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        <title>J Cell Mol Med 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 'J Cell Mol Med' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=J+Cell+Mol+Med&t=J+Cell+Mol+Med&s=Search&f=source]]></link>
        <lastBuildDate>Thu, 18 Mar 2010 16:26:12 +0100</lastBuildDate>
        <item>
            <title>Type-specific dysregulation of matrix metalloproteinases and their tissue inhibitors in end-stage heart failure patients.</title>
            <link>http://www.medworm.com/index.php?rid=3362680&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219015%26dopt%3DAbstract</link>
            <description>In conclusion, this study demonstrated a selective upregulation of MMP-10 and -7 along with a discordant change of TIMP-4, and a positive correlation between MMP-10 levels and the degree of LV dilation in end-stage HF patients. Our findings suggest that type-specific dysregulation of MMPs and TIMPs is associated with LV remodeling in end-stage HF patients, and MMP-10 may act as a novel biomarker for LV remodeling.
    PMID: 20219015 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3362680</comments>
            <pubDate>Tue, 09 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>SKAP2, a novel target of HSF4b, associates with NCK2/F-actin at membrane ruffles and regulates actin reorganization in lens cell.</title>
            <link>http://www.medworm.com/index.php?rid=3362679&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219016%26dopt%3DAbstract</link>
            <description>Authors: Zhou L, Zhang Z, Zheng Y, Zhu Y, Wei Z, Xu H, Tang Q, Kong X, Hu L
    In addition to roles in stress response, heat shock factors (HSFs) play crucial roles in differentiation and development. Heat shock transcription factor 4 (HSF4) deficiency leads to defect in lens epithelial cell (LEC) differentiation and cataract formation. However, the mechanism remains obscure. Here, we identified Src kinase-associated phosphoprotein 2 (SKAP2) as a downstream target of HSF4b and it was highly expressed at the anterior tip of lens elongating fiber cells in vivo. The HSF4-deficient lenses showed reduced SKAP2 expression and defects in actin reorganization. The disassembly of stress fibers and formation of cortical actin fibers are critical for the initiation of LEC differentiation. SKAP2 loca...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3362679</comments>
            <pubDate>Tue, 09 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3362679</guid>        </item>
        <item>
            <title>Differentiation and migration properties of human fetal umbilical cord perivascular cells: potential for lung repair.</title>
            <link>http://www.medworm.com/index.php?rid=3362678&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219017%26dopt%3DAbstract</link>
            <description>Authors: Montemurro T, Andriolo G, Montelatici E, Weissmann G, Crisan M, Colnaghi MR, Rebulla P, Mosca F, P&amp;#xE9;ault B, Lazzari L
    Mesenchymal stem cells (MSC) have been derived from different cultured human tissues, including bone marrow, adipose tissue, amniotic fluid and umbilical cord blood. Only recently was a descendance of MSC from perivascular cells (PC) hypothesized, the latter being defined as CD146+ NG2+ PDGF-Rbeta+ ALP+ CD34- CD45- vWF- CD144-. Herein we studied the properties of PC from a novel source, the fetal human umbilical cord (HUC) collected from pre-term newborns. By immunohistochemistry and flow cytometry we show that pre-term/fetal HUC contain more PC than their full-term counterparts (2.5% versus 0.15%). Moreover, fetal HUCPC express the embryonic cell markers S...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3362678</comments>
            <pubDate>Tue, 09 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3362678</guid>        </item>
        <item>
            <title>Fetal and adult cardiomyocyte progenitor cells have different developmental potential.</title>
            <link>http://www.medworm.com/index.php?rid=3362684&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219011%26dopt%3DAbstract</link>
            <description>Authors: van Vliet P, Smits AM, de Boer TP, Korfage TH, Metz CH, Roccio M, van der Heyden MA, van Veen TA, Sluijter JP, Doevendans PA, Goumans MJ
    In the past years, cardiovascular progenitor cells have been isolated from the human heart and characterized. Up to date, no studies have been reported in which the developmental potential of fetal and adult cardiovascular progenitors was tested simultaneously. However, intrinsic differences will likely affect interpretations regarding progenitor cell potential and application for regenerative medicine. Here we report a direct comparison between human fetal and adult heart-derived cardiomyocyte progenitor cells (CMPCs). We show that fetal and adult CMPCs have distinct preferences to differentiate into mesodermal lineages. Under pro-angiogenic...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3362684</comments>
            <pubDate>Mon, 08 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3362684</guid>        </item>
        <item>
            <title>Promotion of hepatocellular carcinoma metastasis through matrix metalloproteinase activation by epithelial-mesenchymal transition regulator twist1.</title>
            <link>http://www.medworm.com/index.php?rid=3362683&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219012%26dopt%3DAbstract</link>
            <description>Authors: Zhao XL, Sun T, Che N, Sun D, Zhao N, Dong XY, Gu Q, Yao Z, Sun BC
    E-cadherin loss is a key biological mechanism in tumor invasion. As a main regulator of Epithelial-Mesenchymal Transition (EMT) mechanism-mediated invasion and metastasis, Twist1 plays an important role through its regulation of E-cadherin expression. However, whether or not Twist2 has the same function in tumor metastasis remains unclear. The purpose of this study is to investigate the expressions and different roles of Twist1 and Twist2 in human hepatocellular carcinoma (HCC). The expressions of Twist1 and Twist2 in HCC tissue were evaluated by immunohistochemical staining. The role of Twist1 and Twist2 in invasiveness was also evaluated in vitro by using HCC cell lines. Twist1 nuclear over-expression is foun...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3362683</comments>
            <pubDate>Mon, 08 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3362683</guid>        </item>
        <item>
            <title>Microparticles stimulate angiogenesis by inducing ELR(+) CXC-chemokines in synovial fibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=3362682&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219013%26dopt%3DAbstract</link>
            <description>Authors: Reich N, Beyer C, Gelse K, Akhmetshina A, Dees C, Zwerina J, Schett G, Distler O, Distler JH
    Microparticles (MPs) are small membrane-vesicles that accumulate in the synovial fluids of patients with rheumatoid arthritis (RA). In the arthritic joints, MPs induce a pro-inflammatory and invasive phenotype in synovial fibroblasts (SFs). The present study investigated whether activation of SFs by MPs stimulate angiogenesis in the inflamed joints of patients with RA. MPs were isolated from Jurkat cells and U937 cells by differential centrifugation. SFs were co-cultured with increasing numbers of MPs. The effects of supernatants from co-cultures on endothelial cells were studied in vitro and in vivo using MTT assays, annexin V and propidium iodide staining, trans-well migration assays...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3362682</comments>
            <pubDate>Mon, 08 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3362682</guid>        </item>
        <item>
            <title>Vascular function in health and disease review series.</title>
            <link>http://www.medworm.com/index.php?rid=3362681&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219014%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 20219014 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3362681</comments>
            <pubDate>Mon, 08 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3362681</guid>        </item>
        <item>
            <title>Injectable cardiac tissue engineering for the treatment of myocardial infarction.</title>
            <link>http://www.medworm.com/index.php?rid=3328115&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20193036%26dopt%3DAbstract</link>
            <description>Authors: Wang H, Zhou J, Liu Z, Wang C
    Heart disease is a leading cause of morbidity and mortality worldwide. Myocardial infarction leads to permanent loss of cardiac tissue and ultimately heart failure. However, current therapies could only stall the progression of the disease. Thus new therapies are needed to regenerate damaged hearts to overcome poor prognosis of patients with heart failure. The shortage of heart donors is also a factor for innovating new therapies. Although the cardiac performance by cell-based therapy has improved, unsatisfactory cell retention and transplant survival still plague this technique. Since biomaterials can improve the cell retention, survival, and differentiation, cardiac tissue engineering is now being explored as an approach to support cell-based th...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3328115</comments>
            <pubDate>Sat, 27 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3328115</guid>        </item>
        <item>
            <title>Apolipoprotein A-I possesses an anti-obesity effect associated with increase of energy expenditure and upregulation of UCP1 in brown fat.</title>
            <link>http://www.medworm.com/index.php?rid=3328114&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20193037%26dopt%3DAbstract</link>
            <description>Authors: Ruan X, Li Z, Zhang Y, Yang L, Pan Y, Wang Z, Feng GS, Chen Y
    Apolipoprotein A-I (ApoA-I) is the most abundant protein constituent of high density lipoprotein (HDL). Reduced plasma HDL and ApoA-I levels have been found to be associated with obesity and metabolic syndrome in humans. However, whether or not ApoA-I has a direct effect on obesity is largely unknown. Here we analyzed the anti-obesity effect of ApoA-I using two mouse models, a transgenic mouse with overexpression of ApoA-I and the mice administered with an ApoA-I mimetic peptide D-4F. The mice were induced to develop obesity by feeding with high fat diet. Both ApoA-I overexpression and D-4F treatment could significantly reduce white fat mass and slightly improve insulin sensitivity in the mice. Metabolic analyses re...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3328114</comments>
            <pubDate>Sat, 27 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3328114</guid>        </item>
        <item>
            <title>Tumor-associated fibroblasts and mesenchymal stem cells: more similarities than differences.</title>
            <link>http://www.medworm.com/index.php?rid=3316295&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20184663%26dopt%3DAbstract</link>
            <description>Authors: Paunescu V, Bojin FM, Tatu CA, Gavriliuc OI, Rosca A, Gruia AT, Tanasie G, Bunu C, Crisnic D, Gherghiceanu M, Tatu FR, Tatu CS, Vermesan S
    Tumor-associated fibroblasts (TAFs) are part of the tumor stroma, providing functional and structural support for tumor progression and development. The origin and biology of TAFs are poorly understood, but within the tumor environment, TAFs become activated and secrete different paracrine and autocrine factors involved in tumorigenesis. It has been shown that bone marrow mesenchymal stem cells (MSCs) can be recruited into the tumors, where they proliferate and acquire a TAF-like phenotype. We attempted to determine to what extent TAFs characteristics in vitro juxtapose to MSCs' definition, and we showed that TAFs and MSCs share immunopheno...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3316295</comments>
            <pubDate>Wed, 24 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3316295</guid>        </item>
        <item>
            <title>Functions of ICC-like cells in the urinary tract and male genital organs.</title>
            <link>http://www.medworm.com/index.php?rid=3316294&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20184664%26dopt%3DAbstract</link>
            <description>Authors: Hashitani H, Lang RJ
    Interstitial cells of Cajal (ICC)-like cells (ICC-LCs) have been identified in many regions of the urinary tract and male genital organs by immunohistochemical studies and electron microscopy. ICC-LCs are characterized by their spontaneous electrical and Ca(2+) signalling and the cellular mechanisms of their generation have been extensively investigated. Spontaneous activity in ICC-LCs rises from the release of internally stored Ca(2+) and the opening of Ca(2+)-activated Cl(-) channels to generate spontaneous transient depolarizations (STDs) in a manner not fundamentally dependent on Ca(2+) influx through L-type voltage-dependent Ca(2+) channels (VOCCs). Since urogenital ICC-LCs have been identified by their immunoreactivity to Kit (CD117) antibodies, the ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3316294</comments>
            <pubDate>Wed, 24 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3316294</guid>        </item>
        <item>
            <title>Conditional TGF-beta1 treatment increases stem cell-like cell population in myoblasts.</title>
            <link>http://www.medworm.com/index.php?rid=3316296&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20184662%26dopt%3DAbstract</link>
            <description>Authors: Mu X, Li Y
    The limitation in successfully acquiring large populations of stem cell has impeded their application. A new method based on the dedifferentiation of adult somatic cells to generate induced multipotent stem cells would allow us to obtain a large amount of autologous stem cells for regenerative medicine. The current work was proposed to induce a sub-population of cells with characteristics of muscle stem cells from myoblasts through conditional treatment of Transforming Growth Factor (TGF)-beta1. Our results show that a lower concentration of TGF-beta1 is able to promote C2C12 myoblasts to express stem cell markers as well as to repress myogenic proteins, which involves a mechanism of dedifferentiation. Moreover, TGF-beta1 treatment promoted the proliferation-arreste...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3316296</comments>
            <pubDate>Tue, 23 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3316296</guid>        </item>
        <item>
            <title>Hypoxia-induced endothelial secretion of macrophage migration inhibitory factor and role in endothelial progenitor cell recruitment.</title>
            <link>http://www.medworm.com/index.php?rid=3316299&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20178462%26dopt%3DAbstract</link>
            <description>Authors: Simons D, Grieb G, Hristov M, Pallua N, Weber C, Bernhagen J, Steffens G
    Abstract Macrophage migration inhibitory factor (MIF) is a pleiotropic inflammatory cytokine that was recently identified as a non-cognate ligand of the chemokine receptors CXCR2 and CXCR4. MIF is expressed and secreted from endothelial cells (ECs) following atherogenic stimulation, exhibits chemokine-like properties, and promotes the recruitment of leukocytes to atherogenic endothelium. CXCR4 expressed on endothelial progenitor cells (EPCs) and EC-derived CXCL12, the cognate ligand of CXCR4, have been demonstrated to be critical when EPCs are recruited to ischemic tissues. Here we studied whether hypoxic stimulation triggers MIF secretion from ECs and whether the MIF/CXCR4 axis contributes to EPC recruit...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3316299</comments>
            <pubDate>Mon, 22 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3316299</guid>        </item>
        <item>
            <title>Does hepatocyte growth factor/c-Met signal play synergetic role in lung cancer?</title>
            <link>http://www.medworm.com/index.php?rid=3316298&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20178463%26dopt%3DAbstract</link>
            <description>Authors: Wang X, Li K, Chen H, Wang D, Zhang Y, Bai C
    Abstract There is growing evidence that the signal pathway between hepatocyte growth factor (HGF) and its receptor c-Met plays an important role in the development of lung cancer, although the specificity of such role is to be clarified. It seems clear that the HGF/c-Met signal contributes to the metastasis of cancer cells to the lung by stimulating the hyperproduction and overactivation of cytokines and enzymes, e.g. HGF, vascular endothelial growth factor and matrix metalloproteases. The HGF/c-Met signal may act as the candidate responsible for the development of epidermal growth factor receptor (EGFR) kinase inhibitor resistance. Experimental evidence showed that the combination of both EGFR and c-Met inhibitors had synergetic or...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3316298</comments>
            <pubDate>Mon, 22 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3316298</guid>        </item>
        <item>
            <title>The role of HIF prolyl hydroxylases in tumor growth.</title>
            <link>http://www.medworm.com/index.php?rid=3316297&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20178464%26dopt%3DAbstract</link>
            <description>Authors: Jokilehto T, Jaakkola PM
    Abstract Tumor hypoxia is a well-known microenvironmental factor that causes cancer progression and resistance to cancer treatment. This involves multiple mechanisms of which the best-understood ones are mediated through transcriptional gene activation by the hypoxia-inducible factors (HIFs). HIFs in turn are regulated in response to oxygen availability by a family of iron- and 2-oxoglutarate-dependent dioxygenases, the HIF prolyl hydroxylases (PHDs). PHDs inactivate HIFs in normoxia by activating degradation of the HIF-alpha subunit but release HIF activation in poorly oxygenated conditions. The function of HIF in tumors is fairly well characterized but our understanding on the outcome of PHDs in tumors is much more limited. Here we review the functio...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3316297</comments>
            <pubDate>Mon, 22 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3316297</guid>        </item>
        <item>
            <title>Alteration of calcium homeostasis in primary preeclamptic syncytiotrophoblasts: effect on calcium exchange in placenta.</title>
            <link>http://www.medworm.com/index.php?rid=3316300&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20178461%26dopt%3DAbstract</link>
            <description>Conclusion: Calcium homeostasis and transport through placenta is compromised in preeclamptic pregnancies and it appears to be affected by a lack of ATP and an excess of oxidative stress.
    PMID: 20178461 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3316300</comments>
            <pubDate>Fri, 19 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3316300</guid>        </item>
        <item>
            <title>Gene therapy in Alzheimer's disease -potential for disease modification.</title>
            <link>http://www.medworm.com/index.php?rid=3284735&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20158567%26dopt%3DAbstract</link>
            <description>Authors: Nilsson P, Iwata N, Muramatsu SI, Tjernberg LO, Winblad B, Saido TC
    Alzheimer's disease (AD) is the major cause of dementia in the elderly, leading to memory loss and cognitive decline. The mechanism underlying onset of the disease has not been fully elucidated. However, characteristic pathological manifestations include extracellular accumulation and aggregation of the amyloid beta-peptide (Abeta) into plaques and intracellular accumulation and aggregation of hyperphosphorylated tau, forming neurofibrillary tangles. Despite extensive research worldwide, no disease modifying treatment is yet available. In this review, we focus on gene therapy as a potential treatment for AD, and summarize recent work in the field, ranging from proof-of concept studies in animal models to clini...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3284735</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3284735</guid>        </item>
        <item>
            <title>The role of caspase-2 in stress-induced apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=3284734&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20158568%26dopt%3DAbstract</link>
            <description>Authors: Bouchier-Hayes L
    Caspase-2 is the most evolutionarily conserved of all the caspases, yet it has a poorly defined role in apoptotic pathways. This is mainly due to a dearth of techniques to determine the activation status of caspase-2 and the lack of an abnormal phenotype in caspase-2 deficient mice. Nevertheless, emerging evidence suggests that caspase-2 may have important functions in a number of stress-induced cell death pathways, in cell cycle maintenance and regulation of tumor progression. This review discusses recent advances that have been made to help elucidate the true role of this elusive caspase and the potential contribution of caspase-2 to the pathology of human diseases including cancer.
