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        <title>Clinical and Experimental Pharmacology and Physiology 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 'Clinical and Experimental Pharmacology and Physiology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Clinical+and+Experimental+Pharmacology+and+Physiology&t=Clinical+and+Experimental+Pharmacology+and+Physiology&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 14:04:04 +0100</lastBuildDate>
        <item>
            <title>Scavenging of NADPH Oxidase-derived Superoxide Anions Improves Depressed Baroreflex Sensitivity in Spontaneously Hypertensive Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5644040&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22283703%26dopt%3DAbstract</link>
            <description>Authors: GuimarÃ£es DD, Carvalho CC, Braga VA
    Abstract
    1. In pathological conditions such as hypertension, there is impairment in the autonomic control of blood pressure resulting in changes in baroreflex sensitivity. In the present study we tested the hypothesis that acute superoxide scavenging would restore the depressed baroreflex sensitivity (BRS) in spontaneously hypertensive rats (SHR). 2. Male 10-week-old SHR (n=14) and their controls (WKY, n=14) underwent femoral artery and vein catheterization for conscious blood pressure recording and drug administration. BRS was obtained by the drug-induced method using phenylephrine (8 Î¼g/Kg, i.v.) and sodium nitroprusside (25 Î¼g/Kg, i.v.) before and after the administration of tiron (30 mg/Kg, i.v.), a superoxide dismutase mimetic, o...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5644040</comments>
            <pubDate>Fri, 27 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Role of p53-dependent placental apoptosis in the reproductive and developmental toxicities of caffeine in rodents.</title>
            <link>http://www.medworm.com/index.php?rid=5607222&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22243401%26dopt%3DAbstract</link>
            <description>Authors: Huang J, Zhou S, Ping J, Pan X, Liang G, Xu D, Kou H, Bao C, Wang H
    Abstract
    1.â€‚To evaluate the role of placental apoptosis in mediating the reproductive and developmental toxicity of caffeine in rodents. 2.â€‚Female Kunming mice were treated with caffeine (60, 120 and 240 mg/kg per day) before and during pregnancy. The conception rate, maternal bodyweight gain, placental weight and indices of fetal developmental, including the intrauterine growth retardation (IUGR) rate, were determined on gestational day (GD) 18. 3.â€‚Female Wistar rats were treated with caffeine (20, 60 and 180 mg/kg per day) from GD11 to GD20. The IUGR rate, maternal plasma angiotensin (Ang) II and prolactin concentrations, placental pathology, expression of angiotensin AT(1) and AT(2) receptors and ...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5607222</comments>
            <pubDate>Fri, 13 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5607222</guid>        </item>
        <item>
            <title>Lack of effect by CNS active doses of nabilone on capsaicin-induced pain and hyperalgesia.</title>
            <link>http://www.medworm.com/index.php?rid=5580198&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22233155%26dopt%3DAbstract</link>
            <description>Authors: KalliomÃ¤ki J, Philipp A, Baxendale J, Annas P, Karlsten R, Segerdahl M
    Abstract
    1.â€‚The aim was to investigate effects of nabilone on capsaicin-induced pain and hyperalgesia, and on biomarkers of cannabinoid CNS effects. 2.â€‚A randomized, double-blind, placebo-controlled, crossover study was conducted in 30 healthy male volunteers receiving single doses of nabilone 1, 2 or 3 mg. Pain intensity after intradermal capsaicin injections in the forearm was assessed by continuous Visual Analogue Scale (VAS, 0-100 mm). Capsaicin cream was applied to the calf to induce hyperalgesia. Primary hyperalgesia was assessed by measuring heat pain thresholds and secondary hyperalgesia by measuring the area where light tactile stimulation was felt painful. Pain and hyperalgesia were measu...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580198</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580198</guid>        </item>
        <item>
            <title>Oral simvastatin reduces the hypertensive response to air-jet stress.</title>
            <link>http://www.medworm.com/index.php?rid=5580197&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22233179%26dopt%3DAbstract</link>
            <description>In this study we tested the hypothesis that simvastatin affects hemodynamic responses to air-jet stress and intracerebroventricular infusions of vasopressin and angiotensin II. We maintained 12-week-old, male, Sprague Dawley rats either on tap water (control) or on water containing simvastatin 20mg/L, 40mg/L or 60mg/L for four weeks. Subsequently, we measured arterial blood pressure and heart rate at baseline and after air-jet stress, or intracerebroventricular infusions of angiotensin II or vasopressin or their antagonists. 3.â€‚We found no significant difference between the control group and simvastatin groups in baseline mean arterial blood pressure and heart rate. In rats given simvastatin 60mg/L, the hypertensive response to air-jet stress was significantly smaller than in controls as...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580197</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Effect of Amiodarone on Dispersion of Ventricular Repolarization in a Canine Congestive Heart Failure Model.</title>
            <link>http://www.medworm.com/index.php?rid=5580200&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22229329%26dopt%3DAbstract</link>
            <description>Authors: Zhou SX, Fang C, Zheng SX, Zhang YL, Lei J, Wang JF
    Abstract
    1.â€‚The effects of amiodarone on ventricular electrophysiological parameters, especially the dispersion of ventricular repolarization, were investigated in a canine model of congestive heart failure (CHF). 2.â€‚Dogs were randomized to either a control, amiodarone, CHF, or CHF + amiodarone group. Dogs in the CHF and CHF + amiodarone groups underwent 4-5 weeks of rapid ventricular pacing; dogs in the control and amiodarone groups underwent only a sham operation. Amiodarone 20mg/kg/day was administered orally beginning on day 1 post-operatively in the treatment groups, and ventricular electrophysiological variables were evaluated 4-5 weeks after rapid pacing or sham operation. 3.â€‚In CHF dogs, the transmural dispe...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580200</comments>
            <pubDate>Mon, 09 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>The Potential Role of Green Tea Catechins in Various Disease Therapies: Progress and Promise.</title>
            <link>http://www.medworm.com/index.php?rid=5580199&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22229384%26dopt%3DAbstract</link>
            <description>Authors: Mak JC
    Abstract
    1. Green tea (from the plant Camellia sinensis), a beverage whose consumption was started five thousand years ago in China, has important biological and pharmacological properties. 2. The beneficial effects of green tea have been attributed to the presence of phenolic compounds that possess both powerful antioxidant and free iron scavenging activities. Of all the catechins found in green tea [(-)-epicatechin-3-gallate (ECG), (-)-epigallocatechin (EGC), (-)-epicatechin (EC) and (-)-epigallocatechin-3-gallate (EGCG)], EGCG is the most abundant and powerful catechin. 3. It is widely believed that green tea may protect against death from all causes, especially cardiovascular diseases (coronary heart disease and stroke), due to the presence of catechins associat...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580199</comments>
            <pubDate>Mon, 09 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580199</guid>        </item>
        <item>
            <title>Activation of cardiac M(3)  muscarinic acetylcholine receptors has cardioprotective effects against ischaemia-induced arrhythmias.</title>
            <link>http://www.medworm.com/index.php?rid=5580201&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22224440%26dopt%3DAbstract</link>
            <description>Activation of cardiac M(3) muscarinic acetylcholine receptors has cardioprotective effects against ischaemia-induced arrhythmias.
    Clin Exp Pharmacol Physiol. 2012 Jan 7;
    Authors: Wang S, Han HM, Jiang YN, Wang C, Song HX, Pan ZY, Fan K, Du J, Fan YH, Du ZM, Liu Y
    Abstract
    1.â€‚Increasing evidence indicates the important roles of M(3) muscarinic acetylcholine receptors (M(3) mAChR) in the regulation and maintenance of cardiac function and heart disease. In the present study, we investigated whether M(3) mAChR mediates the cardioprotection against ischaemia-induced arrhythmias and the mechanisms involved. 2.â€‚Myocardial ischaemia was established in Wistar rats by occlusion of the left anterior descending coronary artery. Rats were treated with choline (choline chloride; an M...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580201</comments>
            <pubDate>Sat, 07 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580201</guid>        </item>
        <item>
            <title>Berberine ameliorates inflammation in patients with acute coronary syndrome following percutaneous coronary intervention.</title>
            <link>http://www.medworm.com/index.php?rid=5580202&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22220931%26dopt%3DAbstract</link>
            <description>Authors: Meng S, Wang LS, Huang ZQ, Zhou Q, Sun YG, Cao JT, Li YG, Wang CQ
    Abstract
    1.â€‚Inflammation is central to the pathogenesis of acute coronary syndrome (ACS) and is associated with adverse clinical outcomes after percutaneous coronary intervention (PCI). Recent in vitro work from us and others has shown the anti-inflammatory effect of berberine, a main component of the traditional Chinese medicine umbellatine. We further tested whether berberine had beneficial effect on ACS patients following PCI. 2.â€‚130 ACS patients undergoing PCI were recruited in this study. 61 patients were treated with berberine (300mg, 3 times a day, for 30 days) in addition to standard therapy while the remaining patients received standard therapy alone. Circulating inflammatory markers were measur...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580202</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580202</guid>        </item>
        <item>
            <title>The beneficial effect on myocardial perfusion of adenosine in patients treated with primary percutaneous coronary intervention for acute myocardial infarction.</title>
            <link>http://www.medworm.com/index.php?rid=5568556&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214231%26dopt%3DAbstract</link>
            <description>This study investigated the effects of intravenous adenosine on myocardial perfusion and segmental contractile function when used as an adjunct of primary PCI in patients with acute ST segment elevation myocardial infarction (STEMI). 2.â€‚Patients were randomly assigned to receive intravenous adenosine (n=35) or saline (n=34) within 12 h of STEMI. Myocardial contrast echocardiography (MCE) and velocity vector imaging (VVI) were performed 7 days after primary PCI. Serial echocardiography was performed on Days 7 and 30. 3.â€‚Capillary blood volume (A) (6.34Â±1.98 dB vs 5.64Â±1.84 dB, P=0.03) and myocardial blood velocity (Î²) (0.13Â±0.04s(-1) vs 0.1Â±0.04 s(-1) , P=0.01) were higher in the adenosine group than in control patients. Myocardial blood flow (AÃ—Î²) was 0.82Â±0.37 dB/s with adenos...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568556</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568556</guid>        </item>
        <item>
            <title>Chronic exercise partially restores the transmural heterogeneity of action potential duration in left ventricular myocytes of spontaneous hypertensive rats.</title>
            <link>http://www.medworm.com/index.php?rid=5568555&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214260%26dopt%3DAbstract</link>
            <description>Authors: Roman-Campos D, Carneiro-JÃºnior MA, PrÃ­mola-Gomes TN, Silva KA, QuintÃ£o-JÃºnior JF, Gondim AN, Duarte HL, Cruz JS, Natali AJ
    Abstract
    1.â€‚Hypertension leads to electrophysiological changes in the heart. Chronic exercise induced by a treadmill-running program (TRP) is considered as a potential non-pharmacological treatment for hypertension and may have implications in heart remodeling. However, it is not known if TRP is able to improve the electrophysiological properties of the heart in spontaneously hypertensive rats (SHR). In the present study, we tested whether TRP affects the electrical properties of left ventricular (LV) myocytes isolated from different layers of the LV wall of SHR. 2.â€‚Male SHR were divided into exercised (chronic treadmill running for 8 weeks; C...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568555</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568555</guid>        </item>
        <item>
            <title>Schematic diagram of the renal medullary endothelin system. See Nakano and Pollock, pp 104-110.</title>
            <link>http://www.medworm.com/index.php?rid=5568590&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22211564%26dopt%3DAbstract</link>
            <description>Authors: 
    Abstract
    Cover image:â€‚ Schematic diagram of the renal medullary endothelin system. See Nakano and Pollock, pp 104-110. â€¢ â€‚Ca(2+) - sensing receptors in rat myometrium â€¢ â€‚Age-induced changes in sensory neurons â€¢ â€‚Gelatinases and obesity â€¢ â€‚Timing of fructose intake affects body fat â€¢ â€‚Tanshinone IIA attenuates ET-1 expression â€¢ â€‚Frontiers in Research: Salt-Sensitive Hypertension.
    PMID: 22211564 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568590</comments>
            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568590</guid>        </item>
        <item>
            <title>Chlamydia pneumoniae induces a pro-inflammatory phenotype in murine vascular smooth muscle cells independently of elevating reactive oxygen species.</title>
            <link>http://www.medworm.com/index.php?rid=5568589&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22211630%26dopt%3DAbstract</link>
            <description>In conclusion, C. pneumoniae infection increases ROS production in VSMCs independently of Nox activity. While elevated ROS production appears to serve a protective role by limiting the spread of infection, we speculate that this response will be detrimental over the long-term by causing oxidative stress and a smouldering inflammatory response by maintaining C. pneumoniae persistence within the cell. Â© 2011 The Authors Clinical and Experimental Pharmacology and Physiology Â© 2011 Blackwell Publishing Asia Pty Ltd.
    PMID: 22211630 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568589</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568589</guid>        </item>
        <item>
            <title>CB1 cannabinoid receptor mediates glucocorticoid effects on hormone secretion induced by volume and osmotic changes.</title>
            <link>http://www.medworm.com/index.php?rid=5568587&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22211674%26dopt%3DAbstract</link>
            <description>Authors: Ruginsk S, Uchoa E, Elias L, Antunes-Rodrigues J
    Abstract
    This work provides the first in vivo evidence that the CB1 cannabinoid receptor mediates dexamethasone effects on hormone release induced by changes in circulating volume and osmolality in male adult rats. The CB1 antagonist rimonabant potentiated oxytocin (OT) secretion induced by hypertonic extracellular volume expansion (H-EVE) and completely reversed the inhibitory effects of dexamethasone administration under the same experimental conditions. These data suggest that the modulation of OT release by glucocorticoids is mediated by the CB1 receptor. Although dexamethasone did not affect vasopressin (AVP) secretion induced by H-EVE, the administration of rimonabant potentiated AVP release in response to the same sti...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568587</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568587</guid>        </item>
        <item>
            <title>Stat3 - Linking inflammation to (gastrointestinal) tumourigenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5568586&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22211709%26dopt%3DAbstract</link>
            <description>Authors: Ernst M, Putoczki TL
    Abstract
    Tumourigenesis is a multistage process comprising initiation, promotion and progression that is governed by cumulative (epi-)genetic changes. However, tumour initiation, triggered by mutations in proto-oncogenes and/or tumour suppressor genes, is insufficient for the development of cancers. Tumour promotion often depends on the interaction between initiated cells and the microenvironment where excessive abundance of inflammatory mediators, including those of the interleukin (IL-)6/gp130 family, promote their expansion. The activity of most soluble mediators ultimately converge on tumour cells through activation of the latent transcription factors NF-ÎºB and Stat3 to enhance survival of neoplastic cells. In addition, Stat3 also promotes tumour ...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568586</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568586</guid>        </item>
        <item>
            <title>Resveratrol induces gastric cancer cell apoptosis via ROS, but independent of sirtuin1.</title>
            <link>http://www.medworm.com/index.php?rid=5568582&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22211760%26dopt%3DAbstract</link>
            <description>Authors: Wang Z, Li W, Meng X, Jia B
    Abstract
    The currently available chemotherapeutic regimens against gastric cancer are not very effective, leading to high recurrence and poor survival. Resveratrol (RES) is a naturally occurring polyphenol with potent apoptosis-inducing activity. However, the mechanism underlying these findings remains unknown. Human gastric adenocarcinoma SGC7901 cells were treated with RES (0, 25, 50, 100, and 200 Î¼M) for 48 h, and the cellular apoptosis as well as DNA damage were determined. In certain experiments, the cells were incubated with superoxide dismutase (100 U/ml), catalase (300 U/ml), or sirtinol (10 Î¼M) to determine the role of reactive oxygen species and sirtuin1 in resverartol-induced cellular apoptosis. Treatment with RES (50-200 Î¼M) for 4...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568582</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Essential but toxic: Controlling the flux of iron in the body.</title>
            <link>http://www.medworm.com/index.php?rid=5568574&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22211782%26dopt%3DAbstract</link>
            <description>Authors: Anderson GJ, Wang F
    Abstract
    1.â€‚Iron is an essential nutrient, but, since it is toxic when present in excess, its levels in the body are tightly controlled. This regulation is effected by controlling the release of iron into the plasma. 2.â€‚Most iron enters the plasma from macrophages which recycle iron from senescent erythrocytes, but dietary iron absorption and the release of hepatocyte storage iron are other major sources. 3.â€‚Cellular iron export is mediated by the membrane iron transporter ferroportin 1, in conjunction with an iron oxidase. Hephaestin provides this oxidase activity in the intestine, whereas ceruloplasmin is the oxidase used by most other tissues. 4.â€‚The liver-derived peptide hepcidin binds to ferroportin 1 and removes it from the cell surface, t...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568574</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Newcastle Disease Virus: a Promising Agent for Tumor Immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=5568559&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22211810%26dopt%3DAbstract</link>
            <description>Authors: Zhao L, Liu H
    Abstract
    Malignant tumors are a major cause of mortality in humans. Currently employed therapeutic regimens have not much improved survival rates of patients suffering from malignant tumors because of their limited efficacy and side effects. A novel therapeutic approach employs the use of the Newcastle Disease Virus (NDV) that represents an attractive new tool for tumor immunotherapy. The aim of the present review is to highlight the mechanisms and advances that are likely to have considerable impact on NDV virotherapy. There exists significant evidence regarding the oncolytic effects of NDV suggesting its potential use in the treatment of various tumors. Furthermore, clinical trials have suggested that several NDV strains have the potential for cancer viroth...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568559</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568559</guid>        </item>
        <item>
            <title>TGF-Î²/Smad signaling in diabetic nephropathy.</title>
            <link>http://www.medworm.com/index.php?rid=5568558&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22211842%26dopt%3DAbstract</link>
            <description>Authors: Lan HY
    Abstract
    Diabetic nephropathy (DN) is a major diabetic complication and is mediated by TGF-Î²1 via the Smad-dependent and independent signaling pathways. Under diabetic conditions, many pro-fibrotic factors, such as advanced glycation end products (AGE) and angiotensin II can also activate the Smad signaling pathway via the ERK/p38 MAP kinase-Smad signaling cross-talk pathway. Thus, Smads act as signal integrators and interact with other signaling pathways to mediate DN. In the context of renal fibrosis, Smad3 is pathogenic, but Smad2 is protective. Deletion of Smad3 inhibits, but disruption of Smad2 upregulates CTGF and VEGF expression and promotes epithelial-myofibroblast transition (EMT), and endothelial-myofibroblast transition (EndoMT). Smad7 plays a protective...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568558</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568558</guid>        </item>
        <item>
            <title>Low-dose celecoxib improves coronary function after acute myocardial ischaemia in rabbits.</title>
            <link>http://www.medworm.com/index.php?rid=5568557&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22211872%26dopt%3DAbstract</link>
            <description>In conclusion, the experimental evidences suggest that celecoxib exerted its protective effect in a COX-independent manner. Â© 2011 The Authors Clinical and Experimental Pharmacology and Physiology Â© 2011 Blackwell Publishing Asia Pty Ltd.
