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        <title>Basic Research in Cardiology 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 'Basic Research in Cardiology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Basic+Research+in+Cardiology&t=Basic+Research+in+Cardiology&s=Search&f=source]]></link>
        <lastBuildDate>Sun, 21 Mar 2010 14:00:46 +0100</lastBuildDate>
        <item>
            <title>Proatherogenic effects of estradiol in a model of accelerated atherosclerosis in ovariectomized ApoE-deficient mice</title>
            <link>http://www.medworm.com/index.php?rid=3303779&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp3772400u5072m8l%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Clinical studies revealed unfavorable effects of hormone replacement therapy in postmenopausal women despite strong evidence
 for vasoprotective effects of estrogen in animal models. Therefore, an attempt was made to address adverse effects of estradiol
 on atherosclerosis, endothelial function, and thrombosis in a murine model of atherosclerosis. ApoE−/− mice were bilaterally ovariectomized (OVX) and substituted with placebo or 17-β-Estradiol (E2, 1.1 and 6.6&amp;nbsp;μg/day) on Western diet for 90&amp;nbsp;days. Low-dose E2 (1.1&amp;nbsp;μg/day) treatment significantly increased atherosclerotic plaque score, whereas high-dose E2 (6.6&amp;nbsp;μg/day) reduced aortic plaque burden. The proatherosclerotic effects of low-dose E2 were associated with decreased total collagen in ao...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3303779</comments>
            <pubDate>Tue, 23 Feb 2010 07:20:10 +0100</pubDate>
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        <item>
            <title>Blockage of Angiotensin II type 2 receptor prevents thyroxine-mediated cardiac hypertrophy by blocking Akt activation</title>
            <link>http://www.medworm.com/index.php?rid=3273591&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb4j688656135x244%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Although most of effects of Angiotensin II (Ang II) related to cardiac remodelling can be attributed to type 1 Ang II receptor
 (AT1R), the type 2 receptor (AT2R) has been shown to be involved in the development of some cardiac hypertrophy models. In the present study, we investigated
 whether the thyroid hormone (TH) action leading to cardiac hypertrophy is also mediated by increased Ang II levels or by change
 on AT1R and AT2R expression, which could contribute to this effect. In addition, we also evaluated the possible contribution of AT2R in the activation of Akt and in the development of TH-induced cardiac hypertrophy. To address these questions, Wistar rats
 were treated with thyroxine (T4, 0.1&amp;nbsp;mg/kg&amp;nbsp;BW/day, i.p.), with or without AT2R blocker (PD123319)...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3273591</comments>
            <pubDate>Sun, 14 Feb 2010 06:50:24 +0100</pubDate>
            <guid isPermaLink="false">3273591</guid>        </item>
        <item>
            <title>Low intrinsic aerobic exercise capacity and systemic insulin resistance are not associated with changes in myocardial substrate oxidation or insulin sensitivity</title>
            <link>http://www.medworm.com/index.php?rid=3247926&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx3jh364817855043%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In patients, inactivity, obesity and insulin resistance are associated with increased incidence of heart failure. Rats selectively
 bred for low (LCR) intrinsic aerobic exercise capacity show signs of the metabolic syndrome including insulin resistance,
 compared to their counterparts bred for high intrinsic aerobic capacity (HCR). We reasoned that systemic insulin resistance
 in LCR should translate to impaired substrate oxidation and reduced insulin sensitivity in the heart. Isolated hearts were
 perfused in the working mode to analyze cardiac function, substrate oxidation patterns, insulin response, and oxygen consumption.
 After 22 generations of selective breeding, LCR displayed reduction of exercise capacity (LCR vs. HCR: distance 280&amp;nbsp;±&amp;nbsp;12 vs.
 1,968&amp;nb...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247926</comments>
            <pubDate>Fri, 05 Feb 2010 08:42:31 +0100</pubDate>
            <guid isPermaLink="false">3247926</guid>        </item>
        <item>
            <title>Genetic and ultrastructural studies in dilated cardiomyopathy patients: a large deletion in the lamin A/C gene is associated with cardiomyocyte nuclear envelope disruption</title>
            <link>http://www.medworm.com/index.php?rid=3240979&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fgr18583552704xq7%2F</link>
            <description>In this study, we screened a series of 25 unrelated DCM patient
 samples for (a) cardiomyocyte nuclear abnormalities and (b) mutations in LMNA and TMPO as they are two DCM-causing genes that encode proteins involved in maintaining nuclear envelope architecture. Among the 25
 heart samples investigated, we identified major cardiomyocyte nuclear abnormalities in 8 patients. Direct sequencing allowed
 the detection of three heterozygous LMNA mutations (p.D192G, p.Q353K and p.R541S) in three patients. By multiplex ligation-dependant probe amplification (MLPA)/quantitative
 real-time PCR, we found a heterozygous deletion encompassing exons 3–12 of the LMNA gene in one patient. Immunostaining demonstrated that this deletion led to a decrease in lamin A/C expression in cardiomyocytes
 from this...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240979</comments>
            <pubDate>Wed, 03 Feb 2010 06:48:43 +0100</pubDate>
            <guid isPermaLink="false">3240979</guid>        </item>
        <item>
            <title>Reverse rate-dependent changes are determined by baseline action potential duration in mammalian and human ventricular preparations</title>
            <link>http://www.medworm.com/index.php?rid=3240980&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj28x14361831073r%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Class III antiarrhythmic agents exhibit reverse rate-dependent lengthening of the action potential duration (APD). In spite
 of the several theories developed so far to explain this reverse rate-dependency (RRD), its mechanism has not yet been clarified.
 The aim of the present work was to further elucidate the mechanisms responsible for RRD in mammalian ventricular myocardium.
 Action potentials were recorded using conventional sharp microelectrodes from human, canine, rabbit and guinea pig ventricular
 myocardium in a rate-dependent manner varying the cycle length (CL) between 0.3 and 5&amp;nbsp;s. Rate-dependent drug effects were
 studied using agents known to lengthen or shorten action potentials, and these drug-induced changes in APD were correlated
 with baseline APD ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240980</comments>
            <pubDate>Tue, 02 Feb 2010 17:47:10 +0100</pubDate>
            <guid isPermaLink="false">3240980</guid>        </item>
        <item>
            <title>Kinases and phosphatases in ischaemic preconditioning: a re-evaluation</title>
            <link>http://www.medworm.com/index.php?rid=3240981&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fak17686r74118877%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Activation of several protein kinases occurs during myocardial ischaemia and during subsequent reperfusion. In contrast to
 the intensive investigation into the significance of kinase activation in cardioprotection, relatively little is known about
 the role of the phosphatases in this regard. The aim of this study was to re-evaluate the putative roles of PP1 and PP2A in
 ischaemia/reperfusion and in triggering ischaemic preconditioning. Isolated perfused working rat hearts were subjected to
 sustained global (15 or 20&amp;nbsp;min) or regional ischaemia (35&amp;nbsp;min), followed by reperfusion. Hearts were preconditioned using
 global ischaemia (1&amp;nbsp;×&amp;nbsp;5 or 3&amp;nbsp;×&amp;nbsp;5&amp;nbsp;min, alternated with 5&amp;nbsp;min reperfusion). To inhibit both PP1 and PP2A cantharidin (5...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240981</comments>
            <pubDate>Tue, 02 Feb 2010 06:58:14 +0100</pubDate>
            <guid isPermaLink="false">3240981</guid>        </item>
        <item>
            <title>C-kit+ CD45− cells found in the adult human heart represent a population of endothelial progenitor cells</title>
            <link>http://www.medworm.com/index.php?rid=3232818&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb11gl1742225u811%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Although numerous reports support the existence of stem cells in the adult heart, few studies have been conducted using human
 cardiac tissue. Therefore, cells from human cardiac atrial biopsies were analyzed regarding progenitor properties. Expression
 of stem cell markers was analyzed using fluorescence-activated cell sorting. This identified a small population of C-kit+
 cells, which could be further subdivided based on expression of CD45. The C-kit+ CD45+ population was determined to be of
 mast cell identity, while the C-kit+ CD45− population expressed mRNA of the endothelial lineage. Since the number of cells
 obtainable from biopsies was limited, a comparison between directly isolated and monolayer and explant cultured cells, respectively,
 was carried out. Whi...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3232818</comments>
            <pubDate>Mon, 01 Feb 2010 06:45:57 +0100</pubDate>
            <guid isPermaLink="false">3232818</guid>        </item>
        <item>
            <title>PDE5A suppression of acute β-adrenergic activation requires modulation of myocyte beta-3 signaling coupled to PKG-mediated troponin I phosphorylation</title>
            <link>http://www.medworm.com/index.php?rid=3223992&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx013434144788022%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Phosphodiesterase type 5A (PDE5A) inhibitors acutely suppress beta-adrenergic receptor (β-AR) stimulation in left ventricular
 myocytes and hearts. This modulation requires cyclic GMP synthesis via nitric oxide synthase (NOS)-NO stimulation, but upstream
 and downstream mechanisms remain un-defined. To determine this, adult cardiac myocytes from genetically engineered mice and
 controls were studied by video microscopy to assess sarcomere shortening (SS) and fura2-AM fluorescence to measure calcium
 transients (CaT). Enhanced SS from isoproterenol (ISO, 10&amp;nbsp;nM) was suppressed ≥50% by the PDE5A inhibitor sildenafil (SIL,
 1&amp;nbsp;μM), without altering CaT. This regulation was unaltered despite co-inhibition of either the cGMP-stimulated cAMP-esterase
 PDE2 (Bay 60...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3223992</comments>
            <pubDate>Wed, 27 Jan 2010 20:26:04 +0100</pubDate>
            <guid isPermaLink="false">3223992</guid>        </item>
        <item>
            <title>Exposure to cardiomyogenic stimuli fails to transdifferentiate human umbilical cord blood-derived mesenchymal stem cells</title>
            <link>http://www.medworm.com/index.php?rid=3205798&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff6n256348r67l332%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The ability of human umbilical cord blood-derived mesenchymal stem cells (UCBMSCs) to transdifferentiate towards cardiomyocytes
 remains unclear. The aim of this study was to direct UCBMSCs to the cardiac lineage by exposure to: (1) 5-azacytidine (AZ)
 or dimethyl sulfoxide (DMSO); (2) a combination of growth factors involved in early cardiomyogenesis (BMP-2&amp;nbsp;+&amp;nbsp;bFGF&amp;nbsp;+&amp;nbsp;IGF-1);
 (3) the Wnt signaling activators lithium chloride (LiCl) and phorbol-12-myristate-13-acetate (PMA); and (4) direct contact
 with neonatal rat cardiomyocytes. Expression of cardiomyocyte-specific proteins and β-catenin were assessed by quantitative
 RT-PCR, immunofluorescence and Western blot. Cocultures of human UCBMSCs with neonatal rat cardiomyocytes were also analyzed
 for t...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3205798</comments>
            <pubDate>Fri, 22 Jan 2010 03:00:28 +0100</pubDate>
            <guid isPermaLink="false">3205798</guid>        </item>
        <item>
            <title>Direct relationship between levels of TNF-α expression and endothelial dysfunction in reperfusion injury</title>
            <link>http://www.medworm.com/index.php?rid=3205799&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx15q3r4221067176%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;We previously found that myocardial ischemia/reperfusion (I/R) initiates expression of tumor necrosis factor-α (TNF) leading
 to coronary endothelial dysfunction. However, it is not clear whether there is a direct relationship between levels of TNF
 expression and endothelial dysfunction in reperfusion injury. We studied levels of TNF expression by using different transgenic
 animals expressing varying amounts of TNF in I/R. We crossed TNF overexpression (TNF++/++) with TNF knockout (TNF−/−) mice; thus we have a heterozygote population of mice with the expression of TNF “in between” the TNF−/− and TNF++/++ mice. Mouse hearts were subjected to 30&amp;nbsp;min of global ischemia followed by 90&amp;nbsp;min of reperfusion and their vasoactivity before
 and after I/R w...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3205799</comments>
            <pubDate>Fri, 22 Jan 2010 03:00:27 +0100</pubDate>
            <guid isPermaLink="false">3205799</guid>        </item>
        <item>
            <title>Simvastatin in contrast to postconditioning reduces infarct size in hyperlipidemic rabbits: possible role of oxidative/nitrosative stress attenuation</title>
            <link>http://www.medworm.com/index.php?rid=3168697&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F937n83ngl6551t1q%2F</link>
            <description>In conclusion, a 3-week simvastatin treatment
 limits the infarct size and attenuates the oxidative and nitrosative stress both in normo- and in hyper-cholesterolemic rabbits
 subjected to ischemia–reperfusion irrespective of the presence of POC, while POC is effective only in normocholesterolemic
 animals.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0078-3Authors
		Efstathios K. Iliodromitis, University of Athens Second University Department of Cardiology, Medical School, Attikon General Hospital Rimini 1 124 62 Athens GreeceIoanna Andreadou, University of Athens Department of Pharmaceutical Chemistry, School of Pharmacy Panepistimiopolis, Zografou 157 71 Athens GreeceEftihios Prokovas, University of Athens Second University Department of Cardiolo...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3168697</comments>
            <pubDate>Mon, 11 Jan 2010 18:20:11 +0100</pubDate>
            <guid isPermaLink="false">3168697</guid>        </item>
        <item>
            <title>Inhibition of mitochondrial permeability transition pore opening: the holy grail of cardioprotection</title>
            <link>http://www.medworm.com/index.php?rid=3168696&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Frt46130073241111%2F</link>
            <description>Content Type Journal ArticleCategory EditorialDOI 10.1007/s00395-009-0080-9Authors
		Gerd Heusch, University of Essen Medical School Institute for Pathophysiology Hufelandstr. 55 45122 Essen GermanyKerstin Boengler, University of Essen Medical School Institute for Pathophysiology Hufelandstr. 55 45122 Essen GermanyRainer Schulz, University of Essen Medical School Institute for Pathophysiology Hufelandstr. 55 45122 Essen Germany
	

	
		Journal Basic Research in CardiologyOnline ISSN 1435-1803Print ISSN 0300-8428 (Source: Basic Research in Cardiology)</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3168696</comments>
            <pubDate>Mon, 11 Jan 2010 18:20:11 +0100</pubDate>
            <guid isPermaLink="false">3168696</guid>        </item>
        <item>
            <title>HO-1 gene overexpression enhances the beneficial effects of superparamagnetic iron oxide labeled bone marrow stromal cells transplantation in swine hearts underwent ischemia/reperfusion: an MRI study</title>
            <link>http://www.medworm.com/index.php?rid=3121255&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F700408552x1p4514%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;To determine the effect of intracoronary transfer of superparamagnetic iron oxide (SPIO) labeled heme oxygenase-1 (HO-1) overexpressed
 bone marrow stromal cells (BMSCs) in a porcine myocardial ischemia/reperfusion model. Cell apoptosis was assayed and supernatant
 cytokine concentrations were measured in BMSCs that underwent hypoxia/reoxygen in vitro. Female mini-swines that underwent
 1&amp;nbsp;h LAD occlusion followed by 1&amp;nbsp;h reperfusion were randomly allocated to receive intracoronary saline (control), 1&amp;nbsp;×&amp;nbsp;107 SPIO-labeled BMSCs transfected with pcDNA3.1-Lacz plasmid (Lacz-BMSCs), pcDNA3.1-human HO-1 (HO-1-BMSCs), pcDNA3.1-hHO-1
 pretreated with a HO inhibitor, tin protoporphyrin (SnPP, n&amp;nbsp;=&amp;nbsp;10 each). MRI and postmortem histological analysis wer...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3121255</comments>
            <pubDate>Wed, 23 Dec 2009 22:20:31 +0100</pubDate>
            <guid isPermaLink="false">3121255</guid>        </item>
        <item>
            <title>Cardioselective nitric oxide synthase 3 gene transfer protects against myocardial reperfusion injury</title>
            <link>http://www.medworm.com/index.php?rid=3105983&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F4q20v28677798323%2F</link>
            <description>In conclusion, single myocardial NOS3 retroinfusion attenuates I/R injury, and causes a sustained reduction
 in myocardial infarct size and inflammatory cell infiltration. Gene-based strategies to increase NO bioavailability may have
 therapeutic potential in myocardial I/R.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0077-4Authors
		Zsolt Szelid, Flanders Institute for Biotechnology (VIB) Vesalius Research Center Leuven BelgiumPeter Pokreisz, Flanders Institute for Biotechnology (VIB) Vesalius Research Center Leuven BelgiumXiaoshun Liu, Flanders Institute for Biotechnology (VIB) Vesalius Research Center Leuven BelgiumPieter Vermeersch, Flanders Institute for Biotechnology (VIB) Vesalius Research Center Leuven BelgiumGlenn Marsboom, Flanders Institut...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105983</comments>
            <pubDate>Fri, 18 Dec 2009 07:06:12 +0100</pubDate>
            <guid isPermaLink="false">3105983</guid>        </item>
        <item>
            <title>Effects of a protocol of ischemic postconditioning and/or captopril in hearts of normotensive and hypertensive rats</title>
            <link>http://www.medworm.com/index.php?rid=3090283&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa6g260j55r4h86j4%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Brief periods (a few seconds) of cyclic coronary occlusions applied early in reperfusion induce a cardioprotection against
 infarct size, called postconditioning (PostC) in which B2-bradykinin receptors play a pivotal role. Since angiotensin-converting enzyme (ACE) inhibitors reduce degradation of kinins,
 we studied the effects of PostC on infarct size and postischemic myocardial dysfunction in both normotensive (WKY) and spontaneously
 hypertensive rats (SHR) acutely or chronically treated with the ACE inhibitor Captopril. Isolated hearts from SHR and WKY
 rats were subjected to the following protocols: (a) ischemia for 30- and 120-min reperfusion (I/R); (b) I/R&amp;nbsp;+&amp;nbsp;PostC protocol
 (5-cycles 10-s I/R); (c) pretreatment with Captopril for 4-weeks before to subj...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3090283</comments>
            <pubDate>Sun, 13 Dec 2009 06:41:36 +0100</pubDate>
            <guid isPermaLink="false">3090283</guid>        </item>
        <item>
            <title>Anti-inflammatory effect of oxytocin in rat myocardial infarction</title>
            <link>http://www.medworm.com/index.php?rid=3090284&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Flp7u0j3271h1t4m8%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;While an increasing amount of evidence demonstrates the homeostatic functions of the cardiac oxytocin (OT) system, less is
 known about the role of this hormone in the injured heart. The current study examined the effect of OT infusion on cell apoptosis,
 expression of proliferating cell nuclear antigen (PCNA) and inflammation in the acute and subacute phases of myocardial infarction
 (MI). Prior MI male Sprague-Dawley rats were infused subcutaneously with OT 25 or 125&amp;nbsp;ng/(kg&amp;nbsp;h) for 3 or 7&amp;nbsp;days. Saline-treated
 MI and sham-operated rats served as controls. Echocardiography and analysis of cardiac sections were used to disclose OT actions.
 Left ventricular fractional shortening, estimated to be 46.0&amp;nbsp;±&amp;nbsp;1.8% in sham controls, declined to 21.1&amp;nbs...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3090284</comments>
            <pubDate>Sat, 12 Dec 2009 14:16:26 +0100</pubDate>
            <guid isPermaLink="false">3090284</guid>        </item>
        <item>
            <title>Clopidogrel affects leukocyte dependent platelet aggregation by P2Y12 expressing leukocytes</title>
            <link>http://www.medworm.com/index.php?rid=3040903&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy45440728714tngg%2F</link>
            <description>In conclusion, (1) leukocytes influence ADP induced platelet aggregation most likely by expression of the P2Y12 receptor. This interaction is abolished by clopidogrel. Therefore, clopidogrel may act directly on leukocytes via the P2Y12 receptor. (2) Clopidogrel may be under dosed in obese patients.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0073-8Authors
		Philipp Diehl, University-Hospital Freiburg Department of Cardiology and Angiology Hugstetterstr. 55 79106 Freiburg GermanyChristoph Olivier, University-Hospital Freiburg Department of Cardiology and Angiology Hugstetterstr. 55 79106 Freiburg GermanyChristoph Halscheid, University-Hospital Freiburg Department of Cardiology and Angiology Hugstetterstr. 55 79106 Freiburg GermanyThomas Helbing, Unive...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3040903</comments>
            <pubDate>Fri, 27 Nov 2009 07:03:10 +0100</pubDate>
            <guid isPermaLink="false">3040903</guid>        </item>
        <item>
            <title>Adenosine and maximum coronary vasodilation in humans: myth and misconceptions in the assessment of coronary reserve</title>
            <link>http://www.medworm.com/index.php?rid=3040904&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F2278ku4839686402%2F</link>
            <description>Content Type Journal ArticleCategory EditorialDOI 10.1007/s00395-009-0074-7Authors
		Gerd Heusch, Universitätsklinikum Essen Institut für Pathophysiologie Hufelandstr. 55 45122 Essen Germany
	

