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        <title>Am J Pathol 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 Pathol' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Am+J+Pathol&t=Am+J+Pathol&s=Search&f=source]]></link>
        <lastBuildDate>Sun, 21 Mar 2010 15:53:41 +0100</lastBuildDate>
        <item>
            <title>Am J Pathol; +105 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3378612&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222010%252F03%252F12%252021.26%2522%255BMHDA%255D%253A%25222010%252F03%252F18%252013.16%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222010%252F03%252F12%252021.26%2522%255BEDAT%255D%29%29</link>
            <description>105 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3378612</comments>
            <pubDate>Thu, 18 Mar 2010 17:16:02 +0100</pubDate>
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        <item>
            <title>Influenza Virus Receptor Specificity. Disease and Transmission.</title>
            <link>http://www.medworm.com/index.php?rid=3339142&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20203283%26dopt%3DAbstract</link>
            <description>Authors: Garc&amp;#xED;a-Sastre A
    This Commentary discusses the role of influenza virus specificity in viral transmission.
    PMID: 20203283 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3339142</comments>
            <pubDate>Thu, 04 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3339142</guid>        </item>
        <item>
            <title>Lymphangioleiomyoma Cells and Lymphatic Endothelial Cells: Expression of VEGFR-3 in Lymphangioleiomyoma Cell Clusters.</title>
            <link>http://www.medworm.com/index.php?rid=3339141&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20203284%26dopt%3DAbstract</link>
            <description>Authors: Seyama K, Mitani K, Kumasaka T
    This Correspondence addresses the use of LAM and LAM-derived cells in Issaka et al.
    PMID: 20203284 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3339141</comments>
            <pubDate>Thu, 04 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3339141</guid>        </item>
        <item>
            <title>Function of EWS-POU5F1 in Sarcomagenesis and Tumor Cell Maintenance.</title>
            <link>http://www.medworm.com/index.php?rid=3339140&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20203285%26dopt%3DAbstract</link>
            <description>Authors: Fujino T, Nomura K, Ishikawa Y, Makino H, Umezawa A, Aburatani H, Nagasaki K, Nakamura T
    POU5F1 is a transcription factor essential for the self-renewal activity and pluripotency of embryonic stem cells and germ cells. We have previously reported that POU5F1 is fused to EWSR1 in a case of undifferentiated sarcoma with chromosomal translocation t(6;22)(p21;q12). In addition, the EWS-POU5F1 chimeras have been recently identified in human neoplasms of the skin and salivary glands. To clarify the roles of the EWS-POU5F1 chimera in tumorigenesis and tumor cell maintenance, we used small-interfering RNA-mediated gene silencing. Knockdown of EWS-POU5F1 in the t(6;22) sarcoma-derived GBS6 cell line resulted in a significant decrease of cell proliferation because of G1 cell cycle arres...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3339140</comments>
            <pubDate>Thu, 04 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3339140</guid>        </item>
        <item>
            <title>Lack of CXC Chemokine Receptor 3 Signaling Leads to Hypertrophic and Hypercellular Scarring.</title>
            <link>http://www.medworm.com/index.php?rid=3339139&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20203286%26dopt%3DAbstract</link>
            <description>Authors: Yates CC, Krishna P, Whaley D, Bodnar R, Turner T, Wells A
    CXC chemokine receptor 3 (CXCR3) signaling promotes keratinocyte migration while terminating fibroblast and endothelial cell immigration into wounds; this signaling also directs epidermal and matrix maturation. Herein, we investigated the long-term effects of failure to activate the &quot;stop-healing&quot; CXCR3 axis. Full-thickness excisional wounds were created on CXCR3 knockout((-/-)) or wild-type mice and examined at up to 180 days after wounding. Grossly, the CXCR3(-/-) mice presented a thick keratinized scar compared with the wild-type mice in which the scar was scarcely noticeable; histological examination revealed thickening of both the epidermis and dermis. The dermis was disorganized with thick and long collagen fibri...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3339139</comments>
            <pubDate>Thu, 04 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3339139</guid>        </item>
        <item>
            <title>Am J Pathol; +52 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3327410&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222010%252F02%252F20%252008.02%2522%255BMHDA%255D%253A%25222010%252F03%252F03%252013.12%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222010%252F02%252F20%252008.02%2522%255BEDAT%255D%29%29</link>
            <description>52 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2010/03/03PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3327410</comments>
            <pubDate>Wed, 03 Mar 2010 18:12:04 +0100</pubDate>
            <guid isPermaLink="false">3327410</guid>        </item>
        <item>
            <title>Am J Pathol; +17 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3288915&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222010%252F02%252F14%252016.40%2522%255BMHDA%255D%253A%25222010%252F02%252F20%252008.02%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222010%252F02%252F14%252016.40%2522%255BEDAT%255D%29%29</link>
            <description>17 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2010/02/20PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3288915</comments>
            <pubDate>Sat, 20 Feb 2010 13:02:02 +0100</pubDate>
            <guid isPermaLink="false">3288915</guid>        </item>
        <item>
            <title>Am J Pathol; +24 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3198699&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222010%252F01%252F17%252016.30%2522%255BMHDA%255D%253A%25222010%252F01%252F23%252006.30%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222010%252F01%252F17%252016.30%2522%255BEDAT%255D%29%29</link>
            <description>24 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2010/01/23PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3198699</comments>
            <pubDate>Sat, 23 Jan 2010 11:30:02 +0100</pubDate>
            <guid isPermaLink="false">3198699</guid>        </item>
        <item>
            <title>Am J Pathol; +43 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3168073&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222010%252F01%252F10%252006.06%2522%255BMHDA%255D%253A%25222010%252F01%252F13%252023.20%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222010%252F01%252F10%252006.06%2522%255BEDAT%255D%29%29</link>
            <description>43 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2010/01/13PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3168073</comments>
            <pubDate>Thu, 14 Jan 2010 04:20:02 +0100</pubDate>
            <guid isPermaLink="false">3168073</guid>        </item>
        <item>
            <title>Am J Pathol; +19 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3136927&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222009%252F12%252F26%252009.42%2522%255BMHDA%255D%253A%25222010%252F01%252F02%252019.30%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F12%252F26%252009.42%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 Pathol
These pubmed results were generated on 2010/01/02PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136927</comments>
            <pubDate>Sun, 03 Jan 2010 00:30:02 +0100</pubDate>
            <guid isPermaLink="false">3136927</guid>        </item>
        <item>
            <title>Am J Pathol; +24 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3102195&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222009%252F12%252F17%252003.18%2522%255BMHDA%255D%253A%25222009%252F12%252F18%252023.56%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F12%252F17%252003.18%2522%255BEDAT%255D%29%29</link>
            <description>24 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3102195</comments>
            <pubDate>Sat, 19 Dec 2009 04:56:02 +0100</pubDate>
            <guid isPermaLink="false">3102195</guid>        </item>
        <item>
            <title>Am J Pathol; +82 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3093238&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222009%252F12%252F09%252017.12%2522%255BMHDA%255D%253A%25222009%252F12%252F17%252003.18%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F12%252F09%252017.12%2522%255BEDAT%255D%29%29</link>
            <description>82 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2009/12/17PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3093238</comments>
            <pubDate>Thu, 17 Dec 2009 08:18:03 +0100</pubDate>
            <guid isPermaLink="false">3093238</guid>        </item>
        <item>
            <title>Note of concern.</title>
            <link>http://www.medworm.com/index.php?rid=3071961&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19965804%26dopt%3DAbstract</link>
            <description>Authors: Ibdah JA
    
    PMID: 19965804 [PubMed - in process] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3071961</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3071961</guid>        </item>
        <item>
            <title>Cytoprotective Mitochondrial Chaperone TRAP-1 As a Novel Molecular Target in Localized and Metastatic Prostate Cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3045565&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948822%26dopt%3DAbstract</link>
            <description>Authors: Leav I, Plescia J, Goel HL, Li J, Jiang Z, Cohen RJ, Languino LR, Altieri DC
    Molecular chaperones of the heat shock protein-90 (Hsp90) family promote cell survival, but the molecular requirements of this pathway in tumor progression are not understood. Here, we show that a mitochondria-localized Hsp90 chaperone, tumor necrosis factor receptor-associated protein-1 (TRAP-1), is abundantly and ubiquitously expressed in human high-grade prostatic intraepithelial neoplasia, Gleason grades 3 through 5 prostatic adenocarcinomas, and metastatic prostate cancer, but largely undetectable in normal prostate or benign prostatic hyperplasia in vivo. Prostate lesions formed in genetic models of the disease, including the transgenic adenocarcinoma of the mouse prostate and mice carrying pros...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045565</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045565</guid>        </item>
        <item>
            <title>Inducible Nephrin Transgene Expression in Podocytes Rescues Nephrin-Deficient Mice from Perinatal Death.</title>
            <link>http://www.medworm.com/index.php?rid=3045564&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948823%26dopt%3DAbstract</link>
            <description>Authors: Juhila J, Lassila M, Roozendaal R, Lehtonen E, Messing M, Langer B, Kerjaschki D, Verbeek JS, Holthofer H
    Mutations leading to nephrin loss result in massive proteinuria both in humans and mice. Early perinatal lethality of conventional nephrin knockout mice makes it impossible to determine the role of nephrin protein in the adult kidney and in extra-renal tissues. Herein, we studied whether podocyte-specific, doxycycline-inducible, rat nephrin expression can rescue nephrin-deficient mice from perinatal lethality. Fourteen littermates out of 72 lacked endogenous nephrin and expressed transgenic rat nephrin. Six of these rescued mice survived until 6 weeks of age, whereas the nephrin-deficient pups died before the age of 5 days. The rescued mice were smaller, developed proteinu...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045564</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045564</guid>        </item>
        <item>
            <title>EPCs Mobilized and Activated by Neurotrophic Factors May Contribute to Pathologic Neovascularization in Diabetic Retinopathy.</title>
            <link>http://www.medworm.com/index.php?rid=3045563&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948824%26dopt%3DAbstract</link>
            <description>Authors: Liu X, Li Y, Liu Y, Luo Y, Wang D, Annex BH, Goldschmidt-Clermont PJ
    Diabetic retinopathy is characterized by pathological retinal neovascularization. Accumulating evidence has indicated that high levels of circulating endothelial progenitor cells (EPCs) are an important risk factor for neovascularization. Paradoxically, the reduction and dysfunction of circulating EPCs has been extensively reported in diabetic patients. We hypothesized that EPCs are differentially altered in the various vasculopathic complications of diabetes mellitus, exhibiting distinct behaviors in terms of angiogenic response to ischemia and growth factors and potentially playing a potent role in motivating vascular precursors to induce pathological neovascularization. Circulating levels of EPCs from diab...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045563</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045563</guid>        </item>
        <item>
            <title>Experimental Neonatal Status Epilepticus and the Development of Temporal Lobe Epilepsy with Unilateral Hippocampal Sclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=3045562&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948825%26dopt%3DAbstract</link>
            <description>Authors: Dunleavy M, Shinoda S, Schindler C, Ewart C, Dolan R, Gobbo OL, Kerskens CM, Henshall DC
    Hippocampal sclerosis is a common pathological finding in patients with temporal lobe epilepsy, including children, but a causal relationship to early-life seizures remains in question. Neonatal status epilepticus in animals can result in neuronal death within the hippocampus, although macroscopic features of hippocampal shrinkage are not evident at adulthood. Here, we examined electrophysiological and pathological consequences of focally evoked status epilepticus triggered by intra-amygdala microinjection of kainic acid in postnatal day 10 rat pups. Neonatal status epilepticus resulted in extensive neuronal death in the ipsilateral hippocampal CA1 and CA3 subfields and hilus, as assessed ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045562</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045562</guid>        </item>
        <item>
            <title>Cross-Talk between Vascular Endothelial Growth Factor and Matrix Metalloproteinases in the Induction of Neovascularization in Vivo.</title>
            <link>http://www.medworm.com/index.php?rid=3045561&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948826%26dopt%3DAbstract</link>
            <description>Authors: Ebrahem Q, Chaurasia SS, Vasanji A, Qi JH, Klenotic PA, Cutler A, Asosingh K, Erzurum S, Anand-Apte B
    Matrix metalloproteinases (MMPs), a specialized group of enzymes capable of proteolytically degrading extracellular matrix proteins, have been postulated to play an important role in angiogenesis. It has been suggested that MMPs can regulate neovascularization using mechanisms other than simple remodeling of the capillary basement membrane. To determine the interplay between vascular endothelial growth factor (VEGF) and MMPs, we investigated the induction of angiogenesis by recombinant active MMPs and VEGF in vivo. Using a rat corneal micropocket in vivo angiogenesis assay, we observed that the active form of MMP-9 could induce neovascularization in vivo when compared with the...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045561</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045561</guid>        </item>
        <item>
            <title>The Role of Liver Sinusoidal Cells in Hepatocyte-Directed Gene Transfer.</title>
            <link>http://www.medworm.com/index.php?rid=3045560&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948827%26dopt%3DAbstract</link>
            <description>Authors: Jacobs F, Wisse E, De Geest B
    Hepatocytes are a key target for gene therapy of inborn errors of metabolism as well as of acquired diseases such as liver cancer and hepatitis. Gene transfer efficiency into hepatocytes is significantly determined by histological and functional aspects of liver sinusoidal cells. On the one hand, uptake of vectors by Kupffer cells and liver sinusoidal endothelial cells may limit hepatocyte transduction. On the other hand, the presence of fenestrae in liver sinusoidal endothelial cells provides direct access to the space of Disse and allows vectors to bind to receptors on the microvillous surface of hepatocytes. Nevertheless, the diameter of fenestrae may restrict the passage of vectors according to their size. On the basis of lege artis measuremen...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045560</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045560</guid>        </item>
        <item>
            <title>Pigment Epithelium-Derived Factor Inhibits Lysosomal Degradation of Bcl-xL and Apoptosis in HepG2 cells.</title>
            <link>http://www.medworm.com/index.php?rid=3045559&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948828%26dopt%3DAbstract</link>
            <description>Authors: Kawaguchi T, Yamagishi SI, Itou M, Okuda K, Sumie S, Kuromatsu R, Sakata M, Abe M, Taniguchi E, Koga H, Harada M, Ueno T, Sata M
    Pigment epithelium-derived factor (PEDF) has several biological actions on tumor cells, but its effects are cell-type dependent. The aim of this study was to examine the pathophysiological role of PEDF in hepatocellular carcinoma (HCC). PEDF expression was examined in various hepatoma cell lines and human HCC tissues, and was seen in various hepatoma cell lines including HepG2 cells. In human HCC tissues, PEDF expression was higher than in adjacent non-HCC tissues. In addition, serum PEDF levels were higher in HCC patients than in non-HCC patients, and curative treatment of HCC caused significant reductions in serum PEDF levels compared with pretreat...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045559</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045559</guid>        </item>
        <item>
            <title>Methyl Donor Deficiency Affects Fetal Programming of Gastric Ghrelin Cell Organization and Function in the Rat.</title>
            <link>http://www.medworm.com/index.php?rid=3045558&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948829%26dopt%3DAbstract</link>
            <description>We examined the gastric ghrelin system in MDD-induced intrauterine growth retardation. By using specific markers and approaches (such as periodic acid-Schiff, bromodeoxyuridine, homocysteine, terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling, immunostaining, reverse transcription-polymerase chain reaction), we studied the gastric oxyntic mucosa cellular organization and ghrelin gene expression in the mucosa in 20-day-old fetuses and weanling pups, and plasma ghrelin concentration in weanling rat pups of dams either normally fed or deprived of choline, folate, vitamin B6, and vitamin B12 during gestation and suckling periods. MDD fetuses weighed less than controls; the weight deficit reached 57% at weaning (P &amp;lt; 0.001). Both at the end of gestation and at weaning, they p...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045558</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045558</guid>        </item>
        <item>
            <title>CD11c+ Cells Are Required to Prevent Progression from Local Acute Lung Injury to Multiple Organ Failure and Death.</title>
            <link>http://www.medworm.com/index.php?rid=3045557&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948830%26dopt%3DAbstract</link>
            <description>Authors: Milam JE, Erb-Downward JR, Chen GH, Osuchowski MF, McDonald R, Chensue SW, Toews GB, Huffnagle GB, Olszewski MA
    To investigate the role of CD11c(+) cells in endotoxin-induced acute lung injury, wild-type or CD11c-diphtheria toxin receptor transgenic mice were treated with intraperitoneal diphtheria toxin (5 ng/g b.wt.) in the presence or absence of intratracheal lipopolysaccharide (51 mug). Lipopolysaccharide treatment resulted in 100% mortality in CD11c-depleted animals but not in control animals. Analysis of local lung tissue revealed no differences in acute lung injury severity; however, analysis of distal tissues revealed severe damage and necrosis to multiple organs (liver, spleen, and kidneys) in CD11c-diphtheria toxin receptor mice but not in wild-type mice. In addition...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045557</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045557</guid>        </item>
        <item>
            <title>Endometrial Cells Get Side-Tracked. Side Population Cells Promote Epithelial-Mesenchymal Transition in Endometrial Carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=3045556&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948831%26dopt%3DAbstract</link>
            <description>Authors: G&amp;#xF6;tte M
    This Commentary reports on the role of endometrial carcinoma side population cells in epithelial-mesenchymal transition.
