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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>Mon, 06 Feb 2012 16:52:06 +0100</lastBuildDate>
        <item>
            <title>Analysis of molecular mechanisms and anti-tumoral effects of zoledronic acid in breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5619436&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%3D22260151%26dopt%3DAbstract</link>
            <description>Authors: Insalaco L, Gaudio FD, Terrasi M, Amodeo V, Caruso S, Corsini LR, Fanale D, Margarese N, Santini D, Bazan V, Russo A
    Abstract
    Zoledronic acid (ZOL) is the most potent nitrogen-containing bisphosphonate (N-BPs) that strongly binds to bone mineral and acts as a powerful inhibitor of bone resorption, already clinically available for the treatment of patients with osteolytic metastases.Recent data also suggest that ZOL, used in breast cancer, may provide more than just supportive care modifying the course of the disease, though the possible molecular mechanism of action is still unclear. Since breast cancer is one of the primary tumors with high propensity to metastasize to the bone, we investigated, for the first time, differential gene expression profile on MCF-7 breast canc...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5619436</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Amniotic Membrane-Derived Cells Inhibit Proliferation of Cancer Cell Lines by Inducing Cell Cycle Arrest.</title>
            <link>http://www.medworm.com/index.php?rid=5619435&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%3D22260183%26dopt%3DAbstract</link>
            <description>Authors: Magatti M, De Munari S, Vertua E, Parolini O
    Abstract
    Cells derived from the amniotic fetal membrane of human term placenta have drawn particular attention mainly for their plasticity and immunological properties, which render them interesting for stem cell research and cell-based therapeutic applications. In particular, we have previously demonstrated that amniotic mesenchymal tissue cells (AMTC) inhibit lymphocyte proliferation in vitro and suppress the generation and maturation of monocyte-derived dendritic cells. Here we show that AMTC also significantly reduce the proliferation of cancer cell lines of hematopoietic and non-hematopoietic origin, in both cell-cell contact and transwell co-cultures, therefore suggesting the involvement of yet unknown inhibitory soluble f...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5619435</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5619435</guid>        </item>
        <item>
            <title>Glucose can promote a glucocorticoid resistance state.</title>
            <link>http://www.medworm.com/index.php?rid=5619434&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%3D22260204%26dopt%3DAbstract</link>
            <description>Authors: Kassi E, Papavassiliou AG
    Abstract
    It has been shown that ingestion of glucose, amino acids, protein or mixed meals tends to increase serum and salivary cortisol concentrations in healthy adults. Recently, it has been demonstrated that morning glucose ingestion stimulates pulsatile cortisol and adrenocorticotropic hormone (ACTH) secretion, thus elevating their mean concentrations. In light of the above, a question arises: could the frequent food -and specifically glucose- consumption lead to hypercortisolism with possible clinical implications? And can the human body, under normal conditions raise defense mechanisms against the transient hypercortisolism caused by the frequent glucose consumption? Studies have revealed novel mechanisms which are implicated in the glucocort...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5619434</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5619434</guid>        </item>
        <item>
            <title>Ethanol Increases Phosphate-Mediated Mineralization and Osteoblastic Transformation of Vascular Smooth Muscle Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5619433&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%3D22260235%26dopt%3DAbstract</link>
            <description>Authors: Oros M, Zavaczki E, Vadasz C, Jeney V, Tosaki A, Lekli I, Balla G, Nagy L, Balla J
    Abstract
    Vascular calcification is implicated in the pathogenesis of atherosclerosis, diabetes, and chronic kidney disease. Human vascular smooth muscle cells (HSMCs) undergo mineralization in response to elevated levels of inorganic phosphate (Pi) in an active and well-regulated process. This process involves increased activity of alkaline phosphatase and increased expression of core binding factor α-1 (CBF-α1), a bone-specific transcription factor, with the subsequent induction of osteocalcin. It has been shown that heavy alcohol consumption is associated with greater calcification in coronary arteries. The goal of our study was to examine whether ethanol alters mineralization of HSMCs p...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5619433</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5619433</guid>        </item>
        <item>
            <title>Nano-regenerative medicine towards clinical outcome of stem cell and tissue engineering in humans.</title>
            <link>http://www.medworm.com/index.php?rid=5619432&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%3D22260258%26dopt%3DAbstract</link>
            <description>Authors: Arora P, Sindhu A, Dilbaghi N, Chaudhury A, Rajakumar G, Rahuman AA
    Abstract
    Nanotechnology is a fast growing area of research that aims to create nanomaterials or nanostructures development in stem cell and tissue based therapies. Concepts and discoveries from the fields of bio nano research provide exciting opportunities of using stem cells for regeneration of tissues and organs. The application of nanotechnology to stem cell biology would be able to address the challenges of disease therapeutics. This review covers the potential of nanotechnology approaches towards regenerative medicine. Furthermore, it focuses on current aspects of stem and tissue cell engineering. The magnetic nanoparticles-based applications in stem cell research open new frontiers in cell and tissue...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5619432</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5619432</guid>        </item>
        <item>
            <title>Human cardiomyocyte progenitor cells: a short history of nearly everything.</title>
            <link>http://www.medworm.com/index.php?rid=5619431&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%3D22260290%26dopt%3DAbstract</link>
            <description>Authors: van Vliet P, Goumans MJ, Doevendans PA, Sluijter JP
    PMID: 22260290 [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=5619431</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5619431</guid>        </item>
        <item>
            <title>MicroRNA-24 Regulates Cardiac Fibrosis after Myocardial Infarction.</title>
            <link>http://www.medworm.com/index.php?rid=5619430&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%3D22260784%26dopt%3DAbstract</link>
            <description>Authors: Wang J, Huang W, Xu R, Nie Y, Cao X, Meng J, Xu X, Hu S, Zheng Z
    Abstract
    Cardiac fibrosis after myocardial infarction (MI) has been identified as a key factor in the development of heart failure. Although dysregulation of miRNAs is involved in various pathophysiologic processes in the heart, the role of miRNA in fibrosis regulation after MI is unclear. Previously we observed the correlation between fibrosis and the miR-24 expression in hypertrophic hearts, here we assessed how miR-24 regulates fibrosis after MI. Using qRT-PCR, we showed that microRNA-24 was down-regulated in the MI heart, the change in miR-24 expression was closely related to extracellular matrix (ECM) remodeling. In vivo, miR-24 could improve heart function and attenuate fibrosis in the infarct border zo...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5619430</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5619430</guid>        </item>
        <item>
            <title>Cardiac Differentiation of Human Pluripotent Stem Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5619438&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%3D22248065%26dopt%3DAbstract</link>
            <description>Authors: Jiang J, Han P, Zhang Q, Zhao J, Ma Y
    Abstract
    Due to the extremely limited proliferative capacity of adult cardiomyocytes, human embryonic (pluripotent) stem cell derived cardiomyocytes (hESC-CMs) are currently almost the only reliable source of human heart cells which are suited to large-scale production. These cells have the potential for wide-scale application in drug discovery, heart disease research and cell-based heart repair. Embryonic atrial-, ventricular- and nodal-like cardiomyocytes can be obtained from differentiated human embryonic stem cells (hESCs). In recent years, several highly-efficient cardiac differentiation protocols have been developed. Significant progress has also been made on understanding cardiac subtype specification, which is the key to reduci...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5619438</comments>
            <pubDate>Mon, 16 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5619438</guid>        </item>
        <item>
            <title>The non-anticoagulant heparin-like K5 polysaccharide derivative K5-N,OSepi attenuates myocardial ischemia/reperfusion injury.</title>
            <link>http://www.medworm.com/index.php?rid=5619437&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%3D22248092%26dopt%3DAbstract</link>
            <description>In conclusion, we demonstrate that the cardioprotective effect of the non-anticoagulant K5 derivative K5-N,OSepi is secondary to a combination of anti-apoptotic and anti-inflammatory effects. © 2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
    PMID: 22248092 [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=5619437</comments>
            <pubDate>Mon, 16 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5619437</guid>        </item>
        <item>
            <title>Platelet derived growth factor receptor α-positive cells in the tunica muscularis of human colon.</title>
            <link>http://www.medworm.com/index.php?rid=5577382&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%3D22225616%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: Our data suggest that PDGFRα(+) cells may have an important role in transducing inputs from enteric motor neurons. This study identifies reagents and techniques that will allow investigation of this class of interstitial cells and help to develop an understanding of the role of PDGFRα(+) cells in the human GI tract in health and disease. © 2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
    PMID: 22225616 [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=5577382</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577382</guid>        </item>
        <item>
            <title>Dose-Dependent Functional Benefit of Human Cardiosphere Transplantation in Mice with Acute Myocardial Infarction.</title>
            <link>http://www.medworm.com/index.php?rid=5577381&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%3D22225626%26dopt%3DAbstract</link>
            <description>Authors: Shen D, Cheng K, Marbán E
    Abstract
    Despite mounting preclinical and clinical evidence of the beneficial effects of cell-based therapy, optimal cell dosing and delivery approaches have not been identified. Cardiospheres are self-assembling 3D microtissues formed by cardiac stem cells and supporting cell types. The ability of cardiospheres to augment cardiac function has been demonstrated in animal models of ischemic cardiomyopathy. In the present study, we studied the dose-dependence of the benefits of human cardiospheres, delivered via intramyocardial injection, upon cardiac function and ventricular remodeling in SCID mice with acute myocardial infarction. Four doses of cardiospheres were used: 1x10(4) , 5x10(4) , 1x10(5) , and 5x10(5) (expressed as number of plated cardi...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577381</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577381</guid>        </item>
        <item>
            <title>MicroRNA control of myelopoiesis and the differentiation block in Acute Myeloid Leukaemia.</title>
            <link>http://www.medworm.com/index.php?rid=5577380&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%3D22225649%26dopt%3DAbstract</link>
            <description>Authors: Palma CA, Tonna EJ, Ma DF, Lutherborrow M
    Abstract
    In the relatively short period of time since their discovery microRNAs have been shown to control many important cellular functions such as cell differentiation, growth, proliferation and apoptosis. Additionally, microRNAs have been demonstrated as key drivers of many malignancies and can function as either tumour suppressors or oncogenes. The haematopoietic system is not outside the realm of microRNA control with microRNAs controlling aspects of stem cell and progenitor self-renewal and differentiation; with many, if not all haematological disorders associated with aberrant microRNA expression and function. In this review we focus on the current understanding of microRNA control of haematopoiesis and detail the evidence f...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577380</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577380</guid>        </item>
        <item>
            <title>Measuring passive myocardial stiffness in Drosophila melanogaster to investigate diastolic dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=5577379&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%3D22225769%26dopt%3DAbstract</link>
            <description>Authors: Kaushik G, Zambon AC, Fuhrmann A, Bernstein SI, Bodmer R, Engler AJ, Cammarato A
    Abstract
    Aging is marked by a decline in left ventricular diastolic function, which encompasses abnormalities in diastolic relaxation, chamber filling and/or passive myocardial stiffness. Genetic tractability and short life span make Drosophila melanogaster an ideal organism to study the effects of aging on heart function, including senescent-associated changes in gene expression and in passive myocardial stiffness. However, use of the Drosophila heart tube to probe deterioration of diastolic performance is subject to at least two challenges: the extent of genetic homology to mammals and the ability to resolve mechanical properties of the bilayered fly heart, which consists of a ventral muscle...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577379</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577379</guid>        </item>
        <item>
            <title>Rhabdomyosarcomas: an overview on the experimental animal models.</title>
            <link>http://www.medworm.com/index.php?rid=5577378&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%3D22225829%26dopt%3DAbstract</link>
            <description>Authors: Zanola A, Rossi S, Faggi F, Monti E, Fanzani A
    Abstract
    Rhabdomyosarcomas (RMS) are aggressive childhood soft-tissue malignancies deriving from mesenchymal progenitors that are committed to muscle-specific lineages. Despite the histopathological signatures are associated to three main histological variants, termed embryonal, alveolar and pleomorphic, a plethora of genetical and molecular changes are recognized in RMS. Over the years, exposure to carcinogens or ionizing radiations and gene targeting approaches in vivo have greatly contributed to disclose some of the mechanisms underlying RMS onset. In this review, we describe the principal distinct features associated to RMS variants and focus on the current available experimental animal models to point out the molecular de...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577378</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577378</guid>        </item>
        <item>
            <title>A fibronectin-fibrinogen-tropoelastin coating reduces smooth muscle cell growth but improves endothelial cell function.</title>
            <link>http://www.medworm.com/index.php?rid=5577377&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%3D22225866%26dopt%3DAbstract</link>
            <description>Authors: Tersteeg C, Roest M, Mak-Nienhuis EM, Ligtenberg E, Hoefer IE, de Groot PG, Pasterkamp G
    Abstract
    Reendothelialization of the stent surface after PCI is known to be an important determinant of clinical outcome. We compared the effects of biological stent coatings, fibronectin, fibrinogen and tropoelastin, on umbilical vein endothelial cell (HUVEC) and vascular smooth muscle cell (VSMC) characteristics. Umbilical cord arterial segments were cultured on coated surfaces and VSMC outgrowth (indicating proliferation and migration) was measured after 12 days. mRNA was isolated from HUVEC and VSMC cultured on these coatings and gene expression was profiled by QPCR. Procoagulant properties of HUVEC were determined by an indirect chromogenic assay which detects tissue factor activi...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577377</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577377</guid>        </item>
        <item>
            <title>Raf-1 levels determine the migration rate of primary endometrial stromal cells of patients with endometriosis.</title>
            <link>http://www.medworm.com/index.php?rid=5577376&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%3D22225925%26dopt%3DAbstract</link>
            <description>In conclusion, our findings suggest that cellular levels of Raf-1 adjust the threshold of hESC migration in endometriosis. © 2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
    PMID: 22225925 [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=5577376</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577376</guid>        </item>
        <item>
            <title>Large Animal Induced Pluripotent Stem Cells as Pre-Clinical Models For Studying Human Disease.</title>
            <link>http://www.medworm.com/index.php?rid=5577384&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%3D22212700%26dopt%3DAbstract</link>
            <description>Authors: Plews JR, Gu M, Longaker MT, Wu JC
    Abstract
    The derivation of human embryonic stem cells (ESCs) and subsequently human induced pluripotent stem cells (iPSCs) has energized regenerative medicine research and enabled seemingly limitless applications. While small animal models, such as mouse models, have played an important role in the progression of the field, typically, they are poor representations of the human disease phenotype. As an alternative, large animal models should be explored as a potentially better approach for clinical translation of cellular therapies. However, only fragmented information regarding the derivation, characterization, and clinical usefulness of pluripotent large animal cells is currently available. Here we briefly review the latest advances rega...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577384</comments>
            <pubDate>Mon, 02 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577384</guid>        </item>
        <item>
            <title>Identification of F-box only protein 7 as a negative regulator of NF-kappaB signaling.</title>
            <link>http://www.medworm.com/index.php?rid=5577383&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%3D22212761%26dopt%3DAbstract</link>
            <description>Authors: Kuiken HJ, Egan DA, Laman H, Bernards R, Beijersbergen RL, Dirac AM
    Abstract