	
		Journal Basic Research in CardiologyOnline ISSN 1435-1803Print ISSN 0300-8428 (Source: Basic Research in Cardiology)</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3040904</comments>
            <pubDate>Thu, 26 Nov 2009 07:59:06 +0100</pubDate>
            <guid isPermaLink="false">3040904</guid>        </item>
        <item>
            <title>Inhibition of the p38 MAP kinase in vivo improves number and functional activity of vasculogenic cells and reduces atherosclerotic disease progression</title>
            <link>http://www.medworm.com/index.php?rid=2990360&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj1lp326222155521%2F</link>
            <description>In conclusion, this study demonstrates that systemic
 p38 MAP kinase inhibition with SB203580 improves the number and function of vasculogenic cells in an animal model of hypercholesterolemia,
 and reduces atherosclerotic disease progression in ApoE−/− mice.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0072-9Authors
		Florian H. Seeger, Universität Frankfurt Institute for Cardiovascular Regeneration, Centre of Molecular Medicine Haus 25, 4. Stock, Theodor-Stern-Kai 7 60590 Frankfurt GermanyDaniel Sedding, University of Giessen and Marburg GmbH Department of Internal Medicine/Cardiology Giessen GermanyAlexander C. Langheinrich, University of Giessen &amp; Marburg GmbH Department of Diagnostic Radiology Giessen GermanyJudith Haendeler, IUF (Institute f...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2990360</comments>
            <pubDate>Thu, 12 Nov 2009 18:56:56 +0100</pubDate>
            <guid isPermaLink="false">2990360</guid>        </item>
        <item>
            <title>Peroxisome proliferator-activated receptor-γ activation attenuates cardiac fibrosis in type 2 diabetic rats: the effect of rosiglitazone on myocardial expression of receptor for advanced glycation end products and of connective tissue growth factor</title>
            <link>http://www.medworm.com/index.php?rid=2982518&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fd47m8h5220495q15%2F</link>
            <description>This study investigated the effects of the PPAR-γ agonist, rosiglitazone, on myocardial expression of
 RAGE and CTGF, extent of cardiac fibrosis, and left ventricular (LV) diastolic function in type 2 diabetic (T2D) rats. Twenty-week-old
 T2D rats were randomized to treatment with either 20&amp;nbsp;weeks of rosiglitazone (20&amp;nbsp;mg/kg) or saline (n&amp;nbsp;=&amp;nbsp;10 in each group). Serial echocardiographic examinations were performed just before randomization (20&amp;nbsp;weeks) and at study
 completion (40&amp;nbsp;weeks). Fibrosis extent and RAGE and CTGF expression were assessed in previously imaged hearts by picrosirius
 red staining, and by real-time reverse transcriptase-coupled polymerase chain reaction (RT-PCR) and immunoblotting, respectively.
 Results of the latter assessments were further v...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2982518</comments>
            <pubDate>Tue, 10 Nov 2009 08:07:30 +0100</pubDate>
            <guid isPermaLink="false">2982518</guid>        </item>
        <item>
            <title>Depressed expression of MuRF1 and MAFbx in areas remote of recent myocardial infarction: a mechanism contributing to myocardial remodeling?</title>
            <link>http://www.medworm.com/index.php?rid=2936251&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj7646540w352n136%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Ventricular remodeling following myocardial infarction (MI) includes myocardial hypertrophy, a process requiring increased
 protein synthesis and sarcomere assembly. The anti-hypertrophic effect of MuRF1/MafBx, both muscle-specific E3-ubiquitin ligases,
 has been demonstrated in animal experiments and in cultured cardiomyocytes. We assessed MuRF1/MAFbx expression in myocardium
 remote of recently (&amp;lt;2&amp;nbsp;weeks) infarcted regions (MI), compared with patients undergoing coronary artery bypass surgery, with
 normal systolic function and without previous infarction (control or Con). Left ventricular myocardial biopsies were obtained
 from the contralateral normal zone in MI (n&amp;nbsp;=&amp;nbsp;14) patients and from the Con (n&amp;nbsp;=&amp;nbsp;12) group. MuRF-1/MAFbx expression wa...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2936251</comments>
            <pubDate>Mon, 26 Oct 2009 18:07:10 +0100</pubDate>
            <guid isPermaLink="false">2936251</guid>        </item>
        <item>
            <title>Postconditioning with levosimendan reduces the infarct size involving the PI3K pathway and KATP-channel activation but is independent of PDE-III inhibition</title>
            <link>http://www.medworm.com/index.php?rid=2913695&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa6386w8175213600%2F</link>
            <description>In conclusion, levosimendan applied prior to reperfusion
 in acute myocardial infarction significantly reduces the infarct size in an in vivo rat model. This protection involves the
 PI3K pathway and the activation of mitochondrial KATP-channels, but is independent of PDE-III inhibition. This finding may
 open new possibilities for the treatment of patients with acute myocardial infarction using levosimendan, which is an already
 established therapy in cardiogenic shock. Whether the reduction of mortality in cardiogenic shock by levosimendan may in part
 be based on this postconditoning effect remains to be elucidated in clinical setting.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0064-9Authors
		Antje Hönisch, University of Technology Dresden Depa...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2913695</comments>
            <pubDate>Tue, 20 Oct 2009 15:18:08 +0100</pubDate>
            <guid isPermaLink="false">2913695</guid>        </item>
        <item>
            <title>Endothelin-B receptors and ventricular arrhythmogenesis in the rat model of acute myocardial infarction</title>
            <link>http://www.medworm.com/index.php?rid=2905988&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fbh864857273m070g%2F</link>
            <description>We examined the pathophysiologic role of ETB-receptors on ventricular tachyarrhythmias (VT/VF) during myocardial infarction
 (MI). MI was induced by coronary ligation in two animal groups, namely in wild-type (n&amp;nbsp;=&amp;nbsp;63) and in ETB-receptor-deficient (n&amp;nbsp;=&amp;nbsp;61) rats. Using a telemetry recorder, VT/VF episodes were evaluated during phase I (the 1st hour) and phase II (2–24&amp;nbsp;h)
 post-MI, with and without prior β-blockade. Action potential duration at 90% repolarization (APD90) was measured from monophasic
 epicardial recordings and indices of sympathetic activation were assessed using fast-Fourier analysis of heart rate variability.
 Serum epinephrine and norepinephrine were measured with radioimmunoassay. MI size was similar in the two groups. There was
 a marked tempo...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2905988</comments>
            <pubDate>Sat, 17 Oct 2009 08:56:41 +0100</pubDate>
            <guid isPermaLink="false">2905988</guid>        </item>
        <item>
            <title>Mesenchymal stem cell-based prostacyclin synthase gene therapy for pulmonary hypertension rats</title>
            <link>http://www.medworm.com/index.php?rid=2905989&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw23300603648j273%2F</link>
            <description>In conclusion, the gene-engineered MSCs would be a suitable cell vector
 for gene delivery specifically to the PH lung. The allogeneic PCS-MSC transplantation attenuated PH and cardiovascular remodeling,
 and improved the prognosis in PH rats. The MSC-based PCS gene therapy may be a promising strategy for PH treatment.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0065-8Authors
		Kiyoko Takemiya, Kurume University School of Medicine Department of Internal Medicine Division of Cardio-Vascular Medicine 67 Asahimachi Kurume 830-0011 JapanHisashi Kai, Kurume University School of Medicine Department of Internal Medicine Division of Cardio-Vascular Medicine 67 Asahimachi Kurume 830-0011 JapanHideo Yasukawa, Kurume University School of Medicine Department of ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2905989</comments>
            <pubDate>Fri, 16 Oct 2009 17:54:14 +0100</pubDate>
            <guid isPermaLink="false">2905989</guid>        </item>
        <item>
            <title>Role of autoimmunity in dilated cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=2896116&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fum782q50p3545q77%2F</link>
            <description>Content Type Journal ArticleCategory EditorialDOI 10.1007/s00395-009-0069-4Authors
		Ziya Kaya, University of Heidelberg Department of Cardiology 69120 Heidelberg GermanyHugo A. Katus, University of Heidelberg Department of Cardiology 69120 Heidelberg Germany
	