    PMID: 20158568 [PubMed - as supplied by publisher] (Source: J Cell Mol M...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3284734</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3284734</guid>        </item>
        <item>
            <title>Statins potently reduce the cytokine-mediated IL-6 release in SMC / MNC cocultures.</title>
            <link>http://www.medworm.com/index.php?rid=3284733&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20158569%26dopt%3DAbstract</link>
            <description>Authors: Loppnow H, Zhang L, Buerke M, Lautenschl&amp;#xE4;ger M, Chen L, Frister A, Schlitt A, Luther T, Song N, Hofmann B, Rose-John S, Silber RE, M&amp;#xFC;ller-Werdan U, Werdan K
    Inflammatory pathways are involved in the developement of atherosclerosis. Interaction of vessel wall cells and invading monocytes by cytokines may trigger local inflammatory processes. HMG-CoA reductase inhibitors (statins) are a standard medication used in cardiovascular diseases. They are thought to have anti-inflammatory capacities, in addition to their lipid-lowering effects. We investigated the anti-inflammatory effect of statins in the cytokine-mediated-interaction-model of human vascular smooth muscle cells (SMC) and human mononuclear cells (MNC). In this atherosclerosis-related inflammatory model LPS (li...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3284733</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3284733</guid>        </item>
        <item>
            <title>Roles of phospholipase D in phorbol myristate acetate-stimulated neutrophil respiratory burst.</title>
            <link>http://www.medworm.com/index.php?rid=3284732&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20158570%26dopt%3DAbstract</link>
            <description>Authors: Hu T, Liu Z, Shen X
    The phorbol myristate acetate (PMA) stimulated nutrophil respiratory burst has been considered to simply involve the activation of protein kinase C (PKC). However, the PLD activity was also increased by 10-fold in human neutrophils stimulated with 100 nM PMA. Unexpectedly, U73122, an inhibitor of phospholipase C, was found to significantly inhibit PMA-stimulated respiratory burst in human neutrophils. U73122 at the concentrations, which were sufficient to inhibit the respiratory burst completely, caused partial inhibition of the PLD activity but no inhibition on PKC translocation and activation, suggesting that PLD activity is also required in PMA-stimulated respiratory burst. Using 1-butanol, a PLD substrate, to block phosphatidic acid generation, the PMA-...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3284732</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3284732</guid>        </item>
        <item>
            <title>MafA promotes the reprogramming of placenta-derived multipotent stem cells into pancreatic islets-like and insulin-positive cells.</title>
            <link>http://www.medworm.com/index.php?rid=3284731&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20158571%26dopt%3DAbstract</link>
            <description>In this study, we investigate the role of MafA in placenta-derived multipotent stem cells (PDMSCs) that constitutively expressed Oct-4 and Nanog. PDMSCs were isolated and transfected with MafA using a lentivector. Our results showed that overexpression of MafA in PDMSCs significantly upregulated the expression of pancreatic development-related genes (Sox17, Foxa2, Pdx1, and Ngn3). Microarray analysis suggested that the gene expression profile of MafA-overexpressing PDMSCs was similar to that of pancreas and islet tissues. MafA increased the expression levels of the mRNAs of NKx2.2, Glut2, insulin, glucagons, and somatostatin, and further facilitated the differentiation of PDMSCs into insulin-positive cells. The glucose-stimulated responses to insulin and c-peptide production in MafA-overex...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3284731</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3284731</guid>        </item>
        <item>
            <title>Enhanced platelet adhesion induces angiogenesis in intestinal inflammation and inflammatory bowel disease microvasculature.</title>
            <link>http://www.medworm.com/index.php?rid=3284730&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20158572%26dopt%3DAbstract</link>
            <description>In conclusion, PLT adhesion to TNF-alpha-pre-treated HIMEC is mediated by ICAM-1, fractalkine and alpha(v)beta(3), and is associated with VEGF and sCD40L release. These findings suggest that inflamed HIMEC may recruit PLT which, upon release of pro-angiogenic factors, actively contribute to inflammation-induced angiogenesis.
    PMID: 20158572 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3284730</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3284730</guid>        </item>
        <item>
            <title>Oncologist's/hematologist's view on the roles of pathologists for molecular targeted cancer therapy.</title>
            <link>http://www.medworm.com/index.php?rid=3284729&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20158573%26dopt%3DAbstract</link>
            <description>Authors: Keller U, von Bubnoff N, Peschel C, Duyster J
    In the past two decades there has been a tremendous increase in the understanding of the molecular basis of human malignancies. In a variety of neoplasms, specific molecular markers became part of disease classifications and are now routinely used to define specific entities. Molecular analyses discriminate prognostic groups, guide differential treatment strategies and identify targets for molecular defined cancer therapy. A battery of new drugs has been developed to specifically inhibit oncogenic pathways. For an increasing number of solid and hematologic malignancies, the availability of molecular targeted drugs has fundamentally changed treatment algorithms. However, the diagnostic, prognostic and therapeutic impact of selected ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3284729</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3284729</guid>        </item>
        <item>
            <title>Inter-connection between mitochondria and HIFs.</title>
            <link>http://www.medworm.com/index.php?rid=3284728&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20158574%26dopt%3DAbstract</link>
            <description>Authors: Tormos KV, Chandel NS
    The transcription factors hypoxia inducible factor 1 and 2 (HIF-1 and HIF-2) regulate multiple responses to physiological hypoxia such as transcription of the hormone erythropoietin (EPO) to enhance red blood cell proliferation, vascular endothelial growth factor (VEGF) to promote angiogenesis and glycolytic enzymes to increase glycolysis. Recent studies indicate that HIFs also regulate mitochondrial respiration and mitochondrial oxidative stress. Interestingly, mitochondrial metabolism, respiration and oxidative stress also regulate activation of HIFs. In this review we examine the evidence that mitochondria and HIFs are intimately connected to regulate each other resulting in appropriate responses to hypoxia.
    PMID: 20158574 [PubMed - as supplied by ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3284728</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3284728</guid>        </item>
        <item>
            <title>Mankind's first natural stem cell transplant.</title>
            <link>http://www.medworm.com/index.php?rid=3263144&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20141549%26dopt%3DAbstract</link>
            <description>Authors: Tolosa JN, Park DH, Eve DJ, Klasko SK, Borlongan CV, Sanberg PR
    The timing of the umbilical cord clamping at birth is still controversial. In the modern era of medicine, the cord has been clamped early to facilitate resuscitation and stabilization of infants. However, recently delayed cord clamping has been supported by physicians because it allows the physiologic transfer of blood from the placenta to the infant. Many clinical studies have revealed that the delayed cord clamping elevates blood volume and hemoglobin and prevent anemia in infants. Moreover, since it was known that umbilical cord blood contains various valuable stem cells such as hematopoietic stem cells, endothelial cell precursors, mesenchymal progenitors, and multipotent/pluripotent lineage stem cells, the me...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3263144</comments>
            <pubDate>Fri, 05 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3263144</guid>        </item>
        <item>
            <title>Combinatorial interference of toll-like receptor 2 and 4 synergistically stabilizes atherosclerotic plaque in apolipoprotein E-knockout mice.</title>
            <link>http://www.medworm.com/index.php?rid=3248941&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20132416%26dopt%3DAbstract</link>
            <description>In conclusion, combinatorial interference of TLR2 and TLR4 reduces local inflammation and stabilizes plaques more effectively than interference of TLR2 or TLR4 alone.
    PMID: 20132416 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3248941</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3248941</guid>        </item>
        <item>
            <title>Brain Recovery - Towards a Unified Theory.</title>
            <link>http://www.medworm.com/index.php?rid=3248952&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20132405%26dopt%3DAbstract</link>
            <description>Authors: Muresanu DF
    
    PMID: 20132405 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3248952</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3248952</guid>        </item>
        <item>
            <title>Mechanisms in the loss of capillaries in systemic sclerosis: angiogenesis versus vasculogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=3248948&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20132409%26dopt%3DAbstract</link>
            <description>Authors: Manetti M, Guiducci S, Ibba-Manneschi L, Matucci-Cerinic M
    Abstract Systemic sclerosis (SSc, scleroderma) is a chronic, multisystem connective tissue disorder affecting the skin and various internal organs. Although the disease is characterized by a triad of widespread microangiopathy, fibrosis, and autoimmunity, increasing evidence indicates that vascular damage is a primary event in the pathogenesis of SSc. The progressive vascular injury includes persistent endothelial cell activation/damage and apoptosis, intimal thickening, delamination, vessel narrowing and obliteration. These profound vascular changes lead to vascular tone dysfunction and reduced capillary blood flow, with consequent tissue ischemia and severe clinical manifestations, such as digital ulceration or amput...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3248948</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3248948</guid>        </item>
        <item>
            <title>Involvement of beta-adrenergic receptor in synaptic vesicle swelling and implication in neurotransmitter release.</title>
            <link>http://www.medworm.com/index.php?rid=3248947&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20132410%26dopt%3DAbstract</link>
            <description>Authors: Chen Z, Lee JS, Shin L, Cho WJ, Jena BP
    ABSTRACT Secretory vesicle swelling is required for vesicular discharge during cell secretion. The G(alphao)-mediated water channel AQP-6 involvement in synaptic vesicle swelling in neurons has previously been reported. Studies demonstrate that in the presence of GTP, mastoparan, an amphiphilic tetradecapeptide from wasp venom, activates G(o) protein GTPase, and stimulates synaptic vesicle swelling. Stimulation of G proteins is believed to occur via insertion of mastoparan into the phospholipid membrane to form a highly structured alpha-helix that resembles the intracellular loops of G protein-coupled adrenergic receptors. Consequently, the presence of adrenoceptors and the presence of an endogenous beta-adrenergic agonist at the synapti...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3248947</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3248947</guid>        </item>
        <item>
            <title>Interstitial cells of Cajal, macrophages and mast cells in the gut musculature: morphology, distribution, spatial and possible functional interactions.</title>
            <link>http://www.medworm.com/index.php?rid=3248946&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20132411%26dopt%3DAbstract</link>
            <description>Authors: Mikkelsen HB
    Summary Interstitial cells of Cajal (ICC) are recognized as pacemaker cells for gastrointestinal movement and are hypothesized to be mediators of neuromuscular transmission. Intestinal motility disturbances are often associated with a reduced number of ICC and/or ultrastructural damage, sometimes associated with immune cells. Macrophages and mast cells in the intestinal muscularis externa of rodents can be found in close spatial contact with ICC. Macrophages are a constant and regularly distributed cell population in the serosa and at the level of Auerbach's plexus (AP). In human colon, ICC are in close contact with macrophages at the level of AP; suggesting functional interaction. It has therefore been proposed that ICC and macrophages interact. Macrophages and m...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3248946</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3248946</guid>        </item>
        <item>
            <title>Imipramine inhibition of TRPM-like plasmalemmal Mg transport in vascular smooth muscle cells.</title>
            <link>http://www.medworm.com/index.php?rid=3248945&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20132412%26dopt%3DAbstract</link>
            <description>Authors: Hamaguchi Y, Tatematsu Y, Furukawa K, Matsubara T, Nakayama S
    Abstract Depression is associated with vascular disease, such as myocardial infarction and stroke. Pharmacological treatments may contribute to this association. On the other hand, Mg(2+)-deficiency is also known to be a risk factor for the same category of diseases. In the present study, we examined the effect of imipramine on Mg(2+) homeostasis in vascular smooth muscle, especially via melastatin-type transient receptor potential (TRPM)-like Mg(2+)-permeable channels. The intracellular free Mg(2+) concentration ([Mg(2+)](i)) was measured using (31)P-NMR in porcine carotid arteries that express both TRPM6 and TRPM7, the latter being predominant. pH(i) and intracellular phosphorus compounds were simultaneously monit...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3248945</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3248945</guid>        </item>
        <item>
            <title>Gene expression signatures differentiate ovarian/peritoneal serous carcinoma from breast carcinoma in effusions.</title>
            <link>http://www.medworm.com/index.php?rid=3248944&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20132413%26dopt%3DAbstract</link>
            <description>Authors: Davidson B, Stavnes HT, Holth A, Chen X, Yang Y, Shih IM, Wang TL
    Abstract Ovarian/primary peritoneal carcinoma and breast carcinoma are the gynecologic cancers that most frequently involve the serosal cavities. With the objective of improving on the limited diagnostic panel currently available for the differential diagnosis of these two malignancies, as well as to define tumor-specific biological targets, we compared their global gene expression patterns. Gene expression profiles of ten serous ovarian/peritoneal and eight ductal breast carcinoma effusions were analyzed using the HumanRef-8 BeadChip from Illumina. Differentially expressed candidate genes were validated using quantitative real-time PCR and immunohistochemistry. Unsupervised hierarchical clustering using all 54,...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3248944</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3248944</guid>        </item>
        <item>
            <title>Epigenetics in atherosclerosis and inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=3248943&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20132414%26dopt%3DAbstract</link>
            <description>Authors: Wierda RJ, Geutskens SB, Jukema JW, Quax PH, van den Elsen PJ
    Abstract Atherosclerosis is a multifactorial disease with a severe burden on western society. Recent insights into the pathogenesis of atherosclerosis underscore the importance of chronic inflammation in both the initiation and progression of vascular remodelling. Expression of immunoregulatory molecules by vascular wall components within the atherosclerotic lesions is accordingly thought to contribute to the ongoing inflammatory process. Besides genetic factors also epigenetic mechanisms play an essential and fundamental role in the transcriptional control of gene expression. These epigenetic mechanisms change the accessibility of chromatin by DNA methylation and histone modifications. Epigenetic modulators are thu...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3248943</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3248943</guid>        </item>
        <item>
            <title>The contribution of Kv7 channels to pregnant mouse and human myometrial contractility.</title>
            <link>http://www.medworm.com/index.php?rid=3248942&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20132415%26dopt%3DAbstract</link>
            <description>Authors: McCallum LA, Pierce SL, England SK, Greenwood IA, Tribe RM
    Abstract Premature birth accounts for approximately 75% of neonatal mortality and morbidity in the developed world. Despite this, methods for identifying and treating women at risk of preterm labour are limited and many women still present in preterm labour requiring tocolytic therapy to suppress uterine contractility. The aim of this study was to assess the utility of Kv7 channel activators as potential uterine smooth muscle (myometrium) relaxants in tissues from pregnant mice and women. Myometrium was obtained from early and late pregnant mice and from lipopolysaccharide (LPS)-injected mice (day 15 of gestation; model of infection in pregnancy). Human myometrium was obtained at the time of Caesarean section from wome...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3248942</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3248942</guid>        </item>
        <item>
            <title>Gene expression signatures differentiate ovarian/peritoneal serous carcinoma from breast carcinoma in effusions.</title>
            <link>http://www.medworm.com/index.php?rid=3248951&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20132406%26dopt%3DAbstract</link>
            <description>Authors: Davidson B, Stavnes HT, Holth A, Chen X, Yang Y, Shih IM, Wang TL
    Abstract Ovarian/primary peritoneal carcinoma and breast carcinoma are the gynecologic cancers that most frequently involve the serosal cavities. With the objective of improving on the limited diagnostic panel currently available for the differential diagnosis of these two malignancies, as well as to define tumor-specific biological targets, we compared their global gene expression patterns. Gene expression profiles of ten serous ovarian/peritoneal and eight ductal breast carcinoma effusions were analyzed using the HumanRef-8 BeadChip from Illumina. Differentially expressed candidate genes were validated using quantitative real-time PCR and immunohistochemistry. Unsupervised hierarchical clustering using all 54,...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3248951</comments>
            <pubDate>Thu, 28 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3248951</guid>        </item>
        <item>
            <title>Perspectives for the use of structural information and chemical genetics to develop inhibitors of Janus kinases.</title>
            <link>http://www.medworm.com/index.php?rid=3248950&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20132407%26dopt%3DAbstract</link>
            <description>We describe two structural hotspots in the pseudokinase domain of Jak2 that seem to be associated either to myeloproliferation or to lymphoblastic leukaemia, pointing at the involvement of distinct signalling complexes in these disease settings. The different domains of Jaks are discussed as potential drug targets. We present currently available inhibitors targeting Jaks and indicate structural differences in the kinase domains of the different Jaks that may be exploited in the development of specific inhibitors. Moreover, we discuss recent chemical genetic approaches which can be applied to Jaks to better understand the role of these kinases in their biological settings and as drug targets.
    PMID: 20132407 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3248950</comments>
            <pubDate>Thu, 28 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3248950</guid>        </item>
        <item>
            <title>Characterization of smooth muscle differentiation of purified human skeletal muscle derived cells.</title>
            <link>http://www.medworm.com/index.php?rid=3248949&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20132408%26dopt%3DAbstract</link>
            <description>In conclusion, we confirmed the smooth muscle differentiation capability of purified hMDCs. The gene expression of smooth muscle differentiation of purified hMDCs was characterized. These cells may be potential biomaterials for human tissue regeneration.
    PMID: 20132408 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3248949</comments>
            <pubDate>Thu, 28 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3248949</guid>        </item>
        <item>
            <title>Early long-term L-T3 replacement rescues mitochondria and prevents ischemic cardiac remodeling in rats.</title>
            <link>http://www.medworm.com/index.php?rid=3213025&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20100314%26dopt%3DAbstract</link>
            <description>Conclusion. Early and sustained physiological restoration of circulating L-T3 levels after MI halves infarctscar size and prevents the progression towards heart failure. This beneficial effect is likely due to enhanced capillary formation and mitochondrial protection.
