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        <title>Journal of Cellular and Molecular Medicine 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 'Journal of Cellular and Molecular Medicine' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Journal+of+Cellular+and+Molecular+Medicine&t=Journal+of+Cellular+and+Molecular+Medicine&s=Search&f=source]]></link>
        <lastBuildDate>Thu, 09 Feb 2012 16:56:45 +0100</lastBuildDate>
        <item>
            <title>Vestibular Regeneration – Experimental Models and Clinical Implications</title>
            <link>http://www.medworm.com/index.php?rid=5656531&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01540.x</link>
            <description>AbstractTherapies aimed at the protection and/or regeneration of inner ear hair cells are of great interest given the significant monetary and quality of life impact of balance disorders. Different viral vectors have been shown to transfect various cell types in the inner ear. The past decade has provided tremendous advances in the use of adenoviral vectors to achieve targeted treatment delivery. Several routes of delivery have been identified in order to introduce vectors into the inner ear while minimizing injury to surrounding structures. Recently, the transcription factor Atoh1 was determined to play a critical role in hair cell differentiation. Adenoviral‐mediated overexpression of Atoh1 in culture and in vivo has demonstrated the ability to regenerate vestibular hair cells by causi...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5656531</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5656531</guid>        </item>
        <item>
            <title>AL3810, a multi‐tyrosine kinase inhibitor, exhibits potent anti‐angiogenic and antitumor activity via targeting VEGFR, FGFR, and PDGFR</title>
            <link>http://www.medworm.com/index.php?rid=5656530&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01541.x</link>
            <description>AbstractAngiogenesis plays an important role in neoplastic transformation and progression as well as in the metastasis process of most human cancers. Herein, we identified AL3810 as a novel and orally bioavaliable small molecular inhibitor with potent inhibitory activity against multiple tyrosine kinases involved in the process of angiogenesis. We found that AL3810 substantially inhibited the autophosphorylation of VEGFR2, PDGFRβ and FGFR1 in endothelial cells. Moreover, AL3810 exhibited potent anti‐angiogenesis activity, manifested by significant inhibition of microvessel outgrowth of rat arterial ring and chickallantochorion membrane (CAM) in ex vivo angiogenesis models. Daily dosing of AL3810 has shown broad‐spectrum anti‐tumor activity in human kidney, pancreas, liver cancer xen...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5656530</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5656530</guid>        </item>
        <item>
            <title>Genistein as a potential inducer of the anti‐atherogenic enzyme paraoxonase‐1: studies in cultured hepatocytes in vitro and in rat liver in vivo</title>
            <link>http://www.medworm.com/index.php?rid=5656529&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01542.x</link>
            <description>AbstractA number of cardioprotective effects, including the reduction of the LDL particle to oxidation, have been attributed to dietary soy isoflavones. Paraoxonase 1 (PON1), an enzyme mainly synthesized in the liver, may exhibit anti‐atherogenic activity by protecting LDL from oxidation. Thus, dietary and pharmacological inducers of PON1 may reduce cardiovascular disease risk. Using a luciferase reporter gene assay we screened different flavonoids for their ability to induce PON1 in Huh7 hepatocytes in culture. Genistein was the most potent flavonoid regarding its PON1 inducing activity, followed by daidzein, luteolin, isorhamnetin and quercetin. Other flavonoids such as naringenin, cyanidin, malvidin and catechin showed only little or no PON1 inducing activity. Genistein‐mediated PON...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5656529</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5656529</guid>        </item>
        <item>
            <title>A logistic model for the detection of circulating tumor cells in human metastatic colorectal cancer</title>
            <link>http://www.medworm.com/index.php?rid=5656528&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01544.x</link>
            <description>AbstractThe accuracy in the diagnosis of metastatic colorectal cancer (mCRC) represents one of the challenges in the clinical management of patients. The detection of Circulating Tumor Cells (CTC) is becoming a promising alternative to current detection techniques as it focuses on one of the players of the metastatic disease and it should provide with more specific and sensitive detection rates. Here, we describe an improved method of detection of CTC from mCRC patients by combining immune‐enrichment, optimal purification of RNA from very low cell numbers, and the selection of accurate PCR probes. As a result, we obtained a logistic model that combines GAPDH and VIL1 normalized to CD45 rendering powerful results in the detection of CTC from mCRC patients (AUROC value 0.8599). We further ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5656528</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5656528</guid>        </item>
        <item>
            <title>Potential biomarkers in psychiatry: focus on the cholesterol system</title>
            <link>http://www.medworm.com/index.php?rid=5656527&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01543.x</link>
            <description>AbstractMeasuring biomarkers to identify and assess illness is a strategy growing in popularity and relevance. Although already in clinical use for treating and predicting cancer, no biological measurement is used clinically for any psychiatric disorder. Biomarkers could predict the course of a medical problem, and aid in determining how and when to treat. Several studies have indicated that of candidate psychiatric biomarkers detected using proteomic techniques, cholesterol and associated proteins, specifically apolipoproteins (Apos), may be of interest. Cholesterol is necessary for brain development and its synthesis continues at a lower rate in the adult brain. Apos are the protein component of lipoproteins responsible for lipid transport. There is extensive evidence that the levels of ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5656527</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5656527</guid>        </item>
        <item>
            <title>Osteoinduction and survival of osteoblasts and bone‐marrow stromal cells in 3D biphasic calcium phosphate scaffolds under static and dynamic culture conditions</title>
            <link>http://www.medworm.com/index.php?rid=5656526&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01545.x</link>
            <description>AbstractIn many tissue engineering approaches, the basic difference between in vitro and in vivo conditions for cells within three‐dimensional (3D) constructs is the nutrition flow dynamics. To achieve comparable results in vitro, bioreactors are advised for improved cell survival, as they are able to provide a controlled flow through the scaffold. We hypothesize that a bioreactor would enhance long term differentiation conditions of osteogenic cells in 3D scaffolds. To achieve this either primary rat osteoblasts or bone marrow stromal cells (BMSC) were implanted on uniform‐sized biphasic calcium phosphate (BCP) scaffolds produced by a 3D printing method. Three types of culture conditions were applied: static culture without osteoinduction (Group A); static culture with osteoinduction ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5656526</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5656526</guid>        </item>
        <item>
            <title>Drosophila as a Model to Study the Genetic Mechanisms of Obesity‐Associated Heart Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=5664293&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01522.x</link>
            <description>AbstractObesity and cardiovascular disease are among the world's leading causes of death, especially in Western countries where consumption of high caloric food is commonly accompanied by low physical activity. This lifestyle often leads to energy imbalance, obesity, diabetes, and their associated metabolic disorders, including cardiovascular diseases. It has become increasingly recognized that obesity and cardiovascular disease are metabolically linked, and a better understanding of this relationship requires that we uncover the fundamental genetic mechanisms controlling obesity‐related heart dysfunction, a goal that has been difficult to achieve in higher organisms with intricate metabolic complexity. However, the high degree of evolutionary conservation of genes and signaling pathways...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5664293</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5664293</guid>        </item>
        <item>
            <title>Overexpression of mouse TTF‐2 gene causes cleft palate</title>
            <link>http://www.medworm.com/index.php?rid=5656525&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01546.x</link>
            <description>AbstractIn humans, mutations of the gene encoding for thyroid transcription factor‐2 (TTF‐2 or FOXE1) result in Bamforth syndrome. Bamforth syndrome is characterized by agenesis, cleft palate, spiky hair, and choanal atresia. TTF‐2 null mice (TTF‐2‐/‐) also exhibit cleft palate, suggesting its involvement in the palatogenesis. However, the molecular pathology and genetic regulation by TTF2 are largely unknown. In the present study, the recombinant expression vector pBROAD3‐TTF‐2 containing the promoter of the mouse ROSA26 gene was created to form the structural gene of mouse TTF‐2 and was microinjected into the male pronuclei of fertilized ova. Sequence analysis confirmed that the TTF‐2 transgenic mouse model was established successfully. The transgenic mice displayed a...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5656525</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5656525</guid>        </item>
        <item>
            <title>Myocardial regeneration by transplantation of modified endothelial progenitor cells expressing SDF‐1 in a rat model</title>
            <link>http://www.medworm.com/index.php?rid=5643866&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01539.x</link>
            <description>Conclusionintramyocardial application of lentiviral infected EPCs is associated with a significant improvement of myocardial function after infarction, in contrast to an intracoronary application. Histological results revealed a significant augmentation of neovascularization, lower collagen content, higher numbers of inflammatory cells and remarkable alterations of apoptotic/proliferative processes in infarcted areas after cell transplantation.© 2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5643866</comments>
            <pubDate>Tue, 31 Jan 2012 14:52:29 +0100</pubDate>
            <guid isPermaLink="false">5643866</guid>        </item>
        <item>
            <title>The therapeutic effect of Rosuvastatin on cardiac remodeling from hypertrophy to fibrosis during the end‐stage hypertension in rats</title>
            <link>http://www.medworm.com/index.php?rid=5643867&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01536.x</link>
            <description>ConclusionThe present study revealed that old‐aged SHRs developed cardiac remodeling from hypertrophy to fibrosis via cardiac apoptosis during the end stage of hypertensive heart disease. These pathological changes might be the consequence of activation of AT1 Receptor‐PKCβ2/α‐ERK‐c‐fos and AKT‐FOXO1/Bcl‐2/survivin/Caspase3 signaling. Rosuvastatin effectively attenuated the structural changes by reversing the signaling transductions involved.© 2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5643867</comments>
            <pubDate>Mon, 30 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5643867</guid>        </item>
        <item>
            <title>Upregualtion of BMP‐2 antagonizes TGF‐β1/ROCK‐enhanced cardiac fibrotic signaling through activating of Smurf1/Smad6 complex</title>
            <link>http://www.medworm.com/index.php?rid=5643868&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01538.x</link>
            <description>In conclusion, we propose that BMP‐2, as a novel fibrosis antagonizing cytokine, may have potential beneficial effect in attenuating pressure overload‐induced cardiac fibrosis.© 2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5643868</comments>
            <pubDate>Sat, 28 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5643868</guid>        </item>
        <item>
            <title>ENDOGLIN/CD105 is expressed in KIT positive cells in the gut and in gastrointestinal stromal tumours</title>