	
		Journal Basic Research in CardiologyOnline ISSN 1435-1803Print ISSN 0300-8428 (Source: Basic Research in Cardiology)</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2896116</comments>
            <pubDate>Wed, 14 Oct 2009 06:02:04 +0100</pubDate>
            <guid isPermaLink="false">2896116</guid>        </item>
        <item>
            <title>Blockade of NF-κB by pyrrolidine dithiocarbamate attenuates myocardial inflammatory response and ventricular dysfunction following coronary microembolization induced by homologous microthrombi in rats</title>
            <link>http://www.medworm.com/index.php?rid=2896117&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F27t72214ju014g52%2F</link>
            <description>The objective of this study was to evaluate the effects of specific NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) on
 inflammatory response and cardiac function in a rat model of coronary microembolization (CME). CME was developed by injecting
 a suspension of microthrombotic particles (MTPs) into the left ventricle when obstructing the ascending aorta. MTPs were generated
 from the rat clots sized by filtration through 38&amp;nbsp;μm screen. Thirty-two Sprague–Dawley rats served as sham group, 128 CME
 rats were randomized to untreated (CMEU) and PDTC-treated (CMEp) group. Rats in CMEp were administered intraperitoneally with 50, 100, 200&amp;nbsp;mg&amp;nbsp;kg−1&amp;nbsp;day−1 PDTC, respectively, from 1&amp;nbsp;h before to 7&amp;nbsp;days after operation. The rats were sacrificed on day 1, 3, 7, ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2896117</comments>
            <pubDate>Tue, 13 Oct 2009 08:11:01 +0100</pubDate>
            <guid isPermaLink="false">2896117</guid>        </item>
        <item>
            <title>Adrenomedullin is increased in alveolar macrophages and released from the lungs into the circulation in severe heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2896118&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr2g55502n0225356%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Adrenomedullin (AM) is a potent vasorelaxing peptide with natriuretic, diuretic, and growth inhibitory properties. Plasma
 concentrations and myocardial AM expression are increased in heart failure (HF). Since AM and AM binding sites are abundantly
 expressed in the lungs, we investigated to what extent pulmonary AM and AM receptor subtypes [CRLR/RAMP2 (AM1) and CRLR/RAMP3 (AM2)] are changed in HF and whether the lungs contribute to the increased plasma concentrations of AM reported in HF. Pulmonary
 AM mRNA and protein expression were increased by 2.8- and 2.6-fold, respectively, whereas mRNA expression of RAMP2 and CRLR
 was decreased in rats with HF 7&amp;nbsp;days after induction of MI compared to sham-operated rats (P&amp;nbsp;&amp;lt;&amp;nbsp;0.05). Pulmonary AM receptor density...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2896118</comments>
            <pubDate>Tue, 13 Oct 2009 08:11:00 +0100</pubDate>
            <guid isPermaLink="false">2896118</guid>        </item>
        <item>
            <title>PDGF-CC induces tissue factor expression: role of PDGF receptor α/β</title>
            <link>http://www.medworm.com/index.php?rid=2853224&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc29651217p4044u5%2F</link>
            <description>This study
 assesses the impact of PDGF-CC on TF expression in human cells. PDGF-CC concentration-dependently induced TF expression by
 2.5-fold in THP-1 cells, by 2.0-fold in human peripheral blood monocytes, by 1.4-fold in vascular smooth muscle cells, and
 by 2.6-fold in microvascular endothelial cells, but did not affect TF expression in aortic endothelial cells. A similar pattern
 was observed with PDGF-BB. In contrast, PDGF-AA did not alter TF expression in THP-1 cells. TF whole cell activity was induced
 following stimulation with PDGF-BB and PDGF-CC in THP-1 cells. Real-time polymerase chain reaction revealed that PDGF-CC induced
 TF mRNA. PDGF-CC transiently activated p42/44 MAP kinase [extracellular signal-regulated kinase (ERK)], while phosphorylation
 of the MAP kinases c-Jun N...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2853224</comments>
            <pubDate>Wed, 30 Sep 2009 18:21:08 +0100</pubDate>
            <guid isPermaLink="false">2853224</guid>        </item>
        <item>
            <title>Is remodeling the dominant compensatory mechanism in both chronic heart failure with preserved and reduced left ventricular ejection fraction?</title>
            <link>http://www.medworm.com/index.php?rid=2835092&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F113572r832t1j565%2F</link>
            <description>This study examines the individual effects of left ventricular hypertrophy, long-axis shortening and the effect of left ventricular
 remodeling on ejection fraction, end-diastolic volume and stroke volume using a mathematical model of left ventricular contraction.
 Reducing long-axis shortening caused a decline in stroke volume independently of hypertrophy. Increasing concentric left ventricular
 hypertrophy resulted in an increase in ejection fraction secondary to augmented wall thickening. A decline in stroke volume
 occurred despite a preserved ejection fraction when concentric hypertrophy was present. Normalization of stroke volume by
 remodeling resulted in a marked increase in end-diastolic volume in the absence of hypertrophy and an end-diastolic volume
 similar to normal in the pre...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2835092</comments>
            <pubDate>Thu, 24 Sep 2009 16:45:16 +0100</pubDate>
            <guid isPermaLink="false">2835092</guid>        </item>
        <item>
            <title>Obesity-induced insulin resistance causes endothelial dysfunction without reducing the vascular response to hindlimb ischemia</title>
            <link>http://www.medworm.com/index.php?rid=2835091&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh788607737xtl424%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Impairment of vascular growth is a hallmark of diabetic complications but the progression and mechanisms are poorly understood.
 To determine whether obesity and early diabetes impair endothelium-dependent vasodilatation and vascular response to ischemia,
 microvascular function as well as angiogenic responses to ischemia were assessed in young (C57) and 6-month-old lean mice
 (old C57), in obese (db-C57) mice, and in mice suffering an early (db-KsJ) and sustained type&amp;nbsp;2 diabetes (old db-KsJ). Glycemia gradually increased from the db-C57 to the old db-KsJ. Early and established type II diabetes significantly reduced the level of insulin that was significantly increased in
 obese mice. Endothelial function was assessed in isolated resistance arteries while the angio...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2835091</comments>
            <pubDate>Thu, 24 Sep 2009 16:45:16 +0100</pubDate>
            <guid isPermaLink="false">2835091</guid>        </item>
        <item>
            <title>Aldosterone improves contractile function of adult rat ventricular cardiomyocytes in a non-acute way: potential relationship to the calcium paradox of aldosteronism</title>
            <link>http://www.medworm.com/index.php?rid=2810740&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F37031t6145653713%2F</link>
            <description>In conclusion, chronic exposure to aldosterone improves
 the function of cardiomyocytes under basal conditions and electrolyte disturbances that mimic the situation found in heart
 failure patients.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0059-6Authors
		Sibylle Wenzel, Justus-Liebig-University Giessen Physiologisches Institut Aulweg 129 35392 Giessen GermanyIlhan Tastan, Justus-Liebig-University Giessen Physiologisches Institut Aulweg 129 35392 Giessen GermanyYaser Abdallah, Justus-Liebig-University Giessen Physiologisches Institut Aulweg 129 35392 Giessen GermanyRolf Schreckenberg, Justus-Liebig-University Giessen Physiologisches Institut Aulweg 129 35392 Giessen GermanyKlaus-Dieter Schlüter, Justus-Liebig-University Giessen Physiologisches In...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2810740</comments>
            <pubDate>Thu, 17 Sep 2009 23:29:34 +0100</pubDate>
            <guid isPermaLink="false">2810740</guid>        </item>
        <item>
            <title>AMP579 is revealed to be a potent A2b-adenosine receptor agonist in human 293 cells and rabbit hearts</title>
            <link>http://www.medworm.com/index.php?rid=2810742&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F73m8238303528955%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The mixed A1/A2a-adenosine agonist AMP579 given at reperfusion is protective in animal models of myocardial infarction. Receptor-blocking
 studies have indicated that the protection came from an adenosine receptor (AR), but neither A1- nor A2a-selective agonists could duplicate its protection. We recently found that A2b-selective agonists given at reperfusion are protective, and, therefore, tested whether AMP579 might also be an A2b agonist. We used human embryonic kidney cells overexpressing human A2b receptors as an assay system. In these cells, A2b receptor occupancy causes phosphorylation of ERK. AMP579 induced ERK phosphorylation with an EC50 of 250&amp;nbsp;nM and this phosphorylation could be blocked by MRS1754 or PSB1115, two highly selective blockers of human A2b r...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2810742</comments>
            <pubDate>Thu, 17 Sep 2009 12:46:58 +0100</pubDate>
            <guid isPermaLink="false">2810742</guid>        </item>
        <item>
            <title>Humoral anti-proteasomal autoimmunity in dilated cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=2810741&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff444h4183q0qh614%2F</link>
            <description>In conclusion, humoral autoreactive anti-proteasome immune responses appear to be enhanced in DCM. Viral infection
 of the myocardium may be linked to the induction of anti-proteasomal immunity in DCM.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0061-zAuthors
		Antje Voigt, Charité-Universitätsmedizin Campus Mitte Medizinische Klinik für Kardiologie und Angiologie Berlin GermanyKatrin Bartel, Charité-Universitätsmedizin Campus Mitte Medizinische Klinik für Kardiologie und Angiologie Berlin GermanyKarl Egerer, Charité-Universitätsmedizin Medizinische Klinik für Rheumatologie und Immunologie Berlin GermanyChristiane Trimpert, Ernst-Moritz-Arndt-Universität Klinik für Innere Medizin B Greifswald GermanyEugen Feist, Charité-Universitätsmediz...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2810741</comments>
            <pubDate>Thu, 17 Sep 2009 12:46:58 +0100</pubDate>
            <guid isPermaLink="false">2810741</guid>        </item>
        <item>
            <title>K201 improves aspects of the contractile performance of human failing myocardium via reduction in Ca2+ leak from the sarcoplasmic reticulum</title>
            <link>http://www.medworm.com/index.php?rid=2753810&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh921h1382686ru21%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In heart failure, intracellular Ca2+ leak from cardiac ryanodine receptors (RyR2s) leads to a loss of Ca2+ from the sarcoplasmic reticulum (SR) potentially contributing to decreased function. Experimental data suggest that the 1,4-benzothiazepine
 K201 (JTV-519) may stabilise RyR2s and thereby reduce detrimental intracellular Ca2+ leak. Whether K201 exerts beneficial effects in human failing myocardium is unknown. Therefore, we have studied the effects
 of K201 on muscle preparations from failing human hearts. K201 (0.3&amp;nbsp;μM; extracellular [Ca2+]e 1.25&amp;nbsp;mM) showed no effects on contractile function and micromolar concentrations resulted in negative inotropic effects (K201
 1&amp;nbsp;μM; developed tension −9.8&amp;nbsp;±&amp;nbsp;2.5% compared to control group; P&amp;nbsp;&amp;...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2753810</comments>
            <pubDate>Mon, 31 Aug 2009 14:54:30 +0100</pubDate>
            <guid isPermaLink="false">2753810</guid>        </item>
        <item>
            <title>Nitric oxide/cGMP signalling mediates the cardioprotective action of adrenomedullin in reperfused myocardium</title>
            <link>http://www.medworm.com/index.php?rid=2744945&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg23746321v877544%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;We demonstrated previously that adrenomedullin (AM), when given during early reperfusion, limited infarct size in rat heart.
 The present study was undertaken to provide direct evidence of the NO-dependency of AM’s cardioprotective action by assessing
 NO biosynthesis and involvement of the soluble guanylyl cyclase (sGC) pathway. Perfused hearts from male CD-1 mice were subjected
 to 30-min left coronary occlusion and 60-min reperfusion. Infarct size was determined by tetrazolium staining. AM 10 nM was
 administered from 20&amp;nbsp;min after coronary occlusion until 10&amp;nbsp;min after reperfusion. Coronary effluent was analysed for NO2
 − and NO3
 −, and myocardial samples were analysed for NO2
 −, NO3
 −, nitroso-adducts and cGMP concentration. To examine the rol...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2744945</comments>
            <pubDate>Fri, 28 Aug 2009 14:56:57 +0100</pubDate>
            <guid isPermaLink="false">2744945</guid>        </item>
        <item>
            <title>Transcriptional regulation of Pim-1 kinase in vascular smooth muscle cells and its role for proliferation</title>
            <link>http://www.medworm.com/index.php?rid=2742534&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg8k713h60n511102%2F</link>
            <description>This study aimed
 to foster the understanding of Pim-1 expression and regulation in murine VSMC in response to factors typically present within
 the atherosclerotic plaque. While oxidative stress, VEGF-A165 and angiotensin II did not have any effect on Pim-1 expression, VSMC strongly increased (3-fold) Pim-1 mRNA upon stimulation
 with PDGFbb, followed by its protein upregulation. Half life of Pim-1 RNA and protein were determined to be 25&amp;nbsp;min and 6&amp;nbsp;h, respectively.
 PDGFbb induced a strong, 10-fold increase in BrdU-uptake, a marker of proliferation. This was effectively blocked by either Pim-1-specific
 inhibitor quercetagetin or adenovirally introduced Pim-1 shRNA. We further identified the signaling pathways linking PDGFbb to Pim-1 in VSMC: as expected, we determined transcrip...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742534</comments>
            <pubDate>Thu, 27 Aug 2009 15:08:18 +0100</pubDate>
            <guid isPermaLink="false">2742534</guid>        </item>
        <item>
            <title>Long-term treatment with the AT1-receptor antagonist telmisartan inhibits biglycan accumulation in murine atherosclerosis</title>
            <link>http://www.medworm.com/index.php?rid=2728103&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F801wr35wp5458423%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Accumulation of biglycan, a small leucine-rich proteoglycan, in the neointima precedes the retention of lipids and accumulation
 of macrophages during early atherosclerosis. Biglycan is therefore considered a pro-atherogenic proteoglycan that might play
 a key role in atherogenesis. On the other hand biglycan ensures in part establishment of stable collagen networks. Aim of
 the present study was to determine whether telmisartan affects biglycan accumulation in a murine model of accelerated atherosclerosis
 and whether collagen matrix is affected. ApoE−/−-mice on Western diet were chronically (12&amp;nbsp;weeks) treated either with telmisartan (10&amp;nbsp;mg/kg) or hydralazine (500&amp;nbsp;mg/l drinking
 water) and systolic arterial blood pressure was determined by tail cuff ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2728103</comments>
            <pubDate>Sat, 22 Aug 2009 18:58:32 +0100</pubDate>
            <guid isPermaLink="false">2728103</guid>        </item>
        <item>
            <title>Transcriptional and posttranscriptional regulators of biglycan in cardiac fibroblasts</title>
            <link>http://www.medworm.com/index.php?rid=2728104&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F022138k15262603l%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Biglycan, a small leucine-rich proteoglycan, is essential for scar formation and preservation of hemodynamic function after
 myocardial infarction, as shown in biglycan-knockout mice. Because of this important role in cardiac pathophysiology, we aimed
 to identify regulators of biglycan expression and posttranslational modifications in cardiac fibroblasts. Cardiac fibroblasts
 were isolated from neonatal Wistar-Kyoto rats and used in the first passage. Expression of biglycan was analyzed after metabolic
 labeling with [35S]-sulfate by SDS-polyacrylamide gel electrophoresis and molecular sieve chromatography; mRNA expression was examined by Northern
 analysis and real-time RT-PCR. Serum, thrombin, transforming growth factor β1 (TGFβ 1) and platelet-derived growth facto...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2728104</comments>
            <pubDate>Sat, 22 Aug 2009 18:58:31 +0100</pubDate>
            <guid isPermaLink="false">2728104</guid>        </item>
        <item>
            <title>Multi-slice computed tomography with N1177 identifies ruptured atherosclerotic plaques in rabbits</title>
            <link>http://www.medworm.com/index.php?rid=2717488&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F702h00g14l625743%2F</link>
            <description>In conclusion, our results show that N1177
 is a contrast agent that can identify ruptured atherosclerotic plaques.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0052-0Authors
		Jozef Leo Van Herck, Antwerp University Hospital Division of Cardiology Wilrijkstraat 10 2650 Edegem BelgiumGuido R. Y. De Meyer, University of Antwerp Division of Pharmacology Universiteitsplein 1 2610 Wilrijk BelgiumWim Martinet, University of Antwerp Division of Pharmacology Universiteitsplein 1 2610 Wilrijk BelgiumRodrigo A. Salgado, Antwerp University Hospital Division of Radiology Wilrijkstraat 10 2650 Edegem BelgiumBharati Shivalkar, Antwerp University Hospital Division of Cardiology Wilrijkstraat 10 2650 Edegem BelgiumRoel De Mondt, University of Antwerp Division of Che...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2717488</comments>
            <pubDate>Wed, 19 Aug 2009 17:56:32 +0100</pubDate>
            <guid isPermaLink="false">2717488</guid>        </item>
        <item>
            <title>Proteasome inhibitor bortezomib promotes a rupture-prone plaque phenotype in ApoE-deficient mice</title>
            <link>http://www.medworm.com/index.php?rid=2717489&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx28x04237p532625%2F</link>
            <description>In conclusion, our results indicate that an impaired proteasome
 function promotes features of a more rupture-prone plaque phenotype.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0054-yAuthors
		Jozef Leo Van Herck, Antwerp University Hospital Division of Cardiology Wilrijkstraat 10 2650 Edegem BelgiumGuido R. Y. De Meyer, University of Antwerp Division of Pharmacology Universiteitsplein 1 2610 Wilrijk BelgiumWim Martinet, University of Antwerp Division of Pharmacology Universiteitsplein 1 2610 Wilrijk BelgiumHidde Bult, University of Antwerp Division of Pharmacology Universiteitsplein 1 2610 Wilrijk BelgiumChristiaan J. Vrints, Antwerp University Hospital Division of Cardiology Wilrijkstraat 10 2650 Edegem BelgiumArnold G. Herman, University of Antwe...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2717489</comments>
            <pubDate>Wed, 19 Aug 2009 17:56:28 +0100</pubDate>
            <guid isPermaLink="false">2717489</guid>        </item>
        <item>
            <title>Attenuation of infarction in cynomolgus monkeys: preconditioning and postconditioning</title>
            <link>http://www.medworm.com/index.php?rid=2685959&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fvw32t75694510241%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Ischemic pre- (IPC) and post- (IPOC) conditioning are very protective in laboratory animals, but it has not been possible
 to measure their anti-infarct potency in human hearts. Non-human primates are genetically closer to humans than other laboratory
 animals, but until now there have been no studies of IPC or IPOC in any primate species. Accordingly the left anterior descending
 coronary artery of cynomolgus monkeys was occluded for 90&amp;nbsp;min and reperfused for 4&amp;nbsp;h. In control animals, only 44% of the
 risk zone infarcted indicating cynomolgus myocardium is much more resistant to infarction than that of rabbits or rats. The
 regression line for the infarct-risk zone plot was very linear (r&amp;nbsp;=&amp;nbsp;0.99), and intersected the risk zone axis at 0.82&amp;nbsp;cm3. ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2685959</comments>
            <pubDate>Sun, 09 Aug 2009 07:15:20 +0100</pubDate>
            <guid isPermaLink="false">2685959</guid>        </item>
        <item>
            <title>Protein kinase C α and ε phosphorylation of troponin and myosin binding protein C reduce Ca2+ sensitivity in human myocardium</title>
            <link>http://www.medworm.com/index.php?rid=2679772&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fevm4701603618164%2F</link>
            <description>This study was designed to reveal and compare the effects
 of PKCα- and PKCε-mediated phosphorylation on myofilament function in human myocardium. Isometric force was measured at different
 [Ca2+] in single permeabilized cardiomyocytes from failing human left ventricular tissue. Activated PKCα and PKCε equally reduced
 Ca2+ sensitivity in failing cardiomyocytes (ΔpCa50&amp;nbsp;=&amp;nbsp;0.08&amp;nbsp;±&amp;nbsp;0.01). Both PKC isoforms increased phosphorylation of troponin I- (cTnI) and myosin binding protein C (cMyBP-C)
 in failing cardiomyocytes. Subsequent incubation of failing cardiomyocytes with the catalytic subunit of protein kinase A
 (PKA) resulted in a further reduction in Ca2+ sensitivity, indicating that the effects of both PKC isoforms were not caused by cross-phosphorylation of PKA s...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2679772</comments>
            <pubDate>Tue, 04 Aug 2009 19:10:25 +0100</pubDate>
            <guid isPermaLink="false">2679772</guid>        </item>
        <item>
            <title>Effects of muscarinic receptor stimulation on Ca2+ transient, cAMP production and pacemaker frequency of rabbit sinoatrial node cells</title>
            <link>http://www.medworm.com/index.php?rid=2661535&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F1646m40577l72533%2F</link>
            <description>In conclusion, muscarinic receptor stimulation inhibits the Cai2+ transient via a cAMP-dependent signaling pathway. Inhibition of the Cai2+ transient contributes to pacemaker slowing and inhibits Cai2+-stimulated cAMP production. Thus, we provide functional evidence for the contribution of the Cai2+ transient to ACh-induced inhibition of pacemaker activity and cAMP content in rabbit SAN cells.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0048-9Authors
		Marcel M. G. J. van Borren, University of Amsterdam Heart Failure Research Center, Academic Medical Center Amsterdam The NetherlandsArie O. Verkerk, University of Amsterdam Heart Failure Research Center, Academic Medical Center Amsterdam The NetherlandsRonald Wilders, University of Amsterdam Heart Fail...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2661535</comments>
            <pubDate>Tue, 28 Jul 2009 18:57:56 +0100</pubDate>
            <guid isPermaLink="false">2661535</guid>        </item>
        <item>
            <title>Propylthiouracil, independent of its antithyroid effect, promotes vascular smooth muscle cells differentiation via PTEN induction</title>
            <link>http://www.medworm.com/index.php?rid=2642502&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F7mg34977h46376ru%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Propylthiouracil (PTU), independent of its antithyroid effect, is recently found to have an antiatherosclerotic effect. The
 aim of this study is to determine the impact of PTU on phenotypic modulation of vascular smooth muscle cells (VSMCs), as phenotypic
 modulation may contribute to the growth of atherosclerotic lesions and neointimal formation after arterial injury. Propylthiouracil
 reduced neointimal formation in balloon-injured rat carotid arteries. In&amp;nbsp;vitro, PTU may convert VSMCs from a serum-induced
 dedifferentiation state to a differentiated state, as indicated by a spindle-shaped morphology and an increase in the expression
 of SMC differentiation marker contractile proteins, including calponin and smooth muscle (SM)-myosin heavy chain (SM-MHC).
 Transi...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2642502</comments>
            <pubDate>Sat, 25 Jul 2009 10:40:06 +0100</pubDate>
            <guid isPermaLink="false">2642502</guid>        </item>
        <item>
            <title>Sonic hedgehog is a potent chemoattractant for human monocytes: diabetes mellitus inhibits Sonic hedgehog-induced monocyte chemotaxis</title>
            <link>http://www.medworm.com/index.php?rid=2642503&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh6443m7227818716%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The aim of the present study was to evaluate the expression of hedgehog (Hh) signaling molecules and the chemotactic activity
 of Sonic hedgehog (Shh) in monocytes from control (CTR) and diabetic patients with or without coronary artery disease (CAD).
 Previously several studies demonstrated that exogenous administration of Shh can induce angiogenesis and accelerate repair
 of ischemic myocardium and skeletal muscles. Blood samples were collected from (1) CTR (n&amp;nbsp;=&amp;nbsp;25); (2) patients with stable CAD without diabetes mellitus (CAD−DM, n&amp;nbsp;=&amp;nbsp;10); and (3) with stable CAD with DM (CAD+DM, n&amp;nbsp;=&amp;nbsp;15). Monocytes were isolated by Percoll gradient and subjected to PCR and chemotaxis analysis. Hh signaling molecules were
 expressed in human monocytes, an...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2642503</comments>
            <pubDate>Sat, 25 Jul 2009 08:22:17 +0100</pubDate>
            <guid isPermaLink="false">2642503</guid>        </item>
        <item>
            <title>FGF-inducible 14-kDa protein (Fn14) is regulated via the RhoA/ROCK kinase pathway in cardiomyocytes and mediates nuclear factor-kappaB activation by TWEAK</title>
            <link>http://www.medworm.com/index.php?rid=2642504&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F1017845344n85447%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Proinflammatory cytokines, including TNF family members, have been shown to play a critical role in cardiac remodeling. FGF-inducible
 14-kDa protein (Fn14, TNFrsf12a or TWEAKR) is the smallest member of the TNF-receptor family. Currently, little is known about
 the functional role of Fn14 and its only known ligand TNF-like weak inducer of apoptosis (TWEAK) in the heart. We therefore
 evaluated the expression and regulation of Fn14 in cardiomyocytes and in experimental myocardial infarction. In order to study
 the regulation of Fn14, myocardial infarction was induced in CD-1 mice and neonatal rat cardiomyocytes were used for in vitro
 studies. TWEAK and Fn14 were markedly upregulated in the remodeling myocardium after experimental myocardial infarction in
 vivo. Likewis...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2642504</comments>
            <pubDate>Sat, 25 Jul 2009 04:08:51 +0100</pubDate>
            <guid isPermaLink="false">2642504</guid>        </item>
        <item>
            <title>Attenuation of myocardial injury by postconditioning: role of hypoxia inducible factor-1α</title>
            <link>http://www.medworm.com/index.php?rid=2603635&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fmt701162357n70v5%2F</link>
            <description>In conclusion, these data suggest that HIF-1α is involved
 in cardioprotection by PostC and pharmacological augmentation of HIF-1α expression that enhances the infarct-sparing effect
 of PostC; iNOS, the downstream gene of HIF-1α, may participate in signaling pathways in mediating PostC’s protection.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0044-0Authors
		Huan-Xin Zhao, Shanxi Medical University Department of Physiology 56 South Xinjian Road 030001 Taiyuan Shanxi People’s Republic of ChinaXiao-Liang Wang, Shanxi Medical University Department of Physiology 56 South Xinjian Road 030001 Taiyuan Shanxi People’s Republic of ChinaYe-Hong Wang, Shanxi Medical University Department of Physiology 56 South Xinjian Road 030001 Taiyuan Shanxi People...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2603635</comments>
            <pubDate>Tue, 14 Jul 2009 10:01:07 +0100</pubDate>
            <guid isPermaLink="false">2603635</guid>        </item>
        <item>
            <title>Angiotensin type 1 receptor mediates thyroid hormone-induced cardiomyocyte hypertrophy through the Akt/GSK-3β/mTOR signaling pathway</title>
            <link>http://www.medworm.com/index.php?rid=2592332&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fu835314825j53601%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Several studies have implicated the renin angiotensin system in the cardiac hypertrophy induced by thyroid hormone. However,
 whether Angiotensin type 1 receptor (AT1R) is critically required to the development of T3-induced cardiomyocyte hypertrophy as well as whether the intracellular mechanisms that are triggered by AT1R are able to contribute to this hypertrophy model is unknown. To address these questions, we employed a selective small interfering
 RNA (siRNA, 50&amp;nbsp;nM) or an AT1R blocker (Losartan, 1&amp;nbsp;μM) to evaluate the specific role of this receptor in primary cultures of neonatal cardiomyocytes submitted
 to T3 (10&amp;nbsp;nM) treatment. The cardiomyocytes transfected with the AT1R siRNA presented reduced mRNA (90%, P&amp;nbsp;&amp;lt;&amp;nbsp;0.001) and protein (70%,...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2592332</comments>
            <pubDate>Thu, 09 Jul 2009 12:45:07 +0100</pubDate>
            <guid isPermaLink="false">2592332</guid>        </item>
        <item>
            <title>Obesity induced-insulin resistance causes endothelial dysfunction without reducing the vascular response to hindlimb ischemia</title>
            <link>http://www.medworm.com/index.php?rid=2487413&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F642k36207424j284%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Impairment of vascular growth is a hallmark of diabetic complications, but the progression and mechanisms are poorly understood.
 To determine whether obesity and early diabetes impair endothelium-dependent vasodilatation and vascular response to ischemia,
 microvascular function as well as angiogenic responses to ischemia were assessed in young (C57) and 6-month-old lean mice
 (old C57), in obese (db-C57) mice, and in mice suffering an early (db-KsJ) and sustained type 2 diabetes (old db-KsJ). Glycemia gradually increased from the db-C57 to the old db-KsJ. Early and established type II diabetes significantly reduced the level of insulin that was significantly increased in
 obese mice. Endothelial function was assessed in isolated resistance arteries while the angiogeni...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2487413</comments>
            <pubDate>Tue, 23 Jun 2009 06:07:36 +0100</pubDate>
            <guid isPermaLink="false">2487413</guid>        </item>
        <item>
            <title>The eNOS enhancer AVE 9488: a novel cardioprotectant against ischemia reperfusion injury</title>
            <link>http://www.medworm.com/index.php?rid=2487412&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fe649715255vx5v22%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Nitric oxide (NO) is an important regulator of vascular and myocardial function. Cardiac ischemia/reperfusion injury is reduced
 in mice overexpressing endothelial NO synthase (eNOS) suggesting cardioprotection by eNOS. Novel pharmacological substances,
 so called eNOS enhancers, upregulate eNOS expression and thereby increase NO production. We tested the effects of the eNOS
 enhancer AVE 9488 on cardiac ischemia/reperfusion injury in vivo in mice. After treatment with the eNOS enhancer AVE 9488
 (30&amp;nbsp;mg/kg/day) or placebo for one week mice underwent 30&amp;nbsp;min of coronary artery ligation and 24&amp;nbsp;h of reperfusion in vivo.
 Ischemia-reperfusion damage was significantly reduced in mice treated with the eNOS enhancer when compared to placebo treated
 mice (infarct...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2487412</comments>
            <pubDate>Tue, 23 Jun 2009 06:07:36 +0100</pubDate>
            <guid isPermaLink="false">2487412</guid>        </item>
        <item>
            <title>Ischemic postconditioning: experimental models and protocol algorithms</title>
            <link>http://www.medworm.com/index.php?rid=2487414&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F7v01j667438451t6%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Ischemic postconditioning, a simple mechanical maneuver at the onset of reperfusion, reduces infarct size after ischemia/reperfusion.
 After its first description in 2003 by Zhao et al. numerous experimental studies have investigated this protective phenomenon.
 Whereas the underlying mechanisms and signal transduction are not yet understood in detail, infarct size reduction by ischemic
 postconditioning was confirmed in all species tested so far, including man. We have now reviewed the literature with focus
 on experimental models and protocols to better understand the determinants of protection by ischemic postconditioning or lack
 of it. Only studies with infarct size as unequivocal endpoint were considered. In all species and models, the duration of
 index ischemia ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2487414</comments>
            <pubDate>Fri, 19 Jun 2009 06:45:37 +0100</pubDate>
            <guid isPermaLink="false">2487414</guid>        </item>
        <item>
            <title>The cardiac troponin C mutation Leu29Gln found in a patient with hypertrophic cardiomyopathy does not alter contractile parameters in skinned murine myocardium</title>
            <link>http://www.medworm.com/index.php?rid=2470292&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fvv44q1uk32857800%2F</link>
            <description>In conclusion, no major differences in contractile parameters of preparations
 containing hcTnCL29Q compared to hcTnCWT were observed. Therefore, it appears unlikely that hcTnCL29Q induces the development of HCM by affecting the regulation of Ca2+-activated force and interference with PKA-mediated modulation of the Ca2+ sensitivity of contraction.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0038-yAuthors
		Axel Neulen, University of Cologne Institute of Vegetative Physiology Robert-Koch-Strasse 39 50931 Cologne GermanyRobert Stehle, University of Cologne Institute of Vegetative Physiology Robert-Koch-Strasse 39 50931 Cologne GermanyGabriele Pfitzer, University of Cologne Institute of Vegetative Physiology Robert-Koch-Strasse 39 50931 Cologne Germany
...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2470292</comments>
            <pubDate>Tue, 09 Jun 2009 13:06:11 +0100</pubDate>
            <guid isPermaLink="false">2470292</guid>        </item>
        <item>
            <title>Genetic engineering with endothelial nitric oxide synthase improves functional properties of endothelial progenitor cells from patients with coronary artery disease: an in vitro study</title>
            <link>http://www.medworm.com/index.php?rid=2448861&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm805037t2290w683%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Recent studies have reported a marked impairment in the number and functions of endothelial progenitor cells (EPCs) in patients
 with coronary artery disease (CAD). In view of an important role of eNOS in angiogenesis, in the present study, we evaluated
 the effects of eNOS gene transfer in ex vivo expanded EPCs isolated from patients with CAD. The expanded EPCs were transfected
 with mammalian expression vector pcDNA3.1-eNOS containing the full-length human eNOS gene using lipofectamine. About 35–40%
 of the eNOS–EPCs had higher expression of eNOS as compared to untransfected EPCs. EPCs transfected with pcDNA3.0-EGFP, the
 plasmid vector expressing green fluorescent protein (GFP) were used as control. The untransfected, GFP-transfected and eNOS-transfected
 EPCs we...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2448861</comments>
            <pubDate>Fri, 29 May 2009 08:23:19 +0100</pubDate>
            <guid isPermaLink="false">2448861</guid>        </item>
        <item>
            <title>Coronary microvascular resistance: methods for its quantification in humans</title>
            <link>http://www.medworm.com/index.php?rid=2437510&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F381g231187q46377%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Coronary microvascular dysfunction is a topic that has recently gained considerable interest in the medical community owing
 to the growing awareness that microvascular dysfunction occurs in a number of myocardial disease states and has important
 prognostic implications. With this growing awareness, comes the desire to accurately assess the functional capacity of the
 coronary microcirculation for diagnostic purposes as well as to monitor the effects of therapeutic interventions that are
 targeted at reversing the extent of coronary microvascular dysfunction. Measurements of coronary microvascular resistance
 play a pivotal role in achieving that goal and several invasive and noninvasive methods have been developed for its quantification.
 This review is intended to pr...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2437510</comments>
            <pubDate>Tue, 26 May 2009 07:36:01 +0100</pubDate>
            <guid isPermaLink="false">2437510</guid>        </item>
        <item>
            <title>The cannabinoid CB1 receptor antagonist, rimonabant, protects against acute myocardial infarction</title>
            <link>http://www.medworm.com/index.php?rid=2432760&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fq449374721g16542%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;CB1 antagonism is associated with reduced doxorubicin-induced cardiotoxicity and decreased cerebrocortical infarction. Rimonabant,
 a selective CB1 receptor antagonist, was, before it was withdrawn, proposed as a treatment for obesity and reported to reduce cardiovascular
 risk by improving glucose and lipid profiles and raising adiponectin levels. The cardioprotective actions of rimonabant in
 6-week-old C57BL/6J mice fed either high-fat (HFD) or standard diets (STD) for 8&amp;nbsp;weeks were investigated. At 14&amp;nbsp;weeks, mice
 received rimonabant (10&amp;nbsp;mg/kg/day, i.p.) or vehicle for 1&amp;nbsp;week and were then subjected to an in vivo acute myocardial infarction.
 The influence of rimonabant on infarct size (IS) in CB1 knockout (CB1−/−) and wild-type (CB1+/+) mice ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2432760</comments>
            <pubDate>Fri, 22 May 2009 05:47:18 +0100</pubDate>
            <guid isPermaLink="false">2432760</guid>        </item>
        <item>
            <title>Prevention of vasa vasorum neovascularization attenuates early neointima formation in experimental hypercholesterolemia</title>
            <link>http://www.medworm.com/index.php?rid=2429053&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F7403207623625x3l%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Vasa vasorum (VV) neovascularization is a key feature of early atherosclerosis and adds substantial endothelial exchange-surface
 to the coronary vessel wall. Thus, it is conceivable that VV neovascularization favors the entry of pro-inflammatory and pro-atherosclerotic
 blood components into the coronary vessel wall. We sought to investigate the effects of Thalidomide (Th), a potent anti-angiogenic
 drug on vasa vasorum (VV) neovascularization, vessel wall inflammation, and neointima formation in early experimental atherosclerosis.
 Female domestic swine, 3&amp;nbsp;months old, were fed normal (N, n&amp;nbsp;=&amp;nbsp;12) or high-cholesterol diet (HC, n&amp;nbsp;=&amp;nbsp;12) for 3&amp;nbsp;months. In each group six pigs were randomized to 200&amp;nbsp;mg Thalidomide daily for the diet period (...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2429053</comments>
            <pubDate>Thu, 21 May 2009 06:18:56 +0100</pubDate>
            <guid isPermaLink="false">2429053</guid>        </item>
        <item>
            <title>Cardiac dysfunction in an animal model of neonatal asphyxia is associated with increased degradation of MLC1 by MMP-2</title>
            <link>http://www.medworm.com/index.php?rid=2424900&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F906ut3264t662q37%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The purpose of this study was to determine if decreased heart function after hypoxia followed by reoxygenation (H–R) is associated
 with increased degradation of cardiac myosin light chain 1 (MLC1) by matrix metalloproteinase-2 (MMP-2), and to investigate
 the effects of the increased level of peroxynitrite in the hearts of H–R animals on MLC1 degradation by MMP-2. Total of 12
 newborn piglets were acutely instrumented to monitor cardiac function as assessed by stroke volume. Anesthetized piglets were
 block randomized to the normoxic group (n&amp;nbsp;=&amp;nbsp;6), which received ventilation with room air for 6&amp;nbsp;h, or to the H–R group (n&amp;nbsp;=&amp;nbsp;6), which received ventilation with 10–15% oxygen for 2&amp;nbsp;h, followed by reoxygenation with 100% oxygen for 1&amp;nbs...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2424900</comments>
            <pubDate>Tue, 19 May 2009 05:58:02 +0100</pubDate>
            <guid isPermaLink="false">2424900</guid>        </item>
        <item>
            <title>Intracoronary acid infusion as an alternative to ischemic postconditioning in pigs</title>
            <link>http://www.medworm.com/index.php?rid=2418099&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F5n766497g2262007%2F</link>
            <description>In conclusion, in pigs submitted to coronary occlusion, intracoronary acid infusion and postconditioning offered
 protection against cell death only after prolonged coronary occlusion. Both interventions were equally effective, but intracoronary
 acid infusion was associated with high risk of ventricular fibrillation. These results are strongly against translation of
 acidic reperfusion to patients with acute myocardial infarction.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0032-4Authors
		Antonio Rodríguez-Sinovas, Hospital Universitari Vall d’Hebron Laboratorio de Cardiología Experimental, Servicio de Cardiología Barcelona SpainAlberto Cabestrero, Hospital Universitari Vall d’Hebron Laboratorio de Cardiología Experimental, Servicio de Card...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2418099</comments>
            <pubDate>Fri, 15 May 2009 06:09:20 +0100</pubDate>
            <guid isPermaLink="false">2418099</guid>        </item>
        <item>
            <title>Macrophage depletion suppresses sympathetic hyperinnervation following myocardial infarction</title>
            <link>http://www.medworm.com/index.php?rid=2418100&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr6141387k202514j%2F</link>
            <description>The objective of the present study was to determine whether macrophages, which are known to synthesize NGF, are necessary
 for post-infarct cardiac sympathetic sprouting. Ovariectomized female rats received left coronary artery ligation or sham
 operation, followed by intravenous injection of liposomes containing saline vehicle or clodronate, which kills macrophages.
 Sham-operated myocardium contained some sympathetic axons, few myofibroblasts and T cells and no CD-68-positive macrophages.
 In rats receiving saline liposomes through 7&amp;nbsp;days post-ligation, the posterolateral infarct border contained numerous myofibroblasts,
 macrophages and T cells, and sympathetic innervation was increased twofold. Treatment with clodronate liposomes reduced macrophage
 numbers by 69%, while myofibrob...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2418100</comments>
            <pubDate>Wed, 13 May 2009 05:53:29 +0100</pubDate>
            <guid isPermaLink="false">2418100</guid>        </item>
        <item>
            <title>Transcription profiling of HCN-channel isotypes throughout mouse cardiac development</title>
            <link>http://www.medworm.com/index.php?rid=2399743&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj6nxm614m144867n%2F</link>
            <description>In conclusion, substantial changes of HCN isotype transcription throughout cardiac
 development suggest that a regulated pattern of HCN isotypes is required to establish and ensure a stable heart rhythm. Furthermore,
 constantly low HCN transcription in adult myocardium may be required to prevent atrial and ventricular arrhythmogenesis.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0031-5Authors
		Patrick A. Schweizer, Universitätsklinikum Heidelberg, Innere Medizin III Im Neuenheimer Feld 410 69120 Heidelberg GermanyPessah Yampolsky, Max-Planck-Institut für Medizinische Forschung, Abteilung Molekulare Neurobiologie Jahnstr. 29 69120 Heidelberg GermanyRizwan Malik, Max-Planck-Institut für Medizinische Forschung, Abteilung Molekulare Neurobiologie Ja...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2399743</comments>
            <pubDate>Thu, 07 May 2009 06:00:29 +0100</pubDate>
            <guid isPermaLink="false">2399743</guid>        </item>
        <item>
            <title>The role of transient outward K+ current in electrical remodelling induced by voluntary exercise in female rat hearts</title>
            <link>http://www.medworm.com/index.php?rid=2391251&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F12p1tuk8553610m9%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Regular exercise can lead to electrical remodelling of the heart. The cellular mechanisms associated with these changes are
 not well understood, and are difficult to study in human tissue but are important given that exercise is recommended to the
 general population. We have investigated the role played by the transient outward K+ current (I
 to) in the changes in electrical activity seen in response to voluntary exercise training in rats. Female rats undertook 6&amp;nbsp;weeks
 of voluntary wheel running exercise (TRN) or were sedentary controls (SED). Monophasic action potentials (MAPs) were recorded
 from the surface of whole hearts. Whole cell patch clamp recordings of I
 to; mRNA and protein levels of selected targets in sub-epicardial (EPI) and sub-endocardial myoca...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2391251</comments>
            <pubDate>Tue, 05 May 2009 06:12:14 +0100</pubDate>
            <guid isPermaLink="false">2391251</guid>        </item>
        <item>
            <title>Proliferation of neonatal cardiomyocytes by connexin43 knockdown via synergistic inactivation of p38 MAPK and increased expression of FGF1</title>
            <link>http://www.medworm.com/index.php?rid=2357782&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fn461829506812487%2F</link>
            <description>In this study, we examined whether and if so how the knockdown of a gap junction protein Cx43 with
 siRNA produced changes in the proliferative activity of neonatal cardiomyocytes. Cx43-knockdown resulted in a significant
 increase in the proliferation of cardiomyocytes. To clarify the mechanisms behind this increase, we investigated whether the
 activity of mitogen-activated protein kinases (MAPKs) changed on knockdown of Cx43. The knockdown decreased the expression
 of phosphorylated p38 (p-p38) MAPK. In addition, treatment of cardiomyocytes with a p38 MAPK inhibitor significantly increased the proliferative activity.
 Cultures were then co-treated with an inhibitor of p38 MAPK and fibroblast growth factor-1 (FGF1), since Cx43-knockdown significantly
 increased cytosolic FGF1 expression ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2357782</comments>
            <pubDate>Mon, 20 Apr 2009 22:38:05 +0100</pubDate>
            <guid isPermaLink="false">2357782</guid>        </item>
        <item>
            <title>Ischemic injury and the parathyroid hormone-related protein system: friend or foe?</title>
            <link>http://www.medworm.com/index.php?rid=2357784&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fe8073703864j66n1%2F</link>
            <description>Content Type Journal ArticleCategory EDITORIALDOI 10.1007/s00395-009-0784-xAuthors
		Klaus-Dieter Schlüter, Justus-Liebig Universität Physiologisches Institut Aulweg 129 35392 Gießen GermanyRolf Schreckenberg, Justus-Liebig Universität Physiologisches Institut Aulweg 129 35392 Gießen Germany
	

