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        <title>Cardiovascular Toxicology 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 'Cardiovascular Toxicology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Cardiovascular+Toxicology&t=Cardiovascular+Toxicology&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 09:32:33 +0100</lastBuildDate>
        <item>
            <title>Leflunomide-Induced Pulmonary Hypertension in a Young Woman with Rheumatoid Arthritis: A Case Report.</title>
            <link>http://www.medworm.com/index.php?rid=5642910&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22270725%26dopt%3DAbstract</link>
            <description>We present a 28-year-old woman with a history of RA who consulted our hospital because of severe symptomatic pulmonary hypertension. Two years before admission, she was started on leflunomide. Due to previous evidence of the association of leflunomide with pulmonary hypertension, the drug was stopped. The patient became asymptomatic with normal pulmonary arterial pressure within a year. Given the poor prognosis of idiopathic pulmonary arterial hypertension, the recognition of potentially reversible causes is crucial. Until further evidence is available in a patient who develops pulmonary arterial hypertension, stopping leflunomide should be considered.
    PMID: 22270725 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5642910</comments>
            <pubDate>Tue, 24 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>A Case of Caffeine-Induced Coronary Artery Vasospasm of a 17-Year-Old Male.</title>
            <link>http://www.medworm.com/index.php?rid=5578996&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22231478%26dopt%3DAbstract</link>
            <description>We report on a case of a 17-year-old male who presented with angina and an abnormal electrocardiogram (ECG) concerning for ST elevation myocardial infarct. He was found to have diffuse ECG changes and markedly elevated cardiac enzymes. A transthoracic echocardiogram revealed a reduced left ventricular (LV) systolic function as well as segmental wall motion abnormalities consistent with an ischemic insult. The patient admitted to consuming near lethal doses of caffeine immediately preceding his angina. He was diagnosed with coronary vasospasms as a result of stimulant use. During hospitalization, ECG changes resolved, cardiac enzymes started trending downward, and LV systolic function returned to normal, all consistent with stunned myocardium that fully recovered. This case strongly suggest...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578996</comments>
            <pubDate>Wed, 11 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>What are the Values of Using QTc and N-Terminal Fragment of B-Type Natriuretic Peptide as Markers for Early Detection of Acute Antipsychotic Drugs-Induced Cardiotoxicity?</title>
            <link>http://www.medworm.com/index.php?rid=5551636&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22205425%26dopt%3DAbstract</link>
            <description>Authors: Sanaei-Zadeh H
    PMID: 22205425 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5551636</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Toxic Effects of Marijuana on the Cardiovascular System.</title>
            <link>http://www.medworm.com/index.php?rid=5536864&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22194141%26dopt%3DAbstract</link>
            <description>We present a case of marijuana-induced ST segment elevation mimicking Brugada syndrome in a young man. Cannabis can have a multitude of effects on the different organ systems of the body; we take a closer look at its effects on the cardiovascular system, including acute coronary syndrome, arrhythmias and congestive heart failure.
    PMID: 22194141 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536864</comments>
            <pubDate>Fri, 23 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536864</guid>        </item>
        <item>
            <title>Prediction of Anthracycline Cardiotoxicity after Chemotherapy by Biomarkers Kinetic Analysis.</title>
            <link>http://www.medworm.com/index.php?rid=5536865&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22189487%26dopt%3DAbstract</link>
            <description>Authors: Garrone O, Crosetto N, Lo Nigro C, Catzeddu T, Vivenza D, Monteverde M, Merlano M, Feola M
    Abstract
    Anthracyclines are active drugs against breast cancer, but can exert cardiotoxic effects. We analyzed the association between the kinetics of various biomarkers during chemotherapy, and the risk of subsequent cardiac toxicity. 50 patients (49 women) with early breast cancer surgically treated and eligible to anthracycline-based adjuvant chemotherapy were analyzed. The left ventricular ejection fraction (LVEF) together with the plasma concentration of several blood markers was measured at the beginning of anthracycline chemotherapy (t           (0)), 5 months (t           (1)), 16 months (t           (2)), 28 months (t           (3)), and 40 months later (t           (4))...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536865</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536865</guid>        </item>
        <item>