    PMID: 20100314 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3213025</comments>
            <pubDate>Wed, 20 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3213025</guid>        </item>
        <item>
            <title>Oxygen-mediated endocytosis in cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3186310&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20082654%26dopt%3DAbstract</link>
            <description>Authors: Wang Y, Ohh M
    ABSTRACT Solid tumors invariably exhibit regions of hypoxia and upregulation of receptor tyrosine kinases (RTKs) that trigger multiple signal pathways, including those that govern cell proliferation, survival and motility, ultimately contributing to oncogenesis. While past studies have shown hypoxia-dependent transcriptional and translational induction of several RTK expression and their respective ligands, recent evidence suggests that hypoxia regulates RTK signaling through endocytosis, a major deactivation pathway of RTKs. Hypoxia-mediated endocytosis is also thought to modulate the activity of a growing list of other membrane-associated proteins such as integrins and Na,K-ATPase. These recent discoveries underscore the emergence of endocytosis as an important...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186310</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186310</guid>        </item>
        <item>
            <title>beta-adrenergic blockade attenuates cardiac dysfunction and myofibrillar remodeling in congestive heart failure.</title>
            <link>http://www.medworm.com/index.php?rid=3186309&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20082655%26dopt%3DAbstract</link>
            <description>Authors: Machackova J, Sanganalmath SK, Elimban V, Dhalla NS
    Abstract Although beta-adrenoceptor (beta-AR) blockade is an important mode of therapy for congestive heart failure (CHF), subcellular mechanisms associated with its beneficial effects are not clear. Three wks after inducing myocardial infarction (MI), rats were treated daily with or without 20 and 75 mg/kg atenolol, a selective beta(1)-AR antagonist, or propranolol, a nonselective beta-AR antagonist, for 5 wks. Sham operated rats served as controls. All animals were assessed hemodynamically and echocardiographically and the left ventricle (LV) was processed for the determination of myofibrillar ATPase activity, alpha- and beta-myosin heavy chain (MHC) isoforms and gene expression as well as cardiac troponin I (cTnI) phosphor...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186309</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186309</guid>        </item>
        <item>
            <title>Discrepancies between metabolic activity and DNA content as tool to assess cell proliferation in cancer research.</title>
            <link>http://www.medworm.com/index.php?rid=3186308&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20082656%26dopt%3DAbstract</link>
            <description>Authors: Quent VM, Loessner D, Friis T, Reichert JC, Hutmacher DW
    Abstract Cell proliferation is a critical and frequently studied feature of molecular biology in cancer research. Therefore, various assays are available using different strategies to measure cell proliferation. Metabolic assays such as AlamarBlue, WST-1, and MTT, which were originally developed to determine cell toxicity, are being used to assess cell numbers. Additionally, proliferative activity can be determined by quantification of DNA content using fluorophores, such as CyQuant and PicoGreen. Referring to data published in high ranking cancer journals, 945 publications applied these assays over the past 14 years to examine the proliferative behaviour of diverse cell types. Within this study, mainly metabolic assays ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186308</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186308</guid>        </item>
        <item>
            <title>Involvement of HAb18G/CD147 in T cell activation and immunological synapse formation.</title>
            <link>http://www.medworm.com/index.php?rid=3186307&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20082657%26dopt%3DAbstract</link>
            <description>In this report, we demonstrated that HAb18G/CD147 expression on both activated CD4(+) and CD8(+) T cells was up-regulated. In vitro cross-linking of T cells with an anti-HAb18G/CD147 monoclonal antibody (mAb) 5A12 inhibited T cells proliferation upon TCR stimulation. Such co-stimulation inhibited T cell proliferation by down-regulating the expression of CD25 and interleukin 2 (IL-2), decreased production of interleukin 4 (IL-4) but not IFN-gamma. Laser confocal imaging analysis indicated that HAb18G/CD147 was recruited to the immunologic synapse (IS) during T cell activation; triggering HAb18G/CD147 on activated T cells by anti-HAb18G/CD147 mAb 5A12 strongly dispersed the formation of the IS. Further functional studies showed that the ligation of HAb18G/CD147 with mAb 5A12 decreased the ty...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186307</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186307</guid>        </item>
        <item>
            <title>Early defect of transforming growth factor beta-1 formation in Huntington's disease.</title>
            <link>http://www.medworm.com/index.php?rid=3186306&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20082658%26dopt%3DAbstract</link>
            <description>We examined the pharmacological regulation of TGF-beta1 formation in asymptomatic R6/2 mice, where blood TGF-beta1 levels were also reduced. In these R6/2 mice, both the mGlu2/3 metabotropic glutamate receptor agonist, LY379268, and riluzole failed to increase TGF-beta1 formation in the cerebral cortex and corpus striatum, suggesting that a defect in the regulation of TGF-beta1 production is associated with HD. Accordingly, reduced TGF-beta1 mRNA and protein levels were found in cultured astrocytes transfected with mutated exon 1 of the human huntingtin gene, and in striatal knock-in cell lines expressing full-lenght huntingtin with an expanded glutamine repeat. Taken together, our data suggest that plasma TGF-beta1 levels are potential biomarkers of HD development during the asymptomatic ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186306</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186306</guid>        </item>
        <item>
            <title>Basic mechanisms of neurodegeneration: a critical update.</title>
            <link>http://www.medworm.com/index.php?rid=3179107&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20070435%26dopt%3DAbstract</link>
            <description>Authors: Jellinger KA
    Abstract Neurodegenerative diseases are characterized by progressive dysfunction of specific populations of neurons, determining clinical presentation. Neuronal loss is associated with extra- and intra-cellular accumulation of misfolded proteins, the hallmarks of many neurodegenerative proteinopathies. Major basic processes include abnormal protein dynamics due to deficiency of the ubiquitin-proteosome-autophagy system, oxidative stress and free radical formation, mitochondrial dysfunction, impaired bioenergetics, dysfunction of neurotrophins, &quot;neuroinflammatory&quot; processes, and (secondary) disruptions of neuronal Golgi apparatus and axonal transport. These interrelated mechanisms lead to programmed cell death is a long run over many years. Neurodegenerative disord...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3179107</comments>
            <pubDate>Mon, 11 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3179107</guid>        </item>
        <item>
            <title>Differentiation of human adipose-derived stem cells into beating cardiomyocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3179106&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20070436%26dopt%3DAbstract</link>
            <description>Conclusion In conclusion, cell-to-cell interaction was identified as a key inducer for cardiomyogenic differentiation of hASCs. This method was optimized by co-culture with contracting cardiomyocytes and provides a potential cardiac differentiation system to progress applications for cardiac cell therapy or tissue engineering.
    PMID: 20070436 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3179106</comments>
            <pubDate>Mon, 11 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3179106</guid>        </item>
        <item>
            <title>Mechanisms of cellular communication through intercellular protein transfer.</title>
            <link>http://www.medworm.com/index.php?rid=3179105&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20070437%26dopt%3DAbstract</link>
            <description>Authors: Ahmed KA, Xiang J
    Abstract In a multicellular system, cellular communication is a must for orchestration and coordination of cellular events. Advent of the latest analytical and imaging tools has allowed us to enhance our understanding of the intercellular communication. An intercellular exchange of proteins or intact membrane patches is a ubiquitous phenomenon, and has been the subject of renewed interest, particularly in the context of immune cells. Recent evidence implicates that intercellular protein transfers, including trogocytosis is an important mechanism of the immune system to modulate immune responses and transferred proteins can also contribute to pathology. It has been demonstrated that intercellular protein transfer can be through the internalization/ pathway, di...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3179105</comments>
            <pubDate>Mon, 11 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3179105</guid>        </item>
        <item>
            <title>Chagas' disease: an update on immune mechanisms and therapeutic strategies.</title>
            <link>http://www.medworm.com/index.php?rid=3179104&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20070438%26dopt%3DAbstract</link>
            <description>Authors: Boscardin SB, Torrecilhas AC, Manarin R, Revelli S, Rey EG, Tonelli RR, Silber AM
    Abstract The final decade of the 20th century was marked by an alarming resurgence in infectious diseases caused by tropical parasites belonging to the kinetoplastid protozoan order. Among the pathogenic trypanosomatids, some species are of particular interest due to their medical importance. These species include the agent responsible for Chagas' disease, Trypanosoma cruzi. Aproximately 8 to 10 million people are infected in the Americas, and approximately 40 million are at risk. In the present review, we discuss in detail the immune mechanisms elicited during infection by T. cruzi and the effects of chemotherapy in controlling parasite proliferation and on the host immune system.
    PMID: 2007...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3179104</comments>
            <pubDate>Mon, 11 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3179104</guid>        </item>
        <item>
            <title>NSAIDS inhibit in vitro MSC chondrogenesis but not osteogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=3179103&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20070439%26dopt%3DAbstract</link>
            <description>Conclusions. These findings suggest that NSAIDs may inhibit bone formation via blockage of MSC chondrogenic differentiation which is an important intermediate phase in normal endochondral bone formation.
    PMID: 20070439 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3179103</comments>
            <pubDate>Mon, 11 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3179103</guid>        </item>
        <item>
            <title>Cell interactions in bone tissue engineering.</title>
            <link>http://www.medworm.com/index.php?rid=3146788&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20050963%26dopt%3DAbstract</link>
            <description>Authors: Pirraco RP, Marques AP, Reis RL
    Abstract Bone fractures where the innate regenerative bone response is compromised represent between 4 and 8 hundred thousand of the total fracture cases, just in the US. Bone Tissue Engineering (TE) brought the notion that, in cases such as those, it was preferable to boost the healing process of bone tissue instead of just adding artificial parts that could never properly replace the native tissue. However, despite the hype, Bone TE so far could not live up to its promises and new bottom-up approaches are needed. The study of the cellular interactions between the cells relevant for bone biology can be of essential importance to that. In living bone, cells are in a context where communication with adjacent cells is almost permanent. Many fundam...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3146788</comments>
            <pubDate>Sun, 27 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3146788</guid>        </item>
        <item>
            <title>High efficacy and minimal peptide required for the anti-angiogenic and anti-hepatocarcinoma activities of plasminogen K5.</title>
            <link>http://www.medworm.com/index.php?rid=3146787&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20050964%26dopt%3DAbstract</link>
            <description>Authors: Yang X, Cai W, Xu Z, Chen J, Li C, Liu S, Yang Z, Pan Q, Li M, Ma J, Gao G
    [Abstract] Kringle 5(K5) is the fifth kringle domain of human plasminogen and its anti-angiogenic activity is more potent than angiostatin that includes the first four kringle fragment of plasminogen. Our recent study demonstrated that K5 suppressed hepatocarcinoma growth by anti-angiogenesis. To find high efficacy and minimal peptide sequence required for the anti-angiogenic and anti-tumor activities of K5, two deletion mutants of K5 were generated. The amino acid residues outside kringle domain of intact K5 (Pro452-Ala542) were deleted to form K5mut1(Cys462-Cys541). The residue Cys462 was deleted again to form K5mut2(Met463-Cys541). K5mut1 specifically inhibited proliferation, migration and induced ap...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3146787</comments>
            <pubDate>Sun, 27 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3146787</guid>        </item>
        <item>
            <title>Altered expression of claudin family proteins in Alzheimer's disease and vascular dementia brains.</title>
            <link>http://www.medworm.com/index.php?rid=3135848&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20041969%26dopt%3DAbstract</link>
            <description>We report a significant increase in ratio of neurons expressing Cl-2, Cl-5 and Cl-11 in both AD and VaD as compared to aged controls. The ratio of astrocytes expressing Cl-2 and Cl-11 was significantly higher in AD and VaD as compared to aged controls. The ratio of oligodendrocytes expressing Cl-11 was significantly higher in AD and the ratio of oligodendrocytes expressing Cl-2 was significantly higher in VaD as compared to aged controls. Within the cerebral cortex, Cls were selectively expressed by pyramidal neurons, which are the ones responsible for cognitive processes and affected by AD pathology. Our findings suggest a new function of Cl family proteins which might be linked to response to cellular stress.
    PMID: 20041969 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3135848</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3135848</guid>        </item>
        <item>
            <title>Repair of senescent myocardium by mesenchymal stem cells is dependent on the age of donor mice.</title>
            <link>http://www.medworm.com/index.php?rid=3135847&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20041970%26dopt%3DAbstract</link>
            <description>Authors: Khan M, Mohsin S, Khan SN, Riazuddin S
    ABSTRACT Myocardial infarction is one of the leading causes of mortality in aged people. Whether age of donors of mesenchymal stem cell (MSCs) affects its ability to repair the senescent heart tissue is unknown. In the present study, MSCs from young (2 months) and aged (18 months) GFP expressing C57BL/6 mice were characterized with p16(INK4a) and beta-gal associated senescence. Myocardial infarction was produced in 18 month old wild type C57BL/6 mice transplanted with MSCs from young and aged animals in the border of the infarct region. Expression of p16(INK4a) in MSCs from aged animals was significantly higher (21.5%+/- 1.2, p &amp;lt;0.05) as compared to those from young animals (9.2%+/- 2.8). A decline in the tube-forming ability on Matrig...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3135847</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3135847</guid>        </item>
        <item>
            <title>FXR an emerging therapeutic target for the treatment of atherosclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=3135846&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20041971%26dopt%3DAbstract</link>
            <description>Authors: Mencarelli A, Fiorucci S
    Abstract Atherosclerosis is the leading cause of illness and death. Therapeutic strategies aimed at reducing cholesterol plasma levels have shown efficacy in either reducing progression of atherosclerotic plaques and atherosclerosis-related mortality. The farnesoid-X-Receptor (FXR) is a member of metabolic nuclear receptors superfamily activated by bile acids. In entero-hepatic tissues, FXR functions as a bile acid sensor regulating bile acid synthesis, detoxification and excretion. In the liver FXR induces the expression of an atypical nuclear receptor, the small heterodimer partner, which subsequently inhibits the activity of hepatocyte nuclear factor 4a repressing the transcription of cholesterol 7a-hydroxylase, the critical regulatory gene in bile ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3135846</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3135846</guid>        </item>
        <item>
            <title>Molecular characterization and functional properties of cardiomyocytes derived from human inducible pluripotent stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=3135845&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20041972%26dopt%3DAbstract</link>
            <description>Authors: Germanguz I, Sedan O, Zeevi-Levin N, Shtreichman R, Barak E, Ziskind A, Eliyahu S, Meiry G, Amit M, Itskovitz-Eldor J, Binah O
    Abstract In view of the therapeutic potential of cardiomyocytes derived from induced pluripotent stem (iPS) cells (iPS-derived cardiomyocytes), in the present study we investigated in iPS-derived cardiomyocytes, the functional properties related to [Ca(2+)](i) handling and contraction, the contribution of the sarcoplasmic reticulum Ca(2+) release to contraction and the beta-adrenergic inotropic responsiveness. The two iPS clones investigated here were generated through infection of human foreskin fibroblasts (HFF) with retroviruses containing the four human genes: OCT4, Sox2, Klf4 and C-Myc. Our major findings showed that iPS-derived cardiomyocytes: (1...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3135845</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3135845</guid>        </item>
        <item>
            <title>A novel pathway for receptor-mediated post-translational activation of inducible nitric oxide synthase.</title>
            <link>http://www.medworm.com/index.php?rid=3105563&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015194%26dopt%3DAbstract</link>
            <description>Authors: Brovkovych V, Zhang Y, Brovkovych S, Minshall RD, Skidgel RA
    ABSTRACT Inducible nitric oxide synthase (iNOS) is a major source of NO during inflammation whose activity is thought to be controlled primarily at the expression level. The B1 kinin receptor (B1R) post-translationally activates iNOS beyond its basal activity via extracellular signal regulated kinase (ERK)-mediated phosphorylation of Ser(745). Here we identified the signaling pathway causing iNOS activation in cytokine-treated endothelial cells or HEK293 cells transfected with iNOS and B1R. To allow kinetic measurements of NO release, we used a sensitive porphyrinic microsensor (response time = 10 milliseconds; 1 nM detection limit). B1Rs signaled through Gai coupling as ERK and iNOS activation were inhibited by pert...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105563</comments>
            <pubDate>Thu, 10 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105563</guid>        </item>
        <item>
            <title>The kinetochore protein Cenp-F is a potential novel target for zoledronic acid in breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3105562&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015195%26dopt%3DAbstract</link>
            <description>CONCLUSION This is the first report showing a specific effect of zoledronic acid on a protein involved in the regulation of chromosome segregation, identifying Cenp-F as a potential new molecular target for NBPs in tumour cells.