	
		Journal Basic Research in CardiologyOnline ISSN 1435-1803Print ISSN 0300-8428 (Source: Basic Research in Cardiology)</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2357784</comments>
            <pubDate>Mon, 20 Apr 2009 22:38:04 +0100</pubDate>
            <guid isPermaLink="false">2357784</guid>        </item>
        <item>
            <title>Role of extracellular signal-regulated kinase for endothelial progenitor cell dysfunction in coronary artery disease</title>
            <link>http://www.medworm.com/index.php?rid=2332045&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg362476647t0u67p%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In patients with coronary artery disease (CAD), number and function of endothelial progenitor cells (EPCs) are down-regulated.
 The relevant intracellular signalling mechanisms responsible for dysfunction of EPCs in CAD remain poorly characterized. Our
 goal was to examine the regulation of ERK-1/2 by SDF-1 and the role of ERK-1/2 for adhesion in EPCs. Western analysis revealed
 that the chemokine SDF-1 (SDF-1, 100 nM) mediates phosphorylation of ERK-2 after 90&amp;nbsp;s with a maximum after 180–300&amp;nbsp;s in EPCs
 isolated from healthy control subjects, while EPCs from patients with CAD are characterized by a temporally delayed and quantitatively
 markedly attenuated SDF-1-triggered ERK-2-phosphorylation. Functionally, EPCs isolated from patients with CAD display reduce...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2332045</comments>
            <pubDate>Sun, 12 Apr 2009 05:52:05 +0100</pubDate>
            <guid isPermaLink="false">2332045</guid>        </item>
        <item>
            <title>STAT-1 decoy oligodeoxynucleotide inhibition of acute rejection in mouse heart transplants</title>
            <link>http://www.medworm.com/index.php?rid=2332047&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm84621u344458809%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;During acute rejection of cardiac transplants endothelial cell–leukocyte interaction fuelled by co-stimulatory molecules like
 CD40/CD154 may ultimately lead to graft loss. One key player in up-regulating the expression of such pro-inflammatory gene
 products is the interferon-γ-dependent transcription factor STAT-1. Hence down-regulating interferon-γ-stimulated pro-inflammatory
 gene expression in the graft endothelial cells by employing a decoy oligodeoxynucleotide (dODN) neutralising STAT-1 may protect
 the graft. To verify this hypothesis, heterotopic mouse heart transplantation was performed in the allogeneic B10.A(2R) to
 C57BL/6 and syngeneic C57BL/6 to C57BL/6 strain combination without immunosuppression. Graft vessels were pre-treated with
 STAT-1 dODN, mut...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2332047</comments>
            <pubDate>Wed, 08 Apr 2009 08:04:55 +0100</pubDate>
            <guid isPermaLink="false">2332047</guid>        </item>
        <item>
            <title>Reference change values and determinants of variability of NT-proANP and GDF15 in stable chronic heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2332046&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw5755365q2617700%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Biovariability, reference change values (RCV), and index of individuality (IOI) have not been previously described for NT-proANP
 or GDF15. Also, the relation of changes of these markers to other clinical variables or biomarkers is unknown. In 41 patients
 with stable chronic systolic dysfunction, NT-proANP and GDF15 were measured alongside with clinical variables/markers comprising
 NT-proBNP, hsTnT, and hsCRP at four sampling intervals (2&amp;nbsp;weeks, 1-, 2-, 3-month intervals). At 2 weeks, 1-, 2-, and 3-month-follow-up,
 individual NT-proANP variations were 27.1, 22.5, 28.9, 15.6%, respectively, corresponding to RCVs of 53.2, 62.4, 80.2, and
 43.2%, respectively. For GDF15, the respective individual variations were 6.8, 4.1, 5.5, 6.8%, corresponding to RCVs of 18.8,
 ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2332046</comments>
            <pubDate>Wed, 08 Apr 2009 08:04:55 +0100</pubDate>
            <guid isPermaLink="false">2332046</guid>        </item>
        <item>
            <title>Myocardial inflammation and non-ischaemic heart failure: is there a role for C-reactive protein?</title>
            <link>http://www.medworm.com/index.php?rid=2305781&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F00t7wl865xk188h7%2F</link>
            <description>In this study
 we investigated distribution of CRP, the Terminal Complement Complex (C5b-9) and macrophages (CD68) in the myocardium of patients
 suffering from non-ischaemic heart failure and their implication on clinical parameters. Endomyocardial biopsies were taken
 from 66 patients suffering from dilated cardiomyopathy (DCM). Biopsies were analysed by immunohistochemical and immunofluorescent
 staining for CRP, C5b-9 and CD68. Viral DNA/RNA for adenovirus, enterovirus, parvovirus B19 and human herpes virus 6 was detected
 by PCR and Southern blot analysis. Myocardial biopsy findings were correlated with plasma level of hsCRP and NT-proBNP as
 well as echocardiography, exercise test and NYHA class. In 18 (27%) patients, a positive staining for CRP and in 57 (86%)
 patients a positive s...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2305781</comments>
            <pubDate>Fri, 03 Apr 2009 06:57:37 +0100</pubDate>
            <guid isPermaLink="false">2305781</guid>        </item>
        <item>
            <title>Bone marrow-derived cells are not involved in reendothelialized endothelium as endothelial cells after simple endothelial denudation in mice</title>
            <link>http://www.medworm.com/index.php?rid=2305782&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj28rv0263w20v156%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;It has been shown that bone marrow (BM)-derived cells are involved in repaired endothelium induced by a model such as neointima-produced
 wire injury in mice. This has not been shown in a less invasive model that results in simple reendothelialization. A new wire-induced
 simple endothelial denudation model of the common carotid artery (CCA) of mice, which did not form neointima at 14&amp;nbsp;days after
 the operation, was established. At 7&amp;nbsp;days after operation, the CCAs were reendothelialized from the aortic arch and the carotid
 bifurcation but not completely, shown by whole-mount CD31 immunohistochemical staining. Scanning electron microscopy revealed
 that unendothelialized area was covered with platelets. To determine the involvement of BM-derived cells in the re...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2305782</comments>
            <pubDate>Tue, 31 Mar 2009 05:49:21 +0100</pubDate>
            <guid isPermaLink="false">2305782</guid>        </item>
        <item>
            <title>The effects of autoantibodies against the second extracellular loop of α1-adrenoceptor on vasoconstriction</title>
            <link>http://www.medworm.com/index.php?rid=2305783&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl75241443753q61u%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Recent studies have demonstrated the presence of autoantibodies against α1-adrenoceptor (α1-AAB) in the serum of patients with primary hypertension, and that these autoantibodies exert adrenergic-agonist-like effects.
 However, their role in the development of hypertension remains unclear. The current study determined whether α1-AAB can cause vascular contraction, and further investigated the cellular receptors that mediate their vasoactivity. Enzyme-linked
 immunosorbent assay (ELISA) was used to detect α1-AAB in blood samples collected from 73 patients with primary hypertension and 86 normotensive patients. IgGs were purified
 from mixed sera from 25 α1-AAB-positive hypertensive patients and 20 α1-AAB-negative normotensives, respectively. The vasoconstrictive ef...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2305783</comments>
            <pubDate>Sun, 29 Mar 2009 05:51:10 +0100</pubDate>
            <guid isPermaLink="false">2305783</guid>        </item>
        <item>
            <title>Diastolic heart failure: a misNOmer</title>
            <link>http://www.medworm.com/index.php?rid=2305784&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb1rr0111766g9x57%2F</link>
            <description>Content Type Journal ArticleCategory EditorialDOI 10.1007/s00395-009-0025-3Authors
		Gerd Heusch, Universitätsklinikum Essen Direktor des Instituts für Pathophysiologie Hufelandstraße 55 45122 Essen Germany
	

	
		Journal Basic Research in CardiologyOnline ISSN 1435-1803Print ISSN 0300-8428 (Source: Basic Research in Cardiology)</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2305784</comments>
            <pubDate>Sun, 29 Mar 2009 05:51:09 +0100</pubDate>
            <guid isPermaLink="false">2305784</guid>        </item>
        <item>
            <title>The metabolic modulators, Etomoxir and NVP-LAB121, fail to reverse pressure overload induced heart failure in vivo</title>
            <link>http://www.medworm.com/index.php?rid=2276391&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F4476844tkx054222%2F</link>
            <description>In conclusion, pharmacologic induction of substrate-switching is associated with changes in myofibrillar
 isoform expression but does not reverse heart failure in vivo. The improvement of function in vitro deserves further investigation.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0015-5Authors
		Michael Schwarzer, University of Leipzig Heart Center Department of Cardiac Surgery Struempellstr. 39 04289 Leipzig GermanyGloria Faerber, University of Leipzig Heart Center Department of Cardiac Surgery Struempellstr. 39 04289 Leipzig GermanyTilmann Rueckauer, University of Freiburg Department of Cardiovascular Surgery Freiburg GermanyDaniel Blum, University of Leipzig Heart Center Department of Cardiac Surgery Struempellstr. 39 04289 Leipzig GermanyGracjan...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2276391</comments>
            <pubDate>Wed, 18 Mar 2009 07:07:19 +0100</pubDate>
            <guid isPermaLink="false">2276391</guid>        </item>
        <item>
            <title>Regional, age-dependent, and genotype-dependent differences in ventricular action potential duration and activation time in 410 Langendorff-perfused mouse hearts</title>
            <link>http://www.medworm.com/index.php?rid=2276392&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fuv684703557u42v0%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Although numerous studies have reported the effects of genetic alterations on murine electrophysiology, the range of normal
 values for ventricular activation, repolarization, and arrhythmias in mouse hearts is not known. We analyzed right ventricular
 (RV), left ventricular (LV), and septal activation times, monophasic action potential durations (APD), and right ventricular
 effective refractory periods during spontaneous rhythm, induced AV nodal block, right ventricular pacing (100–300&amp;nbsp;ms paced
 cycle length), and programmed stimulation in 410 beating, Langendorff-perfused, wild-type mouse hearts of CD1, DBAC3H, FVBN,
 C57/Bl6, and hybrid backgrounds (age 203&amp;nbsp;±&amp;nbsp;132&amp;nbsp;days). Action potential duration was longer at longer cycle lengths. LV-APD
 prol...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2276392</comments>
            <pubDate>Sat, 14 Mar 2009 13:35:39 +0100</pubDate>
            <guid isPermaLink="false">2276392</guid>        </item>
        <item>
            <title>Effect of insulin and glucose infusion on myocardial infarction size in uraemic rats</title>
            <link>http://www.medworm.com/index.php?rid=2276394&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb75x67p657625762%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The post myocardial infarction (MI) mortality rate is high in renal patients. One possible explanation is the reduced ischemia
 tolerance caused by uraemia. Previous investigations showed larger MI size in uraemic rats when compared with sham-operated
 controls. To explore a possible link between uraemic insulin resistance syndrome and MI size in uraemia, we studied an intervention
 model with administration of insulin and glucose during acute MI in subtotally nephrectomized (SNX) rats and sham-operated
 controls. In 16 SNX rats and 16 sham-operated controls, the left coronary artery was ligated for 60&amp;nbsp;min, followed by reperfusion
 for 90&amp;nbsp;min. To visualize the perfused myocardium, lissamine-green ink was injected. The nonperfused area (lissamine exclusion)
 an...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2276394</comments>
            <pubDate>Sat, 14 Mar 2009 13:35:38 +0100</pubDate>
            <guid isPermaLink="false">2276394</guid>        </item>
        <item>
            <title>Time course and mechanisms of left ventricular systolic and diastolic dysfunction in monocrotaline-induced pulmonary hypertension</title>
            <link>http://www.medworm.com/index.php?rid=2276393&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fkl771w3767h430pt%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Although pulmonary hypertension (PH) selectively overloads the right ventricle (RV), neuroendocrine activation and intrinsic
 myocardial dysfunction have been described in the left ventricle (LV). In order to establish the timing of LV dysfunction
 development in PH and to clarify underlying molecular changes, Wistar rats were studied 4 and 6&amp;nbsp;weeks after subcutaneous injection
 of monocrotaline (MCT) 60&amp;nbsp;mg/kg (MCT-4, n&amp;nbsp;=&amp;nbsp;11; MCT-6, n&amp;nbsp;=&amp;nbsp;11) or vehicle (Ctrl-4, n&amp;nbsp;=&amp;nbsp;11; Ctrl-6, n&amp;nbsp;=&amp;nbsp;11). Acute single beat stepwise increases of systolic pressure were performed from baseline to isovolumetric (LVPiso).
 This hemodynamic stress was used to detect early changes in LV performance. Neurohumoral activation was evaluated by measuring...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2276393</comments>
            <pubDate>Sat, 14 Mar 2009 13:35:38 +0100</pubDate>
            <guid isPermaLink="false">2276393</guid>        </item>
        <item>
            <title>The regulation and control of mitochondrial homeostasis in changing cardiac tolerance to ischemia-reperfusion injury: a focused issue</title>
            <link>http://www.medworm.com/index.php?rid=2239173&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fd48137w77t7620w6%2F</link>
            <description>Content Type Journal ArticleCategory EditorialDOI 10.1007/s00395-009-0005-7Authors
		Michael N. Sack, National Institutes of Health National Heart, Lung and Blood Institute Bethesda MD USAElizabeth Murphy, National Institutes of Health National Heart, Lung and Blood Institute Bethesda MD USARainer Schulz, Universitätsklinikum Essen Institut für Pathophysiologie Essen Germany
	

	
		Journal Basic Research in CardiologyOnline ISSN 1435-1803Print ISSN 0300-8428 (Source: Basic Research in Cardiology)</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2239173</comments>
            <pubDate>Wed, 04 Mar 2009 09:16:26 +0100</pubDate>
            <guid isPermaLink="false">2239173</guid>        </item>
        <item>
            <title>Enhancement of the endothelial NO synthase attenuates experimental diastolic heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2239174&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff21u28224247rgrx%2F</link>
            <description>Abstract
 Background&amp;nbsp;&amp;nbsp;Diastolic heart failure is a rising problem with a high incidence and similar mortality and morbidity compared to patients
 with systolic heart failure. Nevertheless, the underlying pathophysiology is still debated.
 