    PMID: 19948831 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045556</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045556</guid>        </item>
        <item>
            <title>Involvement of L-selectin in Contact Hypersensitivity Responses Augmented by Auditory Stress.</title>
            <link>http://www.medworm.com/index.php?rid=3045555&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948832%26dopt%3DAbstract</link>
            <description>Authors: Bae SJ, Shimizu K, Yozaki M, Yamaoka T, Akiyama Y, Yoshizaki A, Muroi E, Hara T, Ogawa F, Sato S
    Stress affects the pathophysiology of cutaneous immune reactions, including contact hypersensitivity (CH) in individuals sensitized with sensitizing hapten, where local endothelial cell activation plays a critical role. To clarify the effects of stress in cutaneous immune reactions, we selected a CH model using annoying sound as a stress. Furthermore, we conducted the stress experiments by using selectin-deficient mice to determine the involvement of selectin molecules regarding local endothelial activation. Auditory stress augmented CH responses in the present study. Namely, ear thickness and mast cell numbers were significantly increased in stressed CH mice. mRNA expression of pr...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045555</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045555</guid>        </item>
        <item>
            <title>Conditional Deletion of Neuronal Cyclin-Dependent Kinase 5 in Developing Forebrain Results in Microglial Activation and Neurodegeneration.</title>
            <link>http://www.medworm.com/index.php?rid=3045554&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948833%26dopt%3DAbstract</link>
            <description>Authors: Takahashi S, Ohshima T, Hirasawa M, Pareek TK, Bugge TH, Morozov A, Fujieda K, Brady RO, Kulkarni AB
    Neuronal migration disorders are often identified in patients with epilepsy refractory to medical treatment. The prolonged or repeated seizures are known to cause neuronal death; however, the mechanism underlying seizure-induced neuronal death remains to be elucidated. An essential role of cyclin-dependent kinase 5 (Cdk5) in brain development has been demonstrated in Cdk5(-/-) mice, which show neuronal migration defects and perinatal lethality. Here, we show the consequences of Cdk5 deficiency in the postnatal brain by generating Cdk5 conditional knockout mice, in which Cdk5 is selectively eliminated from neurons in the developing forebrain. The conditional mutant mice were via...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045554</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045554</guid>        </item>
        <item>
            <title>Am J Pathol; +30 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2971312&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222009%252F11%252F06%252009.18%2522%255BMHDA%255D%253A%25222009%252F11%252F08%252005.42%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F11%252F06%252009.18%2522%255BEDAT%255D%29%29</link>
            <description>30 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2009/11/08PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2971312</comments>
            <pubDate>Sun, 08 Nov 2009 10:42:02 +0100</pubDate>
            <guid isPermaLink="false">2971312</guid>        </item>
        <item>
            <title>Am J Pathol; +42 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2940193&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222009%252F10%252F24%252011.32%2522%255BMHDA%255D%253A%25222009%252F10%252F30%252000.40%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F10%252F24%252011.32%2522%255BEDAT%255D%29%29</link>
            <description>42 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2009/10/30PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2940193</comments>
            <pubDate>Fri, 30 Oct 2009 04:40:02 +0100</pubDate>
            <guid isPermaLink="false">2940193</guid>        </item>
        <item>
            <title>Am J Pathol; +16 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2880600&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222009%252F10%252F09%252017.08%2522%255BMHDA%255D%253A%25222009%252F10%252F11%252013.12%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F10%252F09%252017.08%2522%255BEDAT%255D%29%29</link>
            <description>16 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2009/10/11PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2880600</comments>
            <pubDate>Sun, 11 Oct 2009 17:12:03 +0100</pubDate>
            <guid isPermaLink="false">2880600</guid>        </item>
        <item>
            <title>Loss-of-Function FERMT1 Mutations in Kindler Syndrome Implicate a Role for Fermitin Family Homolog-1 in Integrin Activation.</title>
            <link>http://www.medworm.com/index.php?rid=2808362&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19762710%26dopt%3DAbstract</link>
            <description>This study provides evidence that fermitin family homolog-1 is implicated in integrin activation and demonstrates that lack of this protein leads to pathological changes beyond focal adhesions, with disruption of several hemidesmosomal components and reduced expression of keratinocyte stem cell markers. These findings collectively provide novel data on the role of fermitin family homolog-1 in skin and further insight into the pathophysiology of Kindler syndrome.
    PMID: 19762710 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2808362</comments>
            <pubDate>Wed, 16 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2808362</guid>        </item>
        <item>
            <title>Role of CD11b+ Macrophages in Intraperitoneal Lipopolysaccharide-Induced Aberrant Lymphangiogenesis and Lymphatic Functionin the Diaphragm.</title>
            <link>http://www.medworm.com/index.php?rid=2808361&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19762711%26dopt%3DAbstract</link>
            <description>Authors: Kim KE, Koh YJ, Jeon BH, Jang C, Han J, Kataru RP, Schwendener RA, Kim JM, Koh GY
    Lymphatic vessels in the diaphragm are essential for draining peritoneal fluid, but little is known about their pathological changes during inflammation. Here we characterized diaphragmatic lymphatic vessels in a peritonitis model generated by daily i.p. administration of lipopolysaccharide (LPS) in mice. Intraperitoneal LPS increased lymphatic density, branching, sprouts, connections, and network formation in the diaphragm in time- and dose-dependent manners. These changes were reversible on discontinuation of LPS administration. The LPS-induced lymphatic density and remodeling occur mainly through proliferation of lymphatic endothelial cells. CD11b(+) macrophages were massively accumulated and ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2808361</comments>
            <pubDate>Wed, 16 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2808361</guid>        </item>
        <item>
            <title>Is Expression or Activation of Src Kinase Associated with Cancer-Specific Survival in ER, PR and HER2-Negative Breast Cancer Patients?</title>
            <link>http://www.medworm.com/index.php?rid=2808360&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19762712%26dopt%3DAbstract</link>
            <description>Authors: Elsberger B, Tan BA, Mitchell TJ, Brown SB, Mallon EA, Tovey SM, Cooke TG, Brunton VG, Edwards J
    The aim of the current study was to assess the expression levels of c-Src and phosphorylated Src kinase in human breast cancers and to establish if these are linked to oestrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 status or patient survival. Tissue microarray technology was used to analyze 314 breast cancer specimens. Immunohistochemistry was performed using antibodies to c-Src, Y419Src, and Y215Src, and expression was assessed using the weighted histoscore method. High cytoplasmic c-Src kinase and high membrane phosphorylated activated Y419Src kinase was associated with decreased disease-specific survival. In contrast, phosphorylated activ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2808360</comments>
            <pubDate>Wed, 16 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2808360</guid>        </item>
        <item>
            <title>An Inducible Cartilage Oligomeric Matrix Protein Mouse Model Recapitulates Human Pseudoachondroplasia Phenotype.</title>
            <link>http://www.medworm.com/index.php?rid=2808359&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19762713%26dopt%3DAbstract</link>
            <description>In this study, we achieved robust expression of human mutant (MT) or wild-type (WT) COMP in mice by using a tetracycline-inducible promoter. Normal growth plate distribution of ECM proteins was observed in 1-month-old WT-COMP and C57BL\\6 control mice. In contrast, the structure of the MT-COMP growth plate recapitulated the findings of human PSACH growth plate morphology, including (1) retention of ECM proteins, (2) intracellular matrix formation in the rER cisternae, and (3) increased chondrocyte apoptosis. Therefore, we have generated the first mouse model to show extensive intracellular retention of ECM proteins recapitulating the human PSACH disease process at the cellular level.
    PMID: 19762713 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2808359</comments>
            <pubDate>Wed, 16 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2808359</guid>        </item>
        <item>
            <title>Role of MKP-1 in Osteoclasts and Bone Homeostasis.</title>
            <link>http://www.medworm.com/index.php?rid=2808358&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19762714%26dopt%3DAbstract</link>
            <description>Authors: Carlson J, Cui W, Zhang Q, Xu X, Mercan F, Bennett AM, Vignery A
    Bone mass is maintained through the complementary activities of osteoblasts and osteoclasts; yet differentiation of either osteoblasts and osteoclasts engages the mitogen-activated protein kinase (MAPK) pathway. The MAPKs are negatively regulated by a family of dual-specificity phosphatases known as the MAPK phosphatases (MKPs). MKP-1 is a stress-responsive MKP that inactivates the MAPKs and plays a central role in macrophages; however, whether MKP-1 plays a role in the maintenance of bone mass has yet to be investigated. We show here, using a genetic approach, that mkp-1(-/-) female mice exhibited slightly reduced bone mass. We found that mkp-1(+/+) and mkp-1(-/-) mice had equivalent levels of bone loss after ov...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2808358</comments>
            <pubDate>Wed, 16 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2808358</guid>        </item>
        <item>
            <title>Kindlin-1 Is Required for RhoGTPase-Mediated Lamellipodia Formation in Keratinocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2808357&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19762715%26dopt%3DAbstract</link>
            <description>Authors: Has C, Herz C, Zimina E, Qu HY, He Y, Zhang ZG, Wen TT, Gache Y, Aumailley M, Bruckner-Tuderman L
    Kindlin-1 is an epithelial-specific member of the novel kindlin protein family, which are regulators of integrin functions. Mutations in the gene that encodes Kindlin-1, FERMT1 (KIND1), cause the Kindler syndrome (KS), a human disorder characterized by mucocutaneous fragility, progressive skin atrophy, ulcerative colitis, photosensitivity, and propensity to skin cancer. Our previous studies indicated that loss of kindlin-1 resulted in abnormalities associated with integrin functions, such as adhesion, proliferation, polarization, and motility of epidermal cells. Here, we disclosed novel FERMT1 mutations in KS and used them, in combination with small-interfering RNA, protein, and i...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2808357</comments>
            <pubDate>Wed, 16 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2808357</guid>        </item>
        <item>
            <title>Am J Pathol; +17 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2769321&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222009%252F09%252F02%252017.50%2522%255BMHDA%255D%253A%25222009%252F09%252F06%252010.00%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F09%252F02%252017.50%2522%255BEDAT%255D%29%29</link>
            <description>17 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2009/09/06PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2769321</comments>
            <pubDate>Sun, 06 Sep 2009 14:00:02 +0100</pubDate>
            <guid isPermaLink="false">2769321</guid>        </item>
        <item>
            <title>Am J Pathol; +18 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2733665&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222009%252F08%252F15%252009.10%2522%255BMHDA%255D%253A%25222009%252F08%252F26%252009.34%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F08%252F15%252009.10%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 Pathol
These pubmed results were generated on 2009/08/26PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2733665</comments>
            <pubDate>Wed, 26 Aug 2009 13:34:02 +0100</pubDate>
            <guid isPermaLink="false">2733665</guid>        </item>
        <item>
            <title>Essential Roles for Early Growth Response Transcription Factor Egr-1 in Tissue Fibrosis and Wound Healing.</title>
            <link>http://www.medworm.com/index.php?rid=2702590&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19679873%26dopt%3DAbstract</link>
            <description>We reported previously that normal fibroblasts stimulated by transforming growth factor-ss showed rapid and transient induction of Egr-1. Moreover, we observed that tissue expression of Egr-1 was elevated in patients with scleroderma, which suggests that Egr-1 may be involved in tissue repair and fibrosis. Here, we investigated matrix remodeling and wound healing in mice harboring gain of function or loss of function mutations of Egr-1. Using the model of bleomycin-induced scleroderma, we found that the early influx of inflammatory cells into the skin and lungs, and the subsequent development of fibrosis in these organs, were markedly attenuated in Egr-1 null mice. Furthermore, full-thickness incisional skin wound healing was impaired, and skin fibroblasts lacking Egr-1 showed reduced migr...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2702590</comments>
            <pubDate>Wed, 12 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2702590</guid>        </item>
        <item>
            <title>Characterization of RAGE, HMGB1, and S100{beta} in Inflammation-Induced Preterm Birth and Fetal Tissue Injury.</title>
            <link>http://www.medworm.com/index.php?rid=2702589&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19679874%26dopt%3DAbstract</link>
            <description>Authors: Buhimschi CS, Baumbusch MA, Dulay AT, Oliver EA, Lee S, Zhao G, Bhandari V, Ehrenkranz RA, Weiner CP, Madri JA, Buhimschi IA
    Immune activation represents an adaptive reaction triggered by both noxious exogenous (microbes) and endogenous [high mobility group box-1 protein (HMGB1), S100 calcium binding proteins] inducers of inflammation. Cell stress or necrosis lead the release of HMGB1 and S100 proteins in the extracellular compartment where they act as damage-associated molecular pattern molecules (or alarmins) by engaging the receptor for advanced glycation end-products (RAGE). Although the biology of RAGE is dictated by the accumulation of damage-associated molecular pattern molecules at sites of tissue injury, the role of RAGE in mediating antenatal fetal injury remains unk...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2702589</comments>
            <pubDate>Wed, 12 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2702589</guid>        </item>
        <item>
            <title>Fenfluramine Disrupts the Mitral Valve Interstitial Cell Response to Serotonin.</title>
            <link>http://www.medworm.com/index.php?rid=2702588&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19679875%26dopt%3DAbstract</link>
            <description>Authors: Connolly JM, Bakay MA, Fulmer JT, Gorman RC, Gorman JH, Oyama MA, Levy RJ
    Serotonin (5HT) receptor signaling and 5HT-related agents, such as the anorexogen fenfluramine (Fen), have been associated with heart valve disease. We investigated the hypothesis that Fen may disrupt mitral valve interstitial cell (MVIC) homeostasis through its effects on mitogenesis and extracellular matrix biosynthesis. Normal and myxomatous mitral valves, both human and canine, were harvested, and primary MVIC cultures were established. 5HT caused increased phosphorylation of extracellular signal-related kinase in MVIC; Fen alone did not. However, Fen combined with 5HT increased the level of MVIC extracellular signal-related kinase, when compared with 5HT alone. In addition, MVIC mitogenesis per (3)H...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2702588</comments>
            <pubDate>Wed, 12 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2702588</guid>        </item>
        <item>
            <title>A Novel Organotypic Model Mimics the Tumor Microenvironment.</title>
            <link>http://www.medworm.com/index.php?rid=2702587&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19679876%26dopt%3DAbstract</link>
            <description>In this study, a novel organotypic model based on human uterine leiomyoma tissue was established and characterized to create a more authentic environment for carcinoma cells. Human tongue squamous cell carcinoma cells (HSC-3) were cultured on top of either collagen or myoma. Organotypic sections were examined by immunohistochemistry and in situ hybridization. The maximal invasion depth of HSC-3 cells was markedly increased in myomas compared with collagen. In myomas, various cell types and ECM components were present, and the HSC-3 cells only expressed ECM molecules in the myoma model. Organotypic media were analyzed by radioimmunoassay, zymography, or Western blotting. During carcinoma cell invasion, matrix metalloprotease-9 production and collagen degradation were enhanced particularly i...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2702587</comments>
            <pubDate>Wed, 12 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2702587</guid>        </item>
        <item>
            <title>Reduced Phosphoinositide 3-Kinase (p110{alpha}) Activation Increases the Susceptibility to Atrial Fibrillation.</title>
            <link>http://www.medworm.com/index.php?rid=2702586&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19679877%26dopt%3DAbstract</link>