    PMID: 20015195 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105562</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105562</guid>        </item>
        <item>
            <title>Tumor hypoxia induces a metabolic shift causing acidosis: a common feature in cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3105561&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015196%26dopt%3DAbstract</link>
            <description>Authors: Chiche J, Brahimi-Horn MC, Pouyss&amp;#xE9;gur J
    Abstract Maintenance of cellular pH homeostasis is fundamental to life. A number of key intracellular pH (pHi) regulating systems including the Na(+)/H(+) exchangers (NHEs), the proton pump (V-ATPase), the monocarboxylate transporters (MCTs), the HCO(3) (-) transporters and exchangers (NBCs, AEs) and the membrane-associated and cytosolic carbonic anhydrases (CAs) cooperate in maintaining a pHi that is permissive for cell survival. A common feature of tumors is acidosis caused by hypoxia (low oxygen tension). In addition to oncogene activation and transformation, hypoxia is responsible for inducing acidosis through a shift in cellular metabolism that generates a high acid load in the tumor microenvironment. However, hypoxia and oncog...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105561</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105561</guid>        </item>
        <item>
            <title>Low-dose taxotere enhances the ability of sorafenib to induce apoptosis in gastric cancer models.</title>
            <link>http://www.medworm.com/index.php?rid=3105560&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015197%26dopt%3DAbstract</link>
            <description>Authors: Tesei A, Leonetti C, Zupi G, Scarsella M, Brigliadori G, Ulivi P, Fabbri F, Arienti C, Amadori D, Passardi A, Silvestrini R, Zoli W
    Abstract Despite the low efficacy of conventional antitumor drugs, chemotherapy remains an essential tool in controlling advanced gastric and esophageal cancers. We aimed to provide a biological rationale based on the sorafenib-taxotere interaction for the clinical treatment of gastric cancer. In vitro experiments were performed on four human gastric cancer cell lines (GK2, AKG, KKP and NCI-N87). Cytotoxicity was evaluated by SRB assay, cell cycle perturbations, apoptosis and mitotic catastrophe were assessed by flow cytometric and microscopic analyses, and protein expression was studied by Western blot. In the in vivo experiments, nude mice xenog...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105560</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105560</guid>        </item>
        <item>
            <title>Clinical outcomes in non-small-cell lung cancer patients with EGFR mutations: pooled analysis.</title>
            <link>http://www.medworm.com/index.php?rid=3105559&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015198%26dopt%3DAbstract</link>
            <description>Authors: Paz-Ares L, Souli&amp;#xE8;res D, Melez&amp;#xED;nek I, Moecks J, Keil L, Mok T, Rosell R, Klughammer B
    Abstract Non-small-cell lung cancer (NSCLC) with mutations in the epidermal growth factor receptor (EGFR) is a distinct subgroup of NSCLCs that is particularly responsive to EGFR tyrosine-kinase inhibitors (TKIs). A weighted pooled analysis of available studies was performed to evaluate clinical outcomes in patients with EGFR-mutated NSCLC who were treated with chemotherapy or EGFR TKIs. Median progression-free survival (PFS) times were pooled from prospective or retrospective studies that evaluated chemotherapy or single-agent EGFR TKIs (erlotinib or gefitinib) in patients with NSCLC and EGFR mutations. Among the studies identified for inclusion in the analysis, 12 evaluated erloti...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105559</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105559</guid>        </item>
        <item>
            <title>Temporal relationship of autophagy and apoptosis in neurons challenged by low molecular weight beta-amyloid peptide.</title>
            <link>http://www.medworm.com/index.php?rid=3105558&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015199%26dopt%3DAbstract</link>
            <description>Authors: Cheung YT, Zhang NQ, Hung CH, Lai CS, Yu MS, So KF, Chang RC
    ABSTRACT Alzheimer's disease (AD) is an aging-related progressive neurodegenerative disorder. Previous studies suggested that various soluble Abeta species are neurotoxic and able to activate autophagy and apoptosis, the type I and type II programmed cell death respectively. However, the sequential and functional relationships between these two cellular events remain elusive. Here we report that low molecular weight Abeta triggered cleavage of caspase 3 and poly (ADP-ribose) polymerase (PARP) to cause neuronal apoptosis in rat cortical neurons. On the other hand, Abeta activated autophagy by inducing autophagic vesicle formation and autophagy related gene 12 (ATG12), and up-regulated the lysosomal machinery for the d...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105558</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105558</guid>        </item>
        <item>
            <title>TFPI-2 silencing increases tumour progression and promotes metalloproteinase 1 and 3 induction through tumour-stromal cell interactions.</title>
            <link>http://www.medworm.com/index.php?rid=3105557&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015200%26dopt%3DAbstract</link>
            <description>This study also reveals for the first time that pulmonary fibroblasts incubated with conditioned media from TFPI-2 silencing cancer cells exhibited increased expression of MMPs, particularly MMP-1, -3 and -7, that are likely involved in lung cancer cell invasion through the surrounding stromal tissue, thus enhancing formation of metastases.
    PMID: 20015200 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105557</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105557</guid>        </item>
        <item>
            <title>Expression of NPP1 is regulated during atheromatous plaque calcification.</title>
            <link>http://www.medworm.com/index.php?rid=3105556&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015201%26dopt%3DAbstract</link>
            <description>Conclusion: Expression of the calcification inhibitor NPP1 is downregulated in calcified atherosclerotic plaques. Our correlation data point to a counter-active mechanism, which in the end turns out to be insufficient to prevent further progression of calcification.
    PMID: 20015201 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105556</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105556</guid>        </item>
        <item>
            <title>Growth factors in ischemic stroke.</title>
            <link>http://www.medworm.com/index.php?rid=3105555&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015202%26dopt%3DAbstract</link>
            <description>Authors: Lanfranconi S, Locatelli F, B Corti S, Candelise L, Comi GP, Baron P, Strazzer S, Bresolin N, Bersano A
    ABSTRACT Data from preclinical and clinical studies provide evidence that colony stimulating factors (CSFs) and other growth factors can improve stroke outcome by reducing stroke damage through their anti-apoptotic and anti-inflammatory effects, and by promoting angiogenesis and neurogenesis. This review provides a critical and up-to-date literature review on CSF use in stroke. We searched for experimental and clinical studies on haemopoietic growth factors such as granulocyte colony stimulating factor (G-CSF), erythropoietin (EPO), granulocyte-macrophage colony stimulating factor (GM-CSF), stem cell factor (SCF), vascular endothelial growth factor (VEGF), stromal cell-deriv...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105555</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105555</guid>        </item>
        <item>
            <title>Small leucine-rich proteoglycans in atherosclerotic lesions: Novel targets of chronic statin treatment?</title>
            <link>http://www.medworm.com/index.php?rid=3105554&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015203%26dopt%3DAbstract</link>
            <description>Conclusions: Long term treatment with rosuvastatin caused pronounced remodelling of atherosclerotic plaque matrix characterized specifically by enrichment with SLRP and formation of a condensed collagen matrix. Therefore, decorin and biglycan might represent novel targets of statin treatment that contribute to a stable plaque phenotype.
    PMID: 20015203 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105554</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105554</guid>        </item>
        <item>
            <title>Ferroportin 1 is expressed basolaterally in rat kidney proximal tubule cells and iron excess increases its membrane trafficking.</title>
            <link>http://www.medworm.com/index.php?rid=3105553&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015204%26dopt%3DAbstract</link>
            <description>Authors: Wolff NA, Liu W, Fenton RA, Lee WK, Th&amp;#xE9;venod F, Smith CP
    Abstract Ferroportin 1 (FPN1) is an iron exporter protein expressed in liver and duodenum, as well as in reticuloendothelial macrophages. Previously, we have shown that Divalent Metal Transporter 1 (DMT1) is expressed in late endosomes and lysosomes of the kidney proximal tubule (PT), the nephron segment responsible for the majority of solute reabsorption. We suggested that following receptor mediated endocytosis of transferrin filtered by the glomerulus, DMT1 exports iron liberated from transferrin into the cytosol. FPN1 is also expressed in the kidney yet its role remains obscure. As a first step towards determining the role of renal FPN1, we localized FPN1 in the PT. FPN1 was found to be located in association wi...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105553</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105553</guid>        </item>
        <item>
            <title>Evidence for the prevention of enthesitis in HLA-B27/hbeta2m transgenic rats treated with a monoclonal antibody against TNFalpha.</title>
            <link>http://www.medworm.com/index.php?rid=3105552&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015205%26dopt%3DAbstract</link>
            <description>Authors: Milia AF, Ibba-Manneschi L, Manetti M, Benelli G, Generini S, Messerini L, Matucci-Cerinic M
    ABSTRACT Transgenic rats with high expression of HLA-B27 and human beta2-microglobulin (B27TR) develop a multisystem inflammatory disease resembling human inflammatory bowel disease (IBD) and spondyloarthritis (SpA). Tumour necrosis factor alpha (TNFalpha has a crucial role in sustaining chronic inflammation in the gut and joints. The aim of this work was to evaluate whether TNFalpha blockade could prevent or reduce the inflammation of peripheral joints in B27TR. A first group of 9-week-old B27TR received anti-TNFalpha mAb or isotypic IgG2a,k up to the age of 18 weeks. An untreated group was monitored up to the age of 18 weeks and then randomly assigned to a 9-week treatment with anti-...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105552</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105552</guid>        </item>
        <item>
            <title>Loss of MTG16a (CBFA2T3), a novel rDNA repressor, leads to increased ribogenesis and disruption of breast acinar morphogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=3067453&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19961547%26dopt%3DAbstract</link>
            <description>Authors: Rossetti S, Hoogeveen AT, Esposito J, Sacchi N
    Human MTG16a (CBFA2T3), a chromatin repressor with nucleolar localization, was described to act as a suppressor of breast tumorigenesis. Here we show that MTG16a is a novel ribosomal gene repressor, which can counteract MYC-driven activation of ribosomal RNA (rRNA) transcription. We also show that either knocking down MTG16a by RNA interference, or sequestering MTG16a outside the nucleolus of human breast epithelial cells, hampers acinar morphogenesis concomitant with upregulation of rRNA synthesis and increased ribogenesis. This is the first demonstration that loss of MTG16a function in the nucleolus of breast epithelial cells can induce morphological and molecular changes typical of breast cancer initiation.
    PMID: 19961547 [...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3067453</comments>
            <pubDate>Wed, 02 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3067453</guid>        </item>
        <item>
            <title>Stem cell-mediated natural tissue engineering.</title>
            <link>http://www.medworm.com/index.php?rid=3036489&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19941631%26dopt%3DAbstract</link>
            <description>Conclusions-Circulating stem cells contributed to the development of a fully differentiated tissue on membranes placed within the left ventricle or descending aorta under physiological conditions. Early cardiomyocyte generation was identified only on membranes positioned within the left ventricle.
    PMID: 19941631 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3036489</comments>
            <pubDate>Sat, 21 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3036489</guid>        </item>
        <item>
            <title>A review on the molecular diagnostics of Lynch Syndrome: A central role for the pathology laboratory.</title>
            <link>http://www.medworm.com/index.php?rid=3033618&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19929944%26dopt%3DAbstract</link>
            <description>Authors: van Lier MG, Wagner A, van Leerdam ME, Biermann K, Kuipers EJ, Steyerberg EW, Dubbink HJ, Dinjens WN
    Lynch Syndrome (LS) is caused by mutations in mismatch repair (MMR) genes and is characterized by a high cumulative risk for the development of mainly colorectal carcinoma and endometrial carcinoma. Early detection of LS is important since surveillance can reduce morbidity and mortality. However, the diagnosis of LS is complicated by the absence of a pre-morbid phenotype and germline mutation analysis is expensive and time-consuming. Therefore it is standard practice to precede germline mutation analysis by a molecular diagnostic work-up of tumours, guided by clinical and pathological criteria, to select patients for germline mutation analysis. In this review we address these m...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3033618</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3033618</guid>        </item>
        <item>
            <title>Intracellular calcium signaling in Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=3033617&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19929945%26dopt%3DAbstract</link>
            <description>Authors: Hermes M, Eichhoff G, Garaschuk O
    More than two decades ago, dysregulation of the intracellular Ca(2+) homeostasis was suggested to underlie the development of Alzheimer's disease (AD). This hypothesis was tested in numerous in vitro studies, which revealed multiple Ca(2+) signaling pathways able to contribute to AD pathology. It remained, however, unclear whether these pathways are also activated in vivo, in cells involved in signal processing in the living brain. Here we review recent data analyzing intracellular Ca(2+) signaling in vivo in the context of previous in vitro findings. We particularly focus on the processes taking place in the immediate vicinity of amyloid plaques and on their possible role for AD-mediated brain dysfunction.
    PMID: 19929945 [PubMed - as supp...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3033617</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3033617</guid>        </item>
        <item>
            <title>Altered distribution of tight junction proteins after intestinal ischemia/reperfusion injury in rats.</title>
            <link>http://www.medworm.com/index.php?rid=3033614&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19929946%26dopt%3DAbstract</link>
            <description>Authors: Li Q, Zhang Q, Wang C, Liu X, Qu L, Gu L, Li N, Li J
    Tight junction (TJ) disruptions have been demonstrated both in vitro and more recently in vivo in infection. However, the molecular basis for changes of TJ during ischemia-reperfusion (I/R) injury is poorly understood. In the present study, intestinal damage was induced by I/R in an animal model. As assessed by TUNEL and PI uptake, we showed that I/R injury induced apoptosis as well as necrosis in rat colon, and the frequency of apoptotic and necrotic cells reached the maximum at 5 h of reperfusion. Immunofluorescence microscopy revealed that claudins 1, 3 and 5 are strongly expressed in the surface epithelial cells of the colon, however, labeling of all three proteins was present diffusely within cells and no longer focused...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3033614</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3033614</guid>        </item>
        <item>
            <title>Targeting histone deacetylases in pancreatic ductal adenocarcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=3033613&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19929947%26dopt%3DAbstract</link>
            <description>Authors: Schneider G, Kr&amp;#xE4;mer OH, Fritsche P, Sch&amp;#xFC;ler S, Schmid RM, Saur D
    Pancreatic ductal adenocarcinoma (PDAC) is a dismal disease with a median survival below six months and a five-year survival rate below 1%. Effective therapies for locally advanced or metastatic tumors are missing and curatively resected patients relapse in over 80% of the cases. Although histone deacetylases (HDACs) are involved in the control of proliferation, apoptosis, differentiation, migration and angiogenesis of cancer cells, knowledge about the expression patterns and functions of individual HDAC isoenzymes in pancreatic cancer is sparse. This review summarizes the roles of HDACs as novel therapeutic targets and the molecular mode of action of HDAC-inhibitors (HDACI) in PDACs. Success of HDACI i...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3033613</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3033613</guid>        </item>
        <item>
            <title>Role for LAMP-2 in endosomal cholesterol transport.</title>
            <link>http://www.medworm.com/index.php?rid=3033612&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19929948%26dopt%3DAbstract</link>
            <description>In this study we show that in cells deficient in both LAMP-1 and LAMP-2 (LAMP-/-), LDL receptor levels and LDL uptake are increased as compared to wild-type cells. However, there is a defect in esterification of both endogenous and LDL cholesterol. These results suggest that LAMP-/- cells have a defect in cholesterol transport to the site of esterification in the endoplasmic reticulum, likely due to defective export of cholesterol out of late endosomes or lysosomes. We also show that cholesterol accumulates in LAMP-2 deficient liver and that over-expression of LAMP-2 retards the lysosomal cholesterol accumulation induced by U18666A. These results point to a critical role for LAMP-2 in endosomal/lysosomal cholesterol export. Moreover, the late endosomal/lysosomal cholesterol accumulation in...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3033612</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3033612</guid>        </item>
        <item>
            <title>Cul4A is an oncogene in malignant pleural mesothelioma.</title>
            <link>http://www.medworm.com/index.php?rid=3033611&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19929949%26dopt%3DAbstract</link>
            <description>Authors: Hung MS, Mao JH, Xu Z, Yang CT, Yu JS, Harvard C, Lin YC, Bravo DT, Jablons DM, You L
    Cullin 4A (Cul4A) is important in cell survival, development, growth, and the cell cycle, but its role in mesothelioma has not been studied. For the first time, we identified amplification of the Cul4A gene in four of five mesothelioma cell lines. Consistent with increased Cul4A gene copy number, we found that Cul4A protein was overexpressed in mesothelioma cells as well. Cul4A protein was also overexpressed in 64% of primary malignant pleural mesothelioma (MPM) tumors. Furthermore, knockdown of Cul4A with shRNA in mesothelioma cells resulted in up-regulation of p21 and p27 tumor suppressor proteins in a p53-independent manner in H290, H28 and MS-1 mesothelioma cell lines. Knockdown of Cul4A ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3033611</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3033611</guid>        </item>
        <item>
            <title>Functionalized self-assembling peptide hydrogel enhance maintenance of hepatocyte activity in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=3000744&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19912437%26dopt%3DAbstract</link>
            <description>Authors: Genov&amp;#xE9; E, Schmitmeier S, Sala A, Borr&amp;#xF3;s S, Bader A, Griffith LG, Semino CE
    ABSTRACT There is a major challenge in maintaining functional hepatocytes in vivo as these cells rapidly lose their metabolic properties in culture. In this work we have developed a bioengineered platform that replaces the use of the collagen I -in the traditional culture sandwich technique- by a defined extracellular matrix analog, the self-assembling peptide hydrogel RAD16-I functionalized with biologically active motifs. Thus, after examining side by side the two culture systems we have found that in both cases hepatocytes acquired similar parenchymal morphology, presence of functional bile canaliculi structures, CYP3A2 induction by dexamethasone, urea production, secretion of proteins such...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3000744</comments>
            <pubDate>Fri, 13 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3000744</guid>        </item>
        <item>
            <title>Human ribosomal protein S13 promotes gastric cancer growth through downregulating p27(Kip1).</title>
            <link>http://www.medworm.com/index.php?rid=3000743&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19912438%26dopt%3DAbstract</link>
            <description>Authors: Guo X, Shi Y, Gou Y, Li J, Han S, Zhang Y, Huo J, Ning X, Sun L, Chen Y, Sun S, Fan D
    Abstract Our previous works revealed that human ribosomal protein S13 (RPS13) was upregulated in multidrug-resistant gastric cancer cells and overexpression of RPS13 could protect gastric cancer cells from drug-induced apoptosis. The present study was designed to explore the role of RPS13 in tumorigenesis and development of gastric cancer. The expression of RPS13 in gastric cancer tissues and normal gastric mucosa was evaluated by immunohistochemical staining and Western blot analysis. It was found RPS13 was expressed at a higher level in gastric cancer tissues than that in normal gastric mucosa. RPS13 was then genetically overexpressed in gastric cancer cells or knocked down by RNA interfere...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3000743</comments>