    The Nuclear factor κB (NF-κB) signaling pathway controls important cellular events such as cell proliferation, differentiation, apoptosis and immune responses. Pathway activation occurs rapidly upon TNFα stimulation and is highly dependent on ubiquitination events. Using cytoplasmic to nuclear translocation of the NF-κB transcription factor family member p65 as a read-out, we screened a synthetic siRNA library targeting enzymes involved in ubiquitin conjugation and de-conjugation for modifiers of regulatory ubiquitination events in NF-κB signaling. We identified F-Box protein only 7 (FBXO7), a component of SCF-ubiquitin ligase complexes, as a negative regulator of NF-κB signaling. FBXO7 bind...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577383</comments>
            <pubDate>Mon, 02 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577383</guid>        </item>
        <item>
            <title>Issue information.</title>
            <link>http://www.medworm.com/index.php?rid=5577388&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%3D22212526%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22212526 [PubMed - in process] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577388</comments>
            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Small molecule regulators of postnatal Nkx2.5 cardiomyoblast proliferation and differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=5577386&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%3D22212626%26dopt%3DAbstract</link>
            <description>Authors: Chen WP, Wu SM
    Abstract
    While recent data have supported the capacity for a neonatal heart to undergo cardiomyogenesis, it is unclear whether these new cardiomyocytes arise from an immature cardiomyoblast population or from the division of mature cardiomyocytes. By following the expression eGFP in an Nkx2.5 enhancer-eGFP transgenic mice, we have identified a population of immature cells that can undergo cardiomyogenic as well as smooth muscle cell differentiation in the neonatal heart. Here, we examined growth factors and small molecule regulators that potentially regulate the proliferation and cardiomyogenic vs smooth muscle cell differentiation of neonatal Nkx2.5-GFP+ cells in vitro. We found that A83-01 (A83), an inhibitor of TGF-βRI, was able to induce an expansion of...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577386</comments>
            <pubDate>Fri, 30 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577386</guid>        </item>
        <item>
            <title>Mitochondrial connexin 43 impacts on respiratory complex I activity and mitochondrial oxygen consumption.</title>
            <link>http://www.medworm.com/index.php?rid=5577385&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%3D22212640%26dopt%3DAbstract</link>
            <description>Authors: Boengler K, Ruiz-Meana M, Gent S, Ungefug E, Soetkamp D, Miro-Casas E, Cabestrero A, Fernandez-Sanz C, Semenzato M, Di Lisa F, Rohrbach S, Garcia-Dorado D, Heusch G, Schulz R
    Abstract
    Connexin 43 (Cx43) is present at the sarcolemma and the inner membrane of cardiomyocyte subsarcolemmal mitochondria (SSM). Lack or inhibition of mitochondrial Cx43 is associated with reduced mitochondrial potassium influx, which might affect mitochondrial respiration. Therefore, we analyzed the importance of mitochondrial Cx43 for oxygen consumption. Acute inhibition of Cx43 in rat left ventricular (LV) SSM by 18α glycyrrhetinic acid (GA) or Cx43 mimetic peptides (Cx43-MP) reduced ADP-stimulated complex I respiration and ATP generation. Chronic reduction of Cx43 in conditional knockout mice ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577385</comments>
            <pubDate>Fri, 30 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577385</guid>        </item>
        <item>
            <title>Cystamine attenuates lupus-associated apoptosis of ventricular tissue by suppressing both intrinsic and extrinsic pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5577387&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%3D22212591%26dopt%3DAbstract</link>
            <description>Authors: Tzang BS, Hsu TC, Kuo CY, Chen TY, Chiang SY, Li SL, Kao SH
    Abstract
    Cystamine, a disulphide metabolite, has been demonstrated to ameliorate various lupus-associated tissue damages by animal models. However, effects of cystamine on apoptosis of cardiac tissue, a main cardiac damage attributing to lupus, are not clear. Therefore, we aimed to investigate whether cystamine possesses anti-apoptotic effects with emphasis on left ventricular (LV) tissue of lupus-prone mice NZB/W-F1. Cystamine treatment was performed by daily intraperitoneal administration. Morphology and apoptotic status of ventricular tissues in the treated mice were assessed by microscopy and TUNEL assay respectively. Levels of apoptotic biomarkers were determined using immunoblot. Our results revealed that cy...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577387</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577387</guid>        </item>
        <item>
            <title>PDGFR-β positive telocytes in skeletal muscle interstitium.</title>
            <link>http://www.medworm.com/index.php?rid=5546113&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%3D22188481%26dopt%3DAbstract</link>
            <description>In conclusion: a) PDGFRβ could be used as a marker for TCs and b) TCs are presumably a transitional population in the complex process of mural cell recruitment during angiogenesis and vascular remodelling. © 2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
    PMID: 22188481 [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=5546113</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5546113</guid>        </item>
        <item>
            <title>Interaction between pathogenic proteins in neurodegenerative disorders.</title>
            <link>http://www.medworm.com/index.php?rid=5530213&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%3D22176890%26dopt%3DAbstract</link>
            <description>Authors: Jellinger KA
    Abstract
    The misfolding and progressive aggregation of specific proteins in selective regions of the nervous system is a seminal occurrence in many neurodegenerative disorders, and the interaction between pathological/toxic proteins to cause neurodegeneration is a hot topic of current neuroscience research. Despite clinical, genetic, and experimental differences, increasing evidence indicates considerable overlap between synucleinopathies, tauopathies and other protein-misfolding diseases. Inclusions, often characteristic hallmarks of these disorders, suggest interactions of pathological proteins enganging common downstream pathways. Novel findings that have shifted our understanding in the role of pathologic proteins in the pathogenesis of Alzheimer, Parkinso...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5530213</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5530213</guid>        </item>
        <item>
            <title>PDGFRα cells in mouse urinary bladder: A new class of interstitial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5530216&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%3D22151424%26dopt%3DAbstract</link>
            <description>In this study, we examined the distribution of PDGFRα(+) cells in the murine urinary bladder and the relation that these cells may have with nerve fibers and smooth muscle cells. PDGFRα(+) cells had a spindle shaped or stellate morphology and often possessed multiple processes that contacted one another forming a loose network. These cells were distributed throughout the bladder wall, being present in the lamina propria as well as throughout the muscularis of the detrusor. PDGFRα(+) cells surrounded and were located between smooth muscle bundles and often came into close morphological association with intramural nerve fibers. These data describe a new class of interstitial cell that express a specific receptor within the bladder wall and provide morphological evidence for a possible neu...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5530216</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5530216</guid>        </item>
        <item>
            <title>Intermittent Hypobaric Hypoxia applicability in myocardial infarction prevention and recovery.</title>
            <link>http://www.medworm.com/index.php?rid=5530215&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%3D22151473%26dopt%3DAbstract</link>
            <description>Authors: Sanchis-Gomar F, Viña J, Lippi G
    Abstract
    Intermittent Hypobaric Hypoxia (IHH) has been the focus of important research in cardioprotection, and it has been associated with several mechanisms. IHH inhibits prolyl hydroxylases (PHD) activity, increasing the stabilization of hypoxia inducible factor-1 (HIF-1) and activating crucial adaptative genes. It has been hence suggested that IHH might be a simple intervention, which may offer a thoughtful benefits to patients with acute myocardial infarction and no complications. Nevertheless, several doubts exist as to whether IHH is a really safe technique, with little to no complications in post-myocardial infarction patients. IHH might produce instead unfavorable changes such as impairment of vascular hemodynamics and hypertensiv...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5530215</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5530215</guid>        </item>
        <item>
            <title>Immunogenicity of allogeneic mesenchymal stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=5530214&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%3D22151542%26dopt%3DAbstract</link>
            <description>Authors: Schu S, Nosov M, O'Flynn L, Shaw G, Treacy O, Barry F, Murphy M, O'Brien T, Ritter T
    Abstract
    Mesenchymal stem cells (MSCs) inhibit proliferation of allogeneic T cells and express low levels of major histocompatibility complex class I (MHCI), MHCII, and vascular adhesion molecule-1 (VCAM-1). We investigated whether their immunosuppressive properties and low immunophenotype protect allogeneic rat MSCs against cytotoxic lysis in vitro and result in a reduced immune response in vivo. Rat MSCs were partially protected against alloantigen-specific cytotoxic T cells in vitro. However, after treatment with IFN-γ and IL-1β, MSCs upregulated MHCI, MHCII, and VCAM-1, and cytotoxic lysis was significantly increased. In vivo, allogeneic T cells but not allogeneic MSCs induced upregu...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5530214</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5530214</guid>        </item>
        <item>
            <title>Erythropoietin attenuates the sequels of ischemic spinal cord injury with enhanced recruitment of CD34(+)  cells in mice.</title>
            <link>http://www.medworm.com/index.php?rid=5530219&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%3D22145921%26dopt%3DAbstract</link>
            <description>Conclusion: Erythropoietin demonstrated neuroprotective effects in the ischemic spinal cord, improving neurologic function and attenuating motor neuron loss. These effects may have been mediated by recruited CD34+ cells, and enhanced expression of brain-derived neurotrophic factor and vascular endothelial growth factor.
    PMID: 22145921 [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=5530219</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5530219</guid>        </item>
        <item>
            <title>Cross-talk between DNA methylation and active histone modifications regulates aberrant expression of ZAP70 in CLL.</title>
            <link>http://www.medworm.com/index.php?rid=5530218&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%3D22151263%26dopt%3DAbstract</link>
            <description>Authors: Amin S, Walsh M, Wilson C, Parker AE, Oscier D, Willmore E, Mann D, Mann J
    Abstract
    Zeta-associated protein of 70 kDa (ZAP70) is a recognised adverse prognostic marker in CLL associated with enhanced B cell receptor signalling, significantly more aggressive disease course and poor overall survival. ZAP70 is ordinarily expressed in T cells where it has a crucial role in T cell receptor signalling, whereas its aberrant expression in CLL leads to enhanced B cell receptor signalling and significantly more aggressive disease course. Although much is known about the activation of ZAP70 following engagement of T cell receptor, there is little data on the regulation of ZAP70 gene expression in normal T cells or CLL. To understand the molecular events underpinning epigenetic regula...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5530218</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5530218</guid>        </item>
        <item>
            <title>Identification of telocytes in the upper lamina propria of the human urinary tract.</title>
            <link>http://www.medworm.com/index.php?rid=5530217&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%3D22151349%26dopt%3DAbstract</link>
            <description>Authors: Gevaert T, De Vos R, Van Der Aa F, Joniau S, van den Oord J, Roskams T, De Ridder D
    Abstract
    The upper lamina propria (ULP) area of interstitial cells (IC) has been studied extensively in bladder, but is rather unexplored in the rest of the urinary tract. This cell layer is intriguing because of the localization directly underneath the urothelium, the intercellular contacts and the close relation with nerve endings and capillaries. In the present study we examine the ULP layer of IC in human renal pelvis, ureter and urethra, and we make a comparison with ULP IC in bladder. Tissue was obtained from normal areas in nephrectomy-, cystectomy- and prostatectomy-specimens, and processed for morphology, immunohistochemistry and electron microscopy. A morphological and immunohisto...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5530217</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5530217</guid>        </item>
        <item>
            <title>Issue information.</title>
            <link>http://www.medworm.com/index.php?rid=5473695&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%3D22123269%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22123269 [PubMed - in process] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473695</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473695</guid>        </item>
        <item>
            <title>Functional consequences of prolactin signaling in endothelial cells: a potential link with angiogenesis in pathophysiology?</title>
            <link>http://www.medworm.com/index.php?rid=5473694&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%3D22128761%26dopt%3DAbstract</link>
            <description>Authors: Reuwer AQ, Nowak-Sliwinska P, Mans LA, van der Loos CM, von der Thüsen JH, Twickler MT, Spek CA, Goffin V, Griffioen AW, Borensztajn KS
    Abstract
    Prolactin is best known as the polypeptide anterior pituitary hormone, which regulates the development of the mammary gland. However, it became clear over the last decade that prolactin contributes to a broad range of pathologies, including breast cancer. Prolactin is also involved in angiogenesis via the release of pro-angiogenic factors by leukocytes and epithelial cells. However, whether prolactin also influences endothelial cells, and whether there are functional consequences of prolactin-induced signaling in the perspective of angiogenesis, remains so far elusive. In the present study, we show that prolactin induces phosphor...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473694</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473694</guid>        </item>
        <item>
            <title>Bone morphogenetic protein receptor 2 in patients with idiopathic portal hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=5473689&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%3D22129439%26dopt%3DAbstract</link>
            <description>Conclusions. We did not detected mutations or rearrangements in the coding region of the BMPR2 gene in our patients with IPH. These findings suggest that, in contrast to IPAH, mutations in BMPR2 are not be involved in the pathogenesis of IPH.
    PMID: 22129439 [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=5473689</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473689</guid>        </item>
        <item>
            <title>Generation of skeletal muscle cells from embryonic and induced pluripotent stem cells as an in vitro model and for therapy of muscular dystrophies.</title>
            <link>http://www.medworm.com/index.php?rid=5473687&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%3D22129481%26dopt%3DAbstract</link>
            <description>Authors: Salani S, Donadoni C, Rizzo F, Bresolin N, Comi GP, Corti S
    Abstract
    Muscular dystrophies (MDs) are a heterogeneous group of inherited disorders characterized by progressive muscle wasting and weakness likely associated with exhaustion of muscle regeneration potential. At present, no cures or efficacious treatments are available for these diseases, but cell transplantation could be a potential therapeutic strategy. Transplantation of myoblasts using satellite cells or other myogenic cell populations has been attempted to promote muscle regeneration, based on the hypothesis that the donor cells repopulate the muscle and contribute to its regeneration. Embryonic stem cells (ESCs) and more recently induced pluripotent stem cells (iPSCs) could generate an unlimited source of d...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473687</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473687</guid>        </item>
        <item>
            <title>Activation of the Prolyl-hydroxylase oxygen-sensing signal cascade leads to AMPK activation in cardiomyocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5473693&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%3D22128786%26dopt%3DAbstract</link>
            <description>Conclusions- We establish for the first time that activation of PHD signal cascade can activate AMPK pathway mainly through a Ca(2+) /CaMKK-dependent mechanism in cardiomyocytes. Furthermore, activation of AMPK plays an essential role in hypoxic protective responses induced by PHI.
    PMID: 22128786 [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=5473693</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473693</guid>        </item>
        <item>
            <title>Repertoire of endothelial progenitor cells mobilized by femoral artery ligation - A nonhuman primate study.</title>
            <link>http://www.medworm.com/index.php?rid=5473692&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%3D22128816%26dopt%3DAbstract</link>
            <description>Authors: Shi Q, Cox LA, Hodara V, Wang XL, Vandeberg JL
    Abstract
    To determine in the baboon model the identities and functional characteristics of endothelial progenitor cells mobilized in response to artery ligation, we collected peripheral blood mononuclear cells before and 3 days after a segment of femoral artery was removed. Our goal was to find EPC subpopulations with highly regenerative capacity. We identified 12 subpopulations of putative EPCs that were altered &amp;gt;1.75 fold; two subpopulations (CD146+/CD54-/CD45- at 6.63 fold, and CD146+/UEA-1-/CD45- at 12.21 fold) were dramatically elevated. To investigate the regenerative capacity of putative EPCs, we devised a new assay that maximally resembled their in vivo scenario, we purified CD34+ and CD146+ cells and co-cultured th...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473692</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473692</guid>        </item>
        <item>
            <title>Effects of valsartan on ventricular arrhythmia induced by programmed electrical stimulation in rats with myocardial infarction.</title>
            <link>http://www.medworm.com/index.php?rid=5473691&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%3D22128836%26dopt%3DAbstract</link>
            <description>CONCLUSIONS Valsartan reduced the incidence of PES induced ventricular arrhythmia, this effect was possibly through modulating the myocardial AT1R and Cx43 expression.
