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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>Thu, 09 Feb 2012 00:42:07 +0100</lastBuildDate>
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            <title>Chlamydophila pneumoniae Infection Induces Alterations in Vascular Contractile Responses.</title>
            <link>http://www.medworm.com/index.php?rid=5571685&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%3D22214836%26dopt%3DAbstract</link>
            <description>Authors: Deniset JF, Hedley TE, Dibrov E, Pierce GN
    Abstract
    Chlamydophila pneumoniae infection has been associated in previous studies with coronary artery disease. The live bacterium has been detected within atherosclerotic plaques and can induce the structural remodeling of the vessel wall. However, the direct effects of infection on the contractile characteristics of the arteries remain unknown. Left anterior descending coronary arteries isolated from porcine hearts were dissected and placed in culture medium for 72 hours before infection with C. pneumoniae. Contractile responses to high molar KCl and u46619 levels and relaxation responses to bradykinin and sodium nitroprusside were assessed at days 5 and 10 postinfection. C. pneumoniae induced decreases in both KCl- and u46619...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571685</comments>
            <pubDate>Sat, 31 Dec 2011 05:00:00 +0100</pubDate>
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            <title>Glucocorticoid-Induced Tumor Necrosis Factor Receptor Family-Related Protein Exacerbates Collagen-Induced Arthritis by Enhancing the Expansion of Th17 Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5571684&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%3D22214837%26dopt%3DAbstract</link>
            <description>In this study, we found that collagen-induced arthritis mice treated with the ligand of GITR (GITRL) displayed an earlier onset of arthritis with a markedly increased severity of arthritic symptoms and joint damage, in which significantly increased Th17 cells in both spleen and draining lymph nodes were observed. Notably, results showed that a marked expansion of Th17 cells with increased RORγt mRNA expression was induced from naïve CD4(+) T cells when cultured with GITRL. Consistently, normal mice that were treated with GITRL were found to display a substantial expansion of splenic Th17 cells. Furthermore, we detected elevated serum levels of GITRL in patients with RA, which were positively correlated with an increase in interleukin-17 production. Taken together, the results from this s...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571684</comments>
            <pubDate>Sat, 31 Dec 2011 05:00:00 +0100</pubDate>
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            <title>Neural Stem Cell Depletion and CNS Developmental Defects After Enteroviral Infection.</title>
            <link>http://www.medworm.com/index.php?rid=5571683&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%3D22214838%26dopt%3DAbstract</link>
            <description>Authors: Ruller CM, Tabor-Godwin JM, Van Deren DA, Robinson SM, Maciejewski S, Gluhm S, Gilbert PE, An N, Gude NA, Sussman MA, Whitton JL, Feuer R
    Abstract
    Coxsackieviruses are significant human pathogens causing myocarditis, meningitis, and encephalitis. We previously demonstrated the ability of coxsackievirus B3 (CVB3) to persist within the neonatal central nervous system (CNS) and to target neural stem cells. Given that CVB3 is a cytolytic virus and may therefore damage target cells, we characterized the potential reduction in neurogenesis within the developing brain and the subsequent developmental defects that occurred after the loss of these essential neural stem cells. Neonatal mice were inoculated with a recombinant CVB3 expressing eGFP (eGFP-CVB3), and alterations in neuro...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571683</comments>
            <pubDate>Sat, 31 Dec 2011 05:00:00 +0100</pubDate>
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            <title>Decreased Proteasomal Activity Causes Age-Related Phenotypes and Promotes the Development of Metabolic Abnormalities.</title>
            <link>http://www.medworm.com/index.php?rid=5571688&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%3D22210478%26dopt%3DAbstract</link>
            <description>Authors: Tomaru U, Takahashi S, Ishizu A, Miyatake Y, Gohda A, Suzuki S, Ono A, Ohara J, Baba T, Murata S, Tanaka K, Kasahara M
    Abstract
    The proteasome is a multicatalytic enzyme complex responsible for the degradation of both normal and damaged proteins. An age-related decline in proteasomal activity has been implicated in various age-related pathologies, including obesity and hepatic steatosis. The relevance of decreased proteasomal activity to aging and age-related diseases remains unclear, however, because suitable animal models are not available. In the present study, we established a transgenic (Tg) mouse model with decreased proteasomal chymotrypsin-like activity. Tg mice exhibited a shortened life span and developed age-related phenotypes. In Tg mice, polyubiquitinated and ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571688</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
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            <title>The NF-κB Subunit c-Rel Stimulates Cardiac Hypertrophy and Fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=5571687&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%3D22210479%26dopt%3DAbstract</link>
            <description>We report for the first time that c-Rel is highly expressed and confined to the nuclei of diseased adult human hearts but is restricted to the cytoplasm of normal cardiac tissues. We conclude that c-Rel-dependent signaling is critical for both cardiac remodeling and hypertrophy. Targeting its activities could offer a novel therapeutic strategy to limit the effects of cardiac disease.
    PMID: 22210479 [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=5571687</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
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            <title>Host-Derived TGFB1 Deficiency Suppresses Lesion Development in a Mouse Model of Endometriosis.</title>
            <link>http://www.medworm.com/index.php?rid=5571686&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%3D22210480%26dopt%3DAbstract</link>
            <description>Authors: Louise Hull M, Zahied Johan M, Hodge WL, Robertson SA, Ingman WV
    Abstract
    Transforming growth factor-β(1) (TGFB1) is a multifunctional cytokine that is abundant in both endometriotic lesions and the peritoneal fluid in women with endometriosis. However, the role of TGFB1 in the development of endometriosis is as yet undefined. In the present study, we investigated the physiologic function of TGFB1 in endometriotic lesion development, using Tgfb1-null mutant mice on a background of severe combined immunodeficiency. Xenotransplantation of human eutopic endometrial tissue resulted in development of endometriosis-like lesions in 63% of ovariectomized estrogen-supplemented Tgfb1-null mutant mice and in 68% of wild-type control mice. Median lesion weight was reduced by 11-fold ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571686</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
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            <title>PTEN Regulates PDGF Ligand Switch for β-PDGFR Signaling in Prostate Cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5571689&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%3D22209699%26dopt%3DAbstract</link>
            <description>In this study, we examined the role of the tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) in the regulation of PDGF expression levels using both a prostate-specific, conditional PTEN-knockout mouse model and mouse prostate epithelial cell lines established from these mice. We found an increase in PDGF D and β-PDGFR expression levels in PTEN-null tumor cells, accompanied by a decrease in PDGF B expression. Among Akt isoforms, increased Akt3 expression was most prominent in mouse PTEN-null cells, and phosphatidylinositol 3-kinase/Akt activity was essential for the maintenance of increased PDGF D and β-PDGFR expression. In vitro deletion of PTEN resulted in a PDGF ligand switch from PDGF B to PDGF D in normal mouse prostate epithelial cells, further demons...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5571689</comments>
            <pubDate>Tue, 27 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>This Month in AJP.</title>
            <link>http://www.medworm.com/index.php?rid=5556676&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%3D22203051%26dopt%3DAbstract</link>
            <description>Authors: 
    Abstract
    The following highlights summarize research articles that are published in the current issue of The American Journal of Pathology.
    PMID: 22203051 [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=5556676</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
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            <title>High Anaplastic Lymphoma Kinase Immunohistochemical Staining in Neuroblastoma and Ganglioneuroblastoma Is an Independent Predictor of Poor Outcome.</title>
            <link>http://www.medworm.com/index.php?rid=5556675&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%3D22203052%26dopt%3DAbstract</link>
            <description>In conclusion, ALK positivity by IHC is an independent, poor prognostic factor in patients with GNBL and NBL. ALK IHC is an easy test suitable for future risk stratification in patients with NBL and GNBL.