            <pubDate>Fri, 13 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3000743</guid>        </item>
        <item>
            <title>Bone marrow-derived cells can acquire cardiac stem cells properties in damaged heart.</title>
            <link>http://www.medworm.com/index.php?rid=3000742&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19912439%26dopt%3DAbstract</link>
            <description>Authors: Barile L, Cerisoli F, Frati G, Gaetani R, Chimenti I, Forte E, Cassinelli L, Spinardi L, Altomare C, Kizana E, Giacomello A, Messina E, Ottolenghi S, Magli MC
    ABSTRACT Experimental data suggest that cell-based therapies may be useful for cardiac regeneration following ischaemic heart disease. Bone marrow (BM) cells have been reported to contribute to tissue repair after myocardial infarction (MI) by a variety of humoral and cellular mechanisms. However, there is no direct evidence, so far, that BM cells can generate Cardiac Stem Cells (CSCs). To investigate whether BM cells contribute to repopulate the Kit+ CSCs pool, we transplanted BM cells from transgenic mice, expressing Green Fluorescent Protein (GFP) under the control of Kit regulatory elements, into wild type irradiated...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3000742</comments>
            <pubDate>Fri, 13 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3000742</guid>        </item>
        <item>
            <title>The CMT4B disease-causing proteins MTMR2 and MTMR13/SBF2 regulate AKT signaling.</title>
            <link>http://www.medworm.com/index.php?rid=3000741&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19912440%26dopt%3DAbstract</link>
            <description>Authors: Berger P, Tersar K, Ballmer-Hofer K, Suter U
    Abstract Charcot-Marie-Tooth disease type 4B is caused by mutations in the genes encoding either the lipid phosphatase Myotubularin-Related-Protein-2 (MTMR2) or its regulatory binding partner MTMR13/SBF2. Mtmr2 dephosphorylates PI-3-P and PI-3,5-P2 to form phosphatidylinositol and PI-5-P, respectively, while Mtmr13/Sbf2 is an enzymatically inactive member of the myotubularin protein family. We have found altered levels of the critical signaling protein AKT in mouse mutants for Mtmr2 and Mtmr13/Sbf2. Thus, we analyzed the influence of Mtmr2 and Mtmr13/Sbf2 on signaling processes. We found that overexpression of Mtmr2 prevents the degradation of the epidermal growth factor receptor (EGFR) and leads to sustained Akt activation whereas ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3000741</comments>
            <pubDate>Fri, 13 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3000741</guid>        </item>
        <item>
            <title>PPARgamma ligands inhibit telomerase activity and hTERT expression through modulation of the Myc/Mad/Max network, in colon cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3000740&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19912441%26dopt%3DAbstract</link>
            <description>In this study, we demonstrated that 15d-PG J2 and rosiglitazone (an endogenous and synthetic PPARgamma ligand, respectively) inhibited hTERT expression and telomerase activity in CaCo-2 colon cancer cells. Moreover, both ligands inhibited c-Myc protein expression and its E-box DNA binding activity. Additionally, Mad1 protein expression and its E-box DNA binding activity were strongly increased by 15d-PG J2 and, to a lesser extent, by rosiglitazone. Sp1 transcription factor expression and its GC-box DNA binding activity were not affected by both PPARgamma ligands. Results obtained by transient transfection of CaCo-2 cells with pmaxFP-Green-PRL plasmid constructs containing the functional hTERT core promoter (including one E-box and five GC-boxes) and its E-box deleted sequences, cloned upst...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3000740</comments>
            <pubDate>Fri, 13 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3000740</guid>        </item>
        <item>
            <title>Functional alterations of myeloid cell subsets in hyperlipidemia: relevance for atherosclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=2985390&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19900213%26dopt%3DAbstract</link>
            <description>Authors: Soehnlein O, Drechsler M, Hristov M, Weber C
    Abstract Atherosclerosis is a chronic inflammatory disease wherein the infiltration of myeloid cells of the vessel wall is a hallmark event. Lymphocytes, platelets and endothelial cells stand out as prominent suspects being involved in atherosclerosis. However, recent advances suggest a crucial role for myeloid leukocytes, specifically monocyte subsets, neutrophils, dendritic cells, and endothelial progenitor cells. These cell types are not just rapidly recruited or already reside in the vascular wall, but also initiate and perpetuate core mechanisms in plaque formation and destabilization. Hyperlipidemia is an independent risk factor for atherosclerosis. Herein, hyperlipidemia skews myeloid cell haemostasis, phenotype, and transcri...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2985390</comments>
            <pubDate>Mon, 09 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2985390</guid>        </item>
        <item>
            <title>Identification of microRNA profiles in docetaxel-resistant human non-small cell lung carcinoma cells (SPC-A1).</title>
            <link>http://www.medworm.com/index.php?rid=2985389&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19900214%26dopt%3DAbstract</link>
            <description>Authors: Rui W, Bing F, Hai-Zhu S, Wei D, Long-Bang C
    Abstract Docetaxel has been used as first-line chemotherapy in advanced NSCLC, but further extensive and effective application is prevented by drug resistance. MicroRNAs (miRNAs) have recently been identified as important posttranscriptional regulators, which are involved in various biological processes. The aim of this study was to identify microRNA expression profiles involved in the development of docetaxel resistance in non-small cell lung carcinoma (NSCLC). Here, microarray chip technology was employed to identify miRNA expression profiles in docetaxel-resistant human NSCLC cell line (SPC-A1/docetaxel). Then, the changes of miRNAs expression (&amp;gt;2-fold compared with control SPC-A1 cell line) were testified by quantitative real...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2985389</comments>
            <pubDate>Mon, 09 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2985389</guid>        </item>
        <item>
            <title>Hypoxia-inducible factors in stem cells and cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2985388&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19900215%26dopt%3DAbstract</link>
            <description>Authors: Mazumdar J, Dondeti V, Simon MC
    Abstract Cellular properties are influenced by complex factors inherent to their microenvironments. While oxygen deprivation (hypoxia) occurs in tumors due to rapid cell proliferation and aberrant blood vessel formation, embryonic cells develop in a naturally occurring hypoxic environment. Cells respond to hypoxia by stabilizing hypoxia-inducible factors (HIFs), which are traditionally viewed to function by altering cellular metabolism and blood vessel architecture. Recently, HIFs have been shown to modulate specific stem cell effectors, such as Notch, Wnt, and Oct4, that control stem cell proliferation, differentiation and pluripotency. Direct molecular links have also been established between HIFs and critical cell signalling pathways such as ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2985388</comments>
            <pubDate>Mon, 09 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2985388</guid>        </item>
        <item>
            <title>Mutant presenilin-1 deregulated peripheral immunity exacerbates alzheimer-like pathology.</title>
            <link>http://www.medworm.com/index.php?rid=2985387&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19900216%26dopt%3DAbstract</link>
            <description>Authors: Zhu Y, Obregon D, Hou H, Giunta B, Erhart J, Fernandez F, Mori T, Nikolic W, Zhao Y, Morgan D, Town T, Tan J
    Abstract Mutations in the presenilin-1 (PS1) gene are independent causes of familial Alzheimer's disease (AD). AD patients have dysregulated immunity, and PS1 mutant mice exhibit abnormal systemic immune responses. To test whether immune function abnormality caused by a mutant human PS1 gene (mhPS1) could modify AD-like pathology, we reconstituted immune systems of AD model mice carrying a mutant human amyloid precursor protein gene (mhAPP; Tg2576 mice) or both mhAPP and mhPS1 genes (PSAPP mice) with allogeneic bone marrow cells. Here, we report a marked reduction in amyloid-beta (Abeta) levels, beta-amyloid plaques, and brain inflammatory responses in PSAPP mice follow...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2985387</comments>
            <pubDate>Mon, 09 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2985387</guid>        </item>
        <item>
            <title>Roles of pathologists in molecular targeted cancer therapy Introduction.</title>
            <link>http://www.medworm.com/index.php?rid=2972237&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19891708%26dopt%3DAbstract</link>
            <description>Authors: Osamura RY
    
    PMID: 19891708 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2972237</comments>
            <pubDate>Wed, 04 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2972237</guid>        </item>
        <item>
            <title>Autoimmunity against type VII collagen in inflammatory bowel disease.</title>
            <link>http://www.medworm.com/index.php?rid=2952876&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19878366%26dopt%3DAbstract</link>
            <description>Authors: Hundorfean G, Neurath MF, Sitaru C
    Abstract Autoimmunity against type VII collagen, an adhesion molecule of the extracellular matrix in epithelial basement membranes, is causing the rare organ-specific epidermolysis bullosa acquisita (EBA). An intriguing association between EBA and inflammatory bowel disease (IBD) has been extensively documented over the last decades, but, due to the very low incidence of EBA, received little attention from physicians involved in the care of patients with IBD. More recently, autoantibodies against type VII collagen have been detected in up to 68% of IBD patients. While these findings suggest that chronic intestinal inflammation in IBD predisposes for autoimmunity against type VII collagen, their relevance for the pathogenesis of both IBD and E...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2952876</comments>
            <pubDate>Sat, 31 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2952876</guid>        </item>
        <item>
            <title>Isthmin is a novel secreted angiogenesis inhibitor that inhibits tumor growth in mice.</title>
            <link>http://www.medworm.com/index.php?rid=2948521&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19874420%26dopt%3DAbstract</link>
            <description>Authors: Xiang W, Ke Z, Zhang Y, Cheng GH, Irwan ID, Sulochana KN, Potturi P, Wang Z, Yang H, Wang J, Zhuo L, Kini RM, Ge R
    Abstract Antiangiogenesis represents a promising therapeutic strategy for the treatment of various malignances. Isthmin is a gene highly expressed in the isthmus of the midbrain-hindbrain organizer in Xenopus with no known functions. It encodes a secreted 60 kDa protein containing a Thrombospondin Type 1 Repeat (TSR) domain in the central region and an Adhesion-associated domain in MUC4 and Other Proteins (AMOP) domain at the C-terminal. In this work, we demonstrate that isthmin is a novel angiogenesis inhibitor. Recombinant mouse isthmin inhibited endothelial cell (EC) capillary network formation on Matrigel through its C-terminal AMOP domain. It also suppressed ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2948521</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2948521</guid>        </item>
        <item>
            <title>Phosphatidylinositol 3-kinase interacts with the glucocorticoid receptor upon TLR2 activation.</title>
            <link>http://www.medworm.com/index.php?rid=2948520&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19874421%26dopt%3DAbstract</link>
            <description>Authors: Arancibia S, Ben&amp;#xED;tez D, N&amp;#xFA;&amp;#xF1;ez LE, Jewell CM, Langjhar P, Candia E, Zapata-Torres G, Cidlowski JA, Gonz&amp;#xE1;lez MJ, Hermoso MA
    ABSTRACT Airway inflammation is a common condition where glucocorticoids (GC) are a well-established therapy. It has been demonstrated that GC stimulate components of innate immunity. Specifically, glucocorticoids up-regulate TLR2 expression and activation upon inflammatory stimuli; however, little is known about the signaling involved in this process. To determine the mechanism by which dexamethasone modulates TLR2-induced cytokine production this signaling pathway was monitored in a lung epithelial cell line exposed to the TLR2 synthetic agonist, Pam(3)-Cys-Ser-Lys(4). These experiments demonstrate that phosphatidylinositol 3-kinase (P...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2948520</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2948520</guid>        </item>
        <item>
            <title>Serially heterotransplanted human prostate tumors as an experimental model.</title>
            <link>http://www.medworm.com/index.php?rid=2948519&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19874422%26dopt%3DAbstract</link>
            <description>Authors: Lopez-Barcons LA
    Abstract Preclinical research on prostate cancer (PC) therapies uses several models to represent the human disease accurately. A common model uses patient prostate tumor biopsies to develop a cell line by serially passaging and subsequent implantation, in immunodeficient mice. An alternative model is direct implantation of patient prostate tumor biopsies into immunodeficient mice, followed by serial passage in vivo. The purpose of this review is to compile data from the more than 30 years of human PC serial heterotransplantation research. Serially heterotransplanted tumors are characterized by evaluating the histopathology of the resulting heterotransplants, including cellular differentiation, karyotype, marker expression, hormone-sensitivity, cellular prolife...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2948519</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2948519</guid>        </item>
        <item>
            <title>Involvement of neuropeptide Y and its Y1 and Y5 receptors in maintaining self-renewal and proliferation of human embryonic stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=2948518&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19874423%26dopt%3DAbstract</link>
            <description>Authors: Son MY, Kim MJ, Yu K, Koo DB, Cho YS
    Abstract Neuropeptide Y (NPY) and NPY receptors are widely expressed in various organs and cell types and have been shown to have pleiotropic functions. However, their presence or role in human embryonic stem cells (hESCs) remains unknown. We now show that undifferentiated hESCs primarily express NPY and its Y1 and Y5 receptors. Inhibition of NPY signaling using either the selective NPY Y1 or Y5 receptor antagonist reduces the maintenance of self-renewal and proliferation of undifferentiated hESCs. We also provide compelling evidence that exogenous NPY supports the long-term growth of undifferentiated hESCs in the absence of feeder cell factors using only knockout serum replacement media. In further, NPY facilitates the use of chemically-de...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2948518</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2948518</guid>        </item>
        <item>
            <title>Exendin-4 regulates pancreatic ABCA1 transcription via CaMKK/CaMKIV pathway.</title>
            <link>http://www.medworm.com/index.php?rid=2948517&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19874424%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: Activation of the CaMKK/CaMKIV cascade by exendin-4 stimulated ABCA1 gene transcription, indicating that exendin-4 plays an important role in insulin secretion and cholesterol ester content in pancreatic beta cells.
    PMID: 19874424 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2948517</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2948517</guid>        </item>
        <item>
            <title>Metformin attenuates ovarian cancer cell growth in an AMP- kinase dispensable manner.</title>
            <link>http://www.medworm.com/index.php?rid=2948516&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19874425%26dopt%3DAbstract</link>
            <description>Authors: Rattan R, Giri S, Hartmann L, Shridhar V
    ABSTRACT Metformin, the most widely used drug for type 2 diabetes activates AMP-activated protein kinase (AMPK), which regulates cellular energy metabolism. Here, we report that ovarian cell lines VOSE, A2780, CP70, C200, OV202, OVCAR3, SKOV3ip, PE01 and PE04 predominantly express -alpha1, -beta1, -gamma1 and -gamma2 isoforms of AMPK subunits. Our studies show that metformin treatment (1) significantly inhibited proliferation of diverse chemo-responsive and -resistant ovarian cancer cell lines (A2780, CP70, C200, OV202, OVCAR3, SKVO3ip, PE01 and PE04), (2) caused cell cycle arrest accompanied by decreased cyclin D1 and increased p21 protein expression, (3) activated AMPK in various ovarian cancer cell lines as evident from increased pho...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2948516</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2948516</guid>        </item>
        <item>
            <title>Dedifferentiation of human articular chondrocytes is associated with alterations in expression patterns of GDF-5 and its receptors.</title>
            <link>http://www.medworm.com/index.php?rid=2948522&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19874419%26dopt%3DAbstract</link>
            <description>Authors: Schlegel W, Albrecht C, Eckl P, Freudenthaler H, Berger A, V&amp;#xE9;csei V, Marlovits S
    Abstract Human articular chondrocytes (HACs) are expanded in monolayer culture in order to obtain sufficient cells for matrix-associated cartilage transplantation (MACT). During this proliferation process, the cells change their shape as well as their expression profile. These changes resemble those that occur during embryogenesis, when the limb anlagen form the interzone that later develops the joint cleft. We analyzed the expression profile of genes that are reportedly important for these changes during embryogenesis within the dedifferentiation process of adult articular chondrocytes. We found GDF-5, BMPR-Ib, and connexin 43 upregulated, as well as a downregulation of BMPR-Ia and noggin. C...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2948522</comments>
            <pubDate>Wed, 28 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2948522</guid>        </item>
        <item>
            <title>Sensing, physiological effects and molecular response to elevated CO(2) levels in eukaryotes.</title>
            <link>http://www.medworm.com/index.php?rid=2944341&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19863692%26dopt%3DAbstract</link>
            <description>Authors: Sharabi K, Lecuona E, Helenius IT, Beitel G, Sznajder JI, Gruenbaum Y
    Abstract Carbon dioxide (CO(2)) is an important gaseous molecule that maintains biosphere homeostasis and is an important cellular signalling molecule in all organisms. The transport of CO(2) through membranes has fundamental roles in most basic aspects of life in both plants and animals. There is a growing interest in understanding how CO(2) is transported into cells, how it is sensed by neurons and other cell types, and in understanding the physiological and molecular consequences of elevated CO(2) levels (hypercapnia) at the cell and organism levels. Human pulmonary diseases and model organisms such as fungi, C. elegans, Drosophila and mice have been proven to be important in understanding of the mechanis...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2944341</comments>
            <pubDate>Fri, 23 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2944341</guid>        </item>
        <item>
            <title>Tissue inhibitor of metalloproteinases-1-induced scattered liver metastasis is mediated by host-derived urokinase-type plasminogen activator.</title>
            <link>http://www.medworm.com/index.php?rid=2944340&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19863693%26dopt%3DAbstract</link>
            <description>Authors: Schr&amp;#xF6;tzlmair F, Kopitz C, Halbgewachs B, Lu F, Alg&amp;#xFC;l H, Br&amp;#xFC;nner N, G&amp;#xE4;nsbacher B, Kr&amp;#xFC;ger A
    ABSTRACT Paradoxically, not only proteinases but also their inhibitors can correlate with bad prognosis of cancer patients, underlining the evolving concept of the protease web as the complex interplay between proteinases, their inhibitors, and effector molecules. Elevated levels of tissue inhibitor of metalloproteinases-1 (TIMP-1) render the liver more susceptible to metastasis by triggering urokinase plasminogen activator (uPA) expression as well as hepatocyte growth factor (HGF) signalling, thereby leading to the fatal scattered infiltration of metastasizing tumour cells throughout the parenchyma of the target organ. Here, we investigated whether host uPA is a ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2944340</comments>
            <pubDate>Fri, 23 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2944340</guid>        </item>
        <item>
            <title>Lipid droplet growth by fusion: insights from freeze-fracture imaging.</title>
            <link>http://www.medworm.com/index.php?rid=2944339&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19863694%26dopt%3DAbstract</link>
            <description>Authors: Robenek H, Severs NJ
    Abstract An understanding of how lipid droplets grow in the cell is important to current human health issues. Homotypic fusion of small lipid droplets to create larger ones is one proposed mechanism though the evidence for this process continues to be debated. By applying the technique of freeze-fracture electron microscopy to cells that have been stimulated to accumulate lipid droplets, we here present images which suggest that at least some large lipid droplets may indeed result from amalgamation of multiple smaller ones. These visual data add significantly to the notion that fusion contributes to lipid droplet growth.