            <description>Authors: Pretorius L, Du XJ, Woodcock EA, Kiriazis H, Lin RC, Marasco S, Medcalf RL, Ming Z, Head GA, Tan JW, Cemerlang N, Sadoshima J, Shioi T, Izumo S, Lukoshkova EV, Dart AM, Jennings GL, McMullen JR
    Atrial fibrillation (AF) is the most common sustained arrhythmia presenting at cardiology departments. A limited understanding of the molecular mechanisms responsible for the development of AF has hindered treatment strategies. The purpose of this study was to assess whether reduced activation of phosphoinositide 3-kinase (PI3K, p110alpha) makes the compromised heart susceptible to AF. Risk factors for AF, including aging, obesity, and diabetes, have been associated with insulin resistance that leads to depressed/defective PI3K signaling. However, to date, there has been no link between...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2702586</comments>
            <pubDate>Wed, 12 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2702586</guid>        </item>
        <item>
            <title>Beta-Catenin Activation Promotes Liver Regeneration after Acetaminophen-Induced Injury.</title>
            <link>http://www.medworm.com/index.php?rid=2702585&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19679878%26dopt%3DAbstract</link>
            <description>Authors: Apte U, Singh S, Zeng G, Cieply B, Virji MA, Wu T, Monga SP
    Acute liver failure (ALF) remains a disease with poor patient outcome. Improved prognosis is associated with spontaneous liver regeneration, which supports the relevance of exploring 'regenerative' therapies. Therefore, the role of the Wnt/beta-catenin pathway in liver regeneration following ALF was investigated. ALF was induced in mice by acetaminophen overdose, which is also a leading cause of liver failure in patients. beta-catenin distribution was also studied in liver sections from acetaminophen-induced ALF patients. A nonlethal dose of acetaminophen, which induces liver regeneration, led to stabilization and activation of beta-catenin for 1 to 12 hours. These data were also verified by increased expression of th...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2702585</comments>
            <pubDate>Wed, 12 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2702585</guid>        </item>
        <item>
            <title>Hypercholesterolemic Mice Exhibit Lymphatic Vessel Dysfunction and Degeneration.</title>
            <link>http://www.medworm.com/index.php?rid=2702584&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19679879%26dopt%3DAbstract</link>
            <description>Authors: Lim HY, Rutkowski JM, Helft J, Reddy ST, Swartz MA, Randolph GJ, Angeli V
    Lymphatic vessels are essential for lipid absorption and transport. Despite increasing numbers of observations linking lymphatic vessels and lipids, little research has been devoted to address how dysregulation of lipid balance in the blood, ie, dyslipidemia, may affect the functional biology of lymphatic vessels. Here, we show that hypercholesterolemia occurring in apolipoprotein E-deficient (apoE(-/-)) mice is associated with tissue swelling, lymphatic leakiness, and decreased lymphatic transport of fluid and dendritic cells from tissue. Lymphatic dysfunction results in part from profound structural abnormalities in the lymphatic vasculature: namely, initial lymphatic vessels were greatly enlarged, and...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2702584</comments>
            <pubDate>Wed, 12 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2702584</guid>        </item>
        <item>
            <title>Neuroendocrine Cancer-Specific Up-Regulating Mechanism of Insulin-Like Growth Factor Binding Protein-2 in Small Cell Lung Cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2702583&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19679880%26dopt%3DAbstract</link>
            <description>In this study, we demonstrate that SCLC cells overexpress insulin-like growth factor binding protein (IGFBP)-2 via NeuroD, a neuroendocrine cell-specific transcription factor. Chromatin immunoprecipitation, electrophoretic mobility shift, and IGFBP-2 promoter assays all revealed that NeuroD binds to the E-box in the 5'-untranslated region of IGFBP-2. A NeuroD transgene in both airway epithelial and NSCLC cells up-regulated the transcription of IGFBP-2 and retarded cell growth. Recombinant IGFBP-2 repressed the growth of both airway epithelial and NSCLC cells in a dose-dependent manner. A NeuroD-specific small interfering RNA repressed IGFBP-2 expression in SCLC, and neutralization of IGFBP-2 and an IGFBP-2-specific small interfering RNA increased SCLC cell growth. Pathological samples of S...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2702583</comments>
            <pubDate>Wed, 12 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2702583</guid>        </item>
        <item>
            <title>Am J Pathol; +42 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2606912&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222009%252F07%252F13%252003.26%2522%255BMHDA%255D%253A%25222009%252F07%252F16%252019.54%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F07%252F13%252003.26%2522%255BEDAT%255D%29%29</link>
            <description>42 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2009/07/16PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2606912</comments>
            <pubDate>Thu, 16 Jul 2009 23:54:02 +0100</pubDate>
            <guid isPermaLink="false">2606912</guid>        </item>
        <item>
            <title>Am J Pathol; +165 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2538856&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222009%252F04%252F09%252010.27%2522%255BMHDA%255D%253A%25222009%252F06%252F27%252017.31%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Pathol%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F04%252F09%252010.27%2522%255BEDAT%255D%29%29</link>
            <description>165 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2538856</comments>
            <pubDate>Sat, 27 Jun 2009 21:31:03 +0100</pubDate>
            <guid isPermaLink="false">2538856</guid>        </item>
        <item>
            <title>Am J Pathol; +32 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2315477&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222009%252F03%252F26%2B12%252E47%2522%255BMHDA%255D%253A%25222009%252F04%252F09%2B10%252E27%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F03%252F26%2B12%252E47%2522%255BEDAT%255D%2529%2529</link>
            <description>32 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2009/04/09PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2315477</comments>
            <pubDate>Thu, 09 Apr 2009 14:27:37 +0100</pubDate>
            <guid isPermaLink="false">2315477</guid>        </item>
        <item>
            <title>Am J Pathol; +37 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2291092&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222009%252F03%252F17%2B13%252E26%2522%255BMHDA%255D%253A%25222009%252F03%252F26%2B12%252E46%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F03%252F17%2B13%252E26%2522%255BEDAT%255D%2529%2529</link>
            <description>37 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2009/03/26PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2291092</comments>
            <pubDate>Thu, 26 Mar 2009 16:46:08 +0100</pubDate>
            <guid isPermaLink="false">2291092</guid>        </item>
        <item>
            <title>Am J Pathol; +16 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2253424&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222009%252F03%252F02%2B07%252E21%2522%255BMHDA%255D%253A%25222009%252F03%252F08%2B08%252E58%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F03%252F02%2B07%252E21%2522%255BEDAT%255D%2529%2529%26itool%3Drss</link>
            <description>16 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2009/03/08PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2253424</comments>
            <pubDate>Sun, 08 Mar 2009 12:58:16 +0100</pubDate>
            <guid isPermaLink="false">2253424</guid>        </item>
        <item>
            <title>Am J Pathol; +16 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2248503&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222009%252F03%252F02%2B07%252E21%2522%255BMHDA%255D%253A%25222009%252F03%252F08%2B08%252E58%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F03%252F02%2B07%252E21%2522%255BEDAT%255D%2529%2529</link>
            <description>16 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2009/03/08PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2248503</comments>
            <pubDate>Sun, 08 Mar 2009 12:58:16 +0100</pubDate>
            <guid isPermaLink="false">2248503</guid>        </item>
        <item>
            <title>Angiotensin II Induces Renal Plasminogen Activator Inhibitor-1 and Cyclooxygenase-2 Expression Posttranscriptionally via Activation of the mRNA-Stabilizing Factor Human-Antigen R.</title>
            <link>http://www.medworm.com/index.php?rid=2226387&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246637%26dopt%3DAbstract</link>
            <description>Authors: Doller A, Gauer S, Sobkowiak E, Geiger H, Pfeilschifter J, Eberhardt W
    Angiotensin (Ang) II-induced fibrosis of the kidney is characterized by the enhanced expression of profibrotic and proinflammatory genes, including the serine protease inhibitor plasminogen activator inhibitor-1 (PAI-1) and cyclooxygenase-2 (COX-2). In addition to transcriptional regulation, both genes are subject to posttranscriptional control by AU-rich destabilizing elements that reside within the 3' untranslated region of the mRNA. We demonstrated that the continuous infusion of AngII in rats induced fibrosis concomitant with a significant increase in glomerular PAI-1 and COX-2 expression levels. Using RNA pull-down assays and electromobility shift assays, we demonstrated the increased binding of the ub...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226387</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226387</guid>        </item>
        <item>
            <title>Mitogen-Activated Protein 3 Kinase 6 Mediates Angiogenic and Tumorigenic Effects via Vascular Endothelial Growth Factor Expression.</title>
            <link>http://www.medworm.com/index.php?rid=2226386&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246638%26dopt%3DAbstract</link>
            <description>Authors: Eto N, Miyagishi M, Inagi R, Fujita T, Nangaku M
    Genome-wide screening using a small interfering RNA (siRNA) library has revealed novel molecules that are involved in a wide range of physiological responses. The expression of vascular endothelial growth factor (VEGF) is increased under hypoxic conditions, and plays a crucial role in tumor angiogenesis and tissue responses to ischemia. Here, we used a siRNA expression vector library to elucidate molecules that modify VEGF expression. Screening using an siRNA library revealed that MAPKKK6 (MEKK6/MAP3K6) regulates VEGF expression under both normoxic and hypoxic conditions in vitro, although the biological function of MAP3K6 remains unknown. Attenuation of VEGF expression by MAP3K6 inhibition was demonstrated by transient transfec...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226386</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226386</guid>        </item>
        <item>
            <title>Lowering Blood Pressure Blocks Mesangiolysis and Mesangial Nodules, but not Tubulointerstitial Injury, in Diabetic eNOS Knockout Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2226385&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246639%26dopt%3DAbstract</link>
            <description>This study could provide insights into the pathogenesis of advanced diabetic nephropathy in the presence of endothelial dysfunction.
    PMID: 19246639 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226385</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226385</guid>        </item>
        <item>
            <title>Large CTG Repeats Trigger p16-Dependent Premature Senescence in Myotonic Dystrophy Type 1 Muscle Precursor Cells.</title>
            <link>http://www.medworm.com/index.php?rid=2226384&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246640%26dopt%3DAbstract</link>
            <description>In this report, we show that these muscle precursor cells containing large CTG expansion sequences have not exhausted their proliferative capacity, but have entered into premature senescence. We demonstrate that an abnormal accumulation of p16 is responsible for this defect because the abolition of p16 activity overcomes early growth arrest and restores an extended proliferative capacity. Our results suggest that the accelerated telomere shortening measured in DM1 cells does not contribute to the aberrant induction of p16. We propose that a cellular stress related to the amplified CTG repeat promotes premature senescence mediated by a p16-dependent pathway in DM1 muscle precursor cells. This mechanism is responsible for the reduced proliferative capacity of the DM1 muscle precursor cells a...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226384</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226384</guid>        </item>
        <item>
            <title>Immunoglobulin Expression in Non-Lymphoid Lineage and Neoplastic Cells.</title>
            <link>http://www.medworm.com/index.php?rid=2226383&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246641%26dopt%3DAbstract</link>
            <description>Authors: Chen Z, Qiu X, Gu J
    It has traditionally been believed that the production of immunoglobulin (Ig) molecules is restricted to B lineage cells. However, immunoglobulin genes and proteins have been recently found in a variety of types of cancer cells, as well as some proliferating epithelial cells and neurons. The immunoglobulin molecules expressed by these cells consist predominantly of IgG, IgM, and IgA, and the light chains expressed are mainly kappa chains. Recombination activating genes 1 and 2, which are required for V(D)J recombination, are also expressed in these cells. Knowledge about the function of these non-lymphoid cell-derived immunoglobulins is limited. Preliminary data suggests that Ig secreted by epithelial cancer cells has some unidentified capacity to promote t...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226383</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226383</guid>        </item>
        <item>
            <title>{beta}-Glycoglycosphingolipid-Induced Alterations of the STAT Signaling Pathways Are Dependent on CD1d and the Lipid Raft Protein Flotillin-2.</title>
            <link>http://www.medworm.com/index.php?rid=2226382&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246642%26dopt%3DAbstract</link>
            <description>Authors: Lalazar G, Ya'acov AB, Livovsky DM, El Haj M, Pappo O, Preston S, Zolotarov L, Ilan Y
    beta-glucosylceramide has been shown to affect natural killer T cell function in models of inflammation. We, therefore, investigated the effects of different beta-glycosphingolipids, including beta-glucosylceramide, on STAT (signal transducers and activators of transcription) signaling pathways and determined whether these effects were mediated by lipid raft microdomains and/or CD1 days molecules. The effects of alpha- and beta-structured ligands on the lipid raft protein flotillin-2 were studied in both natural killer T hybridoma cells and leptin-deficient mice. To determine whether CD1 days was involved in the effects of the beta-glycosphingolipids, an anti-CD1 days blocking antibody was us...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226382</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226382</guid>        </item>
        <item>
            <title>Oxidative Stress-Mediated Mitochondrial Dysfunction Contributes to Angiotensin II-Induced Nonalcoholic Fatty Liver Disease in Transgenic Ren2 Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2226381&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246643%26dopt%3DAbstract</link>
            <description>Authors: Wei Y, Clark SE, Thyfault JP, Uptergrove GM, Li W, Whaley-Connell AT, Ferrario CM, Sowers JR, Ibdah JA
    Emerging evidence indicates that impaired mitochondrial fatty acid beta-oxidation plays a key role in liver steatosis. We have recently demonstrated that increased angiotensin (ANG) II causes progressive hepatic steatosis associated with oxidative stress; however, the underlying mechanisms remain unclear. We hypothesized that ANG II causes hepatic mitochondrial oxidative damage and impairs mitochondrial beta-oxidation, thereby leading to hepatic steatosis. We used the Ren2 rat with elevated endogenous ANG II levels to evaluate mitochondrial ultrastructural changes, gene expression levels, and beta-oxidation. Compared with Sprague-Dawley littermates, Ren2 livers exhibited mito...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226381</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226381</guid>        </item>
        <item>
            <title>Specific Detection of CD56 (NCAM) Isoforms for the Identification of Aggressive Malignant Neoplasms with Progressive Development.</title>
            <link>http://www.medworm.com/index.php?rid=2226380&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246644%26dopt%3DAbstract</link>
            <description>Authors: Gattenl&amp;#xF6;hner S, St&amp;#xFC;hmer T, Leich E, Reinhard M, Etschmann B, V&amp;#xF6;lker HU, Rosenwald A, Serfling E, Bargou RC, Ertl G, Einsele H, M&amp;#xFC;ller-Hermelink HK
    Alternative splicing of transcripts from many cancer-associated genes is believed to play a major role in carcinogenesis as well as in tumor progression. Alternative splicing of one such gene, the neural cell adhesion molecule CD56 (NCAM), impacts the progression, inadequate therapeutic response, and reduced total survival of patients who suffer from numerous malignant neoplasms. Although previous investigations have determined that CD56 exists in three major isoforms (CD56(120kD), CD56(140kD), and CD56(180kD)) with individual structural and functional properties, neither the expression profiles nor the functiona...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226380</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226380</guid>        </item>
        <item>
            <title>Anti-Inflammatory and Renal Protective Actions of Stanniocalcin-1 in a Model of Anti-Glomerular Basement Membrane Glomerulonephritis.</title>
            <link>http://www.medworm.com/index.php?rid=2226379&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246645%26dopt%3DAbstract</link>