            <title>Molecular Analysis of Mitochondrial Compromise in Rodent Cardiomyocytes Exposed Long Term to Nucleoside Reverse Transcriptase Inhibitors (NRTIs).</title>
            <link>http://www.medworm.com/index.php?rid=5514741&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22170576%26dopt%3DAbstract</link>
            <description>Authors: Liu Y, Nguyen P, Baris TZ, Poirier MC
    Abstract
    Despite the highly effective impact of NRTI therapy in patients infected with the human immunodeficiency virus type 1 (HIV-1), long-term treatment has revealed cardiotoxicity, considered to be due to mitochondrial dysfunction. To evaluate mitochondrial damage, and design therapeutic interventions, we established cultures of rat H9c2 and mouse HL-1 cardiomyocytes and exposed them to the NRTIs zidovudine (AZT), and AZT plus didanosine (ddI). Proliferation assays showed that H9c2 cells grew well in 50 μM AZT and 50 μM AZT/50 μM ddI and that HL-1 cells grew well in 10 μM AZT and 10 μM AZT/10 μM ddI. Both types of cells were exposed to the drugs for 39 passages (P), and mitochondrial integrity in the form of oxygen cons...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514741</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514741</guid>        </item>
        <item>
            <title>Bilirubin Attenuates Bufadienolide-Induced Ventricular Arrhythmias and Cardiac Dysfunction in Guinea-Pigs by Reducing Elevated Intracellular Na(+) Levels.</title>
            <link>http://www.medworm.com/index.php?rid=5476286&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22127853%26dopt%3DAbstract</link>
            <description>Authors: Ma H, Zhang J, Jiang J, Zhou J, Xu H, Zhan Z, Wu Q, Duan J
    Abstract
    Bufadienolides, known ligands of the sodium pump, have been shown to inhibit the proliferation of several cancer cell types. However, their development to date as anticancer agents has been impaired by a narrow therapeutic margin resulting from their potential to induce cardiotoxicity. In the present study, we examined the effects of bilirubin, an endogenous antioxidant, on the cardiotoxicity of bufadienolides (derived from toad venom) in guinea-pigs. The results showed that bufadienolides (8 mg/kg) caused ventricular arrhythmias, conduction block, cardiac dysfunction and death in guinea-pigs. Pretreatment with bilirubin (75 and 150 mg/kg) significantly prevented bufadienolide-induced premature ventricul...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5476286</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5476286</guid>        </item>
        <item>
            <title>Is Serum S100B Protein a Biomarker for Amitriptyline-Induced Cardiovascular Toxic Effects?</title>
            <link>http://www.medworm.com/index.php?rid=5382112&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22052576%26dopt%3DAbstract</link>
            <description>Authors: Hocaoglu N, Kalkan S, Buyukdeligoz M, Oransay K, Tuncok Y
    Abstract
    The aim of this study was to assess the role of serum S100B protein as a biomarker for cardiovascular effects in an anesthetized rat model of amitriptyline toxicity. Adult male Wistar rats (n = 28) were randomized into four groups. While the control group received normal saline, the experimental groups received different doses of amitriptyline (0.625 or 0.94 or 1.25 mg/kg/min) infusion. Mean arterial pressure (MAP), heart rate (HR), electrocardiogram parameters, and serum S100B protein levels were recorded during the experiment. Linear Pearson's correlation coefficient was used to examine the association between cardiovascular parameters and serum levels of S100B protein. In the experimental groups, amit...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382112</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382112</guid>        </item>
        <item>
            <title>Bortezomib-Induced Congestive Cardiac Failure in a Patient with Multiple Myeloma.</title>
            <link>http://www.medworm.com/index.php?rid=5282519&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21952908%26dopt%3DAbstract</link>
            <description>Authors: Gupta A, Pandey A, Sethi S
    Abstract
    Bortezomib therapy is known to be associated with neurological side effects and thrombocytopenia. Its cardiac side effects are however not well known. The patient, a 70-year-old woman, with a previous history of myocardial infarction and subsequent coronary stenting, was detected to have multiple myeloma stage IIIa. She was started on Inj. Bortezomib (1.3 mg/m(2)) and Tab. Dexamethasone 40 mg on a weekly basis. She showed good response to therapy. Three days after administration of the 22nd dose of bortezomib, she presented to the hospital with congestive cardiac failure. Echocardiography revealed a drop in the left ventricular ejection fraction from pretreatment levels of 45-50 to 25%. Patient was treated medically for left ventricula...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282519</comments>
            <pubDate>Wed, 28 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282519</guid>        </item>
        <item>
            <title>NAD(P)H: Quinone Oxidoreductase 1 is Induced by Progesterone in Cardiomyocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5282520&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21947872%26dopt%3DAbstract</link>