 
 
 Aim&amp;nbsp;&amp;nbsp;We investigated the effect of pharmacological enhancement of endothelial nitric oxide synthase (eNOS) on experimental diastolic
 heart failure (DHF).
 
 
 
 Methods&amp;nbsp;&amp;nbsp;DHF was induced in 60 DAHL salt-sensitive rats by salt diet in 8-week-old animals. 30 were treated with the eNOS enhancer
 AVE3085 (DHFeNOS) and 30 with placebo (DHF). Rats with normal salt intake served as controls.
 
 
 
 Results and conclusion&amp;nbsp;&amp;nbsp;Diastolic dysfunction with increased diastolic stiffness constant and increased left ventricular...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2239174</comments>
            <pubDate>Tue, 03 Mar 2009 13:28:17 +0100</pubDate>
            <guid isPermaLink="false">2239174</guid>        </item>
        <item>
            <title>Ischemia-reperfusion injury activates early extracellular matrix processing and expression of endostatin in the heart with differential effects of temperature</title>
            <link>http://www.medworm.com/index.php?rid=2239175&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fe9w8354671u1067l%2F</link>
            <description>In conclusion, this blinded study first demonstrated
 that processing of extracellular matrix started early after ischemia-reperfusion and depends on temperature conditions. These
 findings may contribute to a broader understanding of matrix processing after ischemia-reperfusion.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0013-7Authors
		Alexander Lauten, Friedrich-Schiller University Department of Internal Medicine I (Cardiology, Angiology, Pneumology) Erlanger Allee 101 07740 Jena GermanyEwa Majos, University Hospital Cologne Department of Cardiothoracic Surgery Kerpener Str. 62 50937 Cologne GermanyAndre Mühlich, University Hospital Cologne Department of Cardiothoracic Surgery Kerpener Str. 62 50937 Cologne GermanyThorsten Wahlers, University Ho...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2239175</comments>
            <pubDate>Tue, 03 Mar 2009 13:28:16 +0100</pubDate>
            <guid isPermaLink="false">2239175</guid>        </item>
        <item>
            <title>The cardiac sodium channel displays differential distribution in the conduction system and transmural heterogeneity in the murine ventricular myocardium</title>
            <link>http://www.medworm.com/index.php?rid=2239176&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F647q416483277512%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Cardiac sodium channels are responsible for conduction in the normal and diseased heart. We aimed to investigate regional
 and transmural distribution of sodium channel expression and function in the myocardium. Sodium channel Scn5a mRNA and Nav1.5 protein distribution was investigated in adult and embryonic mouse heart through immunohistochemistry and in situ hybridization.
 Functional sodium channel availability in subepicardial and subendocardial myocytes was assessed using patch-clamp technique.
 Adult and embryonic (ED14.5) mouse heart sections showed low expression of Nav1.5 in the HCN4-positive sinoatrial and atrioventricular nodes. In contrast, high expression levels of Nav1.5 were observed in the HCN4-positive and Cx43-negative AV or His bundle, bundle branches...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2239176</comments>
            <pubDate>Tue, 03 Mar 2009 13:28:15 +0100</pubDate>
            <guid isPermaLink="false">2239176</guid>        </item>
        <item>
            <title>The mitochondrial permeability transition pore as a target for preconditioning and postconditioning</title>
            <link>http://www.medworm.com/index.php?rid=2221581&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F5326m0566t6310x5%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The experimental evidence supporting the mitochondrial permeability transition pore (mPTP) as a major mediator of lethal myocardial
 reperfusion injury and therefore a critical target for cardioprotection is persuasive. Although, its molecular identity eludes
 investigators, it is generally accepted that mitochondrial cyclophilin-D, the target for the inhibitory effects of cyclosporine-A
 on the mPTP, is a regulatory component of the mPTP. Animal myocardial infarction studies and a recent clinical proof-of-concept
 study have demonstrated that pharmacologically inhibiting its opening at the onset of myocardial reperfusion reduces myocardial
 infarct size in the region of 30–50%. Interestingly, the inhibition of mPTP opening at this time appears to underpin the infarct...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221581</comments>
            <pubDate>Thu, 26 Feb 2009 12:22:11 +0100</pubDate>
            <guid isPermaLink="false">2221581</guid>        </item>
        <item>
            <title>Nitrite mediates cytoprotection after ischemia/reperfusion by modulating mitochondrial function</title>
            <link>http://www.medworm.com/index.php?rid=2221583&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc8824q847470566w%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Nitrite, once thought to be an inert biomarker of NO formation, is now recognized as an endocrine storage pool of bioactive
 NO. While nitrite mediates a number of hypoxic responses, one of its most robust effects is its ability to confer cytoprotection
 after ischemia/reperfusion in a number of organs and models. The mechanism of this cytoprotection appears to be mediated at
 the level of the mitochondrion. Here we review the studies demonstrating that nitrite is cytoprotective in the heart and describe
 the mechanism of this cytoprotection, which involves the post-translational modification of complex I leading to the modulation
 of mitochondrial reactive oxygen species generation at reperfusion. The mechanism of nitrite-dependent cytoprotection will
 be compared to o...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221583</comments>
            <pubDate>Thu, 26 Feb 2009 12:22:10 +0100</pubDate>
            <guid isPermaLink="false">2221583</guid>        </item>
        <item>
            <title>Cardioprotection requires taking out the trash</title>
            <link>http://www.medworm.com/index.php?rid=2221582&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv05346047555x523%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Autophagy is a critical cellular housekeeping process that is essential for removal of damaged or unwanted organelles and
 protein aggregates. Under conditions of starvation, it is also a mechanism to break down proteins to generate amino acids
 for synthesis of new and more urgently needed proteins. In the heart, autophagy is upregulated by starvation, reactive oxygen
 species, hypoxia, exercise, and ischemic preconditioning, the latter a well-known potent cardioprotective phenomenon. The
 observation that upregulation of autophagy confers protection against ischemia/reperfusion injury and inhibition of autophagy
 is associated with a loss of cardioprotection conferred by pharmacological conditioning suggests that the pathway plays a
 key role in enhancing the heart’...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221582</comments>
            <pubDate>Thu, 26 Feb 2009 12:22:10 +0100</pubDate>
            <guid isPermaLink="false">2221582</guid>        </item>
        <item>
            <title>Cardioprotection and altered mitochondrial adenine nucleotide transport</title>
            <link>http://www.medworm.com/index.php?rid=2221584&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fu758843072l4nr3r%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;It is becoming increasingly clear that mitochondrial dysfunction is critically important in myocardial ischemic injury, and
 that cardioprotective mechanisms must ultimately prevent or attenuate mitochondrial damage. Mitochondria are also essential
 for energy production, and therefore prevention of mitochondrial injury must not compromise oxidative phosphorylation during
 reperfusion. This review will focus on one mitochondrial mechanism of cardioprotection involving inhibition of adenine nucleotide
 transport across the outer mitochondria membrane under de-energized conditions. This slows ATP hydrolysis by the mitochondria,
 and would be expected to lower mitochondrial membrane potential during ischemia, to inhibit calcium uptake during ischemia,
 and potentially to r...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221584</comments>
            <pubDate>Thu, 26 Feb 2009 12:22:08 +0100</pubDate>
            <guid isPermaLink="false">2221584</guid>        </item>
        <item>
            <title>The complex II inhibitor atpenin A5 protects against cardiac ischemia-reperfusion injury via activation of mitochondrial KATP channels</title>
            <link>http://www.medworm.com/index.php?rid=2221585&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ftg7j13873518h7v8%2F</link>
            <description>In conclusion, the specific complex II inhibitor AA5 is the most potent mKATP activator discovered to date, and provides a novel method of activating mKATP channels and protecting the heart from IR injury.
 
	Content Type Journal ArticleCategory Original ContributionDOI 10.1007/s00395-009-0001-yAuthors
		Andrew P. Wojtovich, University of Rochester Medical Center Department of Pharmacology and Physiology Rochester NY USAPaul S. Brookes, University of Rochester Medical Center Department of Anesthesiology Box 604 601 Elmwood Avenue Rochester NY 14642 USA
	

	
		Journal Basic Research in CardiologyOnline ISSN 1435-1803Print ISSN 0300-8428 (Source: Basic Research in Cardiology)</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221585</comments>
            <pubDate>Thu, 26 Feb 2009 12:22:06 +0100</pubDate>
            <guid isPermaLink="false">2221585</guid>        </item>
        <item>
            <title>Autophagy is required for preconditioning by the adenosine A1 receptor-selective agonist CCPA</title>
            <link>http://www.medworm.com/index.php?rid=2221586&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F23851klt501h5701%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;We have shown that the cellular process of macroautophagy plays a protective role in HL-1 cardiomyocytes subjected to simulated
 ischemia/reperfusion (sI/R) (Hamacher-Brady et al. in J Biol Chem 281(40):29776–29787). Since the nucleoside adenosine has
 been shown to mimic both early and late phase ischemic preconditioning, a potent cardioprotective phenomenon, the purpose
 of this study was to determine the effect of adenosine on autophagosome formation. Autophagy is a highly regulated intracellular
 degradation process by which cells remove cytosolic long-lived proteins and damaged organelles, and can be monitored by imaging
 the incorporation of microtubule-associated light chain 3 (LC3) fused to a fluorescent protein (GFP or mCherry) into nascent
 autophagosomes. W...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221586</comments>
            <pubDate>Thu, 26 Feb 2009 12:22:05 +0100</pubDate>
            <guid isPermaLink="false">2221586</guid>        </item>
        <item>
            <title>The mitochondrial permeability transition pore and ischemia-reperfusion injury</title>
            <link>http://www.medworm.com/index.php?rid=2221588&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F161870l5756442p2%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Mitochondrial dysfunction is an underlying cause of ischemia-reperfusion injury. In particular, ischemic injury induces dramatic
 increases in mitochondrial permeability, thereby instigating a chain of events that leads to both apoptotic and necrotic cardiomyocyte
 death. The mitochondrial permeability transition (MPT) pore, a large, non-specific channel that spans the inner mitochondrial
 membrane, is known to mediate the lethal permeability changes that initiate mitochondrial-driven cardiomyocyte death. The
 purpose of this review is to focus on the role of the MPT pore in ischemia-reperfusion injury, the mechanisms involved, and,
 in particular, what we do and do not know regarding the pore’s molecular composition.
 