            <description>We examined the following parameters both at baseline and after anti-glomerular basement membrane antibody treatment: blood pressure; C3a levels; urine output; proteinuria; blood urea nitrogen; and kidney C3 deposition, fibrosis, histological changes, cytokine expression, and number of T cells and macrophages. Compared with wild-type mice, after anti-glomerular basement membrane treatment STC1 transgenic mice exhibited: i) diminished infiltration of inflammatory macrophages in the glomeruli; ii) marked reduction in crescent formation and sclerotic glomeruli; iii) decreased interstitial fibrosis; iv) preservation of kidney function and lower blood pressure; v) diminished C3 deposition in the glomeruli; and vi) reduced expression of macrophage inhibitory protein-2 and transforming growth fac...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226379</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226379</guid>        </item>
        <item>
            <title>Senescent Peritoneal Mesothelial Cells Promote Ovarian Cancer Cell Adhesion. The Role of Oxidative Stress-Induced Fibronectin.</title>
            <link>http://www.medworm.com/index.php?rid=2226378&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246646%26dopt%3DAbstract</link>
            <description>Authors: Ksiazek K, Mikula-Pietrasik J, Korybalska K, Dworacki G, J&amp;#xF6;rres A, Witowski J
    Adhesion of ovarian cancer cells to the peritoneal mesothelium is a key step in the malignant progression of the disease. In an in vitro study, we showed that the adherence of ovarian cancer cells (of the OVCAR-3, SKOV-3, and A2780 cell lines) to senescent human omentum-derived peritoneal mesothelial cells (HOMCs) was greater than to early passage cells. The process was mediated primarily by the increased interaction of the alpha5beta1 integrin on cancer cells with HOMC-associated fibronectin (FN). In comparison with early passage HOMCs, senescent cells exhibited increased FN mRNA expression levels and produced significantly more FN. To assess the effect of senescence-associated oxidative stress...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226378</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226378</guid>        </item>
        <item>
            <title>IDH1 Mutations Are Early Events in the Development of Astrocytomas and Oligodendrogliomas.</title>
            <link>http://www.medworm.com/index.php?rid=2226377&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246647%26dopt%3DAbstract</link>
            <description>Authors: Watanabe T, Nobusawa S, Kleihues P, Ohgaki H
    IDH1 encodes isocitrate dehydrogenase 1, which participates in the citric acid cycle and was recently reported to be mutated in 12% of glioblastomas. We assessed IDH1 mutations in 321 gliomas of various histological types and biological behaviors. A total of 130 IDH1 mutations was detected, and all were located at amino acid residue 132. Of these, 91% were G--&amp;gt;A mutations (Arg--&amp;gt;His). IDH1 mutations were frequent in low-grade diffuse astrocytomas (88%) and in secondary glioblastomas that developed through progression from low-grade diffuse or anaplastic astrocytoma (82%). Similarly, high frequencies of IDH1 mutations were found in oligodendrogliomas (79%) and oligoastrocytomas (94%). Analyses of multiple biopsies from the same...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226377</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226377</guid>        </item>
        <item>
            <title>Lymphotoxin-{alpha} and TNF Have Essential but Independent Roles in the Evolution of the Granulomatous Response in Experimental Leprosy.</title>
            <link>http://www.medworm.com/index.php?rid=2226376&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246648%26dopt%3DAbstract</link>
            <description>Authors: Hagge DA, Saunders BM, Ebenezer GJ, Ray NA, Marks VT, Britton WJ, Krahenbuhl JL, Adams LB
    Recent studies identified an association between genetic variants in the lymphotoxin-alpha (LTalpha) gene and leprosy. To study the influence of LTalpha on the control of experimental leprosy, both low- and high-dose Mycobacterium leprae foot pad (FP) infections were evaluated in LTalpha-deficient chimeric (cLTalpha(-/-)) and control chimeric (cB6) mice. Cellular responses to low-dose infection in cLTalpha(-/-) mice were dramatically different, with reduced accumulation of CD4(+) and CD8(+) lymphocytes and macrophages and failure to form granulomas. Growth of M. leprae was contained for 6 months, but augmented late in infection. In contrast, tumor necrosis factor knockout and tumor necros...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226376</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226376</guid>        </item>
        <item>
            <title>COP9-Associated CSN5 Regulates Exosomal Protein Deubiquitination and Sorting.</title>
            <link>http://www.medworm.com/index.php?rid=2226375&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19246649%26dopt%3DAbstract</link>
            <description>In this study, we show that the COP9 signalosome (CSN)-associated protein CSN5 quantitatively regulated proteins that were sorted into exosomes. Western blot analysis of exosomal proteins indicated that small interfering (si)RNA knockdown of CSN5 results in increased levels of both ubiquitinated and non-ubiquitinated exosomal proteins, including heat shock protein 70, in comparison with exosomes isolated from the supernatants of 293 cells transfected with scrambled siRNA. Furthermore, 293 cells transfected with JAB1/MPN/Mov34 metalloenzyme domain-deleted CSN5 produced exosomes with higher levels of ubiquitinated heat shock protein 70, which did not affect non-ubiquitinated heat shock protein 70 levels. The loss of COP9-associated deubiquitin activity of CSN5 also led to the enhancement of ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2226375</comments>
            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2226375</guid>        </item>
        <item>
            <title>Am J Pathol; +33 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2198728&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222009%252F02%252F18%2B06%252E45%2522%255BMHDA%255D%253A%25222009%252F02%252F20%2B09%252E37%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F02%252F18%2B06%252E45%2522%255BEDAT%255D%2529%2529</link>
            <description>33 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2009/02/20PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2198728</comments>
            <pubDate>Fri, 20 Feb 2009 14:37:47 +0100</pubDate>
            <guid isPermaLink="false">2198728</guid>        </item>
        <item>
            <title>Am J Pathol; +35 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2159502&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222009%252F01%252F31%2B23%252E43%2522%255BMHDA%255D%253A%25222009%252F02%252F05%2B00%252E35%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F01%252F31%2B23%252E43%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 Pathol
These PubMed results were generated on 2009/02/05PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2159502</comments>
            <pubDate>Thu, 05 Feb 2009 05:35:14 +0100</pubDate>
            <guid isPermaLink="false">2159502</guid>        </item>
        <item>
            <title>Proepithelin Regulates Prostate Cancer Cell Biology by Promoting Cell Growth, Migration, and Anchorage-Independent Growth.</title>
            <link>http://www.medworm.com/index.php?rid=2149115&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179604%26dopt%3DAbstract</link>
            <description>This study supports the hypothesis that proepithelin may play a critical role as an autocrine growth factor in the establishment and initial progression of prostate cancer. Furthermore, proepithelin may prove to be a useful clinical marker for the diagnosis of prostate tumors.
    PMID: 19179604 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149115</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149115</guid>        </item>
        <item>
            <title>Aortic Carboxypeptidase-Like Protein Is Expressed in Fibrotic Human Lung and its Absence Protects against Bleomycin-Induced Lung Fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=2149114&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179605%26dopt%3DAbstract</link>
            <description>In this study, we demonstrate that aortic carboxypeptidase-like protein (ACLP), a collagen-associated protein with a discoidin-like domain, is expressed at high levels in human fibrotic lung tissue and human fibroblasts, and that its expression increases markedly in the lungs of bleomycin-injured mice. Importantly, ACLP-deficient mice accumulated significantly fewer myofibroblasts and less collagen in the lung after bleomycin injury, as compared with wild-type controls, despite equivalent levels of bleomycin-induced inflammation. ACLP that is secreted by lung fibroblasts was retained on fibrillar collagen, and ACLP-deficient lung fibroblasts that were cultured on collagen exhibited changes in cell spreading, proliferation, and contraction of the collagen matrix. Finally, the addition of re...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149114</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149114</guid>        </item>
        <item>
            <title>HMGA2 Maintains Oncogenic RAS-Induced Epithelial-Mesenchymal Transition in Human Pancreatic Cancer Cells.</title>
            <link>http://www.medworm.com/index.php?rid=2149113&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179606%26dopt%3DAbstract</link>
            <description>Authors: Watanabe S, Ueda Y, Akaboshi SI, Hino Y, Sekita Y, Nakao M
    Pancreatic cancer is a highly aggressive malignancy due to elevated mitotic activities and epithelial-mesenchymal transition (EMT). Oncogenic RAS and transforming growth factor-beta signaling are implicated in these malignant features. The mechanisms that underlie EMT need to be addressed since it promotes tissue invasion and metastasis. The high-mobility group A protein 2 (HMGA2) is a non-histone chromatin factor that is primarily expressed in undifferentiated tissues and tumors of mesenchymal origin. However, its role in EMT in pancreatic cancer is largely unknown. Here we report that HMGA2 is involved in EMT maintenance in human pancreatic cancer cells. Specific knockdown of HMGA2 inhibited cell proliferation, leadi...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149113</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149113</guid>        </item>
        <item>
            <title>Ribozyme-Mediated Targeting of I{kappa}B{gamma} Inhibits Melanoma Invasion and Metastasis.</title>
            <link>http://www.medworm.com/index.php?rid=2149112&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179607%26dopt%3DAbstract</link>
            <description>We examined the consequences of targeting IkappaBgamma in melanoma cells using a hammerhead ribozyme. We developed stable transformant B16-F10 melanoma cell lines that express a ribozyme that targets mouse IkappaBgamma (IkappaBgamma-144-Rz). Tail-vein injection of B16-F10 cells that stably express IkappaBgamma-144-Rz into mice resulted in a significant reduction of the metastatic potential of these cells. IkappaBgamma-144-Rz-expressing B16 cells were shown to have increased transcriptional activity of nuclear factor-kappaB. We then showed that IkappaBgamma-144-Rz-expressing cells demonstrated both reduced invasion and increased apoptosis, suggesting the existence of pathways through which IkappaBgamma promotes melanoma metastasis. Using gene expression profiling, we identified a differenti...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149112</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149112</guid>        </item>
        <item>
            <title>Prolactin-Growth Factor Crosstalk Reduces Mammary Estrogen Responsiveness Despite Elevated ER{alpha} Expression.</title>
            <link>http://www.medworm.com/index.php?rid=2149111&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179608%26dopt%3DAbstract</link>
            <description>Authors: Arendt LM, Grafwallner-Huseth TL, Schuler LA
    Most breast cancers that occur in women express estrogen receptor alpha (ERalpha). However, a large subset of these cancers either does not initially respond to anti-estrogen therapy or develops resistance to such treatment modalities. One postulated mechanism of this failure is signaling cross talk between hormones and local growth factors. To examine these complex interactions in vivo, we assessed the effects of estrogen on transforming growth factor alpha (TGFalpha)- and prolactin (PRL)-induced mammary tumorigenesis in transgenic mice. Both PRL and estrogen reduced the latency of TGFalpha-induced oncogenesis, resulting in tumors that were variably ERalpha-positive, but were progesterone receptor-negative. However, despite elevate...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149111</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149111</guid>        </item>
        <item>
            <title>Valproic Acid Activates the PI3K/Akt/mTOR Pathway in Muscle and Ameliorates Pathology in a Mouse Model of Duchenne Muscular Dystrophy.</title>
            <link>http://www.medworm.com/index.php?rid=2149110&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179609%26dopt%3DAbstract</link>
            <description>Authors: Gurpur PB, Liu J, Burkin DJ, Kaufman SJ
    Duchenne muscular dystrophy is a lethal neuromuscular disease that currently has no effective therapy. Transgenic overexpression of the alpha7 integrin in mdx/utrn(-/-) mice, a model of Duchenne muscular dystrophy ameliorates the disease. We have isolated and used alpha7(+/-) muscle cells expressing beta-galactosidase, driven by the endogenous alpha7 promoter, to identify compounds that increase alpha7 integrin levels. Valproic acid (VPA) was found to enhance alpha7 integrin levels, induce muscle hypertrophy, and inhibit apoptosis in myotubes by activating the Akt/mTOR/p70S6K pathway. This activation of the Akt pathway occurs within 1 hour of treatment and is mediated by phosphatidylinositol 3-OH kinase. To evaluate the potential use of ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149110</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149110</guid>        </item>
        <item>
            <title>Ezetimibe Is An Inhibitor of Tumor Angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2149109&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179610%26dopt%3DAbstract</link>
            <description>In this study, we used ezetimibe (Zetia), a specific, FDA-approved, cholesterol uptake-blocking drug, in combination with either a hyper- or hypocholesterolemic diet, to show that elevated circulating cholesterol levels promote, whereas a reduction in circulating cholesterol levels retard, the growth of human prostate cancer xenograft tumors in mice. Circulating cholesterol levels also modified tumor angiogenesis; higher cholesterol levels increased microvessel density and other indicators of vascularity. Consistent with these data, the reduction of cholesterol levels also increased the levels of the angiogenesis inhibitor thrombospondin-1 in the xenografts. Our results thus suggest that hypercholesterolemia directly accelerates the growth of prostate carcinomas, and that the pharmacologic...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149109</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149109</guid>        </item>
        <item>
            <title>Dendritic Cell-Nerve Clusters Are Sites of T Cell Proliferation in Allergic Airway Inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=2149108&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179611%26dopt%3DAbstract</link>
            <description>Authors: Veres TZ, Shevchenko M, Krasteva G, Spies E, Prenzler F, Rochlitzer S, Tschernig T, Krug N, Kummer W, Braun A
    Interactions between T cells and dendritic cells in the airway mucosa precede secondary immune responses to inhaled antigen. The purpose of this study was to identify the anatomical locations where dendritic cell-T cell interactions occur, resulting in T cells activation by dendritic cells. In a mouse model of allergic airway inflammation, we applied whole-mount immunohistology and confocal microscopy to visualize dendritic cells and T cells together with nerves, epithelium, and smooth muscle in three dimensions. Proliferating T cells were identified by the detection of the incorporation of the nucleotide analogue 5-ethynyl-2'-deoxyuridine into the DNA. We developed a ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149108</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149108</guid>        </item>
        <item>
            <title>Galectin-3 is Critical for the Development of the Allergic Inflammatory Response in a Mouse Model of Atopic Dermatitis.</title>
            <link>http://www.medworm.com/index.php?rid=2149107&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179612%26dopt%3DAbstract</link>
            <description>Authors: Saegusa J, Hsu DK, Chen HY, Yu L, Fermin A, Fung MA, Liu FT
    Galectin-3 belongs to a family of beta-galactoside-binding animal lectins expressed in several cell types, including epithelial and immune cells. To establish the role of galectin-3 in the development of allergic skin inflammation, we compared inflammatory skin responses of galectin-3-deficient (gal3(-/-)) and wild-type (gal3(+/+)) mice to epicutaneous sensitization with ovalbumin (OVA). OVA-treated gal3(-/-) mice exhibited markedly reduced epidermal thickening, lower eosinophil infiltration, and lower serum IgE levels compared with gal3(+/+) mice. The former evoked lower interleukin-4, but higher interferon-gamma, mRNA expression at OVA-treated skin sites. Moreover, gal3(-/-) splenocytes from OVA-sensitized mice secr...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149107</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149107</guid>        </item>
        <item>
            <title>Critical Roles of Lysosomal Acid Lipase in T Cell Development and Function.</title>
            <link>http://www.medworm.com/index.php?rid=2149106&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179613%26dopt%3DAbstract</link>
            <description>Authors: Qu P, Du H, Wilkes DS, Yan C
    Lysosomal acid lipase (LAL) cleaves cholesteryl esters and triglycerides to generate free fatty acids and cholesterol in lysosomes. In LAL gene-knockout (lal(-/-)) mice, blockage of cholesteryl ester and triglyceride metabolism led to abnormal organization of the thymus and spleen, as well as neutral lipid accumulation in these organs. LAL deficiency impaired T cell development in the thymus. Peripheral T cells were reduced dramatically in lal(-/-) mice, due largely to increased apoptosis and decreased proliferation of lal(-/-) T cells in the thymus and peripheral compartments. These lal(-/-) T cells lost the ability to respond to T cell receptor stimulation, including reduced expression of cell surface receptor CD69, abolishment of T cell prolifer...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149106</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149106</guid>        </item>