    PMID: 22128836 [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=5473691</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473691</guid>        </item>
        <item>
            <title>Endothelial fsh receptor in primary kidney cancer correlates with subsequent response to sunitinib.</title>
            <link>http://www.medworm.com/index.php?rid=5473690&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%3D22129368%26dopt%3DAbstract</link>
            <description>Authors: Siraj MA, Pichon C, Radu A, Ghinea N
    Abstract
    Sunitinib is an antiangiogenic receptor tyrosine kinase inhibitor used to treat advanced metastatic renal cell carcinoma and other types of cancer. Sutent is effective in only approx. 70% of clear cell renal cell carcinoma (CCRCC) patients, has significant adverse side effects, and no method is available to predict which patients will not respond. Our purpose was to explore the possibility of introducing an effective prediction method based on a marker of the tumor vasculature, the Follicle Stimulating Hormone Receptor (FSHR). Fifty patients diagnosed with advanced metastatic CCRCC have been subjected to surgery for removal of the primary tumor and were subsequently treated with sunitinib. After three months of therapy the pati...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473690</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473690</guid>        </item>
        <item>
            <title>Mild hypoxia induced cardiomyocyte hypertrophy via up-regulation of HIF-1α-mediated TRPC signaling.</title>
            <link>http://www.medworm.com/index.php?rid=5473688&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%3D22129453%26dopt%3DAbstract</link>
            <description>Authors: Chu W, Wan L, Zhao D, Qu X, Cai F, Huo R, Wang N, Zhu J, Zhang C, Zheng F, Cai R, Dong D, Lu Y, Yang B
    Abstract
    Hypoxia-inducible factor-1 alpha (HIF-1α) is a central transcriptional regulator of hypoxic response. The present study was designed to investigate the role of HIF-1α in mild hypoxia-induced cardiomyocytes hypertrophy and its underlying mechanism. Mild hypoxia (MH, 10% O(2) ) caused hypertrophy in cultured neonatal rat cardiac myocytes, which was accompanied with increase of HIF-1α mRNA and accumulation of HIF-1α protein in nuclei. Transient receptor potential canonical (TRPC) channels including TRPC3 and TRPC6, except for TRPC1 were increased, and Ca(2+) -calcineurin signals were also enhanced in a time-dependent manner under MH condition. MH-induced cardiom...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473688</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473688</guid>        </item>
        <item>
            <title>Altered apoptosis regulation in kufor-rakeb syndrome patients with mutations in the atp13a2 gene.</title>
            <link>http://www.medworm.com/index.php?rid=5473701&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%3D22117566%26dopt%3DAbstract</link>
            <description>Authors: Radi E, Formichi P, Di Maio G, Battisti C, Federico A
    Abstract
    ATP13A2 gene encodes for a protein of the group 5 P-type ATPase family. ATP13A2 mutations are responsible for Kufor-Rakeb syndrome, a rare autosomal recessive juvenile parkinsonism characterized by the subacute onset of extrapyramidal, pyramidal and cognitive dysfunction with secondary nonresponsiveness to Levodopa. FBXO7 protein is an F-box-containing protein. Recessive FBXO7 mutations are responsible for PARK15, a rare juvenile parkinsonism characterized by progressive neurodegeneration with extrapyramidal and pyramidal system involvement. Our aim was to evaluate apoptosis in cells from two KRS siblings carrying a homozygous ATP13A2 mutation and a heterozygous FBXO7 mutation. We also analysed apoptosis in the...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473701</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473701</guid>        </item>
        <item>
            <title>Myelopoiesis in spleen producing distinct dendritic-like cells.</title>
            <link>http://www.medworm.com/index.php?rid=5473700&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%3D22117595%26dopt%3DAbstract</link>
            <description>Authors: Tan JK, O'Neill HC
    Abstract
    Dendritic cells (DC) represent a heterogeneous class of antigen presenting cells (APC). Previously we reported a distinct myeloid dendritic-like cell present in spleen, as an in vivo counterpart to cells produced in murine spleen long-term cultures (LTC-DC). These cells, named 'L-DC', were found to be functionally and phenotypically distinct from conventional (c)DC, plasmacytoid (p)DC and monocytes. These results suggested that spleen may represent a niche for development of L-DC from endogenous progenitors. Adult murine spleen has now been investigated for the presence of L-DC progenitors. Lineage-negative (Lin)(-) ckit(lo) and Lin(-) ckit(hi) progenitor subsets were identified as candidate populations, and tested for ability to produce L-DC; i...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473700</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473700</guid>        </item>
        <item>
            <title>The Akt1 isoform is an essential mediator of ischemic preconditioning.</title>
            <link>http://www.medworm.com/index.php?rid=5473699&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%3D22117619%26dopt%3DAbstract</link>
            <description>In this study we investigated the specific contribution of Akt1 and Akt2 in cardioprotection against ischemia-reperfusion (I-R) injury. Mice deficient in Akt1 or Akt2 were subjected to in vivo regional myocardial ischemia for 30 minutes followed by reperfusion for 2 hours with or without a prior IPC stimulus. Our results show that mice deficient in Akt1 were resistant to protection with either 1 or 3 cycles of IPC stimulus (42.7±6.5% control versus 38.5±1.9% 1xIPC, N = 6, NS; 41.4±6.3% control versus 32.4±3.2% 3xIPC, N = 10, NS). Western blot analysis, performed on heart samples taken from Akt1(-/-) mice subjected to IPC, revealed an impaired phosphorylation of GSK-3β, a downstream effector of Akt, as well as Erk1/2, the parallel component of the reperfusion injury salvage kinase path...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473699</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473699</guid>        </item>
        <item>
            <title>Pro-inflammatory phenotype of COPD fibroblasts  not compatible with repair in COPD lung.</title>
            <link>http://www.medworm.com/index.php?rid=5473698&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%3D22117690%26dopt%3DAbstract</link>
            <description>In this study, fibroblasts were cultured from lung parenchyma of patients with mild COPD (GOLD 1, n = 5), moderate-severe COPD (GOLD 2-3, n = 12), and controls (non-COPD, n = 5). Measurements were made of proliferation, senescence-associated beta-galactosidase-1, mRNA expression of IL-6, IL-8, MMP-1, tropoelastin and versican, and protein levels for IL-6, IL-8, PGE(2,) tropoelastin, insoluble elastin, and versican. GOLD 2-3 fibroblasts proliferated more slowly (p&amp;lt;0.01), had higher levels of senescence-associated beta-galactosidase-1 (p&amp;lt;0.001) than controls, and showed significant increases in mRNA and/or protein for IL-6 (p&amp;lt;0.05), IL-8 (p&amp;lt;0.01), MMP-1 (p&amp;lt;0.05), PGE(2) (p&amp;lt;0.05), versican (p&amp;lt;0.05) and tropoelastin (p&amp;lt;0.05). mRNA expression and/or protein levels of tro...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473698</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473698</guid>        </item>
        <item>
            <title>Rapamycin inhibits transforming growth factor β induced peritoneal angiogenesis by blocking the secondary hypoxic response.</title>
            <link>http://www.medworm.com/index.php?rid=5473697&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%3D22117756%26dopt%3DAbstract</link>
            <description>Authors: Sekiguchi Y, Zhang J, Patterson S, Liu L, Hamada C, Tomino Y, Margetts PJ
    Abstract
    Patients with end stage kidney disease on peritoneal dialysis often develop progressive scarring of the peritoneal tissues. This manifests as submesothelial thickening and is associated with increased vascularization that leads to ultrafiltration dysfunction. Hypoxia induces a characteristic series of responses including angiogenesis and fibrosis. We investigated the role of hypoxia in peritoneal membrane damage. An adenovirus expressing transforming growth factor (TGF) β was used to induce peritoneal fibrosis. We evaluated the effect of the mTOR inhibitor rapamycin which has been previously shown to block hypoxia inducible factor (HIF) 1α. We also assessed the effect of HIF1α independent...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473697</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473697</guid>        </item>
        <item>
            <title>Pravastatin-induced proangiogenic effects depend upon extracellular FGF-2.</title>
            <link>http://www.medworm.com/index.php?rid=5473696&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%3D22117815%26dopt%3DAbstract</link>
            <description>Authors: Shiota M, Hikita Y, Kawamoto Y, Kusakabe H, Tanaka M, Izumi Y, Nakao T, Miura K, Funae Y, Iwao H
    Abstract
    The HMG-CoA reductase inhibitors (statins) have been shown to exert several protective effects on the vasculature that are unrelated to changes in the cholesterol profile, and to induce angiogenesis. The proangiogenic effect exerted by statins has been attributed to the activation of the PI3K/Akt pathway in endothelial cells; however, it is unclear how statins activate this pathway. Pravastatin-mediated activation of Akt and MAPK occurs rapidly (within 10 min) and at low doses (0.01 μM). Here, we hypothesized that FGF-2 contributes to the proangiogenic effect of statins. We found that pravastatin, a hydrophilic statin, induced phosphorylation of the FGF receptor (FGFR...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473696</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473696</guid>        </item>
        <item>
            <title>Prometheus's Heart: what lies beneath.</title>
            <link>http://www.medworm.com/index.php?rid=5438252&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%3D22099480%26dopt%3DAbstract</link>
            <description>Authors: Barile L, Lionetti V
    Abstract
    A heart attack kills off many cells in the heart. Parts of the heart become thin and fail to contract properly following the replacement of lost cells by scar tissue. However, the notion that the same adult cardiomyocytes beat throughout the lifespan of the organ and organism, without the need for a minimum turnover, gives way to a fascinating investigations. Since the late 1800s, scientists and cardiologists wanted to demonstrate that the cardiomyocytes cannot be generated after the perinatal period in humans. This curiosity has been passed down in subsequent years and has motivated more and more accurate studies in an attempt to exclude the presence of renewed cardiomyocytes in the tissue bordering the ischemic area, and then to confirm the ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438252</comments>
            <pubDate>Wed, 16 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438252</guid>        </item>
        <item>
            <title>Modulation of miroRNA 20b with resveratrol and longevinex is linked with their potent anti-angiogenic action in the ischemic myocardium and synergestic effects of resveratrol and γ-tocotrienol.</title>
            <link>http://www.medworm.com/index.php?rid=5378231&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%3D22050707%26dopt%3DAbstract</link>
            <description>Conclusion: All the interventions treated for 3 weeks lead to significant cardioprotection against ischemia/reperfusion injury. A unique signature of miRNA profile is observed in control heart pretreated with resveratrol or γ-tocotrienol. We have determined specific group of miRNA in heart that have altered during IR injuries. Most of those altered microRNA expressions modulated close to their basal level in resveratrol or longevinex treated I/R rat. Interestingly, resveratrol and γ-tocotrienol resulted in synergestic action.
    PMID: 22050707 [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=5378231</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378231</guid>        </item>
        <item>
            <title>Hypoxia-inducible factor 1-mediated human GATA1 induction promotes erythroid differentiation under hypoxic conditions.</title>
            <link>http://www.medworm.com/index.php?rid=5378227&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%3D22050843%26dopt%3DAbstract</link>
            <description>In this study, we show that hypoxia-induced GATA1 expression is mediated by HIF1 in erythroid cells. Under hypoxic conditions, significantly increased GATA1 mRNA and protein levels were detected in K562 cells and erythroid induction cultures of CD34(+) hematopoietic stem/progenitor cells. Enforced HIF1α expression increased GATA1 expression, while HIF1α knock-down by RNA interference decreased GATA1 expression. In silico analysis revealed one potential hypoxia response element (HRE). The results from reporter gene and mutation analysis suggested that this element is necessary for hypoxic response. Chromatin immunoprecipitation (ChIP)-PCR showed that the putative HRE was recognized and bound by HIF1 in vivo. These results demonstrate that the up-regulation of GATA1 during hypoxia is direc...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378227</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378227</guid>        </item>
        <item>
            <title>Localized colonic stem cell transplantation enhances tissue regeneration in murine colitis.</title>
            <link>http://www.medworm.com/index.php?rid=5378226&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%3D22050903%26dopt%3DAbstract</link>
            <description>Authors: Zhou Q, Price DD, Dreher KL, Pronold B, Callam CS, Sharma J, Verne GN
    Abstract
    Many patients suffer from chronic gastrointestinal diseases characterized by chronic inflammation, increased intestinal permeability, and visceral pain in which there is no definitive treatment. Adult stem cells have recently been used in various disease states to contribute wound healing processes. In the current study we investigated the ability of intra-colonic adult stem cells application to heal colonic inflammation in IL-10(-/-) mice with active colitis. The aims of this study were to determine whether intra-colonic infusion of adult colonic stem cells (local stem cell transplantation): (i) restores intestinal permeability; (ii) attenuates visceral hypersensitivity; (iii) heals murine coli...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378226</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378226</guid>        </item>
        <item>
            <title>Cell-derived microparticles in atherosclerosis: biomarkers and targets for pharmacological modulation?</title>
            <link>http://www.medworm.com/index.php?rid=5378225&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%3D22050954%26dopt%3DAbstract</link>
            <description>Authors: Baron M, Boulanger CM, Staels B, Tailleux A
    Abstract
    Cardiovascular diseases remain an important cause of morbi-mortality. Atherosclerosis, which predisposes to cardiovascular disorders such as myocardial infarction and stroke, develops silently over several decades. Identification of circulating biomarkers to evaluate cardiovascular event risk and pathology prognosis is of particular importance. Microparticles (MPs) are small vesicles released from cells upon apoptosis or activation. MPs are present in blood of healthy individuals. Studies showing a modification of their concentrations in patients with cardiovascular risk factors and after cardiovascular events identify MPs as potential biomarkers of disease. Moreover, the pathophysiological properties of MPs may contribu...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378225</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378225</guid>        </item>
        <item>
            <title>Cardiomyocytes generated from CPVT(D307H)  patients are arrhythmogenic in response to β-adrenergic stimulation.</title>
            <link>http://www.medworm.com/index.php?rid=5378235&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%3D22050625%26dopt%3DAbstract</link>
            <description>Cardiomyocytes generated from CPVT(D307H) patients are arrhythmogenic in response to β-adrenergic stimulation.
    J Cell Mol Med. 2011 Nov 2;
    Authors: Novak A, Barad L, Zeevi-Levin N, Shick R, Shtreichman R, Lorber A, Itskovitz-Eldor J, Binah O
    Abstract
    Sudden cardiac death caused by ventricular arrhythmias is a disastrous event, especially when it occurs in young individuals. Among the 5 major arrhythmogenic disorders occurring in the absence of a structural heart disease is Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT), which is a highly lethal form of inherited arrhythmias. Our study focuses on the autosomal recessive form of the disease caused by the missense mutation D307H in the cardiac calsequestrin gene, CASQ2. Since CASQ2 is a key player in excitation ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378235</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378235</guid>        </item>
        <item>
            <title>Repetitive transplantation of different cell types sequentially improves heart function after infarction.</title>
            <link>http://www.medworm.com/index.php?rid=5378234&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%3D22050647%26dopt%3DAbstract</link>
            <description>In conclusion, repetitive Tx of different cell types after myocardial infarction in rat hearts significantly improved left ventricular function and could represent a feasible option to enhance the benefit of cell therapy.
    PMID: 22050647 [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=5378234</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378234</guid>        </item>
        <item>
            <title>Pancreatic cancer tumor initiating cells: the molecular regulation and therapeutic values.</title>
            <link>http://www.medworm.com/index.php?rid=5378233&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%3D22050663%26dopt%3DAbstract</link>
            <description>Authors: Ni X, Long J, Cen P, Chen L, Yang J, Li M
    Abstract
    Pancreatic cancer is an aggressive solid tumor characterized by its local invasion, early metastasis, and resistance to standard chemotherapy or radiation therapy. Tumor initiating cells (TICs) are not only capable of self-renewal and differentiation, but also play an important role in multidrug resistance, and thus become a popular topic in cancer research especially in pancreatic cancer. In this review, we summarize the current progress of TICs in tumorigenesis, various newly identified surface markers of pancreatic TICs, and the signaling pathways such as EMT, SHH and Notch that regulate TICs. We also discuss the role which microRNA plays in TICs as well as its application in TICs-targeted therapy along with other appro...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378233</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378233</guid>        </item>
        <item>
            <title>Involvement of COX-2/PGE(2)  signaling in hypoxia-induced angiogenic response in endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5378232&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%3D22050691%26dopt%3DAbstract</link>
            <description>Conclusion: Short-term hypoxic treatment enhanced angiogenic capability of ECs, and COX-2/PGE(2) signaling maybe play a critical role in the biological response of ECs to hypoxia.