            <link>http://www.medworm.com/index.php?rid=5635483&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01315.x</link>
            <description>AbstractENDOGLIN/CD105 (ENG) is a transmembrane glycoprotein and an auxiliary unit of the transforming growth factor‐β (TGF‐β); receptor, expressed predominantly in vascular endothelium. Noteworthy, Eng mRNA expression has been reported also in Kit+ interstitial cells of Cajal (ICC) in the mouse intestine. Gastrointestinal stromal tumours (GIST) are thought to derive from ICC. Here we have investigated Eng expression in the KitK641E mouse GIST model, in human GIST and in the Ba/F3 cell model. In wild type (WT) mouse antrum, Eng immunoreactivity (‐ir) was detected in CD34+/CD31+ endothelium and in Kit+ ICC. In KitK641E mice, hyperplasia of Kit+ cells made Eng‐ir even more evident. Quantitative PCR confirmed the increased expression of Eng transcript in KitK641E mice. On human GIST...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5635483</comments>
            <pubDate>Fri, 27 Jan 2012 21:50:41 +0100</pubDate>
            <guid isPermaLink="false">5635483</guid>        </item>
        <item>
            <title>High‐molecular weight Aβ oligomers and protofibrils are the predominant Aβ species in the native soluble protein fraction of the AD brain</title>
            <link>http://www.medworm.com/index.php?rid=5635479&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01306.x</link>
            <description>AbstractAlzheimer’s disease (AD) is characterized by the aggregation and deposition of amyloid β protein (Aβ) in the brain. Soluble Aβ oligomers are thought to be toxic. To investigate the predominant species of Aβ protein that may play a role in AD pathogenesis, we performed biochemical analysis of AD and control brains. Sucrose buffer‐soluble brain lysates were characterized in native form using blue native (BN)‐PAGE and also in denatured form using SDS‐PAGE followed by Western blot analysis. BN‐PAGE analysis revealed a high‐molecular weight smear (&amp;gt;1000 kD) of Aβ42‐positive material in the AD brain, whereas low‐molecular weight and monomeric Aβ species were not detected. SDS‐PAGE analysis, on the other hand, allowed the detection of prominent Aβ monomer and d...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5635479</comments>
            <pubDate>Fri, 27 Jan 2012 21:50:38 +0100</pubDate>
            <guid isPermaLink="false">5635479</guid>        </item>
        <item>
            <title>α‐Lipoic acid attenuates vascular calcification via reversal of mitochondrial function and restoration of Gas6/Axl/Akt survival pathway</title>
            <link>http://www.medworm.com/index.php?rid=5635478&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01294.x</link>
            <description>This study investigated the effect of α‐lipoic acid (ALA), a naturally occurring antioxidant that improves mitochondrial function, on vascular calcification in vitro and in vivo. Calcifying vascular smooth muscle cells (VSMCs) treated with inorganic phosphate (Pi) exhibited mitochondrial dysfunction, as demonstrated by decreased mitochondrial membrane potential and ATP production, the disruption of mitochondrial structural integrity and concurrently increased production of reactive oxygen species. These Pi‐induced functional and structural mitochondrial defects were accompanied by mitochondria‐dependent apoptotic events, including release of cytochrome c from the mitochondria into the cytosol, subsequent activation of caspase‐9 and ‐3, and chromosomal DNA fragmentation. Intrigui...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5635478</comments>
            <pubDate>Fri, 27 Jan 2012 21:50:35 +0100</pubDate>
            <guid isPermaLink="false">5635478</guid>        </item>
        <item>
            <title>Sequential biphasic changes in claudin1 and claudin4 expression are correlated to colorectal cancer progression and liver metastasis</title>
            <link>http://www.medworm.com/index.php?rid=5635477&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01289.x</link>
            <description>In conclusion, sequential biphasic changes in claudin1 and claudin4 expression occur during the homing of rat CC531 CRC cells to the liver. This modulation is reflected by significant changes in claudin expression in human primary and metastatic CRC. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5635477</comments>
            <pubDate>Fri, 27 Jan 2012 21:50:34 +0100</pubDate>
            <guid isPermaLink="false">5635477</guid>        </item>
        <item>
            <title>Elevated levels of hypoxia‐inducible microRNA‐210 in pre‐eclampsia: new insights into molecular mechanisms for the disease</title>
            <link>http://www.medworm.com/index.php?rid=5635476&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01291.x</link>
            <description>AbstractPre‐eclampsia is a leading cause of maternal and foetal morbidity and mortality worldwide. Insufficient uteroplacental oxygenation is believed to be responsible for the disease. However, what molecular events involve in hypoxic responses and how they affect placental development remain unclear. Recently, miRNAs have emerged as a new class of molecules in response to hypoxia. We show here that the expression of microRNA‐210 (mir‐210) is up‐regulated in patients with pre‐eclampsia, as well as in trophoblast cells cultured under hypoxic conditions. Ectopic expression of mir‐210 inhibited the migration and invasion capability of trophoblast cells. Ephrin‐A3 and Homeobox‐A9, which related with cell migration and vascular remodelling, were then experimentally validated as...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5635476</comments>
            <pubDate>Fri, 27 Jan 2012 21:50:32 +0100</pubDate>
            <guid isPermaLink="false">5635476</guid>        </item>
        <item>
            <title>Prometheus’s heart: what lies beneath</title>
            <link>http://www.medworm.com/index.php?rid=5635475&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01487.x</link>
            <description>ConclusionsA 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 human beings. 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 ischaemic area, and then to confirm the dogma of the heart as termina...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5635475</comments>
            <pubDate>Fri, 27 Jan 2012 21:50:29 +0100</pubDate>
            <guid isPermaLink="false">5635475</guid>        </item>
        <item>
            <title>Calcineurin regulation of cytoskeleton organization: a new paradigm to analyse the effects of calcineurin inhibitors on the kidney</title>
            <link>http://www.medworm.com/index.php?rid=5635474&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01398.x</link>
            <description>ConclusionCalcineurin is a serine/threonine phosphatase originally involved in the immune response but is also known for its role as a central mediator in various non‐immunological intracellular signals. The nuclear factor of activated T cell (NFAT) proteins are the most widely described substrates of calcineurin, but ongoing work has uncovered other substrates among which are the cytoskeleton organizing proteins (i.e. cofilin, synaptopodin, WAVE‐1). Control over cytoskeletal proteins is of outmost interest because the phenotypic properties of cells are dependent on cytoskeleton architecture integrity, while rearrangements of the cytoskeleton are implicated in both physiological and pathological processes. Previous works investigating the role of calcineurin on the cytoskeleton have fo...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5635474</comments>
            <pubDate>Fri, 27 Jan 2012 21:50:27 +0100</pubDate>
            <guid isPermaLink="false">5635474</guid>        </item>
        <item>
            <title>Alterations in the contractile phenotype of the bladder: lessons for understanding physiological and pathological remodelling of smooth muscle</title>
            <link>http://www.medworm.com/index.php?rid=5635473&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01368.x</link>
            <description>Abstract• Introduction• Alterations in bladder contractility with normal development• Assessment of bladder function in genetically modified mice• A whole organ perspective on the bladder’s response to pBOO‐ Clinical observations• Experimental observations• In vivo measures of pBOO in a rabbit model• Relating muscle strip studies to whole organ function• Myosin light chain phosphorylation• Regulation of myosin light chain de‐phosphorylation• Alterations in the thick contractile filaments‐ SM1 and SM2 isoforms‐ SM‐B and SM‐A isoforms• Regulatory light chain• Alterations in the thin contractile filaments• Alterations in tension transfer complexThe contractile properties of the urinary bladder are changed by the condition...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5635473</comments>
            <pubDate>Fri, 27 Jan 2012 21:50:25 +0100</pubDate>
            <guid isPermaLink="false">5635473</guid>        </item>
        <item>
            <title>Issue Information</title>
            <link>http://www.medworm.com/index.php?rid=5635472&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01422.x</link>
            <description>(Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5635472</comments>
            <pubDate>Fri, 27 Jan 2012 21:50:24 +0100</pubDate>
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        <item>
            <title>Elevated expression of cav‐1 in a subset of SSc fibroblasts contributes to constitutive Alk1/Smad1 activation</title>
            <link>http://www.medworm.com/index.php?rid=5635470&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01537.x</link>
            <description>In conclusion, this study has revealed an important role of cav‐1 in mediating TGFβ/Smad1 signaling and CCN2 gene expression in healthy and SSc dermal fibroblasts.© 2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5635470</comments>
            <pubDate>Fri, 27 Jan 2012 21:46:01 +0100</pubDate>
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        <item>
            <title>Probing the polygenic basis of cardiomyopathies in Drosophila.</title>
            <link>http://www.medworm.com/index.php?rid=5624816&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01529.x</link>
            <description>AbstractIn trying to understand the causes for congenital heart disease and cardiomyopathies, it is difficult to study polygenic interactions that contribute to the severity of the disease, which is in part due to genetic complexity and generation time of higher organsism that hinder efficient screening for modifiers of primary causes of heart disease. The adult Drosophila heart has recently been established as a model to probe genetic interactions that lead to cardiac dysfunction in this genetically simple and short‐lived organism. This has made it possible to systematically and efficiently screen for polygenic modulators of heart dysfunction inflicted by known heart disease genes. Because heart development and fundamental aspects of cardiac physiology show remarkable evolutionary conse...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624816</comments>
            <pubDate>Mon, 23 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624816</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=5617064&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01534.x</link>
            <description>AbstractNanotechnology 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 engineering.© 2012 The Authors Journal of Cellular and Molecular Medicine © 2012 ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5617064</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5617064</guid>        </item>
        <item>
            <title>Human cardiomyocyte progenitor cells: a short history of nearly everything</title>
            <link>http://www.medworm.com/index.php?rid=5617063&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01535.x</link>
            <description>(Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5617063</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5617063</guid>        </item>
        <item>
            <title>Glucose can promote a glucocorticoid resistance state</title>
            <link>http://www.medworm.com/index.php?rid=5617062&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01532.x</link>
            <description>AbstractIt 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 glucocorticoid receptor (GR)‐mediated action, p...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5617062</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5617062</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=5617061&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01533.x</link>
            <description>AbstractVascular 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 provoked by high Pi. Exposure of HSMCs to ethanol increased extracellular matrix calcification...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5617061</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5617061</guid>        </item>