        <item>
            <title>Aberrant Heparan Sulfate Proteoglycan Localization, Despite Normal Exostosin, in Central Chondrosarcoma.</title>
            <link>http://www.medworm.com/index.php?rid=2149105&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179614%26dopt%3DAbstract</link>
            <description>Authors: Schrage YM, Hameetman L, Szuhai K, Cleton-Jansen AM, Taminiau AH, Hogendoorn PC, Bov&amp;#xE9;e JV
    The tumor suppressor genes EXT1 and EXT2 are involved in the formation of multiple osteochondromas, which can progress to become secondary peripheral chondrosarcomas. The most common chondrosarcoma subtype is primary central chondrosarcoma, which occurs in the medullar cavity of bone. The EXT1/EXT2 protein complex is involved in heparan sulfate proteoglycan (HSPG) biosynthesis, which is important for signal transduction of Indian hedgehog (IHH), WNT, and transforming growth factor (TGF)-beta. The role of EXT and its downstream targets in central chondrosarcomas is currently unknown. EXT1 and EXT2 were therefore evaluated in central chondrosarcomas at both the DNA and mRNA levels. Imm...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149105</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149105</guid>        </item>
        <item>
            <title>Low-Level Expression of MicroRNAs let-7d and miR-205 Are Prognostic Markers of Head and Neck Squamous Cell Carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=2149104&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179615%26dopt%3DAbstract</link>
            <description>In this study, miRNA expression profiles of head and neck squamous cell carcinoma (HNSCC) tumor and adjacent normal tissue were examined by microarray analysis and validated by quantitative TaqMan real-time polymerase chain reaction. Using TaqMan real-time polymerase chain reaction we measured the quantitative associations between a subset of miRNAs identified on microarrays in primary tumors at diagnosis and cancer survival in a cohort of 104 HNSCC patients undergoing treatment with curative intent. The majority of miRNAs exhibiting altered expression in primary human HNSCC tumors (including miR-1, miR-133a, miR-205, and let-7d) show lower expression levels relative to normal adjacent tissue. In contrast, hsa-miR-21 is frequently overexpressed in human HNSCC tumors. Using univariate and m...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149104</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149104</guid>        </item>
        <item>
            <title>Premature Terminal Differentiation and a Reduction in Specific Proteases Associated with Loss of ABCA12 in Harlequin Ichthyosis.</title>
            <link>http://www.medworm.com/index.php?rid=2149103&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19179616%26dopt%3DAbstract</link>
            <description>Authors: Thomas AC, Tattersall D, Norgett EE, O'Toole EA, Kelsell DP
    One of the primary functions of skin is to form a defensive barrier against external infections and water loss. Disrupted barrier function underlies the most severe and often lethal form of recessive congenital ichthyosis, harlequin ichthyosis (HI). HI is associated with mutations in the gene that encodes the ABC transporter protein, ABCA12. We have investigated the morphological and biochemical alterations associated with abnormal epidermal differentiation and barrier formation in HI epidermis. An in vitro model of HI skin using human keratinocytes retrovirally transduced with shRNA targeting ABCA12 in a three-dimensional, organotypic co-culture (OTCC) system has also been developed. A robust reduction in ABCA12 expr...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2149103</comments>
            <pubDate>Thu, 29 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2149103</guid>        </item>
        <item>
            <title>Am J Pathol; +22 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2111824&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222009%252F01%252F10%2B23%252E36%2522%255BMHDA%255D%253A%25222009%252F01%252F17%2B23%252E37%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F01%252F10%2B23%252E36%2522%255BEDAT%255D%2529%2529</link>
            <description>22 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2009/01/17PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2111824</comments>
            <pubDate>Sun, 18 Jan 2009 04:37:08 +0100</pubDate>
            <guid isPermaLink="false">2111824</guid>        </item>
        <item>
            <title>Bone Marrow-Derived Cells Are Not the Origin of the Cancer Stem Cells in Ultraviolet-Induced Skin Cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2094259&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19131588%26dopt%3DAbstract</link>
            <description>Authors: Ando S, Abe R, Sasaki M, Murata J, Inokuma D, Shimizu H
    Several lines of evidence have demonstrated that various cancers are derived from cancer stem cells (CSCs), which are thought to originate from either tissue stem or progenitor cells. However, recent studies have suggested that the origin of CSCs could be bone marrow-derived cells (BMDCs); for example, gastric cancer, which follows persistent gastric inflammation, appears to originate from BMDCs. Although our previous research showed the capability of BMDCs to differentiate into epidermal keratinocytes, it has yet to be determined whether skin CSCs originate from BMDCs. To assess the possibility that BMDCs could be the origin of CSCs in skin squamous cell carcinoma (SCC), we used a mouse model of UVB-induced skin SCC. We ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2094259</comments>
            <pubDate>Thu, 08 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2094259</guid>        </item>
        <item>
            <title>Proteome-Wide Identification of Novel Binding Partners to the Oncogenic Fusion Gene Protein, NPM-ALK, using Tandem Affinity Purification and Mass Spectrometry.</title>
            <link>http://www.medworm.com/index.php?rid=2094258&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19131589%26dopt%3DAbstract</link>
            <description>Authors: Wu F, Wang P, Young LC, Lai R, Li L
    Nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), an oncogenic fusion gene protein that is characteristically found in a subset of anaplastic large cell lymphomas, promotes tumorigenesis through its functional and physical interactions with various biologically important proteins. The identification of these interacting proteins has proven to be useful to further our understanding of NPM-ALK-mediated tumorigenesis. For the first time, we performed a proteome-wide identification of NPM-ALK-binding proteins using tandem affinity purification and a highly sensitive mass spectrometric technique. Tandem affinity purification is a recently developed method that carries a lower background and higher sensitivity compared with the conventional immu...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2094258</comments>
            <pubDate>Thu, 08 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2094258</guid>        </item>
        <item>
            <title>T-Cell Activation Leads to Reduced Collagen Maturation in Atherosclerotic Plaques of Apoe-/- Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2094257&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19131590%26dopt%3DAbstract</link>
            <description>This study aimed to determine the relationship between T-cell-mediated inflammation and collagen turnover in a mouse model of experimental atherosclerosis. Both Apoe(-/-) x CD4dnTbetaRII mice with defective transforming growth factor-beta receptors in T cells (and hence released from tonic suppression of T-cell activation) and lesion size-matched Apoe(-/-) mice were used. Picrosirius red staining showed a lower content of thick mature collagen fibers in lesions of Apoe(-/-) x CD4dnTbetaRII mice, although both groups had similar levels of procollagen type I or III mRNA and total collagen content in lesions. Analysis of both gene expression and protein content showed a significant decrease of lysyl oxidase, the extracellular enzyme needed for collagen cross-linking, in aortas of Apoe(-/-) - ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2094257</comments>
            <pubDate>Thu, 08 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2094257</guid>        </item>
        <item>
            <title>Expression of CD74, the Receptor for Macrophage Migration Inhibitory Factor, in Non-Small Cell Lung Cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2094256&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19131591%26dopt%3DAbstract</link>
            <description>Authors: McClelland M, Zhao L, Carskadon S, Arenberg D
    Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine that is overexpressed in lung cancer. The MIF receptor was recently discovered and found to be the invariant chain of the HLA class II molecule, CD74. We hypothesized that the expression of this receptor-ligand pair in lung cancer is associated with the angiogenic activity and level of CXC chemokine expression in human specimens of non-small cell lung cancer. We, therefore, performed immunolocalization of CD74 and compared it with the localization of MIF in non-small cell lung cancer to determine their respective locations, as well as the relationship between the co-expression of MIF-CD74 and angiogenic CXC chemokines with tumor angiogenesis. We found intens...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2094256</comments>
            <pubDate>Thu, 08 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2094256</guid>        </item>
        <item>
            <title>Collagen fragmentation promotes oxidative stress and elevates matrix metalloproteinase-1 in fibroblasts in aged human skin.</title>
            <link>http://www.medworm.com/index.php?rid=2072157&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116368%26dopt%3DAbstract</link>
            <description>We report here that dermal fibroblasts express increased levels of collagen-degrading matrix metalloproteinases-1 (MMP-1) in aged (&amp;gt;80 years old) compared with young (21 to 30 years old) human skin in vivo. Transcription factor AP-1 and alpha2beta1 integrin, which are key regulators of MMP-1 expression, are also elevated in fibroblasts in aged human skin in vivo. MMP-1 treatment of young skin in organ culture causes fragmentation of collagen fibrils and reduces fibroblast stretch, consistent with reduced mechanical tension, as observed in aged human skin. Limited fragmentation of three-dimensional collagen lattices with exogenous MMP-1 also reduces fibroblast stretch and mechanical tension. Furthermore, fibroblasts cultured in fragmented collagen lattices express elevated levels of MMP-...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072157</comments>
            <pubDate>Thu, 01 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072157</guid>        </item>
        <item>
            <title>Activin-Like Kinase 5 (ALK5) Mediates Abnormal Proliferation of Vascular Smooth Muscle Cells from Patients with Familial Pulmonary Arterial Hypertension and Is Involved in the Progression of Experimental Pulmonary Arterial Hypertension Induced by Monocrotaline.</title>
            <link>http://www.medworm.com/index.php?rid=2072164&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116361%26dopt%3DAbstract</link>
            <description>In this study, we demonstrate that pulmonary artery smooth muscle cells from patients with familial forms of idiopathic PAH exhibit heightened sensitivity to TGF-beta1 in vitro, which can be attenuated after the administration of SB525334. We further demonstrate that SB525334 significantly reverses pulmonary arterial pressure and inhibits right ventricular hypertrophy in a rat model of PAH. Immunohistochemical studies confirmed a significant reduction in pulmonary arteriole muscularization induced by monocrotaline (used experimentally to induce PAH) after treatment of rats with SB525334. Collectively, these data are consistent with a role for the activin receptor-like kinase 5 in the progression of idiopathic PAH and imply that strategies to inhibit activin receptor-like kinase 5 signaling...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072164</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072164</guid>        </item>
        <item>
            <title>Transmembrane Interactions Are Needed for KAI1/CD82-Mediated Suppression of Cancer Invasion and Metastasis.</title>
            <link>http://www.medworm.com/index.php?rid=2072163&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116362%26dopt%3DAbstract</link>
            <description>Authors: Bari R, Zhang YH, Zhang F, Wang NX, Stipp CS, Zheng JJ, Zhang XA
    In transmembrane (TM) domains, tetraspanin KAI1/CD82 contains an Asn, a Gln, and a Glu polar residue. A mutation of all three polar residues largely disrupts the migration-, invasion-, and metastasis-suppressive activities of KAI1/CD82. Notably, KAI1/CD82 inhibits the formation of microprotrusions and the release of microvesicles, while the mutation disrupts these inhibitions, revealing the connections of microprotrusion and microvesicle to KAI1/CD82 function. The TM polar residues are needed for proper interactions between KAI1/CD82 and tetraspanins CD9 and CD151, which also regulate cell movement, but not for the association between KAI1/CD82 and alpha3beta1 integrin. However, KAI1/CD82 still efficiently inhibi...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072163</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072163</guid>        </item>
        <item>
            <title>Massive T-Lymphocyte Infiltration into the Host Stroma Is Essential for Fibroblast Growth Factor-2-Promoted Growth and Metastasis of Mammary Tumors via Neovascular Stability.</title>
            <link>http://www.medworm.com/index.php?rid=2072162&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116363%26dopt%3DAbstract</link>
            <description>Authors: Tsunoda S, Sakurai H, Saito Y, Ueno Y, Koizumi K, Saiki I
    Inflammation in the tumor stroma greatly influences tumor development. In the present study, we investigated the roles of fibroblast growth factor (FGF)-2-induced chronic inflammation in the development of 4T1 murine mammary tumors. Administration of FGF-2 into the tumor inoculation site during the initial phase of tumor growth enhanced tumor growth and pulmonary metastasis as well as microvessel density in tumor tissues in normal but not in nude mice. Infiltration of T lymphocytes and macrophages, recruitment of pericytes/vascular mural cells in neovascular walls, and the expression levels of cyclooxygenase (COX)-2 and vascular endothelial growth factor A (VEGFA) were also enhanced in the FGF-2-activated host stroma of...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072162</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072162</guid>        </item>
        <item>
            <title>A Protein Kinase C{delta}-Dependent Protein Kinase D Pathway Modulates ERK1/2 and JNK1/2 Phosphorylation and Bim-Associated Apoptosis by Asbestos.</title>
            <link>http://www.medworm.com/index.php?rid=2072161&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116364%26dopt%3DAbstract</link>
            <description>Authors: Buder-Hoffmann SA, Shukla A, Barrett TF, Macpherson MB, Lounsbury KM, Mossman BT
    Inhalation of asbestos and oxidant-generating pollutants causes injury and compensatory proliferation of lung epithelium, but the signaling mechanisms that lead to these responses are unclear. We hypothesized that a protein kinase (PK)Cdelta-dependent PKD pathway was able to regulate downstream mitogen-activated protein kinases, affecting pro- and anti-apoptotic responses to asbestos. Elevated levels of phosphorylated PKD (p-PKD) were observed in distal bronchiolar epithelial cells of mice inhaling asbestos. In contrast, PKCdelta-/- mice showed significantly lower levels of p-PKD in lung homogenates and in situ after asbestos inhalation. In a murine lung epithelial cell line, asbestos caused signi...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072161</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072161</guid>        </item>
        <item>
            <title>Glycinergic Innervation of Motoneurons Is Deficient in Amyotrophic Lateral Sclerosis Mice: A Quantitative Confocal Analysis.</title>
            <link>http://www.medworm.com/index.php?rid=2072160&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116365%26dopt%3DAbstract</link>
            <description>Authors: Chang Q, Martin LJ
    Altered motoneuron excitability is involved in amyotrophic lateral sclerosis pathobiology. To test the hypothesis that inhibitory interneuron innervation of spinal motoneurons is abnormal in an amyotrophic lateral sclerosis mouse model, we measured GABAergic, glycinergic, and cholinergic immunoreactive terminals on spinal motoneurons in mice expressing a mutant form of human superoxide dismutase-1 with a Gly93--&amp;gt;Ala substitution (G93A-SOD1) and in controls at different ages. Glutamic acid decarboxylase, glycine transporter-2, and choline acetyltransferase were used as markers for GABAergic, glycinergic, and cholinergic terminals, respectively. Triple immunofluorescent labeling of boutons contacting motoneurons was visualized by confocal microscopy and ana...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072160</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072160</guid>        </item>
        <item>
            <title>A Defective Serca1 Protein Is Responsible for Congenital Pseudomyotonia in Chianina Cattle.</title>
            <link>http://www.medworm.com/index.php?rid=2072159&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116366%26dopt%3DAbstract</link>
            <description>In this study, we provide biochemical evidence for a selective deficiency in SERCA1 protein levels in sarcoplasmic reticulum membranes from affected muscles, although mRNA levels are unaffected. The reduction of SERCA1 levels accounts for the reduced Ca(2+)-ATPase activity without any significant change in Ca(2+)-dependency. The loss of SERCA1 is not compensated for by the expression of the SERCA2 isoform. We believe that Chianina cattle pseudomyotonia might, therefore, be the true counterpart of human Brody's disease, and that bovine species might be used as a suitable animal model.