    PMID: 22050691 [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=5378232</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378232</guid>        </item>
        <item>
            <title>The role of dorsal root ganglia activation and brain derived neurotrophic factor in multiple sclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=5378230&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%3D22050733%26dopt%3DAbstract</link>
            <description>Authors: Zhu W, Frost E, Begum F, Vora P, Au K, Gong Y, Macneil B, Pillai P, Namaka M
    Abstract
    Multiple sclerosis (MS) is characterised by focal destruction of the white matter of the brain and spinal cord. The exact mechanisms underlying the pathophysiology of the disease are unknown. Many studies have shown that MS is predominantly an autoimmune disease with an inflammatory phase followed by a demyelinating phase. Recent studies alongside current treatment strategies, including glatiramer acetate, have revealed a potential role for brain derived neurotrophic factor (BDNF) in MS. However, the exact role of BDNF is not fully understood. We used the experimental autoimmune encephalomyelitis (EAE) model of MS in adolescent female Lewis rats to identify the role of BDNF in disease pro...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378230</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378230</guid>        </item>
        <item>
            <title>Epigenetic control of CCR5 transcript levels in immune cells and modulation by small molecules inhibitors.</title>
            <link>http://www.medworm.com/index.php?rid=5378229&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%3D22050776%26dopt%3DAbstract</link>
            <description>In this study we show that epigenetic changes (i.e. DNA methylation and histone modifications) within the context of the CCR5 P1 promoter region correlate with transcript levels of CCR5 in healthy and in malignant CD4(+) T lymphocytes as well as in CD14(+) monocytes. In normal naïve T cells and CD14(+) monocytes the CCR5 P1 promoter resembles a bivalent chromatin state, with both repressive and permissive histone methylation and acetylation marks. The CCR5 expressing CD14(+) monocytes however show much higher levels of acetylated histone H3 (AcH3) compared to the non-CCR5-expressing naïve T cells. Combined with a highly methylated promoter in CD14(+) monocytes, this indicates a dominant role for AcH3 in CCR5 transcription. We also show that pharmacological interference in the epigenetic ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378229</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378229</guid>        </item>
        <item>
            <title>Inhibition of JAK2/STAT3 signaling induces colorectal cancer cell apoptosis via mitochondrial pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5378228&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%3D22050790%26dopt%3DAbstract</link>
            <description>Authors: Du W, Hong J, Wang YC, Zhang YJ, Wang P, Su WY, Lin YW, Lu R, Zou W, Xiong H, Fang JY
    Abstract
    Abnormalities in the JAK2/STAT3 pathway are involved in the pathogenesis of colorectal cancer (CRC), including apoptosis. However, the exact mechanism by which dysregulated JAK2/STAT3 signaling contributes to the apoptosis has not been clarified. To investigate the role of both JAK2 and STAT3 in the mechanism underlying CRC apoptosis, we inhibited JAK2 with AG490 and depleted STAT3 with a small interfering RNA (siRNA); Our data showed that inhibition of JAK2/STAT3 signaling induced CRC cellular apoptosis via modulating the Bcl-2 gene family, promoting the loss of mitochondrial transmembrane potential (Δψm) and the increase of reactive oxygen species (ROS). In addition, our resu...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378228</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378228</guid>        </item>
        <item>
            <title>Activation of neurokinin-1 receptors up-regulates substance P and neurokinin-1 receptor expression in murine pancreatic acinar cells.</title>
            <link>http://www.medworm.com/index.php?rid=5378236&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%3D22040127%26dopt%3DAbstract</link>
            <description>Authors: Koh YH, Moochhala S, Bian JS, Bhatia M
    Abstract
    Acute pancreatitis (AP) has been associated with an up-regulation of substance P (SP) and neurokinin-1 receptor (NK1R) in the pancreas. Increased SP-NK1R interaction was suggested to be pro-inflammatory during AP. Previously, we showed that caerulein treatment increased SP/NK1R expression in mouse pancreatic acinar cells, but the effect of SP treatment was not evaluated. Pancreatic acinar cells were obtained from pancreas of male swiss mice (25-30g). We measured mRNA expression of preprotachykinin-A (PPTA) and NK1R following treatment of SP (10(-6) M). SP treatment increased PPTA and NK1R expression in isolated pancreatic acinar cells, which was abolished by pretreatment of a selective NK1R antagonist, CP96,345. SP also time ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378236</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378236</guid>        </item>
        <item>
            <title>Issue information.</title>
            <link>http://www.medworm.com/index.php?rid=5359756&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%3D22023249%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22023249 [PubMed - in process] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359756</comments>
            <pubDate>Sun, 30 Oct 2011 23:45:12 +0100</pubDate>
            <guid isPermaLink="false">5359756</guid>        </item>
        <item>
            <title>MicroRNA expression in formalin-fixed paraffin embedded tissue using Real Time Quantitative PCR; the strengths and pitfalls.</title>
            <link>http://www.medworm.com/index.php?rid=5359793&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%3D22003827%26dopt%3DAbstract</link>
            <description>Authors: Dijkstra JR, Mekenkamp LJ, Teerenstra S, De Krijger I, Nagtegaal ID
    Abstract
    MicroRNAs (miRNAs) are a group of small non-coding RNAs with a huge impact in a wide range of biological processes, including cancer. The evidence collected to date demonstrates that miRNAs represent valid diagnostic, prognostic, and predictive markers in cancer. The identification of these miRNA biomarkers in archived tissues has been facilitated by novel development and refinement of detection methodologies. Quantitative real-time reverse-transcription PCR (qRT-PCR) is one of the most common methods used to detect low levels of miRNAs with high sensitivity and specificity. However, several technical parameters should be identified and optimized in order to obtain meaningful and reproducible resu...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359793</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359793</guid>        </item>
        <item>
            <title>Cardiomyogenic differentiation-independent improvement of cardiac function by human cardiomyocyte progenitor cell injection in ischemic mouse hearts.</title>
            <link>http://www.medworm.com/index.php?rid=5359763&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%3D22003890%26dopt%3DAbstract</link>
            <description>Conclusions: Injected hCMPCs engraft into murine infarcted myocardium where they improve LV systolic function and attenuate the ventricular remodeling process 2 weeks post MI. Since no cardiac differentiation of hCMPCs was evident after 2 weeks, the observed beneficial effects were most likely mediated by paracrine factors, targeting amongst others vascular homeostasis. These results demonstrate that hCMPCs can be applied to repair infarcted myocardium without the need to undergo differentiation into cardiomyocytes.
    PMID: 22003890 [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=5359763</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359763</guid>        </item>
        <item>
            <title>Effects of redox modulation by inhibition of Thioredoxin reductase on radiosensitivity and gene expression.</title>
            <link>http://www.medworm.com/index.php?rid=5359762&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%3D22003958%26dopt%3DAbstract</link>
            <description>Authors: Selenius M, Hedman M, Brodin D, Gandin V, Rigobello MP, Flygare J, Marzano C, Bindoli A, Brodin O, Björnstedt M, Fernandes AP
    Abstract
    The thioredoxin system is a promising target when aiming to overcome the problem of clinical radiation resistance. Altered cellular redox-status and redox sensitive thiols contributing to induction of resistance strongly connects the ubiquitous redox enzyme thioredoxin reductase to the cellular response to ionizing radiation. To further investigate possible strategies in combating clinical radiation resistance, human radio-resistant lung cancer cells were subjected to a combination of single fractions of γ-radiation at clinically relevant doses and non-toxic levels of a well-characterized thioredoxin reductase (TrxR) inhibitor, the phosph...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359762</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359762</guid>        </item>
        <item>
            <title>Therapeutic potential of in utero mesenchymal stem cell (MSCs) transplantation in rat fetuses with spina bifida aperta.</title>
            <link>http://www.medworm.com/index.php?rid=5359761&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%3D22004004%26dopt%3DAbstract</link>
            <description>In this study, we successfully devised a prenatal surgical approach and transplanted mesenchymal stem cells (MSCs) to fetal rat spinal column to treat retinoic acid induced NTDs in rat. Transplanted MSCs survived, grew and expressed markers of neurons, glia and myoblasts in the defective spinal cord. MSCs expressed and perhaps induced the surrounding spinal tissue to express neurotrophic factors. In addition, MSC reduced spinal tissue apoptosis in NTD. Our results suggested that prenatal MSC transplantation could treat spinal neuron deficiency in NTDs by the regeneration of neurons and reduced spinal neuron death in the defective spinal cord.
    PMID: 22004004 [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=5359761</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359761</guid>        </item>
        <item>
            <title>Bone marrow mesenchymal stem cells for post-myocardial infarction cardiac repair: micro-RNAs as novel regulators.</title>
            <link>http://www.medworm.com/index.php?rid=5359760&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%3D22004043%26dopt%3DAbstract</link>
            <description>Authors: Wen Z, Zheng S, Zhou C, Yuan W, Wang J, Wang T
    Abstract
    Transplantation of bone marrow-derived mesenchymal stem cells (MSCs) is safe and may improve cardiac function and structural remodeling in patients following myocardial infarction (MI). Cardiovascular cell differentiation and paracrine effects to promote endogenous cardiac regeneration, neovascularization, anti-inflammation, anti-apoptosis, anti-remodeling and cardiac contractility, may contribute to MSC-based cardiac repair following MI. However, current evidence indicates that the efficacy of MSC transplantation was unsatisfactory, due to the poor viability and massive death of the engrafted MSCs in the infarcted myocardium. MicroRNAs are short endogenous, conserved, non-coding RNAs and important regulators involved...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359760</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359760</guid>        </item>
        <item>
            <title>A novel regulation of VEGF expression by HIF-1α and STAT3 in HDM2 transfected prostate cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5359759&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%3D22004076%26dopt%3DAbstract</link>
            <description>Authors: Rathinavelu A, Narasimhan M, Muthumani P
    Abstract
    On the basis of increasing roles for HDM2 oncoprotein in cancer growth and progression, we speculated that HDM2 might play a major role in hypoxia-induced metastatic process. For verification of this hypothesis, wild type LNCaP prostate cancer cells and HDM2 transfected LNCaP-MST (HDM2 stably transfected) cells were studied. The data obtained revealed that the HDM2 transfected LNCaP-MST cells possessed the ability to multiply rapidly and show distinct morphological features compared to non-transfected LNCaP cells. During hypoxia HDM2 expression in the LNCaP and LNCaP-MST cells were significantly increased. The LNCaP-MST cells also expressed higher levels of HIF-1α (hypoxia inducible factor-1α) and p-STAT3 even under the n...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359759</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359759</guid>        </item>
        <item>
            <title>Heat shock protein 27 as a prognostic and predictive biomarker in pancreatic ductal adenocarcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=5359758&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%3D22004109%26dopt%3DAbstract</link>
            <description>Authors: Schäfer C, Seeliger H, Bader DC, Assmann G, Buchner D, Guo Y, Ziesch A, Palagyi A, Ochs S, Laubender RP, Jung A, De Toni EN, Kirchner T, Göke B, Bruns C, Gallmeier E
    Abstract
    A role of heat shock protein 27 (HSP27) as a potential biomarker has been reported in various tumor entities, but comprehensive studies in pancreatic cancer are lacking. Applying tissue microarray (TMA) analysis, we correlated HSP27 protein expression status with clinicopathologic parameters in pancreatic ductal adenocarcinoma specimens from 86 patients. Complementary, we established HSP27 overexpression and RNA-interference models to assess the impact of HSP27 on chemo- and radiosensitivity directly in pancreatic cancer cells. In the TMA study, HSP27 expression was found in 49% of tumor samples. Ap...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359758</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359758</guid>        </item>
        <item>
            <title>The new low-toxic histone deacetylase inhibitor S-(2) induces apoptosis in various acute myeloid leukemia cells.</title>
            <link>http://www.medworm.com/index.php?rid=5359757&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%3D22004558%26dopt%3DAbstract</link>
            <description>Authors: Cellai C, Balliu M, Laurenzana A, Guandalini L, Matucci R, Miniati D, Torre E, Nebbioso A, Carafa V, Altucci L, Romanelli MN, Paoletti F
    Abstract
    Histone deacetylase inhibitors (HDACi) induce tumor cell cycle arrest and/or apoptosis, and some of them are currently used in cancer therapy. Recently, we described a series of powerful HDACi characterized by a 1,4-benzodiazepine (BDZ) ring hybridized with a linear alkyl chain bearing a hydroxamate function as Zn(++) -chelating group. Here, we explored the anti-leukemic properties of three novel hybrids, namely the chiral compounds (S)-2 and (R)-2, and their non-chiral analog 4, which were first comparatively tested in promyelocytic NB4 cells. (S)-2 and partially 4- but not (R)-2 - caused G0/G1 cell-cycle arrest by up-regulating...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359757</comments>
            <pubDate>Mon, 17 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359757</guid>        </item>
        <item>
            <title>Implication of CD38 gene in podocyte epithelial-to-mesenchymal transition and glomerular sclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=5359796&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%3D21992601%26dopt%3DAbstract</link>
            <description>In conclusion, our observations reveal that the normal expression of CD38 importantly contributes to the differentiation and function of podocytes and the defect of this gene expression may be a critical mechanism inducing EMT and consequently resulting in glomerular injury and sclerosis.
    PMID: 21992601 [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=5359796</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359796</guid>        </item>
        <item>
            <title>The plaque protein myozap identified as a novel major component of adhering junctions in endothelia of the blood and the lymph vascular systems.</title>
            <link>http://www.medworm.com/index.php?rid=5359795&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%3D21992629%26dopt%3DAbstract</link>
            <description>Authors: Pieperhoff S, Rickelt S, Heid H, Claycomb WC, Zimbelmann R, Kuhn C, Winter-Simanowski S, Kuhn C, Frey N, Franke WW
    Abstract
    Recently the protein myozap (myocardium-enriched zonula adhaerens protein), a 54-kDa polypeptide, which is not a member of any of the known cytoskeletal and junctional protein multigene families, has been identified as a constituent of the plaques of the composite junctions in the intercalated disks connecting the cardiomyocytes of mammalian hearts. Using a set of novel, highly sensitive and specific antibodies we now report that myozap is also a major constituent of the cytoplasmic plaques of the adherens junctions (AJs) connecting the endothelial cells of the mammalian blood and lymph vascular systems, including the desmoplakin-containing complexus ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5359795</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359795</guid>        </item>
        <item>
            <title>Tracheal telocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5359794&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%3D21992681%26dopt%3DAbstract</link>
            <description>In conclusion, tracheal TC could be involved in the tracheal regulation (e.g. secretion, contractility). The tandem TC-MC deserves further investigations.
    PMID: 21992681 [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=5359794</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5359794</guid>        </item>
        <item>
            <title>Telocytes are the common cell of origin of both PEComas and GISTs: An evidence-supported hypothesis.</title>
            <link>http://www.medworm.com/index.php?rid=5294934&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%3D21977985%26dopt%3DAbstract</link>
            <description>In conclusion we propose that telocytes could be the common cells of origin for both PEComas and GISTs.
    PMID: 21977985 [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=5294934</comments>
            <pubDate>Fri, 07 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5294934</guid>        </item>
        <item>
            <title>Pathophysiology, staging and therapy of severe sepsis in baboon models.</title>
            <link>http://www.medworm.com/index.php?rid=5294953&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%3D21972970%26dopt%3DAbstract</link>
            <description>Authors: Taylor FB, Kinasewitz GT, Lupu F
    Abstract
    We review our baboon models of E. coli sepsis that mimic, respectively, the shock/disseminated intravascular coagulation (DIC) and organ failure variants of severe sepsis, and analyze the pathophysiologic processes that are unique to each. The multistage, multifactorial characteristics of severe sepsis develop as a result of the initial insult, which -depending on its intensity- activates components of the intravascular compartment leading to overwhelming shock/DIC; or initiates a sequence of events involving both the intra- and extravascular (tissues) compartments that lead to organ failure. In the latter case, the disorder passes through two stages: an initial inflammatory/coagulopathic intravascular first stage triggered by E. c...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5294953</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5294953</guid>        </item>
        <item>
            <title>Human versus porcine mesenchymal stromal cells: phenotype, differentiation potential, immunomodulation and cardiac improvement after transplantation.</title>
            <link>http://www.medworm.com/index.php?rid=5294952&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%3D21973026%26dopt%3DAbstract</link>
            <description>Authors: Noort WA, Oerlemans MI, Rozemuller H, Feyen D, Jaksani S, Stecher D, Naaijkens B, Martens AC, Bühring HJ, Doevendans PA, Sluijter JP
    Abstract
    Although Mesenchymal Stromal Cells (MSC) have been applied clinically to treat cardiac diseases, it is unclear how and to which extent transplanted MSC exert their beneficial effects. To address these questions, pre-clinical MSC administrations are needed for which pigs appear to be the species of choice. This requires the use of porcine cells to prevent immune rejection. However, it is currently unknown to what extent porcine MSC (pMSC) resemble human MSC (hMSC). Aim of this study was to compare MSC from porcine bone marrow (BM) with human cells for phenotype, multi-lineage differentiation potential, immune-modulatory capacity and ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5294952</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5294952</guid>        </item>
        <item>
            <title>TNF-α inhibits aquaporin 5 expression in human salivary gland acinar cells via suppression of histone H4 acetylation.</title>
            <link>http://www.medworm.com/index.php?rid=5294951&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%3D21973049%26dopt%3DAbstract</link>
            <description>We examined the expression and activation levels of DNA methyltransferases (Dnmts) in NS-SV-AC cells treated with TNF-α. However, no significant changes were observed in the expression or activation levels of Dnmt1, Dnmt3a, or Dnmt3b. Although we also investigated the role of NF-κB activity in the TNF-α-induced suppression of AQP5 expression in NS-SV-AC cells, we detected similar TNF-α suppression of AQP5 expression in non-transfected cells and in a super-repressor form of IκBα cDNA-transfected cell clones. However, interestingly, chromatin immunoprecipitation analysis demonstrated a remarkable decrease in levels of acetylated histone H4 associated with the AQP5 gene promoter after treatment with TNF-α in NS-SV-AC cells. Therefore, our results may indicate that TNF-α inhibition of ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5294951</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5294951</guid>        </item>
        <item>
            <title>Age-related changes in the contractile and passive arterial properties of murine mesenteric small arteries are altered by caveolin-1 knockout.</title>
            <link>http://www.medworm.com/index.php?rid=5294950&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%3D21973085%26dopt%3DAbstract</link>
            <description>Authors: Hausman N, Martin J, Taggart MJ, Austin C
    Abstract
    Caveolin-1, an integral protein of caveolae, is associated with multiple cardiovascular signalling pathways. Caveolin-1 knockout (KO) mice have a reduced lifespan. As changes in artery structure and function are associated with ageing we have investigated the role of caveolin-1 ablation on age-related changes of small artery contractility and passive mechanical properties. Mesenteric small arteries isolated from 3 and 12 month wild type (WT) and caveolin-1 KO mice were mounted on a pressure myograph and changes in passive and functional arterial properties were continuously monitored. In WT mice ageing was associated with a reduction in arterial contractility to noradrenaline which was reversed by inhibition of nitric oxid...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5294950</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5294950</guid>        </item>
        <item>
            <title>Duodenal expression of iron transport molecules in patients with hereditary hemochromatosis or iron deficiency.</title>
            <link>http://www.medworm.com/index.php?rid=5294949&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%3D21973163%26dopt%3DAbstract</link>
            <description>Authors: Marketa DC, Karolina K, Kamila B, Jitka C, Vaclav H, Jan H, Jitka N, Jana V, Jan K, Jiri H
    Abstract
    Disturbances of iron metabolism are observed in chronic liver diseases. In the present study, we examined gene expression of duodenal iron transport molecules and hepcidin in patients with hereditary hemochromatosis (HHC) (treated and untreated), involving various genotypes (genotypes which represent risk for HHC were examined), and in patients with iron deficiency anemia (IDA). Gene expressions of DMT1, ferroportin, Dcytb, hephaestin, HFE, and TFR1 were measured in duodenal biopsies using real-time PCR and Western blot. Serum hepcidin levels were measured using ELISA. DMT1, ferroportin, and TFR1 mRNA levels were significantly increased in post-phlebotomized hemochromatics r...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5294949</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5294949</guid>        </item>
        <item>
            <title>Human umbilical cord mesenchymal stem cells suppress breast cancer tumorigenesis through direct cell-cell contact and internalization.</title>
            <link>http://www.medworm.com/index.php?rid=5294944&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%3D21973190%26dopt%3DAbstract</link>
            <description>Authors: Chao KC, Yang HT, Chen MW
    Abstract
    The purpose of this study was to investigate how HUMSCs affect breast cancer tumorigenesis. To observe the influence of HUMSCs on tumorigenesis in vitro, we performed a co-culture of MDA MB-231 breast cancer cells with HUMSCs, and a result of HUMSCs on tumorigenesis in vivo was achieved by injection of HUMSCs into NOD/SCID mice following tumor establishment with MDA-MB231. During the co-culture, apoptosis of MDA-MB231 was noted, which was driven either by binding with HUMSC through direct cell-cell contact or by formation of a novel cell-in-cell phenomenon after internalization of HUMSC. Also, treatment with HUMSC injection was efficacious in both in situ and metastatic breast cancers in the animal models. Since HUMSCs were proved to effi...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5294944</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5294944</guid>        </item>
        <item>
            <title>Pharmaceutical regulation of telomerase and its clinical potential.</title>
            <link>http://www.medworm.com/index.php?rid=5294937&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%3D21973217%26dopt%3DAbstract</link>
            <description>Authors: Sprouse AA, Steding CE, Herbert BS
    Abstract
    Telomeres serve the dual function of protecting chromosomes from genomic instability as well as protecting the ends of chromosomes from DNA damage machinery. The enzyme responsible for telomere maintenance is telomerase, an enzyme capable of reverse transcription. Telomerase activity is typically limited to specific cell types. However, telomerase activation in somatic cells serves as a key step toward cell immortalization and cancer. Targeting telomerase serves as a potential cancer treatment with significant therapeutic benefits. Beyond targeting cancers by inhibiting telomerase, manipulating the regulation of telomerase may also provide therapeutic benefit to other ailments, such as those related to aging. This review will int...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5294937</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5294937</guid>        </item>
        <item>
            <title>γ-secretase complexes containing caspase-cleaved presenilin-1 increase intracellular Aβ(42) /Aβ(40)  ratio.</title>
            <link>http://www.medworm.com/index.php?rid=5275031&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%3D21054783%26dopt%3DAbstract</link>
            <description>γ-secretase complexes containing caspase-cleaved presenilin-1 increase intracellular Aβ(42) /Aβ(40) ratio.