            <description>We report here that PG induces NQO1 protein and its activity in a dose-dependent manner. Whereas NQO1 is well known as a target gene of Nrf2 transcription factor due to the presence of antioxidant response element (ARE) in the promoter, PG did not activate the ARE, suggesting Nrf2-independent induction of NQO1. To address the role of NQO1 induction in PG-induced cytoprotection, we tested the effect of NQO1 inducer β-naphthoflavone and inhibitor dicoumarol. Induction of NQO1 by β-naphthoflavone decreased Dox-induced apoptosis and potentiated the protective effect of PG as measured by caspase-3 activity. PG-induced NQO1 activity was inhibited with dicoumarol, which did not affect PG-induced cytoprotection. Dicoumarol treatment alone potentiated Dox-induced caspase-3 activity. These data su...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282520</comments>
            <pubDate>Fri, 23 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282520</guid>        </item>
        <item>
            <title>The History and Future of Probenecid.</title>
            <link>http://www.medworm.com/index.php?rid=5248098&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21938493%26dopt%3DAbstract</link>
            <description>Authors: Robbins N, Koch SE, Tranter M, Rubinstein J
    Abstract
    Probenecid was initially developed with the goal of reducing the renal excretion of antibiotics, specifically penicillin. It is still used for its uricosuric properties in the treatment in gout, but its clinical relevance has sharply fallen and is rarely used today for either. Interestingly, throughout the last 60 years, there have been a host of apparently unrelated studies using probenecid in the clinical and basic research arena, including its potential use in the diagnosis and treatment of depression and its use to prevent fura-2 leakage in calcium transient studies. Recently, it has been shown that it is also an agonist of the Transient Receptor Potential Vanilloid 2 channel. Due to its unique action and new findin...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5248098</comments>
            <pubDate>Thu, 22 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5248098</guid>        </item>
        <item>
            <title>Timely Recognition of Cardiovascular Toxicity by Anticancer Agents: A Common Objective of the Pharmacologist, Oncologist and Cardiologist.</title>
            <link>http://www.medworm.com/index.php?rid=5220007&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21894547%26dopt%3DAbstract</link>
            <description>Authors: Bonura F, Di Lisi D, Novo S, D'Alessandro N
    Abstract
    Both conventional and new anticancer drugs can frequently cause adverse cardiovascular effects, which can span from subclinical abnormalities to serious life-threatening and sometimes fatal events. This review examines the principal basic and clinical elements that may be of profit to identify, prevent and treat such toxicities. Clearly, the accomplishment of such objectives requires the strong commitment and cooperation of different professional figures including, but not limited to, pharmacologists, oncologists and cardiologists. The aspect of anticancer drug cardiotoxicity seems to be somehow underestimated, mainly due to inadequate reporting of adverse reactions from oncology drugs in the post-marketing setting. Thus...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5220007</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5220007</guid>        </item>
        <item>
            <title>Standardized Flavonoid-Rich Eugenia jambolana Seed Extract Retards In Vitro and In Vivo LDL Oxidation and Expression of VCAM-1 and P-Selectin in Atherogenic Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5157851&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21863403%26dopt%3DAbstract</link>
            <description>Authors: Jadeja RN, Thouaojam MC, Sankhari JM, Jain M, Devkar RV, Ramachandran AV
    Abstract
    The present inventory evaluates anti-atherogenic potential of flavonoid-rich Eugenia jambolana seed extract (EJSE) against in vitro low-density lipoprotein (LDL) oxidation, foam cell formation, and atherogenic (ATH) diet-induced experimental atherosclerosis in rats. EJSE was able to prevent in vitro LDL oxidation and oxidized LDL-induced macrophage foam cell formation. Also, EJSE supplementation to ATH rats significantly minimized increment in serum markers of LDL oxidation. The ex vivo oxidation indices were also minimized in LDL of EJSE-treated animals. Microscopic evaluation of thoracic aorta of ATH + EJSE rats recorded minimal evidence of atheromatous plaque formation, accumulation of l...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157851</comments>
            <pubDate>Tue, 23 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157851</guid>        </item>
        <item>
            <title>Cardiac Tissue Injury Resistance During Myocardial Infarction at Adulthood by Developmental Exposure to Cadmium.</title>
            <link>http://www.medworm.com/index.php?rid=5157852&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21858600%26dopt%3DAbstract</link>
            <description>Authors: Zepeda R, Castillo P, Sáez D, Llanos MN, Ronco AM
    Abstract