        <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=5617060&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01531.x</link>
            <description>AbstractCells 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 factor(s) in this “cell growth restraint”. Importa...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5617060</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5617060</guid>        </item>
        <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=5617059&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01527.x</link>
            <description>AbstractZoledronic 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 cancer cells treated with low doses of ZOL (10μM). Microarrays analysis was used to identify, describe and summarize evidences regard...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5617059</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5617059</guid>        </item>
        <item>
            <title>Cardiac Differentiation of Human Pluripotent Stem Cells</title>
            <link>http://www.medworm.com/index.php?rid=5604044&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01528.x</link>
            <description>AbstractDue 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 reducing the heterogeneity of hESC‐CMs, a ma...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5604044</comments>
            <pubDate>Mon, 16 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5604044</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=5568956&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01512.x</link>
            <description>AbstractDespite 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: 1x104, 5x104, 1x105, and 5x105 (expressed as number of plated cardiosphere‐forming cells). Acute (24 hour) cell ret...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568956</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568956</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=5568955&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01514.x</link>
            <description>AbstractIn 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 for the contribution and clinical relevance of aberrant mic...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568955</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568955</guid>        </item>
        <item>
            <title>Measuring passive myocardial stiffness in Drosophila melanogaster to investigate diastolic dysfunction</title>
            <link>http://www.medworm.com/index.php?rid=5568954&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01517.x</link>
            <description>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 layer that covers the contractile cardiomyocytes. Here we argue for wide‐spread use of Drosophila as a...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568954</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568954</guid>        </item>
        <item>
            <title>Rhabdomyosarcomas: an overview on the experimental animal models</title>
            <link>http://www.medworm.com/index.php?rid=5568953&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01518.x</link>
            <description>AbstractRhabdomyosarcomas (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 determinants cooperating to RMS development and progression.© ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568953</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568953</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=5568952&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01519.x</link>
            <description>AbstractReendothelialization 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 activity. The varying stent coatings influence VSMC outgrowth: 31.2±4.0mm2 on fibronectin, 1.6±0.3mm2 on tropoe...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568952</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568952</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=5568951&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01520.x</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 (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568951</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568951</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=5568958&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01521.x</link>
            <description>AbstractThe 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 regarding the derivation and use of large animal iPSCs.©...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568958</comments>
            <pubDate>Mon, 02 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568958</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=5568957&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01524.x</link>
            <description>AbstractThe 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 binds to, and mediates ubiquitin conjugation to cIAP1 and TRAF2, resulting...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568957</comments>
            <pubDate>Mon, 02 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568957</guid>        </item>
        <item>
            <title>Beneficial effects of edaravone, a novel antioxidant, in rats with dilated cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=5624815&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01526.x</link>
            <description>AbstractEdaravone, a novel antioxidant acts by trapping hydroxyl radicals, quenching active oxygen and so on. Its cardioprotective activity against experimental autoimmune myocarditis (EAM) was reported. Nevertheless, it remains to be determined whether edaravone protects against cardiac remodeling in dilated cardiomyopathy (DCM). The present study was undertaken to assess whether edaravone attenuates myocardial fibrosis and examine the effect of edaravone on cardiac function in rats with DCM after EAM. Rat model of EAM was prepared by injection with porcine cardiac myosin. 28 days after immunization, we administered edaravone intraperitoneally at 3 and 10 mg/kg/day to rats for 28 days. The results were compared with vehicle treated rats with DCM. Cardiac function, by hemodynamic and echoc...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624815</comments>
            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624815</guid>        </item>
        <item>
            <title>MicroRNA‐24 Regulates Cardiac Fibrosis after Myocardial Infarction</title>
            <link>http://www.medworm.com/index.php?rid=5617058&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01523.x</link>
            <description>AbstractCardiac 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 zone of the heart 2 weeks after MI through intramyocardial injection of...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5617058</comments>
            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5617058</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=5604043&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2012.01530.x</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 (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5604043</comments>
            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5604043</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=5568950&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01510.x</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 (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568950</comments>
            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568950</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=5556793&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01516.x</link>
            <description>AbstractConnexin 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 (Cx43Cre‐ER(T)/fl + 4‐OHT, 5‐10% of Cx43 protein compared to control Cx43fl/fl mitochondria) reduced ADP‐stimulated complex I respiration of LV SSM to 47.8±2.4 nmol O2/min*mg prote...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5556793</comments>
            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5556793</guid>        </item>
        <item>
            <title>Small molecule regulators of postnatal Nkx2.5 cardiomyoblast proliferation and differentiation</title>
            <link>http://www.medworm.com/index.php?rid=5556794&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01513.x</link>
            <description>AbstractWhile 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 neonatal Nkx2.5‐eGFP+ ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5556794</comments>
            <pubDate>Fri, 30 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5556794</guid>        </item>
        <item>
            <title>A novel copper complex induces paraptosis in colon cancer cells via the activation of ER stress signalling</title>
            <link>http://www.medworm.com/index.php?rid=5549813&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01292.x</link>
            <description>AbstractPlatinum anticancer drugs have been used for three decades despite their serious side effects and the emerging of resistance phenomena. Recently, a phosphine copper(I) complex, [Cu(thp)4][PF6] (CP), gained special attention because of its strong antiproliferative effects. CP killed human colon cancer cells more efficiently than cisplatin and oxaliplatin and it overcame platinum drug resistance. CP preferentially reduced cancer cell viability whereas non‐tumour cells were poorly affected. Colon cancer cells died via a programmed cell death whose transduction pathways were characterized by the absence of hallmarks of apoptosis. The inhibition of 26S proteasome activities induced by CP caused intracellular accumulation of polyubiquitinated proteins and the functional suppression...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549813</comments>
            <pubDate>Thu, 29 Dec 2011 15:19:48 +0100</pubDate>
            <guid isPermaLink="false">5549813</guid>        </item>
        <item>
            <title>Syntaxin 11 marks a distinct intracellular compartment recruited to the immunological synapse of NK cells to colocalize with cytotoxic granules</title>
            <link>http://www.medworm.com/index.php?rid=5549812&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01280.x</link>
            <description>AbstractThe syntaxin 11 (STX11) gene is mutated in a proportion of patients with familial haemophagocytic lymphohistiocytosis (FHL) and exocytosis of cytotoxic granules is impaired in STX11‐deficient NK cells. However, the subcellular localization, regulation of expression and molecular function of STX11 in NK cells and other cytotoxic lymphocytes remain unknown. Here we demonstrate that STX11 expression is strictly controlled by several mechanisms in a cell‐type‐specific manner and that the enzymatic activity of the proteasome is required for STX11 expression in NK cells. In resting NKL cells, STX11 was localized in the cation‐dependent mannose‐6‐phosphate receptor (CD‐M6PR)‐containing compartment, which was clearly distinct from cytotoxic granules or Rab27a‐expressing v...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549812</comments>
            <pubDate>Thu, 29 Dec 2011 15:19:46 +0100</pubDate>
            <guid isPermaLink="false">5549812</guid>        </item>
        <item>
            <title>Embryonic liver fodrin involved in hepatic stellate cell activation and formation of regenerative nodule in liver cirrhosis</title>
            <link>http://www.medworm.com/index.php?rid=5549811&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01290.x</link>
            <description>AbstractTransforming growth factor (TGF) β1 plays a critical role in liver fibrosis. Previous studies demonstrated embryonic liver fodrin (ELF), a β‐spectrin was involved in TGF‐β/Smad signalling pathway as Smad3/4 adaptor. Here we investigate the role of ELF in pathogenesis of liver cirrhosis. In carbon tetrachloride (CCl4)‐induced mice model of liver cirrhosis, ELF is up‐regulated in activated hepatic stellate cells (HSCs), and down‐regulated in regenerative hepatocytes of cirrhotic nodules. In activated HSCs in vitro, reduction of ELF expression mediated by siRNA leads to the inhibition of HSC activation and procollagen I expression. BrdU assay demonstrates that down‐regulation of ELF expression does not inhibit proliferation of activated HSCs in vitro. Immunostaining...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549811</comments>
            <pubDate>Thu, 29 Dec 2011 15:19:45 +0100</pubDate>
            <guid isPermaLink="false">5549811</guid>        </item>
        <item>
            <title>Intestinal metabolite compound K of panaxoside inhibits the growth of gastric carcinoma by augmenting apoptosis via Bid‐mediated mitochondrial pathway</title>
            <link>http://www.medworm.com/index.php?rid=5549810&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01278.x</link>