    J Cell Mol Med. 2011 Oct;15(10):2150-2163
    Authors: Hedskog L, Petersen CA, Svensson AI, Welander H, Tjernberg LO, Karlström H, Ankarcrona M
    Abstract
    Markers for caspase activation and apoptosis have been shown in brains of Alzheimer's disease (AD) patients and AD-mouse models. In neurons, caspase activation is associated with elevated amyloid β-peptide (Aβ) production. Caspases cleave numerous substrates including presenilin-1 (PS1). The cleavage takes place in the large cytosolic loop of PS1-C-terminal fragment (PS1CTF), generating a truncated PS1CTF lacking half of the loop domain (caspCTF). The loop has been shown to possess important regulatory functions with...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275031</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5275031</guid>        </item>
        <item>
            <title>Down-regulated miR-331-5p and miR-27a are associated with chemotherapy resistance and relapse in leukaemia.</title>
            <link>http://www.medworm.com/index.php?rid=5275030&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%3D21070600%26dopt%3DAbstract</link>
            <description>In this study, we used microRNA (miRNA) microarray and qRT-PCR approaches to investigate the expression of miRNAs in three leukaemia cell lines with different degrees of resistance to doxorubicin (DOX) compared with their parent cell line, K562. The expression of miR-331-5p and miR-27a was inversely correlated with the expression of a drug-resistant factor, P-glycoprotein (P-gp), in leukaemia cell lines with gradually increasing resistance. The development of drug resistance is regulated by the expression of the P-gp. Transfection of the K562 and, a human promyelocytic cell line (HL) HL60 DOX-resistant cells with miR-331-5p and miR-27a, separately or in combination, resulted in the increased sensitivity of cells to DOX, suggesting that correction of altered expression of miRNAs may be used...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275030</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5275030</guid>        </item>
        <item>
            <title>Role of HLA-G and NCR in protection of umbilical cord blood haematopoietic stem cells from NK cell mediated cytotoxicity.</title>
            <link>http://www.medworm.com/index.php?rid=5275029&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%3D21073654%26dopt%3DAbstract</link>
            <description>Authors: Wang M, Qiu Y, Wang X, Zhao F, Jin M, Xu M, Rong R, Ge H, Zhang Y, Wang X, Zhu T
    Abstract
    Allogeneic umbilical cord blood haematopoietic stem cells (UCB-HSCs) can be transplanted into a host with the intact innate immunity with limited immuno-reaction, although the mechanisms remain unclear. The present studies aimed at investigating potential mechanisms of allogeneic UCB-HSCs escape from the cytolysis of natural killer (NK) cells. We compared UCB-HSCs ability to protect from NK-mediated cytotoxicity with peripheral blood or bone marrow haematopoietic stem cells (PB-HSCs and BM-HSCs). HSCs expressed lower levels of natural cytotoxicity receptor ligands including NKp30L, NKp44L and NKp46L than monocytes. Blocking these ligands respectively or in combination could increase t...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275029</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5275029</guid>        </item>
        <item>
            <title>The novel Aurora A kinase inhibitor MLN8237 is active in resistant chronic myeloid leukaemia and significantly increases the efficacy of nilotinib.</title>
            <link>http://www.medworm.com/index.php?rid=5275028&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%3D21091633%26dopt%3DAbstract</link>
            <description>Authors: Kelly KR, Ecsedy J, Medina E, Mahalingam D, Padmanabhan S, Nawrocki ST, Giles FJ, Carew JS
    Abstract
    Novel therapies are urgently needed to prevent and treat tyrosine kinase inhibitor resistance in chronic myeloid leukaemia (CML). MLN8237 is a novel Aurora A kinase inhibitor under investigation in multiple phase I and II studies. Here we report that MLN8237 possessed equipotent activity against Ba/F3 cells and primary CML cells expressing unmutated and mutated forms of breakpoint cluster region-Abelson kinase (BCR-ABL). Notably, this agent retained high activity against the T315I and E255K BCR-ABL mutations, which confer the greatest degree of resistance to standard therapy. MLN8237 treatment disrupted cell cycle kinetics, induced apoptosis, caused a dose-dependent reductio...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275028</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5275028</guid>        </item>
        <item>
            <title>A comparison of the biochemical modifications caused by toxic and non-toxic protein oligomers in cells.</title>
            <link>http://www.medworm.com/index.php?rid=5275027&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%3D21155974%26dopt%3DAbstract</link>
            <description>Authors: Zampagni M, Cascella R, Casamenti F, Grossi C, Evangelisti E, Wright D, Becatti M, Liguri G, Mannini B, Campioni S, Chiti F, Cecchi C
    Abstract
    Peptides and proteins can convert from their soluble forms into highly ordered fibrillar aggregates, giving rise to pathological conditions ranging from neurodegenerative disorders to systemic amyloidoses. It is increasingly recognized that protein oligomers forming early in the process of fibril aggregation represent the pathogenic species in protein deposition diseases. The N-terminal domain of the HypF protein from Escherichia coli (HypF-N) has previously been shown to form, under distinct conditions, two types of HypF-N oligomers with indistinguishable morphologies but distinct structural features at the molecular level. Only th...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275027</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5275027</guid>        </item>
        <item>
            <title>Epigenetic regulation of cathepsin L expression in chronic myeloid leukaemia.</title>
            <link>http://www.medworm.com/index.php?rid=5275026&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%3D21496199%26dopt%3DAbstract</link>
            <description>Authors: Samaiya M, Bakhshi S, Shukla AA, Kumar L, Chauhan SS
    Abstract
    The expression and significance of cathepsin L (CTSL) has been extensively studied in solid tumours. However no such information in chronic myeloid leukaemia (CML) was available. We investigated the activity and expression of this protease in peripheral blood mononuclear cells (PBMCs) of 47 adult CML patients. Thirty adults suffering from systemic diseases and 50 healthy volunteers served as controls. The mRNA levels of CTSL, its specific endogenous inhibitor cystatin C and transcriptional up-regulator vascular endothelial growth factor (VEGF) were quantitated by real-time qPCR. CTSL protease activity and its mRNA expression were significantly higher in CML chronic phase (CP) patients compared to CML accelerated...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275026</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5275026</guid>        </item>
        <item>
            <title>Telocytes within human skeletal muscle stem cell niche.</title>
            <link>http://www.medworm.com/index.php?rid=5275025&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%3D21781275%26dopt%3DAbstract</link>
            <description>In this study, we aimed to characterize the properties of human muscle interstitial cells that had the characteristic morphology of telocytes (TCs). Immunocytochemistry and immunofluorescence showed that cells with TC morphology stained positive for c-kit/CD117 and VEGF. C-kit positive TCs were separated with magnetic-activated cell sorting, cultured in vitro and expanded for study. These cells exhibited high proliferation capacity (60% expressed endoglin/CD105 and 80% expressed nuclear Ki67). They also exhibited pluripotent capacity limited to Oct4 nuclear staining. In addition, 90% of c-kit positive TCs expressed VEGF. C-kit negative cells in the MuSCs population exhibited fibroblast-like morphology, low trilineage differential potential and negative VEGF staining. These results suggeste...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275025</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5275025</guid>        </item>
        <item>
            <title>Issue information.</title>
            <link>http://www.medworm.com/index.php?rid=5275024&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%3D21951395%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 21951395 [PubMed - in process] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275024</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5275024</guid>        </item>
        <item>
            <title>Epicardial epithelial to mesenchymal transition in injured heart.</title>
            <link>http://www.medworm.com/index.php?rid=5226954&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%3D21914126%26dopt%3DAbstract</link>
            <description>Authors: Zhou B, Pu WT
    Abstract
    Cre-LoxP-mediated genetic lineage trace has been used to illuminate the cell fate of progenitor cells in vivo. Application of this strategy to the epicardium, a sheet of cells covering the surface of heart, revealed that it dynamically participates in both heart development and postnatal heart repair and regeneration. After myocardial infarction, epicardial cells undergo epithelial-to-mesenchymal transition (EMT) and mainly adopt myofibroblast, fibroblast and smooth muscle cell fates. Here we present the wholemount images that map epicardial EMT following myocardial infarction, taking advantage of an inducible epicardial Cre line and a double fluorescence reporter. While remote epicardium retained its epithelial cell shape, reactivated epicardium in ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5226954</comments>
            <pubDate>Wed, 14 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5226954</guid>        </item>
        <item>
            <title>Ultrastructural differences between diabetic and idiopathic gastroparesis: The NIDDK gastroparesis clinical research consortium (GpCRC)(#†).</title>
            <link>http://www.medworm.com/index.php?rid=5226953&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%3D21914127%26dopt%3DAbstract</link>
            <description>In conclusion, in all the patients TEM showed abnormalities in ICC, nerves and smooth muscle consistent with the delay in gastric emptying. The significant differences found between diabetic and idiopathic gastroparesis offers insight into pathophysiology as well as into potential targeted therapies.
    PMID: 21914127 [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=5226953</comments>
            <pubDate>Wed, 14 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5226953</guid>        </item>
        <item>
            <title>Deep brain stimulation induces rapidly reversible transcript changes in Parkinson's leukocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5226955&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%3D21910823%26dopt%3DAbstract</link>
            <description>Authors: Soreq L, Bergman H, Goll Y, Greenberg DS, Israel Z, Soreq H
    Abstract
    Sub-thalamic deep brain stimulation (DBS) reversibly modulates Parkinson's disease (PD) motor symptoms, providing an unusual opportunity to compare leukocyte transcripts in the same individuals before and after neurosurgery and one hour after stimulus cessation (ON- and OFF-stimulus). Here, we report DBS-induced reversibility and OFF-stimulus restoration in 12 of 16 molecular functions and 3 of 4 biological processes shown to be differentially expressed between PD patients and controls, post-DBS from pre-DBS and OFF from ON states. Intriguingly, 6 of 18 inflammation and immune-related functions exhibited reversibility, and the extent of stimulus-induced changes correlated with the neurological DBS efficac...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5226955</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5226955</guid>        </item>
        <item>
            <title>PED/PEA-15 interacts with the 67 kDa laminin receptor and regulates cell adhesion, migration, proliferation and apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=5216368&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%3D21895963%26dopt%3DAbstract</link>
            <description>Authors: Formisano P, Ragno P, Pesapane A, Alfano D, Alberobello AT, Rea VE, Giusto R, Rossi FW, Beguinot F, Rossi G, Montuori N
    Abstract
    Phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes (PED/PEA-15) is an anti-apoptotic protein whose expression is increased in several human cancers. In addition to apoptosis, PED/PEA-15 is involved in the regulation of other major cellular functions, including cell adhesion, migration, proliferation and glucose metabolism. To further understand the functions of this protein, we performed a yeast two-hybrid screening using PED/PEA-15 as a bait and identified the 67 kDa high affinity laminin receptor (67LR) as an interacting partner. 67LR is a non-integrin cell-surface receptor for the extracellular matrix (ECM), derived from...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5216368</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5216368</guid>        </item>
        <item>
            <title>Elevation of IGF-2 receptor and the possible underlying implications in end-stage heart failure patients before and after heart transplantation.</title>
            <link>http://www.medworm.com/index.php?rid=5216367&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%3D21895964%26dopt%3DAbstract</link>
            <description>Authors: Wei Y, Li J, Huang J, Zhang X, Zhao H, Cui C, Li Y, Hu S
    Abstract
    Up-regulation of insulin-like growth factor 2 receptor (IGF-2R) involved in angiotensin II induced cell apoptosis in cardiomyoblasts, and correlated with cardiomyocyte apoptosis in hypertensive rat hearts. Here, we detected IGF-2R levels and explored the possible underlying implications in end-stage heart failure (HF) patients before and after heart transplantation. Western blot and imunohistochemistry were used to measure cardiac IGF-2R levels. Enzyme-linked immunosorbent assay (ELISA) was used to detect serum IGF-2R and CD8 levels. Labeling of DNA strand breaks and dihydroethidium detection were used to determine cellular apoptosis and reactive oxygen species, respectively. Cardiac IGF-2R levels increased ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5216367</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5216367</guid>        </item>
        <item>
            <title>Regulatory T cell: A protection for tumor cells.</title>
            <link>http://www.medworm.com/index.php?rid=5216365&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%3D21895966%26dopt%3DAbstract</link>
            <description>Authors: Wang Y, Ma Y, Fang Y, Wu S, Liu L, Fu D, Shen X
    Abstract
    Characterized by immunosuppression regulatory T cells (Tregs) plays a key role in maintaining immune tolerance. A growing number of tumors have been found with Tregs accumulating in microenvironment. And patients with high density of Tregs in tumor stroma get a worse prognosis, which suggests that Tregs may inhibit anti-tumor immunity in stroma, resulting in a poor prognosis.. In this paper we demonstrate the accumulation of Tregs in tumor stroma and the possible suppressive mechanisms. We also state the immunotherapy that has being used in animal and clinical trials.