    PMID: 22211872 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568557</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568557</guid>        </item>
        <item>
            <title>Î²-1,3-glucan given orally modulates immunomyelopoietic activity and enhances the resistance of tumor-bearing mice.</title>
            <link>http://www.medworm.com/index.php?rid=5538642&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22150790%26dopt%3DAbstract</link>
            <description>Authors: Torello CO, Souza-Queiroz J, Queiroz ML
    Abstract
    1.â€‚Î²-glucans have been reported as potent adjuvant to stimulate innate and adaptive immune responses. The aim of this study was to determine the immunohematopoietic effects of the oral administration of Imunoglucan(Â®) in normal and Ehrlich ascites tumor (EAT)-bearing mice. 2.â€‚EAT-bearing mice were treated orally with doses of 250, 500 and 1000 mg/kg/day of Imunoglucan(Â®) (Î²-1,3-glucan extracted from Saccharomyces cerevisae) for 18 consecutive days. Treatment started 10 days prior and ended 8 days after tumor inoculation. 3.â€‚Imunoglucan(Â®) (500 and 1000 mg/kg) enhances the life span of EAT-bearing mice and prevented myelosuppression and splenomegaly caused by tumor, due to increased numbers of granulocyte-macrophag...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538642</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538642</guid>        </item>
        <item>
            <title>Hypoxia-inducible Factor 1 Activation from aP2(Fabp4)-Cre Mediated Knockout of Von Hippel-Lindau Gene Leads to Embryonic Lethality.</title>
            <link>http://www.medworm.com/index.php?rid=5538641&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22150821%26dopt%3DAbstract</link>
            <description>Authors: Zhang J, Wang Y, Gao Z, Yun Z, Ye J
    Abstract
    1.â€‚VHL protein (pVHL), an E3 ubiquitin ligase from the Vhl gene, inhibits the transcriptional activity of HIF-1Î± in cells. To gain insight into the HIF-1Î± signaling pathway in adipose tissue, we conducted a study to generate fat-specific Vhl knockout mice. 2.â€‚Cre/loxP technology was used in the knockout study. The mice carrying floxed-Vhl alleles were crossed with aP2-Cre mice, in which the Cre gene is driven by the aP2 (FABP4) gene promoter. 3.â€‚The homozygous knockout (Vhl(f/f) -Cre) mice exhibited embryonic lethality at E14.5 to E18.5. The homozygous embryos suffered from hemorrhages in the brain and liver. HIF-1Î± protein and its target gene protein, vascular endothelial growth factor (VEGF), were increased in the bra...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538641</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538641</guid>        </item>
        <item>
            <title>Role of Renal Medullary Oxidative/Carbonyl stress in Salt Sensitive Hypertension and Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5538644&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22150746%26dopt%3DAbstract</link>
            <description>Authors: Mori T, Ogawa S, Cowely AW, Ito S
    Abstract
    Salt sensitive hypertension is commonly associated with diabetes, obesity and chronic kidney disease. This review focused on renal mechanisms involved in the development of these hypertension. The renal medullary circulation plays an important role in the development of salt sensitive hypertension. In vivo animal studies have demonstrated that the balance between nitric oxide (NO) and reactive oxygen species (ROS) in the renal medulla is an important element of salt sensitive hypertension. The medullary thick ascending limb of Henle (mTAL) in the outer medulla is an important source of NO and ROS production and we have explored the mechanisms that stimulate their production and consequences of NO, O(2)       (-) , and H(2) O(2) up...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538644</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538644</guid>        </item>
        <item>
            <title>Targeting gaseous molecules to protect against cerebral ischaemic injury: Mechanisms and prospects.</title>
            <link>http://www.medworm.com/index.php?rid=5538643&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22150768%26dopt%3DAbstract</link>
            <description>Authors: Zhou J, Wu PF, Wang F, Chen JG
    Abstract
    1.â€‚Ischaemic brain injury is a leading cause of death and disability in many countries. However, the pathological mechanisms underlying ischaemic brain injury, including oxidative stress, calcium overload, excitotoxicity and neuronal apoptosis, are perplexing and this makes it difficult to find effective novel drugs for the treatment of the condition. 2.â€‚Recently, gaseous molecules such as nitric oxide (NO), carbon monoxide (CO), hydrogen sulphide (H(2) S) and hydrogen (H(2) ) have attracted considerable interest because of their physiological and pathophysiological roles in various body systems. Emerging evidence indicates that gaseous molecules are involved in the pathological processes of ischaemic brain damage. 3.â€‚In the pr...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538643</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538643</guid>        </item>
        <item>
            <title>The role of chemical and mechanical stimuli in mediating bone fracture healing.</title>
            <link>http://www.medworm.com/index.php?rid=5496338&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22142430%26dopt%3DAbstract</link>
            <description>Authors: Zhang L, Richardson M, Mendis P
    Abstract
    Bone is a remarkable living tissue that provides a framework for animal body support and motion. However, under excessive loads and deformations, bone is prone is to damage through fracture. Furthermore, once the bone is weakened by osteoporosis, bone fracture can occur even after only minimal trauma. Various techniques have been developed to treat bone fractures. Successful treatment outcomes depend on a fundamental understanding of the biochemical and biomechanical environments of the fracture site. Various cell types (e.g., mesenchymal stem cells, chondrocytes, osteoblasts, and osteoclasts) within the fracture site tightly control the healing process by responding to the chemical and mechanical microenvironment. However, these me...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5496338</comments>
            <pubDate>Mon, 05 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5496338</guid>        </item>
        <item>
            <title>Presenting data: can you follow a recipe?</title>
            <link>http://www.medworm.com/index.php?rid=5463392&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22118575%26dopt%3DAbstract</link>
            <description>Authors: Drummond GB, Tom BD
    PMID: 22118575 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5463392</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5463392</guid>        </item>
        <item>
            <title>Potential mechanisms by which adipose tissue-derived adipokines cause cardiovascular disease. See Li et al., pp 888-896.</title>
            <link>http://www.medworm.com/index.php?rid=5463391&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22118576%26dopt%3DAbstract</link>
            <description>Authors: 
    Abstract
    Cover image:â€‚ Potential mechanisms by which adipose tissue-derived adipokines cause cardiovascular disease. See Li et al., pp 888-896. â€¢ â€‚Contraction and fatigue oxidant status â€¢ â€‚Taurine suppresses LOX-1 expression â€¢ â€‚Multivessel versus single vessel spasm â€¢ â€‚Colour Doppler and cure of vein insufficiency â€¢ â€‚P450 reductase and ROS generation â€¢ â€‚Frontiers in Research: Adipokines and Cardiovascular Disease.
    PMID: 22118576 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5463391</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5463391</guid>        </item>
        <item>
            <title>Early origins of heart disease: Low birth weight and determinants of cardiomyocyte endowment.</title>
            <link>http://www.medworm.com/index.php?rid=5463388&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22126336%26dopt%3DAbstract</link>
            <description>Authors: Botting KJ, Wang KC, Padhee M, McMillen IC, Summers-Pearce B, Rattanatray L, Cutri N, Posterino GS, Brooks DA, Morrison JL
    Abstract
    1.â€‚World-wide epidemiological and experimental animal studies demonstrate that adversity in fetal life, resulting in intrauterine growth restriction (IUGR), programs the offspring for a greater susceptibility to ischemic heart disease and heart failure in adult life. 2.â€‚After cardiogenesis, cardiomyocyte endowment is determined by a range of hormones and signalling pathways that regulate cardiomyocyte proliferation, apoptosis and the timing of multinucleation/terminal differentiation. 3.â€‚The small fetus may have reduced cardiomyocyte endowment due to the impact of suboptimal intrauterine environment on the signalling pathways that regula...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5463388</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5463388</guid>        </item>
        <item>
            <title>Targeting metabolic inflammation in Parkinson's disease: Implications for prospective therapeutic strategies.</title>
            <link>http://www.medworm.com/index.php?rid=5463387&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22126374%26dopt%3DAbstract</link>
            <description>Authors: Lu M, Hu G
    Abstract
    1.â€‚Parkinson's disease (PD) is one of the most common neurodegenerative disorders and is characterized by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Although the aetiology of PD has not been clarified as yet, it believed that ageing, diet, diabetes and adiposity are associated with PD. 2.â€‚Type 2 diabetes and lipid abnormalities share multiple common pathophysiological mechanisms with PD. In particular, inflammation plays a critical role in the destruction of both pancreatic islet Î²-cells and dopaminergic neurons in the substantia nigra. Emerging evidence indicates that dysfunctions of energy metabolism evoke metabolic inflammation, which differs to the narrow concept of inflammation, participating in systemic ...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5463387</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5463387</guid>        </item>
        <item>
            <title>Assessment of Endothelial Function in Atrial Fibrillation: Utility of Peripheral Arterial Tonometry.</title>
            <link>http://www.medworm.com/index.php?rid=5463390&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22118631%26dopt%3DAbstract</link>
            <description>Authors: Wong CX, Lim HS, Schultz CD, Sanders P, Worthley MI, Willoughby SR
    Abstract
    1. Endothelial function is an independent predictor of adverse cardiovascular outcomes. The evaluation of endothelial function via vessel diameters or blood flow changes may be inaccurate during atrial fibrillation (AF) due to non-uniform stroke volumes. 2. Using peripheral arterial tonometry, fifty patients with AF (25 in AF, 25 in sinus rhythm) had digital pulse amplitudes assessed at baseline and during reactive hyperaemia. Hyperaemic responses were compared over varying measurement durations (5, 10 and 15 beats; 30 seconds; and 1 to 10 minutes) to determine the optimal measurement durations. 3. Endothelial responses were significantly decreased (endothelial dysfunction) in patients in AF compar...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5463390</comments>
            <pubDate>Thu, 24 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5463390</guid>        </item>
        <item>
            <title>Discovery of Curcumin, a Component of the Golden Spice, and Its Miraculous Biological Activities.</title>
            <link>http://www.medworm.com/index.php?rid=5463389&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22118895%26dopt%3DAbstract</link>
            <description>Authors: Gupta SC, Patchva S, Koh W, Aggarwal BB
    Abstract
    1. Curcumin is the active ingredient of the dietary spice turmeric and has been consumed for medicinal purposes for thousands of years. Modern science has shown that curcumin modulates various signaling molecules, including inflammatory molecules, transcription factors, enzymes, protein kinases, protein reductases, carrier proteins, cell survival proteins, drug resistance proteins, adhesion molecules, growth factors, receptors, cell-cycle regulatory proteins, chemokines, DNA, RNA, and metal ions. 2. Because of this polyphenol's potential to modulate multiple signaling molecules, it has been reported to possess pleiotropic activities. First shown to have anti-bacterial activity in 1949, curcumin has since been shown to have a...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5463389</comments>
            <pubDate>Thu, 24 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5463389</guid>        </item>
        <item>
            <title>Editorial Update 2012.</title>
            <link>http://www.medworm.com/index.php?rid=5463393&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22098074%26dopt%3DAbstract</link>
            <description>Authors: Evans RG
    PMID: 22098074 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5463393</comments>
            <pubDate>Sun, 20 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5463393</guid>        </item>
        <item>
            <title>Scutellarin inhibits translocation of protein kinase C in diabetic thoracic aorta of the rat.</title>
            <link>http://www.medworm.com/index.php?rid=5427975&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22092277%26dopt%3DAbstract</link>
            <description>Authors: Su Y, Liu W, Ma L, Liu X, Liu Z, Zhu B
    Abstract
    1.â€‚The aims of this study were to explore the effect of scutellarin (Scu) on protein kinase C (PKC) translocation caused by diabetic conditions in diabetic rat thoracic aorta and phorbol-12-myristate-13-acetate (PMA) treatment of cultured thoracic aortic smooth muscle cells. 2.â€‚Diabetes in rats was induced by streptozotozin. The Scu-treated group was made up by diabetic rats administrated through intragavage Scu (0.1g/kg) and an aminoquanidine (AG) -treated group was produced through dietary supplement of 0.1% AG from week-1 of diabetes induction. Thoracic aortic smooth muscle cells were isolated and cultured. The cell fractionations were obtained through ultracentrifugation. The activity of PKC was assayed using an enzym...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427975</comments>
            <pubDate>Wed, 16 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427975</guid>        </item>
        <item>
            <title>Roles of cocaine- and amphetamine-regulated transcript in the central nervous system.</title>
            <link>http://www.medworm.com/index.php?rid=5427978&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22077697%26dopt%3DAbstract</link>
            <description>Authors: Zhang M, Han L, Xu Y
    Abstract
    1.â€‚Cocaine- and amphetamine-regulated transcript (CART), first isolated by from the ovine hypothalamus, is a potential neurotransmitter widely distributed throughout the central and peripheral nervous systems, as well as in endocrine cells in the pituitary and adrenal glands, pancreatic islets and stomach. 2.â€‚Numerous studies have established the role of CART in food intake, maintenance of bodyweight, stress control, reward and pain transmission. Recently, it was demonstrated that CART, as a neurotrophic peptide, had a cerebroprotective against focal ischaemic stroke and inhibited the neurotoxicity of Î²-amyloid protein, which resulted in the concern of CART in the central nervous system (CNS) and neurological diseases. 3.â€‚In fact, littl...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427978</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427978</guid>        </item>
        <item>
            <title>A primer for biomedical scientists on how to execute Model II linear regression analysis.</title>
            <link>http://www.medworm.com/index.php?rid=5427977&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22077731%26dopt%3DAbstract</link>
            <description>Authors: Ludbrook J
    Abstract
    1.â€‚There are two very different ways of executing linear regression analysis. One is Model I, when the x values are fixed by the experimenter. The other is Model II, in which the x values are free to vary and are subject to error. 2.â€‚I have received numerous complaints from biomedical scientists that they have great difficulty in executing Model II linear regression analysis. 3.â€‚This may explain the results of a Google Scholar search, which showed that the authors of articles in journals of physiology, pharmacology and biochemistry rarely use Model II regression analysis. 4.â€‚I repeat my previous arguments in favour of using least products linear regression analysis for Model II regressions. 5.â€‚I review three methods for executing ordinary leas...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427977</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427977</guid>        </item>
        <item>
            <title>Vagal nerve modulation: A promising new therapeutic approach for cardiovascular diseases.</title>
            <link>http://www.medworm.com/index.php?rid=5427976&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22077771%26dopt%3DAbstract</link>
            <description>In conclusion, vagal nerve activation may be a promising new therapeutic approach for the treatment of cardiovascular diseases.
