmenero J, Bataller R, Sancho-Bru P, Dominguez M, Moreno M, Forns X, Bruguera M, Arroyo V, Brenner DA, Gin&amp;#xE8;s P
    Angiotensin II promotes liver fibrogenesis by stimulating non-phagocytic NADPH oxidase (NOX)-induced oxidative stress. Angiotensin II type 1 receptor blockers attenuate experimental liver fibrosis, yet their effects in human liver fibrosis are unknown. We investigated the effects of losartan on the hepatic expression of fibrogenic, inflammatory and NOX genes in patients with chronic hepatitis C (CHC). Fourteen patients with CHC and liver fibrosis received oral losartan (50 mg/day) for 18 months. Liver biopsies were performed at baseline and after treatment. The degree of inflammation and fibrosis was evaluated by histological analysis (METAVIR). Collagen conten...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2638338</comments>
            <pubDate>Wed, 22 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2638338</guid>        </item>
        <item>
            <title>Identification of dynein light chain road block-1 (DYNLRB1) as a novel interaction partner with the human reduced folate carrier (hRFC).</title>
            <link>http://www.medworm.com/index.php?rid=2571434&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19571232%26dopt%3DAbstract</link>
            <description>This study demonstrates for the first time the identification of DYNLRB1 as an interacting protein partner with hRFC. Further, DYNLRB1 appears to influence the function and cell biology of hRFC. Key words: Folate transport, protein-protein interactions, two-hybrid analysis, accessory proteins.
    PMID: 19571232 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2571434</comments>
            <pubDate>Tue, 30 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2571434</guid>        </item>
        <item>
            <title>An imbalance of esophageal effector and regulatory T cell subsets in experimental eosinophilic esophagitis in mice.</title>
            <link>http://www.medworm.com/index.php?rid=2571433&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19571233%26dopt%3DAbstract</link>
            <description>In conclusion, our results suggest that local regulatory interaction of CD45RB(high) and CD45RB(low) CD4(+) T cells may required for protective and pathogenic immunity in EE. Key words: Eosinophils, Esophagitis, T cells, Inflammation.
    PMID: 19571233 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2571433</comments>
            <pubDate>Tue, 30 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2571433</guid>        </item>
        <item>
            <title>Modulation of Ileal Apical Sodium-Dependent Bile Acid Transporter ASBT by Protein Kinase C.</title>
            <link>http://www.medworm.com/index.php?rid=2571432&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19571234%26dopt%3DAbstract</link>
            <description>Authors: Sarwar Z, Annaba F, Dwivedi A, Saksena S, Gill RK, Alrefai WA
    Ileal Apical Sodium-Dependent Bile Acid Transporter (ASBT) is responsible for reabsorbing the majority of bile acids from the intestinal lumen. Rapid adaptation of ASBT function in response to physiological and pathophysiological stimuli is essential for the maintenance of bile acid homeostasis. However, not much is known about molecular mechanisms responsible for acute post-transcriptional regulation of ileal ASBT. Protein kinase C (PKC)-dependent pathway represents a major cell signaling mechanism influencing intestinal epithelial functions. The present studies were, therefore, undertaken to investigate ASBT regulation in intestinal Caco2 monolayers by the well-known PKC activator phorbol ester PMA. Our results sh...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2571432</comments>
            <pubDate>Tue, 30 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2571432</guid>        </item>
        <item>
            <title>Glycine and urea kinetics in non-alcoholic steatohepatitis in human: effect of intralipid infusion.</title>
            <link>http://www.medworm.com/index.php?rid=2571431&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19571235%26dopt%3DAbstract</link>
            <description>Authors: Dasarathy S, Kasumov T, Edmison JM, Gruca LL, Bennett C, Duenas C, Marczewski S, McCullough AJ, Hanson RW, Kalhan SC
    The rate of oxidation of glycine and ureagenesis were quantified in the basal state and in response to an intravenous infusion of intralipid with heparin (IL) in healthy subjects (n=8) and in subjects with non-alcoholic steatohepatitis (NASH) (n=6). During fasting, no significant difference in weight specific rate of appearance (Ra) of glycine, glycine oxidation and urea synthesis was observed. Intralipid infusion resulted in a significant increase in plasma beta-hydroxybutyrate in both groups. The correlation between free fatty acids and beta-hydroxybutyrate concentration in plasma was 0.94 in NASH compared with 0.4 in controls, indicating greater hepatic fatty...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2571431</comments>
            <pubDate>Tue, 30 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2571431</guid>        </item>
        <item>
            <title>Enterocyte-specific epidermal growth factor prevents barrier dysfunction and improves mortality in murine peritonitis.</title>
            <link>http://www.medworm.com/index.php?rid=2571430&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19571236%26dopt%3DAbstract</link>
            <description>Authors: Clark JA, Gan H, Samocha AJ, Fox AC, Buchman TG, Coopersmith CM
    Systemic administration of epidermal growth factor (EGF) decreases mortality in a murine model of septic peritonitis. While EGF can have direct healing effects on the intestinal mucosa, it is unknown whether the benefits of systemic EGF in peritonitis are mediated through the intestine. Here, we demonstrate that enterocyte-specific overexpression of EGF is sufficient to prevent intestinal barrier dysfunction and improve survival in peritonitis. Transgenic FVB/N mice that overexpress EGF exclusively in enterocytes (IFABP-EGF) and wild-type (WT) mice were subjected to either sham laparotomy or cecal ligation and puncture (CLP). Intestinal permeability, expression of the tight junction proteins claudins-1, -2, -3, -4...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2571430</comments>
            <pubDate>Tue, 30 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2571430</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +146 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2533894&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%29%2520AND%2520%25222009%252F04%252F08%252000.53%2522%255BMHDA%255D%253A%25222009%252F06%252F27%252013.22%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Gastrointest%2520Liver%2520Physiol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F04%252F08%252000.53%2522%255BEDAT%255D%29%29</link>
            <description>146 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These pubmed results were generated on 2009/06/27PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533894</comments>
            <pubDate>Sat, 27 Jun 2009 17:22:02 +0100</pubDate>
            <guid isPermaLink="false">2533894</guid>        </item>
        <item>
            <title>Do Corticotropin Releasing Factor-1 Receptors Influence Colonic Transit and Bowel Function in Females with Irritable Bowel Syndrome?</title>
            <link>http://www.medworm.com/index.php?rid=2309694&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19342506%26dopt%3DAbstract</link>
            <description>Conclusions: In women with D-IBS, pexacerfont, 25 or 100 mg QD, does not significantly alter colonic or other regional transit or bowel function. The role of central and peripheral CRF1 receptors in bowel function in IBS-D requires further study. Key words: corticotropin releasing factor, pexacerfont, diarrhea-predominant irritable bowel syndrome, gastrointestinal transit.
    PMID: 19342506 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2309694</comments>
            <pubDate>Thu, 02 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2309694</guid>        </item>
        <item>
            <title>Functional coupling of apical Cl-/HCO3- exchange with CFTR in stimulated HCO3- secretion by guinea pig interlobular pancreatic duct.</title>
            <link>http://www.medworm.com/index.php?rid=2309692&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19342507%26dopt%3DAbstract</link>
            <description>This study demonstrates functional coupling between Cftr and Slc26a6-like Cl(-)/HCO3(-) exchange activity in apical membrane of guinea pig pancreatic interlobular duct. Key words: Slc26, bicarbonate, pancreatic duct, CFTR.