    PMID: 19116366 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072159</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072159</guid>        </item>
        <item>
            <title>Co-Existent Pseudoxanthoma Elasticum and Vitamin K-Dependent Coagulation Factor Deficiency. Compound Heterozygosity for Mutations in the GGCX Gene.</title>
            <link>http://www.medworm.com/index.php?rid=2072158&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116367%26dopt%3DAbstract</link>
            <description>In this study, we investigated a family with two siblings with characteristic features of PXE and vitamin K-dependent coagulation factor deficiency. Mutation analysis identified two GGCX mutations in the affected individuals (p. R83W and p.Q374X); however, no mutations in either ABCC6 or VKORC1 could be found. GGCX encodes a gamma-glutamyl carboxylase necessary for activation of both coagulation factors in the liver and matrix gla protein, which, in fully carboxylated form, is able to prevent ectopic mineralization. Analysis of skin by specific antibodies demonstrated that matrix gla protein was found predominantly in undercarboxylated form and was associated with the mineralized areas in the patients' lesional skin. These observations pathomechanistically suggest that, in our patients, re...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072158</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072158</guid>        </item>
        <item>
            <title>Am J Pathol; +19 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2055327&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F12%252F20%2B02%252E33%2522%255BMHDA%255D%253A%25222008%252F12%252F22%2B00%252E13%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F12%252F20%2B02%252E33%2522%255BEDAT%255D%2529%2529</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 Pathol
These PubMed results were generated on 2008/12/22PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2055327</comments>
            <pubDate>Mon, 22 Dec 2008 05:13:47 +0100</pubDate>
            <guid isPermaLink="false">2055327</guid>        </item>
        <item>
            <title>Am J Pathol; +32 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2051197&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F12%252F18%2B00%252E39%2522%255BMHDA%255D%253A%25222008%252F12%252F20%2B02%252E32%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F12%252F18%2B00%252E39%2522%255BEDAT%255D%2529%2529</link>
            <description>32 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2008/12/20PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2051197</comments>
            <pubDate>Sat, 20 Dec 2008 07:32:53 +0100</pubDate>
            <guid isPermaLink="false">2051197</guid>        </item>
        <item>
            <title>CK2{beta} Is Expressed in Endometrial Carcinoma and Has a Role in Apoptosis Resistance and Cell Proliferation.</title>
            <link>http://www.medworm.com/index.php?rid=2015750&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056846%26dopt%3DAbstract</link>
            <description>Authors: Pallares J, Llobet D, Santacana M, Eritja N, Velasco A, Cuevas D, Lopez S, Palomar-Asenjo V, Yeramian A, Dolcet X, Matias-Guiu X
    Protein kinase CK2 (CK2) is a serine/threonine kinase that participates in important cellular processes. We have recently demonstrated that CK2 plays a role in resistance to TRAIL/Fas-induced apoptosis in endometrial carcinoma (EC) by regulating FLIP. Here, we assessed the immunohistochemical expression of CK2beta in EC and checked its role in cell proliferation and anchorage-independent cell growth. CK2beta immunostaining was assessed in two tissue microarrays, one constructed from paraffin-embedded blocks of 95 ECs and another from 70 samples of normal endometrium. CK2beta expression was correlated with histological type; grade and stage; cell prol...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015750</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015750</guid>        </item>
        <item>
            <title>Expression of Cyclophilin B is Associated with Malignant Progression and Regulation of Genes Implicated in the Pathogenesis of Breast Cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2015749&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056847%26dopt%3DAbstract</link>
            <description>Authors: Fang F, Flegler AJ, Du P, Lin S, Clevenger CV
    Cyclophilin B (CypB) is a 21-kDa protein with peptidyl-prolyl cis-trans isomerase activity that functions as a transcriptional inducer for Stat5 and as a ligand for CD147. To better understand the global function of CypB in breast cancer, T47D cells with a small interfering RNA-mediated knockdown of CypB were generated. Subsequent expression profiling analysis showed that 663 transcripts were regulated by CypB knockdown, and that many of these gene products contributed to cell proliferation, cell motility, and tumorigenesis. Real-time PCR confirmed that STMN3, S100A4, S100A6, c-Myb, estrogen receptor alpha, growth hormone receptor, and progesterone receptor were all down-regulated in si-CypB cells. A linkage analysis of these array...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015749</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015749</guid>        </item>
        <item>
            <title>Development of a Rab9 Transgenic Mouse and Its Ability to Increase the Lifespan of a Murine Model of Niemann-Pick Type C Disease.</title>
            <link>http://www.medworm.com/index.php?rid=2015748&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056848%26dopt%3DAbstract</link>
            <description>Authors: Kaptzan T, West SA, Holicky EL, Wheatley CL, Marks DL, Wang T, Peake KB, Vance J, Walkley SU, Pagano RE
    Niemann-Pick, type C (NP-C) disease is an autosomal recessive neurovisceral storage disorder in which cholesterol and sphingolipids accumulate. There is no specific treatment for this disease, which is characterized by progressive neurological deterioration, sometimes accompanied by hepatosplenomegaly. We and others have shown that overexpression of certain Rab GTPases corrects defective membrane trafficking and reduces lipid storage in cultured NP-C fibroblasts. Here, we tested the possibility that Rab protein overexpression might also have beneficial effects in vivo using a murine model of NP-C. We first generated several lines of transgenic mice that ubiquitously overexpr...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015748</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015748</guid>        </item>
        <item>
            <title>Latent Transforming Growth Factor-{beta}-binding Protein-4 Regulates Transforming Growth Factor-{beta}1 Bioavailability for Activation by Fibrogenic Lung Fibroblasts in Response to Bleomycin.</title>
            <link>http://www.medworm.com/index.php?rid=2015747&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056849%26dopt%3DAbstract</link>
            <description>Authors: Zhou Y, Koli K, Hagood JS, Miao M, Mavalli M, Rifkin DB, Murphy-Ullrich JE
    Recent evidence suggests that subsets of lung fibroblasts differentially contribute to fibrogenic progression. We have previously shown that a subset of rat lung fibroblasts with fibrogenic characteristics [Thy-1 (-) fibroblasts] responds to stimuli (bleomycin, interleukin-4, etc) with increased latent transforming growth factor (TGF)-beta activation, whereas non-fibrogenic Thy-1-expressing [Thy-1 (+)] fibroblasts do not. Activation of latent TGF-beta1 by interstitial lung fibroblasts is critical for fibrogenic responses. To better understand the susceptibility of fibrogenic fibroblasts to the stimulation of TGF-beta activation, we examined the role of latent TGF-beta-binding proteins (LTBPs), key regul...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015747</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015747</guid>        </item>
        <item>
            <title>Heterochromatin Protein 1{gamma} Epigenetically Regulates Cell Differentiation and Exhibits Potential as a Therapeutic Target for Various Types of Cancers.</title>
            <link>http://www.medworm.com/index.php?rid=2015746&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056850%26dopt%3DAbstract</link>
            <description>In this study, we found that HP1gamma levels are decreased during adipocyte differentiation, whereas HP1alpha and beta levels are expressed constitutively during adipogenesis in cultured preadipocyte cells. In addition, ectopic overexpression of HP1gamma inhibited adipogenesis. Furthermore, we did not detect any HP1gamma protein in the differentiated cells of various normal human tissues. These results suggest that the loss of HP1gamma is required for cell differentiation to occur. On the other hand, the methylation levels of lysine 20 (K20) on histone H4 showed a significant correlation with HP1gamma expression in both these preadipocyte cells and normal tissue samples. However, all cancer tissues examined were positive for HP1gamma but were often negative for trimethylated histone H4 K20...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015746</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015746</guid>        </item>
        <item>
            <title>Disruption of Tissue-Specific Fucosyltransferase VII, an Enzyme Necessary for Selectin Ligand Synthesis, Suppresses Atherosclerosis in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2015745&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056851%26dopt%3DAbstract</link>
            <description>In this study, we have determined the role of tissue-specific fucosyltransferase VII (FucT-VII), an enzyme necessary for selectin ligand synthesis, in the development of atherosclerosis. We adopted a scheme of transplanting either FucT-VII(-/-)GFP(+) bone marrow into lethally irradiated low-density lipoprotein receptor low density lipoprotein receptor mice or FucT-VII(+/+) GFP(+) bone marrow into FucT-VII(-/-), low density lipoprotein receptor double-mutant mice to evaluate the roles of E- and P-selectin ligands versus L-selectin ligands, respectively, in diet-induced atherosclerosis. GFP was used to track the transplanted cells. Our results indicate that, compared with controls, selective disruption of E- and P-selectin ligand synthesis resulted in a significant reduction in atheroscleros...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015745</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015745</guid>        </item>
        <item>
            <title>The Protective Role of Per2 Against Carbon Tetrachloride-Induced Hepatotoxicity.</title>
            <link>http://www.medworm.com/index.php?rid=2015744&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19056852%26dopt%3DAbstract</link>
            <description>Authors: Chen P, Li C, Pang W, Zhao Y, Dong W, Wang S, Zhang J
    Period 2 (Per2) is a key component of the core clock oscillator and is involved in regulating a number of different biological processes and pathways. Here we report that Per2 plays a protective role in carbon tetrachloride (CCl4)-induced hepatotoxicity via the modulation of uncoupling protein-2 (Ucp2) gene expression in mice. Hepatic injury after acute CCl4 injection was monitored in both wild-type and Per2-null mice. At the 12-hour time point after CCl4 treatment, many more vacuolations were observed in the liver tissues of Per2-null mice whereas fatty tissue degeneration primarily occurred in the liver tissues of wide-type mice. Serum alanine and aspartate aminotransferase activities were elevated in Per2-null mice compa...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2015744</comments>
            <pubDate>Thu, 04 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2015744</guid>        </item>
        <item>
            <title>Index of Subjects.</title>
            <link>http://www.medworm.com/index.php?rid=1979023&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19022945%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 19022945 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1979023</comments>
            <pubDate>Sun, 23 Nov 2008 06:01:38 +0100</pubDate>
            <guid isPermaLink="false">1979023</guid>        </item>
        <item>
            <title>Index of Authors.</title>
            <link>http://www.medworm.com/index.php?rid=1979022&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19022946%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 19022946 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1979022</comments>
            <pubDate>Sun, 23 Nov 2008 06:01:32 +0100</pubDate>
            <guid isPermaLink="false">1979022</guid>        </item>
        <item>
            <title>Am J Pathol; +32 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1967440&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F11%252F17%2B00%252E07%2522%255BMHDA%255D%253A%25222008%252F11%252F19%2B00%252E11%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F11%252F17%2B00%252E07%2522%255BEDAT%255D%2529%2529</link>
            <description>32 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2008/11/19PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1967440</comments>
            <pubDate>Wed, 19 Nov 2008 05:11:23 +0100</pubDate>
            <guid isPermaLink="false">1967440</guid>        </item>
        <item>
            <title>Am J Pathol; +24 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1926149&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F11%252F01%2B04%252E42%2522%255BMHDA%255D%253A%25222008%252F11%252F02%2B04%252E36%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F11%252F01%2B04%252E42%2522%255BEDAT%255D%2529%2529</link>
            <description>24 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2008/11/02PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1926149</comments>
            <pubDate>Sun, 02 Nov 2008 09:36:17 +0100</pubDate>
            <guid isPermaLink="false">1926149</guid>        </item>
        <item>
            <title>Am J Pathol; +17 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1904891&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F10%252F13%2B04%252E25%2522%255BMHDA%255D%253A%25222008%252F10%252F25%2B04%252E19%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F10%252F13%2B04%252E25%2522%255BEDAT%255D%2529%2529</link>
            <description>17 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2008/10/25PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1904891</comments>
            <pubDate>Sat, 25 Oct 2008 08:19:28 +0100</pubDate>
            <guid isPermaLink="false">1904891</guid>        </item>
        <item>
            <title>Am J Pathol; +30 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1864877&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F10%252F05%2B04%252E39%2522%255BMHDA%255D%253A%25222008%252F10%252F10%2B05%252E16%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F10%252F05%2B04%252E39%2522%255BEDAT%255D%2529%2529</link>
            <description>30 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2008/10/10PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864877</comments>
            <pubDate>Fri, 10 Oct 2008 09:16:43 +0100</pubDate>
            <guid isPermaLink="false">1864877</guid>        </item>
        <item>
            <title>Am J Pathol; +21 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1852274&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F09%252F28%2B05%252E12%2522%255BMHDA%255D%253A%25222008%252F10%252F05%2B04%252E38%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F09%252F28%2B05%252E12%2522%255BEDAT%255D%2529%2529</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 Pathol
These PubMed results were generated on 2008/10/05PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1852274</comments>
            <pubDate>Sun, 05 Oct 2008 08:38:48 +0100</pubDate>
            <guid isPermaLink="false">1852274</guid>        </item>
        <item>
            <title>Am J Pathol; +27 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1828607&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F09%252F25%2B05%252E27%2522%255BMHDA%255D%253A%25222008%252F09%252F26%2B05%252E03%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F09%252F25%2B05%252E27%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 Pathol
These PubMed results were generated on 2008/09/26PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1828607</comments>
            <pubDate>Fri, 26 Sep 2008 09:03:50 +0100</pubDate>
            <guid isPermaLink="false">1828607</guid>        </item>
        <item>
            <title>Am J Pathol; +29 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1823497&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F09%252F17%2B04%252E43%2522%255BMHDA%255D%253A%25222008%252F09%252F25%2B05%252E26%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F09%252F17%2B04%252E43%2522%255BEDAT%255D%2529%2529</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 Pathol
These PubMed results were generated on 2008/09/25PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1823497</comments>
            <pubDate>Thu, 25 Sep 2008 09:26:30 +0100</pubDate>
            <guid isPermaLink="false">1823497</guid>        </item>
        <item>
            <title>Am J Pathol; +16 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1770230&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F08%252F31%2B04%252E14%2522%255BMHDA%255D%253A%25222008%252F09%252F07%2B04%252E16%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F08%252F31%2B04%252E14%2522%255BEDAT%255D%2529%2529</link>
            <description>16 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2008/09/07PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1770230</comments>
            <pubDate>Sun, 07 Sep 2008 08:16:04 +0100</pubDate>
            <guid isPermaLink="false">1770230</guid>        </item>
        <item>
            <title>Am J Pathol; +20 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1693324&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F08%252F04%2B03%252E31%2522%255BMHDA%255D%253A%25222008%252F08%252F10%2B03%252E32%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F08%252F04%2B03%252E31%2522%255BEDAT%255D%2529%2529</link>
            <description>20 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2008/08/10PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1693324</comments>
            <pubDate>Sun, 10 Aug 2008 07:32:45 +0100</pubDate>
            <guid isPermaLink="false">1693324</guid>        </item>
        <item>
            <title>Dlx5, a Positive Regulator of Osteoblastogenesis, is Essential for Osteoblast-Osteoclast Coupling.</title>
            <link>http://www.medworm.com/index.php?rid=1678781&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18669617%26dopt%3DAbstract</link>
            <description>Authors: Samee N, Geoffroy V, Marty C, Schiltz C, Vieux-Rochas M, Levi G, de Vernejoul MC
    The homeodomain protein Dlx5 is an activator of Runx2 (a key regulator of osteogenesis) and is thought to be an important regulator of bone formation. At present, however, the perinatal lethality of Dlx5-null mice has hampered the elucidation of its function in osteogenesis. Here we provide the first analysis of the effects of Dlx5 inactivation on bone development. Femurs of Dlx5-null mouse embryos at the end of gestation exhibit a reduction in both total and trabecular bone volume associated with increased trabecular separation and reduced trabecular number. These parameters are often associated with pathological conditions characterized by reduced osteoblast activity and increased bone resorptio...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1678781</comments>
            <pubDate>Fri, 01 Aug 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1678781</guid>        </item>
        <item>
            <title>Am J Pathol; +26 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1667798&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F07%252F27%2B03%252E23%2522%255BMHDA%255D%253A%25222008%252F07%252F31%2B03%252E54%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F07%252F27%2B03%252E23%2522%255BEDAT%255D%2529%2529</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 Pathol
These PubMed results were generated on 2008/07/31PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1667798</comments>
            <pubDate>Thu, 31 Jul 2008 07:54:55 +0100</pubDate>
            <guid isPermaLink="false">1667798</guid>        </item>
        <item>
            <title>Am J Pathol; +29 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1601984&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F07%252F06%2B03%252E01%2522%255BMHDA%255D%253A%25222008%252F07%252F10%2B03%252E58%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F07%252F06%2B03%252E01%2522%255BEDAT%255D%2529%2529</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 Pathol
These PubMed results were generated on 2008/07/10PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1601984</comments>
            <pubDate>Thu, 10 Jul 2008 07:58:51 +0100</pubDate>
            <guid isPermaLink="false">1601984</guid>        </item>
        <item>
            <title>Am J Pathol; +16 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1550213&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F06%252F18%2B15%252E58%2522%255BMHDA%255D%253A%25222008%252F06%252F28%2B12%252E01%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F06%252F18%2B15%252E58%2522%255BEDAT%255D%2529%2529</link>
            <description>16 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2008/06/28PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1550213</comments>
            <pubDate>Sat, 28 Jun 2008 16:01:55 +0100</pubDate>
            <guid isPermaLink="false">1550213</guid>        </item>
        <item>
            <title>Am J Pathol; +27 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1517813&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F06%252F07%2B16%252E26%2522%255BMHDA%255D%253A%25222008%252F06%252F14%2B16%252E47%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F06%252F07%2B16%252E26%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 Pathol
These PubMed results were generated on 2008/06/14PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1517813</comments>
            <pubDate>Sat, 14 Jun 2008 20:47:51 +0100</pubDate>
            <guid isPermaLink="false">1517813</guid>        </item>
        <item>
            <title>CCAAT/Enhancer Binding Protein {beta} Is a Major Mediator of Inflammation and Viral Replication in the Gastrointestinal Tract of Simian Immunodeficiency Virus-Infected Rhesus Macaques.</title>
            <link>http://www.medworm.com/index.php?rid=1498992&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535173%26dopt%3DAbstract</link>
            <description>Authors: Mohan M, Aye PP, Borda JT, Alvarez X, Lackner AA
    The gastrointestinal tract (GIT) is a major target of infection with human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV). Chronic GIT disease and inflammation are common sequelae to HIV/SIV infection. Nonetheless, the molecular mechanisms that cause and maintain GIT dysfunction remain unclear. We investigated the contribution of CCAAT/enhancer-binding protein beta (C/EBPbeta) to GIT disease and viral replication in jejunum and colon collected at necropsy from 12 SIV-infected (group 1), or 10 uninfected macaques with chronic diarrhea (group 2), and 9 uninfected control macaques (group 3). All group 1 and 2 macaques had chronic diarrhea, wasting, and colitis, but group 1 animals had more severe lesions in th...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498992</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498992</guid>        </item>
        <item>
            <title>Interleukin-1 Receptor Type I Signaling Critically Regulates Infarct Healing and Cardiac Remodeling.</title>
            <link>http://www.medworm.com/index.php?rid=1498991&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535174%26dopt%3DAbstract</link>
            <description>In conclusion, IL-1 signaling is essential for activation of inflammatory and fibrogenic pathways in the healing infarct, playing an important role in the pathogenesis of remodeling after infarction. Thus, interventional therapeutics targeting the IL-1 system may have great benefits in myocardial infarction.