    PMID: 22077771 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427976</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427976</guid>        </item>
        <item>
            <title>Mitochondria as a Source and Target of Lipid Peroxidation Products in Healthy and Diseased Heart.</title>
            <link>http://www.medworm.com/index.php?rid=5427979&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22066679%26dopt%3DAbstract</link>
            <description>Authors: Anderson EJ, Katunga LA, Willis MS
    Abstract
    1.â€‚The heart is a highly oxidative organ in which cardiomyocyte turnover is virtually absent, making it particularly vulnerable to accumulation of lipid peroxidation products (LPPs) formed as a result of oxidative damage. 2.â€‚Reactive oxygen and nitrogen species are the most common electrophiles formed during lipid peroxidation and lead to the formation of both stable and unstable lipid peroxidation products (LPPs). Of the LPPs formed, highly reactive aldehydes are a well-recognized causative factor in aging and age-associated diseases including cardiovascular disease and diabetes. 3.â€‚Recent studies have identified that the mitochondria are both a primary source and target of LPPs, with specific emphasis on aldehydes in card...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427979</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427979</guid>        </item>
        <item>
            <title>Inhibition of 11Î²-Hydroxysteroid Dehydrogenase I by carbenoxolone affects glucose homeostasis and obesity in db/db mice.</title>
            <link>http://www.medworm.com/index.php?rid=5427980&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22060140%26dopt%3DAbstract</link>
            <description>Authors: Dhanesha N, Joharapurkar A, Shah G, Kshirsagar S, Dhote V, Sharma A, Jain M
    Abstract
    1 â€‚Elevated 11beta-HSD1 in liver and adipose tissue is one of the major causes of metabolic syndrome. High expression of 11beta-HSD1 contributes significantly to the diabetic phenotype in db/db mice. The purpose of the present study was to test the effect of pharmacological inhibition of 11beta-HSD1 inhibition by carbenoxolone in db/db mice, a genetic model of diabetes. 2 â€‚Inhibition of 11beta-HSD1 by carbenoxolone was evaluated in liver homogenates. The conversion of cortisone to cortisol was reduced by 21% at 0.4Î¼M, 48% at 0.8 Î¼M, 82% at 1.6 Î¼M, and 95% at 3.2 Î¼M, of carbenoxolone, respectively. 3 â€‚Female db/db mice were dosed orally with carbenoxolone (10, 25 and 50 mg/kg, twi...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427980</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427980</guid>        </item>
        <item>
            <title>Unmasking the Janus Faces of Autophagy in Obesity-Associated Insulin Resistance and Cardiac Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=5427981&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22053892%26dopt%3DAbstract</link>
            <description>Authors: Xu X, Ren J
    Abstract
    1.â€‚Autophagy is an intracellular, lysosomal-dependent process involved in the turnover of long-lived proteins, damaged organelles, and other subcellular structures. The autophagic process is known to play an essential role in the maintenance of cellular homeostasis and results from recent studies also indicate an important role in the pathogenesis of human diseases including cancer, cardiovascular diseases, obesity, diabetes mellitus and aging. 2.â€‚Because of the pivotal role of autophagy in the regulation of adipogenesis, obesity and insulin sensitization, research efforts have focused on elucidating the role of autophagy in metabolic syndrome. The mammalian target of rapamycin (mTOR) is a key regulator of cell growth and is characterized by a comp...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427981</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427981</guid>        </item>
        <item>
            <title>Discontinuous tight junctions in the ipsilateral thalamus after middle cerebral artery occlusion in rat. See Li et al, pp 776-782.</title>
            <link>http://www.medworm.com/index.php?rid=5363531&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22017751%26dopt%3DAbstract</link>
            <description>Authors: 
    Abstract
    Cover image:â€‚ Discontinuous tight junctions in the ipsilateral thalamus after middle cerebral artery occlusion in rat. See Li et al, pp 776-782. â€¢ â€‚Pumping ions â€¢ â€‚Pet ownership and cardiovascular risk â€¢ â€‚Propofol and LPS-induced kidney injury â€¢ â€‚Tight junction lesion in thalamus â€¢ â€‚Dalteparin increases ROTEM(Â®) parameters.
    PMID: 22017751 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363531</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363531</guid>        </item>
        <item>
            <title>Timing of Fructose Intake: An Important Regulator of Adiposity.</title>
            <link>http://www.medworm.com/index.php?rid=5363528&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22032284%26dopt%3DAbstract</link>
            <description>Authors: Morris M, Araujo IC, Pohlman RL, Marques MC, Rodwan NS, Farah VM
    Abstract
    1.â€‚Overconsumption of fructose produces glucose intolerance, autonomic abnormalities, and renal dysfunction and may be related to the worldwide epidemic of obesity and diabetes. 2.â€‚Experiments were conducted to determine whether the time period (light or dark) of fructose consumption influenced the pathological consequences. C57BL mice were given standard chow and assigned to one of three groups: Controlâ€ƒ(n=10, water 24h); FL (n=11, 10% fructose solution during 12h light period); and FD (n=11, 10% fructose solution during 12h dark period). 3.â€‚There was a time-related increase in body weight (BW) (p&amp;lt;0.0001). Body fat as measured with Echo-MRI showed a greater increase in the FL group as com...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363528</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363528</guid>        </item>
        <item>
            <title>Tanshinone IIA Attenuates Cyclic Strain-Induced Endothelin-1 Expression in Human Umbilical Vein Endothelial Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5363527&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22032308%26dopt%3DAbstract</link>
            <description>This study provides important new insights into the molecular pathways that may contribute to the beneficial effects of tanshinone IIA in the cardiovascular system.
    PMID: 22032308 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363527</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363527</guid>        </item>
        <item>
            <title>Effect of gelatinase inhibition on adipogenesis and adipose tissue development.</title>
            <link>http://www.medworm.com/index.php?rid=5363529&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22026722%26dopt%3DAbstract</link>
            <description>Authors: Van Hul M, Bauters D, Himmelreich U, Kindt N, Noppen B, Vanhove M, Lijnen HR
    Abstract
    1.â€‚The potential of the matrix metalloproteinase (MMP) inhibitor ABT-518 to affect preadipocyte differentiation in vitro and adipose tissue development in vivo was investigated using mouse models of adipogenesis and obesity. 2.â€‚Differentiation of 3T3-F442A preadipocytes into mature adipocytes was enhanced in a dose-dependent manner by addition of ABT-518. This was associated with increased expression of the adipogenic markers aP2, PPAR-Î³ and adiponectin. 3.â€‚Feeding 5 weeks old male wild-type mice with a high fat diet with or without addition of ABT-518 (to achieve a dose of 100 mg/kg/day) for 16 weeks, resulted in a significant reduction of body weight throughout the experimental p...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363529</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363529</guid>        </item>
        <item>
            <title>Age-related changes in TASK channel expression in rat dorsal root ganglion neurons.</title>
            <link>http://www.medworm.com/index.php?rid=5363532&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22017174%26dopt%3DAbstract</link>
            <description>This study was performed to identify postnatal changes in the expression of TASK channels in DRG neurons. 2 â€‚TASK channel (TASK-1, TASK-2, and TASK-3) expression levels were compared between neonatal (postnatal day 1 or 2, P1-2) and adult (postnatal day 120, P120) rat DRGs using semiquantitative PCR, western blot analysis, immunostaining, and the patch-clamp technique. 3 â€‚The mRNA and protein levels of TASK-2 were down-regulated, whereas TASK-3 was up-regulated in the P120 DRGs. Changes in TASK-1 expression levels were not consistent in terms of mRNA and protein expression. Single-channel recordings showed very low TASK-2- and TASK-3-like channel expression in P1-2 DRG neurons (âˆ¼10% in TASK-2 and âˆ¼3% in TASK-3). In P120 DRGs, the detection of TASK-2-like channels decreased, whereas...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363532</comments>
            <pubDate>Fri, 21 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363532</guid>        </item>
        <item>
            <title>Andrographolide and its analogues: versatile bioactive molecules for combating inflammation and cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5363530&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22017767%26dopt%3DAbstract</link>
            <description>Authors: Lim CW, Chan TK, Ng DS, Sagineedu SR, Stanslas J, Wong WF
    Abstract
    1.â€‚Andrographis paniculata (Burm.f.) Nees is a herbaceous plant in the family of Acanthaceae commonly known as &quot;King of Bitters&quot;. It is widely used for centuries in Asian countries like China, India, Thailand and Malaysia for the treatment of sore throat, flu and upper respiratory tract infection. 2.â€‚Andrographolide, 14-deoxy-11,12-didehydroandrographolide and neoandrographolide are examples of the major labdane diterpenoids isolated from A. paniculata. These bioactive molecules have displayed varying degrees of anti-inflammatory and anti-cancer activities in both in-vitro and in-vivo experimental models of inflammation and cancer. 3.â€‚Extensive libraries of andrographolide analogues have been synthesi...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363530</comments>
            <pubDate>Fri, 21 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363530</guid>        </item>
        <item>
            <title>Immunohistochemical and functional studies on calcium-sensing receptors in rat uterine smooth muscle.</title>
            <link>http://www.medworm.com/index.php?rid=5363534&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22013999%26dopt%3DAbstract</link>
            <description>Authors: Pistilli MJ, Petrik JJ, Holloway AC, Crankshaw DJ
    Abstract
    1.â€‚Activation of calcium-sensing receptors (CaS) leads to relaxation of vascular smooth muscle. However, the role of CaS in uterine smooth muscle is unknown. Therefore the purpose of this study was to investigate the expression and function of CaS in the uterus. 2.â€‚The expression of CaS in the oestrogen-dominated rat's uterus was investigated using immunohistochemistry. The effects of putative CaS ligands on oxytocin-induced contractions of longitudinally-oriented uterine strips from oestrogen-dominated rats were determined at reduced extracellular Ca(2+) concentrations using conventional organ bath techniques. 3.â€‚Immunohistochemical evidence showed the presence of CaS in endometrium and the smooth muscle lay...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363534</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363534</guid>        </item>
        <item>
            <title>Cardiorenal Syndrome: Pathophysiology, Preclinical Models, Management and Potential Role of Uraemic Toxins.</title>
            <link>http://www.medworm.com/index.php?rid=5363533&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22014026%26dopt%3DAbstract</link>
            <description>Authors: Liu S, Lekawanvijit S, Kompa AR, Wang BH, Kelly DJ, Krum H
    Abstract
    1.â€‚Cardiorenal syndrome (CRS) describes the primary dysfunction in either the kidney or heart that initiates the combined impairments of both organs. The heart and the kidney exert reciprocal control of the respective function to maintain constant blood volume and organ perfusion under continuously changing conditions. 2.â€‚The pathophysiology of CRS is not fully understood, but appears to be caused by a complex combination of hemodynamic, neurohormonal, immunological and biochemical feedback pathways. Amongst these pathways, the contributory role of uraemic toxins that accumulate in CRS has been under-explored. One such toxin, indoxyl sulfate, has been found to have direct adverse effects on relevant ca...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363533</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363533</guid>        </item>
        <item>
            <title>Protective Effect of Ligustrazine Against Myocardial Ischaemia Reperfusion in Rats: Role Of Endothelial Nitric Oxide Synthase.</title>
            <link>http://www.medworm.com/index.php?rid=5363537&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22004361%26dopt%3DAbstract</link>
            <description>Authors: Lv L, Jiang SS, Xu J, Gong JB, Cheng Y
    Abstract
    1. The aim of the present study was to determine whether ligustrazine (2,3,5,6-tetramethylpyrazine, TMP) exerts a cardioprotective effect during myocardial ischaemia reperfusion (IR), and to investigate the underlying mechanisms and the role of endothelial nitric oxide synthase (eNOS) in cardioprotection. 2. Sprague-Dawley rats were divided into a sham group and 5 IR groups: IR control, TMP pre-treated, TMP+wortmannin [a phosphatidylinositol 3-kinase (PI3K) inhibitor], L-NAME (a NOS inhibitor), and TMP+L-NAME. IR was produced by 35 min of regional ischaemia followed by 120 min of reperfusion. Myocardial infarct size, oxidative stress, myocardial apoptosis, nitric oxide (NO) production, and expression of phosphorylated protein...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363537</comments>
            <pubDate>Mon, 17 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363537</guid>        </item>
        <item>
            <title>Effects of magnolol on vascular contraction in rat aortic rings.</title>
            <link>http://www.medworm.com/index.php?rid=5363536&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22004427%26dopt%3DAbstract</link>
            <description>In conclusion, magnolol reduces vascular contraction through inhibition of RhoA/Rho-kinase pathway in endothelium-denuded rat aorta.
    PMID: 22004427 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363536</comments>
            <pubDate>Mon, 17 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363536</guid>        </item>
        <item>
            <title>Active chemicalâ€ƒcompounds of Traditional Chinese Medicine Herba leonuri: implications for cardiovascular diseases.</title>
            <link>http://www.medworm.com/index.php?rid=5363535&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22004449%26dopt%3DAbstract</link>
            <description>Authors: Liu XH, Pan LL, Zhu YZ
    Abstract
    1 Herba leonuri, a famous Chinese traditional medicine, has a long history of development and application in China. In particular, Herba leonuri has been widely used in gynecological and obstetrical disorders for thousands of years, but recent studies have shown that the effects of Herba leonuri are versatile. 2 Herba leonuri contains several active components including alkaloids, flavonoids, diterpenes compounds, fatty acid, etc. The recent studies have shown that the beneficial effects of these molecules are versatile, such as coronary artery disease and cerebral ischemia. These molecules may become novel candidates for drug discovery and development. 3 This review aims to give an overview of the chemical composition, focusing on biologica...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363535</comments>
            <pubDate>Mon, 17 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363535</guid>        </item>
        <item>
            <title>Regulation of growth factors associated cell migration by C-phycocyanin scaffold in dermal wound healing.</title>
            <link>http://www.medworm.com/index.php?rid=5363538&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21995435%26dopt%3DAbstract</link>
            <description>In conclusion, biodegradable C-pc scaffold may help to serve as an alternate scaffold material for wound healing.
    PMID: 21995435 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363538</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363538</guid>        </item>
        <item>
            <title>Effect of Fluvoxamine on the Pharmacokinetics of Zolpidem: A Two-Treatment Period Study in Healthy Volunteers.</title>
            <link>http://www.medworm.com/index.php?rid=5363539&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21985609%26dopt%3DAbstract</link>
            <description>Authors: Vlase L, Popa A, Neag M, Muntean D, Achim M, LeucuÅ£a SE
    Abstract
    1 â€‚Our objective was to evaluate a possible pharmacokinetic interaction between zolpidem and fluvoxamine in healthy volunteers. 2 â€‚The study consisted of 2 periods: Period 1 (Reference), when each volunteer received a single dose of 5 mg zolpidem and Period 2 (Test), when each volunteer received a single dose of 5 mg zolpidem and 100 mg fluvoxamine. Between the two periods, the subjects were treated for 6 days with a single daily dose of 100 mg fluvoxamine. 3 â€‚Pharmacokinetic parameters of zolpidem administered in each treatment period were calculated using non-compartmental analysis and the data from two periods were compared to determine statistically significant differences. 4 â€‚In the two periods ...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363539</comments>
            <pubDate>Mon, 10 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363539</guid>        </item>
        <item>
            <title>Aberrant Regulation and Function of Src-Family Tyrosine Kinases - their potential contributions to Glutamate-Induced Neurotoxicity.</title>
            <link>http://www.medworm.com/index.php?rid=5363543&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21973029%26dopt%3DAbstract</link>
            <description>Authors: Hossain MI, Kamaruddin MA, Cheng HC
    Abstract
    1 â€‚Excitotoxicity, a major cause of neuronal death in acute and chronic neurodegenerative diseases and conditions such as stroke and Parkinson's disease, is initiated by over-stimulation of glutamate receptors leading to calcium overload in the affected neurons. The sustained high concentration of intracellular calcium constitutively activates a host of enzymes, notably the calcium-activated proteases calpains, neuronal nitric oxide synthase (nNOS) and NADPH oxidase (NOX) to antagonize the cell survival signalling pathways and induce cell death. 2 â€‚Upon over-activation by calcium, calpains catalyzes limited proteolysis of specific cellular proteins to modulate their functions; nNOS produces excessive amount of nitric oxide w...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363543</comments>
            <pubDate>Tue, 04 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363543</guid>        </item>
        <item>
            <title>Effects of transient overexpression or knockdown of cytochrome P450 reductase on reactive oxygen species generation and hypoxia-reoxygenation injury in liver cells.</title>
            <link>http://www.medworm.com/index.php?rid=5363542&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21973081%26dopt%3DAbstract</link>
            <description>Authors: Pillai VC, Snyder RO, Gumaste U, Thekkumkara TJ, Mehvar R
    Abstract
    1 â€‚Literature data suggest that the electron-donating enzyme cytochrome P450 reductase (CPR) may act as a source of reactive oxygen species (ROS). However, the role of CPR in pathophysiologic conditions associated with oxidative stress is unknown. The aim of this study was to study the role of CPR in the generation of ROS and cellular injury under basal conditions and after simulated in vitro ischemia-reperfusion (IR). 2 â€‚Plasmid DNA or siRNA approaches were used to transiently overexpress or knockdown human CPR gene in rat liver epithelial (WB-F344) or human hepatoblastoma (HepG2) cells, respectively. The generation of ROS and/or cellular injury was then studied under the basal conditions and after sim...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363542</comments>
            <pubDate>Tue, 04 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363542</guid>        </item>
        <item>
            <title>Leptin and the regulation of endothelial function in physiological and pathological conditions.</title>
            <link>http://www.medworm.com/index.php?rid=5363541&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21973116%26dopt%3DAbstract</link>
            <description>Authors: BeÅ‚towski J
    Abstract
    1 â€‚Obesity and the accompanying metabolic syndrome are among the most important causes of cardiovascular pathologies associated with endothelial dysfunction such as arterial hypertension and atherosclerosis. This detrimental effect of obesity is mediated in part by excessive production of adipose tissue hormone, leptin. 2 â€‚In physiological conditions leptin induces endothelium-dependent vasorelaxation by stimulating nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). Leptin activates endothelial NO synthase through the mechanism involving AMP-stimulated protein kinase (AMPK) and protein kinase B/Akt, which phosphorylates eNOS at Ser(1177) increasing its activity. 3 â€‚In pathological conditions such as obesity and metabolic sy...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363541</comments>
            <pubDate>Tue, 04 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363541</guid>        </item>
        <item>
            <title>Effect of cross-fostering on renal antioxidant/oxidant status and development of hypertension in spontaneously hypertensive rats.</title>
            <link>http://www.medworm.com/index.php?rid=5363540&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21973174%26dopt%3DAbstract</link>
            <description>This study therefore examined the effect of cross-fostering and in-fostering of 1-day old offspring between SHR and WKY dams on renal antioxidant/oxidant status and systolic blood pressure (SBP). SBP and renal antioxidant/oxidant status in the offspring were determined from the age of 4 to 16 weeks. 3 â€‚Cross-fostered SHR had significantly lower SBP than in-fostered SHR at 6, 8 and 12 weeks, but not at 16 weeks (126.5 Â± 0.7 vs 143.5Â± 2.4; 138.1 Â± 1.3 vs 159.6 Â± 1.4; 173.5 Â± 1.7 vs 183.5 Â± 2.1; and 199.2 Â± 2.3 vs 194.1 Â± 3.2 mmHg at 6, 8, 12 and 16 weeks respectively). No difference in SBP was evident between cross-fostered and in-fostered WKY rats. Levels of thiobarbiturate reactive substances (TBARS), protein carbonyl, total antioxidant status (TAS), and activities of superoxide ...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5363540</comments>
            <pubDate>Tue, 04 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5363540</guid>        </item>
        <item>
            <title>Heme oxygenase-1 could mediate the protective effects of hyperbaric oxygen preconditioning against hepatic ischemia-reperfusion injury in rats.</title>
            <link>http://www.medworm.com/index.php?rid=5284119&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21711378%26dopt%3DAbstract</link>
            <description>In conclusion, HBO preconditioning can protect the liver against I/R injury and it appears that this effect might be mediated by the induction of HO-1.