    PMID: 19342507 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2309692</comments>
            <pubDate>Thu, 02 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2309692</guid>        </item>
        <item>
            <title>A Guide to Ussing Chamber Studies of Mouse Intestine.</title>
            <link>http://www.medworm.com/index.php?rid=2309690&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19342508%26dopt%3DAbstract</link>
            <description>Authors: Clarke LL
    The Ussing chamber provides a physiological system to measure the transport of ions, nutrients and drugs across various epithelial tissues. One of the most studied epithelium is the intestine which has provided several landmark discoveries regarding the mechanisms of ion transport processes. Adaptation of this method to mouse intestine adds the dimension of investigating genetic loss- or gain-of-function as a means to identify proteins or processes affecting transepithelial transport. In this review, the principles underlying the use of Ussing chambers are outlined including limitations and advantages of the technique. With an emphasis on mouse intestinal preparations, the review covers chamber design, commercial equipment sources, tissue preparation, step-by-step in...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2309690</comments>
            <pubDate>Thu, 02 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2309690</guid>        </item>
        <item>
            <title>Interleukin-1 Participates in the Progression from Liver Injury to Fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=2309688&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19342509%26dopt%3DAbstract</link>
            <description>In this study, we first established a temporal relationship between IL-1, MMPs, HSC activation, and early fibrosis. The roles of IL-1 and MMP-9 in HSC activation and fibrogenesis were determined by mice deficient of these genes. After liver injury, IL-1, MMP-9, and MMP-13 levels were found to be elevated prior to the onset of HSC activation and fibrogenesis. IL-1 receptor-deficient mice exhibited ameliorated liver damage, and reduced fibrogenesis. Similarly, advanced fibrosis, as determined by type-I and -III collagen mRNA expression and fibrotic septa, was partially attenuated by the deficiency of IL-1. In the early phase of liver injury, the MMP-9, MMP-13, and TIMP-1 expression correlated well with IL-1 levels. In injured livers, MMP-9 was predominantly co-localized to desmin-positive ce...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2309688</comments>
            <pubDate>Thu, 02 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2309688</guid>        </item>
        <item>
            <title>Inflammatory NF{kappa}B activation promotes hepatic apolipoprotein B100 secretion: Evidence for a link between hepatic inflammation and lipoprotein production.</title>
            <link>http://www.medworm.com/index.php?rid=2309687&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19342510%26dopt%3DAbstract</link>
            <description>Authors: Tsai J, Zhang R, Qiu W, Su Q, Naples M, Adeli K
    Insulin resistant states are commonly associated with chronic inflammation and hepatic overproduction of apolipoprotein B100 (apoB100) leading to hypertriglyceridemia and a metabolic dyslipidemic profile. Molecular mechanisms linking hepatic inflammatory cascades and the pathways of apoB100-lipoprotein production are however unknown. In the present study, we employed a diet-induced insulin resistant hamster model as well as cell culture studies to investigate the potential link between activation of hepatic inflammatory nuclear factor kappaB (NFkappaB) signaling cascade and the synthesis and secretion of apoB100-containing lipoproteins. Using an established insulin resistant animal model, the fructose-fed hamster, we found that f...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2309687</comments>
            <pubDate>Thu, 02 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2309687</guid>        </item>
        <item>
            <title>Role of iron in the pathogenesis of cysteamine-induced duodenal ulceration in rats.</title>
            <link>http://www.medworm.com/index.php?rid=2309686&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19342511%26dopt%3DAbstract</link>
            <description>Authors: Khomenko T, Szabo S, Deng X, Ishikawa H, Anderson GJ, McLaren GD
    Cysteamine induces perforating duodenal ulcers in rats within 24-48 hr. This reducing aminothiol generates hydrogen peroxide in the presence of transition metals (e.g., ferric iron), producing oxidative stress, which may contribute to organ-specific tissue damage. Since most intestinal iron absorption takes place in the proximal duodenum, we hypothesized that cysteamine may disrupt regulation of mucosal iron transport, and iron may facilitate cysteamine-induced duodenal ulceration. We show here that cysteamine-induced ulceration was aggravated by pretreatment of rats with Fe(3+) or Fe(2+) compounds, which elevated the iron concentration in duodenal mucosa. In contrast, feeding rats an iron-deficient diet was asso...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2309686</comments>
            <pubDate>Thu, 02 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2309686</guid>        </item>
        <item>
            <title>Cross-inhibition Between Nicotinic Acetylcholine Receptors and P2X Receptors in Myenteric Neurons and HEK-293 cells.</title>
            <link>http://www.medworm.com/index.php?rid=2309613&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19342512%26dopt%3DAbstract</link>
            <description>Authors: Decker DA, Galligan JJ
    The enteric nervous system (ENS) controls gut function. P2X and nicotinic acetylcholine receptors (nAChRs) are ligand-gated cation channels that mediate fast synaptic excitation in the ENS. Close molecular coupling in enteric neuronal membranes contributes to a mutually inhibitory interaction between these receptors; this effect is called cross-inhibition. We studied the molecular mechanisms responsible for cross-inhibition. Whole-cell patch clamp techniques were used to measure P2X- and nAChR-mediated currents in cultured enteric neurons and HEK-293 cells. In cultured myenteric neurons, ACh (3 mM) and ATP (1 mM) co-application evoked an inward current that was only 57 +/- 6% (P &amp;lt; 0.05) of the predicted current that would have occurred if the two popu...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2309613</comments>
            <pubDate>Thu, 02 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2309613</guid>        </item>
        <item>
            <title>Putative role for actin organization status in the dynamic localization of canalicular carriers under oxidative stress conditions.</title>
            <link>http://www.medworm.com/index.php?rid=2309696&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19332616%26dopt%3DAbstract</link>
            <description>Authors: S&amp;#xE1;nchez Pozzi EJ, Roma MG
    
    PMID: 19332616 [PubMed - in process] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2309696</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2309696</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +38 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2269905&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%2529%2BAND%2B%25222009%252F03%252F08%2B10%252E01%2522%255BMHDA%255D%253A%25222009%252F03%252F14%2B23%252E24%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F03%252F08%2B10%252E01%2522%255BEDAT%255D%2529%2529%26itool%3Drss</link>
            <description>38 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These PubMed results were generated on 2009/03/14PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2269905</comments>
            <pubDate>Sun, 15 Mar 2009 03:24:33 +0100</pubDate>
            <guid isPermaLink="false">2269905</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +38 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2263778&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%2529%2BAND%2B%25222009%252F03%252F08%2B10%252E01%2522%255BMHDA%255D%253A%25222009%252F03%252F14%2B23%252E24%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F03%252F08%2B10%252E01%2522%255BEDAT%255D%2529%2529</link>
            <description>38 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These PubMed results were generated on 2009/03/14PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2263778</comments>
            <pubDate>Sun, 15 Mar 2009 03:24:33 +0100</pubDate>
            <guid isPermaLink="false">2263778</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +18 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2238598&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%2529%2BAND%2B%25222009%252F02%252F22%2B06%252E58%2522%255BMHDA%255D%253A%25222009%252F02%252F28%2B10%252E21%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F02%252F22%2B06%252E58%2522%255BEDAT%255D%2529%2529%26itool%3Drss</link>
            <description>18 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These PubMed results were generated on 2009/02/28PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2238598</comments>
            <pubDate>Sat, 28 Feb 2009 15:21:39 +0100</pubDate>
            <guid isPermaLink="false">2238598</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +18 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2221105&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%2529%2BAND%2B%25222009%252F02%252F22%2B06%252E58%2522%255BMHDA%255D%253A%25222009%252F02%252F28%2B10%252E21%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F02%252F22%2B06%252E58%2522%255BEDAT%255D%2529%2529</link>
            <description>18 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These PubMed results were generated on 2009/02/28PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221105</comments>
            <pubDate>Sat, 28 Feb 2009 15:21:39 +0100</pubDate>
            <guid isPermaLink="false">2221105</guid>        </item>
        <item>
            <title>Distinct SOX9 Levels Differentially Mark Stem/Progenitor Populations and Enteroendocrine Cells of the Small Intestine Epithelium.</title>
            <link>http://www.medworm.com/index.php?rid=2204025&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19228882%26dopt%3DAbstract</link>
            <description>Authors: Formeister EJ, Sionas AL, Lorance DK, Barkley CL, Lee GH, Magness ST
    SOX transcription factors have the capacity to modulate stem/progenitor cell proliferation and differentiation in a dose-dependent manner. SOX9 is expressed in the small intestine epithelial stem cell zone, therefore, we hypothesized differential levels of SOX9 may exist, influencing proliferation and/or differentiation of the small intestine epithelium. Sox9 expression levels in the small intestine were investigated using a Sox9(EGFP) transgenic mouse. Sox9(EGFP) levels correlate with endogenous SOX9 levels, which are expressed at two steady-state levels, termed Sox9(EGFPLO) and Sox9(EGFPHI). Crypt-based columnar cells are Sox9(EGFPLO) and demonstrate enriched expression of the stem cell marker, Lgr5. Sox9(E...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2204025</comments>
            <pubDate>Thu, 19 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2204025</guid>        </item>
        <item>
            <title>Schlafen-3, A Novel Gene, Regulates Colonic Mucosal Growth during Aging.</title>
            <link>http://www.medworm.com/index.php?rid=2204024&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19228883%26dopt%3DAbstract</link>
            <description>In conclusion, our current study demonstrates that several genes involved in proliferation and apoptosis are differentially expressed in the colonic mucosa of young and aged rats. Schlafen-3, a novel negative regulator of growth, which is markedly downregulated in the colonic mucosa of the aged, may play a role in regulating colonic mucosal growth during aging. Key words: Aging, Gastrointestinal Mucosa, Proliferation, Cancer.