    PMID: 19863694 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2944339</comments>
            <pubDate>Fri, 23 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2944339</guid>        </item>
        <item>
            <title>Preservation of TSPO by chronic intermittent hypobaric hypoxia confers antiarrhythmic activity.</title>
            <link>http://www.medworm.com/index.php?rid=2944338&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19863695%26dopt%3DAbstract</link>
            <description>Authors: Li J, Xu J, Xiao J, Zhang H, Liang D, Liu Y, Zhang Y, Liu Y, Wen W, Hu Y, Yu Z, Yan B, Jiang B, Zhou ZN, Chen YH
    Abstract Abnormal activation of mitochondrial translocator protein (TSPO) contributes to arrhythmogenesis during cardiac metabolic compromise; however, its role in the antiarrhythmic activities of chronic hypoxia adaptation remains unclear. Our results demonstrated that 80% of normoxic rats developed ischemic VF, whereas this condition was seldom observed in rats with 14-days of chronic intermittent hypobaric hypoxia (CIHH). TSPO stimulation or inhibition affected the arrhythmias incidence in normoxic rats, but did not change the CIHH-mediated antiarrhythmic effects. Abrupt and excessive elevation of TSPO activity was positively linked to ischemic VF, and CIHH prese...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2944338</comments>
            <pubDate>Fri, 23 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2944338</guid>        </item>
        <item>
            <title>Ox-LDL modifies the behavior of bone marrow stem cells and impairs their endothelial differentiation via inhibition of Akt phosphorylation.</title>
            <link>http://www.medworm.com/index.php?rid=2944335&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19863696%26dopt%3DAbstract</link>
            <description>In conclusion, ox-LDL promotes apoptosis and inhibits Oct-4 expression and self-renewal of MAPCs, and impairs their endothelial differentiation via suppression of Akt signaling.
    PMID: 19863696 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2944335</comments>
            <pubDate>Fri, 23 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2944335</guid>        </item>
        <item>
            <title>Maternal thyroid hormones are transcriptionally active during embryo-fetal development: results from a novel transgenic mouse model.</title>
            <link>http://www.medworm.com/index.php?rid=2944334&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19863697%26dopt%3DAbstract</link>
            <description>Conclusions: our results provide in vivo direct evidence that during embryonic life and before the onset of FTF, maternal THs are transcriptionally active through the action of embryonic TRs. This model may have clinical relevance and may be employed to design endpoint assays for new molecules affecting THs action.
    PMID: 19863697 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2944334</comments>
            <pubDate>Fri, 23 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2944334</guid>        </item>
        <item>
            <title>Native LDL-induced oxidative stress in human proximal 1 tubular cells: multiple players involved.</title>
            <link>http://www.medworm.com/index.php?rid=2944332&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19863698%26dopt%3DAbstract</link>
            <description>This study aimed to examine the effects of native non oxidized LDL on cellular oxidative metabolism in cultured human proximal tubular cells. By means of confocal microscopy imaging combined to respirometric and enzymatic assays it is shown that purified native LDL caused a marked increase of cellular ROS production which was mediated by activation of NADPH oxidase(s) and by mitochondrial dysfunction by means of a ROS-induced ROS release mechanism. The LDL-dependent mitochondrial alterations comprised inhibition of the respiratory chain activity, enhanced ROS production, uncoupling of the oxidative phosphorylation efficiency, collapse of the mtDeltaPsi, increased Ca(2+) uptake and loss of cytochrome c. All the above LDL-induced effects were completely abrogated by chelating extracellular C...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2944332</comments>
            <pubDate>Fri, 23 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2944332</guid>        </item>
        <item>
            <title>Metabolic profiling reveals key metabolic features of renal cell carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=2917278&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19845817%26dopt%3DAbstract</link>
            <description>Authors: Catchpole G, Platzer A, Weikert C, Kempkensteffen C, Johannsen M, Krause H, Jung K, Miller K, Willmitzer L, Selbig J, Weikert S
    Abstract Recent evidence suggests that metabolic changes play a pivotal role in the biology of cancer and in particular renal cell carcinoma (RCC). Here, a global metabolite profiling approach was applied to characterize the metabolite pool of RCC and normal renal tissue. Advanced decision tree models were applied to characterize the metabolic signature of RCC and to explore features of metastasized tumors. The findings were validated in a second independent dataset. Vitamin E derivates and metabolites of glucose, fatty acid, and inositol phosphate metabolism determined the metabolic profile of RCC. Alpha-tocopherol, hippuric acid, myoinositol, fructo...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2917278</comments>
            <pubDate>Mon, 19 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2917278</guid>        </item>
        <item>
            <title>Telomere attrition and genomic instability in xeroderma pigmentosum type-B deficient fibroblasts under oxidative stress.</title>
            <link>http://www.medworm.com/index.php?rid=2912565&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19840190%26dopt%3DAbstract</link>
            <description>Authors: Ting AP, Low GK, Gopalakrishnan K, Hande MP
    ABSTRACT Xeroderma Pigmentosum B (XPB/ ERCC3/ p89) is an ATP-dependent 3'--&amp;gt;5' directed DNA helicase involved in basal RNA transcription and the nucleotide excision repair pathway (NER). While the role of NER in alleviating oxidative DNA damage has been acknowledged it remains poorly understood. To study the involvement of XPB in repair of oxidative DNA damage, we utilised primary fibroblasts from a patient suffering from Xeroderma Pigmentosum with Cockayne Syndrome and Hydrogen Peroxide (H(2)O(2)) to induce oxidative stress. Mutant cells retained higher viability and cell cycle dysfunction after H(2)O(2) exposure. Cytokinesis blocked micronucleus assay revealed increased genome instability induced by H(2)O(2). Single cell gel ele...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2912565</comments>
            <pubDate>Thu, 15 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2912565</guid>        </item>
        <item>
            <title>Assessment of tumor hypoxia for prediction of response to therapy and cancer prognosis.</title>
            <link>http://www.medworm.com/index.php?rid=2912564&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19840191%26dopt%3DAbstract</link>
            <description>Authors: Jubb AM, Buffa FM, Harris AL
    Abstract Tumor cells exploit both genetic and adaptive means to survive and proliferate in hypoxic microenvironments, resulting in the outgrowth of more aggressive tumor cell clones. Direct measurements of tumor oxygenation, and surrogate markers of the hypoxic response in tumors (for instance, hypoxia inducible factor-1alpha, carbonic anhydrase 9 and glucose transporter-1) are well-established prognostic markers in solid cancers. However, individual markers do not fully capture the complex, dynamic and heterogeneous hypoxic response in cancer. To overcome this, expression profiling has been employed to identify hypoxia signatures in cohorts or models of human cancer. Several of these hypoxia signatures have demonstrated prognostic significance in ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2912564</comments>
            <pubDate>Thu, 15 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2912564</guid>        </item>
        <item>
            <title>Ankyrin protein networks in membrane formation and stabilization.</title>
            <link>http://www.medworm.com/index.php?rid=2912560&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19840192%26dopt%3DAbstract</link>
            <description>Authors: Cunha SR, Mohler PJ
    Abstract In eukaryotic cells, ankyrins serve as adaptor proteins that link membrane proteins to the underlying cytoskeleton. These adaptor proteins form protein complexes consisting of integral membrane proteins, signaling molecules, and cytoskeletal components. With their modular architecture and ability to interact with many proteins, ankyrins organize and stabilize these protein networks, thereby establishing the infrastructure of membrane domains with specialized functions. To this end, ankyrin collaborates with a number of proteins including cytoskeletal proteins, cell adhesion molecules, and large structural proteins. This review addresses the targeting and stabilization of protein networks related to ankyrin interactions with the cytoskeletal protein...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2912560</comments>
            <pubDate>Thu, 15 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2912560</guid>        </item>
        <item>
            <title>Aldehyde dehydrogenase activity promotes survival of human muscle precursor cells.</title>
            <link>http://www.medworm.com/index.php?rid=2912559&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19840193%26dopt%3DAbstract</link>
            <description>Authors: Jean E, Laoudj-Chenivesse D, Notarnicola C, Rouger K, Serratrice N, Bonnieu A, Gay S, Bacou F, Duret C, Carnac G
    ABSTRACT Aldehyde dehydrogenases (ALDH) are a family of enzymes that efficiently detoxify aldehydic products generated by reactive oxygen species and might therefore participate in cell survival. Since ALDH activity has been used to identify normal and malignant cells with stem cell properties, we asked whether human myogenic precursor cells (myoblasts) could be identified and isolated based on their levels of ALDH activity. Human muscle explant-derived cells were incubated with ALDEFLUOR, a fluorescent substrate for ALDH, and we determined by flow cytometry the level of enzyme activity. We found that ALDH activity positively correlated with the myoblast-CD56 positi...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2912559</comments>
            <pubDate>Thu, 15 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2912559</guid>        </item>
        <item>
            <title>A systems biology perspective on sVEGFR1: its biological function, pathogenic role &amp; therapeutic use.</title>
            <link>http://www.medworm.com/index.php?rid=2912554&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19840194%26dopt%3DAbstract</link>
            <description>A systems biology perspective on sVEGFR1: its biological function, pathogenic role &amp; therapeutic use.
    J Cell Mol Med. 2009 Oct 16;
    Authors: Wu FT, Stefanini MO, Gabhann FM, Kontos CD, Annex BH, Popel AS
    Abstract Angiogenesis is the growth of new capillaries from pre-existent microvasculature. A wide range of pathological conditions, from atherosclerosis to cancer, can be attributed to either excessive or deficient angiogenesis. Central to the physiological regulation of angiogenesis is the vascular endothelial growth factor (VEGF) system - its ligands and receptors (VEGFRs) are thus prime molecular targets of pro-angiogenic and anti-angiogenic therapies. Of growing interest as a prognostic marker and therapeutic target in angiogenesis-dependent diseases is soluble VEGF rece...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2912554</comments>
            <pubDate>Thu, 15 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2912554</guid>        </item>
        <item>
            <title>Plasma gelsolin facilitates interaction between beta(2) glycoprotein I and alpha5beta1 integrin.</title>
            <link>http://www.medworm.com/index.php?rid=2912553&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19840195%26dopt%3DAbstract</link>
            <description>In this study, we identified plasma gelsolin as a protein associated with beta(2)GPI by using immunoaffinity chromatography and mass spectrometric analysis. An in vivo binding assay showed that endogenous beta(2)GPI interacts with plasma gelsolin, which binds to integrin alpha5beta1 through fibronectin. The tethering of beta(2)GPI to monoclonal anti-beta(2)GPI autoantibody on the cell surface was enhanced in the presence of plasma gelsolin. Immunoblot analysis demonstrated that p38 MAPK protein was phosphorylated by monoclonal anti-beta(2)GPI antibody treatment, and its phosphorylation was attenuated in the presence of anti-integrin alpha5beta1 antibody. Furthermore, focal adhesion kinase (FAK), a downstream molecule of the fibronectin-integrin signaling pathway, was phosphorylated by anti...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2912553</comments>
            <pubDate>Thu, 15 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2912553</guid>        </item>
        <item>
            <title>FHL1 interacts with estrogen receptors and regulates breast cancer cell growth.</title>
            <link>http://www.medworm.com/index.php?rid=2912550&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19840196%26dopt%3DAbstract</link>
            <description>Authors: Ding L, Niu C, Zheng Y, Xiong Z, Liu Y, Lin J, Sun H, Huang K, Yang W, Li X, Ye Q
    Abstract Four and a half LIM protein 1 (FHL1) belongs to the LIM-only protein family and plays important roles in muscle growth and carcinogenesis. However, the biological function of FHL1 remains largely unknown. Here, we show that FHL1 physically and functionally interacted with estrogen receptors (ERs), which are involved in breast cancer development and progression. FHL1 bound specifically to the activation function-1 (AF1) domain of ER. Physical interaction of FHL1 and ER is required for FHL1 repression of estrogen-responsive gene transcription. FHL1 affected recruitment of ER to an estrogen-responsive promoter and ER binding to an estrogen-responsive element. Over-expression of FHL1 in brea...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2912550</comments>
            <pubDate>Thu, 15 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2912550</guid>        </item>
        <item>
            <title>Glomerular parietal epithelial cells of adult murine kidney undergo EMT to generate cells with traits of renal progenitors.</title>
            <link>http://www.medworm.com/index.php?rid=2912549&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19840197%26dopt%3DAbstract</link>
            <description>Authors: Chandra V, Phadnis S, Bhonde R
    ABSTRACT Glomerular parietal epithelial cells (GPECs) are known to revert to embryonic phenotype in response to renal injury. However, the mechanism of de-differentiation in GPECs and the underlying cellular processes are not fully understood. In the present study, we show that cultured GPECs of adult murine kidney undergo epithelial-mesenchymal transition (EMT) to generate cells, which express CD24, CD44 and CD29 surface antigens. Characterization by qRT-PCR and immunostaining of these clonogenic cells demonstrate that they exhibit metastable phenotype with co-expression of both epithelial (cytokeratin-18) and mesenchymal (vimentin) markers. Transcript analysis by qRT-PCR revealed high expression of metanephric mesenchymal (Pax2, WT-1, SIX-1, EY...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2912549</comments>
            <pubDate>Thu, 15 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2912549</guid>        </item>
        <item>
            <title>Androgen receptor coactivator p44/Mep50 in breast cancer growth and invasion.</title>
            <link>http://www.medworm.com/index.php?rid=2912548&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19840198%26dopt%3DAbstract</link>
            <description>In this report, we examined the expression and function of p44 in breast cancer. In addition to being an AR coactivator, p44 also functions as an ER coactivator. In contrast to findings in prostate cancer, the expression of p44 shows strong cytoplasmic expression in morphologically normal terminal ductal lobular units, while nuclear p44 is observed in both ductal carcinoma in situ (DCIS) and invasive carcinoma. Further, overexpression of nuclear-localized p44 stimulates proliferation and invasion in MCF7 breast cancer cells in the presence of estrogen and is ERalpha-dependent. These findings strongly suggest that p44 plays a role in mediating the effects of hormones during tumorigenesis in breast.
    PMID: 19840198 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2912548</comments>
            <pubDate>Thu, 15 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2912548</guid>        </item>
        <item>
            <title>Breast Cancer Cell Growth Inhibition by Phenethyl Isothiocyanate is Associated with Downregulation of Estrogen Receptor-alpha36.</title>
            <link>http://www.medworm.com/index.php?rid=2912567&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19840189%26dopt%3DAbstract</link>
            <description>Authors: Kang L, Wang ZY
    The dietary isothiocyanates (ITCs) exhibit strong chemopreventive activities for varieties of neoplasms including breast cancer. However, the molecular mechanisms underlying ITC function in breast cancer cells have not been well established. Here, we found that phenethyl isothiocyanate (PEITC) acted more potently than the &quot;pure&quot; antiestrogen ICI 182,780 to inhibit the growth of estrogen receptor (ER)-positive breast cancer MCF7 and H3396 cells and ER-negative MDA-MB-231 and SK-BR-3 cells. PEITC reduced the steady state levels of ER-alpha and it's novel variant, ER-alpha36 in a dose-and time-dependent manner and inhibited estrogen-induced activation of the MAPK/ERK 1/2 signaling pathway. However, ICI 182,780 that is potent in destabilization of ER-alpha protein,...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2912567</comments>
            <pubDate>Wed, 14 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2912567</guid>        </item>
        <item>
            <title>Targeting and retention of HPV16 E7 to the endoplasmic reticulum enhances immune tumor protection.</title>
            <link>http://www.medworm.com/index.php?rid=2887448&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818090%26dopt%3DAbstract</link>
            <description>Authors: Loera-Arias MJ, Mart&amp;#xED;nez-P&amp;#xE9;rez AG, Barrera-Hern&amp;#xE1;ndez A, Ibarra-Obreg&amp;#xF3;n ER, Gonz&amp;#xE1;lez-Sald&amp;#xED;var G, Mart&amp;#xED;nez-Ortega JI, Rosas-Taraco A, Villanueva-Olivo A, Esparza-Gonz&amp;#xE1;lez SC, Villatoro-Hernandez J, Saucedo-C&amp;#xE1;rdenas O, Montes-de-Oca-Luna R
    ABSTRACT The endoplasmic reticulum (ER) is where the Major Histocompatibility Complex (MHC) Class I molecules are loaded with epitopes to cause an immune cellular response. Most of the protein antigens are degraded in the cytoplasm to amino acids and few epitopes reach the ER. Antigen targeting of this organelle by Calreticulin fusion avoids this degradation and enhances the immune response. We constructed a recombinant adenovirus to express the E7 antigen with an ER-targeting signal peptide (SP) plu...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887448</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887448</guid>        </item>
        <item>
            <title>Effect of irreversibly glycated LDL in human vascular smooth muscle cells: Lipid loading, oxidative and inflammatory stress.</title>
            <link>http://www.medworm.com/index.php?rid=2887447&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818091%26dopt%3DAbstract</link>
            <description>In conclusion, AGE-LDL activates hSMC (increasing CD36, LRP1, RAGE), inducing a pro-oxidant state (activation of NADPHox), lipid accumulation and a pro-inflammatory state (expression of MCP-1). These results may partly explain the contribution of AGE-LDL and hSMC to the accelerated atherosclerosis in diabetes.