            <description>AbstractCompound K (20‐O‐β‐D‐glucopyranosyl‐20(S)‐protopanaxadiol, CK), an intestinal bacterial metabolite of panaxoside, has been shown to inhibit tumour growth in a variety of tumours. However, the mechanisms involved are largely unknown. We use human gastric carcinoma cell lines BGC823, SGC7901 and human gastric carcinoma xenograft in nude mice as models to study the mechanisms of CK in gastric cancers. We found that CK significantly inhibits the viabilities of BGC823 and SGC7901 cells in dose‐ and time‐dependent manners. CK‐induced BGC823 and SGC7901 cells apoptosis and cell cycle arrest in G2 phase by up‐regulation of p21 and down‐regulation of cdc2 and cyclin B1. Further studies show that CK induces apoptosis in BGC823 and SGC7901 cells mainly through mitochond...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549810</comments>
            <pubDate>Thu, 29 Dec 2011 15:19:41 +0100</pubDate>
            <guid isPermaLink="false">5549810</guid>        </item>
        <item>
            <title>Proteomic analysis of metabolic, cytoskeletal and stress response proteins in human heart failure</title>
            <link>http://www.medworm.com/index.php?rid=5549809&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01336.x</link>
            <description>In this study, we performed exhaustive global proteomic surveys of cardiac ventricle isolated from failing and non‐failing human hearts, and determined the regulatory pathway to uncover the mechanism underlying heart failure. Two‐dimensional gel electrophoresis (2‐DE) coupled with tandem mass spectrometry was used to identify differentially expressed proteins in specimens from failing (n = 9) and non‐failing (n = 6) human hearts. A total of 25 proteins with at least 1.5‐fold change in the failing heart were identified; 15 proteins were up‐regulated and 10 proteins were down‐regulated. The altered proteins belong to three broad functional categories: (i) metabolic [e.g. NADH dehydrogenase (ubiquinone), dihydrolipoamide dehydrogenase, and the cytochrome c oxidase subunit]...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549809</comments>
            <pubDate>Thu, 29 Dec 2011 15:19:36 +0100</pubDate>
            <guid isPermaLink="false">5549809</guid>        </item>
        <item>
            <title>Multifaceted role of nitric oxide in an in vitro mouse neuronal injury model: transcriptomic profiling defines the temporal recruitment of death signalling cascades</title>
            <link>http://www.medworm.com/index.php?rid=5549808&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01288.x</link>
            <description>AbstractNitric oxide is implicated in the pathogenesis of various neuropathologies characterized by oxidative stress. Although nitric oxide has been reported to be involved in the exacerbation of oxidative stress observed in several neuropathologies, existent data fail to provide a holistic description of how nitrergic pathobiology elicits neuronal injury. Here we provide a comprehensive description of mechanisms contributing to nitric oxide induced neuronal injury by global transcriptomic profiling. Microarray analyses were undertaken on RNA from murine primary cortical neurons treated with the nitric oxide generator DETA‐NONOate (NOC‐18, 0.5 mM) for 8–24 hrs. Biological pathway analysis focused upon 3672 gene probes which demonstrated at least a ±1.5‐fold expression in a minimum...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549808</comments>
            <pubDate>Thu, 29 Dec 2011 15:19:34 +0100</pubDate>
            <guid isPermaLink="false">5549808</guid>        </item>
        <item>
            <title>Issue Information</title>
            <link>http://www.medworm.com/index.php?rid=5549807&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01421.x</link>
            <description>(Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549807</comments>
            <pubDate>Thu, 29 Dec 2011 15:19:26 +0100</pubDate>
            <guid isPermaLink="false">5549807</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=5549806&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01511.x</link>
            <description>AbstractCystamine, 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 cystamine significantly attenuated the apoptosis of LV tissues in NZB/W...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549806</comments>
            <pubDate>Thu, 29 Dec 2011 15:15:14 +0100</pubDate>
            <guid isPermaLink="false">5549806</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=5501146&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01506.x</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 neuromodu...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5501146</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5501146</guid>        </item>
        <item>
            <title>Immunogenicity of allogeneic mesenchymal stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5501145&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01509.x</link>
            <description>AbstractMesenchymal 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 upregulation of the activation markers CD25 and CD71 as well as downregulation of CD62L on CD4+ T ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5501145</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5501145</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=5483154&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01489.x</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. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5483154</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5483154</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=5483153&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01503.x</link>
            <description>AbstractZeta‐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 regulation of ZAP70 gene in CLL, we have defined ZAP70 promoter region and outlined the regions c...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5483153</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5483153</guid>        </item>
        <item>
            <title>PDGFR‐β positive telocytes in skeletal muscle interstitium</title>
            <link>http://www.medworm.com/index.php?rid=5533476&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01505.x</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 (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5533476</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5533476</guid>        </item>
        <item>
            <title>Interaction between pathogenic proteins in neurodegenerative disorders</title>
            <link>http://www.medworm.com/index.php?rid=5520418&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01507.x</link>
            <description>AbstractThe 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, Parkinson, Huntington, and prion dise...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5520418</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5520418</guid>        </item>
        <item>
            <title>Intermittent Hypobaric Hypoxia applicability in myocardial infarction prevention and recovery</title>
            <link>http://www.medworm.com/index.php?rid=5501144&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01508.x</link>
            <description>AbstractIntermittent 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 hypertensive response, increased risk of hemoconcentratio...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5501144</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5501144</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=5483152&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01504.x</link>
            <description>AbstractThe 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 immunohistochemical phenotype for the ULP IC was assessed and region‐dependent differences were looked for...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5483152</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5483152</guid>        </item>
        <item>
            <title>Bone morphogenetic protein receptor 2 in patients with idiopathic portal hypertension</title>
            <link>http://www.medworm.com/index.php?rid=5465226&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01496.x</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. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5465226</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5465226</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=5465225&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01498.x</link>
            <description>AbstractMuscular 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 differentiated cell types, including myogenic cells. Here we review the literat...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5465225</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5465225</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=5465224&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01499.x</link>
            <description>AbstractProlactin 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 phosphorylation of ERK1/2 and STAT5 and induces tube formation of endothelial cells on Matrigel. These effects are blocked by a specific prolactin receptor ant...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5465224</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5465224</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=5465231&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01495.x</link>
            <description>AbstractSunitinib 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 patients were categorized as “responsive”, “stable”...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5465231</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5465231</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=5465230&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01497.x</link>
            <description>AbstractHypoxia‐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% O2) 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 Ca2+‐calcineurin signals were also enhanced in a time‐dependent manner under MH condition. MH‐induced cardiomyocytes hypertrophy, TRPC up‐regulation and enhanced Ca2+‐calcineurin signals were inhibited by a HIF...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5465230</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5465230</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=5465229&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01500.x</link>
            <description>Conclusions‐ We establish for the first time that activation of PHD signal cascade can activate AMPK pathway mainly through a Ca2+/CaMKK‐dependent mechanism in cardiomyocytes. Furthermore, activation of AMPK plays an essential role in hypoxic protective responses induced by PHI. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5465229</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5465229</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=5465228&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01501.x</link>
            <description>AbstractTo 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 them with basal and mobilized peripheral blood mononucl...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5465228</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5465228</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=5465227&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01502.x</link>
            <description>CONCLUSIONS Valsartan reduced the incidence of PES induced ventricular arrhythmia, this effect was possibly through modulating the myocardial AT1R and Cx43 expression. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5465227</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5465227</guid>        </item>
        <item>
            <title>Corrigendum</title>
            <link>http://www.medworm.com/index.php?rid=5454108&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01466.x</link>
            <description>(Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454108</comments>
            <pubDate>Tue, 29 Nov 2011 10:33:15 +0100</pubDate>
            <guid isPermaLink="false">5454108</guid>        </item>
        <item>
            <title>Epicardial epithelial‐to‐mesenchymal transition in injured heart</title>
            <link>http://www.medworm.com/index.php?rid=5454107&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01450.x</link>
            <description>AbstractCre‐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 the infarcted region s...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454107</comments>
            <pubDate>Tue, 29 Nov 2011 10:33:14 +0100</pubDate>
            <guid isPermaLink="false">5454107</guid>        </item>
        <item>
            <title>Palmitoylethanolamide counteracts reactive astrogliosis induced by β‐amyloid peptide</title>
            <link>http://www.medworm.com/index.php?rid=5454106&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01267.x</link>