    PMID: 22203052 [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=5556675</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
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            <title>Adenovirus-Mediated Gene Transfer of Transforming Growth Factor β1 to the Renal Glomeruli Leads to Proteinuria.</title>
            <link>http://www.medworm.com/index.php?rid=5556674&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%3D22203053%26dopt%3DAbstract</link>
            <description>In this study, we used an adenovirus vector to transfer active TGFβ1 to the glomeruli of rat kidneys. Transient TGFβ1 overexpression induced significant proteinuria, podocyte foot process effacement, nephrin down-regulation, and nephrinuria. The expression of synaptopodin was also significantly down-regulated by TGFβ1. Increased glomerular expression of Snail, suggestive of an in vivo dedifferentiation process, was associated with a loss of podocyte epithelial markers. The expression of angiopoietin-1 and angiopoietin-2 was significantly increased in TGFβ1-transfected glomeruli, and TGFβ1 increased the expression of the angiopoietin receptor, Tie2, in podocyte cell culture. TGFβ1 down-regulated nephrin and synaptopodin expression in podocytes in cell culture; this effect was reversed...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5556674</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Co-Regulation of Transcellular and Paracellular Leak Across Microvascular Endothelium by Dynaminand Rac.</title>
            <link>http://www.medworm.com/index.php?rid=5556673&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%3D22203054%26dopt%3DAbstract</link>
            <description>Authors: Armstrong SM, Khajoee V, Wang C, Wang T, Tigdi J, Yin J, Kuebler WM, Gillrie M, Davis SP, Ho M, Lee WL
    Abstract
    Increased permeability of the microvascular endothelium to fluids and proteins is the hallmark of inflammatory conditions such as sepsis. Leakage can occur between (paracellular) or through (transcytosis) endothelial cells, yet little is known about whether these pathways are linked. Understanding the regulation of microvascular permeability is essential for the identification of novel therapies to combat inflammation. We investigated whether transcytosis and paracellular leakage are co-regulated. Using molecular and pharmacologic approaches, we inhibited transcytosis of albumin in primary human microvascular endothelium and measured paracellular permeability. Bl...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5556673</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Chemokine Receptor CCR1 Disruption Limits Renal Damage in a Murine Model of Hemolytic Uremic Syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=5556672&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%3D22203055%26dopt%3DAbstract</link>
            <description>Authors: Ramos MV, Auvynet C, Poupel L, Rodero M, Mejias MP, Panek CA, Vanzulli S, Combadiere C, Palermo M
    Abstract
    Shiga toxin (Stx)-producing Escherichia coli is the main etiological agent that causes hemolytic uremic syndrome (HUS), a microangiopathic disease characterized by hemolytic anemia, thrombocytopenia, and acute renal failure. Although direct cytotoxic effects on endothelial cells by Stx are the primary pathogenic event, there is evidence that indicates the inflammatory response mediated by polymorphonuclear neutrophils and monocytes as the key event during HUS development. Because the chemokine receptor CCR1 participates in the pathogenesis of several renal diseases by orchestrating myeloid cell kidney infiltration, we specifically addressed the contribution of CCR1 in...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5556672</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
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            <title>Collagen VI Ablation Retards Brain Tumor Progression Due to Deficits in Assembly of the Vascular Basal Lamina.</title>
            <link>http://www.medworm.com/index.php?rid=5556679&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%3D22200614%26dopt%3DAbstract</link>
            <description>Authors: You WK, Bonaldo P, Stallcup WB
    Abstract
    To investigate the importance of the vascular basal lamina in tumor blood vessel morphogenesis and function, we compared vessel development, vessel function, and progression of B16F10 melanoma tumors in the brains of wild-type and collagen VI-null mice. In 7-day tumors in the absence of collagen VI, the width of the vascular basal lamina was reduced twofold. Although the ablation of collagen VI did not alter the abundance of blood vessels, a detailed analysis of the number of either pericytes or endothelial cells (or pericyte coverage of endothelial cells) showed that collagen VI-dependent defects during the assembly of the basal lamina have negative effects on both pericyte maturation and the sprouting and survival of endothelial ce...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5556679</comments>
            <pubDate>Fri, 23 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Inflammation-Induced Lymph Node Lymphangiogenesis Is Reversible.</title>
            <link>http://www.medworm.com/index.php?rid=5556678&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%3D22200615%26dopt%3DAbstract</link>
            <description>In this study, we therefore used a well-established mouse model of inflammation in the skin to investigate whether lymphatic vessels in the lymph nodes regress on resolution of inflammation. Our data reveal that the lymphatic network indeed regresses on the resolution of inflammation and that we can image this process by anti-LYVE-1 immuno-PET.
    PMID: 22200615 [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=5556678</comments>
            <pubDate>Fri, 23 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Promotion of Lymphatic Integrity by Angiopoietin-1/Tie2 Signaling during Inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=5556677&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%3D22200616%26dopt%3DAbstract</link>
            <description>Authors: Kajiya K, Kidoya H, Sawane M, Matsumoto-Okazaki Y, Yamanishi H, Furuse M, Takakura N
    Abstract
    The cutaneous lymphatic system plays a major role in tissue fluid homeostasis and inflammation of the skin. Although several lymphangiogenic factors are known to be involved in the formation of lymphatic vessels, the molecular mechanisms that maintain lymphatic integrity and control the functional drainage of interstitial fluid and resolution of inflammation remain unknown. Here we show that angiopoietin-1 (Ang-1) enhances lymphatic integrity and function during inflammation. Ang-1 transgenic mice under the control of keratin-14 (K14-Ang1) showed attenuated edema formation and inflammation after UV B (UVB) exposure. After UVB irradiation, blood vascular permeability was inhibited ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5556677</comments>
            <pubDate>Fri, 23 Dec 2011 05:00:00 +0100</pubDate>
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            <title>Am J Pathol; +78 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5521224&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%25222011%252F11%252F27%252006.36%2522%255BMHDA%255D%253A%25222011%252F12%252F20%252012.06%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%25222011%252F11%252F27%252006.36%2522%255BEDAT%255D%29%29</link>
            <description>78 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 2011/12/20PubMed, 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=5521224</comments>
            <pubDate>Tue, 20 Dec 2011 17:06:02 +0100</pubDate>
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        <item>
            <title>Am J Pathol; +24 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5430482&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%25222011%252F11%252F09%252018.45%2522%255BMHDA%255D%253A%25222011%252F11%252F21%252010.18%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%25222011%252F11%252F09%252018.45%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 2011/11/21PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5430482</comments>
            <pubDate>Mon, 21 Nov 2011 15:18:04 +0100</pubDate>
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            <title>Am J Pathol; +73 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5385884&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%25222011%252F10%252F21%252023.54%2522%255BMHDA%255D%253A%25222011%252F11%252F09%252018.45%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%25222011%252F10%252F21%252023.54%2522%255BEDAT%255D%29%29</link>
            <description>73 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 2011/11/09PubMed, 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=5385884</comments>
            <pubDate>Wed, 09 Nov 2011 23:45:01 +0100</pubDate>
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        <item>
            <title>Am J Pathol; +25 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5335743&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%25222011%252F10%252F06%252010.39%2522%255BMHDA%255D%253A%25222011%252F10%252F21%252023.54%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%25222011%252F10%252F06%252010.39%2522%255BEDAT%255D%29%29</link>
            <description>25 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2011/10/21PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5335743</comments>
            <pubDate>Sat, 22 Oct 2011 03:54:53 +0100</pubDate>
            <guid isPermaLink="false">5335743</guid>        </item>
        <item>
            <title>Am J Pathol; +70 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5287875&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%25222011%252F10%252F01%252008.00%2522%255BMHDA%255D%253A%25222011%252F10%252F06%252010.39%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%25222011%252F10%252F01%252008.00%2522%255BEDAT%255D%29%29</link>
            <description>70 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 2011/10/06PubMed, 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=5287875</comments>
            <pubDate>Thu, 06 Oct 2011 14:39:43 +0100</pubDate>
            <guid isPermaLink="false">5287875</guid>        </item>
        <item>
            <title>Am J Pathol; +78 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5270215&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%25222011%252F09%252F21%252009.52%2522%255BMHDA%255D%253A%25222011%252F10%252F01%252008.00%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%25222011%252F09%252F21%252009.52%2522%255BEDAT%255D%29%29</link>
            <description>78 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 2011/10/01PubMed, 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=5270215</comments>
            <pubDate>Sat, 01 Oct 2011 12:00:02 +0100</pubDate>
            <guid isPermaLink="false">5270215</guid>        </item>
        <item>
            <title>Am J Pathol; +56 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5182615&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%25222011%252F08%252F27%252023.44%2522%255BMHDA%255D%253A%25222011%252F09%252F02%252016.04%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%25222011%252F08%252F27%252023.44%2522%255BEDAT%255D%29%29</link>
            <description>56 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 2011/09/02PubMed, 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=5182615</comments>
            <pubDate>Fri, 02 Sep 2011 20:04:01 +0100</pubDate>
            <guid isPermaLink="false">5182615</guid>        </item>
        <item>
            <title>Am J Pathol; +22 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5169313&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%25222011%252F08%252F22%252019.04%2522%255BMHDA%255D%253A%25222011%252F08%252F27%252023.44%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%25222011%252F08%252F22%252019.04%2522%255BEDAT%255D%29%29</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 2011/08/27PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5169313</comments>