    PMID: 21895966 [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=5216365</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5216365</guid>        </item>
        <item>
            <title>Experimental acute myocardial infarction: telocytes involvement in neo-angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5216363&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%3D21895968%26dopt%3DAbstract</link>
            <description>Authors: Manole CG, Cismasiu V, Gherghiceanu M, Popescu LM
    Abstract
    We used rat experimental myocardial infarction to study the ultrastructural recovery, especially neo-angiogenesis in the infarction border zone. We were interested in the possible role(s) of telocytes (TCs), a novel type of interstitial cell very recently discovered in myocardim (see www.telocytes.com). Indeed, electron microscopy, immunocytochemistry, and analyses of several proangiogenic microRNAs provided evidence for TC involvement in neo-angiogenesis after myocardial infarction. Electron microscopy showed the close spatial association of TCs with neoangiogenetic elements. Higher resolution provided the following information: a) the intercellular space between the abluminal face of endothelium and its surroundi...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5216363</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5216363</guid>        </item>
        <item>
            <title>Immune response to human embryonic stem cell-derived cardiac progenitors and adipose-derived stromal cells.</title>
            <link>http://www.medworm.com/index.php?rid=5216366&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%3D21895965%26dopt%3DAbstract</link>
            <description>Conclusion. ADSC express an immunomodulatory effect that limits both alloantigen and mitogen-induced lymphocyte responses. Furthermore, lymphocytes from patients with CAD are low responders to conventional stimuli, possibly because of their age and disease-associated treatment regimens. We propose that, in combination, these factors may limit the in vivo immunogenicity of cardiac progenitors co-implanted with ADSC in patients with CAD.
    PMID: 21895965 [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=5216366</comments>
            <pubDate>Mon, 05 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5216366</guid>        </item>
        <item>
            <title>Molecular mechanisms controlling CFTR gene expression in the airway.</title>
            <link>http://www.medworm.com/index.php?rid=5216364&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%3D21895967%26dopt%3DAbstract</link>
            <description>Authors: Zhang Z, Ott CJ, Lewandowsa MA, Leir SH, Harris A
    Abstract
    The low levels of CFTR gene expression and paucity of CFTR protein in human airway epithelial cells are not easily reconciled with the pivotal role of the lung in cystic fibrosis pathology. Previous data suggested that the regulatory mechanisms controlling CFTR gene expression might be different in airway epithelium in comparison to intestinal epithelium where CFTR mRNA and protein is much more abundant. Here we examine chromatin structure and modification across the CFTR locus in primary human tracheal (HTE) and bronchial (NHBE) epithelial cells and airway cell lines including 16HBE14o- and Calu3. We identify regions of open chromatin that appear selective for primary airway epithelial cells and show that several ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5216364</comments>
            <pubDate>Fri, 02 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5216364</guid>        </item>
        <item>
            <title>Angiostatic kinase inhibitors to sustain photodynamic angio-occlusion.</title>
            <link>http://www.medworm.com/index.php?rid=5192085&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%3D21880113%26dopt%3DAbstract</link>
            <description>Authors: Nowak-Sliwinska P, Weiss A, Beijnum JR, Wong TJ, Ballini JP, Lovisa B, Bergh HV, Griffioen AW
    Abstract
    Targeted angiostatic therapy receives major attention for the treatment of cancer and exudative age-related macular degeneration (AMD). Photodynamic therapy (PDT) has been used as an effective clinical approach for these diseases. Since PDT can cause an angiogenic response in the treated tissue, combination of PDT with anti-angiogenic compounds should lead to improved therapy. The current study was undertaken to test the clinically used small molecule kinase inhibitors Nexavar(®) (sorafenib), Tarceva(®) (erlotinib), and Sutent(®) (sunitinib) for this purpose, and compare the results to the combination of Visudyne(®) -PDT with Avastin(®) (bevacizumab) treatment. When ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192085</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192085</guid>        </item>
        <item>
            <title>Issue information.</title>
            <link>http://www.medworm.com/index.php?rid=5192067&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%3D21884404%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 21884404 [PubMed - in process] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192067</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192067</guid>        </item>
        <item>
            <title>SNARE complex-mediated degranulation in mast cells.</title>
            <link>http://www.medworm.com/index.php?rid=5192084&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%3D21880114%26dopt%3DAbstract</link>
            <description>Authors: Woska JR, Gillespie ME
    Abstract
    Mast cell function and dysregulation is important in the development and progression of allergic and autoimmune disease. Identifying novel proteins involved in mast cell function and disease progression is the first step in the design of new therapeutic strategies. SNAREs [soluble N-ethylmaleimide-sensitive factor attachment protein receptors] are a family of proteins demonstrated to mediate the transport and fusion of secretory vesicles to the membrane in mast cells, leading to the subsequent release of the vesicle cargo through an exocytotic mechanism. The functional role[s] of specific SNARE family member complexes in mast cell degranulation has not been fully elucidated. Here, we review recent and historical data on the expression, forma...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192084</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192084</guid>        </item>
        <item>
            <title>Identification of new cancer biomarkers based on aberrant mucin glycoforms by in situ Proximity Ligation.</title>
            <link>http://www.medworm.com/index.php?rid=5192073&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%3D21883895%26dopt%3DAbstract</link>
            <description>In conclusion, application of the PLA technique allowed sensitive detection of specific aberrant mucin glycoforms in cancer, increasing specificity to the use of antibodies either to the mucin protein backbone or the O-glycan haptens alone.
    PMID: 21883895 [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=5192073</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192073</guid>        </item>
        <item>
            <title>Everolimus is an active agent in medullary thyroid cancer: a clinical and in vitro study.</title>
            <link>http://www.medworm.com/index.php?rid=5192072&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%3D21883896%26dopt%3DAbstract</link>
            <description>Authors: Faggiano A, Ramundo V, Dicitore A, Castiglioni S, Borghi MO, Severino R, Ferolla P, Crinò L, Abbruzzese A, Sperlongano P, Caraglia M, Ferone D, Hofland L, Colao A, Vitale G
    Abstract
    Everolimus, an mTOR inhibitor, which has been demonstrated to induce antitumor effects in different types of neuroendocrine tumors, has never been evaluated in patients with medullary thyroid cancer (MTC). The aim of this study was to evaluate the in vitro and in vivo effects of everolimus in combination with octreotide in MTC. Two patients with progressive metastatic MTC and high calcitonin levels were treated with everolimus 5-10 mg/day. Both patients were under treatment with octreotide LAR at the study entry. An in vitro study was also performed to assess everolimus effects on MTC cell lin...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192072</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192072</guid>        </item>
        <item>
            <title>Analysis of microdissected neurons by (18) O mass spectrometry reveals altered protein expression in alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=5192071&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%3D21883897%26dopt%3DAbstract</link>
            <description>Authors: Hashimoto M, Bogdanovic N, Nakagawa H, Volkmann I, Aoki M, Winblad B, Sakai J, Tjernberg LO
    Abstract
    It is evident that the symptoms of Alzheimer's disease (AD) are derived from severe neuronal damage, and especially pyramidal neurons in the hippocampus are affected pathologically. Here, we analyzed the proteome of hippocampal neurons, isolated from postmortem brains by laser capture microdissection. By using (18) O labeling and mass spectrometry, the relative expression levels of 150 proteins in AD and controls were estimated. Many of the identified proteins are involved in transcription and nucleotide binding, glycolysis, heat-shock response, microtubule stabilization, axonal transport or inflammation. The proteins showing the most altered expression in AD were selected ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192071</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192071</guid>        </item>
        <item>
            <title>Basement membrane collagen type IV expression by human mesenchymal stem cells during adipogenic differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=5192070&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%3D21883898%26dopt%3DAbstract</link>
            <description>Authors: Sillat T, Saat R, Pöllänen R, Hukkanen M, Takagi M, Konttinen YT
    Abstract
    During adipogenic differentiation human mesenchymal stem cells (hMSC) produce collagen type IV. In immunofluorescence staining differentiating hMSCs started to express collagen type IV when Oil Red O-positive fat droplets appeared intracellularly. Quantitative real time-polymerase chain reaction confirmed progressive increase of collagen type IV α1 and α2 mRNA levels over time, 18.6- and 12.2-fold by day 28, respectively, whereas the copy numbers of α3-α6 mRNAs remained rather stable and low. Type IV collagen was in confocal laser scanning microscopy seen around adipocytes, where also laminins and nidogen were found, suggesting pericellular deposition of all key components of the fully develope...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192070</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192070</guid>        </item>
        <item>
            <title>Lysophosphatidylcholine inhibits membrane-associated SNARE complex disassembly.</title>
            <link>http://www.medworm.com/index.php?rid=5192077&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%3D21883893%26dopt%3DAbstract</link>
            <description>Authors: Shin L, Wang S, Lee JS, Flack A, Mao G, Jena BP
    Abstract
    In cells, NSF (N-ethylmaleimide-sensitive factor)-attachment protein receptors called SNAREs are involved in membrane fusion. In neurons for example, target membrane proteins SNAP-25 and syntaxin called t-SNAREs present at the presynaptic membrane, and a synaptic VAMP (vesicle-associated membrane protein) or v-SNARE, is part of the conserved protein complex involved in neurotransmission. Cholesterol and LPC (L-α-Lysophosphatidylcholine) are known to contribute to the negative and positive curvature respectively of membranes. In the present study, using purified recombinant neuronal membrane-associated SNAREs, we demonstrate for the first time that membrane-curvature-influencing lipids profoundly influence SNARE comp...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192077</comments>
            <pubDate>Sun, 28 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192077</guid>        </item>
        <item>
            <title>Endocytosis and intracellular processing of platelet microparticles by brain endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5192075&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%3D21883894%26dopt%3DAbstract</link>
            <description>In conclusion, PMP are taken up by active endocytosis in HBEC, involving mechanisms consistent with both phagocytosis and macropinocytosis. These findings identify new processes by which PMP could modify endothelial cell phenotype and functions.
    PMID: 21883894 [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=5192075</comments>
            <pubDate>Sun, 28 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192075</guid>        </item>
        <item>
            <title>Altered distribution of interstitial cells and innervation in the rat urinary bladder following spinal cord injury.</title>
            <link>http://www.medworm.com/index.php?rid=5192083&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%3D21883887%26dopt%3DAbstract</link>
            <description>Conclusions IC populations in bladder wall were decreased five weeks post-SCI, accompanied with reduced innervation, smooth muscle hypertrophy and increased compliance. These novel findings indicate that bladder wall remodelling post-SCI affects the integrity of interactions between smooth muscle, nerves and IC, with compromised IC populations. Correlation between IC reduction and a hypercompliant phenotype suggests that disruption to bladder IC contribute to pathophysiological processes underpinning the dysfunctional SCI bladder.
    PMID: 21883887 [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=5192083</comments>
            <pubDate>Wed, 24 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192083</guid>        </item>
        <item>
            <title>Selection of disease-specific biomarkers by integrating inflammatory mediators with clinical informatics in AECOPD patients: a preliminary study.</title>
            <link>http://www.medworm.com/index.php?rid=5192081&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%3D21883889%26dopt%3DAbstract</link>
            <description>Conclusion: There is a disease-specific profile of inflammatory mediators in COPD and AECOPD patients which may have a potential diagnostics together with clinical informatics of patients. Our preliminary study suggested that integration of proteomics with clinical informatics can be a new way to validate and optimize disease-special biomarkers.
    PMID: 21883889 [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=5192081</comments>
            <pubDate>Wed, 24 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192081</guid>        </item>
        <item>
            <title>Bone marrow mesenchymal stem cells can differentiate and assume corneal keratocyte phenotype.</title>
            <link>http://www.medworm.com/index.php?rid=5192080&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%3D21883890%26dopt%3DAbstract</link>
            <description>Authors: Liu H, Zhang J, Liu CY, Hayashi Y, Kao WW
    Abstract
    It remains elusive as to what bone marrow (BM) cell types infiltrate into injured and/or diseased tissues and subsequently differentiate to assume the phenotype of residential cells, e.g., neurons, cardiac myocytes, keratocytes, etc., to repair damaged tissue. Here, we examined the possibility of whether BM cell invasion via circulation into uninjured and injured corneas could assume a keratocyte phenotype, using chimeric mice generated by transplantation of enhanced green fluorescent protein (EGFP)+ BM cells into keratocan null (Kera(-/-) ) and lumican null (Lum(-/-) ) mice. EGFP+ BM cells assumed dendritic cell morphology, but failed to synthesize corneal-specific keratan sulfate proteoglycans, i.e., KS-lumican and KS-ke...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192080</comments>
            <pubDate>Wed, 24 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192080</guid>        </item>
        <item>
            <title>αV integrins and TGF-β induced EMT; a circle of regulation.</title>
            <link>http://www.medworm.com/index.php?rid=5192079&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%3D21883891%26dopt%3DAbstract</link>
            <description>Authors: Mamuya FA, Duncan MK
    Abstract
    Transforming Growth Factor-beta (TGF-β) has roles in embryonic development, the prevention of inappropriate inflammation and tumor suppression. However, TGF-β signaling also regulates pathological epithelial to-mesenchymal transition (EMT), inducing or progressing a number of diseases ranging from inflammatory disorders, to fibrosis and cancer. However, TGF-β signaling does not proceed linearly but rather induces a complex network of cascades that mutually influence each other and cross-talk with other pathways to successfully induce EMT. Particularly, there is substantial evidence for cross-talk between αV integrins and TGF-β during EMT, and anti-integrin therapeutics are under development as treatments for TGF-β-related disorders. Howe...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192079</comments>
            <pubDate>Wed, 24 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192079</guid>        </item>
        <item>
            <title>Cardiomyocytes derived from human embryonic and induced pluripotent stem cells: comparative ultrastructure.</title>
            <link>http://www.medworm.com/index.php?rid=5192082&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%3D21883888%26dopt%3DAbstract</link>
            <description>In conclusion, iPSC and hESC differentiate into cardiomyocytes of comparable ultrastructure, thus supporting the notion that iPSC offer a viable option for an autologous cell source for cardiac regenerative therapy.
    PMID: 21883888 [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=5192082</comments>
            <pubDate>Tue, 23 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192082</guid>        </item>
        <item>
            <title>Trichostatin A induces 5-lipoxygenase promoter activity and mRNA expression via inhibition of histone deacetylase 2 and 3.</title>
            <link>http://www.medworm.com/index.php?rid=5192078&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%3D21883892%26dopt%3DAbstract</link>
            <description>Authors: Pufahl L, Katryniok C, Schnur N, Sorg BL, Metzner J, Grez M, Steinhilber D
    Abstract
    5-lipoxygenase (5-LO) is the key enzyme in the formation of leukotrienes. We have previously shown that the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) activates 5-LO transcription via recruitment of Sp1, Sp3 and RNA polymerase II to the proximal promoter. In order to identify the HDACs involved in the regulation of 5-LO promoter activity isoform-specific HDAC inhibitors were applied. 5-LO promoter activity and mRNA expression was upregulated by the class I HDAC inhibitors apicidin and MS-275 but not by class II inhibitors. Knockdown of HDAC 1, 2 and 3 revealed that HDAC2 and HDAC3 but not HDAC1 is involved in the upregulation of 5-LO mRNA expression. In order to analyze the c...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192078</comments>
            <pubDate>Tue, 23 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5192078</guid>        </item>
        <item>
            <title>Oncostatin M decreases interleukin-1β secretion by human synovial fibroblasts and attenuates an acute inflammatory reaction in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5173915&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%3D21854541%26dopt%3DAbstract</link>
            <description>Authors: Dumas A, Lagarde S, Laflamme C, Pouliot M
    Abstract
    Oncostatin M (OSM) is a pleiotropic cytokine of the IL-6 family and displays both pro-inflammatory and anti-inflammatory activities. We studied the impact of OSM on the gene activation profile of human synovial cells, which play a central role in the progression of inflammatory responses in joints. In synovial cells stimulated with Escherichia coli lipopolysaccharide and recombinant human granulocyte-macrophage colony-stimulating factor, recombinant human OSM and native OSM secreted by human granulocytes both reduced the gene expression and secretion of IL-1β and CXCL8, but increased that of IL-6 and CCL2. This impact on synovial cell activation was not obtained using IL-6 or LIF. Signal transducer and activator of transc...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173915</comments>
            <pubDate>Thu, 18 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5173915</guid>        </item>
        <item>
            <title>Cyclic AMP increases COX-2 expression via mitogen activated kinase in human myometrial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5173914&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%3D21854542%26dopt%3DAbstract</link>
            <description>Authors: Chen L, Sooranna SR, Lei K, Kandola M, Bennett PR, Liang Z, Grammatopoulos D, Johnson MR
    Abstract
    Cyclic AMP (cAMP) is the archetypal smooth muscle relaxant, mediating the effects of many hormones and drugs. However, recently PGI(2) , acting via cAMP/PKA, was found to increase contraction-associated protein expression in myometrial cells and to promote oxytocin-driven myometrial contractility. Cyclo-oxygenase-2 (COX-2) is the rate-limiting enzyme in prostaglandin synthesis, which is critical to the onset and progression of human labour. We have investigated the impact of cAMP on myometrial COX-2 expression, synthesis and activity. Three cAMP agonists (8-bromo-cAMP, forskolin and rolipram) increased COX-2 mRNA expression and further studies confirmed that this was associate...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173914</comments>
            <pubDate>Thu, 18 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5173914</guid>        </item>
        <item>
            <title>Tyrosine kinase gene fusions in cancer: translating mechanisms into targeted therapies.</title>
            <link>http://www.medworm.com/index.php?rid=5173913&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%3D21854543%26dopt%3DAbstract</link>
            <description>Authors: Medves S, Demoulin JB
    Abstract
    Tyrosine kinase fusion genes represent an important class of oncogenes associated with leukemia and solid tumors. They are produced by translocations and other chromosomal rearrangements of a subset of tyrosine kinase genes, including ABL, PDGFRA, PDGFRB, FGFR1, SYK, RET, JAK2 and ALK. Based on recent findings, this review discusses the common mechanisms of activation of these fusion genes. Enforced oligomerization and inactivation of inhibitory domains are the two key processes that switch on the kinase domain. Activated tyrosine kinase fusions then signal via an array of transduction cascades which are largely shared. In addition, the fusion partner provides a scaffold for the recruitment of proteins that contribute to signaling, protein st...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173913</comments>
            <pubDate>Thu, 18 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5173913</guid>        </item>
        <item>
            <title>Injectable biodegradable hydrogels for embryonic stem cell transplantation: improved cardiac remodeling and function of myocardial infarction.</title>
            <link>http://www.medworm.com/index.php?rid=5140642&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%3D21838774%26dopt%3DAbstract</link>
            <description>This study suggest the potential of a method for heart regeneration involving oligo(poly(ethylene glycol) fumarate) hydrogels for stem cell encapsulation and transplantation.