    PMID: 21711378 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284119</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284119</guid>        </item>
        <item>
            <title>Rho kinase inhibition by fasudil exerts antioxidant effects in hypercholesterolemic rats.</title>
            <link>http://www.medworm.com/index.php?rid=5284118&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21711379%26dopt%3DAbstract</link>
            <description>Authors: Ma Z, Zhang J, Ji E, Cao G, Li G, Chu L
    Abstract
    1.â€‚The inhibition of Rho kinase (ROCK) ameliorates many cardiovascular dysfunctions, but the role of ROCK in oxidative stress in hypercholesterolemic rats has not been explored. The aim of the current study was to investigate the antioxidant effects and the potential related mechanisms of fasudil, a selective ROCK inhibitor, in high-cholesterol diet (HCD)-induced hypercholesterolemic rats. 2.â€‚Hypercholesterolemia was induced in rats by feeding with a HCD for 4â€ƒweeks. Starting from day 15, physiological saline (1â€ƒmL/100â€ƒg) or ROCK inhibitor, fasudil (10 or 30â€ƒmg/kg), was injected intraperitoneally for another 14â€ƒdays. 3.â€‚The results showed that fasudil significantly suppressed ROCK activity, potently elevated ...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284118</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284118</guid>        </item>
        <item>
            <title>Multiple factors are required for the prediction of metabolic syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=5284117&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21711380%26dopt%3DAbstract</link>
            <description>Authors: Kawada T
    PMID: 21711380 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284117</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284117</guid>        </item>
        <item>
            <title>Are threshold levels of signal transduction required for the protective effect of cilostazol against cardiac ischaemia-reperfusion injury?</title>
            <link>http://www.medworm.com/index.php?rid=5284116&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21711382%26dopt%3DAbstract</link>
            <description>Authors: Reis F
    PMID: 21711382 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284116</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284116</guid>        </item>
        <item>
            <title>Nitric oxide synthase activity in the abdominal aorta of rats is decreased after 4â€ƒweeks of simulated microgravity.</title>
            <link>http://www.medworm.com/index.php?rid=5284115&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21711383%26dopt%3DAbstract</link>
            <description>Authors: Ren XL, Zhang R, Zhang YY, Liu H, Yu JW, Cai Y, Wang ZC, Purdy RE, Ma J
    Abstract
    1.â€‚The aim of the present study was to investigate the effects of simulated microgravity on the arterial dilatory responsiveness and l-arginine (l-Arg)-nitric oxide (NO)-cGMP pathway in the abdominal aorta of rats. 2.â€‚Twenty healthy male Sprague-Dawley were randomly divided into control and simulated microgravity groups. Rats in the simulated microgravity group were subjected to hindlimb unweighting (HU). After 4â€ƒweeks, arterial dilatory responsiveness was examined in vitro in isolated abdominal aortic rings. Western blotting was used to measure endothelial (e) and inducible (i) NO synthase (NOS) protein content. Total concentrations of nitrate and nitrite (NO(x) ), the stable metabolite...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284115</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284115</guid>        </item>
        <item>
            <title>Cardiac ischaemic stress: Cardiomyocyte Ca(2+) , sex and sex steroids.</title>
            <link>http://www.medworm.com/index.php?rid=5284114&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21722161%26dopt%3DAbstract</link>
            <description>Authors: Bell JR, Mellor KM, Wollermann AC, Delbridge LM
    Abstract
    1.â€‚Important sex differences exist in ischaemic heart disease. Oestrogen has been conventionally regarded as providing a cardioprotective benefit and testosterone frequently perceived to exert a deleterious effect. However, there is accumulating evidence that argues against this simple dichotomy, suggesting that the influence of oestrogen and testosterone conferring benefit or detriment may be context specific. 2.â€‚Cardiomyocyte calcium (Ca(2+) ) loading is recognized to be a major factor in acute ischaemia-reperfusion pathology, promoting cell death, contractile dysfunction and arrhythmogenic activity. Ca(2+) /calmodulin-dependent kinase II (CaMKII) is a mediator of many of the cardiomyocyte Ca(2+) -related patho...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284114</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284114</guid>        </item>
        <item>
            <title>Elevation of liver enzymes within the normal limits and metabolic syndrome: reply.</title>
            <link>http://www.medworm.com/index.php?rid=5284113&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21729144%26dopt%3DAbstract</link>
            <description>Authors: Gao X, Xia M
    PMID: 21729144 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284113</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284113</guid>        </item>
        <item>
            <title>Representative images of left ventricular myocytes from Wistar Kyoto (WKY, left) and spontaneously hypertensive rats (SHR, right) labelled with antibodies raised against the calcium-ATPase SERCA2a (red) and the sarcolemmal sodium-calcium exchanger (NCX, green). See Ward et al., pp 711-716.</title>
            <link>http://www.medworm.com/index.php?rid=5284112&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951297%26dopt%3DAbstract</link>
            <description>Authors: 
    Abstract
    Cover image:â€‚ Representative images of left ventricular myocytes from Wistar Kyoto (WKY, left) and spontaneously hypertensive rats (SHR, right) labelled with antibodies raised against the calcium-ATPase SERCA2a (red) and the sarcolemmal sodium-calcium exchanger (NCX, green). See Ward et al., pp 711-716. â€¢ â€‚Cilostazol reduces myocardial infarct size â€¢ â€‚HF enhances PV arrhythmogenesis â€¢ â€‚NOS in simulated microgravity â€¢ â€‚Fasudil exerts antioxidant effects â€¢ â€‚Losartan diminishes schistosomal liver fibrosis â€¢ â€‚Proceedings of the Australian Physiological Society Symposium: Stress, disease and Ca -2+ management: The cardiovascular challenge.
    PMID: 21951297 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284112</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284112</guid>        </item>
        <item>
            <title>X-Ray Fluorescence Elemental Mapping and Microscopy to Follow Hepatic Disposition of A GD-Based MRI Contrast Agent.</title>
            <link>http://www.medworm.com/index.php?rid=5284111&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21957877%26dopt%3DAbstract</link>
            <description>In this study, we applied XRF techniques at macro and micro level to perform drug distribution studies on ex vivo models to confirm the hepatobiliary disposition of the Gd-based MRI contrast agent B22956/1. 2 â€‚Gd presence was selectively quantified allowing the determination of the time dependent disappearance of the drug from blood and its hepatic accumulation in mice after administration. Elemental mapping highlighted the drug distribution differences between healthy and diseased livers. XRF microanalyses demonstrated that in CCl(4) induced hepatitis B22956/1 has greatly reduced hepatic accumulation revealed as a twenty-fold reduction of Gd presence. Moreover a significant increase of Fe presence was found in steatotic compared to healthy livers, in line with the disease features. 3 â€...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284111</comments>
            <pubDate>Thu, 29 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284111</guid>        </item>
        <item>
            <title>Leptin and cardiovascular diseases.</title>
            <link>http://www.medworm.com/index.php?rid=5284110&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21957899%26dopt%3DAbstract</link>
            <description>Authors: Hou N, Luo JD
    Abstract
    1.â€‚Leptin is a 16-kDa hormone, synthesized primarily by adipocyte, which acts as a key factor for maintenance of energy homeostasis in central and peripheral tissues. In most obese individuals, serum leptin levels are increased and correlate with the individual's body mass index. 2.â€‚Abundant investigations ranging from clinical and animal model studies to in vitro analyses demonstrate that leptin plays a pivotal role in obesity-related cardiovascular diseases (CVD). Hyperleptinemia has been confirmed to be a predictor of acute cardiovascular events. However, some studies have shown that leptin has a cardioprotective effect in leptin-deficient models. These data suggest the influences of leptin on the pathophysiology of cardiovascular diseases are...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284110</comments>
            <pubDate>Thu, 29 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284110</guid>        </item>
        <item>
            <title>Application of Color Doppler in Encircling Constriction of Superficial Femoral Vein in Primary Deep Venous Insufficiency of the Lower Limbs.</title>
            <link>http://www.medworm.com/index.php?rid=5284109&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21957940%26dopt%3DAbstract</link>
            <description>In conclusion, our data suggest that application of color Doppler in encircling constriction of superficial femoral vein may enhance surgical pertinence and improve surgical effect for PDVI.
    PMID: 21957940 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284109</comments>
            <pubDate>Thu, 29 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284109</guid>        </item>
        <item>
            <title>Reply from Gordon B. Drummond and Brian D. M. Tom.</title>
            <link>http://www.medworm.com/index.php?rid=5284121&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21933228%26dopt%3DAbstract</link>
            <description>Authors: Drummond GB, Tom BD
    PMID: 21933228 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284121</comments>
            <pubDate>Wed, 21 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284121</guid>        </item>
        <item>
            <title>Assessment of the pharmacokinetics and platelet aggregation inhibitory effects of a novel intravenous formulation of clopidogrel in humans.</title>
            <link>http://www.medworm.com/index.php?rid=5284120&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21933229%26dopt%3DAbstract</link>
            <description>Authors: Cushing DJ, Souney PF, Cooper WD, Mosher GL, Adams MP, Machatha S, Zhang B, Kowey PR
    Abstract
    1.â€‚PM103 is an intravenous formulation of clopidogrel being developed as an alternative to oral clopidogrel in order to provide for dosing flexibility in the emergent clinical setting. This first-in-human study assessed the pharmacokinetic and pharmacodynamic effects of PM103 and its safety in 144 healthy human subjects. 2.â€‚This was a randomized, open-label, parallel-group trial. Single intravenous doses of PM103 (0.1, 1.0, 10, 30, 100, or 300 mg) were administered to each group (N=24 subjects per group). Platelet aggregation was assessed at baseline, 15, 30 minutes, and 2, 5, 24 hours. Determination of clopidogrel, clopidogrel carboxylic acid metabolite, and the clopidogrel t...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284120</comments>
            <pubDate>Wed, 21 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284120</guid>        </item>
        <item>
            <title>The SRR rs391300 G/A polymorphism influences the therapeutic efficacy of metformin in Chinese patients with type 2 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5284125&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21933224%26dopt%3DAbstract</link>
            <description>Authors: Dong M, Gong ZC, Dai XP, Lei GH, Lu HB, Fan L, Qu J, Zhou HH, Liu ZQ
    Abstract
    1.â€‚The aim of the study was to investigate the association of the serine racemase (SRR) rs391300 G/A polymorphism with the risk of type 2 diabetes mellitus (T2DM) and to assess the impacts of the polymorphism on the therapeutic efficacy of metformin in Chinese patients. 2.â€‚A case-control study of 402 patients with T2DM and 171 healthy controls was conducted. The SRR rs391300 polymorphism was genotyped in all participants using the ABI 3700 automated sequencer. Forty-four recent-onset T2DM patients with different rs391300 genotypes were selected to receive 500 mg metformin orally daily for 12 consecutive weeks as monotherapy. Serum fasting plasma glucose (FPG), postprandial plasma glucose (PPG...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284125</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284125</guid>        </item>
        <item>
            <title>Multivessel versus Single Vessel Spasm as Assessed by Intracoronary Acetylcholine Provocation Test in Korean Patients.</title>
            <link>http://www.medworm.com/index.php?rid=5284124&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21933225%26dopt%3DAbstract</link>
            <description>Authors: Park JY, Rha SW, Jin Z, Poddar KL, Ramasamy S, Chen KY, Li YJ, Choi BG, Ryu SK, Choi JW, Song EJ, Ryou JW, Elnagar A, Kim YK, Na JO, Choi CU, Lim HE, Kim JW, Kim EJ, Park CG, Seo HS, Oh DJ
    Abstract
    1.â€‚Coronary artery spasm (CAS) is known to be a major cause of myocardial ischemia, and multivessel coronary spasm (MVS) in particular is likely to induce more severe and prolonged myocardial ischemia than single vessel spasm (SVS). 2.â€‚A total of 1082 consecutive patients without significant coronary artery disease who underwent acetylcholine (ACh) provocation test between March 2004 and April 2009 were analyzed. The patients were divided into three groups: MVS (n=275), SVS (n=376), and non CAS (n=431). We assessed the differences in clinical and angiographic characteristics...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284124</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284124</guid>        </item>
        <item>
            <title>Taurine suppresses oxidative stress-potentiated LOX-1 expression and restenosis in balloon injured rabbit iliac artery.</title>
            <link>http://www.medworm.com/index.php?rid=5284123&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21933226%26dopt%3DAbstract</link>
            <description>This study was designed to investigate the effects of taurine on intimal thickening and LOX-1 expression in normal and oxidative settings. 2.â€‚Balloon injury was performed in the iliac artery and oxidative stress was induced by buthionine sulfoximine (BSO, 75 mg/kg b. wt., s.c), a specific inhibitor of glutathione synthesis, for 14 days. 3.â€‚Taurine (1% in drinking water, w/v) preserved the levels of plasma antioxidants and lowered the increased blood pressure induced by BSO. The stenosis rate of 29.92% in the placebo group increased to 72.20% in the BSO Group, which was then significantly reduced to 42.21% by taurine (P &amp;lt; 0.001, n = 5). LOX-1 was shown to be localized in both intimal and medial area of the iliac artery. Taurine reduced the increased expression of LOX-1 by BSO, both i...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284123</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284123</guid>        </item>
        <item>
            <title>Statistical perspectives: all together NOT.</title>
            <link>http://www.medworm.com/index.php?rid=5284122&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21933227%26dopt%3DAbstract</link>
            <description>Authors: Hopkins WG, Batterham AM, Impellizzeri FM, Pyne DB, Rowlands DS
    PMID: 21933227 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284122</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284122</guid>        </item>
        <item>
            <title>Overexpression of cationic amino acid transporter-1 increases nitric oxide production in hypoxic human pulmonary microvascular endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5235029&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21923750%26dopt%3DAbstract</link>
            <description>Authors: Cui H, Chen B, Chicoine LG, Nelin LD
    Abstract
    1.â€‚The endogenous production of and/or the bioavailability of nitric oxide (NO) is decreased in pulmonary hypertensive diseases. L-arginine (L-arg) is the substrate for NO synthase (NOS). L-arg is transported into cells via the cationic amino acid transporters (CAT), of which there are two isoforms in endothelial cells, CAT-1 and CAT-2. 2.â€‚To test the hypothesis that hypoxia will decrease CAT expression and L-arg uptake resulting in decreased NO production in human pulmonary microvascular endothelial cells (hPMVEC), cells were incubated in either normoxia (21% O(2) , 5% CO(2) , balance N(2) ) or hypoxia (1% O(2) , 5% CO(2) , balance N(2) ). 3.â€‚The hPMVEC incubated in hypoxia had 80% less NO production than cells incubated...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5235029</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5235029</guid>        </item>
        <item>
            <title>Association of the time course of pulmonary arterial hypertension with changes in oxidative stress in the left ventricle.</title>
            <link>http://www.medworm.com/index.php?rid=5235028&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21923751%26dopt%3DAbstract</link>