    It has been suggested that prenatal exposure to cadmium may alter the cardiovascular function during adulthood. Using the left coronary artery ligation model of acute myocardial infarction, we studied the cardiac function of female adult offspring rats exposed to cadmium (30 ppm) during gestation. The cardiac ischemic zone in the control and cadmium-exposed groups was measured 72 h post-ligation using the TPT staining technique. Offspring from cadmium-treated dams showed a significantly smaller infarcted area compared with the control group (7.1 ± 1.5 vs. 19.6 ± 2.8%, P ≤ 0.05). We also performed echocardiographic and biochemical studies, which positively correlated with the differences observed previo...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157852</comments>
            <pubDate>Fri, 19 Aug 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Mechanistic Clues in the Protective Effect of Ellagic Acid Against Apoptosis and Decreased Mitochondrial Respiratory Enzyme Activities in Myocardial Infarcted Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5142153&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21822950%26dopt%3DAbstract</link>
            <description>In this study, we are reporting the mechanism of protective action of ellagic acid with respect to apoptosis and mitochondrial respiratory enzymes. Ellagic acid (7.5 and 15 mg/kg) was administered orally as a pretreatment for 10 days. Then, isoproterenol (100 mg/kg) was injected subcutaneously to rats at an interval of 24 h for 2 days. Myocardial infarction was quantified by planimetry. Apoptosis was measured by apoptotic gene expressions. The levels of mitochondrial respiratory enzymes were also measured. Isoproterenol-induced myocardial infarcted rats showed increased infarct size, a decrease in myocardial expression of the Bcl-2 gene and an increase in myocardial expression of the BAX gene. Fas ligand and caspases were markedly elevated along with compromised respiratory marker enz...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142153</comments>
            <pubDate>Sat, 06 Aug 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Dietary Selenium (Se) and Vitamin E (V(E)) Supplementation Modulated Methylmercury-Mediated Changes in Markers of Cardiovascular Diseases in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5142154&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21822669%26dopt%3DAbstract</link>
            <description>This study examined the effects of Se and V(E) supplementation on MeHg-mediated systemic oxidative stress, antioxidant defense, inflammation, and endothelial dysfunction in an animal model. Male Sprague-Dawley rats were fed a starch-based casein diet or the same diet supplemented with 1 or 3 mg Se/kg diet and with or without 250 or 750 mg V(E)/kg diet. After 28 days of dietary treatment, rats were gavaged with 0 or 3 mg MeHg/kg BW for 14 consecutive days. Results suggested that exposure to MeHg may increase the risk of cardiovascular disease by decreasing circulating paraoxonase-1 activities, increasing serum oxidized low density lipoprotein levels, and associated systemic inflammation and endothelial dysfunction as reflected by increased leukocyte counts and serum levels of intercellu...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142154</comments>
            <pubDate>Fri, 05 Aug 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>NAD(P)H:Quinone Oxidoreductase 1 and its Potential Protective Role in Cardiovascular Diseases and Related Conditions.</title>
            <link>http://www.medworm.com/index.php?rid=5106771&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21818552%26dopt%3DAbstract</link>
            <description>Authors: Zhu H, Li Y
    NAD(P)H:quinone oxidoreductase (NQO) represents a family of flavoproteins that catalyze the two-electron reduction of quinones and their derivatives. In mammalian systems, there are two members of NQO, namely, NQO1 and NQO2. NQO1 utilizes NAD(P)H, whereas NQO2 employs dihydronicotinamide riboside (NRH) as the electron donors. In addition to the well-documented action in reducing quinone compounds and preventing the formation of reactive oxygen species, NQO enzymes, especially NQO1 also possess other important biological activities. These include anti-inflammatory effects, direct scavenging of superoxide anion radicals, and stabilization of p53 and other tumor suppressors. Recently, multiple studies in animal models demonstrated a potential role for NQO1 in protecti...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106771</comments>
            <pubDate>Thu, 04 Aug 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Toxicological Insight from AP-1 Silencing Study on Proliferation, Migration, and Dedifferentiation of Rat Vascular Smooth Muscle Cell.</title>
            <link>http://www.medworm.com/index.php?rid=5106770&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21818553%26dopt%3DAbstract</link>