	Content Type Journal ArticleCategory ReviewDOI ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221588</comments>
            <pubDate>Thu, 26 Feb 2009 12:22:04 +0100</pubDate>
            <guid isPermaLink="false">2221588</guid>        </item>
        <item>
            <title>Targeting malonyl CoA inhibition of mitochondrial fatty acid uptake as an approach to treat cardiac ischemia/reperfusion</title>
            <link>http://www.medworm.com/index.php?rid=2221587&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F1u10137764022r31%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Cardiovascular disease is the major cause of death and disability in the world, with ischemic heart disease accounting for
 the vast majority of this health problem. Current treatments for ischemic heart disease are primarily aimed at either increasing
 blood and oxygen supply to the heart or decreasing the heart’s oxygen demand. A novel treatment strategy involves increasing
 the efficiency of oxygen use by the heart. During and following ischemia, the heart can become inefficient in using oxygen,
 due in part to an excessive use of fatty acids as a source of fuel. One potential strategy to increase cardiac efficiency
 is to inhibit this use of fatty acid oxidation as a fuel source, while stimulating the use of glucose oxidation as a fuel
 source, which allows the he...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221587</comments>
            <pubDate>Thu, 26 Feb 2009 12:22:04 +0100</pubDate>
            <guid isPermaLink="false">2221587</guid>        </item>
        <item>
            <title>Mitochondrial pathways for ROS formation and myocardial injury: the relevance of p66Shc and monoamine oxidase</title>
            <link>http://www.medworm.com/index.php?rid=2221589&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg707322l8105v47x%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Although mitochondria are considered the most relevant site for the formation of reactive oxygen species (ROS) in cardiac
 myocytes, a major and unsolved issue is where ROS are generated in mitochondria. Respiratory chain is generally indicated
 as a main site for ROS formation. However, other mitochondrial components are likely to contribute to ROS generation. Recent
 reports highlight the relevance of monoamine oxidases (MAO) and p66Shc. The importance of these systems in the irreversibility of ischemic heart injury will be discussed along with the cardioprotective
 effects elicited by both MAO inhibition and p66Shc knockout. Finally, recent evidence will be reviewed that highlight the relevance of mitochondrial ROS formation also in myocardial
 failure and atheroscle...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221589</comments>
            <pubDate>Thu, 26 Feb 2009 12:22:03 +0100</pubDate>
            <guid isPermaLink="false">2221589</guid>        </item>
        <item>
            <title>Presence of connexin 43 in subsarcolemmal, but not in interfibrillar cardiomyocyte mitochondria</title>
            <link>http://www.medworm.com/index.php?rid=2221590&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F810656v447l8rvt1%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Cardiomyocytes contain subsarcolemmal (SSM) and interfibrillar (IFM) mitochondria, which differ in their respiratory and calcium
 retention capacity. Connexin 43 (Cx43) is located at the inner membrane of SSM, and Cx43 is involved in the cardioprotection
 by ischemic preconditioning (IP). The function of Cx43-formed channels is regulated in part by phosphorylation at residues
 in the carboxy terminus of Cx43. The aim of the present study was (1) to investigate whether Cx43 is also present in IFM,
 and (2) to characterize its spatial orientation in the inner mitochondrial membrane (IMM). Confirming previous findings, ADP-stimulated
 respiration was greater in IFM than in SSM from rat ventricles. In preparations from rats and mice not contaminated with sarcolemmal
 protei...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221590</comments>
            <pubDate>Thu, 26 Feb 2009 12:22:02 +0100</pubDate>
            <guid isPermaLink="false">2221590</guid>        </item>
        <item>
            <title>Inadvertent phosphorylation of survival kinases in isolated perfused hearts: a word of caution</title>
            <link>http://www.medworm.com/index.php?rid=2172143&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F7820l164k77v2267%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The isolated perfused heart is an important model in cardiovascular research. We hypothesized that the perfusion procedure
 per se will phosphorylate some protein kinases important in pre- and postconditioning. Isolated hearts were Langendorff-perfused
 for 20&amp;nbsp;min with or without an intraventricular balloon (rats and mice), or in the working heart mode (mice) and compared to
 non-perfused controls with respect to protein phosphorylation. Rat hearts were also perfused for 20 and 50&amp;nbsp;min in the Langendorff
 mode to investigate the effect of perfusion time on phosphorylation. Western blot analysis showed that perfusion per se induced
 a massive phosphorylation of ERK 1/2, P38-MAPK, JNK, AMPK, but decreased phosphorylation of AKT in the isolated rat and mouse
 hear...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2172143</comments>
            <pubDate>Sat, 07 Feb 2009 13:32:00 +0100</pubDate>
            <guid isPermaLink="false">2172143</guid>        </item>
        <item>
            <title>Ischemic injury activates PTHrP and PTH1R expression in human ventricular cardiomyocytes</title>
            <link>http://www.medworm.com/index.php?rid=2163102&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F4554um75810714j6%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The PTHrP/PTH1R signalling system induces calciotropic and myorelaxant effects on the vascular system and plays critical roles
 in the development of the cardiovascular system. In animal models, PTHrP exerts important effects on heart rate and contractility,
 particularly under ischemic conditions, while, in human hearts, the expression of PTHrP by cardiomyocytes remains to be defined
 in both normal and ischemic conditions. The present study has been conducted on 101 autoptical cases and confirmed on nine
 explanted hearts in order to analyze the expression of the PTHrP/PTH1R system by ventricular myocardium in respect to morphological
 aspects of the myocardial ischemic damage, myofiber hypertrophy and disarray, coronarosclerosis, age and sex. Immunohistochemistry
 sh...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2163102</comments>
            <pubDate>Wed, 04 Feb 2009 10:45:29 +0100</pubDate>
            <guid isPermaLink="false">2163102</guid>        </item>
        <item>
            <title>Effects of the NO donor sodium nitroprusside on oxygen consumption and energetics in rabbit myocardium</title>
            <link>http://www.medworm.com/index.php?rid=2163104&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fbq3196367033p788%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Nitric oxide (NO) has influence on various cellular functions. Little is known of the influence of NO on myocardial energetics.
 In the present study oxygen consumption and mechanical parameters of isometrically contracting rabbit papillary muscles (1&amp;nbsp;Hz
 stimulation frequency) were investigated at varying interventions while maintaining physiological conditions (37°C; 2.5&amp;nbsp;mM
 Ca2+) to study the effects of NO on energetics. The NO donor sodium nitroprusside (SNP) showed a negative inotropic effect. SNP
 decreased the maximal force in normal rabbit muscle strips by 30%, the force time integral (FTI) by 40% and the relaxation
 time by 20%. In addition the oxygen consumption decreased by 60%, a notably disproportional decrease compared to the mechanical
 paramet...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2163104</comments>
            <pubDate>Wed, 04 Feb 2009 10:45:26 +0100</pubDate>
            <guid isPermaLink="false">2163104</guid>        </item>
        <item>
            <title>Impact of myocardial inflammation on cytosolic and mitochondrial creatine kinase activity and expression</title>
            <link>http://www.medworm.com/index.php?rid=2163103&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F3773785j6844q601%2F</link>
            <description>We examined the myocardial creatine kinase (CK) system, which connects mitochondrial ATP-producing and cytosolic ATP-consuming
 processes and is thus of central importance to the cellular energy homeostasis. The time course of expression and enzymatic
 activity of mitochondrial (mtCK) and cytosolic CK (cytCK) was investigated in Coxsackievirus B3 (CVB3)-infected SWR mice,
 which are susceptible to the development of chronic myocarditis. In addition, cytCK activity and isoform expression were analyzed
 in biopsies from patients with chronic inflammatory heart disease (n&amp;nbsp;=&amp;nbsp;22). Cardiac CVB3 titer in CVB3-infected mice reached its maximum at 4&amp;nbsp;days post-infection (pi) and became undetectable
 at 28&amp;nbsp;days pi; cardiac inflammation cumulated 14&amp;nbsp;days pi but persisted throu...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2163103</comments>
            <pubDate>Wed, 04 Feb 2009 10:45:26 +0100</pubDate>
            <guid isPermaLink="false">2163103</guid>        </item>
        <item>
            <title>Changes in cellular contractility and cytokines profile during 
 Trypanosoma cruzi
 infection in mice</title>
            <link>http://www.medworm.com/index.php?rid=2163105&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F2l45760r52507358%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;
 Trypanosoma cruzi, an intracellular protozoan parasite infecting a wide variety of vertebrates, is the agent responsible for Chagas’ disease.
 This pathology often results in severe inflammatory heart condition and it is one of the major causes of dilated cardiomyopathy
 leading to heart failure in Latin America. Nevertheless, little is known about the changes in isolate cardiac myocytes contractility
 during the development of this pathology. Here we report a relationship between cytokines profile of mice infected with T. cruzi and the modifications in the cellular contractility pattern. We found that cellular contractility, measured as fractional
 shortening, showed a complex behavior. The changes were evaluated during the acute phase (15, 30 and 45&amp;nbsp;dpi) and ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2163105</comments>
            <pubDate>Wed, 04 Feb 2009 10:45:25 +0100</pubDate>
            <guid isPermaLink="false">2163105</guid>        </item>
        <item>
            <title>Vascular control in humans: focus on the coronary microcirculation</title>
            <link>http://www.medworm.com/index.php?rid=2163106&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F92648g310663p371%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Myocardial perfusion is regulated by a variety of factors that influence arteriolar vasomotor tone. An understanding of the
 physiological and pathophysiological factors that modulate coronary blood flow provides the basis for the judicious use of
 medications for the treatment of patients with coronary artery disease. Vasomotor properties of the coronary circulation vary
 among species. This review highlights the results of recent studies that examine the mechanisms by which the human coronary
 microcirculation is regulated in normal and disease states, focusing on diabetes. Multiple pathways responsible for myogenic
 constriction and flow-mediated dilation in human coronary arterioles are addressed. The important role of endothelium-derived
 hyperpolarizing factors, t...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2163106</comments>
            <pubDate>Wed, 04 Feb 2009 10:45:22 +0100</pubDate>
            <guid isPermaLink="false">2163106</guid>        </item>
        <item>
            <title>Regulation of platelet glycoprotein VI (GPVI) surface expression and of soluble GPVI in patients with atrial fibrillation (AF) and acute coronary syndrome (ACS)</title>
            <link>http://www.medworm.com/index.php?rid=2163107&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg274m12vx404t612%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;Platelet GPVI surface expression is decreased in patients with AF and ACS compared to patients with SR and ACS. Nonvalvular
 AF is related to indices of chronic platelet activation and might be responsible for a down-regulation of GPVI receptor density
 on platelets, while soluble GPVI was increased in ACS and AF accordingly.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-009-0779-7Authors
		Boris Bigalke, Eberhard-Karls-Universität Tübingen Medizinische Klinik III, Klinik für Kardiologie und Kreislauferkrankungen Otfried-Müller-Straße 10 72076 Tübingen GermanyKonstantinos Stellos, Eberhard-Karls-Universität Tübingen Medizinische Klinik III, Klinik für Kardiologie und Kreislauferkrankungen Otfried-Müller-Straße 10 72076 ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2163107</comments>
            <pubDate>Wed, 04 Feb 2009 10:45:18 +0100</pubDate>
            <guid isPermaLink="false">2163107</guid>        </item>
        <item>
            <title>Role of the Innate Immune System in Acute Viral Myocarditis</title>
            <link>http://www.medworm.com/index.php?rid=2128334&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F91x27l8k313r4536%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Although the adaptive immune system is thought to play an important role in the pathogenesis of viral myocarditis, the role
 of the innate immune system has not been well defined. To address this deficiency, we employed a unique line of mice that
 harbor a genomic “knock in” of a mutated TNF gene lacking the AU rich element (TNFARE/ARE) that is critical for TNF mRNA stability and translation, in order to examine the contribution of the innate immune system
 in encephalomyocarditis-induced myocarditis (EMCV). Heterozygous mice (TNFARE/+) were infected with 500 plaque-forming units of EMCV. TNFARE/+mice had a significantly higher 14-day mortality and myocardial inflammation when compared to littermate control mice. Virologic
 studies showed that the viral load at 14&amp;n...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2128334</comments>
            <pubDate>Thu, 22 Jan 2009 08:51:18 +0100</pubDate>
            <guid isPermaLink="false">2128334</guid>        </item>
        <item>
            <title>The angiotensin–calcineurin–NFAT pathway mediates stretch-induced up-regulation of matrix metalloproteinases-2/-9 in atrial myocytes</title>
            <link>http://www.medworm.com/index.php?rid=2111990&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F425528331643pxx1%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;Our results present new insights in molecular mechanisms of ECM remodeling activity of atrial myocytes exposed to static stretch.
 The AT1-Cn-NFAT pathway is a potential mediator of MMP activation.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0772-6Authors
		Erol Saygili, University Hospital Rheinisch Westfälische Technische Hochschule Aachen Dept. of Cardiology, Medical Clinic I Pauwelsstraße 30 52074 Aachen GermanyObaida R. Rana, University Hospital Rheinisch Westfälische Technische Hochschule Aachen Dept. of Cardiology, Medical Clinic I Pauwelsstraße 30 52074 Aachen GermanyChristian Meyer, University Hospital Rheinisch Westfälische Technische Hochschule Aachen Dept. of Cardiology, Medical Clinic I Pauwelsstraße 30 52...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2111990</comments>
            <pubDate>Fri, 16 Jan 2009 12:52:12 +0100</pubDate>
            <guid isPermaLink="false">2111990</guid>        </item>
        <item>
            <title>The S1P2 receptor expressed in human platelets is linked to the RhoA-Rho kinase pathway and is down regulated in type 2 diabetes</title>
            <link>http://www.medworm.com/index.php?rid=2104049&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fe81k230852j52r13%2F</link>
            <description>This study was undertaken to examine S1P receptor expression in human platelets
 as well as potential changes associated with type 2 diabetes. S1P2 receptor expression (Western blotting) was detected in washed human platelets from healthy volunteers. Stimulation of these
 platelets with exogenous S1P led to a concentration-dependent increase in intracellular Ca2+ as well as to platelet aggregation. The S1P-induced increase in Ca2+ was sensitive to the S1P2 receptor antagonist JTE-013 but not the S1P1/3 antagonist VPC23019. Both antagonists reduced the aggregation stimulated by S1P in a non-additive manner. S1P also elicited
 the translocation of RhoA to the membrane and RhoA activity was inhibited (by 50%) by the S1P receptor antagonists. Platelets
 from patients with type 2 diabetes demon...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2104049</comments>
            <pubDate>Tue, 13 Jan 2009 08:14:29 +0100</pubDate>
            <guid isPermaLink="false">2104049</guid>        </item>
        <item>
            <title>The effect of enhanced gap junctional conductance on ventricular conduction in explanted hearts from patients with heart failure</title>
            <link>http://www.medworm.com/index.php?rid=2104050&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw613q0n761587470%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;Rotigaptide applied to hearts of patients with end-stage HF shortened RPs normalized conduction curves and increased conduction
 parallel to fiber direction. However, in 50% of the hearts local slowing of conduction with destabilization of conduction
 (curves) occurs at sites close to the stimulation site, when activation is perpendicular to fiber direction.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0771-7Authors
		Rob F. Wiegerinck, Center for Heart Failure Research, Academic Medical Center Rm K2-112 Experimental Cardiology Group (ECG), Dept. of Experimental Cardiology Meibergdreef 9 1105 AZ Amsterdam The NetherlandsJacques M. T. de Bakker, Center for Heart Failure Research, Academic Medical Center Rm K2-112 Experimental ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2104050</comments>
            <pubDate>Tue, 13 Jan 2009 08:14:25 +0100</pubDate>
            <guid isPermaLink="false">2104050</guid>        </item>
        <item>
            <title>Beta2-integrin activation on T cell subsets is an independent prognostic factor in unstable angina pectoris</title>
            <link>http://www.medworm.com/index.php?rid=2104051&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl0t1280404q27237%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;Quantitative assessment of T cell beta2-integrin activation allows to identify high risk patients with UA and sC without established
 MI; furthermore, it is associated with incidence of future cardiovascular events independent of conventional risk factors
 (troponin, hsCRP).
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0770-8Authors
		Mathias H. Konstandin, Ruprecht-Karls-University Dept. of Cardiology Im Neuenheimer Feld 410 69120 Heidelberg GermanyHülya Aksoy, Ruprecht-Karls-University Dept. of Cardiology Im Neuenheimer Feld 410 69120 Heidelberg GermanyGuido H. Wabnitz, Ruprecht-Karls-University Institute for Immunology Heidelberg GermanyChristian Volz, Ruprecht-Karls-University Dept. of Cardiology Im Neuenheimer Feld 410 ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2104051</comments>
            <pubDate>Tue, 13 Jan 2009 08:14:23 +0100</pubDate>
            <guid isPermaLink="false">2104051</guid>        </item>
        <item>
            <title>Improved left ventricular function after transplantation of microspheres and fibroblasts in a rat model of myocardial infarction</title>
            <link>http://www.medworm.com/index.php?rid=2104052&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc7g2q85n2071n0mu%2F</link>
            <description>In this study we investigated the effect of several cell types and microspheres (uniform polystyrene
 microspheres, 10&amp;nbsp;µm diameter) transplanted 4&amp;nbsp;weeks after induction of myocardial infarction in a rat model. Eight weeks after
 intramyocardial application of fibroblasts and microspheres, left ventricular function was significantly improved as demonstrated
 by isolated heart studies (Langendorff) and echocardiographic findings (LVDP fibroblasts 129&amp;nbsp;±&amp;nbsp;32.9&amp;nbsp;mmHg, LVDP microspheres
 119.2&amp;nbsp;±&amp;nbsp;24.1&amp;nbsp;mmHg, fractional shortening (FS) microspheres 38.9&amp;nbsp;±&amp;nbsp;4.6%, FS fibroblasts 36.84&amp;nbsp;±&amp;nbsp;6.05%) in contrast to injection
 of macrophages or medium alone (LVDP medium 67&amp;nbsp;±&amp;nbsp;22.6&amp;nbsp;mmHg, LVDP macrophages 75.9&amp;nbsp;±&amp;nbsp;24.8&amp;nbsp;m...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2104052</comments>
            <pubDate>Tue, 13 Jan 2009 08:14:19 +0100</pubDate>
            <guid isPermaLink="false">2104052</guid>        </item>
        <item>
            <title>Tyrosine hydroxylase phosphorylation after naloxone-induced morphine withdrawal in the left ventricle</title>
            <link>http://www.medworm.com/index.php?rid=2064880&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr44377p15158v441%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Our previous studies have shown that morphine withdrawal induced hyperactivity of cardiac noradrenergic pathways. The purpose
 of the present study was to evaluate the effects of morphine withdrawal on site-specific tyrosine hydroxylase (TH) phosphorylation
 in the rat left ventricle. Dependence on morphine was induced by a 7-day s.c. implantation of morphine pellets. Morphine withdrawal
 was precipitated on day 8 by an injection of naloxone (2&amp;nbsp;mg/kg, s.c.). TH phosphorylation was determined by quantitative blot
 immunolabelling using phosphorylation state-specific antibodies. Ninety min after naloxone administration to morphine-dependent
 rats there was an increase in phospho-Ser40-TH (139.0&amp;nbsp;±&amp;nbsp;13%, P&amp;nbsp;&amp;lt;&amp;nbsp;0.05) and Ser31-TH (135.5&amp;nbsp;±&amp;nbsp...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2064880</comments>
            <pubDate>Tue, 23 Dec 2008 07:57:47 +0100</pubDate>
            <guid isPermaLink="false">2064880</guid>        </item>
        <item>
            <title>Tribute to Wolfgang Schaper on the occasion of his 75th birthday</title>
            <link>http://www.medworm.com/index.php?rid=2059645&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp5721205127x7665%2F</link>
            <description>Content Type Journal ArticleCategory EDITORIALDOI 10.1007/s00395-008-0766-4Authors
		Gerd Heusch
	

	
		Journal Basic Research in CardiologyOnline ISSN 1435-1803Print ISSN 0300-8428
	
		Journal Volume Volume 104
	
		Journal Issue Volume 104, Number 1 / January, 2009 (Source: Basic Research in Cardiology)</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2059645</comments>
            <pubDate>Sun, 21 Dec 2008 08:28:48 +0100</pubDate>
            <guid isPermaLink="false">2059645</guid>        </item>
        <item>
            <title>On the occasion of Wolfgang Schaper’s 75th birthday</title>
            <link>http://www.medworm.com/index.php?rid=2059644&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F844756771p1j17p4%2F</link>
            <description>Content Type Journal ArticleCategory EDITORIALDOI 10.1007/s00395-008-0767-3Authors
		Kerstin BoenglerIvo BuschmannElisabeth DeindlMartin GottwikHans Martin HoffmeisterWulf ItoHermann KleinManfred MauserChristoph NienaberVera Regitz-ZagrosekStefan Sack
	

	
		Journal Basic Research in CardiologyOnline ISSN 1435-1803Print ISSN 0300-8428
	
		Journal Volume Volume 104
	
		Journal Issue Volume 104, Number 1 / January, 2009 (Source: Basic Research in Cardiology)</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2059644</comments>
            <pubDate>Sun, 21 Dec 2008 08:28:48 +0100</pubDate>
            <guid isPermaLink="false">2059644</guid>        </item>
        <item>
            <title>Collateral circulation</title>
            <link>http://www.medworm.com/index.php?rid=2059646&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx71qj0843030h19m%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Following an arterial occlusion outward remodeling of pre-existent inter-connecting arterioles occurs by proliferation of
 vascular smooth muscle and endothelial cells. This is initiated by deformation of the endothelial cells through increased
 pulsatile fluid shear stress (FSS) caused by the steep pressure gradient between the high pre-occlusive and the very low post-occlusive
 pressure regions that are interconnected by collateral vessels. Shear stress leads to the activation and expression of all
 NOS isoforms and NO production, followed by endothelial VEGF secretion, which induces MCP-1 synthesis in endothelium and in
 the smooth muscle of the media. This leads to attraction and activation of monocytes and T-cells into the adventitial space
 (peripheral collateral ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2059646</comments>
            <pubDate>Sun, 21 Dec 2008 08:28:47 +0100</pubDate>
            <guid isPermaLink="false">2059646</guid>        </item>
        <item>
            <title>Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion?</title>
            <link>http://www.medworm.com/index.php?rid=2059647&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F58957r6120272621%2F</link>
            <description>In conclusion, T3
 administration at reperfusion can improve postischaemic recovery of function while limiting apoptosis. This may constitute
 a paradigm of a positive inotropic agent with anti-apoptotic action suitable for supporting hemodynamics in the clinical setting
 of ischaemia-reperfusion.
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0758-4Authors
		Constantinos Pantos, University of Athens Dept. of Pharmacology 75 Mikras Asias Ave. 11527 Goudi, Athens GreeceIordanis Mourouzis, University of Athens Dept. of Pharmacology 75 Mikras Asias Ave. 11527 Goudi, Athens GreeceTheodosios Saranteas, University of Athens Dept. of Pharmacology 75 Mikras Asias Ave. 11527 Goudi, Athens GreeceGuillaume Clavé, Quidd Saint Etienne du Rouvray Rouen FranceHeidi L...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2059647</comments>
            <pubDate>Sun, 21 Dec 2008 08:28:45 +0100</pubDate>
            <guid isPermaLink="false">2059647</guid>        </item>
        <item>
            <title>Green and black tea are equally potent stimuli of NO production and vasodilation: new insights into tea ingredients involved</title>
            <link>http://www.medworm.com/index.php?rid=2059648&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc0528336818jl2r4%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Epidemiological studies suggest that consumption of tea is associated with beneficial cardiovascular effects. Since different
 types of tea are consumed throughout the world, a question of much interest is whether green tea is superior to black tea
 in terms of cardiovascular protection. We therefore compared the effects of green and black tea on nitric oxide (NO) production
 and vasodilation and elucidated the tea compounds involved. We chose a highly fermented black tea and determined concentrations
 of individual tea compounds in both green and black tea of the same type (Assam). The fermented black tea was almost devoid
 of catechins. However, both teas stimulated eNOS activity and phosphorylation in bovine aortic endothelial cells (BAEC) as
 well as vasorelaxation ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2059648</comments>
            <pubDate>Sun, 21 Dec 2008 08:28:44 +0100</pubDate>
            <guid isPermaLink="false">2059648</guid>        </item>
        <item>
            <title>Postconditioning cardioprotection against infarct size and post-ischemic systolic dysfunction is influenced by gender</title>
            <link>http://www.medworm.com/index.php?rid=1984387&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh423361612g061x8%2F</link>
            <description>In conclusion IS, contracture and PSD
 are differently affected by gender, depending on ischemia duration. Yet, reduction of IS induced by PostC depends on the extension
 of IS induced by index-ischemia. While in female hearts reduction of PSD paralleled IS reduction, in male it does not occur.
 Results suggest that improvement of systolic function is mainly due to the anti-necrotic rather than to the anti-stunning
 effect exerted by PostC.
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0762-8Authors
		Claudia Penna, Università di Torino Dip. to di Scienze Cliniche e Biologiche Regione Gonzole 10 10043 Orbassano TO ItalyFrancesca Tullio, Università di Torino Dip. to di Scienze Cliniche e Biologiche Regione Gonzole 10 10043 Orbassano TO ItalyAnnalisa M...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1984387</comments>
            <pubDate>Sun, 23 Nov 2008 06:48:01 +0100</pubDate>
            <guid isPermaLink="false">1984387</guid>        </item>
        <item>
            <title>Protection of peroxiredoxin II on oxidative stress-induced cardiomyocyte death and apoptosis</title>
            <link>http://www.medworm.com/index.php?rid=1984386&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F225720u717311r87%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Peroxiredoxin II, a cytosolic isoform of the antioxidant enzyme family, has been implicated in cancer-associated cell death
 and apoptosis, but its functional role in the heart remains to be elucidated. Interestingly, the expression levels of peroxiredoxin
 II were decreased in mouse hearts upon ischemia-reperfusion, while they were elevated in two genetically modified hyperdynamic
 hearts with phospholamban ablation or protein phosphatase 1 inhibitor 1 overexpression. To delineate the functional significance
 of altered peroxiredoxin II expression, adenoviruses encoding sense or antisense peroxiredoxin II were generated; cardiomyocytes
 were infected, and then subjected to H2O2 treatment to mimic oxidative stress-induced cell death and apoptosis. H2O2 stimulation resul...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1984386</comments>
            <pubDate>Sun, 23 Nov 2008 06:48:01 +0100</pubDate>
            <guid isPermaLink="false">1984386</guid>        </item>
        <item>
            <title>Oxidative stress induces myeloperoxidase expression in endocardial endothelial cells from patients with chronic heart failure</title>
            <link>http://www.medworm.com/index.php?rid=1984388&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F1k2t12j882523371%2F</link>
            <description>This study demonstrates for the
 first time that EEC can express MPO after oxidative stress, both in vitro and in vivo, followed by accumulation of 3-chlorotyrosine,
 an end product of oxidative stress. Deregulation of endothelial functions may contribute to the development of a number of
 cardiovascular diseases, including CHF. The results also highlight the notion that endothelium is not only a target but also
 a key player in oxidative-driven cardiovascular stress.
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0761-9Authors
		Giampiero La Rocca, Università degli Studi di Palermo Sezione di Anatomia Umana, Dipto. di Medicina Sperimentale Via del Vespro 129 90127 Palermo ItalyAntonino Di Stefano, Fondazione S. Maugeri, IRCCS Laboratorio di Citoimmuno...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1984388</comments>
            <pubDate>Sun, 23 Nov 2008 06:48:00 +0100</pubDate>
            <guid isPermaLink="false">1984388</guid>        </item>
        <item>
            <title>Modulation of L-type Ca2+ channel current density and inactivation by β-adrenergic stimulation during murine cardiac embryogenesis</title>
            <link>http://www.medworm.com/index.php?rid=1911067&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F41qu715n02346173%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;These results imply that β-adrenergic modulation becomes of importance especially during fetal heart development. CDI and
 VDI of I
 CaL are modulated by β-adrenergic stimulation in fetal but not in early embryonic mouse cardiomyocytes. Furthermore our data
 suggest important changes of the L-type Ca2+ channel protein, and/or maturation of the Ca2+-induced Ca2+ release (CICR) machinery.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0755-7Authors
		Filomain Nguemo, University of Cologne Institute of Neurophysiology Cologne GermanyPhilipp Sasse, University of Bonn Institute of Physiology I, Life and Brain Center Bonn GermanyBernd K. Fleischmann, University of Bonn Institute of Physiology I, Life and Brain Center Bonn GermanyAl...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1911067</comments>
            <pubDate>Sat, 25 Oct 2008 08:38:56 +0100</pubDate>
            <guid isPermaLink="false">1911067</guid>        </item>
        <item>
            <title>Guggulsterone, an anti-inflammatory phytosterol, inhibits tissue factor and arterial thrombosis</title>
            <link>http://www.medworm.com/index.php?rid=1911066&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc5441022609v1203%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;Guggulsterone inhibits TF expression in vascular cells as well as thrombus formation in vivo; moreover, it impairs vascular
 smooth muscle cell activation. Hence, this phytosterol offers novel therapeutic options, in particular in inflammatory diseases
 associated with an increased risk of thrombosis.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0757-5Authors
		Catherine Gebhard, University of Zurich Cardiovascular Research, Institute of Physiology Winterthurerstraße 190 8057 Zürich SwitzerlandSimon F. Stämpfli, University of Zurich Cardiovascular Research, Institute of Physiology Winterthurerstraße 190 8057 Zürich SwitzerlandCaroline E. Gebhard, University of Zurich Cardiovascular Research, Institute of Physiology Wint...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1911066</comments>
            <pubDate>Sat, 25 Oct 2008 08:38:56 +0100</pubDate>
            <guid isPermaLink="false">1911066</guid>        </item>
        <item>
            <title>Innate immunity and myocardial adaptation to ischemia</title>
            <link>http://www.medworm.com/index.php?rid=1894172&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F282728704823204t%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Myocardial adaptation to ischemia in the form of ischemic preconditioning is clinically attractive, but not directly usable
 until molecular mimics are discovered. A growing body of evidence indicates that events underlying myocardial adaptation to
 ischemia may either involve, or be parallel to, signaling of the innate immune response. Preconditioning-like protection of
 the heart can be evoked through giving cytokines or fragments of bacterial walls. A possible role for cytokines, toll-like
 receptors, and nuclear factor kappa B for evoking ischemic preconditioning are discussed. Through stimulating innate immunity,
 there is potential to bring preconditioning into the clinics in a reasonable time frame. The possibility that the underlying
 protective response may inv...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1894172</comments>
            <pubDate>Sun, 19 Oct 2008 10:11:57 +0100</pubDate>
            <guid isPermaLink="false">1894172</guid>        </item>
        <item>
            <title>Aging-associated insulin resistance predisposes to hypertension and its reversal by exercise: the role of vascular vasorelaxation to insulin</title>
            <link>http://www.medworm.com/index.php?rid=1894171&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj03w568864k12222%2F</link>
            <description>In conclusion, these results demonstrate that endothelial
 dysfunction in response to insulin, but not insulin’s positive inotropic effects, plays an important role in the development
 of aging-related hypertension. The reversal of hypertensive response to insulin by exercise is most likely associated with
 improved insulin sensitivity in an eNOS-dependent manner and reduced oxidative and nitrative stresses.
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0754-8Authors
		Qiu-Xia Li, Shaanxi Normal University Institution of Physical Education Xi’an 710062 ChinaZheng-Ying Xiong, Shaanxi Normal University Institution of Physical Education Xi’an 710062 ChinaBai-Ping Hu, Shaanxi Normal University Institution of Physical Education Xi’an 710062 ChinaZhe...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1894171</comments>
            <pubDate>Sun, 19 Oct 2008 10:11:57 +0100</pubDate>
            <guid isPermaLink="false">1894171</guid>        </item>
        <item>
            <title>A novel-1364A/C aquaporin 5 gene promoter polymorphism influences the responses to salt loading of the renin-angiotensin-aldosterone system and of blood pressure in young healthy men</title>
            <link>http://www.medworm.com/index.php?rid=1870278&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj017622785061357%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;A novel single nucleotide polymorphism in the AQP5 gene promoter alters AQP5 expression in different in vitro systems and cells, and is associated with alterations of variables
 of the RAAS both in young healthy males and in patients with coronary artery disease.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0750-zAuthors
		Michael Adamzik, Universitätsklinikum Essen Klinik für Anästhesiologie und Intensivmedizin Hufelandstraße 55 45122 Essen GermanyUlrich H. Frey, University Hospital Essen, University of Duisburg–Essen Dept. of Anesthesiology and Intensive Care Medicine Essen GermanyKathrin Bitzer, University Hospital Essen, University of Duisburg-Essen Institute of Pharmacogenetics Essen GermanyHeinz Jakob, University ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1870278</comments>
            <pubDate>Fri, 10 Oct 2008 07:57:56 +0100</pubDate>
            <guid isPermaLink="false">1870278</guid>        </item>
        <item>
            <title>TNF-α induced shedding of the endothelial glycocalyx is prevented by hydrocortisone and antithrombin</title>
            <link>http://www.medworm.com/index.php?rid=1855560&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F7331r11764311328%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;Both hydrocortisone and antithrombin clearly preserve the endothelial glycocalyx in the face of inflammatory degradation initiated
 by TNF-α, however, with different mechanisms. This is an important new facet in the pathophysiology and therapy of sepsis,
 since preservation of the glycocalyx should help prevent vasoconstriction, tissue edema as well as leukocyte and platelet
 adhesion, thus mitigating inflammation and tissue hypoxia.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0749-5Authors
		Daniel Chappell, Ludwig-Maximilians University Clinic of Anaesthesiology Nussbaumstraße 20 80336 Munich GermanyKlaus Hofmann-Kiefer, Ludwig-Maximilians University Clinic of Anaesthesiology Nussbaumstraße 20 80336 Munich GermanyMatth...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1855560</comments>
            <pubDate>Sat, 04 Oct 2008 09:27:55 +0100</pubDate>
            <guid isPermaLink="false">1855560</guid>        </item>
        <item>
            <title>Effects of atorvastatin on calcium-regulating proteins: a possible mechanism to repair cardiac dysfunction in spontaneously hypertensive rats</title>
            <link>http://www.medworm.com/index.php?rid=1855561&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx3284250240xg148%2F</link>
            <description>In this study, we investigated the effect of atorvastatin on cardiac function in spontaneously hypertensive
 rats (SHRs), focusing in particular on its impact on the expression of sarcoplasmic reticulum Ca2+-adenosine triphosphatase (SERCA2a), phospholamban (PLB) and its phosphorylated form (phosphorylated PLB), all of which are
 Ca2+ regulatory proteins in myocardium. SHRs showed decreases in gene expression of SERCA2a and phosphorylated PLB, and reduction
 in SERCA activity in the left ventricular myocardium, as well as reduced cardiac function, compared to age-matched Wistar
 Kyoto rats (WKYs). Furthermore, we showed that in SHRs atorvastatin preserved cardiac dysfunction accompanied by positive
 alterations in calcium regulatory proteins, with up-regulation in expression of SERCA2a and...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1855561</comments>
            <pubDate>Sat, 04 Oct 2008 09:27:54 +0100</pubDate>
            <guid isPermaLink="false">1855561</guid>        </item>
        <item>
            <title>Propylthiouracil, independent of its antithyroid effect, decreases VSMC collagen expression</title>
            <link>http://www.medworm.com/index.php?rid=1840426&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg2n615687235345m%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Propylthiouracil (PTU), in addition to its antithyroid effect, is recently found to have a potent antiatherosclerotic effect.
 Because collagen accumulation is the major contributor to the growth of atherosclerotic lesions and the neointimal formation
 after arterial injury, the aim of this study is to investigate the impact of PTU on collagen regulation. In the rat carotid
 injury model, PTU administration reversed the up-regulation of collagen in the neointima induced by balloon injury. In vitro,
 vascular smooth muscle cells (VSMCs), the main origin of arterial collagen, were treated with PTU. Propylthiouracil caused
 a concentration-dependent decrease in collagen I and III steady-state protein and mRNA levels, as determined by immuno-cytochemistry,
 Western, and/or ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1840426</comments>
            <pubDate>Sat, 27 Sep 2008 14:05:59 +0100</pubDate>
            <guid isPermaLink="false">1840426</guid>        </item>
        <item>
            <title>Identification of mutational hot spots in 
 LMNA
 encoding lamin A/C in patients with familial dilated cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=1805797&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fn5338787122162p8%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The familial form of dilated cardiomyopathy (DCM) occurs in about 20%–50% of DCM cases. It is a heterogenous genetic disease:
 mutations in more than 20 different genes have been shown to cause familial DCM. LMNA, encoding the nuclear membrane protein lamin A/C, is one of the most inportant disease gene for that disease. Therefore,
 we analyzed the LMNA gene in a large cohort of 73 patients with familial DCM. Clinical examination (ECG, echocardiography, and catheterization)
 was followed by genetic characterization of LMNA by direct sequencing. We detected five heterozygous missense mutations (prevalence 7%) in five different families characterized
 by severe DCM and heart failure with conduction system disease necessitating pacemaker implantation and heart transplant...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1805797</comments>
            <pubDate>Tue, 16 Sep 2008 09:36:56 +0100</pubDate>
            <guid isPermaLink="false">1805797</guid>        </item>
        <item>
            <title>Impaired interaction between platelets and endothelial progenitor cells in diabetic patients</title>
            <link>http://www.medworm.com/index.php?rid=1790005&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F3523841510887810%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;This editorial focuses on new data on the role of platelets of the recruitment of endothelial progenitor cells to sites of
 vascular lesion and their differentiation into endothelium. Questions of further research are raised.
 