            <description>AbstractEmerging evidence indicates that astrogliosis is involved in the pathogenesis of neurodegenerative disorders. Our previous findings suggested cannabinoids and Autacoid Local Injury Antagonism Amides (ALIAmides) attenuate glial response in models of neurodegeneration. The present study was aimed at exploring palmitoylethanolamide (PEA) ability to mitigate β‐amyloid (Aβ)‐induced astrogliosis. Experiments were carried out to investigate PEA’s (10−7M) effects upon the expression and release of pro‐inflammatory molecules in rat primary astrocytes activated by soluble Aβ1–42 (1 μg/ml) as well as to identify mechanisms responsible for such actions. The effects of Aβ and exogenous PEA on the astrocyte levels of the endocannabinoidsand of endogenous ALIAmides were also stud...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454106</comments>
            <pubDate>Tue, 29 Nov 2011 10:32:54 +0100</pubDate>
            <guid isPermaLink="false">5454106</guid>        </item>
        <item>
            <title>Intracerebral transplantation of foetal neural stem cells improves brain dysfunction induced by intracerebral haemorrhage stroke in mice</title>
            <link>http://www.medworm.com/index.php?rid=5454105&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01259.x</link>
            <description>AbstractIntracerebral haemorrhage (ICH) can lead to secondary insults and severe neurological deficits. Transplantation of neural stem cells (NSCs) was suggested as an alternative to improve ICH‐induced neurological dysfunction. The present study aimed at investigating the therapeutic role and long‐term survival of foetal NSCs and potential role of foetal NSCs‐produced factors in ICH. Our results demonstrated that foetal NSCs could differentiate into neural axons and dendrites and astrocytes in both in vitro and in vivo conditions, demonstrated by positive double or triple staining with Hoechst, neuronal specific nuclear protein, neurofilaments and glial fibrillary acidic protein. Intracerebral transplantation of foetal NSCs 3 days after ICH induction by intrastriatal adminis...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454105</comments>
            <pubDate>Tue, 29 Nov 2011 10:32:47 +0100</pubDate>
            <guid isPermaLink="false">5454105</guid>        </item>
        <item>
            <title>Nox2 and Nox4 mediate tumour necrosis factor‐α‐induced ventricular remodelling in mice</title>
            <link>http://www.medworm.com/index.php?rid=5454104&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01261.x</link>
            <description>In this study, we investigated whether TNF‐α‐induced ventricular remodelling was mediated by Nox2 and/or Nox4. An intravenous injection of murine TNF‐α was administered to a group of mice and saline injection was administered to controls. Echocardiography was performed on days 1, 7 and 28 post‐injection. Ventricular tissue was used to determine gene and protein expression of Nox2, Nox4, ANP, interleukin (IL)‐1β, IL‐2, IL‐6, TNF‐α and to measure ROS. Nox2 and Nox4 siRNA were used to determine whether or not Nox2 and Nox4 mediated TNF‐α‐induced ROS and upregulation of IL‐1β and IL‐6 in adult human cardiomyocytes. Echocardiography showed a significant increase in left ventricular end‐diastolic and left ventricular end‐systolic diameters, and a significant dec...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454104</comments>
            <pubDate>Tue, 29 Nov 2011 10:32:44 +0100</pubDate>
            <guid isPermaLink="false">5454104</guid>        </item>
        <item>
            <title>Adipose‐derived stem cells accelerate neovascularization in ischaemic diabetic skin flap via expression of hypoxia‐inducible factor‐1α</title>
            <link>http://www.medworm.com/index.php?rid=5454103&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01313.x</link>
            <description>In this study, the authors explored the feasibility of applying human adipose‐derived stem cells (ASCs) to increase the viability of random‐patterned skin flaps in streptozotocin‐induced diabetic mice. ASCs were isolated from the fresh human lipoaspirates and expanded ex vivo for three passages. After the elevation of caudally based random‐patterned skin flaps (3 cm long and 1 cm wide), ASCs suspensions were then injected into the flap (group A). Media containing no ASCs were similarly injected as a control (group B), although nothing was injected into the flap base of mice in control group C. Flap assessments were carried out at post‐operative day 7 for evaluation of flap viability. The flap survival rate of group A was significantly higher than those of groups B and C, wher...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454103</comments>
            <pubDate>Tue, 29 Nov 2011 10:32:39 +0100</pubDate>
            <guid isPermaLink="false">5454103</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=5454102&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01461.x</link>
            <description>In conclusion we propose that telocytes could be the common cells of origin for both PEComas and GISTs. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454102</comments>
            <pubDate>Tue, 29 Nov 2011 10:32:37 +0100</pubDate>
            <guid isPermaLink="false">5454102</guid>        </item>
        <item>
            <title>Issue Information</title>
            <link>http://www.medworm.com/index.php?rid=5454101&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01474.x</link>
            <description>(Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454101</comments>
            <pubDate>Tue, 29 Nov 2011 10:32:33 +0100</pubDate>
            <guid isPermaLink="false">5454101</guid>        </item>
        <item>
            <title>Pravastatin‐induced proangiogenic effects depend upon extracellular FGF‐2</title>
            <link>http://www.medworm.com/index.php?rid=5454095&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01494.x</link>
            <description>AbstractThe 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) in human umbilical vein endothelial cells. SU5402, an inhibitor of FGFR, abolished pravastatin‐induced PI...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454095</comments>
            <pubDate>Tue, 29 Nov 2011 10:28:13 +0100</pubDate>
            <guid isPermaLink="false">5454095</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=5454100&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01488.x</link>
            <description>AbstractATP13A2 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 patients’ healthy parents. Peripheral blood lymphocytes from ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454100</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5454100</guid>        </item>
        <item>
            <title>Myelopoiesis in spleen producing distinct dendritic‐like cells</title>
            <link>http://www.medworm.com/index.php?rid=5454099&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01490.x</link>
            <description>AbstractDendritic 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)−ckitlo and Lin−ckithi progenitor subsets were identified as candidate populations, and tested for ability to produce L‐DC; in vitro upon co‐cultu...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454099</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5454099</guid>        </item>
        <item>
            <title>The Akt1 isoform is an essential mediator of ischemic preconditioning</title>
            <link>http://www.medworm.com/index.php?rid=5454098&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01491.x</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 kin...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454098</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5454098</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=5454097&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01492.x</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, PGE2, 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), PGE2 (p&amp;lt;0.05), versican (p&amp;lt;0.05) and tropoelastin (p&amp;lt;0.05). mRNA express...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454097</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5454097</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=5454096&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01493.x</link>
            <description>AbstractPatients 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 independently using an adenovirus expressing active HIF1α. To identify the TGFβ1 independent effects ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5454096</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5454096</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=5375484&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01480.x</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. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375484</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5375484</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=5375483&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01484.x</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...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375483</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5375483</guid>        </item>
        <item>
            <title>Localized colonic stem cell transplantation enhances tissue regeneration in murine colitis</title>
            <link>http://www.medworm.com/index.php?rid=5375482&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01485.x</link>
            <description>AbstractMany 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 colitis. IL‐10−/− mice with active colitis were transplanted with adult stem c...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375482</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5375482</guid>        </item>
        <item>
            <title>Cardiomyocytes generated from CPVTD307H patients are arrhythmogenic in response to β‐adrenergic stimulation</title>
            <link>http://www.medworm.com/index.php?rid=5375491&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01476.x</link>
            <description>AbstractSudden 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 contraction coupling, the derangements in intracellular Ca2+ handling may cause delayed afterdepolarizations (DADs) which constitute the mechanism underlying CPVT. To investigate catecholamine‐induced arrhythmias in the CASQ2 mutated cells, we generated for ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375491</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5375491</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=5375490&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01477.x</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. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375490</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5375490</guid>        </item>
        <item>
            <title>Pancreatic cancer tumor initiating cells: the molecular regulation and therapeutic values</title>
            <link>http://www.medworm.com/index.php?rid=5375489&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01478.x</link>
            <description>AbstractPancreatic 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 approaches. (Source: Journal of Cellular and Molecular Medici...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375489</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5375489</guid>        </item>
        <item>
            <title>Involvement of COX‐2/PGE2 signaling in hypoxia‐induced angiogenic response in endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=5375488&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01479.x</link>
            <description>Conclusion: Short‐term hypoxic treatment enhanced angiogenic capability of ECs, and COX‐2/PGE2 signaling maybe play a critical role in the biological response of ECs to hypoxia. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375488</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5375488</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=5375487&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01481.x</link>
            <description>AbstractMultiple 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 progression. DRG and spinal cords were harvested for protein and gene expression analysis every 3 ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375487</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5375487</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=5375486&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01482.x</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 repres...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375486</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5375486</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=5375485&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01483.x</link>
            <description>AbstractAbnormalities 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 results demonstrated that the translocation of cytochrome c (Cyt c), caspase activation and cleavage of po...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375485</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5375485</guid>        </item>