            <pubDate>Sun, 28 Aug 2011 03:44:03 +0100</pubDate>
            <guid isPermaLink="false">5169313</guid>        </item>
        <item>
            <title>Am J Pathol; +27 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5126908&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%25222011%252F07%252F30%252015.15%2522%255BMHDA%255D%253A%25222011%252F08%252F13%252023.30%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%25222011%252F07%252F30%252015.15%2522%255BEDAT%255D%29%29</link>
            <description>27 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2011/08/13PubMed, 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=5126908</comments>
            <pubDate>Sun, 14 Aug 2011 03:30:04 +0100</pubDate>
            <guid isPermaLink="false">5126908</guid>        </item>
        <item>
            <title>Am J Pathol; +76 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5078794&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%25222011%252F07%252F16%252001.45%2522%255BMHDA%255D%253A%25222011%252F07%252F30%252015.15%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%25222011%252F07%252F16%252001.45%2522%255BEDAT%255D%29%29</link>
            <description>76 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 2011/07/30PubMed, 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=5078794</comments>
            <pubDate>Sat, 30 Jul 2011 19:15:02 +0100</pubDate>
            <guid isPermaLink="false">5078794</guid>        </item>
        <item>
            <title>Am J Pathol; +26 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5029553&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%25222011%252F06%252F30%252016.00%2522%255BMHDA%255D%253A%25222011%252F07%252F16%252001.45%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%25222011%252F06%252F30%252016.00%2522%255BEDAT%255D%29%29</link>
            <description>26 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2011/07/16PubMed, 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=5029553</comments>
            <pubDate>Sat, 16 Jul 2011 05:45:07 +0100</pubDate>
            <guid isPermaLink="false">5029553</guid>        </item>
        <item>
            <title>Am J Pathol; +71 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4984801&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%25222011%252F06%252F16%252011.30%2522%255BMHDA%255D%253A%25222011%252F06%252F30%252016.00%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%25222011%252F06%252F16%252011.30%2522%255BEDAT%255D%29%29</link>
            <description>71 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 2011/06/30PubMed, 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=4984801</comments>
            <pubDate>Thu, 30 Jun 2011 20:00:02 +0100</pubDate>
            <guid isPermaLink="false">4984801</guid>        </item>
        <item>
            <title>Am J Pathol; +47 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4929564&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%25222011%252F06%252F02%252003.45%2522%255BMHDA%255D%253A%25222011%252F06%252F16%252011.30%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%25222011%252F06%252F02%252003.45%2522%255BEDAT%255D%29%29</link>
            <description>47 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 2011/06/16PubMed, 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=4929564</comments>
            <pubDate>Thu, 16 Jun 2011 15:30:26 +0100</pubDate>
            <guid isPermaLink="false">4929564</guid>        </item>
        <item>
            <title>Am J Pathol; +93 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4885173&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%25222011%252F05%252F18%252021.45%2522%255BMHDA%255D%253A%25222011%252F06%252F02%252003.45%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%25222011%252F05%252F18%252021.45%2522%255BEDAT%255D%29%29</link>
            <description>93 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 2011/06/02PubMed, 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=4885173</comments>
            <pubDate>Thu, 02 Jun 2011 07:45:02 +0100</pubDate>
            <guid isPermaLink="false">4885173</guid>        </item>
        <item>
            <title>Am J Pathol; +117 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4780972&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%25222011%252F04%252F05%252003.15%2522%255BMHDA%255D%253A%25222011%252F05%252F04%252013.45%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%25222011%252F04%252F05%252003.15%2522%255BEDAT%255D%29%29</link>
            <description>117 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 2011/05/04PubMed, 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=4780972</comments>
            <pubDate>Wed, 04 May 2011 17:45:02 +0100</pubDate>
            <guid isPermaLink="false">4780972</guid>        </item>
        <item>
            <title>Am J Pathol; +87 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4676062&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%25222011%252F03%252F21%252022.15%2522%255BMHDA%255D%253A%25222011%252F04%252F05%252003.15%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%25222011%252F03%252F21%252022.15%2522%255BEDAT%255D%29%29</link>
            <description>87 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 2011/04/05PubMed, 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=4676062</comments>
            <pubDate>Tue, 05 Apr 2011 07:15:05 +0100</pubDate>
            <guid isPermaLink="false">4676062</guid>        </item>
        <item>
            <title>Am J Pathol; +119 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4615709&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%25222011%252F03%252F07%252008.15%2522%255BMHDA%255D%253A%25222011%252F03%252F21%252022.15%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%25222011%252F03%252F07%252008.15%2522%255BEDAT%255D%29%29</link>
            <description>119 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 2011/03/21PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4615709</comments>
            <pubDate>Tue, 22 Mar 2011 02:15:03 +0100</pubDate>
            <guid isPermaLink="false">4615709</guid>        </item>
        <item>
            <title>Am J Pathol; +47 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4554924&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%25222011%252F02%252F07%252003.00%2522%255BMHDA%255D%253A%25222011%252F03%252F07%252008.15%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%25222011%252F02%252F07%252003.00%2522%255BEDAT%255D%29%29</link>
            <description>47 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 2011/03/07PubMed, 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=4554924</comments>
            <pubDate>Mon, 07 Mar 2011 13:15:05 +0100</pubDate>
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        <item>
            <title>Am J Pathol; +99 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4442268&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%25222011%252F01%252F21%252004.30%2522%255BMHDA%255D%253A%25222011%252F02%252F07%252003.00%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%25222011%252F01%252F21%252004.30%2522%255BEDAT%255D%29%29</link>
            <description>99 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 2011/02/07PubMed, 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=4442268</comments>
            <pubDate>Mon, 07 Feb 2011 08:00:02 +0100</pubDate>
            <guid isPermaLink="false">4442268</guid>        </item>
        <item>
            <title>Am J Pathol; +76 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4378113&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%252F12%252F17%252010.40%2522%255BMHDA%255D%253A%25222011%252F01%252F21%252004.30%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%252F12%252F17%252010.40%2522%255BEDAT%255D%29%29</link>
            <description>76 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 2011/01/21PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Pathol)</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4378113</comments>
            <pubDate>Fri, 21 Jan 2011 09:30:03 +0100</pubDate>
            <guid isPermaLink="false">4378113</guid>        </item>
        <item>
            <title>Am J Pathol; +225 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4289501&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%252F12%252F07%252020.40%2522%255BMHDA%255D%253A%25222010%252F12%252F17%252010.40%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%25222010%252F12%252F07%252020.40%2522%255BEDAT%255D%29%29</link>
            <description>225 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 2010/12/17PubMed, 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=4289501</comments>
            <pubDate>Fri, 17 Dec 2010 15:40:10 +0100</pubDate>
            <guid isPermaLink="false">4289501</guid>        </item>
        <item>
            <title>Am J Pathol; +66 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4033738&amp;cid=s_28450_32_f&amp;fid=28450&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%26debug%3Dpubmeddembup%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Pathol%29%2520AND%2520%25222010%252F09%252F26%252014.15%2522%255BMHDA%255D%253A%25222010%252F10%252F06%252012.15%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%252F09%252F26%252014.15%2522%255BEDAT%255D%29%29</link>
            <description>66 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 2010/10/06PubMed, 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=4033738</comments>
            <pubDate>Wed, 06 Oct 2010 16:15:03 +0100</pubDate>
            <guid isPermaLink="false">4033738</guid>        </item>
        <item>
            <title>Unexpected Vascular Enrichment of SCO1 over SCO2 in Mammalian Tissues. Implications for Human Mitochondrial Disease.</title>
            <link>http://www.medworm.com/index.php?rid=4002581&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%3D20864674%26dopt%3DAbstract</link>
            <description>Authors: Brosel S, Yang H, Tanji K, Bonilla E, Schon EA
    Mammalian SCO1 and SCO2 are evolutionarily-related copper-binding proteins that are required for the assembly of cytochrome c oxidase (COX), a mitochondrial respiratory chain complex, but the exact roles that they play in the assembly process are unclear. Mutations in both SCO1 and SCO2 are associated with distinct clinical phenotypes as well as tissue-specific COX deficiency, but the reason for such tissue specificity is unknown. We show in this study that although both genes are expressed ubiquitously in all mouse and human tissues examined, surprisingly, SCO1 localizes predominantly to blood vessels, whereas SCO2 is barely detectable in this tissue. To our knowledge, SCO1 is the first known example of a mitochondrial protein th...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4002581</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4002581</guid>        </item>
        <item>
            <title>Neuroserpin Protects Neurons from Ischemia-Induced Plasmin-Mediated Cell Death Independently of Tissue-Type Plasminogen Activator Inhibition.</title>
            <link>http://www.medworm.com/index.php?rid=4002580&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%3D20864675%26dopt%3DAbstract</link>
            <description>Authors: Wu J, Echeverry R, Guzman J, Yepes M
    The serine proteinase tissue-type plasminogen activator (tPA) and the serine proteinase inhibitor neuroserpin are both expressed in areas of the brain with the highest vulnerability to hypoxia/ischemia. In vitro studies show that neuroserpin inhibits tPA and, to a lesser extent, urokinase-type plasminogen activator and plasmin. Experimental middle cerebral artery occlusion (MCAO) increases tPA activity and neuroserpin expression in ischemic tissue, and genetic deficiency of tPA or either treatment with or overexpression of neuroserpin decreases the volume of the ischemic lesion following MCAO. These findings have led to the hypothesis that neuroserpin's neuroprotection is mediated by inhibition of tPA's alleged neurotoxic effect. Ischemic p...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4002580</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4002580</guid>        </item>