    PMID: 19228883 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2204024</comments>
            <pubDate>Thu, 19 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2204024</guid>        </item>
        <item>
            <title>Hepatocyte nuclear factor-4{alpha} and bile acids regulate human concentrative nucleoside transporter-1 gene expression.</title>
            <link>http://www.medworm.com/index.php?rid=2204023&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19228884%26dopt%3DAbstract</link>
            <description>Authors: Klein K, Kullak-Ublick GA, Wagner M, Trauner M, Eloranta JJ
    The concentrative nucleoside transporter-1 (CNT1) is a member of the solute carrier 28 (SLC28) gene family, and is expressed in the liver, intestine, and kidneys. CNT1 mediates the uptake of naturally occurring pyrimidine nucleosides, but also nucleoside analogues used in anticancer and antiviral therapy. Thus, expression levels of CNT1 may affect the pharmacokinetics of these drugs and the outcome of drug therapy. Because little is known about the transcriptional regulation of human CNT1 gene expression, we have characterized the CNT1 promoter with respect to DNA response elements and their binding factors. The transcriptional start site of the CNT1 gene was determined by 5'-RACE. In silico analysis revealed the exis...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2204023</comments>
            <pubDate>Thu, 19 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2204023</guid>        </item>
        <item>
            <title>Threonine-deficient diets induced changes in hepatic bioenergetics.</title>
            <link>http://www.medworm.com/index.php?rid=2204022&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19228885%26dopt%3DAbstract</link>
            <description>Authors: Ross-Inta CM, Zhang YF, Almendares A, Giulivi C
    Diets de fi cient in an indispensable amino acid are known to suppress food intake in rats. Few studies were focused at understanding how amino acid deficient diets may elicit biochemical changes at the mitochondrial level. The goal of this study was to evaluate mitochondrial function in rats fed diets with 0.00%, 0.18%, 0.36%, and 0.87% Thr (set at 0 %, 30%, 60% and 140% of Thr requirement for growth). Here, it is described for the first time, that Thr-deficient diets induce a specific uncoupling of mitochondria in liver, especially with NADH-linked substrates, not observed in heart (except for Thr-devoid diet). The advantage of this situation would be to provide more ATP to support growth and maintenance when high-quality prote...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2204022</comments>
            <pubDate>Thu, 19 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2204022</guid>        </item>
        <item>
            <title>Knockdown of ATP8B1 expression leads to specific down-regulation of the bile acid sensor FXR in HepG2 cells. Effect of the FXR agonist GW4064.</title>
            <link>http://www.medworm.com/index.php?rid=2204021&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19228886%26dopt%3DAbstract</link>
            <description>Authors: Martinez-Fernandez P, Hierro L, Jara P, Alvarez L
    Farnesoid X receptor (FXR) is a bile acid-sensing nuclear receptor that controls bile acid homeostasis. It has been suggested that down-regulation of FXR contributes to the pathogenesis of an inherited disorder of bile secretion caused by mutations in ATP8B1. We have investigated the relationship between ATP8B1 knockdown and FXR down-regulation in the human hepatoblastoma cell line HepG2. Transfection of HepG2 cells with ATP8B1 small interfering RNA (siRNA) duplexes led to a 60% reduction in the endogenous levels of ATP8B1 mRNA and protein, and a concomitant decrease in FXR mRNA and protein content, as well as in FXR phosphorylation. This decrease was accompanied by a marked reduction in mRNA levels of a subset of FXR targets, ...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2204021</comments>
            <pubDate>Thu, 19 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2204021</guid>        </item>
        <item>
            <title>Tumor necrosis factor-alpha impairs intestinal phosphate absorption in colitis.</title>
            <link>http://www.medworm.com/index.php?rid=2166638&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19196948%26dopt%3DAbstract</link>
            <description>Conclusions: Intestinal phosphate absorption mediated by NaPi-IIb protein is reduced in colitis. This inhibition is mediated by proinflammatory cytokine, TNF-alpha, through a novel molecular mechanism involving TNF-alpha/EGFR interaction. Key words: TNBS colitis, Caco-2 cells, TNF-, NaPi-IIb.
    PMID: 19196948 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2166638</comments>
            <pubDate>Thu, 05 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2166638</guid>        </item>
        <item>
            <title>Attenuation of Experimental Hepatopulmonary Syndrome in Endothelin B Receptor-deficient Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2166637&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19196949%26dopt%3DAbstract</link>
            <description>In conclusion, ETB receptor deficiency inhibits lung Akt/eNOS activation and prevents the onset of experimental HPS after CBDL. This effect is independent of inhibition of pulmonary intravascular monocyte accumulation. These results demonstrate that ET-1/ETB receptor signaling plays a key role in the initiation of experimental HPS. Key words: common bile duct ligation, endothelin-1, endothelin B receptor, endothelial nitric oxide synthase.
    PMID: 19196949 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2166637</comments>
            <pubDate>Thu, 05 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2166637</guid>        </item>
        <item>
            <title>cAMP-GEF cytoprotection by Src tyrosine kinase activation of phosphoinositide -3 -kinase p110 {beta}/{alpha} in rat hepatocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2166636&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19196950%26dopt%3DAbstract</link>
            <description>Conclusion: Activation of cAMP-GEFs results in phosphorylation of Src-TYK and Akt and activation of the p110beta/alpha subunits of PI3K. Maximal cAMP-GEF mediated Akt phosphorylation as well as protection from bile acid induced apoptosis requires activation of Src-TYK and the EGFR. These studies support the existence of 2 pathways: cAMP-GEF/ Rap/ Src/PI3Kbeta/Akt and cAMP-GEF/Rap/Src/EGFR/PI3Kalpha/Akt both of which are necessary for maximal cytoprotective effect of cAMP-GEFs in hepatocytes. Key words: bile acids, apoptosis, Rap, Akt.
    PMID: 19196950 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2166636</comments>
            <pubDate>Thu, 05 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2166636</guid>        </item>
        <item>
            <title>The effect of eating on lower esophageal sphincter electrical activity.</title>
            <link>http://www.medworm.com/index.php?rid=2166635&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19196951%26dopt%3DAbstract</link>
            <description>In conclusion, the beginning and duration of a meal are identified by distinct, easily recognizable changes in the amplitude of LES electrical activity. These changes depend on the type of the substance being swallowed and are most prominent with solid food. Changes in LES electrical activity can potentially be used for automatic eating detection. Key words: Lower Esophageal Sphincter, eating detection, esophageal motility, myoelectrical activity.
    PMID: 19196951 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2166635</comments>
            <pubDate>Thu, 05 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2166635</guid>        </item>
        <item>
            <title>Short-term adaptation of postprandial lipoprotein secretion and intestinal gene expression to a high fat diet.</title>
            <link>http://www.medworm.com/index.php?rid=2166634&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19196952%26dopt%3DAbstract</link>
            <description>SHORT-TERM ADAPTATION OF POSTPRANDIAL LIPOPROTEIN SECRETION AND INTESTINAL GENE EXPRESSION TO A HIGH FAT DIET.