	Content Type Journal ArticleCategory INVITED EDITORIALDOI 10.1007/s00395-008-0747-7Authors
		Petra Kleinbongard, Universitätsklinikum Essen, Universität Duisburg-Essen Institut für Pathophysiologie Hufelandstraße 55 45122 Essen GermanyArtur-Aron Weber, Universitätsklinikum Essen, Universität Duisburg-Essen Institut für Pharmakologie Essen Germany
	

	
		Journal Basic Research in CardiologyOnline ISSN 1435-1803Print ISSN 0300-8428 (Source: Basic Research in Cardiology)</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1790005</comments>
            <pubDate>Fri, 12 Sep 2008 08:09:52 +0100</pubDate>
            <guid isPermaLink="false">1790005</guid>        </item>
        <item>
            <title>Impact of atherosclerotic plaque composition on coronary microembolization during percutaneous coronary interventions</title>
            <link>http://www.medworm.com/index.php?rid=1790006&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj54lv102675g2g35%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;Patients with large NC in culprit lesions may experience more myocardial injury from peri-interventional microembolization.
 IVUS-RF assessment before PCI has the potential to identify lesions at particular high risk which may help to tailor PCI.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0745-9Authors
		Dirk Böse, University of Duisburg-Essen Dept. of Cardiology, West German Heart Center Hufelandstraße 55 45122 Essen GermanyClemens von Birgelen, Medisch Spectrum Twente Dept. of Cardiology Enschede The NetherlandsXiu Ying Zhou, University of Duisburg-Essen Dept. of Cardiology, West German Heart Center Hufelandstraße 55 45122 Essen GermanyAxel Schmermund, Cardioangiologisches Centrum Bethanien Dept. of Cardiology Frankfu...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1790006</comments>
            <pubDate>Fri, 12 Sep 2008 08:09:51 +0100</pubDate>
            <guid isPermaLink="false">1790006</guid>        </item>
        <item>
            <title>Activation of sphingosine kinase by muscarinic receptors enhances NO-mediated and attenuates EDHF-mediated vasorelaxation</title>
            <link>http://www.medworm.com/index.php?rid=1778649&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F249n6un142p87746%2F</link>
            <description>In this study we investigated whether sphingosine kinase, the enzyme responsible for S1P synthesis, plays
 a role in muscarinic receptor-mediated NO production and vascular relaxation in different blood vessel types. For this purpose,
 sphingosine kinase translocation and sphingolipid-dependent NO-production after muscarinic receptor stimulation were assessed
 in an endothelial cell line. Furthermore, we used the sphingosine kinase inhibitor N,N-dimethylsphingosine (DMS) to investigate the role of sphingosine kinase in the relaxant responses to the muscarinic agonist
 methacholine (MCh) in isolated rat aorta and mesenteric arteries. Activation of M3-receptors in an endothelial cell line induced a fast translocation of YFP-tagged sphingosine kinase-1 from the cytosol to
 the plasma membrane...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1778649</comments>
            <pubDate>Mon, 08 Sep 2008 16:13:53 +0100</pubDate>
            <guid isPermaLink="false">1778649</guid>        </item>
        <item>
            <title>Limitation of myocardial infarct size in the clinical setting: current status and challenges in translating animal experiments into clinical therapy</title>
            <link>http://www.medworm.com/index.php?rid=1729217&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb762304733243757%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;This review takes a critical look at the current effectiveness of reperfusion therapy for acute myocardial infarction and
 at the potential for cardioprotective agents to improve it. Reperfusion alone limits the median value of infarct size to approximately
 50% of the ischemic region. However, the range of infarct sizes is very wide, and one-fourth of these patients have more than
 75% of the ischemic zone infarcted despite successful coronary reperfusion. Available studies suggest that mortality and morbidity
 is increased when more than 20% of the left ventricle is infarcted. Therefore, to be effective infarct size-limiting therapy
 would have to reduce infarction to or below this 20% target. To achieve this goal in the quartile of patients with the biggest
 infarcts...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1729217</comments>
            <pubDate>Thu, 21 Aug 2008 09:26:18 +0100</pubDate>
            <guid isPermaLink="false">1729217</guid>        </item>
        <item>
            <title>Impaired endothelial progenitor cell function predicts age-dependent carotid intimal thickening</title>
            <link>http://www.medworm.com/index.php?rid=1713595&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa667np1533w24685%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;Impaired EPC function may lead to accelerated vascular remodeling due to chronic impairment of endothelial maintenance.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0742-zAuthors
		Stefanie Keymel, RWTH University Hospital Aachen Medical Clinic I, Dept. of Medicine, Division of Cardiology, Pulmonology, and Vascular Medicine Pauwelstraße 30 52074 Aachen GermanyChristoph Kalka, Swiss Cardiovascular Center, Inselspital, University Hospital Dept. of Vascular Medicine Bern SwitzerlandTienush Rassaf, RWTH University Hospital Aachen Medical Clinic I, Dept. of Medicine, Division of Cardiology, Pulmonology, and Vascular Medicine Pauwelstraße 30 52074 Aachen GermanyYerem Yeghiazarians, University of California Division of Cardiology ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1713595</comments>
            <pubDate>Fri, 15 Aug 2008 06:49:54 +0100</pubDate>
            <guid isPermaLink="false">1713595</guid>        </item>
        <item>
            <title>Intravenous infusion of mesenchymal stem cells enhances regional perfusion and improves ventricular function in a porcine model of myocardial infarction</title>
            <link>http://www.medworm.com/index.php?rid=1713594&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj7061886v6281464%2F</link>
            <description>In conclusion, these data demonstrate that intravenous delivery of MSCs during early reperfusion augments
 vasculogenesis, enhances regional perfusion, and improves post-infarct ventricular function. The results suggest that intravenous
 infusion of MSCs is an effective modality for the treatment of ischemia/reperfusion induced myocardial injury.
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0741-0Authors
		Michael E. Halkos, Emory Crawford Long Hospital Cardiothoracic Research Laboratory, Division of Cardiothoracic Surgery 550 Peachtree Street, NE Atlanta GA 30308 USAZhi-Qing Zhao, Emory Crawford Long Hospital Cardiothoracic Research Laboratory, Division of Cardiothoracic Surgery 550 Peachtree Street, NE Atlanta GA 30308 USAFaraz Kerendi, Emory Crawfo...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1713594</comments>
            <pubDate>Fri, 15 Aug 2008 06:49:54 +0100</pubDate>
            <guid isPermaLink="false">1713594</guid>        </item>
        <item>
            <title>Transforming growth factor beta inhibition increases mortality and left ventricular dilatation after myocardial infarction</title>
            <link>http://www.medworm.com/index.php?rid=1654953&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F42512g0711067423%2F</link>
            <description>Abstract
 Background&amp;nbsp;&amp;nbsp;Transforming growth factor (TGF)-β is a locally generated cytokine involved in healing processes and tissue fibrosis, all
 relevant for cardiac remodeling and the development of heart failure after myocardial infarction (MI). However, data regarding
 the function of TGF-β after ischemic injury are inconclusive.
 
 
 
 Methods and results&amp;nbsp;&amp;nbsp;We tested the effect of TGF-β inhibition by application of a blocking antibody in mice with MI. Starting 1&amp;nbsp;week before or
 5&amp;nbsp;days after coronary artery ligation mice were treated with intraperitoneal injections of an anti-TGF-β (5&amp;nbsp;mg/kg bodyweight
 1D11, Genzyme) or control antibody. Mortality over 8&amp;nbsp;weeks was significantly higher in the groups treated with the anti-TGF-β
 antibody. Both, ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1654953</comments>
            <pubDate>Thu, 24 Jul 2008 09:02:49 +0100</pubDate>
            <guid isPermaLink="false">1654953</guid>        </item>
        <item>
            <title>Effects of unipolar stimulation on voltage and calcium distributions in the isolated rabbit heart</title>
            <link>http://www.medworm.com/index.php?rid=1642137&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F23qm60354n954128%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;Changes in the [Ca2+]
 i
 distribution correlate with the behavior of the V
 m distribution for S1–S2 coupling intervals longer than 20&amp;nbsp;ms; at shorter intervals S2 creates more heterogeneous [Ca2+]
 i
 distribution in comparison with V
 m. Stimulation in diastole and at very short coupling intervals caused V
 m–[Ca2+]
 i
 uncoupling at the regions of positive polarization (virtual cathode).
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0740-1Authors
		Veniamin Y. Sidorov, Vanderbilt University Dept. of Biomedical Engineering Nashville TN USAMark R. Holcomb, Vanderbilt University Dept. of Physics and Astronomy VU Station B 351807 Nashville TN 37235-1807 USAMarcella C. Woods, Vanderbilt University Dept. of Biomedical E...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1642137</comments>
            <pubDate>Sun, 20 Jul 2008 06:23:13 +0100</pubDate>
            <guid isPermaLink="false">1642137</guid>        </item>
        <item>
            <title>Acidosis, oxygen, and interference with mitochondrial permeability transition pore formation in the early minutes of reperfusion are critical to postconditioning’s success</title>
            <link>http://www.medworm.com/index.php?rid=1630507&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff118357696428405%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Repetitive cycles of reflow/reocclusion in the initial 2&amp;nbsp;min following release of a prolonged coronary occlusion, i.e., ischemic
 postconditioning (IPoC), salvages ischemic myocardium. We have proposed that the intermittent ischemia prevents formation
 of mitochondrial permeability transition pores (MPTP) by maintaining an acidic myocardial pH for several minutes until survival
 kinases can be activated. To determine other requisites of IPoC, isolated rabbit hearts were subjected to 30&amp;nbsp;min of regional
 myocardial ischemia and 120&amp;nbsp;min of reperfusion. Infarct size was determined by staining with triphenyltetrazolium chloride.
 During the first 2&amp;nbsp;min of reperfusion the perfusate was either at pH 7.4 following equilibration with 95% O2/5% CO2, pH 6.9 fol...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630507</comments>
            <pubDate>Tue, 15 Jul 2008 07:04:57 +0100</pubDate>
            <guid isPermaLink="false">1630507</guid>        </item>
        <item>
            <title>Advanced glycation end products depress function of endothelial progenitor cells via p38 and ERK 1/2 mitogen-activated protein kinase pathways</title>
            <link>http://www.medworm.com/index.php?rid=1624994&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy765531p838u4q13%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;AGE-HSA could promote atherosclerosis by upregulating EPCs RAGE expressions and promoting EPCs apoptosis via p38, ERK MAPK
 pathways, activation of NF-κB might also play a role in this process.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0738-8Authors
		Chengbo Sun, 2nd Hospital Affiliated to the Second Military Medical University Dept. of Cardiology Shanghai People’s Republic of ChinaChun Liang, 2nd Hospital Affiliated to the Second Military Medical University Dept. of Cardiology Shanghai People’s Republic of ChinaYusheng Ren, 2nd Hospital Affiliated to the Second Military Medical University Dept. of Cardiology Shanghai People’s Republic of ChinaYi Zhen, 2nd Hospital Affiliated to the Second Military Medical Universi...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1624994</comments>
            <pubDate>Sat, 12 Jul 2008 07:55:36 +0100</pubDate>
            <guid isPermaLink="false">1624994</guid>        </item>
        <item>
            <title>Contribution of 
 I
 Kr and 
 I
 K1 to ventricular repolarization in canine and human myocytes: is there any influence of action potential duration?</title>
            <link>http://www.medworm.com/index.php?rid=1593305&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm255575736261246%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;The results indicate that action potential configuration fails to influence the amplitude of I
 Kr and I
 K1 during the ventricular action potential in dogs and humans, suggesting that rate-dependent changes in action potential duration
 are not likely related to rate-dependent alterations in I
 Kr or I
 K1 kinetics in these species.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0730-3Authors
		Norbert Jost, University of Szeged Dept. of Pharmacology and Pharmacotherapy Szeged HungaryKároly Acsai, University of Szeged Dept. of Pharmacology and Pharmacotherapy Szeged HungaryBalázs Horváth, University of Debrecen Dept. of Physiology Nagyerdei krt 98 4012 Debrecen HungaryTamás Bányász, University of Debrecen Dept. of Physi...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1593305</comments>
            <pubDate>Sun, 06 Jul 2008 06:58:56 +0100</pubDate>
            <guid isPermaLink="false">1593305</guid>        </item>
        <item>
            <title>Ischemia-reperfusion injury and cardioprotection: investigating PTEN, the phosphatase that negatively regulates PI3K, using a congenital model of PTEN haploinsufficiency</title>
            <link>http://www.medworm.com/index.php?rid=1593304&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw296800jh3542718%2F</link>
            <description>In conclusion, PTEN haploinsufficiency alone does not induce cardioprotection in this model; however, it reduces the threshold
 of protection induced by IPC.
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0735-yAuthors
		Hilary K. Siddall, The Hatter Cardiovascular Institute, University College London Hospital and Medical School 67 Chenies Mews London WC1E 6HX UKClare E. Warrell, The Hatter Cardiovascular Institute, University College London Hospital and Medical School 67 Chenies Mews London WC1E 6HX UKDerek M. Yellon, The Hatter Cardiovascular Institute, University College London Hospital and Medical School 67 Chenies Mews London WC1E 6HX UKMihaela M. Mocanu, The Hatter Cardiovascular Institute, University College London Hospital and Medical School 67 ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1593304</comments>
            <pubDate>Sun, 06 Jul 2008 06:58:56 +0100</pubDate>
            <guid isPermaLink="false">1593304</guid>        </item>
        <item>
            <title>Impaired interaction of platelets with endothelial progenitor cells in patients with cardiovascular risk factors</title>
            <link>http://www.medworm.com/index.php?rid=1593306&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F58r4h3h362167624%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;Healthy volunteer-derived platelets provide a source of soluble factors to improve the number and function of EPC from patients
 with cardiovascular risk factors, particularly diabetes mellitus.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0734-zAuthors
		Elisabeth Dernbach, University of Frankfurt Molecular Cardiology, Dept. of Internal Medicine III Theodor-Stern-Kai 7 60590 Frankfurt GermanyVoahanginirina Randriamboavonjy, University of Frankfurt Vascular Signalling Group, Dept. of Cardiovascular Physiology Frankfurt GermanyIngrid Fleming, University of Frankfurt Vascular Signalling Group, Dept. of Cardiovascular Physiology Frankfurt GermanyAndreas M. Zeiher, University of Frankfurt Molecular Cardiology, Dept. of Internal M...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1593306</comments>
            <pubDate>Sun, 06 Jul 2008 06:58:54 +0100</pubDate>
            <guid isPermaLink="false">1593306</guid>        </item>
        <item>
            <title>The role of inflammatory cytokines in endothelial dysfunction</title>
            <link>http://www.medworm.com/index.php?rid=1581718&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F0732l63841617056%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Clinical and experimental data support a link between endothelial dysfunction and inflammation. Inflammatory cytokines are
 important protagonists in formation of atherosclerotic plaque, eliciting effects throughout the atherosclerotic vessel. Importantly,
 the development of atherosclerotic lesions, regardless of the risk factor, e.g., diabetes, hypertension, obesity, is characterized
 by disruption in normal function of the endothelial cells. Endothelial cells, which line the internal lumen of the vasculature,
 are part of a complex system that regulates vasodilation and vasoconstriction, growth of vascular smooth muscle cells, inflammation,
 and hemostasis, maintaining a proper blood supply to tissues and regulating inflammation and coagulation. Current concepts
 sug...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1581718</comments>
            <pubDate>Fri, 04 Jul 2008 05:58:25 +0100</pubDate>
            <guid isPermaLink="false">1581718</guid>        </item>
        <item>
            <title>Persistent beneficial effect of postconditioning against infarct size: role of mitochondrial KATP channels during reperfusion</title>
            <link>http://www.medworm.com/index.php?rid=1581717&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F81177rn048qlq342%2F</link>
            <description>This study tested the hypothesis that inhibition of myocardial injury and modulation of mitochondrial dysfunction by postconditioning
 (Postcon) after 24&amp;nbsp;h of reperfusion is associated with activation of KATP channels. Thirty dogs undergoing 60&amp;nbsp;min of ischemia and 24&amp;nbsp;h of reperfusion (R) were randomly divided into four groups: Control:
 no intervention at R; Postcon: three cycles of 30&amp;nbsp;s R alternating with 30&amp;nbsp;s re-occlusion were applied at R; 5-hydroxydecanoate
 (5-HD): the mitochondrial KATP channel blocker was infused 5&amp;nbsp;min before Postcon; HMR1098: the sarcolemmal KATP channel blocker was administered 5&amp;nbsp;min before Postcon. After 24&amp;nbsp;h of R, infarct size was smaller in Postcon relative to Control
 (27&amp;nbsp;±&amp;nbsp;4%* Vs. 39&amp;nbsp;±&amp;nbsp;2% of area a...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1581717</comments>
            <pubDate>Fri, 04 Jul 2008 05:58:25 +0100</pubDate>
            <guid isPermaLink="false">1581717</guid>        </item>
        <item>
            <title>Clinical translation of cardioprotective strategies</title>
            <link>http://www.medworm.com/index.php?rid=1581716&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg0127x83q4477n25%2F</link>
            <description>Content Type Journal ArticleCategory MEETING REPORTDOI 10.1007/s00395-008-0736-xAuthors
		Derek J. Hausenloy, University College London Hospitals and Medical School The Hatter Institute and Center for Cardiology Grafton Way London WC1E 6DB UKDerek M. Yellon, University College London Hospitals and Medical School The Hatter Institute and Center for Cardiology Grafton Way London WC1E 6DB UK
	