    PMID: 18535174 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498991</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498991</guid>        </item>
        <item>
            <title>Regulation of Skp2-p27 Axis by the Cdh1/Anaphase-Promoting Complex Pathway in Colorectal Tumorigenesis.</title>
            <link>http://www.medworm.com/index.php?rid=1498990&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535175%26dopt%3DAbstract</link>
            <description>Authors: Fujita T, Liu W, Doihara H, Wan Y
    Abrogated entry into S phase is a common hallmark of cancer cells. Skp2, a subunit of ubiquitin ligase, is critical for regulating the G1/S transition. Uncontrolled Skp2 activity is detected frequently in human tumors, often correlated with poor prognosis. Current studies have suggested that the regulation of Skp2 turnover is mediated by another critical ubiquitin ligase, the anaphase-promoting complex (APC), in association with its substrate-specific factor Cdh1. To dissect the potential role of Cdh1/APC in tumorigenesis through the degradation of Skp2, we analyzed the Cdh1/APC-Skp2-p27 axis in colorectal tumorigenesis using a human tumor array and biochemical analyses. Our results show that the percentage of Cdh1- and p27-positive samples in...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498990</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498990</guid>        </item>
        <item>
            <title>Integrin-Linked Kinase in the Vascular Smooth Muscle Cell Response to Injury.</title>
            <link>http://www.medworm.com/index.php?rid=1498989&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535176%26dopt%3DAbstract</link>
            <description>Authors: Ho B, Hou G, Pickering JG, Hannigan G, Langille BL, Bendeck MP
    Integrin-mediated interactions between smooth muscle cells (SMCs) and the extracellular matrix regulate cell migration and proliferation during neointimal hyperplasia. Integrin-linked kinase (ILK) is a serine-threonine kinase and scaffolding molecule that acts downstream of integrin receptors to modulate cell adhesion; therefore, we examined ILK function in SMCs during wound repair. Silencing of ILK expression with siRNA in vitro decreased cell adhesion to fibronectin and accelerated both cell proliferation and wound closure in the cell monolayer; it also resulted in the rearrangement of focal adhesions and diminished central actin stress fibers. Akt and GSK3beta are ILK substrates that are important in cell motili...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498989</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498989</guid>        </item>
        <item>
            <title>Amelioration of Experimental Autoimmune Encephalomyelitis in IL-4R{alpha}-/- Mice Implicates Compensatory Up-Regulation of Th2-Type Cytokines.</title>
            <link>http://www.medworm.com/index.php?rid=1498988&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535177%26dopt%3DAbstract</link>
            <description>Authors: Gaupp S, Cannella B, Raine CS
    The cytokine receptor interleukin (IL)-4R, expressed by lymphocytes, is well known for its role in immunomodulatory signaling and has also been documented on oligodendrocytes, suggesting involvement in glial cell interactions. In the present study, we investigated the clinical course and pathology of experimental autoimmune encephalomyelitis in mice demonstrating deletion of IL-4R and found a correlation with cytokine expression during acute and chronic disease. Wild-type (WT) littermates served as controls. Although IL-4R(-/-) mice displayed a milder course throughout, they showed comparable pathology to WT in the acute phase. However, during the chronic phase, IL-4R(-/-) mice exhibited extensive remyelination and an apparent increase in oligoden...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498988</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498988</guid>        </item>
        <item>
            <title>CD4 T Cells Mediate Axonal Damage and Spinal Cord Motor Neuron Apoptosis in Murine P0106-125-Induced Experimental Autoimmune Neuritis.</title>
            <link>http://www.medworm.com/index.php?rid=1498987&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535178%26dopt%3DAbstract</link>
            <description>In conclusion, P0106-125-induced experimental autoimmune neuritis is a CD4 T cell-mediated autoimmune disease that affects both the peripheral and central nervous systems.
    PMID: 18535178 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498987</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498987</guid>        </item>
        <item>
            <title>Inhibition of Proteasome Activity Promotes the Correct Localization of Disease-Causing {alpha}-Sarcoglycan Mutants in HEK-293 Cells Constitutively Expressing {beta}-, {gamma}-, and {delta}-Sarcoglycan.</title>
            <link>http://www.medworm.com/index.php?rid=1498986&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535179%26dopt%3DAbstract</link>
            <description>Authors: Gastaldello S, D'Angelo S, Franzoso S, Fanin M, Angelini C, Betto R, Sandon&amp;#xE0; D
    Sarcoglycanopathies are progressive muscle-wasting disorders caused by genetic defects of four proteins, alpha-, beta-, gamma-, and delta-sarcoglycan, which are elements of a key transmembrane complex of striated muscle. The proper assembly of the sarcoglycan complex represents a critical issue of sarcoglycanopathies, as several mutations severely perturb tetramer formation. Misfolded proteins are generally degraded through the cell's quality-control system; however, this can also lead to the removal of some functional polypeptides. To explore whether it is possible to rescue sarcoglycan mutants by preventing their degradation, we generated a heterologous cell system, based on human embryonic k...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498986</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498986</guid>        </item>
        <item>
            <title>Down Syndrome Fibroblast Model of Alzheimer-Related Endosome Pathology. Accelerated Endocytosis Promotes Late Endocytic Defects.</title>
            <link>http://www.medworm.com/index.php?rid=1498985&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535180%26dopt%3DAbstract</link>
            <description>Authors: Cataldo AM, Mathews PM, Boiteau AB, Hassinger LC, Peterhoff CM, Jiang Y, Mullaney K, Neve RL, Gruenberg J, Nixon RA
    Endocytic dysfunction is an early pathological change in Alzheimer's disease (AD) and Down's syndrome (DS). Using primary fibroblasts from DS individuals, we explored the interactions among endocytic compartments that are altered in AD and assessed their functional consequences in AD pathogenesis. We found that, like neurons in both AD and DS brains, DS fibroblasts exhibit increased endocytic uptake, fusion, and recycling, and trafficking of lysosomal hydrolases to rab5-positive early endosomes. Moreover, late endosomes identified using antibodies to rab7 and lysobisphosphatidic acid increased in number and appeared as enlarged, perinuclear vacuoles, resembling t...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498985</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498985</guid>        </item>
        <item>
            <title>Fas-Ligand-Induced Apoptosis of Respiratory Epithelial Cells Causes Disruption of Postcanalicular Alveolar Development.</title>
            <link>http://www.medworm.com/index.php?rid=1498984&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535181%26dopt%3DAbstract</link>
            <description>Authors: De Paepe ME, Gundavarapu S, Tantravahi U, Pepperell JR, Haley SA, Luks FI, Mao Q
    Premature infants are at risk for bronchopulmonary dysplasia, a complex condition characterized by impaired alveolar development and increased alveolar epithelial apoptosis. The functional involvement of pulmonary apoptosis in bronchopulmonary dysplasia- associated alveolar disruption remains undetermined. The aims of this study were to generate conditional lung-specific Fas-ligand (FasL) transgenic mice and to determine the effects of FasL-induced respiratory epithelial apoptosis on alveolar remodeling in postcanalicular lungs. Transgenic (TetOp)7-FasL responder mice, generated by pronuclear microinjection, were bred with Clara cell secretory protein (CCSP)-rtTA activator mice. Doxycycline (Dox) ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498984</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498984</guid>        </item>
        <item>
            <title>Role of the Peroxynitrite-Poly(ADP-Ribose) Polymerase Pathway in Human Disease.</title>
            <link>http://www.medworm.com/index.php?rid=1498983&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535182%26dopt%3DAbstract</link>
            <description>Authors: Pacher P, Szabo C
    Throughout the last 2 decades, experimental evidence from in vitro studies and preclinical models of disease has demonstrated that reactive oxygen and nitrogen species, including the reactive oxidant peroxynitrite, are generated in parenchymal, endothelial, and infiltrating inflammatory cells during stroke, myocardial and other forms of reperfusion injury, myocardial hypertrophy and heart failure, cardiomyopathies, circulatory shock, cardiovascular aging, atherosclerosis and vascular remodeling after injury, diabetic complications, and neurodegenerative disorders. Peroxynitrite and other reactive species induce oxidative DNA damage and consequent activation of the nuclear enzyme poly(ADP-ribose) polymerase 1 (PARP-1), the most abundant isoform of the PARP enz...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498983</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498983</guid>        </item>
        <item>
            <title>C-C Chemokine Receptor 5 on Pulmonary Fibrocytes Facilitates Migration and Promotes Metastasis via Matrix Metalloproteinase 9.</title>
            <link>http://www.medworm.com/index.php?rid=1498982&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535183%26dopt%3DAbstract</link>
            <description>Authors: van Deventer HW, Wu QP, Bergstralh DT, Davis BK, O'Connor BP, Ting JP, Serody JS
    Previously, our group has used a B16-F10 melanoma model to show that C-C chemokine receptor 5 (CCR5) knockout (CCR5(-/-)) mice form fewer pulmonary metastases than wild-type mice. This advantage can be eliminated by injecting CCR5(-/-) mice with wild-type pulmonary mesenchymal cells before tumor injection. In this article, we present the mechanisms underlying this finding. First, we demonstrate that wild-type mesenchymal cells migrate to CCL4 more efficiently in vitro than CCR5(-/-) cells. Wild-type mesenchymal cells were also 3.6 (1.85 to 5.85) times more efficient than CCR5(-/-) cells at migrating into the lung after intravenous injection (P &amp;lt; 0.01). The injection of wild-type but not CCR5(-/...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498982</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498982</guid>        </item>
        <item>
            <title>Inhibition of Chronic and Acute Skin Inflammation by Treatment with a Vascular Endothelial Growth Factor Receptor Tyrosine Kinase Inhibitor.</title>
            <link>http://www.medworm.com/index.php?rid=1498981&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535184%26dopt%3DAbstract</link>
            <description>Authors: Halin C, Fahrngruber H, Meingassner JG, Bold G, Littlewood-Evans A, Stuetz A, Detmar M
    Although vascular remodeling is a hallmark of many chronic inflammatory disorders, antivascular strategies to treat these conditions have received little attention to date. We investigated the effects of a newly identified vascular endothelial growth factor (VEGF) receptor tyrosine-kinase inhibitor, NVP-BAW2881, on endothelial cell function in vitro and its anti-inflammatory activity in different animal models. NVP-BAW2881 inhibited proliferation, migration, and tube formation by human umbilical vein endothelial cells and lymphatic endothelial cells in vitro. In a transgenic mouse model of psoriasis, NVP-BAW2881 reduced the number of blood and lymphatic vessels and infiltrating leukocytes in...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498981</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498981</guid>        </item>
        <item>
            <title>Enrichment of C-Terminal Fragments in TAR DNA-Binding Protein-43 Cytoplasmic Inclusions in Brain but not in Spinal Cord of Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=1498980&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18535185%26dopt%3DAbstract</link>
            <description>Authors: Igaz LM, Kwong LK, Xu Y, Truax AC, Uryu K, Neumann M, Clark CM, Elman LB, Miller BL, Grossman M, McCluskey LF, Trojanowski JQ, Lee VM
    TAR DNA-binding protein (TDP-43) has been recently described as a major pathological protein in both frontotemporal dementia with ubiquitin-positive inclusions (FTLD-U) and amyotrophic lateral sclerosis. However, little is known about the relative abundance and distribution of different pathological TDP-43 species, which include hyperphosphorylated, ubiquitinated, and N-terminally cleaved TDP-43. Here, we developed novel N-terminal (N-t) and C-terminal (C-t)-specific TDP-43 antibodies and performed biochemical and immunohistochemical studies to analyze cortical, hippocampal, and spinal cord tissue from frontotemporal dementia with ubiquitin-posi...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1498980</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1498980</guid>        </item>
        <item>
            <title>The tuberous sclerosis complex regulates trafficking of glucose transporters and glucose uptake.</title>
            <link>http://www.medworm.com/index.php?rid=1479634&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18511518%26dopt%3DAbstract</link>
            <description>Authors: Jiang X, Kenerson H, Aicher L, Miyaoka R, Eary J, Bissler J, Yeung RS
    Human cancers often display an avidity for glucose, a feature that is exploited in clinical staging and response monitoring by using (18)F-fluoro-deoxyglucose (FDG) positron emission tomography. Determinants of FDG accumulation include tumor blood flow, glucose transport, and glycolytic rate, but the underlying molecular mechanisms are incompletely understood. The phosphoinositide-3 kinase/Akt/mammalian target of rapamycin complex (mTORC) 1 pathway has been implicated in this process via the hypoxia-inducible factor alpha-dependent expression of vascular endothelial growth factor and glycolytic enzymes. Thus, we predicted that tumors with elevated mTORC1 activity would be accompanied by high FDG uptake. We t...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1479634</comments>
            <pubDate>Sat, 31 May 2008 14:21:00 +0100</pubDate>
            <guid isPermaLink="false">1479634</guid>        </item>
        <item>
            <title>Index of Subjects.</title>
            <link>http://www.medworm.com/index.php?rid=1479633&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18511519%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 18511519 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1479633</comments>
            <pubDate>Sat, 31 May 2008 14:20:57 +0100</pubDate>
            <guid isPermaLink="false">1479633</guid>        </item>
        <item>
            <title>Index of Authors.</title>
            <link>http://www.medworm.com/index.php?rid=1479632&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18511520%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 18511520 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1479632</comments>
            <pubDate>Sat, 31 May 2008 14:20:55 +0100</pubDate>
            <guid isPermaLink="false">1479632</guid>        </item>
        <item>
            <title>Suppression by CD4+CD25+ Regulatory T Cells Is Dependent on Expression of Heme Oxygenase-1 in Antigen-Presenting Cells.</title>
            <link>http://www.medworm.com/index.php?rid=1479636&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18511516%26dopt%3DAbstract</link>
            <description>We examined if impaired regulatory T cell (Treg) function contributes to the immunoregulatory defects observed in HO-1(-/-) mice. HO-1(-/-) mice exhibited a significantly higher proportion of Foxp3-expressing cells among total CD4(+) and CD4(+)CD25(+) cells in comparison to HO-1(+/+) mice, and HO-1(-/-) Treg cells were at least as effective as HO-1(+/+) Treg cells in suppressing proliferation of effector T cells in vitro from either HO-1(+/+) or HO-1(-/-) mice. However, the absence of HO-1 in antigen-presenting cells abolished the suppressive activity of Treg cells on effector T cells. These findings demonstrate that HO-1 activity in antigen-presenting cells is important for Treg-mediated suppression, providing an explanation for the apparent defect in immune regulation in HO-1(-/-) mice.