    Am J Physiol Gastrointest Liver Physiol. 2009 Feb 5;
    Authors: Hernandez-Vallejo SJ, Alqub M, Luquet S, Cruciani-Guglielmacci C, Delerive P, Lobaccaro JM, Kalopissis AD, Chambaz J, Rousset M, Lacorte JM
    Western diet is characterized by a hypercaloric and hyperlipidic intake, enriched in saturated fats, that is associated with the increased occurrence of metabolic diseases. To cope with this overload of dietary lipids, the intestine, which delivers dietary lipids to the body, has to adapt its capacity in lipid absorption and lipoprotein synthesis. We have studied the early effects of a high fat diet (HFD) on intestinal lipid metabolism in mice. After seven days of HFD, m...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2166634</comments>
            <pubDate>Thu, 05 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2166634</guid>        </item>
        <item>
            <title>Interleukin-1{beta} contributes via nitric oxide to the up-regulation and functional activity of the zinc transporter Zip14 (Slc39A14) in murine hepatocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2149149&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179618%26dopt%3DAbstract</link>
            <description>Authors: Lichten LA, Liuzzi JP, Cousins RJ
    Zinc metabolism during chronic disease is dysregulated by inflammatory cytokines. Experiments with IL 6 (interleukin 6) knockout mice show that LPS regulates expression of the zinc transporter, Zip14, by a mechanism that is partially independent of IL 6. The LPS induced model of sepsis may occur by a mechanism signaled by NO (nitric oxide) as a secondary messenger. To address the hypothesis that NO can modulate Zip14 expression, we treated primary hepatocytes from wild type mice with the NO donor SNAP (s nitroso n acetyl penicillamine). After treatment with SNAP, steady state Zip14 mRNA levels displayed a maximal increase after 8 h, and a concomitant increase in the transcriptional activity of the gene. Chromatin immunoprecipitation documented...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149149</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149149</guid>        </item>
        <item>
            <title>Very high aquaporin-1 facilitated water permeability in mouse gallbladder.</title>
            <link>http://www.medworm.com/index.php?rid=2149148&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179619%26dopt%3DAbstract</link>
            <description>VERY HIGH AQUAPORIN-1 FACILITATED WATER PERMEABILITY IN MOUSE GALLBLADDER.
    Am J Physiol Gastrointest Liver Physiol. 2009 Jan 29;
    Authors: Li L, Zhang H, Ma T, Verkman AS
    Water transport across gallbladder epithelium is driven by osmotic gradients generated from active salt absorption and secretion. Aquaporin (AQP) water channels have been proposed to facilitate transepithelial water transport in gallbladder and to modulate bile composition. We found strong AQP1 immunofluorescence at the apical membrane of mouse gallbladder epithelium. Transepithelial osmotic water permeability (Pf) was measured in freshly isolated gallbladder sacs from the kinetics of luminal calcein self-quenching in response to an osmotic gradient. Pf was very high (0.12 cm/s) in gallbladders from wildtype mi...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149148</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149148</guid>        </item>
        <item>
            <title>Delineating the signals by which repetitive deformation stimulates intestinal epithelial migration across fibronectin.</title>
            <link>http://www.medworm.com/index.php?rid=2149147&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179620%26dopt%3DAbstract</link>
            <description>Authors: Gayer CP, Chaturvedi LS, Wang S, Alston B, Basson MD
    Repetitive strain stimulates intestinal epithelial migration across fibronectin via FAK, Src, and ERK, although how these signals act and interact remains unclear. We hypothesized that PI3K is central to this pathway. We subjected Caco-2 and IEC-6 cells to 10 cycles/minute deformation on flexible fibronectin-coated membranes, assayed migration by wound closure, and signaling by immunoblots. Strain stimulated PI3K, AKT, GSK, and p38 phosphorylation. Blocking each kinase prevented strain stimulation of migration. Blocking PI3K prevented strain-stimulated ERK and p38 phosphorylation. Blocking AKT did not. Downstream, blocking PI3K, AKT, or ERK inhibited strain-induced GSK-Ser9 phosphorylation. Upstream of AKT, reducing FAK or R...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149147</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149147</guid>        </item>
        <item>
            <title>Tissue factor-dependent coagulation contributes to alpha-naphthylisothiocyanate-induced cholestatic liver injury in mice.</title>
            <link>http://www.medworm.com/index.php?rid=2149146&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179621%26dopt%3DAbstract</link>
            <description>Authors: Luyendyk JP, Cantor GH, Kirchhofer D, Mackman N, Copple BL, Wang R
    Separation of concentrated bile acids from hepatic parenchymal cells is a key function of the bile duct epithelial cells (BDECs) that form intrahepatic bile ducts. Using co-immunostaining, we found that tissue factor (TF), the principal activator of coagulation, colocalized with cytokeratin 19, a marker of BDECs in the adult mouse liver. BDEC injury induced by xenobiotics such as alpha-naphthylisothiocyanate (ANIT) causes cholestasis, inflammation and hepatocellular injury. We tested the hypothesis that acute ANIT-induced cholestatic hepatitis is associated with TF-dependent activation of coagulation, and determined the role of TF in ANIT hepatotoxicity. Treatment of mice with ANIT (60 mg/kg) caused multifocal ...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149146</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149146</guid>        </item>
        <item>
            <title>Lysophosphatidyl choline modulates mechanosensitive L-type Ca2+ current in circular smooth muscle cells from human jejunum.</title>
            <link>http://www.medworm.com/index.php?rid=2149145&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179622%26dopt%3DAbstract</link>
            <description>Authors: Kraichely RE, Strege PR, Sarr MG, Kendrick ML, Farrugia G
    The L-type Ca(2+) channel expressed in gastrointestinal smooth muscle is mechanosensitive. Direct membrane stretch and shear stress results in increased Ca(2+) entry into the cell. The mechanism for mechanosensitivity is not known, and mechanosensitivity is not dependent on an intact cytoskeleton. The aim of this study was to determine whether L-type Ca(2+) channel mechanosensitivity is dependent on tension in the lipid bilayer in human jejunal circular muscle myocytes. Whole cell currents were recorded in the amphotericin perforated-patch configuration and lysophosphatidyl choline (LPC), lysophosphatidic acid (LPA) and choline used to alter differentially the tension in the lipid bilayer. Shear stress (perfusion at 10 ...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149145</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149145</guid>        </item>
        <item>
            <title>Secretory effects of a luminal bitter tastant and expressions of bitter taste receptors, T2Rs, in the human and rat large intestine.</title>
            <link>http://www.medworm.com/index.php?rid=2149144&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179623%26dopt%3DAbstract</link>
            <description>In conclusion, these results suggest that the T2R ligand, 6-PTU, evokes anion secretion and such response is regulated by prostaglandins. This luminal bitter sensing mechanism may be important for host defense in the GI tract. Key words: intestinal chemosensing, taste receptor type 2, prostaglandin E2, transepithelial ion transport.