    PMID: 21838774 [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=5140642</comments>
            <pubDate>Thu, 11 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5140642</guid>        </item>
        <item>
            <title>Central Zone of Myocardial Infarction: a neglected target area for heart cell therapy.</title>
            <link>http://www.medworm.com/index.php?rid=5140641&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%3D21838808%26dopt%3DAbstract</link>
            <description>Authors: Jin P, Wang E, Wang YH, Huang W, Kuang W, Sun C, Hu S, Zhang H
    Abstract
    The purpose of this study was to investigate the fate of transplanted cells in the central zone of myocardial infarction (MI), and to clarify the relationship between the injection-site impact and the efficacy of cell therapy. MI was created by coronary ligation in female rats. Three weeks later, 3-million labeled male bone-marrow mesenchymal stem cells (BMSCs) were directly injected into the border (BZC group) or central zone (CZC group) of MI area. As a control, culture medium was injected into the same sites. Cell survival was evaluated by quantitative real-time polymerase chain reaction, and apoptosis was assayed with TUNEL and caspase-3 staining. Four weeks after transplantation, heart function an...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5140641</comments>
            <pubDate>Thu, 11 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5140641</guid>        </item>
        <item>
            <title>Change in hepatocyte growth factor concentration promote mesenchymal stem cell-mediated osteogenic regeneration.</title>
            <link>http://www.medworm.com/index.php?rid=5140643&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%3D21831134%26dopt%3DAbstract</link>
            <description>This study aimed to determine the mechanisms by which different concentrations of HGF regulate MSC proliferation and osteogenic differentiation, and validate the mechanism in an animal model of early stage avascular necrosis of femoral head (ANFH). Our results demonstrate that a low concentration of HGF (20 ng/mL) preferentially promotes MSC osteogenic differentiation through increased c-Met expression and phosphorylation, Akt pathway activation, and increased expression of p27, Runx2, and Osterix. In contrast, a high concentration of HGF (100 ng/mL) strongly induced proliferation by inducing strong activation of the ERK1/2 signaling pathway. As validated by animal experiments, high localized expression of HGF achieved by transplantation of HGF transgenic MSCs into ANFH rabbits increased t...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5140643</comments>
            <pubDate>Tue, 09 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5140643</guid>        </item>
        <item>
            <title>Endoplasmic reticulum stress and insulin resistance post-trauma: similarities to type 2 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5140645&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%3D21812914%26dopt%3DAbstract</link>
            <description>Authors: Jeschke MG, Boehning D
    Abstract
    Type 2 diabetes, a rapidly growing disease of modern etiology, has a profound impact on morbidity and mortality. Explosions in the understanding of the underlying cellular mechanisms which lead to type 2 diabetes have recently been elucidated. In particular, the central role of endoplasmic reticulum stress (ER stress) and the unfolding protein response (UPR) in insulin resistance in type 2 diabetes has recently been discovered. We hypothesize that ER stress and UPR are not only central for type 2 diabetes but also for stress-induced diabetes. We review here the evidence that post-burn insulin resistance and hyperglycemia have pathophysiologic mechanisms in common with type 2 diabetes. These recent discoveries not only highlight the importanc...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5140645</comments>
            <pubDate>Tue, 02 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5140645</guid>        </item>
        <item>
            <title>Modification of a novel angiogenic peptide, AG30, for the development of novel therapeutic agents.</title>
            <link>http://www.medworm.com/index.php?rid=5140644&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%3D21812915%26dopt%3DAbstract</link>
            <description>Authors: Nakagami H, Nishikawa T, Tamura N, Maeda A, Hibino H, Mochizuki M, Shimosato T, Moriya T, Morishita R, Tamai K, Tomono K, Kaneda Y
    Abstract
    We previously identified a novel angiogenic peptide, AG30, with antibacterial effects that could serve as a foundation molecule for the design of wound healing drugs. Toward clinical application, in this study we have developed a modified version of the AG30 peptide characterized by improved antibacterial and angiogenic action, thus establishing a lead compound for a feasibility study. Since AG30 has an α-helix structure with a number of hydrophobic and cationic amino acids, we designed a modified AG30 peptide by replacing several of the amino acids. The replacement of cationic amino acids (yielding a new molecule, AG30/5C), but not h...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5140644</comments>
            <pubDate>Tue, 02 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5140644</guid>        </item>
        <item>
            <title>Telocytes in trachea and lungs.</title>
            <link>http://www.medworm.com/index.php?rid=5095135&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%3D21810171%26dopt%3DAbstract</link>
            <description>In conclusion, this study shows the presence in trachea and lungs of a peculiar type of cells, which fulfills the criteria for TC.
    PMID: 21810171 [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=5095135</comments>
            <pubDate>Tue, 02 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5095135</guid>        </item>
        <item>
            <title>Trivanillic polyphenols with anticancer cytostatic effects through the targeting of multiple kinases and intracellular Ca(2+) release.</title>
            <link>http://www.medworm.com/index.php?rid=5095171&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%3D21810170%26dopt%3DAbstract</link>
            <description>Authors: Lamoral-Theys D, Wauthoz N, Heffeter P, Mathieu V, Jungwirth U, Lefranc F, Nève J, Dubois J, Dufrasne F, Amighi K, Berger W, Gailly P, Kiss R
    Cancer cells exhibit deregulation of multiple cellular signaling pathways and treatments of various types of cancers with polyphenols are promising. We recently reported the synthesis of a series of 33 novel divanillic and trivanillic polyphenols that displayed anticancer activity, at least in vitro, through inhibiting various kinases. The current study revealed that minor chemical modifications of a trivanillate scaffold could convert cytotoxic compounds into cytostatic ones. Compound 13c, a tri-chloro derivative of trivanillic ester, displayed marked inhibitory activities against FGF-, VEGF-, EGF- and Src-related kinases, all of which...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5095171</comments>
            <pubDate>Mon, 01 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5095171</guid>        </item>
        <item>
            <title>Issue information.</title>
            <link>http://www.medworm.com/index.php?rid=5046743&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%3D21752187%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 21752187 [PubMed - in process] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5046743</comments>
            <pubDate>Thu, 21 Jul 2011 22:45:58 +0100</pubDate>
            <guid isPermaLink="false">5046743</guid>        </item>
        <item>
            <title>Tight junction proteins expression and modulation in immune cells and multiple sclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=5046742&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%3D21762372%26dopt%3DAbstract</link>
            <description>This study highlights a potential role of leukocyte TJPs in physiological states, and autoimmunity and suggests they should be further evaluated as biomarkers for aberrant immune activity and response to therapy in immune-mediated diseases such as MS.
    PMID: 21762372 [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=5046742</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5046742</guid>        </item>
        <item>
            <title>HMGB-1 induces c-kit(+) cell microvascular rolling and adhesion via both toll-like receptor-2 and toll like receptor-4 of endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5046741&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%3D21762373%26dopt%3DAbstract</link>
            <description>Conclusion HMGB-1 mediates c-kit(+) cell recruitment via endothelial TLR-2 and -4.
    PMID: 21762373 [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=5046741</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5046741</guid>        </item>
        <item>
            <title>Cardiomyocyte death induced by ischemic/hypoxic stress is differentially affected by distinct purinergic P2 receptors.</title>
            <link>http://www.medworm.com/index.php?rid=5046740&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%3D21762374%26dopt%3DAbstract</link>
            <description>Conclusions: Overall, these findings indicate a role for ATP and its receptors in modulating cardiomyocyte damage during ischemic/hypoxic stress.
    PMID: 21762374 [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=5046740</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5046740</guid>        </item>
        <item>
            <title>Mesenchymal stem cells show radioresistance in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5046739&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%3D21762375%26dopt%3DAbstract</link>
            <description>Authors: Singh S, Kloss FR, Brunauer R, Schimke M, Jamnig A, Greiderer-Kleinlercher B, Klima G, Rentenberger J, Auberger T, Hächl O, Rasse M, Gassner R, Lepperdinger G
    Irradiation impacts on the viability and differentiation capacity of tissue-borne mesenchymal stem cells (MSC), which play a pivotal role in bone regeneration. As a consequence of radiotherapy, bones may develop osteoradionecrosis. When irradiating human bone-derived MSC in vitro with increasing doses, the cells' self-renewal capabilities were greatly reduced. Mitotically stalled cells were still capable of differentiating into osteoblasts and preadipocytes. As a large animal model comparable to the clinical situation pig mandibles were subjected to fractionized radiation of 2×9 Gy within one week. This treatment mimic...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5046739</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5046739</guid>        </item>
        <item>
            <title>Contribution of genetic and dietary insulin resistance to Alzheimer phenotype in APP/PS1 transgenic mice.</title>
            <link>http://www.medworm.com/index.php?rid=5046738&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%3D21762376%26dopt%3DAbstract</link>
            <description>Authors: Hiltunen M, Khandelwal VK, Yaluri N, Tiilikainen T, Tusa M, Koivisto H, Krzisch M, Vepsäläinen S, Mäkinen P, Kemppainen S, Miettinen P, Haapasalo A, Soininen H, Laakso M, Tanila H
    According to epidemiological studies, type-2 diabetes increases the risk of Alzheimer's disease. Here, we induced hyperglycemia in mice over-expressing mutant amyloid precursor protein and presenilin-1 (APdE9) either by cross-breeding them with pancreatic insulin-like growth factor 2 (IGF-2) over-expressing mice or by feeding them with high-fat diet. Glucose and insulin tolerance tests revealed significant hyperglycemia in mice over-expressing IGF-2, which was exacerbated by high-fat diet. However, sustained hyperinsulinemia and insulin resistance were observed only in mice co-expressing IGF-2 and...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5046738</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5046738</guid>        </item>
        <item>
            <title>miR-145 is differentially regulated by TGFβ1 and ischemia and targets disabled-2 expression and wnt/β-catenin activity.</title>
            <link>http://www.medworm.com/index.php?rid=5046737&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%3D21762377%26dopt%3DAbstract</link>
            <description>Authors: Mayorga ME, Penn MS
    The effect of wnt/β-catenin signaling in the response to acute myocardial infarction (AMI) remains controversial. The membrane receptor adaptor protein Disabled-2 (Dab2) is a tumor suppressor protein and has a critical role in stem cell specification. We recently demonstrated that down-regulation of Dab2 regulates cardiac protein expression and wnt/β-catenin activity in mesenchymal stem cells (MSC) in response to TGFβ1. While Dab2 expression has been shown to have effects in stem cells and tumor suppression the molecular mechanisms regulating is expression are still undefined. We identified putative binding sites for miR-145 in the 3'-UTR of Dab2. In MSC in culture we observed that TGFβ1 treatment led to rapid and sustained up-regulation of pri-miR-145....</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5046737</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5046737</guid>        </item>
        <item>
            <title>Lucifer yellow - an angel rather than the Devil.</title>
            <link>http://www.medworm.com/index.php?rid=5046744&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%3D21740513%26dopt%3DAbstract</link>
            <description>Authors: Hanani M
    The fluorescent dye Lucifer yellow (LY) was introduced in 1978, and has been extremely useful in studying cell structure and communications. This dye has been used mostly for labeling cells by intracellular injection from microelectrodes. This review describes the numerous applications of LY, with emphasis on the enteric nervous system and interstitial cells of Cajal. Of particular importance is the dye coupling method, which enables the detection of cell coupling by gap junctions.