            <description>This study investigates the time course of pulmonary arterial hypertension (PAH) due to monocrotaline (MCT) and its association with cardiac function and oxidative stress markers in the left ventricle (LV). 2.â€‚Male Wistar rats were divided into six groups: 7 days, 21 days, and 31 days for both control and MCT groups. Following echocardiographic analysis, the heart was removed. The LV was separated and homogenized to analyze oxidized-to-total glutathione ratio and thioredoxin reductase (TrxR) activity as well as hydrogen peroxide (H(2) O(2) ) and ascorbic acid levels. 3.â€‚There was significant (P &amp;lt; 0.01) cardiac and right ventricle (RV) hypertrophy and pulmonary congestion in the MCT 21 d and 31 d groups. Echocardiography showed a change in the flow wave of the pulmonary artery at 21 ...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5235028</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5235028</guid>        </item>
        <item>
            <title>Hypoadiponectinemia in Type 2 Diabetes: Molecular Mechanisms and Clinical Significance.</title>
            <link>http://www.medworm.com/index.php?rid=5235031&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21916932%26dopt%3DAbstract</link>
            <description>Authors: Su H, Lau WB, Ma XL
    Abstract
    1.â€‚This review focuses upon the regulatory mechanisms of adiponectin (APN) gene expression during physiologic conditions, and both the clinical significance and underlying molecular mechanisms of hypoadiponectinemia during pathologic conditions. 2.â€‚APN is a versatile cardiovascular protective factor. It plays an important role in regulating insulin sensitivity and energy homeostasis, with anti-inflammatory and anti-atherosclerotic properties. 3.â€‚APN gene expression is down-regulated in both obesity and type 2 diabetes mellitus. Hypoadiponectinemia is an independent risk factor for coronary artery disease in type 2 diabetic patients. 4.â€‚Exogenous supplementation of recombinant APN attenuates insulin resistance, improving metabolic disord...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5235031</comments>
            <pubDate>Wed, 14 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5235031</guid>        </item>
        <item>
            <title>Neurodegeneration in Familal Amyloidotic Polyneuropathy.</title>
            <link>http://www.medworm.com/index.php?rid=5235030&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21916933%26dopt%3DAbstract</link>
            <description>Authors: Gasperini RJ, Small DH
    Abstract
    1.â€‚Familial amyloid polyneuropathies (FAP) constitute a group of inherited amyloidoses that affect peripheral nerves. One common form of FAP is caused by transthyretin (TTR) misfolding and deposition in the peripheral nervous system, leading to neuronal toxicity and death. 2.â€‚The molecular mechanisms responsible for this toxicity are unclear, however there is good biochemical and histopathological evidence that the toxicity of TTR mutations is correlated to their aggregation state. In addittion, neuronal calcium dysregulation is a mechanism that has been suggested to drive the pathogenesis of FAP. 3.â€‚Amyloidogenic TTR mutations cause significant calcium influx via L-type calcium channels in neuronal cell lines, while in primary sensory...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5235030</comments>
            <pubDate>Wed, 14 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5235030</guid>        </item>
        <item>
            <title>Changes in nitric oxide and free radical levels in rat gastrocnemius muscle during contraction and fatigue.</title>
            <link>http://www.medworm.com/index.php?rid=5221585&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21913957%26dopt%3DAbstract</link>
            <description>Authors: Ibrahim MY, Ashour OM
    Abstract
    1. The ratio of nitric oxide (NO) to free radicals is critical during skeletal muscle contraction. Changes in this ratio have been suggested to play a role in muscle fatigue. 2. The aim of the present study was to investigate the changes in NO and free radicals during tetanic and subtetanic contraction and fatigue in the gastrocnemius muscle of adult male Wistar rats. 3. Rats were subjected to either low- or high-frequency stimulation (10 and 100 Hz, respectively) of the right gastrocnemius muscle. Both groups were further subdivided into untreated (0.9% NaCl solution), N(G) -nitro-l-arginine methyl ester (l-NAME)-treated and reduced glutathione (GSH)-treated groups. Rats were administered their treatments intraperitoneally 30 min prior to el...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221585</comments>
            <pubDate>Tue, 13 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221585</guid>        </item>
        <item>
            <title>Salt-sensitive hypertension: Introduction.</title>
            <link>http://www.medworm.com/index.php?rid=5221584&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21913958%26dopt%3DAbstract</link>
            <description>Authors: Nakano D, Mori T
    Abstract
    Hypertension is a major risk factor of cardiovascular events. Although the scientific understanding of hypertension and therapeutic tools for its treatment have dramatically progressed since the middle of the 20(th) century, we have not fully understood the disease and it is difficult to halt the clinical course of disease in patients with essential hypertension. It is still unclear how salt triggers increased blood pressure, how the autonomic nervous system can become imbalanced by chronically high salt intake, and the factors associated with high salt intake which hinder the ability of the kidneys mediate salt balance. To highlight some of the major recent advances in salt-sensitive hypertension research, we are publishing a special section in t...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221584</comments>
            <pubDate>Tue, 13 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221584</guid>        </item>
        <item>
            <title>Adipokines in inflammation, insulin resistance and cardiovascular disease.</title>
            <link>http://www.medworm.com/index.php?rid=5221586&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21910745%26dopt%3DAbstract</link>
            <description>Authors: Li ZY, Wang P, Miao CY
    Abstract
    1. Obesity is a major determinant of cardiovascular disease (CVD). Studies in the past two decades have shown that adipose tissue is not merely an inert energy reserve of triglycerides, but also an active endocrine organ. 2. Adipose tissue can produce and secrete numerous bioactive peptides and/or proteins termed adipokines. These secretory factors are involved in the regulation of local and systemic inflammation and insulin sensitivity in a paracrine and/or endocrine manner. Inflammation and insulin resistance (IR) play critical roles in the obesity-linked development of CVD, such as atherosclerosis, hypertension and restenosis. 3. In the present minireview, we summarize the relationship between inflammation and IR, as well as their contrib...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221586</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221586</guid>        </item>
        <item>
            <title>GAPDH: A common enzyme with uncommon functions.</title>
            <link>http://www.medworm.com/index.php?rid=5221589&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21895736%26dopt%3DAbstract</link>
            <description>Authors: Nicholls C, Li H, Liu JP
    Abstract
    1. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) has long been recognized as an important enzyme for energy metabolism and the production of ATP and pyruvate through anaerobic glycolysis in the cytoplasm. 2. Recent studies have shown that GAPDH has multiple functions independent of its role in energy metabolism. While increased GAPDH gene expression and enzymatic function is associated with cell proliferation and tumorigenesis, conditions such as oxidative stress impair GAPDH catalytic activity and lead to cellular ageing and apoptosis,. 3. While the mechanism(s) of GAPDH influence on cellular proliferation remain unclear, much evidence has been accrued demonstrating a variety of interacting partners for GAPDH, including proteins, vario...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221589</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221589</guid>        </item>
        <item>
            <title>Mitochondrial decay in aging: 'Qi-invigorating' schisandrin B as a hormetic agent for mitigating age-related diseases.</title>
            <link>http://www.medworm.com/index.php?rid=5221588&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21895737%26dopt%3DAbstract</link>
            <description>Authors: Leong PK, Chen N, Ko KM
    Abstract
    1. The 'Mitochondrial Free Radical Theory of Aging' (MFRTA) proposes a primary role of mitochondrial reactive oxygen species (ROS) in the aging process. The 'Reductive Hotspot Hypothesis of Mammalian Aging' serves as a supplement to the MFRTA by explaining how the relatively few cells that have lost oxidative phosphorylation capacity due to mitochondrial DNA mutations can be toxic to the rest of the body and result in the development of age-related diseases. 2. Schisandrin B (Sch B), which can induce a glutathione antioxidant response and a heat shock response via the redox-sensitive signaling pathways, is a hormetic agent potentially useful for increasing the resistance of tissues to oxidative damage. The enhancement in cellular/mitochondr...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221588</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221588</guid>        </item>
        <item>
            <title>Human Epicardial Fat: what is new and what is missing?</title>
            <link>http://www.medworm.com/index.php?rid=5221587&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21895738%26dopt%3DAbstract</link>
            <description>Authors: Sacks HS, Fain JN
    Abstract
    1. Putative physiological functions of human epicardial adipose tissue [EAT] include lipid storage for the energy needs of the myocardium; thermoregulation whereby brown fat components of EAT generate heat by non-shivering thermogenesis in response to core cooling; neuroprotection of the cardiac autonomic ganglia and nerves; and regulation of vasomotion and luminal size of the coronary arteries. Under pathophysiological circumstances, EAT may play an adverse paracrine role in cardiac arrhythmias and in lipotoxic cardiomyopathy but of major current interest is its hypothetical role as an immunological organ contributing to inflammation around coronary artery disease [CAD]. 2. The amount of EAT measured either by echocardiographic thickness over th...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221587</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221587</guid>        </item>
        <item>
            <title>Smooth muscle progenitor cells stained for a-smooth muscle actin (green) and the chemokine receptor CXCR4 (red). See Liu et al pp 586-591.</title>
            <link>http://www.medworm.com/index.php?rid=5195566&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21884193%26dopt%3DAbstract</link>
            <description>Authors: 
    Abstract
    Cover image:â€‚ Smooth muscle progenitor cells stained for a-smooth muscle actin (green) and the chemokine receptor CXCR4 (red). See Liu et al pp 586-591 â€¢ â€‚Advances in stroke in 2010 â€¢ â€‚Aldosterone synthase gene and hypertension â€¢ â€‚Aliskiren, bradykinin and tissue kallikrein â€¢ â€‚ABCC1 polymorphism and lung cancer â€¢ â€‚Non-Î²(2) effects of clenbuterol on soleus muscle â€¢ â€‚Gelatinases and adiposity.
    PMID: 21884193 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195566</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195566</guid>        </item>
        <item>
            <title>Statistics, probability, significance, likelihood: words mean what we define them to mean.</title>
            <link>http://www.medworm.com/index.php?rid=5195565&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21884194%26dopt%3DAbstract</link>
            <description>Authors: Drummond GB, Tom BD
    PMID: 21884194 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195565</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195565</guid>        </item>
        <item>
            <title>Mechanism of alcohol-induced impairments in renal development: Could it be reduced retinoic acid?</title>
            <link>http://www.medworm.com/index.php?rid=5195568&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21883382%26dopt%3DAbstract</link>
            <description>In this study we proposed that the ethanol-induced inhibition of ureteric branching morphogenesis and glomerular development in the cultured rat kidney would be ameliorated by co-culture with exogenous retinoic acid, and that examining the expression profile of key genes involved in the development of the kidney would provide insights into potential molecular pathways involved. 3. Whole rat metanephroi cultured in the presence of exogenous retinoic acid without ethanol appeared larger and had significantly more ureteric branch points, tips and glomeruli than metanephroi cultured in control media. Those cultured in the presence of ethanol alone (0.2%) had 20% fewer ureteric branch points, tips and glomeruli, which was ameliorated by co-culture with retinoic acid. 4. Gene expression analysis...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195568</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195568</guid>        </item>
        <item>
            <title>Frontiers in Research: Adipokines and Cardiovascular Disease.</title>
            <link>http://www.medworm.com/index.php?rid=5195567&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21883383%26dopt%3DAbstract</link>
            <description>Authors: Miao CY
    PMID: 21883383 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195567</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195567</guid>        </item>
        <item>
            <title>Regulation of Stem Cell Differentiation in Adipose Tissue by Chronic Inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=5195569&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21883381%26dopt%3DAbstract</link>
            <description>Authors: Ye J, Gimble JM
    Abstract
    1. Recent studies suggest that a local hypoxic response leads to chronic inflammation in adipose tissue of obese individuals. The adipose tissue hypoxia may reflect a compensatory failure in the local vasculature system in response to obesity. 2. Studies suggest that inflammation stimulates angiogenesis and inhibits adipocyte activities in a feedback manner within the obese adipose tissue. Adipose-derived stem cells (ASCs) are able to differentiate into multiple linages of progenitor cells for adipocytes, endothelial cells, fibroblasts and pericytes. Differentiation of ASCs into those progenitors is regulated by the adipose tissue microenvironment. 3. As a major factor in the microenvironment, inflammation may favor ASC differentiation into the end...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195569</comments>
            <pubDate>Sun, 28 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195569</guid>        </item>
        <item>
            <title>Linkage between Twist1 and Bmi1: molecular mechanism of cancer metastasis/stemness and clinical implications.</title>
            <link>http://www.medworm.com/index.php?rid=5195571&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21883379%26dopt%3DAbstract</link>
            <description>Authors: Wu CY, Hung JJ, Wu KJ
    Abstract
    1. Cancer metastasis is the major cause of cancer-related death in spite of the significant improvement in multimodality cancer therapy. Epithelial-mesenchymal transition (EMT), a major mechanism of cancer metastasis, is a process which generates cells with stem cell-like properties (cancer stemness). 2. Cancer stemness is a concept that describes a minor population of cells (cancer stem cells) residing within a tumor, which are able to self-renew and are resistant to conventional therapy. The mechanisms delineating the generation of cancer stemness and its connection to cancer metastasis remain largely unknown. 3. Twist1 is an EMT regulator and its increased expression, which also possesses prognostic significance in various human cancers, h...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195571</comments>
            <pubDate>Sat, 27 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195571</guid>        </item>
        <item>
            <title>Cell biology of Smad2/3 linker region phosphorylation in vascular smooth muscle.</title>
            <link>http://www.medworm.com/index.php?rid=5195572&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21883378%26dopt%3DAbstract</link>
            <description>Authors: Rezaei HB, Kamato D, Ansari G, Osman N, Little PJ
    Abstract
    1.â€‚The Transforming Growth Factor Î² (TGF-Î²) superfamily of ligands regulate a diverse set of cellular functions. TGF-Î² induces its biological effects through type I and type II transmembrane receptors which have serine/threonine kinase activities and weak tyrosine kinase activity. In vascular smooth muscle TGF-Î² binds to the TGF-Î² type II receptor (TÎ²RII) at the cell surface recruiting the type I receptor (TÎ²RI) to form a heterocomplex. Consequently, after phosphorylation and activation of TÎ²RI, the transcription factors R-Smad2 and Smad3 are recruited and activated through phosphorylation of C terminal residues. Smad2/3 and co-Smad4 have overall similar structures consisting of three regions an N-termina...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195572</comments>
            <pubDate>Mon, 22 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195572</guid>        </item>
        <item>
            <title>Dalteparin dose-dependently increases ROTEMÂ® thrombelastography parameters only at supratherapeutic anti-factor Xa levels: an in-vitro study.</title>
            <link>http://www.medworm.com/index.php?rid=5195570&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21883380%26dopt%3DAbstract</link>
            <description>In conclusion, the results indicate that the thrombelastograph ROTEM(Â®) can detect the anticoagulant effects of dalteparin only at supratherapeutic levels of anti-factor Xa.