    PMID: 19818091 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887447</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887447</guid>        </item>
        <item>
            <title>BiP, an endoplasmic reticulum chaperone, modulates the development of morphine antinociceptive tolerance.</title>
            <link>http://www.medworm.com/index.php?rid=2887446&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818092%26dopt%3DAbstract</link>
            <description>We examined knock-in mice expressing a mutant BiP with the retrieval sequence deleted in order to elucidate physiological processes that are sensitive to BiP functions. We tested the thermal antinociceptive effect of morphine in heterozygous mutant BiP mice in a hot plate test. Paw withdrawal latencies before and after a single administration of morphine were not significantly different between the wild-type and mutant BiP mice. Repeated morphine administration caused the development of morphine tolerance in the wild-type mice. The activation of glycogen synthase kinase 3beta (GSK3beta) was associated with morphine tolerance, since an inhibitor of GSK3beta prevented it. On the other hand, the mutant BiP mice showed less morphine tolerance, and the activation of GSK3beta was suppressed in t...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887446</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887446</guid>        </item>
        <item>
            <title>A link between the accumulation of DNA damage and loss of multipotency of human mesenchymal stromal cells.</title>
            <link>http://www.medworm.com/index.php?rid=2887445&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818093%26dopt%3DAbstract</link>
            <description>Authors: Alves H, Munoz-Najar U, de Wit J, Renard AJ, Hoeijmakers JH, Sedivy JM, van Blitterswijk C, de Boer J
    Abstract Human mesenchymal stromal cells (hMSCs) represent and attractive cell source for clinic applications. Besides being mutipotent, recent clinical trials suggest that they secrete both trophic and immunomodulatory factors, allowing allogenic MSCs to be used in a wider variety of clinical situations. The yield of prospective isolation is however very low, making expansion a required step towards clinical applications. Unfortunately, this leads to a significant decrease in their stemness. To identify the mechanism behind loss of multipotency, hMSCs were expanded until replicative senescence and the concomitant molecular changes were characterized at regular intervals. We o...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887445</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887445</guid>        </item>
        <item>
            <title>Transport characteristics of a novel peptide platform for CNS therapeutics.</title>
            <link>http://www.medworm.com/index.php?rid=2887444&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818094%26dopt%3DAbstract</link>
            <description>Authors: Bertrand Y, Currie JC, Demeule M, R&amp;#xE9;gina A, Ch&amp;#xE9; C, Abulrob A, Fatehi D, Sartelet H, Gabathuler R, Castaigne JP, Stanimirovic D, B&amp;#xE9;liveau R
    ABSTRACT New and effective therapeutics that cross the blood-brain barrier (BBB) are critically needed for treatment of many brain diseases. We characterize here a novel drug development platform that is broadly applicable for the development of new therapeutics with increased brain penetration. The platform is based on the Angiopep-2 peptide, a sequence derived from ligands that bind to low-density lipoprotein receptor-related protein-1 (LRP-1), a receptor expressed on the BBB. Fluorescent imaging studies of a Cy5.5Angiopep-2 conjugate and immunohistochemical studies of injected Angiopep-2 in mice demonstrated efficient tran...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887444</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887444</guid>        </item>
        <item>
            <title>Mechanisms of intermittent hypoxia-induced hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=2887443&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818095%26dopt%3DAbstract</link>
            <description>Authors: Gonz&amp;#xE1;lez Bosc LV, Resta T, Walker B, Kanagy NL
    Exposing rodents to brief episodes of hypoxia mimics the hypoxemia and the cardiovascular and metabolic effects observed in patients with obstructive sleep apnea (OSA), a condition that affects between 5% to 20% of the population. Apart from daytime sleepiness, OSA is associated with a high incidence of systemic and pulmonary hypertension, peripheral vascular disease, stroke and sudden cardiac death. The development of animal models to study sleep apnea has provided convincing evidence that recurrent exposure to intermittent hypoxia has significant vascular and hemodynamic impacts that explain much of the cardiovascular morbidity and mortality observed in patients with sleep apnea. However, the molecular and cellular mechanis...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887443</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887443</guid>        </item>
        <item>
            <title>Platelet microparticle levels: A biomarker of thromboangiitis obliterans (Buerger's disease) exacerbation.</title>
            <link>http://www.medworm.com/index.php?rid=2887442&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818096%26dopt%3DAbstract</link>
            <description>Authors: Darnige L, Helley D, Fischer AM, Emmerich J, Smadja DM, Fiessinger JN
    
    PMID: 19818096 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887442</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887442</guid>        </item>
        <item>
            <title>Epigenetic modulation of the protein kinase a RIIalpha (PRKAR2A) gene by histone deacetylases 1 &amp; 2 in human smooth muscle cells.</title>
            <link>http://www.medworm.com/index.php?rid=2887441&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818097%26dopt%3DAbstract</link>
            <description>Epigenetic modulation of the protein kinase a RIIalpha (PRKAR2A) gene by histone deacetylases 1 &amp; 2 in human smooth muscle cells.
    J Cell Mol Med. 2009 Oct 10;
    Authors: Karolczak-Bayatti M, Loughney AD, Robson SC, Europe-Finner GN
    Abstract Recently we reported that the expression of the PKA regulatory subunit RIIalpha is dynamically regulated in human smooth muscle cells of the uterus. We showed that expression levels of mRNA/protein were substantially increased during pregnancy and decreased upon labour, changes that were mirrored by particulate type II PKA activity. This implied an important role for RIIalpha in maintaining uterine quiescence during pregnancy. Consequently the purpose of the present study was to identify potential mechanisms by which expression of the RIIa...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887441</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887441</guid>        </item>
        <item>
            <title>Zoledronic acid repolarizes tumor-associated macrophages and inhibits mammary carcinogenesis by targeting the mevalonate pathway.</title>
            <link>http://www.medworm.com/index.php?rid=2887440&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818098%26dopt%3DAbstract</link>
            <description>Authors: Coscia M, Quaglino E, Iezzi M, Curcio C, Pantaleoni F, Riganti C, Holen I, M&amp;#xF6;nkk&amp;#xF6;nen H, Boccadoro M, Forni G, Musiani P, Bosia A, Cavallo F, Massaia M
    ABSTRACT It is unknown whether zoledronic acid at clinically relevant doses is active against tumors not located in bone. Mice transgenic for the activated ErbB-2 oncogene were treated with a cumulative number of doses equivalent to that recommended in humans. A significant increase in tumor-free and overall survival was observed in mice treated with zoledronic acid. At clinically compatible concentrations, zoledronic acid modulated the mevalonate pathway and affected protein prenylation in both tumor cells and macrophages. A marked reduction in the number of tumor associated macrophages was paralleled by a significant...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887440</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887440</guid>        </item>
        <item>
            <title>Characterization of the expression of HTm4 (MS4A3), a cell cycle regulator, in human peripheral blood cells and normal and malignant tissues.</title>
            <link>http://www.medworm.com/index.php?rid=2887439&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818099%26dopt%3DAbstract</link>
            <description>Authors: Kutok JL, Yang X, Folkerth R, Adra CN
    Abstract HTm4 (MS4A3) is a member of a family of four-transmembrane proteins designated MS4A. MS4A proteins fulfill diverse functions, acting as cell surface signaling molecules and intracellular adapter proteins. Early reports demonstrated that HTm4 is largely restricted to the hematopoietic lineage, and is involved in cell cycle control, via a regulatory interaction with the KAP phosphatase, Cyclin A and CDK2. Here we describe the expression pattern of HTm4 in peripheral blood cells using gene expression microarray technology, and in normal fetal and adult human tissues, as well as adult human cancers, using tissue microarray technology. Using oligonucleotide microarrays to evaluate HTm4 mRNA, all peripheral blood cell types demonstrated...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887439</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887439</guid>        </item>
        <item>
            <title>Familial and Racial Determinants of Tumor Suppressor Genes Promoter Hypermethylation in Breast Tissues from Healthy Women.</title>
            <link>http://www.medworm.com/index.php?rid=2864503&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19799643%26dopt%3DAbstract</link>
            <description>Conclusions: Gene promoter hypermethylation was commonly found in healthy breast tissues from women without cancer, indicating that these events are frequent and early lesions. Race and family history of cancer increase the likelihood of these early events.
    PMID: 19799643 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2864503</comments>
            <pubDate>Fri, 02 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2864503</guid>        </item>
        <item>
            <title>Hematopoietic stem cells in spleen have distinct differentiative potential for antigen presenting cells.</title>
            <link>http://www.medworm.com/index.php?rid=2864502&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19799644%26dopt%3DAbstract</link>
            <description>In this study, neonatal spleen showed multilineage hematopoietic reconstitution in mouse chimeras, rather than specific or restricted ability to differentiate into L-DC. However, the representation of individual APC subsets was found to be unequal in chimeras partially reconstituted with donor cells, such that more donor-derived progeny were seen for L-DC than for myeloid and cDC subsets. The ability of HSC in spleen to develop into L-DC was indicated by a strong bias in the subset size of these cells over other splenic APC subsets. This type of evidence supports a model whereby spleen represents an important site for hematopoiesis of this distinct DC subset. The conditions under which hematopoiesis of L-DC occurs in spleen, or the progenitors involved, will require further investigation.
...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2864502</comments>
            <pubDate>Fri, 02 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2864502</guid>        </item>
        <item>
            <title>Functional characterization of the progestagen-associated endometrial protein gene in human melanoma.</title>
            <link>http://www.medworm.com/index.php?rid=2864501&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19799645%26dopt%3DAbstract</link>
            <description>Authors: Ren S, Liu S, Howell PM, Zhang G, Pannell L, Samant R, Shevde-Samant L, Tucker JA, Fodstad O, Riker AI
    Abstract Utilizing gene microarray profiling of melanoma samples, we have recently identified a novel gene over-expressed in both thick primary and metastatic melanomas. This gene, progestagen-associated endometrial protein (PAEP), has never before been implicated in the oncogenic processes of melanoma, with its true function in oncogenesis and tumor progression relatively unknown. Over-expression of the PAEP gene in freshly procured thick primary and metastatic melanoma samples (58%) and daughter cell lines (77%) is confirmed by quantitative RT-PCR, immunohistochemisty, Western blotting and mass spectrometric analysis. We hypothesize that PAEP gene over-expression is involve...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2864501</comments>
            <pubDate>Fri, 02 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2864501</guid>        </item>
        <item>
            <title>Co-ordinated autophagy with resveratrol and gamma-tocotrienol confers synergetic cardioprotection.</title>
            <link>http://www.medworm.com/index.php?rid=2864499&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19799646%26dopt%3DAbstract</link>
            <description>This study compared two dietary phytochemicals, grape-derived resveratrol and palm oil-derived gamma-tocotrienol, either alone or in combination, on the contribution of autophagy in cardioprotection during ischemia and reperfusion. Sprague Dawley rats weighing between 250-300 gm were randomly assigned to one of the following groups: vehicle, ischemia/reperfusion (I/R), resveratrol+I/R, gamma-tocotrienol+I/R, resveratrol+gamma-tocotrienol+I/R. For resveratrol treatments, the rats were gavaged with resveratrol [2.5 mg/kg] for 15 days while for gamma-tocotrienol experiments the rats were gavaged with gamma-tocotrienol [0.3 mg/kg] for 30 days. For the combined resveratrol +gamma-tocotrienol experiments, the rats were gavaged with gamma-tocotrienol for 15 days, and then gavaging continued with ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2864499</comments>
            <pubDate>Fri, 02 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2864499</guid>        </item>
        <item>
            <title>Mesenchymal stem cells modified to express lentivirus-TNFalpha-Tumstatin inhibit the growth of prostate cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2864498&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19799647%26dopt%3DAbstract</link>
            <description>Authors: Zhang X, Xu W, Qian H, Zhu W, Zhang R
    Abstract Mesenchymal stem cells (MSCs) are a potential novel delivery system for cell-based gene therapies. Although TNFalpha has been shown to have antitumor activity, its use for therapy is limited by its systemic toxicity. For the present study, we designed lentivirus-mediated signal peptide TNFalpha-Tumstatin(45-132)-expressing mesenchymal stem cells (SPTT-MSCs) as a novel anticancer approach. We evaluated the effects of this approach on human prostate cancer cells (PC3 and LNCaP) by co-culturing them with either SPTT-MSCs or supernatants from their culture medium in vitro. The antitumor effects and possible mechanisms of action of SPTT-MSCs were then determined in PC3 cells in vivo. The results showed that efficient TNFalpha-Tumstatin...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2864498</comments>
            <pubDate>Fri, 02 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2864498</guid>        </item>
        <item>
            <title>Translational up-regulation of Aurora-A in EGFR-overexpressed cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2864497&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19799648%26dopt%3DAbstract</link>
            <description>In this study, we demonstrated that EGF signaling increased the Aurora-A protein expression in EGFR-overexpressed colorectal cancer cell lines via increasing the translational efficiency. In addition, the overexpression of EGFR was also associated with higher expression of Aurora-A in clinical colorectal samples. Activation of the PI3K/Akt/mTOR and MEK/ERK pathways mediated the effect of EGF induced translational up-regulation. Besides, only the splicing variants containing exon 2 of Aurora-A mRNA showed increased interaction with the translational complex to synthesize Aurora-A protein under EGF stimulus. Besides, the exon 2 containing splicing variants were the major Aurora-A splicing form expressed in human colorectal cancers. Taken together, our results propose a novel regulatory mecha...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2864497</comments>
            <pubDate>Fri, 02 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2864497</guid>        </item>
        <item>
            <title>The actin filament cross-linker L-plastin confers resistance to TNF-alpha in MCF-7 breast cancer cells in a phosphorylation-dependent manner.</title>
            <link>http://www.medworm.com/index.php?rid=2864496&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19799649%26dopt%3DAbstract</link>
            <description>Authors: Janji B, Vallar L, Al-Tanoury Z, Bernardin F, Vetter G, Schaffner-Reckinger E, Berchem G, Friederich E, Chouaib S
    Abstract We used a TNF-resistant breast adenocarcinoma MCF-7 cell line to investigate the involvement of the actin cytoskeleton in the mechanism of cell resistance to this cytokine. We found that TNF-resistance correlates with the loss of cell epithelial properties and the gain of a mesenchymal phenotype, reminiscent of an epithelial-to-mesenchymal transition (EMT). Morphological changes were associated with a profound reorganization of the actin cytoskeleton and with a change in the repertoire of expressed actin cytoskeleton genes and EMT markers, as revealed by DNA microarray-based expression profiling. L-plastin, an F-actin cross-linking and stabilizing protein,...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2864496</comments>
            <pubDate>Fri, 02 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2864496</guid>        </item>
        <item>
            <title>Aberrant human leukocyte antigen-G expression and its clinical relevance in hepatocellular carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=2864495&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19799650%26dopt%3DAbstract</link>
            <description>Authors: Lin A, Chen HX, Zhu CC, Zhang X, Xu HH, Zhang JG, Wang Q, Zhou WJ, Yan WH
    Abstract The clinical relevance of human leukocyte antigen-G (HLA-G) has been postulated in malignancies. Hepatocellular carcinoma (HCC) is a major contributor to cancer incidence and mortality worldwide; however, potential roles of HLA-G in HCC remain unknown. In the current study, HLA-G expression in 219 primary HCC lesions and their adjacent non-tumorous samples was analyzed with immuno- histochemistry. Correlations between HLA-G expression and various clinical parameters were evaluated. Meanwhile, functional analysis of transfected cell surface HLA-G expression on NK cell cytolysis was performed in vitro. HLA-G expression was observed in 50.2% (110/219) of primary HCC lesions, and undetectable in cor...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2864495</comments>
            <pubDate>Fri, 02 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2864495</guid>        </item>
        <item>
            <title>Neurotrophic factors promote cholinergic differentiation in human embryonic stem cell-derived neurons.</title>
            <link>http://www.medworm.com/index.php?rid=2864494&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19799651%26dopt%3DAbstract</link>
            <description>Authors: Nilbratt M, Porras O, Marutle A, Hovatta O, Nordberg A
    ABSTRACT Cholinergic neurotransmission is essential for many important functions in the brain, including cognitive mechanisms. Here we demonstrate that human embryonic stem (hES) cells differentiate into a population of neuronal cells that express the cholinergic enzyme choline acetyltransferase (ChAT) and homeobox proteins specifying neuronal progenitors of ventral telencephalic lineage. These differentiated cells express transcripts for cholinergic alpha3, alpha4 and alpha7 nicotinic acetylcholine receptor (nAChR) subunits and for M1, M2 and M3 muscarinic acetylcholine receptor (mAChR) subtypes. Stimulation with brain-derived neurotrophic factor, neurotrophin-3, ciliary neurotrophic factor and nerve growth factor increas...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2864494</comments>
            <pubDate>Fri, 02 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2864494</guid>        </item>
        <item>
            <title>Stem cells for stress urinary incontinence: the adipose promise.</title>
            <link>http://www.medworm.com/index.php?rid=2864493&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19799652%26dopt%3DAbstract</link>
            <description>Authors: Roche R, Festy F, Fritel X
    Abstract Stress urinary incontinence (SUI), the most common type of incontinence in women, is a frequent and costly ailment responsible for an alteration to the quality of life. While medical treatment give some rather deceiving results, surgical techniques that include colposuspension or tension-free vaginal tape, employed in cases of urethral support defect, give a 5 year cure rate of more than 80%. However, these techniques could lead to complications or recurrence of symptoms. Recently, the initiation of urethral cell therapy has been undertaken by doctors and researchers. One principal source of autologous adult stem cells is generally used: muscle precursor cells (MPCs) which are the progenitors of skeletal muscle cells. Recently, a few researc...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2864493</comments>
            <pubDate>Fri, 02 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2864493</guid>        </item>
        <item>
            <title>Molecular risk stratification in advanced heart failure patients.</title>
            <link>http://www.medworm.com/index.php?rid=2856094&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19793385%26dopt%3DAbstract</link>
            <description>Conclusions: Gene expression profiling has the potential to reproducibly detect heart failure patients with highest heart failure severity with high sensitivity and specificity. In addition, not only LV but also RV samples could be used for molecular risk stratification with similar predictive power.