        <item>
            <title>Cotinine Exposure Increases Fallopian Tube PROKR1 Expression via Nicotinic AChR{alpha}-7. A Potential Mechanism Explaining the Link between Smoking and Tubal Ectopic Pregnancy.</title>
            <link>http://www.medworm.com/index.php?rid=4002579&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%3D20864676%26dopt%3DAbstract</link>
            <description>Authors: Shaw JL, Oliver E, Lee KF, Entrican G, Jabbour HN, Critchley HO, Horne AW
    Tubal ectopic pregnancy (EP) is the most common cause of maternal mortality in the first trimester of pregnancy; however, its etiology is uncertain. In EP, embryo retention within the Fallopian tube (FT) is thought to be due to impaired smooth muscle contractility (SMC) and alterations in the tubal microenvironment. Smoking is a major risk factor for EP. FTs from women with EP exhibit altered prokineticin receptor-1 (PROKR1) expression, the receptor for prokineticins (PROK). PROK1 is angiogenic, regulates SMC, and is involved in intrauterine implantation. We hypothesized that smoking predisposes women to EP by altering tubal PROKR1 expression. Sera/FT were collected at hysterectomy (n = 21). Serum levels...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4002579</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4002579</guid>        </item>
        <item>
            <title>Toll-Like Receptor (TLR) 2 and TLR9 Expressed in Trigeminal Ganglia are Critical to Viral Control During Herpes Simplex Virus 1 Infection.</title>
            <link>http://www.medworm.com/index.php?rid=4002578&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%3D20864677%26dopt%3DAbstract</link>
            <description>Authors: Lima GK, Zolini GP, Mansur DS, Freire Lima BH, Wischhoff U, Astigarraga RG, Dias MF, Silva MD, BÃ©la SR, do Valle Antonelli LR, Arantes RM, Gazzinelli RT, BÃ¡fica A, Kroon EG, Campos MA
    Herpes simplex virus 1 (HSV-1) is a neurotropic DNA virus that is responsible for several clinical manifestations in humans, including encephalitis. HSV-1 triggers toll-like receptors (TLRs), which elicit cytokine production. Viral multiplication and cytokine expression in C57BL/6 wild-type (WT) mice infected with HSV-1 were evaluated. Virus was found in the trigeminal ganglia (TG), but not in the brains of animals without signs of encephalitis, between 2 and 6 days postinfection (d.p.i.). Cytokine expression in the TG peaked at 5 d.p.i. TLR9(-/-) and TLR2/9(-/-) mice were more susceptible ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4002578</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4002578</guid>        </item>
        <item>
            <title>Collagen XIII Induced in Vascular Endothelium Mediates {alpha}1{beta}1 Integrin-Dependent Transmigration of Monocytes in Renal Fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=4002577&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%3D20864678%26dopt%3DAbstract</link>
            <description>In this study, we report the identification of collagen XIII as a ligand that facilitates this selective recruitment of Î±1Î²1 integrin-positive monocytes. Collagen XIII is absent in the vascular endothelium from normal renal cortex and abundant in Alport renal cortex. Neutralizing antibodies against the binding site in collagen XIII for Î±1Î²1 integrin selectively block VLA1-positive monocyte migration in transwell assays. Injection of these antibodies into Alport mice slows monocyte recruitment and protects against renal fibrosis. Thus, the induction of collagen XIII in endothelial cells of Alport kidneys mediates the selective recruitment of Î±1Î²1 integrin-positive monocytes and may potentially serve as a therapeutic target for inflammatory diseases in which lymphocyte/mono...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4002577</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4002577</guid>        </item>
        <item>
            <title>CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models.</title>
            <link>http://www.medworm.com/index.php?rid=4002576&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%3D20864679%26dopt%3DAbstract</link>
            <description>Authors: Lee S, Varvel NH, Konerth ME, Xu G, Cardona AE, Ransohoff RM, Lamb BT
    Microglia, the primary immune effector cells in the brain, continually monitor the tissue parenchyma for pathological alterations and become activated in Alzheimer's disease. Loss of signaling between neurons and microglia via deletion of the microglial receptor, CX3CR1, worsens phenotypes in various models of neurodegenerative diseases. In contrast, CX3CR1 deficiency ameliorates pathology in murine stroke models. To examine the role of CX3CR1 in Alzheimer's disease-related Î²-amyloid pathology, we generated APPPS1 and R1.40 transgenic mouse models of Alzheimer's disease deficient for CX3CR1. Surprisingly, CX3CR1 deficiency resulted in a gene dose-dependent reduction in Î²-amyloid deposition in both the ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4002576</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4002576</guid>        </item>
        <item>
            <title>Dual Roles of CD40 on Microbial Containment and the Development of Immunopathology in Response to Persistent Fungal Infection in the Lung.</title>
            <link>http://www.medworm.com/index.php?rid=4002575&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%3D20864680%26dopt%3DAbstract</link>
            <description>In this study, we performed a comparative analysis of cryptococcal infection in wild-type versus CD40-deficient mice (in a C57BL/6 genetic background) to define two important roles of CD40 in the modulation of fungal clearance as well as Th2-mediated immunopathology. First, CD40 promoted microanatomic containment of the organism within the lung tissue. This protective effect was associated with: i) a late reduction in fungal burden within the lung; ii) a late accumulation of lung leukocytes, including macrophages, CD4(+) T cells, and CD8+ T cells; iii) both early and late production of tumor necrosis factor-Î± and interferon-Î³ by lung leukocytes; and iv) early IFN-Î³ production at the site of T cell priming in the regional lymph nodes. In the absence of CD40, systemic cryptococcal d...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4002575</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4002575</guid>        </item>
        <item>
            <title>CD44 Deficiency Is Associated with Increased Bacterial Clearance but Enhanced Lung Inflammation During Gram-Negative Pneumonia.</title>
            <link>http://www.medworm.com/index.php?rid=4002574&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%3D20864681%26dopt%3DAbstract</link>
            <description>In conclusion, the absence of CD44 affects various components and phases of the host response during Klebsiella pneumonia, reducing bacterial outgrowth and dissemination and enhancing pulmonary pathology during lethal infection, and diminishing the resolution of lung inflammation during sublethal infection.
    PMID: 20864681 [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=4002574</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4002574</guid>        </item>
        <item>
            <title>Hepatocyte Proliferation During Liver Regeneration Is Impaired in Mice with Methionine Diet-Induced Hyperhomocysteinemia.</title>
            <link>http://www.medworm.com/index.php?rid=4002573&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%3D20864682%26dopt%3DAbstract</link>
            <description>In this report, we investigated the effect of homocysteine on liver regeneration. Our results demonstrated that mice with HHcy exhibited an impairment in liver regeneration after partial hepatectomy, as measured by immunohistochemical staining of proliferation cell nuclear antigen and bromodeoxyuridine incorporation. Impaired proliferation was also correlated with reduced cyclin D1 induction and elevated expression levels of both p53 and p21(Cip1). In addition, the phosphorylation of Akt, which plays an essential role in normal regeneration responses, was attenuated during the early phases of liver regeneration in HHcy mice. Our results also indicated that the cAMP/protein kinase A pathway mediated the inhibitory effect of homocysteine on liver regeneration. These findings provide evidence...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4002573</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4002573</guid>        </item>
        <item>
            <title>Role of Cystatin C in Neuroprotection and Its Therapeutic Implications.</title>
            <link>http://www.medworm.com/index.php?rid=4002572&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%3D20864683%26dopt%3DAbstract</link>
            <description>Authors: D'Adamio L
    This Commentary discusses the role of Cystatin C in Neuroprotection and its Therapeutic Implications.
    PMID: 20864683 [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=4002572</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4002572</guid>        </item>
        <item>
            <title>Local Mesenchymal Stem/Progenitor Cells Are a Preferential Target for Initiation of Adult Soft Tissue Sarcomas Associated with p53 and Rb Deficiency.</title>
            <link>http://www.medworm.com/index.php?rid=4002571&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%3D20864684%26dopt%3DAbstract</link>
            <description>Authors: Choi J, Curtis SJ, Roy DM, Flesken-Nikitin A, Nikitin AY
    The cell of origin and pathogenesis of the majority of adult soft tissue sarcomas (STS) remains poorly understood. Because mutations in both the P53 and RB tumor suppressor genes are frequent in STS in humans, we inactivated these genes by Cre-loxP-mediated recombination in mice with floxed p53 and Rb. Ninety-three percent of mice developed spindle cell/pleomorphic sarcomas after a single subcutaneous injection of adenovirus carrying Cre-recombinase. Similar to human STS, these sarcomas overexpress Cxcr4, which contributes to their invasive properties. Using irradiation chimeras generated by transplanting bone marrow cells from mice carrying either the Rosa26Stop(loxP)LacZ or the Z/EG reporter, as well as the floxed p53 ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4002571</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4002571</guid>        </item>
        <item>
            <title>Am J Pathol; +24 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3960249&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%252F09%252F02%252003.27%2522%255BMHDA%255D%253A%25222010%252F09%252F12%252009.18%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%25222010%252F09%252F02%252003.27%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 2010/09/12PubMed, 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=3960249</comments>
            <pubDate>Sun, 12 Sep 2010 13:18:02 +0100</pubDate>
            <guid isPermaLink="false">3960249</guid>        </item>
        <item>
            <title>SCG10 Expression on Activation of Hepatic Stellate Cells Promotes Cell Motility Through Interference with Microtubules.</title>
            <link>http://www.medworm.com/index.php?rid=3923209&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%3D20802173%26dopt%3DAbstract</link>
            <description>In conclusion, the de novo expression of SCG10 by hepatic stellate cells may play a major role in cellular mechanisms associated with HSC activation, namely cell motility and division, through interference with microtubules. SCG10 may represent a potential molecular target for anti-fibrosis therapies.