    PMID: 21740513 [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=5046744</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5046744</guid>        </item>
        <item>
            <title>Unfolded proteins and Endoplasmic Reticulum stress in neurodegenerative disorders.</title>
            <link>http://www.medworm.com/index.php?rid=4999084&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%3D21722302%26dopt%3DAbstract</link>
            <description>Authors: Doyle KM, Kennedy D, Gorman AM, Gupta S, Healy SJ, Samali A
    The stimuli for neuronal cell death in neurodegenerative disorders are multi-factorial and may include genetic predisposition, environmental factors, cellular stressors such as oxidative stress and free radical production, bioenergy failure, glutamate-induced excitotoxicity, neuroinflammation, disruption of Ca(2+) -regulating systems, mitochondrial dysfunction and misfolded protein accumulation. Cellular stress disrupts functioning of the endoplasmic reticulum, a critical organelle for protein quality control, leading to induction of the Unfolded Protein Response (UPR). ER stress may contribute to neurodegeneration in a range of neurodegenerative disorders. This review summarizes the molecular events occurring during ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999084</comments>
            <pubDate>Sun, 03 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999084</guid>        </item>
        <item>
            <title>Role of endothelial nitric oxide synthase (eNOS) in chronic stress-promoted tumor growth.</title>
            <link>http://www.medworm.com/index.php?rid=4999083&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%3D21722303%26dopt%3DAbstract</link>
            <description>Authors: Barbieri A, Palma G, Rosati A, Giudice A, Falco A, Petrillo A, Petrillo M, Bimonte S, Benedetto MD, Esposito G, Stiuso P, Abbruzzese A, Caraglia M, Arra C
    Accumulating evidence suggest that chronic stress can be a cofactor for the initiation and progression of cancer. Here we evaluated the role of endothelial nitric oxide synthase (eNOS) in stress-promoted tumor growth of murine B16F10 melanoma cell line in C57BL/6 mice. Animals subjected to restraint stress showed increased levels ACTH, enlarged adrenal glands, reduced thymus weight and a 3.61 fold increase in tumor growth in respect to no-stressed animals. Tumor growth was significantly reduced in mice treated with the beta antagonist propranolol. Tumor samples obtained from stressed mice displayed high levels of VEGF protei...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999083</comments>
            <pubDate>Sun, 03 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999083</guid>        </item>
        <item>
            <title>Type 2 diabetic Obese db/db mice are refractory to myocardial ischemic postconditioning In Vivo: potential role for Hsp20, F(1) -ATPase δ, and Echs1.</title>
            <link>http://www.medworm.com/index.php?rid=4999082&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%3D21722304%26dopt%3DAbstract</link>
            <description>Authors: Zhu SG, Xi L, Kukreja RC
    Ischemic postconditioning (PostC) is a clinically relevant cardioprotective modality that has been confirmed in many species including human. It remains unknown if PostC can still protect heart in Type 2 diabetes, a rapidly growing disease in the world. The present study investigated the efficacy of PostC in the leptin receptor deficient db/db mice, which possess Type 2 diabetic characteristics including obesity, hyperglycemia, and hyperleptinemia. Adult male C57BL/6J wild-type (WT) and db/db mice were anesthetized, mechanically ventilated, and subjected to left coronary artery occlusion for 30 min followed by 24 hrs of reperfusion. For the PostC groups, the hearts underwent 6 cycles of 10 sec of reperfusion and 10 sec of re-occlusion at the onset of r...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999082</comments>
            <pubDate>Sun, 03 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999082</guid>        </item>
        <item>
            <title>Regulation of the (pro)renin-renin receptor in cardiac remodeling.</title>
            <link>http://www.medworm.com/index.php?rid=4999081&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%3D21722305%26dopt%3DAbstract</link>
            <description>Authors: Mahmud H, Silljé HH, Cannon MV, van Gilst WH, de Boer RA
    The (pro)renin-renin receptor, (P)RR, was discovered as an important novel component of the renin angiotensin system (RAS). The functional significance of (P)RR is widely studied in renal and vascular pathologies and has sparked interest for a potential role in cardiovascular disease. To investigate the role of (P)RR in cardiac pathophysiology, we aimed to assess (P)RR regulation in adverse cardiac remodeling of the failing heart. In particular, we evaluated the expression of (P)RR in different models of heart failure and across different species. Significantly increased levels of (P)RR mRNA were found in post myocardial infarcted (MI) hearts of rats (1.6-fold, P&amp;lt;0.05) and mice (5-fold, P&amp;lt;0.01), as well as in tran...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999081</comments>
            <pubDate>Sun, 03 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999081</guid>        </item>
        <item>
            <title>Issue information.</title>
            <link>http://www.medworm.com/index.php?rid=4999092&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%3D21696540%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 21696540 [PubMed - in process] (Source: J Cell Mol Med)</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999092</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999092</guid>        </item>
        <item>
            <title>Caveolin induces cardioprotection through epigenetic regulation.</title>
            <link>http://www.medworm.com/index.php?rid=4999086&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%3D21707918%26dopt%3DAbstract</link>
            <description>Authors: Das M, Das S, Lekli I, Das DK
    Lipid rafts represent a sub-compartment of the plasma membrane that coordinate and regulate varieties of signaling processes while caveolins are the integral membrane protein of the lipid raft. Recent evidence demonstrated the pivotal role of caveolins in cardioprotection against ischemic injury although their mechanism of action is not clear. However, new understanding of epigenetic modification during ischemia reperfusion suggests additional targeted approaches that have not been explored before. To study the role of caveolin on epigenetic regulation, isolated mouse heart was prepared from wild type (WT) and caveolin-1 knock-out (Cav-1 KO) mouse and preconditioned them with 4 cyclic episodes of ischemia/ reperfusion followed by 30 min global isc...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999086</comments>
            <pubDate>Mon, 27 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999086</guid>        </item>
        <item>
            <title>Enhanced mobilisation of the bone marrow derived circulating progenitor cells by intracoronary freshly isolated bone marrow cells transplantation in patients with acute myocardial infarction.</title>
            <link>http://www.medworm.com/index.php?rid=4999090&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%3D21707914%26dopt%3DAbstract</link>
            <description>Authors: Turan RG, Bozdag-T I, Turan CH, Ortak J, Akin I, Kische S, Schneider H, Rauchhaus M, Rehders TC, Kleinfeldt T, Belu C, Amen S, Hermann T, Yokus S, Brehm M, Steiner S, Chatterjee T, Sahin K, Nienaber CA, Ince H
    Autologous bone marrow cell transplantation (BMCs-Tx) is a promising novel option for treatment of cardiovascular disease. We analyzed in a randomized controlled study the influence of the intracoronary autologous freshly isolated BMCs-Tx on the mobilisation of BM-CPCs in patients with acute myocardial infarction (AMI). 62 patients with AMI were randomized to either freshly isolated BMCs-Tx or to a control group without cell therapy. Peripheral blood (PB) concentrations of CD34/45(+) and CD133/45(+) circulating progenitor cells were measured by flow cytometry in 42 AMI p...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999090</comments>
            <pubDate>Thu, 23 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999090</guid>        </item>
        <item>
            <title>Caveolins in rhabdomyosarcoma.</title>
            <link>http://www.medworm.com/index.php?rid=4999089&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%3D21707915%26dopt%3DAbstract</link>
            <description>Authors: Rossi S, Poliani PL, Missale C, Monti E, Fanzani A
    Caveolins are scaffolding proteins that play a pivotal role in numerous processes, including caveolae biogenesis, vesicular transport, cholesterol homeostasis and regulation of signal transduction. There are three different isoforms (Cav-1, -2 and -3) that form homo- and hetero-aggregates at the plasma membrane and modulate the activity of a number of intracellular binding proteins. Cav-1 and Cav-3, in particular, are respectively expressed in the reserve elements (e.g. satellite cells) and in mature myofibers of skeletal muscle and their expression interplay characterizes the switch from muscle precursors to differentiated elements. Recent findings have shown that caveolins are also expressed in rhabdomyosarcoma, a group of h...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999089</comments>
            <pubDate>Thu, 23 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999089</guid>        </item>
        <item>
            <title>C-peptide promotes lesion development in a mouse model of arteriosclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=4999088&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%3D21707916%26dopt%3DAbstract</link>
            <description>Conclusions: Our results demonstrate that elevated C-peptide levels promote inflammatory cell infiltration and lesion development in ApoE-deficient mice without having metabolic effects. These data obtained in a mouse model of arteriosclerosis support the hypothesis that C-peptide may have an active role in atherogenesis in patients with diabetes and insulin resistance.
    PMID: 21707916 [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=4999088</comments>
            <pubDate>Thu, 23 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999088</guid>        </item>
        <item>
            <title>Alterations in the contractile phenotype of the bladder; lessons for understanding physiological and pathological remodeling of smooth muscle.</title>
            <link>http://www.medworm.com/index.php?rid=4999087&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%3D21707917%26dopt%3DAbstract</link>
            <description>Authors: Zderic SA, Chacko S
    The contractile properties of the urinary bladder are changed by the conditions of normal development and partial bladder outlet obstruction. This change in the contractile phenotype is accompanied by changes in the regulatory cascades and filaments that regulate contractility. This reviews focuses on such changes during the course of normal development and in response to obstruction. Our goal is to discuss the experimental evidence that has accumulated from work in animal models and correlate these findings with the human voiding phenotype.
    PMID: 21707917 [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=4999087</comments>
            <pubDate>Thu, 23 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999087</guid>        </item>
        <item>
            <title>Transcriptional insights on the regenerative mechanics of axotomized neurons in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=4999085&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%3D21711447%26dopt%3DAbstract</link>
            <description>Authors: Jeremy Ng JM, Chen MJ, Leung JY, Peng ZF, Manikandan J, Qi RZ, Chuah MI, West AK, Vickers JC, Lu J, Cheung NS, Chung RS
    Axotomized neurons have the innate ability to undergo regenerative sprouting but this is often impeded by the inhibitory central nervous system environment. To gain mechanistic insights into the key molecular determinates that specifically underlie neuronal regeneration at a transcriptomic level, we have undertaken a DNA microarray study on mature cortical neuronal clusters maintained in vitro at 8, 15, 24 and 48hrs following complete axonal severance. A total of 305 genes, each with a minimum fold change of ±1.5 for at least one out of the four time points and which achieved statistical significance (one-way ANOVA, p&amp;lt;0.05), were identified by DAVID and c...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999085</comments>
            <pubDate>Thu, 23 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999085</guid>        </item>
        <item>
            <title>The effect of myosin RLC phosphorylation in normal and cardiomyopathic mouse hearts.</title>
            <link>http://www.medworm.com/index.php?rid=4999091&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%3D21696541%26dopt%3DAbstract</link>
            <description>In this study, we have examined the effects of MLCK-phosphorylation of transgenic (Tg)-mouse cardiac muscle preparations expressing the D166V (aspartic acid to valine)-RLC mutation, identified to cause familial hypertrophic cardiomyopathy with malignant outcomes. Our previous work with Tg-D166V mice demonstrated a large increase in the Ca(2+) sensitivity of contraction, reduced maximal ATPase and force, and a decreased level of endogenous RLC phosphorylation. Based on studies demonstrating the beneficial and/or protective effects of cardiac myosin phosphorylation for heart function, we hypothesized that an ex vivo phosphorylation of Tg-D166V cardiac muscle may rescue the detrimental contractile phenotypes observed earlier at the level of single myosin molecules and in Tg-D166V papillary mu...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999091</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999091</guid>        </item>
        <item>
            <title>Deletion of PLCB1 gene in schizophrenia affected patients.</title>
            <link>http://www.medworm.com/index.php?rid=4999097&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%3D21692983%26dopt%3DAbstract</link>
            <description>Authors: Lo Vasco VR, Cardinale G, Polonia P
    A prevalence of 1% in the general population and approximately 50% concordance rate in monozygotic twins was reported for schizophrenia, suggesting that genetic predisposition affecting neurodevelopmental processes might combine with environmental risk factors. A multitude of pathways seems to be involved in the etiology and/or pathogenesis of schizophrenia, including dopaminergic, serotoninergic, muscarinic and glutamatergic signaling. The phosphoinositide signal transduction system and related phosphoinositide-specific phospholipase C (PI-PLC) enzymes seem to represent a point of convergence in these networking pathways during the development of selected brain regions. The existence of a susceptibility locus on the short arm of chromosome ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999097</comments>
            <pubDate>Tue, 21 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999097</guid>        </item>
        <item>
            <title>Anti-inflammatory potential of allyl-isothiocyanate-role of Nrf2, NFκB and microRNA-155.</title>
            <link>http://www.medworm.com/index.php?rid=4999095&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%3D21692985%26dopt%3DAbstract</link>
            <description>Authors: Wagner AE, Boesch-Saadatmandi C, Dose J, Schultheiss G, Rimbach G
    In the present study the underlying mechanisms of the potential anti-inflammatory properties of allyl-isothiocyanate (AITC) were analysed in vitro and in vivo. Murine RAW264.7 macrophages stimulated with lipopolysaccharide (LPS) were supplemented with increasing concentrations of AITC. In addition C57BL/6 mice (n = 10 per group) were fed a pro-inflammatory high fat diet and AITC was administered orally via gavage for 7 days. Biomarkers of inflammation were determined both in cultured cells and in mice. AITC significantly decreased tumor necrosis factor α mRNA levels and its secretion in LPS stimulated RAW264.7 macrophages. Furthermore gene expression of other pro-inflammatory markers including interleukin 1β a...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999095</comments>
            <pubDate>Tue, 21 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999095</guid>        </item>
        <item>
            <title>Genetic polymorphisms and MicroRNAs: new direction in molecular epidemiology of solid cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4999100&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%3D21692980%26dopt%3DAbstract</link>
            <description>Authors: Slaby O, Bienertova-Vasku J, Svoboda M, Vyzula R
    MicroRNAs (miRNAs) are small non-coding RNAs which regulate gene expression. Single nucleotide polymorphisms (SNPs) may occur in miRNA biogenesis pathway genes, pri-miRNA, pre-miRNA or a mature miRNA sequence. Such polymorphisms may be functional with respect to biogenesis and actions of mature miRNA. Specific SNPs were identified in predicted miRNA target sites within 3' untranslated regions of mRNAs. These SNPs have a potential to affect the efficiency of miRNA binding to the target sites or can create or disrupt binding sites. Resulting gene dysregulation may involve changes in phenotype and may eventually prove critical for the susceptibility to cancer and its onset as well as for estimates of prognosis and therapy response....</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999100</comments>
            <pubDate>Mon, 20 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999100</guid>        </item>
        <item>
            <title>How do tenascins influence the birth and life of a malignant cell?</title>
            <link>http://www.medworm.com/index.php?rid=4999099&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%3D21692981%26dopt%3DAbstract</link>
            <description>Authors: Brellier F, Chiquet-Ehrismann R
    Tenascins are large glycoproteins found in embryonic and adult extracellular matrices. Of the four family members, two have been shown to be overexpressed in the microenvironment of solid tumors: tenascin-C and tenascin-W. The regular presence of these proteins in tumors suggests a role in tumorigenesis which has been investigated intensively for tenascin-C and recently for tenascin-W as well. In this review, we follow a malignant cell starting from its birth through its potential metastatic journey and describe how tenascin-C and tenascin-W contribute to these successive steps of tumorigenesis. We consider the importance of the mechanical aspect in tenascin signaling. Furthermore, we discuss studies describing tenascin-C as an important compone...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999099</comments>
            <pubDate>Mon, 20 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999099</guid>        </item>
        <item>
            <title>Water channels in platelet volume regulation.</title>
            <link>http://www.medworm.com/index.php?rid=4999098&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%3D21692982%26dopt%3DAbstract</link>
            <description>Authors: Lee JS, Agrawal S, Turkovich MV, Taatjes DJ, Walz DA, Jena BP
    The regulation of platelet volume significantly affects its function. Since water is the major molecule in cells and its active transport via water channels called aquaporins (AQPs) have been implicated in cellular and organelle volume regulation, the presence of water channels in platelets and their potential role in platelet volume regulation was investigated. G protein-mediated AQP regulation in secretory vesicle swelling has previously been reported in neurons and in pancreatic acinar cells. Mercuric chloride has been demonstrated to inhibit most AQPs except AQP6, which is stimulated by the compound. Exposure of platelets to HgCl(2) induced swelling in a dose-dependent manner, suggesting the presence of AQP6 in ...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999098</comments>
            <pubDate>Mon, 20 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999098</guid>        </item>
        <item>
            <title>K(ATP) channel agonists preserve connexin43 protein in infarcted rats by a protein kinase c-dependent pathway.</title>
            <link>http://www.medworm.com/index.php?rid=4999096&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%3D21692984%26dopt%3DAbstract</link>
            <description>Authors: Lee TM, Lin CC, Lien HY, Chen CC
    Downward remodeling of gap junctional proteins between myocytes may trigger ventricular arrhythmia after myocardial infarction. We have demonstrated that ATP-sensitive potassium (K(ATP) ) channel agonists attenuated postinfarction arrhythmias. However, the involved mechanisms remain unclear. The purpose of this study was to determine whether K(ATP) channel agonists can attenuate arrhythmias through preserving protein kinase C (PKC)-ɛ-dependent connexin43 level after myocardial infarction. Male Wistar rats after ligating coronary artery were randomized to either vehicle, nicorandil, pinacidil, glibenclamide, or a combination of nicorandil and glibenclamide or pinacidil and glibenclamide for 4 weeks. To elucidate the role of PKCɛ in the modulat...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999096</comments>
            <pubDate>Mon, 20 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999096</guid>        </item>
        <item>
            <title>Profilin1 facilitates staurosporine-triggered apoptosis by stabilizing the integrin β1-actin complex in breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4999094&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%3D21692986%26dopt%3DAbstract</link>
            <description>Authors: Yao W, Yu X, Fang Z, Yin P, Zhao C, Li N, Wang L, Li Z, Zha X
    Profilin1 (Pfn1) functions as a tumor suppressor against malignant phenotypes of cancer cells. A minimum level of Pfn1 is critical for the differentiation of human epithelial cells, and its lower expression correlates with the tumorigenesis of breast cancer cells and tissues. However, the molecular mechanisms underlying its antitumor action remain largely unknown. In the current study, we found that stable expression of ectopic Pfn1 sensitized the breast cancer cell line MDA-MB-468 to apoptosis induced by staurosporine, a widely used natural apoptosis-inducing agent. Pfn1 overexpression could also upregulate the expression of integrin α5β1, which has been shown to inhibit the transformed phenotype of cancer cells....</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4999094</comments>
            <pubDate>Mon, 20 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999094</guid>        </item>
        <item>
            <title>MiR-210: an important player in the pathogenesis of preeclampsia?</title>
            <link>http://www.medworm.com/index.php?rid=4999093&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%3D21692987%26dopt%3DAbstract</link>
            <description>Authors: Liu C, Zhou Y, Zhang Z
    
    PMID: 21692987 [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=4999093</comments>
            <pubDate>Mon, 20 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4999093</guid>        </item>
        <item>
            <title>Inducible hydrogen sulfide synthesis in chondrocytes and mesenchymal progenitor cells: is h(2) S a novel cytoprotective mediator in the inflamed joint?</title>
            <link>http://www.medworm.com/index.php?rid=4953519&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%3D21679296%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: These data suggest CSE is an inducible source of H(2) S in cultured HAC and MPC. H(2) S may represent a novel endogenous mechanism of cytoprotection in the inflamed joint, suggesting a potential opportunity for therapeutic intervention.
    PMID: 21679296 [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=4953519</comments>
            <pubDate>Thu, 16 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4953519</guid>        </item>
        <item>
            <title>Autoantibody signatures: progress and perspectives for early cancer detection.</title>
            <link>http://www.medworm.com/index.php?rid=4953521&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%3D21651719%26dopt%3DAbstract</link>
            <description>Authors: Desmetz C, Mange A, Maudelonde T, Solassol J
    Becoming invasive is a crucial step in cancer development, and the early spread of tumor cells is usually undetected by current imaging technologies. In patients with cancer and no signs of overt metastases, sensitive methods have been developed to identify circulating autoantibodies and their antigen counterparts in several cancers. These technologies are often based on proteomic approaches, and recent advances in protein and antibody microarrays have greatly facilitated the discovery of new antibody biomarkers in sera from cancer patients. Interestingly, in a clinical application setting, combinations of multiple autoantibody reactivities into panel assays have recently been proposed as relevant screening tests and validated in se...</description>
            <author>J Cell Mol Med</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4953521</comments>
            <pubDate>Wed, 08 Jun 2011 23:00:00 +0100</pubDate>
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