    PMID: 19179623 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149144</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149144</guid>        </item>
        <item>
            <title>Lactobacillus reuteri ingestion prevents hyperexcitability of colonic DRG neurons induced by noxious stimuli.</title>
            <link>http://www.medworm.com/index.php?rid=2149143&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179624%26dopt%3DAbstract</link>
            <description>Authors: Ma X, Mao YK, Wang B, Huizinga JD, Bienenstock J, Kunze WA
    Lactobacillus species ingestion can decrease autonomic responses and spinal fibre discharge to nociceptive colorectal distension (CRD), even in the absence of inflammation. The present study aimed to determine if dorsal root ganglion (DRG) somas could be a locus where the anti-nociceptive probiotic may have an effect. Healthy rats were fed with Lactobacillus reuteri, or vehicle control for 9 days whereupon they were anaesthetised and intermittent distal colonic CRD at 80 mmHg distension was either performed for 1 hr, or not. The animals were immediately sacrificed and patch clamp recordings taken after isolation and overnight culture from those DRG that projected to the distal colon. CRD increased both the threshold fo...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149143</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149143</guid>        </item>
        <item>
            <title>Stimulation of Mucosal Secretion by Lubiprostone (SPI-0211) in Guinea Pig Small Intestine and Colon.</title>
            <link>http://www.medworm.com/index.php?rid=2149142&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179625%26dopt%3DAbstract</link>
            <description>Authors: Fei G, Wang YZ, Liu S, Hu HZ, Wang GD, Qu MH, Wang XY, Xia Y, Sun X, Bohn LM, Cooke HJ, Wood JD
    Actions of lubiprostone, a selective type-2 chloride channel activator, on mucosal secretion were investigated in guinea pig small intestine and colon. Flat-sheet preparations were mounted in Ussing flux chambers for recording short-circuit current (Isc) as a marker for electrogenic chloride secretion. Lubiprostone, applied to the small intestinal mucosa in 8 concentrations ranging from 1 to 3000nM, evoked increases in Isc in concentration-dependent manner with an EC50 of 42.5nM. Lubiprostone, applied to the mucosa of the colon in 8 concentrations ranging from 1 to 3000nM evoked increases in Isc in concentration-dependent manner with an EC50 of 31.7nM. Blockade of enteric nerves by ...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149142</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149142</guid>        </item>
        <item>
            <title>Regulation of the proprotein convertase subtilisin/ kexin type 9 in intestinal epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=2149141&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179626%26dopt%3DAbstract</link>
            <description>Authors: Leblond F, Seidah NG, Precourt LP, Delvin E, Dominguez M, Levy E
    Proprotein convertase subtilisin/kexin type 9 (PCSK9) posttranslationally promotes the degradation of the low-density lipoprotein receptor (LDLr) in hepatocytes and increases plasma LDL cholesterol. It is not clear, however, whether PCSK9 plays a role in the small intestine. Here, we characterized the patterns of variations of PCSK9 and LDLr in fully differentiated Caco-2/15 cells as a function of various potential effectors. Cholesterol (100 microM) solubilised in albumin or micelles significantly down-regulated PCSK9 gene (30%, p&amp;lt;0,05) and protein expression (50%, p&amp;lt;0,05), surprisingly in concert with a decrease in LDLr protein levels (45%, p&amp;lt;0,05). 25-hydroxycholesterol (50 microM) treated cells also ...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149141</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149141</guid>        </item>
        <item>
            <title>Small Molecule Inhibitors of Divalent Metal Transporter-1.</title>
            <link>http://www.medworm.com/index.php?rid=2149140&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179627%26dopt%3DAbstract</link>
            <description>This study characterizes important pharmacological tools that can be used to probe DMT1's mechanism of iron transport and its role in iron metabolism. Key words: Iron, Divalent Metal Transporter-1, Iron Transport Inhibitors.
    PMID: 19179627 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149140</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149140</guid>        </item>
        <item>
            <title>Signaling pathway via TNF{alpha}/NF{kappa}B in intestinal epithelial cells may be directly involved in colitis-associated carcinogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2149139&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179628%26dopt%3DAbstract</link>
            <description>Authors: Onizawa M, Nagaishi T, Kanai T, Nagano KI, Oshima S, Nemoto Y, Yoshioka A, Totsuka T, Okamoto R, Nakamura T, Sakamoto N, Tsuchiya K, Aoki K, Ohya K, Yagita H, Watanabe M
    Treatment with anti-TNFalpha mAb has been accepted as a successful maintenance therapy for patients with inflammatory bowel diseases (IBD). Moreover, it has been recently reported that blockade of TNF receptor (TNFR) 1 signaling in infiltrating hematopoietic cells may prevent the development of colitis-associated cancer (CAC). However, it remains unclear whether the TNFalpha signaling in epithelial cells is involved in the development of CAC. To investigate this, we studied the effects of anti-TNFalpha mAb in an animal model of CAC by administration of azoxymethane (AOM) followed by sequential dextran sodium s...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149139</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149139</guid>        </item>
        <item>
            <title>Mitochondrial DNA, Gastrointestinal Motor and Sensory Functions in Health and Functional Gastrointestinal Disorders.</title>
            <link>http://www.medworm.com/index.php?rid=2111884&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19147801%26dopt%3DAbstract</link>
            <description>Authors: Camilleri M, Carlson P, Zinsmeister AR, McKinzie S, Busciglio IA, Burton DD, Zaki EA, Boles RG
    Nerve, muscle and inflammatory cells involved in gastrointestinal (GI) function have high-energy requirements, and are affected in mitochondrial disorders. Familial aggregation of irritable bowel syndrome (IBS) frequently involves mothers and their children. Since mitochondrial DNA (mtDNA) is maternally inherited, mtDNA single nucleotide polymorphisms (SNPs) could confer risk to the development of IBS. The mtDNA SNPs, 16519C&amp;gt;T and 3010G&amp;gt;A, are associated with migraine and childhood cyclic vomiting syndrome. Our hypothesis is that these mtDNA SNPs are associated with functional GI disorders (FGIDs) and GI functions. The mt genome was first tested for the 7028C polymorphism (defi...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2111884</comments>
            <pubDate>Thu, 15 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2111884</guid>        </item>
        <item>
            <title>Kruppel-like factor 4 regulates adaptive expression of the zinc transporter ZIP4 (Slc39A4) in mouse small intestine.</title>
            <link>http://www.medworm.com/index.php?rid=2111883&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19147802%26dopt%3DAbstract</link>
            <description>Authors: Cousins RJ, Liuzzi JP, Guo L, Chang SM
    Epithelial cells of the small intestine are the site of zinc absorption. Intestinal uptake of zinc is inversely proportional to the dietary supply of this essential micronutrient. The mechanism responsible for this adaptive differential in apical zinc transport is not known. The zinc transporter Zip4 (SLC39A4) is essential for adequate enteric zinc uptake. In mice Zip4 expression is up-regulated at low zinc intakes with a concomitant ZIP4 localization to the apical enterocyte plasma membrane. With the present experiments, we show that the zinc finger transcription factor, KLF4, produced in high abundance in the intestine, is expressed at elevated levels when low zinc diets are provided to mice. Using a murine intestinal epithelial cell (I...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2111883</comments>
            <pubDate>Thu, 15 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2111883</guid>        </item>
        <item>
            <title>Pancreatic secretory trypsin inhibitor is a major motogenic and protective factor in human breast milk.</title>
            <link>http://www.medworm.com/index.php?rid=2111882&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19147803%26dopt%3DAbstract</link>
            <description>Conclusions: PSTI is secreted into human milk at concentrations which have probable pathophysiological relevance. Key words: repair, injury, nutrition.
    PMID: 19147803 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2111882</comments>
            <pubDate>Thu, 15 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2111882</guid>        </item>
        <item>
            <title>Expression and Sub-cellular Localization of BNIP3 in Hypoxic Hepatocytes and Liver Stress.</title>
            <link>http://www.medworm.com/index.php?rid=2111881&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19147804%26dopt%3DAbstract</link>
            <description>Authors: Metukuri MR, Beer-Stolz D, Namas RA, Dhupar R, Torres A, Loughran PA, Jefferson BS, Tsung A, Billiar TR, Vodovotz Y, Zamora R
    We have previously demonstrated that the Bcl-2/adenovirus EIB 19kD-interacting protein 3 (BNIP3), a cell death-related member of the Bcl-2 family, is upregulated in vitro and in vivo in both experimental and clinical settings of redox stress, and that nitric oxide (NO) downregulates its expression. Here, we sought to examine the expression and localization of BNIP3 in murine hepatocytes and in a murine model of hemorrhagic shock (HS) and ischemia/reperfusion (I/R). Freshly isolated mouse hepatocytes were exposed to 1% hypoxia for 6 hr followed by reoxygenation for 18 hr, and protein was isolated for Western blot analysis. Hepatocytes grown on coverslips...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2111881</comments>
            <pubDate>Thu, 15 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2111881</guid>        </item>
        <item>
            <title>Lactobacillus reuteri prevents colitis by reducing P-selectin-associated leukocyte- and platelet-endothelial cell interactions.</title>
            <link>http://www.medworm.com/index.php?rid=2111880&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19147805%26dopt%3DAbstract</link>
            <description>Authors: Schreiber O, Petersson J, Phillipson M, Perry MA, Roos S, Holm L
    Recent findings indicate that DSS induced colitis is associated with a prothrombogenic phenotype, with P-selectin playing a major role in platelet recruitment. Probiotics have been suggested to ameliorate colonic inflammation. We therefore investigated how treatment with L. reuteri influenced P-selectin expression, leukocyte and platelet endothelial cell interactions, and colitis severity in DSS treated rats. Rats were divided into four groups; non-treated, DSS treated (5% in drinking water for 9 days), L. reuteri and L. reuteri and DSS treated. The rats were anesthetized with Inactin (120 mg/kg i.p.) and the dual radiolabeled monoclonal antibody technique was used to quantify P-selectin expression. Leukocyte-end...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2111880</comments>
            <pubDate>Thu, 15 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2111880</guid>        </item>
        <item>
            <title>Hepatocyte nuclear factor-4{alpha} regulates human cellular retinol-binding protein type II gene expression in intestinal cells.</title>
            <link>http://www.medworm.com/index.php?rid=2111879&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19147806%26dopt%3DAbstract</link>
            <description>Authors: Yamaguchi N, Miyamoto S, Ogura Y, Goda T, Suruga K
    Cellular retinol-binding protein type II (CRBPII) is abundantly expressed in the small intestinal enterocytes of many vertebrates and plays important physiological roles in intestinal absorption, transport and metabolism of vitamin A. In the present study, we investigated regulation of human CRBPII gene expression using human intestinal Caco-2 BBe cells. We found that the human CRBPII gene contained a direct-repeat 1 (DR-1)-like nuclear receptor response element in the proximal promoter region, and that endogenous hepatocyte nuclear factor-4alpha (HNF-4alpha) was a major transcription factor binding to the DR-1-like element. Co-transfection of HNF-4alpha expression vector transactivated the human CRBPII gene promoter activity,...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2111879</comments>
            <pubDate>Thu, 15 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2111879</guid>        </item>
        <item>
            <title>Methods for Measurement of Gastric Motility.</title>
            <link>http://www.medworm.com/index.php?rid=2111878&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19147807%26dopt%3DAbstract</link>
            <description>This article reviews the tests most commonly available in practice and research to evaluate in vivo the gastric functions of emptying, accommodation, contractility, and myoelectrical activity. The rationale for testing, the relative strengths and weaknesses of each test, and technical details are summarized. We also briefly indicate the applications and validations of the tests for use in experimental animal studies.