    PMID: 20802173 [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=3923209</comments>
            <pubDate>Thu, 26 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3923209</guid>        </item>
        <item>
            <title>Cytomegalovirus Infection Leads to Microvascular Dysfunction and Exacerbates Hypercholesterolemia-Induced Responses.</title>
            <link>http://www.medworm.com/index.php?rid=3923208&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%3D20802174%26dopt%3DAbstract</link>
            <description>This study determined whether CMV also impairs microvascular homeostasis and synergizes with hypercholesterolemia to exaggerate these responses. Intravital microscopy was used to assess endothelium-dependent and -independent arteriolar vasodilation and venular leukocyte and platelet adhesion in mice after injection with either mock inoculum or murine CMV (mCMV). Mice were fed a normal (ND) or high-cholesterol (HC) diet beginning at 5 weeks postinfection (p.i.), or a HC diet for the final 4 weeks of infection. mCMV-ND mice exhibited impaired endothelium-dependent vasodilation versus mock-ND at 9 and 12 weeks and endothelium-independent arteriolar dysfunction by 24 weeks. Transient mild leukocyte adhesion occurred in mCMV-ND venules at 7 and 21 weeks p.i. HC alone caused temporary arteriolar...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3923208</comments>
            <pubDate>Thu, 26 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3923208</guid>        </item>
        <item>
            <title>Trophoblast- and Vascular Smooth Muscle Cell-Derived MMP-12 Mediates Elastolysis during Uterine Spiral Artery Remodeling.</title>
            <link>http://www.medworm.com/index.php?rid=3923207&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%3D20802175%26dopt%3DAbstract</link>
            <description>In this study, we sought to identify the elastolytic proteases involved in this process. Primary first-trimester cytotrophoblasts (CTBs) derived from the placenta exhibited intracellular and membrane-associated elastase activity; membrane-associated activity was primarily attributable to matrix metalloproteinases (MMP). Indeed, Affymetrix microarray analysis and immunocytochemistry implicated MMP-12 (macrophage metalloelastase) as a key mediator of elastolysis. Cultured human aortic smooth muscle cells (HASMCs) exhibited constitutive membrane-associated elastase activity and inducible intracellular elastase activity; these cells also expressed MMP-12 protein. Moreover, a specific inhibitor of MMP-12 significantly reduced CTB- and HASMC-mediated elastolysis in vitro, to 31.7 +/- 10.9% and 2...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3923207</comments>
            <pubDate>Thu, 26 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3923207</guid>        </item>
        <item>
            <title>The Role of Vascular Endothelial Growth Factor-Induced Activation of NADPH Oxidase in Choroidal Endothelial Cells and Choroidal Neovascularization.</title>
            <link>http://www.medworm.com/index.php?rid=3923206&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%3D20802176%26dopt%3DAbstract</link>
            <description>We reported previously that Rac1 activation was necessary for choroidal endothelial cell migration across the retinal pigment epithelium, a critical step in the development of vision-threatening neovascular age-related macular degeneration. Here we explored the roles of Rac1 and NADPH oxidase activation in response to vascular endothelial growth factor treatment in vitro and in a model of laser-induced choroidal neovascularization. We found that vascular endothelial growth factor induced the activation of Rac1 and of NADPH oxidase in cultured human choroidal endothelial cells. Further, vascular endothelial growth factor led to heightened generation of reactive oxygen species from cultured human choroidal endothelial cells, which was prevented by the NADPH oxidase inhibitors, apocynin and d...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3923206</comments>
            <pubDate>Thu, 26 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3923206</guid>        </item>
        <item>
            <title>FTY720 Regulates Bone Marrow Egress of Eosinophils and Modulates Late-Phase Skin Reaction in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3923195&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%3D20802177%26dopt%3DAbstract</link>
            <description>Authors: Sugita K, Kabashima K, Sakabe JI, Yoshiki R, Tanizaki H, Tokura Y
    Eosinophilia in the blood and skin is frequently observed in patients with certain inflammatory skin diseases, such as atopic dermatitis. However, the mechanism underlying eosinophil circulation and the role of eosinophils in cutaneous immune responses remain unclear. In repeated hapten application-induced cutaneous responses in BALB/c mice, the administration of FTY720 before the last challenge decreased the number of skin-infiltrating eosinophils and reduced the late-phase reaction. A similar reduction of the late-phase reaction was observed by a sphingosine-1-phosphate G protein-coupled receptor (S1P1)-selective agonist, SEW2871. We monitored numerous alterations of eosinophils in the blood, spleen, bone marr...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3923195</comments>
            <pubDate>Thu, 26 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3923195</guid>        </item>
        <item>
            <title>TLR2-Mediated Expansion of MDSCs Is Dependent on the Source of Tumor Exosomes.</title>
            <link>http://www.medworm.com/index.php?rid=3923188&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%3D20802178%26dopt%3DAbstract</link>
            <description>In this study, we show that exosomes released from tumor cells re-isolated from syngeneic mice are capable of inducing interleukin-6 in a Toll-like receptor 2-independent manner, whereas the data generated from exosomes of tumor cells having undergone numerous in vitro passages induce interleukin-6 in a Toll-like receptor 2-dependent manner. This discrepancy may be due to the source of tumor cells used to generate the exosomes for this study. These results suggest that exosomes released from tumor cells that are not within a tumor microenvironment may not realistically represent the role of tumor exosomes in vivo. This is an important consideration since frequently passing tumor cells in vivo is an accepted practice for studying tumor exosome-mediated inflammatory responses.
    PMID: 2080...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3923188</comments>
            <pubDate>Thu, 26 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3923188</guid>        </item>
        <item>
            <title>Focal Adhesion Assembly in Myofibroblasts Fosters a Microenvironment that Promotes Tumor Growth.</title>
            <link>http://www.medworm.com/index.php?rid=3923187&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%3D20802179%26dopt%3DAbstract</link>
            <description>Authors: Kang N, Yaqoob U, Geng Z, Bloch K, Liu C, Gomez T, Billadeau D, Shah V
    Cells within the tumor microenvironment influence tumor growth through multiple mechanisms. Pericytes such as hepatic stellate cells are an important cell within the tumor microenvironment; their transformation into highly motile myofibroblasts leads to angiogenesis, stromal cell recruitment, matrix deposition, and ensuing tumor growth. Thus, a better understanding of mechanisms that regulate motility of pericytes is required. Focal adhesions (FAs) form a physical link between the extracellular environment and the actin cytoskeleton, a requisite step for cell motility. FAs contain a collection of proteins including the Ena/VASP family member, vasodilator-stimulated phosphoprotein (VASP); however, a role for...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3923187</comments>
            <pubDate>Thu, 26 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3923187</guid>        </item>
        <item>
            <title>Adaptive Calcified Matrix Response of Dental Pulp to Bacterial Invasion Is Associated with Establishment of a Network of Glial Fibrillary Acidic Protein+/Glutamine Synthetase+ Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3923182&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%3D20802180%26dopt%3DAbstract</link>
            <description>We report evidence for anatomical and functional changes of dental pulp in response to bacterial invasion through dentin that parallel responses to noxious stimuli reported in neural crest-derived sensory tissues. Sections of resin-embedded carious adult molar teeth were prepared for immunohistochemistry, in situ hybridization, ultrastructural analysis, and microdissection to extract mRNA for quantitative analyses. In odontoblasts adjacent to the leading edge of bacterial invasion in carious teeth, expression levels of the gene encoding dentin sialo-protein were 16-fold greater than in odontoblasts of healthy teeth, reducing progressively with distance from this site of the carious lesion. In contrast, gene expression for dentin matrix protein-1 by odontoblasts was completely suppressed in...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3923182</comments>
            <pubDate>Thu, 26 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3923182</guid>        </item>
        <item>
            <title>BRAF Mutation Is Rare in Advanced-Stage Low-Grade Ovarian Serous Carcinomas.</title>
            <link>http://www.medworm.com/index.php?rid=3923181&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%3D20802181%26dopt%3DAbstract</link>
            <description>In this study, we found that advanced-stage, low-grade ovarian serous carcinomas both with and without adjacent serous borderline tumor shared similar regions of loss of heterozygosity. We then analyzed 91 ovarian tumor samples for mutations in TP53, BRAF, and KRAS. TP53 mutations were not detected in any serous borderline tumors (n = 30) or low-grade serous carcinomas (n = 43) but were found in 73% of high-grade serous carcinomas (n = 18). BRAF (n = 9) or KRAS (n = 5) mutation was detected in 47% of serous borderline tumors, but among the low-grade serous carcinomas (39 stage III, 2 stage II, and 2 stage I), only one (2%) had a BRAF mutation and eight (19%) had a KRAS mutation. The low frequency of BRAF mutations in advanced-stage, low-grade serous carcinomas, which contrasts with previou...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3923181</comments>
            <pubDate>Thu, 26 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3923181</guid>        </item>
        <item>