    PMID: 21883380 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195570</comments>
            <pubDate>Mon, 22 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195570</guid>        </item>
        <item>
            <title>Decrease of Tight Junction Integrity in the Ipsilateral Thalamus during the Acute Stage after Focal Infarction and Ablation of Cerebral Cortex in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5142767&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21851377%26dopt%3DAbstract</link>
            <description>This study investigated tight junction-related proteins and tight junction (TJ) microstructure in the ipsilateral thalamus during the acute stage after middle cerebral artery occlusion (MCAO) and cortical aspiration lesion (CAL) in rats. 2.â€‚MCAO or CAL was induced in 36 hypertensive and normotensive rats, and another 18 rats in each group were submitted to a sham operation. ZO-1, occludin, and albumin were detected by western blotting at 12 h and 24 h after the operation. TJ microstructure was observed using electron microscopy, and albumin location in the ipsilateral thalamus was examined by double immunostaining of albumin(+) /occludin(+) and albumin(+) /NeuN(+) at 24 h after the surgery. 3.â€‚At 24 h after MCAO or CAL, occludin expression reduced to 78.4% or 81.3% compared to the cont...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142767</comments>
            <pubDate>Wed, 17 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142767</guid>        </item>
        <item>
            <title>Pumping ions.</title>
            <link>http://www.medworm.com/index.php?rid=5142771&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21848638%26dopt%3DAbstract</link>
            <description>Authors: Clarke RJ, Fan X
    Abstract
    1.â€‚This is a concise review of the field of ion pumping from the perspective of the authors. 2.â€‚The period covered spans the discovery of Na(+) and K(+) concentration gradients across animal cell membranes by Carl Schmidt in the 1850s, through the isolation of the Na(+) ,K(+) -ATPase by Skou in 1957 (for which he was awarded the 1997 Nobel Prize in Chemistry), to the publication of the first crystal structure of the enzyme in 2007 and beyond. 3.â€‚Contributions of the authors' research group to the resolution of the questions of the mechanism of the allosteric role of ATP within the Na(+) ,K(+) -ATPase reaction cycle and how protomeric versus diprotomeric states of the enzyme influence its kinetics are discussed within the context of the resea...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142771</comments>
            <pubDate>Tue, 16 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142771</guid>        </item>
        <item>
            <title>Adipokines and Thrombosis.</title>
            <link>http://www.medworm.com/index.php?rid=5142770&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21848866%26dopt%3DAbstract</link>
            <description>Authors: SchÃ¤fer K, Konstantinides S
    Abstract
    1. Obesity is a major risk factor for cardiovascular disease. An increased body-mass index (BMI) is associated with venous thromboembolism, myocardial infarction, stroke, and stent thrombosis after percutaneous interventions. Studies in mouse models of obesity and induced arterial or venous thrombosis have provided insights into the mechanisms involved. 2. Besides an elevation in circulating levels of fibrinogen, factor VII, and plasminogen activator inhibitor (PAI)-1, changes in platelet biology and function may underlie the increased (athero)thrombotic risk in obesity. They include elevated platelet counts, an increase in mean platelet volume, an increased platelet aggregatory response to agonists, and a reversible resistance to the ...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142770</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142770</guid>        </item>
        <item>
            <title>Presynaptic muscarinic and adenosine receptors involved in 2 Hz-induced train-of-four fade caused by antinicotinic neuromuscular relaxants in the rat.</title>
            <link>http://www.medworm.com/index.php?rid=5142769&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21848867%26dopt%3DAbstract</link>
            <description>In this study, we evaluated the TOF(fade) caused by antinicotinic neuromuscular relaxants (hexamethonium, D-tubocurarine, vecuronium, and rocuronium) as the ratio between the muscle tension produced in the rat diaphragm by the fourth over the first stimulus of a train-of-four stimuli delivered to the phrenic nerve trunk at a frequency of 2 Hz. 3. All antinicotinic agents, except hexamethonium, decreased the amplitude of muscle tension during the first stimulus. Hexamethonium, D-tubocurarine-, vecuronium-, and rocuronium-induced TOF(fade) were attenuated by pirenzepine (10 nM, a M(1) antagonist), methoctramine (1 Î¼M, a M(2) antagonist), and DPCPX (2.5 nM, a A(1) antagonist). Blockade of the A(2A) receptor with ZM241385 (10 nM) partially reversed the TOF(fade) induced by D-tubocurarine, vec...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142769</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142769</guid>        </item>
        <item>
            <title>Effects of the cannabinoid antagonist SR 141716 on sexual and motor behavior in receptive female rats.</title>
            <link>http://www.medworm.com/index.php?rid=5142768&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21848907%26dopt%3DAbstract</link>
            <description>Authors: Zavatti M, Carnevale G, Benelli A, Zanoli P
    Abstract
    1. The aim of the present study was to investigate the influence of the cannabinoid antagonist/inverse agonist SR 141716 (SR) on receptive behavior and sexual motivation of female rats. 2. Partner preference, receptivity and proceptivity were evaluated in ovariectomized females primed with estrogen and progesterone and administered intraperitoneally with SR (1-2.5 mg/kg) 20 min prior to testing. 3. In the partner preference test, a reduced interest in both stimulus animals was detected in rats treated with SR at both dosages, but no influence on preference score was observed. In the receptivity test a pronounced reduction in lordosis quotient and lordosis rating as well in the percentage of receptive females was found in...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142768</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142768</guid>        </item>
        <item>
            <title>TW (Tripterygium wilfordii) bioactive compounds as anti-cancer and anti-inflammatory agents.</title>
            <link>http://www.medworm.com/index.php?rid=5142772&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21834865%26dopt%3DAbstract</link>
            <description>Authors: Wong KF, Yi Y, Luk JM
    Abstract
    1. Bioactive compounds from medicinal plants with anti-cancer and anti-inflammatory effects have become key resources in drug discovery fields for treatment of various malignancies and immunological disorders. 2. Tripterygium wilfordii (TW) is a medicinal plant showing profound immuno-suppressive effect, and have been used in herbal regimen for treatment of immunological diseases for thousand years in China. 3. The procedures for the isolation and characterization of TW bioactive compounds have been well established. Over the past three decades, more than 46 diterpenoids, 20 new triterpenoids, 26 alkaloids and other small molecules have been identified from TW. 4. Triptolide, celastrol, and tripchlorolide are among the bioactive compounds con...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142772</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142772</guid>        </item>
        <item>
            <title>Protective effects of propofol on endotoxemia-induced acute kidney injury in rats.</title>
            <link>http://www.medworm.com/index.php?rid=5111840&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21824173%26dopt%3DAbstract</link>
            <description>This study examined the protective effects of propofol on endotoxemia-induced acute kidney injury in rats. 2. A rat model of endotoxemia was established using lipopolysaccharide. We determined the effects of propofol administration before, during, and after lipopolysaccharide-induced endotoxemia on expression of aquaporin-2, tumor necrosis factor-Î±, intercellular adhesion molecule-1, caspase-3, Bcl-2, and Bax using RT-PCR, western blotting, and immunocytochemistry. Renal morphology, superstructure, and apoptosis and renal function were also assessed. 3. We observed normal renal tubular structure in the propofol pre-treatment group, but lipopolysaccharide treatment led to changes in renal tissue morphology. Propofol treatment improved renal function in lipopolysaccharide-treated rats. Pret...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111840</comments>
            <pubDate>Mon, 08 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111840</guid>        </item>
        <item>
            <title>Naja nigricollis CMS-9 enhances mitochondria-mediated death pathway in adaphostin-treated human leukemia U937 cells.</title>
            <link>http://www.medworm.com/index.php?rid=5111835&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21824174%26dopt%3DAbstract</link>
            <description>Authors: Chen YJ, Wang JJ, Chang LS
    1. The aim of the present study is to explore the effect of Naja nigricollis phospholipase A(2) , CMS-9, on adaphostin-induced death of human leukemia U937 cells. 2. Leukemia U937 cells (Bcr/Abl-negative cells) were treated with adaphostin and CMS-9 in the present study. The effect of CMS-9, adaphostin and the combination of CMS-9 and adaphostin on cell viability, reactive oxygen species (ROS) generation, intracellular Ca(2+) concentration ([Ca(2+) ]i), p38 MAPK activation, inactivation of Akt and ERK, mitochondrial membrane potential (Î”Î¨m) and Bcl-2 family proteins of U937 cells were analyzed. 3. Either adaphostin or CMS-9 induced apoptosis of U937 cells, characterized by dissipation of Î”Î¨m and ROS generation. Co-treatment with CMS-9 further inc...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111835</comments>
            <pubDate>Mon, 08 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111835</guid>        </item>
        <item>
            <title>The application of complementary luminescent and fluorescent imaging techniques to visualize nuclear and cytoplasmic Ca(2+) -signalling during the in vivo differentiation of slow muscle cells in zebrafish embryos under normal and dystrophic conditions.</title>
            <link>http://www.medworm.com/index.php?rid=5111897&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21824171%26dopt%3DAbstract</link>
            <description>Authors: Webb SE, Cheung CC, Chan CM, Love DR, Miller AL
    1. Evidence is accumulating for a role for Ca(2+) signalling in the differentiation and development of embryonic skeletal muscle. 2. Imaging of intact, normally developing transgenic zebrafish that express the protein component of the Ca(2+) -sensitive complex, aequorin, specifically in skeletal muscle, show that two distinct periods of spontaneous synchronized Ca(2+) transients occur in the trunk: at âˆ¼17.5 hours post-fertilization (hpf)-19.5 hpf (termed signalling period, SP1); and after âˆ¼23 hpf (termed SP2). These periods of intense Ca(2+) signalling activity are separated by a quiet period. 3. Higher resolution confocal imaging of embryos loaded with the fluorescent Ca(2+) reporter, calcium green-1 dextran, show that the C...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111897</comments>
            <pubDate>Sun, 07 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111897</guid>        </item>
        <item>
            <title>Pet ownership and cardiovascular risk reduction: Supporting evidence, conflicting data, and underlying mechanisms.</title>
            <link>http://www.medworm.com/index.php?rid=5111888&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21824172%26dopt%3DAbstract</link>
            <description>Authors: Arhant-Sudhir K, Arhant-Sudhir R, Sudhir K
    1. It is widely believed that pet ownership is beneficial to humans, and that some of this benefit is through favorable effects on cardiovascular risk. In this review, we critically examine the evidence in support of this hypothesis, and present the available data with respect to major cardiovascular risk factors. 2. There is evidence that dog owners are less sedentary and have lower blood pressure, plasma cholesterol and triglycerides, attenuated responses to laboratory induced mental stress, and improved survival following myocardial infarction compared to non-pet owners. 3. However, conflicting data exist with regard to the association between pet ownership and each of these risk factors. 4. Numerous non-cardiovascular effects of p...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111888</comments>
            <pubDate>Sun, 07 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111888</guid>        </item>
        <item>
            <title>Physiological concentration of glucocorticoids inhibit proliferation of adult rat cardiac fibroblasts induced by pro-inflammatory cytokines: roles of ERK1/2 and NF-ÎºB.</title>
            <link>http://www.medworm.com/index.php?rid=5111898&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21819443%26dopt%3DAbstract</link>
            <description>In conclusion, these results indicate that physiological concentration of hydrocortisone can inhibit inflammation-induced proliferation of cardiac fibroblasts by preventing activation of ERK1/2 and NF-ÎºB.
    PMID: 21819443 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111898</comments>
            <pubDate>Thu, 04 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111898</guid>        </item>
        <item>
            <title>Platelet activation, oxidative stress and overexpression of inducible nitric oxide synthase in moderate heart failure.</title>
            <link>http://www.medworm.com/index.php?rid=5111907&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21806669%26dopt%3DAbstract</link>
            <description>Authors: de Meirelles LR, de Castro Resende A, Matsuura C, Salgado A, Pereira NR, Cascarelli PG, Mendes-Ribeiro AC, Brunini TM
    1. Chronic heart failure (CHF) is a common disabling disorder associated with thromboembolic events, and the full understanding of its genesis remains to be discovered. Nitric oxide (NO), derived from vascular endothelium and platelets, has an important role in the physiological regulation of blood flow. It is generated from the amino acid L-arginine by using the NO synthase (NOS) enzymes. 2. The main objective of this study was to investigate NO production and its relationship to platelet aggregation, oxidative stress, inflammation and related amino acids in patients with moderate CHF. The expression and activity of NOS isoforms were analysed by Western Blotti...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111907</comments>
            <pubDate>Mon, 01 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111907</guid>        </item>
        <item>
            <title>Triple immunostaining for c-MYC (green), proliferating cell nuclear antigen (PCNA; red) and 4',6'-diamidino-2-phyenylindole (DAPI) in serum starved L6 cells 12 h after treatment with leukaemia inhibitory factor (LIF). See Srikuea et al, pp 501-509.</title>
            <link>http://www.medworm.com/index.php?rid=5111937&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21790717%26dopt%3DAbstract</link>
            <description>Authors: 
    Cover image:â€‚ Triple immunostaining for c-MYC (green), proliferating cell nuclear antigen (PCNA; red) and 4',6'-diamidino-2-phyenylindole (DAPI) in serum starved L6 cells 12 h after treatment with leukaemia inhibitory factor (LIF). See Srikuea et al, pp 501-509. â€¢ â€‚NOS uncoupling and LV dysfunction â€¢ â€‚Contusion and LIF expression in rat muscle â€¢ â€‚Tetrodotoxin alleviates acute heroin syndrome â€¢ â€‚Octreotide inhibits thin afferents â€¢ â€‚ Protective effects of probucol.
    PMID: 21790717 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111937</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111937</guid>        </item>
        <item>
            <title>How can we tell if frogs jump further?</title>
            <link>http://www.medworm.com/index.php?rid=5111931&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21790718%26dopt%3DAbstract</link>
            <description>Authors: Drummond GB, Tom BD
    
    PMID: 21790718 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111931</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111931</guid>        </item>
        <item>
            <title>The developmental origins of obesity-related hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=5111914&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21801195%26dopt%3DAbstract</link>
            <description>Authors: Henry SL, Barzel B, Wood-Bradley RJ, Burke SL, Head GA, Armitage JA
    1. In the past 30 years the prevalence of obesity and overweight have doubled and it is now estimated that globally, over 500 million adults are obese and a further billion adults are overweight. Obesity is a cardiovascular risk factor and some studies suggest that up to 70% of cases of essential hypertension may be attributable, in part, to obesity. Increasingly, evidence supports a view that obesity-related hypertension may be driven by altered hypothalamic signaling which results in inappropriately high appetite and sympathetic nerve activity to the kidney. 2. In addition to the adult risk factors for obesity and hypertension, the environment encountered in early life may &quot;programme&quot; the development of obes...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111914</comments>
            <pubDate>Sun, 31 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111914</guid>        </item>
        <item>
            <title>Comparison of the organization of t-tubules, sarcoplasmic reticulum and ryanodine receptors in rat and human ventricular myocardium.</title>
            <link>http://www.medworm.com/index.php?rid=5111919&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21790719%26dopt%3DAbstract</link>
            <description>Authors: Jayasinghe ID, Crossman DJ, Soeller C, Cannell MB
    1. It is apparent from the literature that there are significant differences in excitation-contraction (EC) coupling between species, particularly in the density of calcium transporting proteins in the t-system and SR Ca release channels. Unfortunately, there is a lack of information on how the principal structures that link electrical excitation to the activation of calcium-induced calcium release (CICR) are different between human and animal models (particularly rat). 2. Comparison of wheat germ agglutin and caveolin-3 labelling revealed a non-uniform distribution of surface membrane glycosylation in rat, rabbit and human and that the rat t-system appeared more complex in geometry than the latter species. Analysis of the t-sy...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111919</comments>
            <pubDate>Sun, 24 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111919</guid>        </item>
        <item>
            <title>Arrhythmogenic pulmonary vein myocardium in heart failure.</title>
            <link>http://www.medworm.com/index.php?rid=5111942&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21781146%26dopt%3DAbstract</link>
            <description>Authors: Boukens BJ, Baartscheer A, Higa S
    
    PMID: 21781146 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111942</comments>
            <pubDate>Thu, 21 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111942</guid>        </item>
        <item>
            <title>Potential antifibrotic effects of at1 receptor antagonist, losartan, and/or praziquantel on acute and chronic experimental liver fibrosis induced by schistosoma mansoni.</title>
            <link>http://www.medworm.com/index.php?rid=5111946&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21762203%26dopt%3DAbstract</link>
            <description>In conclusion, losartan has a promising antifibrotic action and could be introduced as a therapeutic tool with PZQ especially in acute schistosomal hepatic fibrosis.