    PMID: 19147807 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2111878</comments>
            <pubDate>Thu, 15 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2111878</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +27 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2086316&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%2529%2BAND%2B%25222009%252F01%252F03%2B01%252E38%2522%255BMHDA%255D%253A%25222009%252F01%252F08%2B00%252E30%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F01%252F03%2B01%252E38%2522%255BEDAT%255D%2529%2529</link>
            <description>27 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These PubMed results were generated on 2009/01/08PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2086316</comments>
            <pubDate>Thu, 08 Jan 2009 05:30:52 +0100</pubDate>
            <guid isPermaLink="false">2086316</guid>        </item>
        <item>
            <title>Low-dose inhaled carbon monoxide attenuates the remote intestinal inflammatory response elicited by hindlimb ischemia-reperfusion.</title>
            <link>http://www.medworm.com/index.php?rid=2072399&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19114681%26dopt%3DAbstract</link>
            <description>The objectives of this study were to determine if low-dose inhaled CO reduces remote intestinal leukocyte recruitment, proinflammatory cytokine expression, and oxidative stress elicited by hindlimb ischemia-reperfusion (I/R). Male mice underwent 1 h of hindlimb ischemia, followed by 3 h of reperfusion. Throughout reperfusion, mice were exposed to AIR or AIR + CO (250 ppm). Following reperfusion, the distal ileum was exteriorized to assess the intestinal inflammatory response by quantifying leukocyte rolling and adhesion in submucosal postcapillary venules with the use of intravital microscopy. Ileum samples were also analyzed for proinflammatory cytokine expression [tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta] and malondialdehyde (MDA) with the use of enzyme-linked immunos...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072399</comments>
            <pubDate>Thu, 01 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072399</guid>        </item>
        <item>
            <title>Early but not late administration of Glucagon-Like Peptide-2 following ileo-cecal resection augments putative intestinal stem cell expansion.</title>
            <link>http://www.medworm.com/index.php?rid=2072398&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19118113%26dopt%3DAbstract</link>
            <description>This study shows that in mice, GLP-2 promotes jejunal pISC expansion only in the period immediately following ICR. This is associated with increased IGF-I and accelerated adaptive increases in mucosal mass. These data provide clinical rationale relevant to the optimal timing of GLP-2 in patients with intestinal failure. Key words: Glucagon-Like Peptide-2, Intestinal Stem Cell, Intestinal Adaptation.
    PMID: 19118113 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072398</comments>
            <pubDate>Wed, 31 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072398</guid>        </item>
        <item>
            <title>Lymphocyte-derived interferon-{gamma} mediates ischemia-reperfusion induced leukocyte and platelet adhesion in intestinal microcirculation.</title>
            <link>http://www.medworm.com/index.php?rid=2072397&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19118114%26dopt%3DAbstract</link>
            <description>Authors: Osman M, Russell JM, Granger DN
    Although previous studies have implicated lymphocytes in the gut microvascular and inflammatory responses to ischemia-reperfusion (I/R), the lymphocyte population and lymphocyte-derived products that mediate these responses have not been defined. Platelet and leukocyte adhesion was measured in intestinal postcapillary venules of wild type (WT) mice and mice genetically deficient in either CD4+ T-cells (CD4(-/-)), CD8+ T-cells (CD8(-/-)), B-cells (B-cell(-/-)) or interferon-gamma (IFN-gamma(-/-)) subjected to 45 min of ischemia and 4 hrs reperfusion. The I/R-induced platelet and leukocyte recruitment responses were also evaluated following adoptive transfer of WT splenocytes into CD4(-/-), CD8(-/-), B-cell(-/-), and IFN-gamma(-/-) mice. WT mice e...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072397</comments>
            <pubDate>Wed, 31 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072397</guid>        </item>
        <item>
            <title>Short food deprivation inhibits orexin receptor 1 expression and orexin-A induced intracellular calcium signaling in acutely isolated duodenal enterocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2072396&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19118115%26dopt%3DAbstract</link>
            <description>Conclusions. Induction of intracellular calcium signaling in isolated duodenal enterocytes is mediated primarily by OX1R receptors. Short (overnight) food deprivation markedly depresses receptor expression and inhibits orexin-A induced increases in [Ca(2+)]i. Studies of enterocyte signaling and intestinal secretion requires particular evaluation regarding feeding status. Key words: (Ala11, D-Leu15)-orexin-B, bicarbonate secretion, fasting, feeding.
    PMID: 19118115 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072396</comments>
            <pubDate>Wed, 31 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072396</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +35 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2045205&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%2529%2BAND%2B%25222008%252F12%252F07%2B01%252E38%2522%255BMHDA%255D%253A%25222008%252F12%252F18%2B01%252E38%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F12%252F07%2B01%252E38%2522%255BEDAT%255D%2529%2529</link>
            <description>35 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These PubMed results were generated on 2008/12/18PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2045205</comments>
            <pubDate>Thu, 18 Dec 2008 06:38:10 +0100</pubDate>
            <guid isPermaLink="false">2045205</guid>        </item>
        <item>
            <title>Sodium channel mutation in the irritable bowel syndrome: Evidence for an ion channelopathy.</title>
            <link>http://www.medworm.com/index.php?rid=2015955&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056759%26dopt%3DAbstract</link>
            <description>In conclusion, the G298S-SCN5A missense mutation caused a marked reduction of whole cell Na(+) current and loss-of-function of Nav1.5 and suggests SCN5A as a candidate gene in the pathophysiology of IBS. Key words: SCN5A, Nav1.5, channelopathy, current density.
    PMID: 19056759 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015955</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015955</guid>        </item>
        <item>
            <title>Lymphatic and Portal Vein Absorption of Organochlorine Compounds in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2015954&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056760%26dopt%3DAbstract</link>
            <description>We report here methodology that allows a direct measurement of portal vein absorption that is independent of these assumptions. Mesenteric lymph was diverted from rats by cannulation. Portal blood was sampled after duodenal infusion of a bolus of compound of interest along with a portal absorption marker, 3-O-methylglucose. Since lymph was diverted, the appearance in portal blood was solely the result of portal absorption. Absorption was quantified by the areas under the curve for the compound and marker. Portal absorption was a function of the octanol/water partition coefficients for four organochlorine compounds: hexachlorobenzene; pentachlorophenol; DDT; and its metabolite, DDE. Key words: portal vein, mesenteric lymph duct, organochlorines, DDT, DDE.