        <item>
            <title>Prometheus's Heart: what lies beneath</title>
            <link>http://www.medworm.com/index.php?rid=5417673&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01487.x</link>
            <description>AbstractA 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 dogma of the heart as terminally differ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417673</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417673</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=5375492&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01475.x</link>
            <description>AbstractAcute 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 (10−6M). 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 dependently increased protein expression of NK...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375492</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5375492</guid>        </item>
        <item>
            <title>Cell‐derived microparticles in atherosclerosis: biomarkers and targets for pharmacological modulation?</title>
            <link>http://www.medworm.com/index.php?rid=5375481&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01486.x</link>
            <description>AbstractCardiovascular 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 contribute to atherosclerosis development. In addition, pharmacologi...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375481</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5375481</guid>        </item>
        <item>
            <title>NK receptors, Substance P, Ano1 expression and ultrastructural features of the muscle coat in Cav‐1−/− mouse ileum</title>
            <link>http://www.medworm.com/index.php?rid=5355413&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01333.x</link>
            <description>AbstractCaveolin (Cav)‐1 is an integral membrane protein of caveolae playing a crucial role in various signal transduction pathways. Caveolae represent the sites for calcium entry and storage especially in smooth muscle cells (SMC) and interstitial cells of Cajal (ICC). Cav‐1−/− mice lack caveolae and show abnormalities in pacing and contractile activity of the small intestine. Presently, we investigated, by transmission electron microscopy (TEM) and immunohistochemistry, whether the absence of Cav‐1 in Cav‐1−/− mouse small intestine affects ICC, SMC and neuronal morphology, the expression of NK1 and NK2 receptors, and of Ano1 (also called Dog1 or TMEM16A), an essential molecule for slow wave activity in gastrointestinal muscles. ICC were also labelled with c‐Kit and tach...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5355413</comments>
            <pubDate>Fri, 28 Oct 2011 02:47:20 +0100</pubDate>
            <guid isPermaLink="false">5355413</guid>        </item>
        <item>
            <title>The anticancer flavonoid chrysin induces the unfolded protein response in hepatoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5355412&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01244.x</link>
            <description>In this study, we aimed to determine the effects of chrysin on hepatoma cells and roles of the ER‐resident protein GRP78 (glucose‐regulated protein 78) in its action. Also, we investigated the effects of green tea polyphenol (‐)‐epigallocatechin‐3‐gallate (EGCG), a natural GRP78 inhibitor, on the sensitivity of hepatoma cells to chrysin. Here, we report that chrysin inhibits hepatoma cells growth and induces apoptosis in a dose‐dependent manner. Chrysin induces GRP78 overexpression, X‐box binding protein‐1 splicing and eukaryotic initiation factor 2α phosphorylation, hallmarks of the unfolded protein response. GRP78 knockdown potentiates chrysin‐induced caspase‐7 cleavage in hepatoma cells and enhances chrysin‐induced apoptosis. EGCG overcomes chrysin‐induced GRP...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5355412</comments>
            <pubDate>Fri, 28 Oct 2011 02:47:16 +0100</pubDate>
            <guid isPermaLink="false">5355412</guid>        </item>
        <item>
            <title>Regulation of dynamin‐2 assembly–disassembly and function through the SH3A domain of intersectin‐1s</title>
            <link>http://www.medworm.com/index.php?rid=5355411&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01226.x</link>
            <description>AbstractIntersectin‐1s (ITSN‐1s), a five Src homology 3 (SH3) domain‐containing protein, is critically required for caveolae and clathrin‐mediated endocytosis (CME), due to its interactions with dynamin (dyn). Of the five SH3A‐E domains, SH3A is unique because of its high affinity for dyn and potent inhibition of CME. However, the molecular mechanism by which SH3A integrates in the overall function of ITSN‐1s to regulate the endocytic process is not understood. Using biochemical and functional approaches as well as high‐resolution electron microscopy, we show that SH3A exogenously expressed in human lung endothelial cells caused abnormal endocytic structures, distorted caveolae clusters, frequent staining‐dense rings around the caveolar necks and 60% inhibition of caveolae ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5355411</comments>
            <pubDate>Fri, 28 Oct 2011 02:47:12 +0100</pubDate>
            <guid isPermaLink="false">5355411</guid>        </item>
        <item>
            <title>Immunosuppressive effect of bone marrow‐derived mesenchymal stem cells in inflammatory microenvironment favours the growth of B16 melanoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5355410&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01215.x</link>
            <description>In this study, we investigated the mechanism of MSCs favouring tumour escape from immunologic surveillance in inflammatory microenvironment. We first compared the promotive capacity of bone marrow‐derived MSCs on B16 melanoma cells growth in vivo, pre‐incubated or not with the inflammatory cytokines interferon (IFN)‐γ and tumour necrosis factor (TNF)‐α. We showed that the development of B16 melanoma cells is faster when co‐injected with MSCs pre‐incubated with IFN‐γ and TNF‐α compared with control groups. Moreover, tumour incidence increases obviously in allogeneic recipients when B16 melanoma cells were co‐injected with MSCs pre‐incubated with IFN‐γ and TNF‐α. We then demonstrated that the immunosuppressive function of MSCs was elicited by IFN‐γ and TNF‐...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5355410</comments>
            <pubDate>Fri, 28 Oct 2011 02:47:09 +0100</pubDate>
            <guid isPermaLink="false">5355410</guid>        </item>
        <item>
            <title>Catalase activity prevents exercise‐induced up‐regulation of vasoprotective proteins in venous tissue</title>
            <link>http://www.medworm.com/index.php?rid=5355409&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01227.x</link>
            <description>This study sought to investigate the effects of two different training protocols on the expression of eNOS and extracellular superoxide dismutase (ecSOD) in venous and lung tissue and to evaluate the underlying molecular mechanisms. C57Bl/6 mice underwent voluntary exercise or forced physical activity. Changes of vascular mRNA and protein levels and activity of eNOS, ecSOD and catalase were determined in aorta, heart, lung and vena cava. Both training protocols similarly increased relative heart weight and resulted in up‐regulation of aortic and myocardial eNOS. In striking contrast, eNOS expression in vena cava and lung remained unchanged. Likewise, exercise up‐regulated ecSOD in the aorta and in left ventricular tissue but remained unchanged in lung tissue. Catalase expression in lun...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5355409</comments>
            <pubDate>Fri, 28 Oct 2011 02:47:05 +0100</pubDate>
            <guid isPermaLink="false">5355409</guid>        </item>
        <item>
            <title>Issue Information</title>
            <link>http://www.medworm.com/index.php?rid=5355408&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01453.x</link>
            <description>(Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5355408</comments>
            <pubDate>Fri, 28 Oct 2011 02:46:55 +0100</pubDate>
            <guid isPermaLink="false">5355408</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=5330695&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01467.x</link>
            <description>AbstractMicroRNAs (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 results. The purpose of this review is to describe some of these technical paramet...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5330695</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5330695</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=5330694&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01468.x</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. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5330694</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5330694</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=5330693&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01469.x</link>
            <description>AbstractThe 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 phosphine gold(I) compound [Au(SCN)(PEt3)]. The combination of the TrxR‐inhibitor and ionizing radiation reduced the surviving fractions an...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5330693</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5330693</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=5330692&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01470.x</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. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5330692</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5330692</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=5330691&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01471.x</link>
            <description>AbstractTransplantation 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 in numerous facets of cardiac pathophysiologic proce...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5330691</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5330691</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=5330690&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01472.x</link>
            <description>AbstractOn 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 normoxic conditions compared to the non‐...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5330690</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5330690</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=5330696&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01464.x</link>
            <description>AbstractHistone 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 cyclin G2 and p21 expression and down‐regulating cyclin D2 expression, and also apoptosis as assessed by cell morphology and cytofl...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5330696</comments>
            <pubDate>Mon, 17 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5330696</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=5310792&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01462.x</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. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5310792</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5310792</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=5310791&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01463.x</link>
            <description>AbstractRecently 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 adhaerentes of the virgultar cells of lymph node sinus. In light and electron microscopic immunolocalization experiments we sho...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5310791</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5310791</guid>        </item>
        <item>
            <title>Pathophysiology, staging and therapy of severe sepsis in baboon models</title>
            <link>http://www.medworm.com/index.php?rid=5292968&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01454.x</link>
            <description>AbstractWe 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. coli, followed by an extravascular second stag...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5292968</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5292968</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=5292967&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01455.x</link>