    PMID: 21762203 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111946</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111946</guid>        </item>
        <item>
            <title>Acute inhibitory effects of clenbuterol on force, Ca(2+) transients and action potentials in rat soleus may not involve the Î²(2) -adrenoceptor pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5111949&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21752065%26dopt%3DAbstract</link>
            <description>Authors: Head SI, Ha TN
    1.â€‚Clenbuterol, a Î²(2) -adrenoceptor agonist, can have inhibitory and myotoxic effects on slow-twitch muscles. Clenbuterol is lipophilic and may enter into the intracellular compartment, and because of this, it is likely that clenbuterol will have different effects to classical Î²(2) -adrenoceptor agonists such as terbutaline. The aim of the present study is to investigate clenbuterol's effect on force, intracellular [Ca(2+) ] and electrophysiology, and the role of the Î²(2) -adrenoceptor pathway in these effects. 2.â€‚Simultaneous measurements of isometric force and [Ca(2+) ](i) were made from small bundles of rat soleus muscle fibres in which several superficial fibres had been pressure-injected with the fluorescence Ca(2+) indicator Indo-1. The muscle's el...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111949</comments>
            <pubDate>Tue, 12 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111949</guid>        </item>
        <item>
            <title>Hyperbaric oxygen preconditioning: what remains between hypoxia and hyperoxia?</title>
            <link>http://www.medworm.com/index.php?rid=5111952&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21749437%26dopt%3DAbstract</link>
            <description>Authors: Mik EG
    
    PMID: 21749437 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5111952</comments>
            <pubDate>Mon, 11 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5111952</guid>        </item>
        <item>
            <title>MRP1/ABCC1 polymorphism Arg723Gln (2168G&gt;A) is associated with lung cancer susceptibility in Chinese population.</title>
            <link>http://www.medworm.com/index.php?rid=5019098&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21736601%26dopt%3DAbstract</link>
            <description>Authors: Yin JY, Han LF, Huang Q, Xu XJ, Zhou HH, Liu ZQ
    1. Our previous in vitro study showed that the Arg723Gln (2168G&amp;gt;A) polymorphism significantly reduced multidrug resistance-associated protein 1 (MRP1/ABCC1) induced multidrug resistance. The present study aims to further investigate the association of this polymorphism with lung cancer susceptibility and chemotherapy response in a Chinese population. 2. A total of 77 lung cancer patients (54 male, 23 female) and 71 cancer-free controls (49 male, 22 female) were enrolled in this study. Genomic DNA was extracted from peripheral blood and all samples were genotyped using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. 3. The subjects carrying the 723Gln (A) allele have a 3.4 fold increased...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019098</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019098</guid>        </item>
        <item>
            <title>Aliskiren increases bradykinin and tissue kallikrein mRNA levels in the heart.</title>
            <link>http://www.medworm.com/index.php?rid=5019078&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21736602%26dopt%3DAbstract</link>
            <description>Authors: Campbell DJ, Zhang Y, Kelly DJ, Gilbert RE, McCarthy DJ, Shi W, Smyth GK
    1.â€‚Aliskiren is a renin inhibitor with IC(50) of 0.6 nmol/L for human renin, 4.5 nmol/L for mouse renin, and 80 nmol/L for rat renin. 2.â€‚We compared the effects of aliskiren (10 mg/kg/day), angiotensin converting enzyme inhibitor perindopril (0.2 mg/kg/day), and their combination, on angiotensin and bradykinin peptides in female heterozygous (mRen-2)27 rats, transgenic for the mouse renin gene. 3.â€‚All 3 treatments produced similar reductions in systolic blood pressure, heart weight, and plasma aldosterone levels and reduced angiotensin II levels in lung, but only perindopril and the combination reduced angiotensin II levels in kidney of (mRen-2)27 rats. By contrast, aliskiren and the combination, bu...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019078</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019078</guid>        </item>
        <item>
            <title>Elevation of liver enzymes within the normal limits and metabolic syndrome: Response to Kawada.</title>
            <link>http://www.medworm.com/index.php?rid=5019099&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21729144%26dopt%3DAbstract</link>
            <description>Authors: Gao X, Xia M
    
    PMID: 21729144 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019099</comments>
            <pubDate>Tue, 05 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019099</guid>        </item>
        <item>
            <title>Cardiac ischemic stress: cardiomyocyte Ca2+, sex and sex steroids.</title>
            <link>http://www.medworm.com/index.php?rid=5019102&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21722161%26dopt%3DAbstract</link>
            <description>Authors: Bell JR, Mellor KM, Wollermann AC, Delbridge LM
    1. Important sex differences exist in ischemic heart disease. Estrogen has been conventionally regarded as providing a cardioprotective benefit and testosterone frequently perceived to exert a deleterious effect. However, there is accumulating evidence which argues against this simple dichotomy, suggesting that the influence of estrogen and testosterone conferring benefit or detriment may be context specific. 2. Cardiomyocyte calcium (Ca(2+) ) loading is recognized to be a major factor in acute ischemia/reperfusion pathology, promoting cell death, contractile dysfunction and arrhythmogenic activity. Ca(2+) /calmodulin-dependent kinase II (CaMKII) is a mediator of many of the cardiomyocyte Ca(2+) -related pathologies in ischemia/r...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019102</comments>
            <pubDate>Sun, 03 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019102</guid>        </item>
        <item>
            <title>Advances in stroke care and research in 2010.</title>
            <link>http://www.medworm.com/index.php?rid=5019101&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21722162%26dopt%3DAbstract</link>
            <description>Authors: Wang CJ, Wang CX, Zhang L, Wang YL, Wang YJ
    1. There have been many advances in stroke research and care over the past year. The aim of the present review is to highlight the significant advances that are likely to have considerable impact on the direction of future investigations and models of clinical practice. 2. In terms of the acute treatment of stroke, there is now Level I evidence for the use of thrombolysis in the treatment of ischaemic stroke. The results of clinical trials suggest potential new treatments for stroke of inherited origin, whereas other potential treatments have been suggested following the identification of a novel mechanism of emboli clearance by extravasation. Clinical guidelines have also been updated, with tight blood pressure control advocated in ...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019101</comments>
            <pubDate>Sun, 03 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019101</guid>        </item>
        <item>
            <title>Effects of a maternal diet supplemented with chocolate and fructose beverage during gestation and lactation on rat dams and their offspring.</title>
            <link>http://www.medworm.com/index.php?rid=5019100&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21722163%26dopt%3DAbstract</link>
            <description>Authors: Zhang ZY, Zeng JJ, Kjaergaard M, Guan N, Raun K, Nilsson C, Wang MW
    1. High-fat and high-energy diet during pregnancy leads to a risk for long-term consequences on fetal development as well as postnatal health of offspring. To investigate the effects of such diet on fetal programming, we established a high-energy intake pregnant rat model using chocolate and fructose beverage as supplement to a normal chow diet. 2. Pregnant Sprague-Dawley rats were assigned to either chow (control) or a diet supplemented with chocolate and fructose throughout gestation and lactation. The male F1 pups received normal chow diet after weaning. Physiological or pathological changes in dams and pups, e.g., glucose and lipid metabolism, were evaluated. 3. Our study suggests that dams, offered high-f...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019100</comments>
            <pubDate>Sun, 03 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019100</guid>        </item>
        <item>
            <title>Proposed pathophysiological mechanisms of bovine serum albumin (BSA)-induced membranous nephropathy. See Ronco &amp; Debiec, pp 410-416.</title>
            <link>http://www.medworm.com/index.php?rid=5019111&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21702764%26dopt%3DAbstract</link>
            <description>Authors: 
    Cover image:â€‚ Proposed pathophysiological mechanisms of bovine serum albumin (BSA)-induced membranous nephropathy. See Ronco &amp; Debiec, pp 410-416. â€¢ â€‚NHE3 and acidification in epididymal fluid â€¢ â€‚Mediators of von Bezold-Jarisch reflex actions of BNP â€¢ â€‚Sulfur dioxide and calcium channel â€¢ â€‚Chelation in GaAs intoxication â€¢ â€‚Antithrombotic effects of TB-II â€¢ â€‚Effect of ACh on oocyte maturation â€¢ â€‚Frontiers in Research: Chronic Kidney Disease.
    PMID: 21702764 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019111</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019111</guid>        </item>
        <item>
            <title>Heme oxygenase 1 may mediate the protective effects of hyperbaric oxygen preconditioning against hepatic ischemia-reperfusion injury in rats.</title>
            <link>http://www.medworm.com/index.php?rid=5019109&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21711378%26dopt%3DAbstract</link>
            <description>In conclusion, HBO preconditioning can protect the liver against I/R injury and it appears that this effect may be mediated by the induction of HO-1.
    PMID: 21711378 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019109</comments>
            <pubDate>Mon, 27 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019109</guid>        </item>
        <item>
            <title>Rho kinase inhibition by fasudil exerts anti-oxidant effects in hypercholesterolemic rats.</title>
            <link>http://www.medworm.com/index.php?rid=5019107&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21711379%26dopt%3DAbstract</link>
            <description>Authors: Ma Z, Zhang J, Ji E, Cao G, Li G, Chu L
    1. Inhibition of Rho kinase (ROCK) ameliorates many cardiovascular dysfunctions, but the role of ROCK in oxidative stress in hypercholesterolemic rats has not been explored. The aim of the current study was to investigate the anti-oxidant effects and the potential related mechanisms of fasudil, a selective ROCK inhibitor, in high cholesterol diet (HCD)-induced hypercholesterolemic rats. 2. Hypercholesterolemia was induced in rats by feeding with a HCD for 4 weeks. Starting from day 15, physiological saline (1 ml/100 g) or ROCK inhibitor fasudil (10 or 30 mg/kg) was injected intraperitoneally (i.p.) for another 14 days. 3. The results showed that fasudil significantly suppressed ROCK activity, potently elevated the activities of anti-oxid...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019107</comments>
            <pubDate>Mon, 27 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019107</guid>        </item>
        <item>
            <title>Multiple factors are required for prediction of metabolic syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=5019106&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21711380%26dopt%3DAbstract</link>
            <description>Authors: Kawada T
    
    PMID: 21711380 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019106</comments>
            <pubDate>Mon, 27 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019106</guid>        </item>
        <item>
            <title>Mechanisms of reduced contractility in an animal model of hypertensive heart failure.</title>
            <link>http://www.medworm.com/index.php?rid=5019105&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21711381%26dopt%3DAbstract</link>
            <description>Authors: Ward ML, Crossman DJ, Cannell MB
    1. Alterations in intracellular Ca(2+) homeostasis have frequently been implicated as underlying the contractile dysfunction of failing hearts. Contraction in cardiac muscle is due to a balance between sarcolemmal (SL) and sarcoplasmic reticulum (SR) Ca(2+) transport which has been studied in single cells and small tissue samples. However, many studies have not used physiological temperatures and pacing rates, and this could be problematic given different temperature dependencies and kinetics for transport processes. 2. The spontaneously hypertensive rat (SHR) and their age-matched Wistar Kyoto controls (WKY) provide an animal model of hypertensive failure with many features in common to heart failure in humans. Steady-state measurements of Ca(...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019105</comments>
            <pubDate>Mon, 27 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019105</guid>        </item>
        <item>
            <title>Are threshold levels of signal transduction required for the protective effect of cilostazol against cardiac ischaemia reperfusion injury?</title>
            <link>http://www.medworm.com/index.php?rid=5019104&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21711382%26dopt%3DAbstract</link>
            <description>Authors: Reis F
    
    PMID: 21711382 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019104</comments>
            <pubDate>Mon, 27 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019104</guid>        </item>
        <item>
            <title>Nitric oxide synthase activity in the abdominal aorta of rats is decreased after 4 weeks of simulated microgravity.</title>
            <link>http://www.medworm.com/index.php?rid=5019103&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21711383%26dopt%3DAbstract</link>
            <description>Authors: Ren XL, Zhang R, Zhang YY, Liu H, Yu JW, Cai Y, Wang ZC, Purdy RE, Ma J
    The aim of this work was to investigate the effects of simulated microgravity on the arterial dilatory responsiveness and L-arginine (L-Arg)-nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathway in the abdominal aorta of rats. Twenty healthy male Sprague-Dawley (SD) rats were randomly divided into control and simulated microgravity groups. Rats in the simulated microgravity group were subjected to hindlimb unweighting (HU). After 4 weeks, arterial dilatory responsiveness was examined in vitro by using isolated abdominal aortic rings. Western blotting was used to measure the endothelial NO synthase (eNOS) and inducible NOS (iNOS) protein content. Total concentrations of nitrate and nitrite (NOx), ...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5019103</comments>
            <pubDate>Mon, 27 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5019103</guid>        </item>
        <item>
            <title>Arterial remodeling following pressure overload by aortic constriction: An overlooked and potentially fertile research area.</title>
            <link>http://www.medworm.com/index.php?rid=4971260&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21692825%26dopt%3DAbstract</link>
            <description>Authors: Du XJ, Kiriazis H, Dart AM
    
    PMID: 21692825 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971260</comments>
            <pubDate>Tue, 21 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971260</guid>        </item>
        <item>
            <title>Calcium-sensing receptors induce apoptosis during simulated ischemia-reperfusion in BRL cells.</title>
            <link>http://www.medworm.com/index.php?rid=4971259&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21692826%26dopt%3DAbstract</link>
            <description>In conclusion, increased CaSR expression plays a vital role in apoptosis induced by I/R injury, which mechanism is related with calcium overload, and activation of mitochondrial and MAPK apoptotic pathways. Regulation of CaSR activity may serve as a novel pharmacological target to prevent and treat liver disease.
    PMID: 21692826 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971259</comments>
            <pubDate>Tue, 21 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971259</guid>        </item>
        <item>
            <title>Emerging Clinical and Experimental Evidence for the Role ofLipocalin-2 in Metabolic Syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=4971261&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21689137%26dopt%3DAbstract</link>
            <description>Authors: Jang YS, Lee JH, Wang Y, Sweeney G
    The inflammatory state which is associated with the current pandemic of obesity has been established as an important contributing pathogenic factor to the increased prevalence of the so called metabolic syndrome. Many studies have focused on the contribution of various adipokines to this phenomenon and here we provide an update on the emerging evidence that the pro-inflammatory factor lipocalin-2 may influence various aspects of the metabolic syndrome. Previous reports indicate a positive correlation of serum lipocalin-2 with fasting glucose, homeostasis model assessment of insulin resistance (HOMA-IR) index, and the inflammatory marker high-sensitivity C-reactive protein, even after adjustment for BMI, suggesting that it is an independent ri...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971261</comments>
            <pubDate>Sun, 19 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971261</guid>        </item>
        <item>
            <title>Association of the aldosterone synthase gene -344T&gt;C polymorphism with essential hypertension and glucose homeostasis: A case-control study in a Han Chinese population.</title>
            <link>http://www.medworm.com/index.php?rid=4971263&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21682760%26dopt%3DAbstract</link>
            <description>Authors: Li XM, Ling Y, Lu DR, Lu ZQ, Yi QL, Liu Y, Chen HY, Gao X
    Aldosterone is a hormone that affects both blood pressure and glucose homeostasis. We studied the association of the aldosterone synthase gene (CYP11B2) polymorphism -344T&amp;gt;C with essential hypertension (EH) and glucose homeostasis in people in China. We investigated the polymorphism -344T&amp;gt;C in CYP11B2 using a case-control study design (1059 cases and 1120 controls). Genotyping was performed by matrix-assisted laser desorption/ionization time-of-flight mass spectroscopy using a MassARRAY platform. The aldosterone synthase gene -344T&amp;gt;C polymorphism was found to be associated with EH (odds ratio, 1.252; 95% confidence interval, 1.067-1.468; P(add) , 0.006). The -344C variant was found to be significantly associate...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971263</comments>
            <pubDate>Thu, 16 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971263</guid>        </item>
        <item>
            <title>NMDA - receptor modulators block hyperalgesia induced by acute low dose morphine.</title>
            <link>http://www.medworm.com/index.php?rid=4971262&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21682761%26dopt%3DAbstract</link>
            <description>Authors: Gupta LK, Gupta R, Tripathi CD
    Following opioid-induced antinociception in mice, hyperalgesic responses may be observed. The current study was designed to evaluate the effect of different NMDA receptor modulators (magnesium, dextromethorphan, D-serine) on the development of morphine-induced hyperalgesia. The tail-flick test in mice was used to assess the effects of morphine alone and in combination with NMDA receptor modulators. Administration of a single low- dose (2 mg/kg) of morphine produced antinociception which was followed by hyperalgesia in mice. Administration of magnesium sulphate (5 mg/kg) and D-serine (10 mg/kg) alone produced a transient antinociceptive response while dextromethorphan (10 mg/kg) alone produced a relatively delayed onset and prolonged antinocicepti...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971262</comments>
            <pubDate>Thu, 16 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971262</guid>        </item>
        <item>
            <title>Heart Failure Enhances Arrhythmogenesis in Pulmonary Veins.</title>
            <link>http://www.medworm.com/index.php?rid=4971266&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21671985%26dopt%3DAbstract</link>
            <description>This study aimed to investigate the impact of HF on the electrical remodeling of the pulmonary veins (PVs) and left atrium (LA). The electrical activity was recorded in LAs and PVs from control rabbits and rabbits with rapid ventricular pacing-induced HF, using a multielectrode array system, and conventional microelectrodes. Compared with the control-PVs (n=21), the HF-PVs (n=13) had a higher incidence and frequency of rapid pacing-induced spontaneous activity (85% vs. 29%, P=0.005; 3.5Â±0.2 vs. 1.7Â±0.1 Hz, P&amp;lt;0.001) and high-frequency irregular electrical activity (92% vs. 38%, P=0.01; 23Â±1 vs. 19Â±1 Hz, P=0.003), greater depolarized resting membrane potential (-59Â±1 vs. -70Â±2 mV, P&amp;lt;0.001), higher incidence of early afterdepolarizations (EAD, 69% vs. 6%, P=0.001) and delayed afte...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971266</comments>
            <pubDate>Tue, 14 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971266</guid>        </item>
        <item>
            <title>Phenotype and differentiation of bone marrow-derived smooth muscle progenitor cells.</title>
            <link>http://www.medworm.com/index.php?rid=4971265&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21671986%26dopt%3DAbstract</link>
            <description>Authors: Liu Y, Liu M, Niu W, Luo Y, Zhang B, Li Z
    Smooth muscle progenitor cells (SPC) are undifferentiated vascular smooth muscle cells implicated in many hyperplastic diseases of the blood vessels. However, few in vitro studies have investigated the characteristics of SPC. In the present study, we constructed a recombinant plasmid with the enhanced green fluorescent protein (GFP) gene and a rat SM22Î± promoter, which was exclusively promoted in a smooth muscle cell lineage. Constructs were then transferred into adherent mononuclear cells derived from rat bone marrow. After 3 days, GFP-positive cells, which should be SPC, were isolated by flow cytometry. Flow cytometric analysis and dual immunofluorescent staining revealed that the GFP-positive cells expressed both Î±-smooth muscle a...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971265</comments>
            <pubDate>Tue, 14 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971265</guid>        </item>
        <item>
            <title>Cilostazol protects the heart against ischaemia reperfusion injury in a rabbit model of myocardial infarction: Focus on adenosine, nitric oxide and mitochondrial KATP channels.</title>
            <link>http://www.medworm.com/index.php?rid=4971264&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21679220%26dopt%3DAbstract</link>
            <description>This study examined whether cilostazol reduces the myocardial infarct size and to investigated its mechanism in a rabbit model of myocardial infarction. 2)â€‚Japanese white rabbits underwent 30 min of coronary occlusion, followed by 48 hours of reperfusion. Cilostazol (1 and 5 mg/kg) or vehicle was intravenously administered 5 min before ischaemia. 8-p-Sulfophenyl theophylline (8SPT, an adenosine receptor blocker, 7.5 mg/kg), NÏ‰-nitro-L-arginine methylester (L-NAME, an NOS inhibitor, 10 mg/kg), or 5-hydroxydecanoic acid sodium salt (5-HD, a mitochondrial KATP channel blocker, 5 mg/kg) was intravenously administered 5 min before cilostazol injection. Infarct size was determined as a percentage of the risk area. 3)â€‚The myocardial interstitial levels of adenosine and nitrogen oxide (NOx) d...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971264</comments>
            <pubDate>Tue, 14 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971264</guid>        </item>
        <item>
            <title>Effect of weight loss on gelatinase levels in obese mice.</title>
            <link>http://www.medworm.com/index.php?rid=4971267&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21671984%26dopt%3DAbstract</link>
            <description>Authors: Van Hul M, Lijnen HR
    Gelatinases (MMP-2 and MMP-9) may play a role in development and structural organization of adipose tissue. Obese mice were subjected to caloric restriction (from 82 to 27 kJ/day) during 6 weeks, in order to investigate the effect of drastic weight loss on gelatinase mRNA, protein and activity levels. Caloric restriction resulted in significantly lower body weight as well as subcutaneous (SC) and gonadal (GON) fat mass (all p &amp;lt; 0.001). The expression of MMP-2 mRNA was significantly upregulated in both SC (3.3-fold) and GON (2.2-fold) adipose tissues, however, without significant effect on total MMP-2 protein levels in fat tissues or in plasma. In contrast, MMP-9 mRNA expression in SC or GON fat was not affected by caloric restriction, whereas protein le...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4971267</comments>
            <pubDate>Mon, 13 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4971267</guid>        </item>
        <item>
            <title>Neuroprotective effects of estrogen against oxidative toxicity through activation of GPR30 receptor.</title>
            <link>http://www.medworm.com/index.php?rid=4922743&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21645039%26dopt%3DAbstract</link>
            <description>Authors: Liu SB, Han J, Zhang N, Tian Z, Li XB, Zhao MG
    1.â€‚17-Î²-estradiol (E2) plays a critical role in neuroprotection through both genomic and nongenomic mechanisms. The aim of the present study was to investigate the role of G-protein-coupled receptor 30 (GPR30), a new kind of estrogen receptor, in the neuroprotection against oxidative insult. 2.â€‚The neuroprotection evoked by GPR30 stimulation was examined in cultured cortical neurons. Hoechst 33258/PI double staining, flow cytometric analysis, and Western blotting were applied to assess neuronal apoptosis induced by H(2) O(2) . 3.â€‚We found that the GPR30 agonist G1 and E2 attenuated apoptosis induced by H(2) O(2) exposure. Furthermore, G1 (1 nM) or E2 (1 nM) significantly increased the levels of phosphorylated ERK1/2 (p-ERK1...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922743</comments>
            <pubDate>Sun, 05 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922743</guid>        </item>
        <item>
            <title>Celecoxib Does Not Alter Cardiovascular and Renal Function During Dietary Salt Loading.</title>
            <link>http://www.medworm.com/index.php?rid=4922746&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21631568%26dopt%3DAbstract</link>
            <description>In conclusion, blood pressure and renal function were not adversely affected by celecoxib, even during dietary salt loading. These findings support current guidelines suggesting minimal cardiovascular risks associated with short-term, low-dose use of celecoxib in young to middle-aged adults.