    PMID: 19793385 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2856094</comments>
            <pubDate>Tue, 29 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2856094</guid>        </item>
        <item>
            <title>Enhanced neointimal hyperplasia and carotid artery remodeling in sequestosome 1 deficient mice.</title>
            <link>http://www.medworm.com/index.php?rid=2847270&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19780870%26dopt%3DAbstract</link>
            <description>Authors: Sugimoto R, Warabi E, Katayanagi S, Sakai S, Uwayama J, Yanagawa T, Watanabe A, Harada H, Kitamura K, Noguchi N, Yoshida H, Siow RC, Mann GE, Ishii T
    Abstract Deficiency in the signal adaptor protein sequestosome 1 (SQSTM1/A170/p62) in mice exhibits mature-onset obesity accompanied by insulin and leptin resistance. We previously established that redox sensitive transcription factor Nrf2 upregulates SQSTM1 expression in response to atherogenic stimuli or laminar shear stress in vascular cells, and here examine role of SQSTM1 in neointimal hyperplasia and vascular remodeling in vivo following carotid artery ligation. Neointimal hyperplasia was markedly enhanced at ligation sites after 3 weeks in SQSTM1(-/-) compared with wild type mice. The intimal area and stenotic ratio were r...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847270</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847270</guid>        </item>
        <item>
            <title>Recruitment of endogenous bone marrow mesenchymal stem cells towards injured liver.</title>
            <link>http://www.medworm.com/index.php?rid=2847269&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19780871%26dopt%3DAbstract</link>
            <description>Authors: Chen Y, Xiang LX, Shao JZ, Pan RL, Wang YX, Dong XJ, Zhang GR
    Abstract Background Recent studies suggest that mesenchymal stem cells (MSCs) possess a greater differentiation potential than once thought and that they have the capacity to regenerate damaged tissues/organs. However, the evidence is insufficient, and the mechanism governing the recruitment and homing of MSCs to these injured sites is not well understood. Methods We first examined the MSCs circulating in peripheral blood and then performed chemotaxis, wound-healing, and tubule-formation assays to investigate the migration capability of mouse bone marrow MSCs (mBM-MSCs) in response to liver-injury signals. In addition, BM-MSCs from donor EGFP-transgenic male mice were transplanted into liver-injured co-isogenic fema...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847269</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847269</guid>        </item>
        <item>
            <title>Ovarian Cancer Cytoreduction Induces Changes in T Cell Population Subsets Reducing Immunosuppression.</title>
            <link>http://www.medworm.com/index.php?rid=2847268&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19780872%26dopt%3DAbstract</link>
            <description>In conclusion, we demonstrate in ovarian cancer that primary debulking is associated with a reduction of circulating T(reg) and an increase in CD8 T cell function. Debulking plays a beneficial systemic effect by reverting immunosuppression and restoring immunological fitness.
    PMID: 19780872 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847268</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847268</guid>        </item>
        <item>
            <title>Calcineurin A-beta is required for hypertrophy but not matrix expansion in the diabetic kidney.</title>
            <link>http://www.medworm.com/index.php?rid=2834986&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19778355%26dopt%3DAbstract</link>
            <description>In conclusion, loss of the beta isoform of calcineurin is sufficient to reproduce beneficial aspects of cyclosporine on diabetic renal hypertrophy but not matrix expansion. Therefore, while multiple signals appear to regulate matrix, calcineurin beta appears to be a central mechanism involved in organ hypertrophy.
    PMID: 19778355 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2834986</comments>
            <pubDate>Tue, 22 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2834986</guid>        </item>
        <item>
            <title>Anti-CD44 induces apoptosis in T lymphoma via mitochondrial depolarization.</title>
            <link>http://www.medworm.com/index.php?rid=2824509&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19765170%26dopt%3DAbstract</link>
            <description>Authors: Rajasagi M, von Au A, Singh R, Hartmann N, Z&amp;#xF6;ller M, Marhaba R
    Abstract A blockade of CD44 can interfere with hematopoietic and leukemic stem cell homing, the latter being considered as a therapeutic option in hematological malignancies. We here aimed to explore the molecular mechanism underlying the therapeutic efficacy of anti-CD44. We noted that in irradiated mice reconstituted with a bone marrow cell transplant, anti-CD44 exerts a stronger effect on hematopoietic reconstitution than on T lymphoma (EL4) growth. Nonetheless, in the non-reconstituted mouse anti-CD44 suffices for a prolonged survival of EL4-bearing mice, where anti-CD44-prohibited homing actively drives EL4 cells into apoptosis. In vitro, a CD44 occupancy results in a 2-4-fold increase in apoptotic EL4 ce...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2824509</comments>
            <pubDate>Thu, 17 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2824509</guid>        </item>
        <item>
            <title>Bone Marrow-Derived Cells in the Tumor Microenvironment Contain Cells with Primitive Hematopoietic Phenotype.</title>
            <link>http://www.medworm.com/index.php?rid=2824508&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19765171%26dopt%3DAbstract</link>
            <description>Authors: Deak E, G&amp;#xF6;ttig S, R&amp;#xFC;ster B, Paunescu V, Seifried E, Gille J, Henschler R
    Abstract Infiltration of bone marrow-derived cells is part of the angiogenic switch required for uncontrolled tumor growth. However, the nature of the tumor-infiltrating cells from bone marrow has not been fully elucidated. To investigate the phenotype of bone marrow-derived cells within a tumor, we employed the Lewis Lung Carcinoma (LLC) murine tumor model. We followed bone marrow-derivation of tumor-infiltrating cells through transplantation of CD45.2 bone marrow cells into pre-irradiated CD45.1 mice. We found robust CD45.2 donor type chimerism in bone marrow and blood of CD45.1 recipient tumor bearing mice. Flow cytometric analysis of LLC tumors showed, in addition to previously described pro...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2824508</comments>
            <pubDate>Thu, 17 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2824508</guid>        </item>
        <item>
            <title>Affinity pulldown of gamma-secretase and associated proteins from human and rat brain.</title>
            <link>http://www.medworm.com/index.php?rid=2804905&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19754663%26dopt%3DAbstract</link>
            <description>Authors: Teranishi Y, Hur JY, Welander H, Fr&amp;#xE5;nberg J, Aoki M, Winblad B, Frykman S, Tjernberg LO
    Abstract gamma-Secretase is a transmembrane protease complex responsible for the processing of a multitude of type 1 transmembrane proteins, including APP and Notch. A functional complex is dependent on the assembly of four proteins; presenilin (PS), nicastrin, Aph-1 and Pen-2. Little is known about how the substrates are selected by gamma-secretase, but it has been suggested that gamma-secretase associated proteins (GSAPs) could be of importance. For instance, it was recently reported from studies in cell lines that TMP21, a transmembrane protein involved in trafficking, binds to gamma-secretase and regulates the processing of APP-derived substrates without affecting Notch cleavage. H...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2804905</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2804905</guid>        </item>
        <item>
            <title>Genetic Characterisation of Breast Cancer and Implications for Clinical Management.</title>
            <link>http://www.medworm.com/index.php?rid=2804904&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19754664%26dopt%3DAbstract</link>
            <description>Authors: Geyer FC, Lopez-Garcia MA, Lambros MB, Reis-Filho JS
    Abstract Breast cancer is a genetic disease caused by the accumulation of mutations in neoplastic cells. In the last few years, high-throughput microarray-based molecular analysis has provided increasingly more coherent information about the genetic aberrations in breast cancer. New biomarkers and molecular techniques are slowly becoming part of the diagnostic and prognostic armamentarium available for pathologists and oncologists to tailor the therapy for breast cancer patients. In this review we will focus on the contribution of breast cancer somatic genetics to our understanding of breast cancer biology and its impact on breast cancer patient management.
    PMID: 19754664 [PubMed - as supplied by publisher] (Source: J Ce...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2804904</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2804904</guid>        </item>
        <item>
            <title>Chromosomal instability correlates with poor outcome in patients with myelodysplastic syndromes irrespectively of the cytogenetic risk group.</title>
            <link>http://www.medworm.com/index.php?rid=2804903&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19754665%26dopt%3DAbstract</link>
            <description>In conclusion, elevated CIN levels may be valuable as an early indicator of poor prognosis in MDS, hence corroborating the concept of CIN as a driving force in tumor progression.
    PMID: 19754665 [PubMed - as supplied by publisher] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2804903</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2804903</guid>        </item>
        <item>
            <title>TNF-alpha mediated signal transduction pathway is a major determinant of apoptosis in dilated cardiomyopathy.</title>
            <link>http://www.medworm.com/index.php?rid=2804902&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19754666%26dopt%3DAbstract</link>
            <description>This study examined the hypothesis that cardiac dysfunction and apoptosis in the cardiomyopathic hamsters were associated with tumor necrosis factor-alpha (TNF-alpha)-mediated signaling pathway involving the activation of some pro-apoptotic proteins and/or deactivation of some antiapoptotic proteins. Echocardiographic assessment of 31 week old hamsters indicated an increase in the internal dimension of the left ventricle as well as decreases in the ejection fraction, fractional shortening, and cardiac output without any evidence of cardiac hypertrophy. Increased level of TNF-alpha and apoptosis in cardiomyopathic hearts were accompanied by increased protein content for protein kinase C (PKC) -alpha and -epsilon isozymes as well as caspases 3 and 9. Phosphorylated protein content for p38 MA...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2804902</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2804902</guid>        </item>
        <item>
            <title>Monocyte Transplantation for Neural and Cardiovascular Ischemia Repair.</title>
            <link>http://www.medworm.com/index.php?rid=2804901&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19754667%26dopt%3DAbstract</link>
            <description>Authors: Sanberg PR, Park DH, Kuzmin-Nichols N, Cruz E, Hossne NA, Buffolo E, Willing AE
    Abstract Neovascularization is an integral process of inflammatory reactions and subsequent repair cascades in tissue injury. Monocytes/macrophages play a key role in the inflammatory process including angiogenesis as well as the defense mechanisms by exerting microbicidal and immunomodulatory activity. Current studies have demonstrated that recruited monocytes/macrophages aid in regulating angiogenesis in ischemic tissue, tumors, and chronic inflammation. In terms of neovascularization followed by tissue regeneration, monocytes/macrophages should be highly attractive for cell-based therapy compared to any other stem cells due to their considerable advantages: non-oncogenic, non-teratogenic, multip...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2804901</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2804901</guid>        </item>
        <item>
            <title>Imatinib inhibits vascular smooth muscle proteoglycan synthesis and reduces ldl binding in vitro and aortic lipid deposition in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=2804900&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19754668%26dopt%3DAbstract</link>
            <description>IMATINIB INHIBITS VASCULAR SMOOTH MUSCLE PROTEOGLYCAN SYNTHESIS AND REDUCES LDL BINDING IN VITRO AND AORTIC LIPID DEPOSITION IN VIVO.
    J Cell Mol Med. 2009 Sep 14;
    Authors: Ballinger ML, Osman N, Hashimura K, de Haan JB, Jandeleit-Dahm K, Allen T, Tannock LR, Rutledge JC, Little PJ
    ABSTRACT The &quot;response to retention&quot; hypothesis of atherogenesis proposes that proteoglycans bind and retain low density lipoproteins (LDL) in the vessel wall. Platelet derived growth factor (PDGF) is strongly implicated in atherosclerosis and stimulates proteoglycan synthesis. Here we investigated the action of the PDGF receptor inhibitor imatinib on PDGF-mediated proteoglycan biosynthesis in vitro, lipid deposition in the aortic wall in vivo and the carotid artery ex vivo. In human vSMCs, imatinib i...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2804900</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2804900</guid>        </item>
        <item>
            <title>Helicobacter pylori urease activates blood platelets through a lipoxygenase-mediated pathway.</title>
            <link>http://www.medworm.com/index.php?rid=2804899&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19754669%26dopt%3DAbstract</link>
            <description>Authors: Wassermann GE, Olivera-Severo D, Uberti AF, Carlini CR
    Abstract The bacterium Helicobacter pylori causes peptic ulcers and gastric cancer in humans by mechanisms yet not fully understood. H. pylori produces urease which neutralizes the acidic medium permitting its survival in the stomach. We have previously shown that ureases from jackbean, soybean or Bacillus pasteurii induce blood platelet aggregation independently of their enzyme activity by a pathway requiring platelet secretion, activation of calcium channels and lipoxygenase-derived eicosanoids. We investigated whether H. pylori urease displays platelet-activating properties and defined biochemical pathways involved in this phenomenon. For that the effects of purified recombinant H. pylori (HPU) added to rabbit platelets...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2804899</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2804899</guid>        </item>
        <item>
            <title>Role of AKT-Glycogen Synthase Kinase axis in Monocyte Activation in Humans with and without Type 2 Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=2804898&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19754670%26dopt%3DAbstract</link>
            <description>Authors: Nandy D, Asmann YW, Mukhopadhyay D, Basu A
    Monocyte activation by chemokines is a vital trigger for initiation of atherosclerotic process. Circulating levels of Platelet Activating Factor (PAF), a recognized chemokine, is known to be increased in type 2 diabetes that is linked to accelerated atherosclerosis. To explore the molecular basis we examined the signaling pathways involved in PAF induced monocyte activation. PAF increased migration in monocytes obtained from THP-1 cells, nondiabetic and diabetic subjects that was blocked by AKT inhibition. It did so by phosphorylation of GSK-3betaS(9) which was completely blocked by AKT inhibition. Additionally, PAF induced GSK-3beta phosphorylation was linked to Rac-1 activation and Rho-A inactivation leading to migration. Paradoxica...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2804898</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2804898</guid>        </item>
        <item>
            <title>Resistin competes with lipopolysaccharide for binding to Toll-like receptor 4.</title>
            <link>http://www.medworm.com/index.php?rid=2804897&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19754671%26dopt%3DAbstract</link>
            <description>Authors: Tarkowski A, Bjersing J, Shestakov A, Bokarewa MI
    Abstract. Toll-like receptors (TLRs) are a family of cellular structures activated by recognition of pathogen associated molecular sequences. The activation of TLRs triggers a variety of intracellular mechanisms aiming to protect the host from the invading microorganisms. Lipopolysaccharide (LPS) is the main ligand for TLR4. Here we show that resistin, a cystein-rich protein believed to regulate carbohydrate metabolism, competes with LPS for binding to TLR4. Binding of recombinant resistin to human myeloid and epithelial cells was assessed by flow cytometry and its co-precipitation with TLR4 was demonstrated. Antibodies against TLR4 abolished resistin binding to human leukocytes and cytokine production by PBMC in response to re...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2804897</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2804897</guid>        </item>
        <item>
            <title>Acceleration of muscle regeneration by local injection of muscle-specific microRNAs in rat skeletal muscle injury model.</title>
            <link>http://www.medworm.com/index.php?rid=2804896&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19754672%26dopt%3DAbstract</link>
            <description>Authors: Nakasa T, Ishikawa M, Shi M, Shibuya H, Adachi N, Ochi M
    Abstract MicroRNA (miRNA)s are a class of non-coding RNAs that regulate gene expression post-transcriptionally. Muscle-specific miRNA, miRNA (miR)-1, miR-133 and miR-206 play a crucial role in the regulation of muscle development and homeostasis. Muscle injuries are a common muscloskeletal disorder, and the most effective treatment has not been established yet. The purpose of this study was to demonstrate that a local injection of double-stranded (ds) miR-1, miR-133 and 206 can accelerate muscle regeneration in a rat skeletal muscle injury model. After the laceration of the rat tibialis anterior muscle, ds miR-1, 133 and 206 mixture mediated atelocollagen was injected into the injured site. The control group was injected...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2804896</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2804896</guid>        </item>
        <item>
            <title>Chemical and molecular mechanisms of antioxidants: Experimental approaches and model systems.</title>
            <link>http://www.medworm.com/index.php?rid=2804895&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19754673%26dopt%3DAbstract</link>
            <description>Authors: L&amp;#xFC; JM, Lin PH, Yao Q, Chen C
    ABSTRACT Free radicals derived from oxygen, nitrogen and sulfur molecules in the biological system are highly active to react with other molecules due to their unpaired electrons. These radicals are important part of groups of molecules called reactive oxygen/nitrogen species (ROS/RNS), which are produced during cellular metabolism and functional activities and have important roles in cell signaling, apoptosis, gene expression and ion transportation. However, excessive ROS attack bases in nucleic acids, amino acid side chains in proteins and double bonds in unsaturated fatty acids, and cause oxidative stress, which can damage DNA, RNA proteins and lipids resulting in an increased risk for cardiovascular disease, cancer, autism, and other disea...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2804895</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2804895</guid>        </item>
        <item>
            <title>Microselection - Affinity Selecting Antibodies against a Single Rare Cell in a Heterogeneous Population.</title>
            <link>http://www.medworm.com/index.php?rid=2804894&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19754674%26dopt%3DAbstract</link>
            <description>Authors: S&amp;#xF8;rensen MD, Agerholm IE, Christensen B, K&amp;#xF8;lvraa S, Kristensen P
    Rare cells not normally present in the peripheral bloodstream, such as circulating tumor cells, have potential applications for development of non-invasive methods for diagnostics or follow up. Obtaining these cells however require some means of discrimination, achievable by cell type specific antibodies. Here we have generated a microselection method allowing antibody selection, by phage display, targeting a single cell in a heterogeneous population. One K562 cell (female origin) was positioned on glass-slide among millions of lymphocytes from male donor, identifying the K562 cell by FISH (XX). Several single cell selections were performed on such individual slides. The phage particles bound to the tar...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
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            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
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            <title>Structure of membrane-associated neuronal SNARE complex: Implication in neurotransmitter release.</title>
            <link>http://www.medworm.com/index.php?rid=2782557&amp;cid=s_30454_67_f&amp;fid=30454&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19737333%26dopt%3DAbstract</link>
            <description>Authors: Cho WJ, Shin L, Ren G, Jena BP
    Abstract To enable fusion between biological membranes, t-SNAREs and v-SNARE present in opposing bilayers, interact and assemble in a circular configuration forming ring-complexes, which establish continuity between the opposing membranes, in presence of calcium ions. The size of a t-/v-SNARE ring complex is dictated by the curvature of the opposing membrane. Hence smaller vesicles form small SNARE-ring complexes, as opposed to large vesicles. Neuronal communication depends on the fusion of 40-50 nm in diameter membrane-bound synaptic vesicles containing neurotransmitters at the nerve terminal. At the presynaptic membrane, 12-17 nm in diameter cup-shaped neuronal porosomes are present where synaptic vesicles transiently dock and fuse. Studies dem...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
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            <pubDate>Mon, 07 Sep 2009 23:00:00 +0100</pubDate>
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