            <title>A{beta} Accelerates the Spatiotemporal Progression of Tau Pathology and Augments Tau Amyloidosis in an Alzheimer Mouse Model.</title>
            <link>http://www.medworm.com/index.php?rid=3923180&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%3D20802182%26dopt%3DAbstract</link>
            <description>Authors: Hurtado DE, Molina-Porcel L, Iba M, Aboagye AK, Paul SM, Trojanowski JQ, Lee VM
    Senile plaques formed by beta-amyloid peptides (Abeta) and neurofibrillary tangles (NFTs) formed by hyperphosphorylated tau, a microtubule-associated protein, are the hallmark lesions of Alzheimer's disease (AD) in addition to loss of neurons. While several transgenic (Tg) mouse models have recapitulated aspects of AD-like Abeta and tau pathologies, a spatiotemporal mapping paradigm for progressive NFT accumulation is urgently needed to stage disease progression in AD mouse models. Braak and co-workers developed an effective and widely used NFT staging paradigm for human AD brains. The creation of a Braak-like spatiotemporal staging scheme for tau pathology in mouse models would facilitate mechanis...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3923180</comments>
            <pubDate>Thu, 26 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3923180</guid>        </item>
        <item>
            <title>Blockade of Endothelin-1 with a Novel Series of 1,3,6-Trisubstituted-2-Carboxy-Quinol-4-Ones Controls Infection-Associated Preterm Birth.</title>
            <link>http://www.medworm.com/index.php?rid=3923179&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%3D20802183%26dopt%3DAbstract</link>
            <description>Authors: Olgun NS, Patel HJ, Stephani R, Lengyel I, Reznik SE
    Preterm birth (PTB) currently accounts for 13% of all births in the United States, with the leading cause of PTB being maternal infection. Endothelin-1, an extremely potent vasoconstrictor capable of increasing myometrial smooth muscle tone, has been shown to be up-regulated in the setting of infection in pregnancy, ultimately leading to PTB. In previous work, we have shown that infection-associated PTB is controlled in our murine model by using phospharamidon, an endothelin-converting enzyme-1 inhibitor; knocking down endothelin-converting enzyme-1 mRNA; or blocking the binding of endothelin-1 to the endothelin-A (ETA) receptor with either BQ-123 or with HJP-272, the 6-OH compound of our series of novel synthetic (ETA) rece...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3923179</comments>
            <pubDate>Thu, 26 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3923179</guid>        </item>
        <item>
            <title>Am J Pathol; +16 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3896383&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%252F08%252F18%252020.18%2522%255BMHDA%255D%253A%25222010%252F08%252F24%252012.27%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%252F08%252F18%252020.18%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 2010/08/24PubMed, 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=3896383</comments>
            <pubDate>Tue, 24 Aug 2010 16:27:02 +0100</pubDate>
            <guid isPermaLink="false">3896383</guid>        </item>
        <item>
            <title>Am J Pathol; +23 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3799707&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%252F07%252F21%252011.42%2522%255BMHDA%255D%253A%25222010%252F07%252F29%252020.57%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%252F07%252F21%252011.42%2522%255BEDAT%255D%29%29</link>
            <description>23 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2010/07/29PubMed, 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=3799707</comments>
            <pubDate>Fri, 30 Jul 2010 00:57:02 +0100</pubDate>
            <guid isPermaLink="false">3799707</guid>        </item>
        <item>
            <title>Tumor Lymphangiogenesis and Metastasis to Lymph Nodes Induced by Cancer Cell Expression of Podoplanin.</title>
            <link>http://www.medworm.com/index.php?rid=3740892&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%3D20616339%26dopt%3DAbstract</link>
            <description>Authors: Cueni LN, Hegyi I, Shin JW, Albinger-Hegyi A, Gruber S, Kunstfeld R, Moch H, Detmar M
    The membrane glycoprotein podoplanin is expressed by several types of human cancers and might be associated with their malignant progression. Its exact biological function and molecular targets are unclear, however. Here, we assessed the relevance of tumor cell expression of podoplanin in cancer metastasis to lymph nodes, using a human MCF7 breast carcinoma xenograft model. We found that podoplanin expression promoted tumor cell motility in vitro and, unexpectedly, increased tumor lymphangiogenesis and metastasis to regional lymph nodes in vivo, without promoting primary tumor growth. Importantly, high cancer cell expression levels of podoplanin correlated with lymph node metastasis and reduc...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740892</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3740892</guid>        </item>
        <item>
            <title>CD137 Is Required for M Cell Functional Maturation but Not Lineage Commitment.</title>
            <link>http://www.medworm.com/index.php?rid=3740891&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%3D20616340%26dopt%3DAbstract</link>
            <description>Authors: Hsieh EH, Fernandez X, Wang J, Hamer M, Calvillo S, Croft M, Kwon BS, Lo DD
    Mucosal immune surveillance depends on M cells that reside in the epithelium overlying Peyer's patch and nasopharyngeal associated lymphoid tissue to transport particles to underlying lymphocytes. M cell development is associated with B lymphocytes in a basolateral pocket, but the interactions between these cells are poorly understood. In a cell culture model of M cell differentiation, we found lymphotoxin/tumor necrosis factor alpha induction of CD137 (TNFRSF9) protein on intestinal epithelial cell lines, raising the possibility that CD137 on M cells in vivo might interact with CD137L expressed by B cells. Accordingly, while CD137-deficient mice produced UEA-1+ M cell progenitors in nasopharyngeal ass...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740891</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3740891</guid>        </item>
        <item>
            <title>Natural Killer Cells Promote Tissue Injury and Systemic Inflammatory Responses During Fatal Ehrlichia-Induced Toxic Shock-Like Syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=3740890&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%3D20616341%26dopt%3DAbstract</link>
            <description>In this study, we examined the relative contributions of natural killer (NK) and NKT cells in Ehrlichia-induced toxic shock. Lethal ehrlichial infection in wild-type mice induced a decline in NKT cell numbers, and late expansion and migration of activated NK cells to the liver, a main infection site that coincided with development of hepatic injury. The spatial and temporal changes in NK and NKT cells in lethally infected mice correlated with higher NK cell cytotoxic activity, higher expression of cytotoxic molecules such as granzyme B, higher production of interferon-gamma and tumor necrosis factor-alpha, increased hepatic infiltration with CD8alphaCD11c(+) dendritic cells and CD8(+)T cells, decreased splenic CD4(+)T cells, increased serum concentrations of IL-12p40, IL-18, RANTES, and mo...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740890</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3740890</guid>        </item>
        <item>
            <title>Mast Cells Are Novel Independent Prognostic Markers in Prostate Cancer and Represent a Target for Therapy.</title>
            <link>http://www.medworm.com/index.php?rid=3740889&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%3D20616342%26dopt%3DAbstract</link>
            <description>Authors: Johansson A, Rudolfsson S, Hammarsten P, Halin S, Pietras K, Jones J, Stattin P, Egevad L, Granfors T, WikstrÃ¶m P, Bergh A
    Mast cells affect growth in various human tumors, but their role in prostate cancer (PC) is unclear. Here, we identify mast cells as independent prognostic markers in PC using a large cohort of untreated PC patients with a long follow-up. By analyzing mast cells in different tissue compartments, our data indicate that intratumoral and peritumoral mast cells have anti- opposed to protumor properties. Intratumoral mast cells negatively regulate angiogenesis and tumor growth, whereas peritumoral mast cells stimulate the expansion of human prostate tumors. We also observed mast cell recruitment particularly to the peritumoral compartment in men during the f...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740889</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3740889</guid>        </item>
        <item>
            <title>Impaired Autophagy in Sporadic Inclusion-Body Myositis and in Endoplasmic Reticulum Stress-Provoked Cultured Human Muscle Fibers.</title>
            <link>http://www.medworm.com/index.php?rid=3740888&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%3D20616343%26dopt%3DAbstract</link>
            <description>We report for the first time that in s-IBM, lysosomal enzyme activities of cathepsin D and B were decreased 60% (P &amp;lt; 0.01) and 40% (P &amp;lt; 0.05), respectively. We also detected two indicators of increased autophagosome maturation, the presence of LC3-II and decreased mammalian target of rapamycin-mediated phosphorylation of p70S6 kinase. Moreover, in cultured human muscle fibers, ERS induction significantly decreased activities of cathepsins D and B, increased levels of LC3-II, decreased phosphorylation of p70S6 kinase, and decreased expression of VMA21, a chaperone for assembly of lysosomal V-ATPase. We conclude that in s-IBM muscle, decreased lysosomal proteolytic activity might enhance accumulation of misfolded proteins, despite increased maturation of autophagosomes, and that ERS is...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740888</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3740888</guid>        </item>
        <item>
            <title>Tubular Overexpression of Transforming Growth Factor-{beta}1 Induces Autophagy and Fibrosis but not Mesenchymal Transition of Renal Epithelial Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3740887&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%3D20616344%26dopt%3DAbstract</link>
            <description>In conclusion, overexpression of TGF-beta1 in renal tubules in vivo induces interstitial proliferation, tubular autophagy, and fibrosis, but not epithelial-to-mesenchymal transition.