    PMID: 21631568 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922746</comments>
            <pubDate>Tue, 31 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922746</guid>        </item>
        <item>
            <title>Epidermal growth factor receptor signaling mediates growth hormone-induced growth of chondrocytes from sex hormone-inhibited adolescent rats.</title>
            <link>http://www.medworm.com/index.php?rid=4922745&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21631569%26dopt%3DAbstract</link>
            <description>Authors: Pan SN, Ma HM, Su Z, Zhang CX, Zhu SY, Du ML
    Growth hormone (GH) has been demonstrated to overcome the inappropriate deceleration of growth rate in central precocious puberty (CPP) children treated with gonadotropin releasing hormone analog (GnRHa). However, the underlying mechanisms remain largely unclear. In the present study, we investigate the potential involvement of the epidermal growth factor receptor (EGFR) pathway in the growth promotion by GH using in vitro cultured growth plate chondrocytes isolated from adolescent rats treated with GnRHa. The chondrocytes were stimulated with GH in the presence or absence of Janus tyrosine kinase 2 (JAK2) inhibitor AG490, EGFR kinase inhibitor AG1478, Erk activation inhibitor U0126 or a neutralizing antibody against EGF (EGF-Ab). T...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922745</comments>
            <pubDate>Tue, 31 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922745</guid>        </item>
        <item>
            <title>NAMPT -3186C/T polymorphism influences repaglinide response in Chinese patients with type 2 diabetes mellitus.</title>
            <link>http://www.medworm.com/index.php?rid=4922744&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21631570%26dopt%3DAbstract</link>
            <description>Authors: Sheng FF, Dai XP, Qu J, Lei GH, Lu HB, Wu J, Xu XJ, Pei Q, Dong M, Liu YZ, Zhou HH, Liu ZQ
    1. We identified the associations of NAMPT -3186 C/T and -948G/T polymorphisms with risk of type 2 diabetes mellitus (T2DM) and their impacts on efficacy of repaglinide in Chinese Han T2DM patients. 2. 170 patients with T2DM and 129 healthy controls were genotyped for NAMPT -948G&amp;gt;T and -3186C&amp;gt;T polymorphisms. Thirty-five patients with different genotype of NAMPT -3186 C/T and the same OATP1B1 521 T/C genotypes were randomly selected and underwent an 8-week preprandial repaglinide treatment (1mg, 3 times daily). Serum fasting plasma glucose (FPG), postprandial plasma glucose (PPG), glycated hemoglobin (HbAlc), fasting serum insulin (FINS), postprandial serum insulin (PINS), triglyce...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4922744</comments>
            <pubDate>Tue, 31 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4922744</guid>        </item>
        <item>
            <title>First molar of a six-week-old mouse over-expressing human fibroblast growth factor 23, stained with haematoxylin-eosin. See Chen et al., pp 395-402.</title>
            <link>http://www.medworm.com/index.php?rid=4877069&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21605141%26dopt%3DAbstract</link>
            <description>Authors: 
    Cover image:â€‚ First molar of a six-week-old mouse over-expressing human fibroblast growth factor 23, stained with haematoxylin-eosin. See Chen et al., pp 395-402. â€¢ â€‚PPARÎ³ downregulates sEH in heart â€¢ â€‚Fluoxetine inhibits PAH by OPN downregulation â€¢ â€‚Liver enzymes and metabolic syndrome â€¢ â€‚Effects of NO on A(2A) R and ACh in the RVLM â€¢ â€‚Fasudil and cardiac fibroblast functions â€¢ â€‚Effect of fibroblast growth factor 23 on teeth.
    PMID: 21605141 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4877069</comments>
            <pubDate>Mon, 30 May 2011 07:30:55 +0100</pubDate>
            <guid isPermaLink="false">4877069</guid>        </item>
        <item>
            <title>Data interpretation: using probability.</title>
            <link>http://www.medworm.com/index.php?rid=4877068&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21605142%26dopt%3DAbstract</link>
            <description>Authors: Drummond GB, Vowler SL
    
    PMID: 21605142 [PubMed - in process] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4877068</comments>
            <pubDate>Mon, 30 May 2011 07:30:27 +0100</pubDate>
            <guid isPermaLink="false">4877068</guid>        </item>
        <item>
            <title>Effect of an acute mechanical stimulus on aortic structure in the transverse aortic constriction mouse model.</title>
            <link>http://www.medworm.com/index.php?rid=4877067&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21615773%26dopt%3DAbstract</link>
            <description>In conclusion, aortic structure undergoes considerable remodeling by an acute mechanical stimulus in the TAC model, mainly in the adventitia. Upregulation of Î±-SM-actin and extracellular matrix components accompanied by macrophage infiltration might contribute to adventitial modification in TAC mice.
    PMID: 21615773 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4877067</comments>
            <pubDate>Wed, 25 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4877067</guid>        </item>
        <item>
            <title>A possible role for the thioredoxin system in the protective effects of probucol in the pancreatic islets of diabetic rats.</title>
            <link>http://www.medworm.com/index.php?rid=4877066&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21615774%26dopt%3DAbstract</link>
            <description>Authors: Liu JH, Liu DF, Wang NN, Lin HL, Mei X
    1.â€‚Probucol, a lipid-lowering agent with potent antioxidant action, has been shown to protect diabetic pancreatic islets by an unknown mechanism. Thioredoxin-interacting protein (TXNIP), an endogenous inhibitor of the ubiquitous thiol oxidoreductase, thioredoxin (TRX), has been associated with oxidative stress in diabetic rat islets. The present study aimed to examine the effects of probucol on diabetic islet function and expression of TRX and TXNIP. 2.â€‚Thirty rats were randomly assigned to a normal control group, a diabetic group, and a probucol-treated diabetic group. After 8 weeks' treatment with probucol (500 mg/kg Â· day), plasma malonaldehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) levels were measured by chemical ...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4877066</comments>
            <pubDate>Wed, 25 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4877066</guid>        </item>
        <item>
            <title>Inhibition of octreotide on the capsaicin-induced activation of C and AÎ´ afferent fibers in rat hairy skin in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=4877070&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21595740%26dopt%3DAbstract</link>
            <description>This study investigated whether the somatostatin receptor (SSTR) agonist octreotide could inhibit the activation of dorsal skin afferent fibers induced by local injection of capsaicin in the rat. 2. Single unit activity from AÎ´ mechano-heat sensitive (AMH, n = 41) and C mechano-heat sensitive (CMH, n = 30) afferents was recorded following their isolation in thin filaments from the dorsal cutaneous nerve branches. The effect of subcutaneous octreotide injection on the change in discharge rate and mechanical threshold induced by capsaicin was determined. 3. Capsaicin (0.05%) injection into the edge of receptive field of both AMH and CMH units increased their discharge rate and decreased their mechanical threshold. Pre-injection of octreotide inhibited these responses, and co-application of ...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4877070</comments>
            <pubDate>Thu, 19 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4877070</guid>        </item>
        <item>
            <title>Indomethacin abolishes core temperature but neither cardiovascular nor renal responses to lipopolysaccharide in conscious lambs.</title>
            <link>http://www.medworm.com/index.php?rid=4877073&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21585420%26dopt%3DAbstract</link>
            <description>INDOMETHACIN ABOLISHES CORE TEMPERATURE BUT NEITHER CARDIOVASCULAR NOR RENAL RESPONSES TO LIPOPOLYSACCHARIDE IN CONSCIOUS LAMBS.
    Clin Exp Pharmacol Physiol. 2011 May 17;
    Authors: Smith FG, Fewell JE, Qi W
    (1). Core temperature (Tc), cardiovascular, and renal responses to lipopolysaccharide (LPS) as well as the role of endogenously produced prostaglandins (PG's) in influencing these responses were investigated in conscious, chronically instrumented lambs. (2). Tc, mean arterial pressure (MAP), heart rate (HR), renal blood flow (RBF), and several parameters of renal function were measured for 30 min before and for 5 h after intravenous (I.V.) injection of 0.03 Î¼gÂ·kg(-1) of the LPS Salmonella abortus equi (SAE, n=9) or saline vehicle (n=9). (3). Tc increased after LPS with a lat...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4877073</comments>
            <pubDate>Mon, 16 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4877073</guid>        </item>
        <item>
            <title>Leukemia inhibitory factor is expressed in rat gastrocnemius after contusion and increases proliferation of rat myoblasts via c-Myc signalling.</title>
            <link>http://www.medworm.com/index.php?rid=4877072&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21585421%26dopt%3DAbstract</link>
            <description>Authors: Srikuea R, Esser KA, Pholpramool C
    Leukemia inhibitory factor (LIF) was demonstrated to play an important role during muscle regeneration. The regenerative capacity in muscles of LIF knockout was impaired compared to wild-type mice after contusion injury. To clarify whether LIF modulates muscle regeneration by regulation of myogenic precursor cell activity, we have studied LIF expression and myogenic precursor cell activity in Wistar rat gastrocnemius muscle at various times after contusion injury using immunohistochemistry in vivo and the direct effect of LIF on rat myoblast cell line (L6) in vitro. After contusion injury, a transient up-regulation of LIF, LIF receptors and STAT3 (a downstream pathway of LIF to enhance cell proliferation) mRNA expression were observed. A mark...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4877072</comments>
            <pubDate>Mon, 16 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4877072</guid>        </item>
        <item>
            <title>The role of mineralocorticoid action in the brain in salt-sensitive hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=4877071&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21585422%26dopt%3DAbstract</link>
            <description>Authors: Oki K, Gomez-Sanchez EP, Gomez-Sanchez CE
    The mechanisms by which excessive salt causes hypertension involve more than retention of sodium and water by the kidneys and are far from clear. Mineralocorticoids act centrally to increase salt appetite, sympathetic drive and vasopressin release, resulting in hypertension that is prevented by the central infusion of mineralocorticoid receptor (MR) antagonists. The MR has similar affinity for aldo and the glucocorticoids corticosterone or cortisol. Specificity is conferred in transport epithelia by the co-localization of the MR with 11Î²-hydroxysteroid dehydrogenase type 2. Co-expression also occurs in some neurons, notably those of the nucleus tractus solitarius that are activated by sodium depletion and aldo and mediate salt seeking...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4877071</comments>
            <pubDate>Mon, 16 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4877071</guid>        </item>
        <item>
            <title>Tetrodotoxin Alleviates Acute Heroin Withdrawal Syndrome: A Multicenter, Randomized, Double-blind and Placebo-controlled Study.</title>
            <link>http://www.medworm.com/index.php?rid=4877075&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21575032%26dopt%3DAbstract</link>
            <description>In conclusion, this clinical trial shows that TTX (5 Î¼g and 10 Î¼g given 3 times daily) is effective in alleviating opiate withdrawal symptoms with few side effects.
    PMID: 21575032 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4877075</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4877075</guid>        </item>
        <item>
            <title>The effect of clazosentan, a selective endothelin A receptor antagonist, and tezosentan, a dual endothelin A/B antagonist, on pulsatile shear stress induced constriction of the iliac in the anaesthetised pig.</title>
            <link>http://www.medworm.com/index.php?rid=4877074&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21575033%26dopt%3DAbstract</link>
            <description>In conclusion, an increase in pulsatile shear stress causes vasoconstriction of the pig iliac artery which is attenuated by dual endothelin receptor antagonism, but not by specific endothelin A blockade.
    PMID: 21575033 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4877074</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4877074</guid>        </item>
        <item>
            <title>Inhibition of Nitric Oxide Synthase Uncoupling by Sepiapterin Improves Left Ventricular Function in Streptozotocin-induced Diabetic Mice.</title>
            <link>http://www.medworm.com/index.php?rid=4824213&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21554376%26dopt%3DAbstract</link>
            <description>Authors: Jo H, Otani H, Jo F, Shimazu T, Okazaki T, Yoshioka K, Fujita M, Kosaki A, Iwasaka T
    The uncoupling of nitric oxide synthase (NOS) has been implicated in the pathogenesis of left ventricular (LV) dysfunction in diabetes mellitus (DM). We investigated the role of NOS uncoupling in oxidative/nitrosative stress and LV dysfunction in the diabetic mouse heart. DM was induced in wild-type (WT), eNOS knockout (eNOS-/-), iNOS knockout (iNOS-/-), and nNOS knockout (nNOS-/-) mice by streptozotocin (STZ) treatment. iNOS but not eNOS or nNOS expression was increased in the diabetic heart. Malondialdehyde (MDA), 4-hydroxy-noneal (HNE) and nitrotyrosine (NT) as markers of oxidative/nitrosative stress increased in the diabetic mouse heart, but the increase in oxidative/nitrosative stress was...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4824213</comments>
            <pubDate>Sun, 08 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4824213</guid>        </item>
        <item>
            <title>Renal Tubulointerstitial Hypoxia: Cause and Consequence of Kidney Dysunction.</title>
            <link>http://www.medworm.com/index.php?rid=4824216&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21545630%26dopt%3DAbstract</link>
            <description>Authors: Palm F, Nordquist L
    1. Intrarenal oxygen availability is the balance between supply, mainly dependent on renal blood flow, and demand, determined by the basal metabolic demand and the energy-requiring tubular electrolyte transport. Renal blood flow is maintained within close limits in order to sustain stable glomerular filtration, so increased intrarenal oxygen consumption is likely to cause tissue hypoxia. 2. The increased oxygen consumption is closely linked to increased oxidative stress, which increases mitochondrial oxygen usage and reduces tubular electrolyte transport efficiency; both contributing to increased total oxygen consumption. 3. Tubulointerstitial hypoxia stimulates productions of collagen I and Î±-smooth muscle actin, indications of increased fibrogenesis. Fur...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
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            <pubDate>Wed, 04 May 2011 23:00:00 +0100</pubDate>
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            <title>Acetylcholine controls mouse oocyte maturation through down-regulation of cAMP.</title>
            <link>http://www.medworm.com/index.php?rid=4824215&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21545631%26dopt%3DAbstract</link>
            <description>Authors: Yoon SY, Choe C, Kim EJ, Kim CW, Han J, Kang D
    Acetylcholine (ACh) plays an important role in the oocyte activation and embryonic development in mice. However, the role of ACh in mouse oocyte maturation has not been addressed. The effect of ACh on maturation processes of murine germinal vesicle (GV)-intact oocytes (oocytes(GV) ) exposed to 3-isobutyl-1-methylxanthine (IBMX), an inhibitor of cyclic nucleotide phosphodiesterase was evaluated morphologically and immunologically. The IBMX inhibits the resumption of meiosis by preventing cAMP breakdown. At the start of the in vitro culture, 100% of the oocytes were at the GV stage. After 18 hours of culture, 95.0 Â± 3.0%, 0%, and 85.8 Â± 10.2% of oocytes had passed the GV stage in the control, IBMX, and IBMX + ACh groups, respectiv...</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
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            <pubDate>Wed, 04 May 2011 23:00:00 +0100</pubDate>
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            <title>Frontiers in Research: Chronic Kidney Disease Introduction: hearing footsteps of the future.</title>
            <link>http://www.medworm.com/index.php?rid=4824214&amp;cid=s_32541_13_f&amp;fid=32541&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21545632%26dopt%3DAbstract</link>
            <description>Authors: Nangaku M, Nishiyama A
    
    PMID: 21545632 [PubMed - as supplied by publisher] (Source: Clinical and Experimental Pharmacology and Physiology)</description>
            <author>Clinical and Experimental Pharmacology and Physiology</author>
            <type>journals</type>
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            <pubDate>Wed, 04 May 2011 23:00:00 +0100</pubDate>
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