    PMID: 19056760 [PubMed - as sup...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015954</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015954</guid>        </item>
        <item>
            <title>In vivo imaging of zebrafish digestive organ function using multiple quenched fluorescent reporters.</title>
            <link>http://www.medworm.com/index.php?rid=2015953&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056761%26dopt%3DAbstract</link>
            <description>Authors: Hama K, Provost E, Baranowski TC, Rubinstein AL, Anderson JL, Leach SD, Farber SA
    Optical clarity of larvae makes the zebrafish ideal for real-time analyses of vertebrate organ function through the use of fluorescent reporters of enzymatic activities. A key function of digestive organs is to couple the generation of enzymes with mechanical processes that enable nutrient availability and absorption. However, it has been extremely difficult, and in many cases not possible, to directly observe digestive processes in a live vertebrate. Here we describe a new method to visualize intestinal protein and lipid processing simultaneously in live zebrafish larvae using a quenched fluorescent protein (EnzChek) and phospholipid (PED6). By employing these reagents, we found that wild-type l...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015953</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015953</guid>        </item>
        <item>
            <title>Nutrient-driven incretin secretion into intestinal lymph is different between diabetic, Goto-Kakizaki rats and Wistar rats.</title>
            <link>http://www.medworm.com/index.php?rid=2015952&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056762%26dopt%3DAbstract</link>
            <description>Conclusions. After administration of a carbohydrate-containing meal, GK rats were unable to mount as robust a response of both GIP and GLP-1 compared to Wistar rats, a phenomenon not seen after a lipid meal. We propose a similar, glucose-mediated incretin secretion pathway defect of both K and L cells in GK rats. Key words: glucagon-like peptide-1 (GLP-1), gastric inhibitory polypeptide (GIP), enteroendocrine cell, lymph.
    PMID: 19056762 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015952</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015952</guid>        </item>
        <item>
            <title>Cyclooxygenase Type 1 (COX-1) vs. Cyclooxygenase Type 2 (COX-2) as a Determinant of the Basal Tone in the Internal Anal Sphincter.</title>
            <link>http://www.medworm.com/index.php?rid=2015951&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056763%26dopt%3DAbstract</link>
            <description>Authors: De Godoy MA, Rattan N, Rattan S
    Prostanoids, produced endogenously via cyclooxygenases, have been implicated in the sustained contraction of different smooth muscles. The two major types of cyclooxygenases are COX-1 and COX-2. The COX subtype involved in the basal state of the internal anal sphincter (IAS) smooth muscle tone is not known. To identify the COX subtype, we examined the effect of COX-1 vs. COX-2 selective inhibitors, SC-560 and rofecoxib respectively, on the rat IAS basal tone. We also determined the effect of selective deletion of COX-1 and COX-2 genes on the murine IAS basal tone. Data show that SC-560 causes significantly more efficacious and potent concentration-dependent decreases in the IAS tone as compared with rofecoxib. Supporting these data, significantl...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015951</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015951</guid>        </item>
        <item>
            <title>Transplantation of basic fibroblast growth factor-pretreated adipose tissue-derived stromal cells enhances regression of liver fibrosis in mice.</title>
            <link>http://www.medworm.com/index.php?rid=2015950&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056764%26dopt%3DAbstract</link>
            <description>Authors: Kamada Y, Yoshida Y, Saji Y, Fukushima J, Tamura S, Kiso S, Hayashi N
    Adipose tissue-derived stromal cells (ADSC) potentially differentiate into various cell types similar to bone marrow-derived mesenchymal stromal cells (BMSC). Unlike BMSC, ADSC can be harvested easily and repeatedly. However, the advantages of ADSC for cell transplantation in liver disease remain unclear. To investigate this, we developed a novel culture system for ADSC, as well as effective methods for transplantation of ADSC into mice liver. ADSC were isolated from subcutaneous adipose tissues of male C57BL6/J mice and cultured on plastic dishes with or without basic fibroblast growth factor (bFGF). In the in vivo study, ADSC isolated from GFP-transgenic mice were transplanted into carbon tetrachloride-inj...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015950</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015950</guid>        </item>
        <item>
            <title>Functional coupling of the down regulated in adenoma Cl-/base exchanger DRA and the apical sodium/hydrogen exchangers NHE2 and NHE3.</title>
            <link>http://www.medworm.com/index.php?rid=2015949&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056765%26dopt%3DAbstract</link>
            <description>Authors: Musch MW, Arvans DL, Wu GD, Chang EB
    Non-nutrient dependent salt absorption across the brush border membrane of intestinal epithelial cells is primarily mediated by coupled apical Na(+)-H(+) (aNHE) and anion exchange transport, the latter suspected of being mediated by DRA (Down-Regulated in Adenoma, SLC26A3) that is defective in congenital chloridorrhea. To investigate DRA in greater detail and determine if DRA and NHE activities can be coupled, (22)Na(+) and (36)Cl(-) uptake were measured in Caco2BBE colon cells infected with the tet-off-inducible DRA transgene. Under basal conditions, DRA activity was low in normal and infected Caco2BBE cells in the presence of tetracycline, whereas NHE activities could be easily detected. When apical NHE activity was increased by transfect...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015949</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015949</guid>        </item>
        <item>
            <title>Epidermal Growth Factor receptor is involved in enterocyte anoikis through the dismantling of E-cadherin-mediated junctions.</title>
            <link>http://www.medworm.com/index.php?rid=2015948&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056766%26dopt%3DAbstract</link>
            <description>Authors: Lugo-Martinez VH, Petit CS, Fouquet S, Le Beyec J, Chambaz J, Pin&amp;#xE7;on-Raymond M, Cardot P, Thenet S
    Enterocytes of the intestinal epithelium are continually regenerated. They arise from precursor cells in crypts, migrate along villi, and finally die, 3 to 4 days later, when they reach the villus apex. Their death is thought to occur by anoikis, a form of apoptosis induced by cell detachment, but the mechanism of this process remains poorly understood. We have previously shown that a key event in the onset of anoikis in normal enterocytes detached from the basal lamina is the disruption of adherens junctions mediated by E-cadherin. Here we have further investigated the mechanisms underlying this disassembly of the adherens junctions. We show that disruption of the junctions...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015948</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015948</guid>        </item>
        <item>
            <title>Atorvastatin attenuates angiotensin ii-induced inflammatory actions in the liver.</title>
            <link>http://www.medworm.com/index.php?rid=2015947&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056767%26dopt%3DAbstract</link>
            <description>ATORVASTATIN ATTENUATES ANGIOTENSIN II-INDUCED INFLAMMATORY ACTIONS IN THE LIVER.
    Am J Physiol Gastrointest Liver Physiol. 2008 Dec 4;
    Authors: Moreno M, Ramalho LN, Sancho-Bru P, Ruiz-Ortega M, Ramalho F, Abraldes JG, Colmenero J, Dominguez M, Egido J, Arroyo V, Gines P, Bataller R
    Statins exert beneficial effects in chronically damaged tissues. Angiotensin II (Ang II) participates in liver fibrogenesis by inducing oxidative stress, inflammation and transforming growth factor beta1 (TGF-beta1) expression. We investigate whether Ator modulates Ang II-induced pathogenic effects in the liver. Male Wistar rats were infused with saline or Ang II (100 ng/Kg/min) for 4 weeks through a subcutaneous osmotic pump. Rats received either vehicle or Ator (5 mg/Kg/day) by gavage. Angiotensin...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015947</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015947</guid>        </item>
        <item>
            <title>Loss of p21Waf1/cip1/Sdi1 enhances intestinal stem cell survival following radiation injury.</title>
            <link>http://www.medworm.com/index.php?rid=2015946&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056768%26dopt%3DAbstract</link>
            <description>In conclusion, deletion of p21 results in protection of crypt stem/progenitor cells from IR induced cell death. Furthermore the increase in crypt survival is associated with increased numbers of Msi-1 and survivin expressing cells in regenerative crypts. Key words: p21, musashi-1, gamma irradiation, survivin, crypt survival.