    PMID: 20616344 [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=3740887</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3740887</guid>        </item>
        <item>
            <title>Role of Cripto-1 in Stem Cell Maintenance and Malignant Progression.</title>
            <link>http://www.medworm.com/index.php?rid=3740886&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%3D20616345%26dopt%3DAbstract</link>
            <description>Authors: Bianco C, Rangel MC, Castro NP, Nagaoka T, Rollman K, Gonzales M, Salomon DS
    Cripto-1 is critical for early embryonic development and, together with its ligand Nodal, has been found to be associated with the undifferentiated status of mouse and human embryonic stem cells. Like other embryonic genes, Cripto-1 performs important roles in the formation and progression of several types of human tumors, stimulating cell proliferation, migration, epithelial to mesenchymal transition, and tumor angiogenesis. Several studies have demonstrated that cell fate regulation during embryonic development and cell transformation during oncogenesis share common signaling pathways, suggesting that uncontrolled activation of embryonic signaling pathways might drive cell transformation and tumor p...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740886</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3740886</guid>        </item>
        <item>
            <title>The DNA Damage-Binding Protein XPC Is a Frequent Target for Inactivation in Squamous Cell Carcinomas.</title>
            <link>http://www.medworm.com/index.php?rid=3740885&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%3D20616346%26dopt%3DAbstract</link>
            <description>Authors: de Feraudy S, Ridd K, Richards LM, Kwok PY, Revet I, Oh D, Feeney L, Cleaver JE
    XPC, the main damage-recognition protein responsible for nucleotide excision repair of UVB damage to DNA, is lost or mutated in xeroderma pigmentosum group C (XP-C), a rare inherited disease characterized by high incidence and early onset of non-melanoma and melanoma skin cancers. The high incidence of skin cancers in XP-C patients suggests that loss of expression of XPC protein might also provide a selective advantage for initiation and progression of similar cancers in non XP-C patients in the general population. To test whether XPC is selectively lost in squamous cell carcinomas from non XP-C patients, we examined XPC expression by immunohistochemistry on a tissue microarray with 244 tissue core...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740885</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3740885</guid>        </item>
        <item>
            <title>Gastrointestinal Tract Disorder in Natriuretic Peptide Receptor B Gene Mutant Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3740884&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%3D20616347%26dopt%3DAbstract</link>
            <description>Authors: Sogawa C, Abe A, Tsuji T, Koizumi M, Saga T, Kunieda T
    Natriuretic peptide receptor B (NPR-B), which has high affinity for C-type natriuretic peptide (CNP) and synthesizes intracellular cGMP, may be involved in gastrointestinal tract (GIT) regulation. A mutant allele of the NPR-B-encoding gene (Npr2) is responsible for the phenotype of the short-limb dwarfism (SLW) mouse. Homozygosity for this autosomal-recessive gene (slw/slw) leads to dwarfism and death before weaning because of milk retention in the stomach and intestinal distention. To elucidate the relationship between CNP/NPR-B signaling and GIT function, we investigated the association between Npr2 mutation and the GIT phenotype in slw/slw mice. The pylorus and large intestine of the mutants did not respond to CNP stimu...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740884</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3740884</guid>        </item>
        <item>
            <title>Therapeutic Effects of Vitamin D Analogs on Cardiac Hypertrophy in Spontaneously Hypertensive Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3740883&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%3D20616348%26dopt%3DAbstract</link>
            <description>Authors: Kong J, Kim GH, Wei M, Sun T, Li G, Liu SQ, Li X, Bhan I, Zhao Q, Thadhani R, Li YC
    Vitamin D inhibits renin expression and blocks the compensatory induction of renin associated with the use of renin-angiotensin system inhibitors. Here we test the therapeutic effects of two commonly used vitamin D analogs and their combination with losartan on the development of left ventricular hypertrophy. One-month-old male spontaneously hypertensive rats were treated with vehicle, losartan, paricalcitol, doxercalciferol, a combination of losartan and paricalcitol, or a combination of losartan and doxercalciferol for 2 months. Blood pressure was markedly reduced by losartan, but not by paricalcitol or doxercalciferol alone. Echocardiograpy demonstrated a 65 to 80% reduction in left ventricu...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740883</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3740883</guid>        </item>
        <item>
            <title>Morphine Suppresses Tumor Angiogenesis through a HIF-1{alpha}/p38MAPK Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3740882&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%3D20616349%26dopt%3DAbstract</link>
            <description>In this study, morphine was administered at a clinically relevant analgesic dose to assess tumor cell-induced angiogenesis and subcutaneous tumor growth in nude mice using mouse Lewis lung carcinoma cells (LLCs). Implantation of mice with a continuous slow-release morphine pellet achieved morphine plasma levels within 250-400 ng/ml (measured using a radioimmunoassay, Coat-A-Count Serum Morphine) and was sufficient to significantly reduce tumor cell-induced angiogenesis and tumor growth when compared with placebo treatment. Morphometric analysis for blood vessel formation further confirmed that morphine significantly reduced blood vessel density (P &amp;lt; 0.003), vessel branching (P &amp;lt; 0.05), and vessel length (P &amp;lt; 0.002) when compared with placebo treatment. Morphine's effect was abolis...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3740882</comments>
            <pubDate>Wed, 07 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3740882</guid>        </item>
        <item>
            <title>Vascular-Leukocyte Interactions. Mechanisms of Human Decidual Spiral Artery Remodeling in Vitro.</title>
            <link>http://www.medworm.com/index.php?rid=3678976&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%3D20558572%26dopt%3DAbstract</link>
            <description>Authors: Hazan AD, Smith SD, Jones RL, Whittle W, Lye SJ, Dunk CE
    Transformation of uterine spiral arteries is critical for healthy human pregnancy. We recently proposed a role for maternal leukocytes in decidual spiral artery remodeling and suggested that matrix metalloprotease (MMP) activity contributed to the destruction of the arterial wall. In the current study we used our first trimester placental-decidual co-culture (PDC) model to define the temporal relationship and test the mechanistic aspects of this process. PDC experiments were assessed by image analysis over a six-day time-course for degree of vascular transformation and leukocyte distribution around progressively remodeled arterioles. We observed rapid transformation in PDCs associated with loss of vascular smooth muscle ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3678976</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3678976</guid>        </item>
        <item>
            <title>Atheromas Feel the Pressure. Biomechanical Stress and Atherosclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=3678975&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%3D20558573%26dopt%3DAbstract</link>
            <description>Authors: Pyle AL, Young PP
    Atherosclerosis, a chronic vascular disease, is the underlying cause of over half the deaths in the United States each year. Variations in local vascular hemodynamics predispose select sites in the vasculature to atherosclerosis, and the atherosclerotic lesions, in turn alter the biomechanical functioning of the local microenvironment, the consequences of which are not well understood on a molecular level. Further progress in the field of atherosclerosis will require an understanding of the relationship between biomechanics, the tissue microenvironment, and the cellular and molecular response to these factors. This review summarizes this field, particularly within the context of the vascular smooth muscle cell.
    PMID: 20558573 [PubMed - as supplied by publ...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3678975</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3678975</guid>        </item>
        <item>
            <title>Mesenchymal Stem Cells, Used As Bait, Disclose Tissue Binding Sites. A Tool in the Search for the Niche?</title>
            <link>http://www.medworm.com/index.php?rid=3678974&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%3D20558574%26dopt%3DAbstract</link>
            <description>In conclusion, we developed a cell-bait strategy to unmask renal stem cell binding sites, which may potentially shed light on the MSC niche(s) and its characteristics.