...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1479636</comments>
            <pubDate>Thu, 29 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1479636</guid>        </item>
        <item>
            <title>Cleavage of Type II Collagen by Cathepsin K in Human Osteoarthritic Cartilage.</title>
            <link>http://www.medworm.com/index.php?rid=1479635&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18511517%26dopt%3DAbstract</link>
            <description>Authors: Dejica VM, Mort JS, Laverty S, Percival MD, Antoniou J, Zukor DJ, Poole AR
    Cathepsin K is a cysteine protease of the papain family that cleaves triple-helical type II collagen, the major structural component of the extracellular matrix of articular cartilage. In osteoarthritis (OA), the anabolic/catabolic balance of articular cartilage is disrupted with the excessive cleavage of collagen II by collagenases or matrix metalloproteinases. A polyclonal antibody against a C-terminal neoepitope (C2K) generated in triple-helical type II collagen by the proteolytic action of cathepsin K was prepared and used to develop an enzyme-linked immunosorbent assay to study the generation of this epitope and the effects of its presence in normal adult and osteoarthritic femoral condylar articul...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1479635</comments>
            <pubDate>Thu, 29 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1479635</guid>        </item>
        <item>
            <title>Absence of Smad3 Induces Neutrophil Migration after Cutaneous Irradiation. Possible Contribution to Subsequent Radioprotection.</title>
            <link>http://www.medworm.com/index.php?rid=1468733&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18502822%26dopt%3DAbstract</link>
            <description>Authors: Flanders KC, Ho BM, Arany PR, Stuelten C, Mamura M, Paterniti MO, Sowers A, Mitchell JB, Roberts AB
    Our previous work showed that 6 weeks after cutaneous irradiation, mice null (knockout, KO) for Smad3, a cytoplasmic downstream mediator of transforming growth factor-beta, demonstrate less epidermal acanthosis and dermal inflammation than wild-type (WT) Smad3 mice. Analysis of the kinetics of inflammation showed that 6 to 8 hours after skin irradiation, there was a transient sevenfold increase in neutrophil influx in Smad3 KO mice compared with WT. Herein we describe bone marrow transplantation and skin grafting between WT and KO mice to assess the contribution of the neutrophil genotype compared with that of irradiated skin to the induction of neutrophil migration after irradi...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1468733</comments>
            <pubDate>Fri, 23 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1468733</guid>        </item>
        <item>
            <title>Expression of the Epstein-Barr Virus-Encoded Epstein-Barr Virus Nuclear Antigen 1 in Hodgkin's Lymphoma Cells Mediates Up-Regulation of CCL20 and the Migration of Regulatory T Cells.</title>
            <link>http://www.medworm.com/index.php?rid=1468732&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18502823%26dopt%3DAbstract</link>
            <description>Authors: Baumforth KR, Birgersdotter A, Reynolds GM, Wei W, Kapatai G, Flavell JR, Kalk E, Piper K, Lee S, Machado L, Hadley K, Sundblad A, Sjoberg J, Bjorkholm M, Porwit AA, Yap LF, Teo S, Grundy RG, Young LS, Ernberg I, Woodman CB, Murray PG
    In approximately 50% of patients with Hodgkin's lymphoma (HL), the Epstein-Barr virus (EBV), an oncogenic herpesvirus, is present in tumor cells. After microarray profiling of both HL tumors and cell lines, we found that EBV infection increased the expression of the chemokine CCL20 in both primary Hodgkin and Reed-Sternberg cells and Hodgkin and Reed-Sternberg cell-derived cell lines. Additionally, this up-regulation could be mediated by the EBV nuclear antigen 1 protein. The higher levels of CCL20 in the supernatants of EBV-infected HL cell line...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1468732</comments>
            <pubDate>Fri, 23 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1468732</guid>        </item>
        <item>
            <title>Hepatocyte Growth Factor Exerts Its Anti-Inflammatory Action by Disrupting Nuclear Factor-{kappa}B Signaling.</title>
            <link>http://www.medworm.com/index.php?rid=1468731&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18502824%26dopt%3DAbstract</link>
            <description>Authors: Giannopoulou M, Dai C, Tan X, Wen X, Michalopoulos GK, Liu Y
    Renal inflammation, characterized by the influx of inflammatory cells, is believed to play a critical role in the initiation and progression of a wide range of chronic kidney diseases. Here, we show that hepatocyte growth factor (HGF) inhibited renal inflammation and proinflammatory chemokine expression by disrupting nuclear factor (NF)-kappaB signaling. In vivo, HGF gene delivery inhibited interstitial infiltration of inflammatory T cells and macrophages, and suppressed expression of both RANTES (regulated on activation, normal T cell expressed and secreted) and monocyte chemoattractant protein-1 in a mouse model of obstructive nephropathy. In vitro, HGF abolished RANTES induction in human kidney epithelial cells, w...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1468731</comments>
            <pubDate>Fri, 23 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1468731</guid>        </item>
        <item>
            <title>Am J Pathol; +27 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1445194&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F05%252F10%2B19%252E10%2522%255BMHDA%255D%253A%25222008%252F05%252F16%2B10%252E23%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F05%252F10%2B19%252E10%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 Pathol
These PubMed results were generated on 2008/05/16PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1445194</comments>
            <pubDate>Fri, 16 May 2008 14:23:01 +0100</pubDate>
            <guid isPermaLink="false">1445194</guid>        </item>
        <item>
            <title>Am J Pathol; +46 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1433477&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F05%252F07%2B16%252E32%2522%255BMHDA%255D%253A%25222008%252F05%252F10%2B19%252E09%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F05%252F07%2B16%252E32%2522%255BEDAT%255D%2529%2529</link>
            <description>46 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These PubMed results were generated on 2008/05/10PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1433477</comments>
            <pubDate>Sat, 10 May 2008 23:09:20 +0100</pubDate>
            <guid isPermaLink="false">1433477</guid>        </item>
        <item>
            <title>Endogenous Hydrogen Peroxide Regulates Glutathione Redox via Nuclear Factor Erythroid 2-Related Factor 2 Downstream of Phosphatidylinositol 3-Kinase during Muscle Differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=1425433&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18458092%26dopt%3DAbstract</link>
            <description>In conclusion, endogenous H2O2 generated during muscle differentiation not only functions as a signaling molecule, but also regulates the GSH redox state via activation of the Nrf2-GCL/GR-GSH signaling pathway downstream of phosphatidylinositol 3-kinase.
    PMID: 18458092 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1425433</comments>
            <pubDate>Mon, 05 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1425433</guid>        </item>
        <item>
            <title>Adding Fuel to the Fire: Methamphetamine Enhances HIV Infection.</title>
            <link>http://www.medworm.com/index.php?rid=1425432&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18458093%26dopt%3DAbstract</link>
            <description>Authors: Potula R, Persidsky Y
    This Commentary examines the ability of methamphetamine to enhance HIV-1 infection in human macrophages, shedding new light on the drug's role in augmenting HIV-1 replication and immunopathogenesis.
    PMID: 18458093 [PubMed - as supplied by publisher] (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1425432</comments>
            <pubDate>Mon, 05 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1425432</guid>        </item>
        <item>
            <title>Expression and Maintenance of Mitochondrial DNA. New Insights into Human Disease Pathology.</title>
            <link>http://www.medworm.com/index.php?rid=1425431&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18458094%26dopt%3DAbstract</link>
            <description>Authors: Shadel GS
    Mitochondria are central players in cellular energy metabolism and, consequently, defects in their function result in many characterized metabolic diseases. Critical for their function is mitochondrial DNA (mtDNA), which encodes subunits of the oxidative phosphorylation complexes essential for cellular respiration and ATP production. Expression, replication, and maintenance of mtDNA require factors encoded by nuclear genes. These include not only the primary machinery involved (eg, transcription and replication components) but also those in signaling pathways that mediate or sense alterations in mitochondrial function in accord with changing cellular needs or environmental conditions. Mutations in these contribute to human disease pathology by mechanisms that are bei...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1425431</comments>
            <pubDate>Mon, 05 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1425431</guid>        </item>
        <item>
            <title>Methamphetamine Enhances HIV Infection of Macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=1425430&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18458095%26dopt%3DAbstract</link>
            <description>This study examined whether meth is able to enhance HIV infection of macrophages, the primary target site for the virus. Meth treatment resulted in a significant and dose-dependent increase of HIV reverse transcriptase activity in human blood monocyte-derived macrophages. Dopamine D1 receptor antagonists (SCH23390 and SKF83566) blocked this meth-mediated increase in the HIV infectivity of macrophages. Investigation of the underlying mechanisms of meth action showed that meth up-regulated the expression of the HIV entry co-receptor CCR5 on macrophages. Additionally, meth inhibited the expression of endogenous interferon-alpha and signal transducer and activator of transcription-1 in macrophages. These findings provide direct in vitro evidence to support the possibility that meth may functio...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1425430</comments>
            <pubDate>Mon, 05 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1425430</guid>        </item>
        <item>
            <title>Multiple Pathogenic Roles of Microvasculature in Inflammatory Bowel Disease: A Jack of All Trades.</title>
            <link>http://www.medworm.com/index.php?rid=1425429&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18458096%26dopt%3DAbstract</link>
            <description>Authors: Deban L, Correale C, Vetrano S, Malesci A, Danese S
    The etiology of Crohn's disease and ulcerative colitis, the two major forms of inflammatory bowel disease (IBD), is still largely unknown. However, it is now clear that the abnormalities underlying pathogenesis of intestinal inflammation are not restricted to those mediated by classic immune cells but also involve nonimmune cells. In particular, advances in vascular biology have outlined a central and multifaceted pathogenic role for the microcirculation in the initiation and perpetuation of IBD. The microcirculation and its endothelial lining play a crucial role in mucosal immune homeostasis through tight regulation of the nature and magnitude of leukocyte migration from the intravascular to the interstitial space. Chronical...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1425429</comments>
            <pubDate>Mon, 05 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1425429</guid>        </item>
        <item>
            <title>L-Arginine Decreases Inflammation and Modulates the Nuclear Factor-{kappa}B/Matrix Metalloproteinase Cascade in Mdx Muscle Fibers.</title>
            <link>http://www.medworm.com/index.php?rid=1425428&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18458097%26dopt%3DAbstract</link>
            <description>Authors: Hnia K, Gayraud J, Hugon G, Ramonatxo M, De La Porte S, Matecki S, Mornet D
    Duchenne muscular dystrophy (DMD) is a lethal, X-linked disorder associated with dystrophin deficiency that results in chronic inflammation, sarcolemma damage, and severe skeletal muscle degeneration. Recently, the use of L-arginine, the substrate of nitric oxide synthase (nNOS), has been proposed as a pharmacological treatment to attenuate the dystrophic pattern of DMD. However, little is known about signaling events that occur in dystrophic muscle with L-arginine treatment. Considering the implication of inflammation in dystrophic processes, we asked whether L-arginine inhibits inflammatory signaling cascades. We demonstrate that L-arginine decreases inflammation and enhances muscle regeneration in t...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1425428</comments>
            <pubDate>Mon, 05 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1425428</guid>        </item>
        <item>
            <title>Am J Pathol; +18 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1368225&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F04%252F09%2B15%252E43%2522%255BMHDA%255D%253A%25222008%252F04%252F12%2B15%252E16%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F04%252F09%2B15%252E43%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 Pathol
These PubMed results were generated on 2008/04/12PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1368225</comments>
            <pubDate>Sat, 12 Apr 2008 19:16:01 +0100</pubDate>
            <guid isPermaLink="false">1368225</guid>        </item>
        <item>
            <title>Am J Pathol; +25 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1359756&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F04%252F05%2B07%252E18%2522%255BMHDA%255D%253A%25222008%252F04%252F09%2B15%252E42%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F04%252F05%2B07%252E18%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 Pathol
These PubMed results were generated on 2008/04/09PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1359756</comments>
            <pubDate>Wed, 09 Apr 2008 19:42:57 +0100</pubDate>
            <guid isPermaLink="false">1359756</guid>        </item>
        <item>
            <title>Am J Pathol; +27 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1346844&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPathol%2529%2BAND%2B%25222008%252F03%252F29%2B17%252E08%2522%255BMHDA%255D%253A%25222008%252F04%252F03%2B10%252E23%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPathol%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F03%252F29%2B17%252E08%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 Pathol
These PubMed results were generated on 2008/04/03PubMed, 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 Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1346844</comments>
            <pubDate>Thu, 03 Apr 2008 14:23:48 +0100</pubDate>
            <guid isPermaLink="false">1346844</guid>        </item>
        <item>
            <title>Antiprion Prophylaxis by Gene Transfer of a Soluble Prion Antagonist.</title>
            <link>http://www.medworm.com/index.php?rid=1335937&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18372425%26dopt%3DAbstract</link>
            <description>Authors: Genoud N, Ott D, Braun N, Prinz M, Schwarz P, Suter U, Trono D, Aguzzi A
    Prion diseases are untreatable neurodegenerative disorders characterized by accumulation of PrP(Sc), an aggregated isoform of the normal prion protein PrP(C). Here, we delivered the soluble prion antagonist PrP-Fc2 to the brains of mice by lentiviral gene transfer. Although na&amp;#xEF;ve mice developed scrapie at 175 +/- 5 days postintracerebral prion inoculation (dpi), gene transfer before inoculation delayed disease onset by 72 +/- 4 days. At 170 days postintracerebral prion inoculation, PrP(Sc) accumulation and prion infectivity in PrPFc-treated brains were reduced by 3.6 and 4.2 logs, respectively. When PrP-Fc2 was delivered 30 days after prion inoculation, survival of the treated animals was extended by...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1335937</comments>
            <pubDate>Thu, 27 Mar 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1335937</guid>        </item>
        <item>
            <title>Retinal Dysfunction and Progressive Retinal Cell Death in SOD1-Deficient Mice.</title>
            <link>http://www.medworm.com/index.php?rid=1335936&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18372426%26dopt%3DAbstract</link>
            <description>Authors: Hashizume K, Hirasawa M, Imamura Y, Noda S, Shimizu T, Shinoda K, Kurihara T, Noda K, Ozawa Y, Ishida S, Miyake Y, Shirasawa T, Tsubota K
    The superoxide dismutase (SOD) family is a major antioxidant system, and deficiency of Cu,Zn-superoxide dismutase (SOD1) in mice leads to many different phenotypes that resemble accelerated aging. The purpose of this study was to examine the morphology and physiology of the sensory retina in Sod1(-/-) mice. The amplitudes of the a- and b-waves of electroretinograms elicited by stimuli of different intensity were reduced in senescent Sod1(-/-) mice, and this reduction in amplitude was more pronounced with increasing age. Retinal morphometric analyses showed a reduced number of nuclei in both the inner nuclear cell layer and outer nuclear cell...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1335936</comments>
            <pubDate>Thu, 27 Mar 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1335936</guid>        </item>
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