    PMID: 19056768 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015946</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015946</guid>        </item>
        <item>
            <title>Corrigendum.</title>
            <link>http://www.medworm.com/index.php?rid=2015945&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056769%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 19056769 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015945</comments>
            <pubDate>Mon, 01 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015945</guid>        </item>
        <item>
            <title>Increased glial glutamate transporter EAAT2 expression reduces visceral nociceptive response in mice.</title>
            <link>http://www.medworm.com/index.php?rid=1979235&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19023027%26dopt%3DAbstract</link>
            <description>Authors: Lin Y, Tian G, Roman K, Handy C, Travers JB, Lin CL, Stephens Jr RL
    Visceral hypersensitivity is the leading complaint of functional bowel disorders. Central sensitization mediated by glutamate receptor activation is implicated in pathophysiology of visceral pain. The glial glutamate transporter EAAT2 is the principal mediator of glutamate clearance to terminate glutamate-mediated responses. Transgenic mice over-expressing human EAAT2 (EAAT2 mice), which exhibited a 2-fold enhanced glutamate uptake, showed 39% less writhing response to intraperitoneal acetic acid than non-transgenic littermates. Moreover, EAAT2 transgenic mice showed a 53-64% reduction in visceromotor response (VMR) to colo-rectal distension (CRD) when assessing the response to graded increase in pressures. Co...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1979235</comments>
            <pubDate>Thu, 20 Nov 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1979235</guid>        </item>
        <item>
            <title>Synchronized Gastric Electrical Stimulation Improves Vagotomy-induced Impairment in Gastric Accommodation via the Nitrergic Pathway in Dogs.</title>
            <link>http://www.medworm.com/index.php?rid=1979234&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19023028%26dopt%3DAbstract</link>
            <description>Conclusions: SGES with appropriate parameters restores gastric accommodation and improves gastric slow waves impaired by vagotomy. The improvement in gastric accommodation with SGES is mediated via the nitrergic pathway. Combined with previously reported findings (enhanced antral contractions and accelerated gastric emptying) and findings in this study (improved gastric accommodation and slow waves), SGES may be a viable therapy for gastroparesis. Key words: gastric accommodation, gastric electrical stimulation, gastric slow waves, gastric tone, gastroparesis.
    PMID: 19023028 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1979234</comments>
            <pubDate>Thu, 20 Nov 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1979234</guid>        </item>
        <item>
            <title>Decreased heart rate variability in patients with cirrhosis relates to the presence and severity of hepatic encephalopathy.</title>
            <link>http://www.medworm.com/index.php?rid=1979233&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19023029%26dopt%3DAbstract</link>
            <description>Conclusions: The changes observed in HRV and in neuropsychiatric status in patients with cirrhosis are significantly correlated, possibly reflecting a common pathogenic mechanism mediated by inflammatory cytokines. Key words: Hepatic encephalopathy, cirrhosis, heart rate variability, cytokine.
    PMID: 19023029 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1979233</comments>
            <pubDate>Thu, 20 Nov 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1979233</guid>        </item>
        <item>
            <title>Hepatocyte Growth Factor Regulates the Development of Highly Pure Cultured Chief Cells from Rat Stomach by Stimulating Chief Cell Proliferation in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=1979232&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19023030%26dopt%3DAbstract</link>
            <description>Authors: Tashima K, Zhang S, Ragasa R, Nakamura E, Seo JH, Muvaffak A, Hagen SJ
    The physiology of gastric epithelial cells is often studied using cancer cell lines, which may, or may not provide information relevant to normal cells. Because few models exist to study chief cell physiology, in vitro, our purpose was to develop primary cultured chief cells from rodent species that are structurally and functionally similar to native chief cells. For this, isolated chief cells from the rat stomach, purified by counterflow elutriation and density gradient centrifugation, were grown in media with growth factors. Purity and the continuity of tight junctions were determined and permeability, viability, TER, cell number and proliferation, and pepsinogen secretion in response to carbachol were me...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1979232</comments>
            <pubDate>Thu, 20 Nov 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1979232</guid>        </item>
        <item>
            <title>Requirement of Notch activation during regeneration of the intestinal epithelia.</title>
            <link>http://www.medworm.com/index.php?rid=1979231&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19023031%26dopt%3DAbstract</link>
            <description>This study showed the critical involvement of Notch signaling during intestinal tissue regeneration, regulating differentiation, proliferation and anti-microbial response of the epithelial cells. Thus, Notch signaling is a key intracellular molecular pathway for the proper reconstruction of the intestinal epithelia. Key words: Intestinal epithelial cells, PLA2G2A, goblet cells, ulcerative colitis.
    PMID: 19023031 [PubMed - as supplied by publisher] (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1979231</comments>
            <pubDate>Thu, 20 Nov 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1979231</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +25 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1867628&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%2529%2BAND%2B%25222008%252F10%252F05%2B05%252E08%2522%255BMHDA%255D%253A%25222008%252F10%252F11%2B04%252E57%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F10%252F05%2B05%252E08%2522%255BEDAT%255D%2529%2529</link>
            <description>25 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These PubMed results were generated on 2008/10/11PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1867628</comments>
            <pubDate>Sat, 11 Oct 2008 08:57:45 +0100</pubDate>
            <guid isPermaLink="false">1867628</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +23 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1832401&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%2529%2BAND%2B%25222008%252F09%252F21%2B04%252E55%2522%255BMHDA%255D%253A%25222008%252F09%252F27%2B05%252E09%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F09%252F21%2B04%252E55%2522%255BEDAT%255D%2529%2529</link>
            <description>23 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These PubMed results were generated on 2008/09/27PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1832401</comments>
            <pubDate>Sat, 27 Sep 2008 09:09:46 +0100</pubDate>
            <guid isPermaLink="false">1832401</guid>        </item>
        <item>
            <title>Am J Physiol Gastrointest Liver Physiol; +23 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1781845&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%2529%2BAND%2B%25222008%252F09%252F10%2B04%252E53%2522%255BMHDA%255D%253A%25222008%252F09%252F11%2B05%252E01%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BGastrointest%2BLiver%2BPhysiol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F09%252F10%2B04%252E53%2522%255BEDAT%255D%2529%2529</link>
            <description>23 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Gastrointest Liver Physiol
These PubMed results were generated on 2008/09/11PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Gastroi...)</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1781845</comments>
            <pubDate>Thu, 11 Sep 2008 09:01:21 +0100</pubDate>
            <guid isPermaLink="false">1781845</guid>        </item>
        <item>
            <title>Overexpression of progesterone receptor B increases sensitivity of human colon muscle cells to progesterone.</title>
            <link>http://www.medworm.com/index.php?rid=1778417&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18776045%26dopt%3DAbstract</link>
            <description>Authors: Cheng L, Pricolo V, Biancani P, Behar J
    Colon muscle strips and cells from female patients with slow-transit constipation (STC) exhibit impaired motility, signal transduction abnormalities characterized by downregulation of G(q/11) and upregulation of G(s) proteins, decreased cyclooxygenase (COX)-1 and thromboxane (Tx)B(2) levels, increased COX-2 and PGE(2) levels, and overexpression of progesterone receptors (PGR). Progesterone (P(4)) treatment of normal cells reproduced these motility and signal transduction abnormalities. The purpose of the study was to examine whether overexpression of PGR-B reproduces these abnormalities by rendering the cells more sensitive to physiological concentrations of P(4). Cultured human colon muscle was transfected with a plasmid DNA expressing ...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1778417</comments>
            <pubDate>Mon, 01 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1778417</guid>        </item>
        <item>
            <title>Effects of cholecystokinin-58 on type 1 cholecystokinin receptor function and regulation.</title>
            <link>http://www.medworm.com/index.php?rid=1778416&amp;cid=s_30378_17_f&amp;fid=30378&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18776046%26dopt%3DAbstract</link>
            <description>Authors: Wu SV, Harikumar KG, Burgess RJ, Reeve JR, Miller LJ
    Cholecystokinin, like many peptide hormones, is present as multiple molecular forms. CCK-58 has been identified as the dominant form in the circulation, whereas most of the studies of CCK-receptor interactions have been performed with CCK-8. Despite both sharing the pharmacophoric region of CCK, representing its carboxy terminal heptapeptide amide, studies in vivo have demonstrated biological diversity of action of the two peptides, with CCK-58, but not CCK-8, stimulating pancreatic fluid secretion and lengthening the interval between meals. Here, we have directly studied the ability of these two CCK peptides to bind to the type 1 CCK receptor and to stimulate it to elicit an intracellular calcium response. The calcium respo...</description>
            <author>Am J Physiol Gastroi...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1778416</comments>
            <pubDate>Mon, 01 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1778416</guid>        </item>
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