    PMID: 20558574 [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=3678974</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3678974</guid>        </item>
        <item>
            <title>A Differentiation-Based MicroRNA Signature Identifies Leiomyosarcoma as a Mesenchymal Stem Cell-Related Malignancy.</title>
            <link>http://www.medworm.com/index.php?rid=3678973&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%3D20558575%26dopt%3DAbstract</link>
            <description>Authors: Danielson LS, Menendez S, Stephan-Otto Attolini C, Guijarro MV, Bisogna M, Wei J, Socci ND, Levine DA, Michor F, Hernando E
    Smooth muscle (SM) is a spontaneously contractile tissue that provides physical support and function to organs such as the uterus. Uterine smooth muscle-related neoplasia comprise common well-differentiated benign lesions called leiomyomas (ULM), and rare, highly aggressive and pleomorphic tumors named leiomyosarcomas (ULMS). MicroRNAs (miRNAs) are small non-coding RNAs that play essential roles in normal cellular development and tissue homeostasis that can be used to accurately subclassify different tumor types. Here, we demonstrate that miRNAs are required for full smooth muscle cell (SMC) differentiation of bone marrow-derived human mesenchymal stem ce...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3678973</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3678973</guid>        </item>
        <item>
            <title>Long-Term Expression of Tissue-Inhibitor of Matrix Metalloproteinase-1 in the Murine Central Nervous System Does Not Alter the Morphological and Behavioral Phenotype but Alleviates the Course of Experimental Allergic Encephalomyelitis.</title>
            <link>http://www.medworm.com/index.php?rid=3678972&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%3D20558576%26dopt%3DAbstract</link>
            <description>Authors: Althoff GE, Wolfer DP, Timmesfeld N, Kanzler B, Schrewe H, Pagenstecher A
    Tissue inhibitors of metalloproteinases (TIMPs) are a family of closely related proteins that inhibit matrix metalloproteinases (MMPs). In the central nervous system (CNS), TIMPs 2, 3, and 4 are constitutively expressed at high levels, whereas TIMP1 can be induced by various stimuli. Here, we studied the effects of constitutive expression of TIMP1 in the CNS in transgenic mice. Transgene expression started prenatally and persisted throughout lifetime at high levels. Since MMP activity has been implicated in CNS development, in proper function of the adult CNS, and in inflammatory disorders, we investigated Timp1-induced CNS alterations. Despite sufficient MMP inhibition, high expressor transgenic mice ha...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3678972</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3678972</guid>        </item>
        <item>
            <title>In Vivo Assessment of Acute UVB Responses in Normal and Xeroderma Pigmentosum (XP-C) Skin-Humanized Mouse Models.</title>
            <link>http://www.medworm.com/index.php?rid=3678971&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%3D20558577%26dopt%3DAbstract</link>
            <description>Authors: GarcÃ­a M, Llames S, GarcÃ­a E, Meana A, Cuadrado N, Recasens M, Puig S, Nagore E, Illera N, Jorcano JL, Del Rio M, Larcher F
    In vivo studies of UVB effects on human skin are precluded by ethical and technical arguments on volunteers and inconceivable in cancer-prone patients such as those affected with Xeroderma Pigmentosum (XP). Establishing reliable models to address mechanistic and therapeutic matters thus remains a challenge. Here we have used the skin-humanized mouse system that circumvents most current model constraints. We assessed the UVB radiation effects including the sequential changes after acute exposure with respect to timing, dosage, and the relationship between dose and degree-sort of epidermal alteration. On Caucasian-derived regenerated skins, UVB irradi...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3678971</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3678971</guid>        </item>
        <item>
            <title>Richard (Dick) Gregory Lynch, M.D., 1934-2009.</title>
            <link>http://www.medworm.com/index.php?rid=3678970&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%3D20558578%26dopt%3DAbstract</link>
            <description>Authors: Sobel ME
    This In Memoriam highlights the life of Dr. Richard (Dick) G. Lynch.
    PMID: 20558578 [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=3678970</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3678970</guid>        </item>
        <item>
            <title>Deregulated Expression of the Polycomb-Group Protein SUZ12 Target Genes Characterizes Mantle Cell Lymphoma.</title>
            <link>http://www.medworm.com/index.php?rid=3678969&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%3D20558579%26dopt%3DAbstract</link>
            <description>Authors: MartÃ­n-PÃ©rez D, SÃ¡nchez E, Maestre L, Suela J, Vargiu P, Di Lisio L, MartÃ­nez N, Alves J, Piris MA, SÃ¡nchez-Beato M
    Polycomb proteins are known to be of great importance in human cancer pathogenesis. SUZ12 is a component of the Polycomb PRC2 complex that, along with EZH2, is involved in embryonic stem cell differentiation. EZH2 plays an essential role in many cancer types, but an equivalent involvement of SUZ12 has not been as thoroughly demonstrated. Here we show that SUZ12 is anomalously expressed in human primary tumors, especially in mantle cell lymphoma (MCL), pulmonary carcinomas and melanoma, and is associated with gene locus amplification in some cases. Using MCL as a model, functional and genomic studies demonstrate that SUZ12 loss compromises cell viab...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3678969</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3678969</guid>        </item>
        <item>
            <title>Adipose Tissue-Derived Mesenchymal Stem Cells Facilitate Hematopoiesis In Vitro and In Vivo. Advantages Over Bone Marrow-Derived Mesenchymal Stem Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3678968&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%3D20558580%26dopt%3DAbstract</link>
            <description>In this study, we extensively evaluated the hematopoiesis-supporting properties of ADSCs, which are largely unknown. In vitro coculture and progenitor assays showed that ADSCs generated significantly more granulocytes and progenitor cells from human hematopoietic stem cells (HSCs) than BMSCs. We found that ADSCs express the chemokine CXCL12, a critical regulator of hematopoiesis, at levels that are three fold higher than those with BMSCs. The addition of a CXCL12 receptor antagonist resulted in a lower yield of granulocytes from ADSC layers, whereas the addition of recombinant CXCL12 to BMSC cocultures promoted the growth of granulocytes. In vivo cell homing assays showed that ADSCs facilitated the homing of mouse HSCs to the BM better than BMSCs. ADSCs injected into the BM cavity of fatal...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3678968</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3678968</guid>        </item>
        <item>
            <title>Suppression of SLC11A2 Expression Is Essential to Maintain Duodenal Integrity During Dietary Iron Overload.</title>
            <link>http://www.medworm.com/index.php?rid=3678967&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%3D20558581%26dopt%3DAbstract</link>
            <description>Authors: Shirase T, Mori K, Okazaki Y, Itoh K, Yamamoto M, Tabuchi M, Kishi F, Jiang L, Akatsuka S, Nakao K, Toyokuni S
    Iron is essential for the survival of mammals, but iron overload causes fibrosis and carcinogenesis. Reduced iron absorption and regulated release into circulation in duodenal mucosa constitute two major mechanisms of protection against dietary iron overload; however, their relative contribution remains elusive. To study the significance of the former process, we generated SLC11A2 transgenic mice (TGs) under the control of the chicken beta-actin promoter. TGs were viable and fertile, and displayed no overt abnormalities up to 20 months. No significant difference in iron concentration was observed in major solid organs between TGs and their wild-type littermates, sugge...</description>
            <author>Am J Pathol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3678967</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3678967</guid>        </item>
        <item>
            <title>Am J Pathol; +50 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3649512&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%252F06%252F05%252016.18%2522%255BMHDA%255D%253A%25222010%252F06%252F11%252008.03%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%252F06%252F05%252016.18%2522%255BEDAT%255D%29%29</link>
            <description>50 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 2010/06/11PubMed, 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=3649512</comments>
            <pubDate>Fri, 11 Jun 2010 12:03:02 +0100</pubDate>
            <guid isPermaLink="false">3649512</guid>        </item>
        <item>
            <title>Am J Pathol; +23 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3589140&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%252F05%252F19%252010.24%2522%255BMHDA%255D%253A%25222010%252F05%252F22%252014.12%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%252F05%252F19%252010.24%2522%255BEDAT%255D%29%29</link>
            <description>23 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Pathol
These pubmed results were generated on 2010/05/22PubMed, 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=3589140</comments>
            <pubDate>Sat, 22 May 2010 18:12:02 +0100</pubDate>
            <guid isPermaLink="false">3589140</guid>        </item>
        <item>
            <title>Am J Pathol; +22 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3479534&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%252F04%252F13%252017.38%2522%255BMHDA%255D%253A%25222010%252F04%252F17%252011.42%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%25222010%252F04%252F13%252017.38%2522%255BEDAT%255D%29%29</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 2010/04/17PubMed, 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=3479534</comments>
            <pubDate>Sat, 17 Apr 2010 15:42:02 +0100</pubDate>
            <guid isPermaLink="false">3479534</guid>        </item>
        <item>
            <title>Am J Pathol; +17 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3444585&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%252F31%252015.18%2522%255BMHDA%255D%253A%25222010%252F04%252F08%252003.02%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%252F03%252F31%252015.18%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 2010/04/08PubMed, 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=3444585</comments>
            <pubDate>Thu, 08 Apr 2010 07:02:04 +0100</pubDate>
            <guid isPermaLink="false">3444585</guid>        </item>
        <item>
            <title>Am J Pathol; +16 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3395951&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%252F18%252013.16%2522%255BMHDA%255D%253A%25222010%252F03%252F24%252004.16%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%252F18%252013.16%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 2010/03/24PubMed, 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=3395951</comments>
            <pubDate>Wed, 24 Mar 2010 08:16:02 +0100</pubDate>
            <guid isPermaLink="false">3395951</guid>        </item>
        <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>
            <guid isPermaLink="false">3378612</guid>        </item>
        <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>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>
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            <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>
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            <pubDate>Thu, 26 Feb 2009 05:00:00 +0100</pubDate>
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