            <description>AbstractAlthough 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 the effect on cardiac function after transplantation in a mouse model of myocardial infarction. Flow cytometric analysis revealed that pMSC expres...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5292967</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5292967</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=5292966&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01456.x</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 indic...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5292966</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5292966</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=5292965&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01457.x</link>
            <description>AbstractCaveolin‐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 oxide synthase (NOS) with L‐NNA. Similarly, in 3 mon...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5292965</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5292965</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=5292964&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01458.x</link>
            <description>AbstractDisturbances 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 relative to controls. mRNAs of all tested molecules were significantly increased in patients with IDA comp...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5292964</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5292964</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=5292963&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01459.x</link>
            <description>AbstractThe 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 efficaciously suppress breast ca...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5292963</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5292963</guid>        </item>
        <item>
            <title>Pharmaceutical regulation of telomerase and its clinical potential</title>
            <link>http://www.medworm.com/index.php?rid=5292962&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01460.x</link>
            <description>AbstractTelomeres 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 introduce human telomeres and telomerase and discuss pha...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5292962</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5292962</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=5330689&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01473.x</link>
            <description>AbstractA 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. Applying univariate analyses, a significant correlation was found between HSP27 expression and survival. In the multivariate Cox‐regression model, HSP27 expression emerged as an inde...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5330689</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5330689</guid>        </item>
        <item>
            <title>Tracheal telocytes</title>
            <link>http://www.medworm.com/index.php?rid=5310790&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01465.x</link>
            <description>In conclusion, tracheal TC could be involved in the tracheal regulation (e.g. secretion, contractility). The tandem TC‐MC deserves further investigations. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5310790</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5310790</guid>        </item>
        <item>
            <title>Telocytes are the common cell of origin of both PEComas and GISTs</title>
            <link>http://www.medworm.com/index.php?rid=5292961&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01461.x</link>
            <description>In conclusion we propose that telocytes could be the common cells of origin for both PEComas and GISTs (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5292961</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5292961</guid>        </item>
        <item>
            <title>Epigenetic regulation of cathepsin L expression in chronic myeloid leukaemia</title>
            <link>http://www.medworm.com/index.php?rid=5257316&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01203.x</link>
            <description>AbstractThe 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 phase/blast crisis (AP/BC) patients and controls (P≤ 0.001). VEG...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5257316</comments>
            <pubDate>Tue, 27 Sep 2011 02:54:25 +0100</pubDate>
            <guid isPermaLink="false">5257316</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=5257315&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01213.x</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 expressi...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5257315</comments>
            <pubDate>Tue, 27 Sep 2011 02:54:22 +0100</pubDate>
            <guid isPermaLink="false">5257315</guid>        </item>
        <item>
            <title>γ‐secretase complexes containing caspase‐cleaved presenilin‐1 increase intracellular Aβ42/Aβ40 ratio</title>
            <link>http://www.medworm.com/index.php?rid=5257314&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01208.x</link>
            <description>AbstractMarkers 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 regard to Aβ40 and Aβ42 production. Previously, we have demonstrated that γ‐secretase complexes are active during apoptosis regardless of caspase cleavage in the PS1CTF‐loop. Here, a PS1/PS2‐knockout mouse blastocyst‐derived cell line was used ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5257314</comments>
            <pubDate>Tue, 27 Sep 2011 02:54:20 +0100</pubDate>
            <guid isPermaLink="false">5257314</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=5257313&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01239.x</link>
            <description>AbstractPeptides 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 the oligomer type exposing hydrophobic surfaces and possessing sufficient structural plasticity is toxic (type A), whereas the other type is benign ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5257313</comments>
            <pubDate>Tue, 27 Sep 2011 02:54:14 +0100</pubDate>
            <guid isPermaLink="false">5257313</guid>        </item>
        <item>
            <title>Mesothelial cell differentiation into osteoblast‐ and adipocyte‐like cells</title>
            <link>http://www.medworm.com/index.php?rid=5257312&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01212.x</link>
            <description>In conclusion, these studies confirm that mesothelial cells have the capacity to differentiate into osteoblast‐ and adipocyte‐like cells, providing definitive evidence of their multipotential nature. These data strongly support mesothelial cell differentiation as the potential source of different tissue types in MM tumours and other serosal pathologies, and add support for the use of mesothelial cells in regenerative therapies. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5257312</comments>
            <pubDate>Tue, 27 Sep 2011 02:54:12 +0100</pubDate>
            <guid isPermaLink="false">5257312</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=5257311&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01218.x</link>
            <description>AbstractNovel 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 reduction in the expression of the large inhibitor of apoptosis protein Apollon, and produced a morphological...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5257311</comments>
            <pubDate>Tue, 27 Sep 2011 02:54:07 +0100</pubDate>
            <guid isPermaLink="false">5257311</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=5257310&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01214.x</link>
            <description>AbstractAllogeneic 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 the resistance of HSCs against NK cell mediated cytotoxicity. High expression of HLA...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5257310</comments>
            <pubDate>Tue, 27 Sep 2011 02:54:04 +0100</pubDate>
            <guid isPermaLink="false">5257310</guid>        </item>
        <item>
            <title>Issue Information</title>
            <link>http://www.medworm.com/index.php?rid=5257309&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01452.x</link>
            <description>(Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5257309</comments>
            <pubDate>Tue, 27 Sep 2011 02:53:59 +0100</pubDate>
            <guid isPermaLink="false">5257309</guid>        </item>
        <item>
            <title>Epicardial epithelial to mesenchymal transition in injured heart</title>
            <link>http://www.medworm.com/index.php?rid=5217715&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01450.x</link>
            <description>AbstractCre‐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 the infarcted region sho...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5217715</comments>
            <pubDate>Wed, 14 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5217715</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=5217716&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01444.x</link>
            <description>AbstractSub‐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 efficacy, suggesting mechanistic implications. A minimal list of 29...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5217716</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5217716</guid>        </item>
        <item>
            <title>Experimental acute myocardial infarction: telocytes involvement in neo‐angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=5204224&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01449.x</link>
            <description>AbstractWe 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 surrounding TCs is frequently less than 50 nm; b) TCs establish multiple ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5204224</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5204224</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=5204223&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01411.x</link>
            <description>AbstractPhosphoprotein 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 the dimerization of a 37 kDa cytosolic precursor (37LRP). The 67LR is highly expressed in human cancers and widely recogniz...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5204223</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5204223</guid>        </item>
        <item>
            <title>Regulatory T cell: A protection for tumor cells</title>
            <link>http://www.medworm.com/index.php?rid=5204225&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01437.x</link>
            <description>AbstractCharacterized 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. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5204225</comments>
            <pubDate>Mon, 05 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5204225</guid>        </item>
        <item>
            <title>Ultrastructural differences between diabetic and idiopathic gastroparesis</title>
            <link>http://www.medworm.com/index.php?rid=5217714&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01451.x</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. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5217714</comments>
            <pubDate>Thu, 01 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5217714</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=5204222&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01414.x</link>
            <description>AbstractUp‐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 in end‐stage HF patients (n = 11) compared with non‐f...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5204222</comments>
            <pubDate>Thu, 01 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5204222</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=5194789&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01435.x</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. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194789</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5194789</guid>        </item>
        <item>
            <title>Angiostatic kinase inhibitors to sustain photodynamic angio‐occlusion</title>
            <link>http://www.medworm.com/index.php?rid=5191232&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01440.x</link>
            <description>AbstractTargeted 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 topically applied to the chicken chorioallantoic membrane (CAM) at embryo development day (EDD) 7, a clear inhibition ...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5191232</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5191232</guid>        </item>
        <item>
            <title>Molecular mechanisms controlling CFTR gene expression in the airway</title>
            <link>http://www.medworm.com/index.php?rid=5191231&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01439.x</link>
            <description>AbstractThe 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 of these are enriched for a histone modification (H3K4me1) that is...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5191231</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5191231</guid>        </item>