	
		Journal Basic Research in CardiologyOnline ISSN 1435-1803Print ISSN 0300-8428 (Source: Basic Research in Cardiology)</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1581716</comments>
            <pubDate>Fri, 04 Jul 2008 05:58:25 +0100</pubDate>
            <guid isPermaLink="false">1581716</guid>        </item>
        <item>
            <title>Maturation-induces endothelial dysfunction via vascular inflammation in diabetic mice</title>
            <link>http://www.medworm.com/index.php?rid=1581719&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp0642r02203800j3%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;We hypothesized that maturation-induced vascular inflammation produces endothelial dysfunction in type II diabetes and TNFα
 plays a key role in triggering inflammation in the development of diabetes. In control (Db/db) mice aged 6, 12, 18 and 24&amp;nbsp;weeks,
 sodium nitroprusside (SNP) and acetylcholine (ACh) induced dose-dependent vasodilation, and dilation to ACh was blocked by
 the NO synthase inhibitor N
 G-monomethyl-l-arginine. In type II diabetic (db/db) mice at age of 12, 18 and 24&amp;nbsp;weeks, ACh or flow-induced dilation was blunted compared
 to Db/db; endothelial function is normal at 6&amp;nbsp;weeks of age in db/db Vs. control mice, but SNP produced comparable dilation
 at age of 6, 12, 18 and 24&amp;nbsp;weeks. Decrements in endothelial function in db/db mice prog...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1581719</comments>
            <pubDate>Fri, 04 Jul 2008 05:58:24 +0100</pubDate>
            <guid isPermaLink="false">1581719</guid>        </item>
        <item>
            <title>Reduced calcium responsiveness characterizes contractile dysfunction following coronary microembolization</title>
            <link>http://www.medworm.com/index.php?rid=1550860&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F4j6qk484782g5187%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;The ME-induced myocardial dysfunction is not related to an altered calcium sensitivity, but is characterized by a reduced
 maximal contractile force.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0732-1Authors
		Andreas Skyschally, University School of Medicine Institute of Pathophysiology Essen GermanyPetra Gres, University School of Medicine Institute of Pathophysiology Essen GermanyPatrick van Caster, University School of Medicine Institute of Pathophysiology Essen GermanyAnita van de Sand, University School of Medicine Institute of Pathophysiology Essen GermanyKerstin Boengler, University School of Medicine Institute of Pathophysiology Essen GermanyRainer Schulz, University School of Medicine Institute of Pathophysiology E...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1550860</comments>
            <pubDate>Wed, 25 Jun 2008 07:57:52 +0100</pubDate>
            <guid isPermaLink="false">1550860</guid>        </item>
        <item>
            <title>Inhibiting matrix metalloproteinase-2 reduces protein release into coronary effluent from isolated rat hearts during ischemia-reperfusion</title>
            <link>http://www.medworm.com/index.php?rid=1481595&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F4009572031r18082%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;MMP inhibition not only reduces cardiac mechanical dysfunction but also reduces endothelial damage resulting from cardiac
 I/R injury.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0727-yAuthors
		Justyna Fert-Bober, University of Saskatchewan Dept. of Pharmacology, College of Medicine 107 Wiggins Road Saskatoon SK S7N 5E5 CanadaHernando Leon, University of Alberta Dept. of Pediatrics and Pharmacology Edmonton AB CanadaJolanta Sawicka, University of Saskatchewan Dept. of Pharmacology, College of Medicine 107 Wiggins Road Saskatoon SK S7N 5E5 CanadaRashpal S. Basran, University of Saskatchewan Dept. of Medicine, Division of Cardiology Saskatoon SK CanadaRichard M. Devon, University of Saskatchewan Dept. of Anatomy and Cell Biol...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1481595</comments>
            <pubDate>Fri, 30 May 2008 05:59:52 +0100</pubDate>
            <guid isPermaLink="false">1481595</guid>        </item>
        <item>
            <title>Signal transducer and activator of transcription 3 is involved in the cardioprotective signalling pathway activated by insulin therapy at reperfusion</title>
            <link>http://www.medworm.com/index.php?rid=1469180&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv03gm4tmvk786tt4%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;Insulin-induced cardioprotection at reperfusion occurs through activation of STAT3. Inhibiting STAT3 by AG490, or STAT3 depletion
 in cardiac myocytes affects activation of Akt, suggesting close interaction between STAT3 and Akt in the cardioprotective
 signalling pathway activated by insulin treatment at reperfusion.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0728-xAuthors
		Britt N. Fuglesteg, University of Tromsø Dept. of Medical Physiology, Faculty of Medicine 9037 Tromsø NorwayNaushaad Suleman, University of Cape Town Hatter Institute for Cardiovascular Research, Dept. of Medicine, Faculty of Health Sciences Cape Town South AfricaCrina Tiron, University of Bergen Dept. of Biomedicine, Faculty of Medicine Bergen Norwa...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1469180</comments>
            <pubDate>Sat, 24 May 2008 06:54:24 +0100</pubDate>
            <guid isPermaLink="false">1469180</guid>        </item>
        <item>
            <title>TGF-β1 enhances cardiomyogenic differentiation of skeletal muscle-derived adult primitive cells</title>
            <link>http://www.medworm.com/index.php?rid=1469181&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Flk002572j8665510%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The optimal medium for cardiac differentiation of adult primitive cells remains to be established. We quantitatively compared
 the efficacy of IGF-1, dynorphin B, insulin, oxytocin, bFGF, and TGF-β1 in inducing cardiomyogenic differentiation. Adult
 mouse skeletal muscle-derived Sca1+/CD45-/c-kit-/Thy-1+ (SM+) and Sca1-/CD45-/c-kit-/Thy-1+ (SM-) cells were cultured in basic
 medium (BM; DMEM, FBS, IGF-1, dynorphin B) alone and BM supplemented with insulin, oxytocin, bFGF, or TGF-β1. Cardiac differentiation
 was evaluated by the expression of cardiac-specific markers at the mRNA (qRT-PCR) and protein (immunocytochemistry) levels.
 BM+TGF-β1 upregulated mRNA expression of Nkx2.5 and GATA-4 after 4&amp;nbsp;days and Myl2 after 9&amp;nbsp;days. After 30&amp;nbsp;days, BM+TGF-β1 ind...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1469181</comments>
            <pubDate>Sat, 24 May 2008 06:54:23 +0100</pubDate>
            <guid isPermaLink="false">1469181</guid>        </item>
        <item>
            <title>Activation of kappa-opioid receptors at reperfusion affords cardioprotection in both rat and mouse hearts</title>
            <link>http://www.medworm.com/index.php?rid=1469182&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F41561715j4131111%2F</link>
            <description>This study was aimed at delineating the time course of κ-OR-mediated protection in two experimental
 models: an in vivo rat model of regional myocardial infarction (30&amp;nbsp;min of left coronary artery occlusion with 120&amp;nbsp;min of reperfusion),
 and an in vitro perfused murine heart model (undergoing 25&amp;nbsp;min of global ischemia and 45&amp;nbsp;min of reperfusion). In the rat model,
 the selective κ-OR agonist U50, 488 (0.1&amp;nbsp;mg/kg, IV bolus), administered either 10&amp;nbsp;min prior to ischemia or 5&amp;nbsp;min prior to
 reperfusion, significantly reduced infarct size (38&amp;nbsp;±&amp;nbsp;3% and 43&amp;nbsp;±&amp;nbsp;2% infarct size/area-at-risk (IS/AAR), respectively; P&amp;nbsp;&amp;lt;&amp;nbsp;0.05) compared to untreated rats (56&amp;nbsp;±&amp;nbsp;1% IS/AAR). Administration of U50, 488 10&amp;nbsp;s after onset of re...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1469182</comments>
            <pubDate>Sat, 24 May 2008 06:54:21 +0100</pubDate>
            <guid isPermaLink="false">1469182</guid>        </item>
        <item>
            <title>NO and PGI2 in coronary endothelial dysfunction in transgenic mice with dilated cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=1397382&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl7275t7l02l8kjp4%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;In the mouse model of dilated cardiomyopathy, endothelial dysfunction in coronary circulation is present in the late but not
 the early stage of heart failure pathology and is characterized by a decrease in NO bioavailability and a compensatory increase
 in PGI2. Both the decrease in NO activity and the increase in PGI2 activity may result from excessive O2
 − production by cardiac NADPH oxidase in Tgαq*44 hearts.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0723-2Authors
		Lukasz Drelicharz, Jagiellonian University Medical College Dept. of Experimental Pharmacology, Chair of Pharmacology Grzegorzecka 16 Krakow 31-531 PolandValery Kozlovski, Jagiellonian University Medical College Dept. of Experimental Pharmacology, Chair...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1397382</comments>
            <pubDate>Wed, 23 Apr 2008 16:19:23 +0100</pubDate>
            <guid isPermaLink="false">1397382</guid>        </item>
        <item>
            <title>Platelet GPVI binds to collagenous structures in the core region of human atheromatous plaque and is critical for atheroprogression in vivo</title>
            <link>http://www.medworm.com/index.php?rid=1397384&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F433146wm5w414q3h%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Platelet adhesion to the atherosclerotic vascular wall induces thrombosis and boosters vascular inflammation and atheroprogression.
 In the present study we studied the binding of the platelet collagen receptor glycoprotein (GP) VI to human atherosclerotic
 plaques (AP) and the role of GPVI-mediated platelet adhesion for atheroprogression. Soluble GPVI-Fc fusion protein bound to
 immobilized collagen type I, collagen type III, and predominantly to the core region of human carotid atheromatous plaques.
 The pattern of GPVI-Fc binding was similar to the immunostaining pattern of collagen type III and differed from the immunostaining
 of collagen type I, which was more intense in the cap than in the core. Plaque-induced platelet aggregation in stirred blood
 and platelet a...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1397384</comments>
            <pubDate>Wed, 23 Apr 2008 16:19:22 +0100</pubDate>
            <guid isPermaLink="false">1397384</guid>        </item>
        <item>
            <title>The association of coronary flow changes and inflammatory indices to ischaemia–reperfusion microvascular damage and left ventricular remodelling</title>
            <link>http://www.medworm.com/index.php?rid=1397383&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc729256x1885j339%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;Changes of mean diastolic CF and IL-6 cs are associated with alterations in myocardial microvascular integrity after ischaemia–reperfusion
 and may be used as a predictor of myocardial dysfunction.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0720-5Authors
		Dimitris Bramos, Athens Medical School, “Alexandra” Hospital Dept. of Clinical Therapeutics Athens GreeceIgnatios Ikonomidis, Athens Medical School, “Alexandra” Hospital Dept. of Clinical Therapeutics Athens GreeceNikolaos Tsirikos, Athens Medical School, “Alexandra” Hospital Dept. of Clinical Therapeutics Athens GreeceGiorgios Kottis, Athens Medical School, “Alexandra” Hospital Dept. of Clinical Therapeutics Athens GreeceVasiliki Kostopoulou, Athens Med...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1397383</comments>
            <pubDate>Wed, 23 Apr 2008 16:19:22 +0100</pubDate>
            <guid isPermaLink="false">1397383</guid>        </item>
        <item>
            <title>Genes in congenital heart disease: atrioventricular valve formation</title>
            <link>http://www.medworm.com/index.php?rid=1362221&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F4rlv1l232v285740%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Through the use of animal studies, many candidate genes (mainly encoding transcriptional factors and receptors) have been
 implicated in the development of congenital heart disease. Thus far, only a minority of these genes have been shown to carry
 mutations associated with congenital disease in humans, e.g., GATA 4, TBX-5, NOTCH1 and NKX2-5. Mutations in these genes can cause a variety of cardiac defects even within the same family. Conversely, similar phenotypes
 are observed for different gene mutations suggesting a common pathway. Multiple genes and genetic pathways have been related
 to atrioventricular valve formation, although most of these genes have not yet been demonstrated as causative in human atrioventricular
 valve defects. Key pathways include the epiderm...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1362221</comments>
            <pubDate>Tue, 08 Apr 2008 07:12:57 +0100</pubDate>
            <guid isPermaLink="false">1362221</guid>        </item>
        <item>
            <title>Platelets in regenerative medicine</title>
            <link>http://www.medworm.com/index.php?rid=1362223&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fkt82018672056217%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Stem and progenitor cells have evolved as the central cell type in regenerative medicine. This focussed approach may, however,
 sometimes narrow the point of view. Recently, platelets have been shown to strongly influence progenitor cell biology and
 to serve as regenerative cells themselves. Platelets represent an important recruitment factor for circulating progenitor
 cells. Furthermore, they modulate progenitor cell chemotaxis, migration and differentiation. Platelets are crucial for the
 regeneration of parenchymatous organs such as the liver. Moreover, in the clinical setting, platelets are already applied
 for the restoration of connective and bone tissue. However, also adverse effects can be mediated by platelets and progenitor
 cells exposed to platelets, inclu...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1362223</comments>
            <pubDate>Tue, 08 Apr 2008 07:12:56 +0100</pubDate>
            <guid isPermaLink="false">1362223</guid>        </item>
        <item>
            <title>Regional and temporal heterogeneity of postsystolic wall thickening is associated with left ventricular asynchrony in normal and experimental stunned myocardium</title>
            <link>http://www.medworm.com/index.php?rid=1362222&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fuv80227013x20u93%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;The present study demonstrates that location of ischemia and wall interactions produce discrepancies in PSWT between anterior
 and posterior walls in stunned myocardium.
 
 
 
	Content Type Journal ArticleCategory ORIGINAL CONTRIBUTIONDOI 10.1007/s00395-008-0716-1Authors
		Laurence Lucats, INSERM U 841 Equipe 03 Faculté de Médecine Université Paris 12 Laboratoire de Pharmacologie 8, rue du Général Sarrail 94010 Créteil Cedex FranceXavier Monnet, INSERM U 841 Equipe 03 Faculté de Médecine Université Paris 12 Laboratoire de Pharmacologie 8, rue du Général Sarrail 94010 Créteil Cedex FranceAlain Bizé, INSERM U 841 Equipe 03 Faculté de Médecine Université Paris 12 Laboratoire de Pharmacologie 8, rue du Général Sarrail 94010 Créteil Cedex FranceValérie ...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1362222</comments>
            <pubDate>Tue, 08 Apr 2008 07:12:56 +0100</pubDate>
            <guid isPermaLink="false">1362222</guid>        </item>
        <item>
            <title>Redox signaling triggers protection during the reperfusion rather than the ischemic phase of preconditioning</title>
            <link>http://www.medworm.com/index.php?rid=1313865&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F91h3847310375144%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In ischemic preconditioning (IPC) brief ischemia/reperfusion renders the heart resistant to infarction from any subsequent
 ischemic insult. Protection results from binding of surface receptors by ligands released during the preconditioning ischemia.
 The downstream pathway involves redox signaling as IPC will not protect in the presence of a free radical scavenger. To determine
 when in the IPC protocol the redox signaling occurs, seven groups of isolated rabbit hearts were studied. All hearts underwent
 30 min of coronary branch occlusion and 2 h of reperfusion. IPC groups were subjected to 5 min of regional ischemia followed
 by 10 min of reperfusion prior to the 30-min coronary occlusion. The Control group had only the 30-min occlusion and 2-h reperfusion.
 In the s...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1313865</comments>
            <pubDate>Tue, 18 Mar 2008 08:15:44 +0100</pubDate>
            <guid isPermaLink="false">1313865</guid>        </item>
        <item>
            <title>Slow contractions characterize failing rat hearts</title>
            <link>http://www.medworm.com/index.php?rid=1313864&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh26v02g14r288w61%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The reduced power of the failing heart can be ascribed to a combination of reduced force and slower contraction. We hypothesized
 that these two properties are due to different cellular mechanisms. We measured contraction parameters both in vivo and in
 isolated left ventricular (LV) cardiomyocytes from a rat model of post infarction congestive heart failure (CHF). ECG was
 measured simultaneously with echocardiography and LV pressure, respectively. Shortening and shortening velocity (SV) in isolated
 cardiomyocytes were measured during different stimulation protocols. LV end diastolic pressure (LVEDP) was 24.6 ± 0.7 mmHg
 in CHF. LV systolic pressure was decreased by 20%, maximum rate of pressure development in the LV (+dP/dt
 max) by 36% and time in systole increased...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1313864</comments>
            <pubDate>Tue, 18 Mar 2008 08:15:44 +0100</pubDate>
            <guid isPermaLink="false">1313864</guid>        </item>
        <item>
            <title>Age-dependent endothelial dysfunction is associated with failure to increase plasma nitrite in response to exercise</title>
            <link>http://www.medworm.com/index.php?rid=1313867&amp;cid=s_33458_7_f&amp;fid=33458&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fq8m5g88357n720g9%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Age-dependent alterations of the vessel wall may predispose older individuals to increased cardiovascular pathology. Aging
 is associated with an impaired bioactivity of nitric oxide (NO). Plasma nitrite reflects NO-synthase activity under fasting
 conditions and is an important storage pool of NO. To test the hypothesis that aging is associated with an impaired capacity
 of the vasculature to increase plasma nitrite during exercise, 29 young and 28 old healthy individuals (25 ± 1 years and 58
 ± 2 years; P &amp;lt; 0.001) without major cardiovascular risk factors were enrolled. Exercise stress was similar in both groups. Baseline nitrite
 did not differ (107 ± 8 vs. 82 ± 10 nmol/l, young vs. old; n.s.) although a trend toward higher nitrite levels in young individuals
...</description>
            <author>Basic Research in Cardiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1313867</comments>
            <pubDate>Tue, 18 Mar 2008 08:15:43 +0100</pubDate>
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