        <item>
            <title>SNARE complex‐mediated degranulation in mast cells</title>
            <link>http://www.medworm.com/index.php?rid=5179238&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01443.x</link>
            <description>AbstractMast 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, formation, and localization of variou...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5179238</comments>
            <pubDate>Wed, 31 Aug 2011 03:21:38 +0100</pubDate>
            <guid isPermaLink="false">5179238</guid>        </item>
        <item>
            <title>Radiosensitization of glioma cells by modulation of Met signalling with the hepatocyte growth factor neutralizing antibody, AMG102</title>
            <link>http://www.medworm.com/index.php?rid=5173960&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01122.x</link>
            <description>AbstractThe hepatocyte growth factor (HGF)/Met signalling pathway is up‐regulated in many cancers, with downstream mediators playing a role in DNA double strand break repair. Previous studies have shown increased radiosensitization of tumours through modulation of Met signalling by genetic methods. We investigated the effects of the anti‐HGF monoclonal antibody, AMG102, on the response to ionizing radiation in a model of glioblastoma multiforme in vitro and in vivo. Radiosensitivity was evaluated in vitro in the U‐87 MG human glioma cell line. Met activation was measured by Western blot, and the effect on survival following radiation was evaluated by clonogenic assay. Mechanism of cell death was evaluated by apoptosis and mitotic catastrophe assays. DNA damage was quantitat...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173960</comments>
            <pubDate>Tue, 30 Aug 2011 02:45:48 +0100</pubDate>
            <guid isPermaLink="false">5173960</guid>        </item>
        <item>
            <title>Rapid clinical‐scale propagation of mesenchymal stem cells using cultures initiated with immunoselected bone marrow CD105+ cells</title>
            <link>http://www.medworm.com/index.php?rid=5173959&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01157.x</link>
            <description>AbstractCurrent clinical protocols used for isolation and purification of mesenchymal stem cells (MSC) are based on long‐term cultures starting with bone marrow (BM) mononuclear cells. Using a commercially available immunoselection kit for enrichment of MSC, we investigated whether culture of enriched BM‐CD105+ cells could provide an adequate number of pure MSC in a short time for clinical use in the context of graft versus host disease and graft failure/rejection. We isolated a mean of 5.4 × 105 ± 0.9 × 105 CD105+ cells from 10 small volume (10–25 ml) BM samples achieving an enrichment &amp;gt;100‐fold in MSC. Seeding 2 × 103 immunoselected cells/cm2 we were able to produce 2.5 × 108 ± 0.7 × 108 MSC from cultures with autologous serum enriched medium within 3 weeks....</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173959</comments>
            <pubDate>Tue, 30 Aug 2011 02:45:46 +0100</pubDate>
            <guid isPermaLink="false">5173959</guid>        </item>
        <item>
            <title>In vitro and in vivo properties of distinct populations of amniotic fluid mesenchymal progenitor cells</title>
            <link>http://www.medworm.com/index.php?rid=5173958&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01180.x</link>
            <description>AbstractHuman mesenchymal progenitor cells (MPCs) are considered to be of great promise for use in tissue repair and regenerative medicine. MPCs represent multipotent adherent cells, able to give rise to multiple mesenchymal lineages such as osteoblasts, adipocytes or chondrocytes. Recently, we identified and characterized human second trimester amniotic fluid (AF) as a novel source of MPCs. Herein, we found that early colonies of AF‐MPCs consisted of two morphologically distinct adherent cell types, termed as spindle‐shaped (SS) and round‐shaped (RS). A detailed analysis of these two populations showed that SS‐AF‐MPCs expressed CD90 antigen in a higher level and exhibited a greater proliferation and differentiation potential. To characterize better the molecular identity of thes...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173958</comments>
            <pubDate>Tue, 30 Aug 2011 02:45:41 +0100</pubDate>
            <guid isPermaLink="false">5173958</guid>        </item>
        <item>
            <title>MicroRNA‐107, an oncogene microRNA that regulates tumour invasion and metastasis by targeting DICER1 in gastric cancer</title>
            <link>http://www.medworm.com/index.php?rid=5173957&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01194.x</link>
            <description>In conclusion, our results suggested that miR‐107, an oncogene miRNA promoting gastric cancer metastasis through down‐regulation of DICER1. Inhibition of miR‐107 or restoration of DICER1 may represent a new potential therapeutic target for gastric cancer treatment. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173957</comments>
            <pubDate>Tue, 30 Aug 2011 02:45:41 +0100</pubDate>
            <guid isPermaLink="false">5173957</guid>        </item>
        <item>
            <title>The reconstruction of lung alveolus‐like structure in collagen‐matrigel/microcapsules scaffolds in vitro</title>
            <link>http://www.medworm.com/index.php?rid=5173956&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01189.x</link>
            <description>This study attempted to use collagen–Matrigel as extracellular matrix (ECM) to supply cells with three‐dimensional (3D) culture condition and employ alginate‐poly‐l‐lysine‐alginate (APA) microcapsules to control the formation of alveolus‐like structure in vitro. We tested mice foetal pulmonary cells (FPCs) by immunohistochemistry after 2D culture. The alveolus‐like structure was reconstructed by seeding FPCs in collagen–Matrigel mixed with APA microcapsules 1.5 ml. A self‐made mould was used to keep the structure from contraction. Meanwhile, it provided static stretch to the structure. After 7, 14 and 21 days of culture, the alveolus‐like structure was analysed histologically and immunohistochemically, or by scanning transmission electron microscopy (TEM). We also o...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173956</comments>
            <pubDate>Tue, 30 Aug 2011 02:45:40 +0100</pubDate>
            <guid isPermaLink="false">5173956</guid>        </item>
        <item>
            <title>Pre‐clinical and clinical significance of heparanase in Ewing’s sarcoma</title>
            <link>http://www.medworm.com/index.php?rid=5173955&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2010.01190.x</link>
            <description>AbstractHeparanase is an endoglycosidase that specifically cleaves heparan sulphate side chains of heparan sulphate proteoglycans, activity that is strongly implicated in cell migration and invasion associated with tumour metastasis, angiogenesis and inflammation. Heparanase up‐regulation was documented in an increasing number of human carcinomas, correlating with reduced post‐operative survival rate and enhanced tumour angiogenesis. Expression and significance of heparanase in human sarcomas has not been so far reported. Here, we applied the Ewing’s sarcoma cell line TC71 and demonstrated a potent inhibition of cell invasion in vitro and tumour xenograft growth in vivo upon treatment with a specific inhibitor of heparanase enzymatic activity (compound SST0001, non‐anticoag...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173955</comments>
            <pubDate>Tue, 30 Aug 2011 02:45:38 +0100</pubDate>
            <guid isPermaLink="false">5173955</guid>        </item>
        <item>
            <title>Class IIa HDACs: from important roles in differentiation to possible implications in tumourigenesis</title>
            <link>http://www.medworm.com/index.php?rid=5173954&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01321.x</link>
            <description>ConclusionsHistone deacetylases (HDACs) are important regulators of gene expression. Specific structural features and distinct regulative mechanisms rationalize the separation of the 18 different human HDACs into four classes. The class II comprises a heterogeneous group of nuclear and cytosolic HDACs involved in the regulation of several cellular functions, not just limited to transcriptional repression. In particular, HDAC4, 5, 7 and 9 belong to the subclass IIa and share many transcriptional partners, including members of the MEF2 family. Genetic studies in mice have disclosed the fundamental contribution of class IIa HDACs to specific developmental/differentiation pathways. In this review, we discuss about the recent literature, which hints a role of class IIa HDACs in the development,...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173954</comments>
            <pubDate>Tue, 30 Aug 2011 02:45:37 +0100</pubDate>
            <guid isPermaLink="false">5173954</guid>        </item>
        <item>
            <title>Dimeric MHC‐peptides inserted into an immunoglobulin scaffold as new immunotherapeutic agents</title>
            <link>http://www.medworm.com/index.php?rid=5173953&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01319.x</link>
            <description>Abstract• Introduction• In vitro activation of antigen specific T cells by DEF containing peptides derived from foreign antigens• In vitro activation of auto‐reactive T cells by DEF containing peptides derived from self‐antigens• In vivo effect of DEF chimeras on prevention and reversal of autoimmune diseases• Perspectives for the utilization of DEF molecules as a new modality in the treatment of autoimmune diseasesThe interactions of the T cell receptor (TCR) with cognate MHC‐peptide and co‐stimulatory molecules expressed at surface of antigen presenting cells (APC) leads to activation or tolerance of T cells. The development of molecular biological tools allowed for the preparation of soluble MHC‐peptide molecules as surrogate for the APC. A decade ago...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173953</comments>
            <pubDate>Tue, 30 Aug 2011 02:45:36 +0100</pubDate>
            <guid isPermaLink="false">5173953</guid>        </item>
        <item>
            <title>Possible implications of insulin resistance and glucose metabolism in Alzheimer’s disease pathogenesis</title>
            <link>http://www.medworm.com/index.php?rid=5173952&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01318.x</link>
            <description>ConclusionsType 2 diabetes mellitus (DM) appears to be a significant risk factor for Alzheimer disease (AD). Insulin and insulin‐like growth factor‐1 (IGF‐1) also have intense effects in the central nervous system (CNS), regulating key processes such as neuronal survival and longevity, as well as learning and memory. Hyperglycaemia induces increased peripheral utilization of insulin, resulting in reduced insulin transport into the brain. Whereas the density of brain insulin receptor decreases during age, IGF‐1 receptor increases, suggesting that specific insulin‐mediated signals is involved in aging and possibly in cognitive decline. Molecular mechanisms that protect CNS neurons against β‐amyloid‐derived‐diffusible ligands (ADDL), responsible for synaptic deterioration und...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173952</comments>
            <pubDate>Tue, 30 Aug 2011 02:45:34 +0100</pubDate>
            <guid isPermaLink="false">5173952</guid>        </item>
        <item>
            <title>Issue Information</title>
            <link>http://www.medworm.com/index.php?rid=5173951&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01392.x</link>
            <description>(Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5173951</comments>
            <pubDate>Tue, 30 Aug 2011 02:45:33 +0100</pubDate>
            <guid isPermaLink="false">5173951</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=5179242&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01436.x</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. (Source: Journal of Cellular and Molecular Medicine)</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5179242</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5179242</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=5179241&amp;cid=s_38736_67_f&amp;fid=38736&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1111%252Fj.1582-4934.2011.01438.x</link>
            <description>AbstractEverolimus, 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 lines (TT and MZ‐CRC‐1 cells). A tumor response was observed in both patients. Serum calcitonin decreased by 86% in patient 1 and by 42% in patient 2. In TT and MZ‐CRC‐1 cells, everolim...</description>
            <author>Journal of Cellular and Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5179241</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5179241</guid>        </item>
    </channel>
</rss>