            <description>The objectives of this study were to determine toxicological effects of AP-1 silencing study on proliferation, migration, and dedifferentiation of rat vascular smooth muscle cell. To suppress the expression of AP-1 gene, AP-1 siRNA was used to interfere post-transcription in rat primary VSMCs. To observe the expression of SM α-actin and downstream genes of AP-1, the activity of cell matrix metal proteinases and the migration ability of VSMC was examined by a modified Boyden chamber assay. Effects of AP-1 siRNA on proliferation and differentiation in rat VSMCs were evaluated by cell cycle analysis, DNA synthesis, MTT-test, and immunofluorescence. The results showed that the level of SM α-actin protein expression was increased. AP-1 siRNA also significantly decreased the MTT extinction val...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106770</comments>
            <pubDate>Thu, 04 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5106770</guid>        </item>
        <item>
            <title>Effects of Everolimus in Combination with Sildenafil in Monocrotaline-induced Pulmonary Hypertension in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5106772&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21811847%26dopt%3DAbstract</link>
            <description>Authors: Ilgin S, Burukoglu D, Atli O, Sirmagul B
    In our study, we investigated the efficacy of everolimus in combination with sildenafil on hemodynamic and morphological parameters in rats with monocrotaline-induced pulmonary hypertension (PH). Right ventricular pressure (RVP), right ventricular hypertrophy, and the response to vasoconstrictor and vasodilator agents in pulmonary arteries as evaluated by myography and histopathological changes were compared among the groups. RVP and right ventricle/body weight ratios were increased in non-treated monocrotaline groups versus the controls; these increased ratios were decreased in the treated groups and were similar to control values. The contractile responses to endothelin-1 in the pulmonary arteries were decreased in the non-treated mon...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106772</comments>
            <pubDate>Tue, 02 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5106772</guid>        </item>
        <item>
            <title>Supplemental Studies for Cardiovascular Risk Assessment in Safety Pharmacology: A Critical Overview.</title>
            <link>http://www.medworm.com/index.php?rid=5106773&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21805209%26dopt%3DAbstract</link>
            <description>Authors: Picard S, Goineau S, Guillaume P, Henry J, Hanouz JL, Rouet R
    Safety Pharmacology studies for the cardiovascular risk assessment, as described in the ICH S7A and S7B guidelines, appear as being far from sufficient. The fact that almost all medicines withdrawn from the market because of life-threatening tachyarrhythmias (torsades-de-pointes) were shown as hERG blockers and QT interval delayers led the authorities to focus mainly on these markers. However, other surrogate biomarkers, e.g., TRIaD (triangulation, reverse-use-dependence, instability and dispersion of ventricular repolarization), have been identified to more accurately estimate the drug-related torsadogenic risk. In addition, more attention should be paid to other arrhythmias, not related to long QT and nevertheless...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106773</comments>
            <pubDate>Fri, 29 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5106773</guid>        </item>
        <item>
            <title>Salutary Effect of Cassia auriculata L. Leaves on Hyperglycemia-Induced Atherosclerotic Environment in Streptozotocin Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5106774&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21800129%26dopt%3DAbstract</link>
            <description>Authors: Gupta S, Sharma SB, Singh UR, Bansal SK
    Diabetes mellitus is very often associated with dyslipidemia, increased oxidative stress and endothelial dysfunction that could develop atherosclerosis and consequently cardiovascular diseases. Medicinal plants with reputed traditional use to treat diabetes and cardiovascular diseases might provide valuable drugs. Therefore, the present study was designed to evaluate anti-atherosclerotic potential of aqueous extract of Cassia auriculata L. leaves in streptozotocin (STZ)-induced diabetic rats. The rats were rendered diabetic by STZ (45 mg/kg, ip). Diabetic rats were orally administered C. auriculata leaf extract at 400 mg/kg dose daily for 21 days. The supplementation of extract to the diabetic rats produced significant reduction in fa...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106774</comments>
            <pubDate>Thu, 28 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5106774</guid>        </item>
        <item>
            <title>N-acetylcysteine Offers Cardioprotection by Decreasing Cardiac Lipid Hydroperoxides and 8-Isoprostane Level in Isoproterenol-Induced Cardiotoxicity in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5106775&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21796404%26dopt%3DAbstract</link>
            <description>In conclusion, the study proves that NAC has a strong cardioprotective effect against isoproterenol-induced cardiac changes. NAC decreases isoproterenol-induced LPO and IP levels in the heart tissue and prevented free radicals-induced damage to the myocardium.
    PMID: 21796404 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106775</comments>
            <pubDate>Wed, 27 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5106775</guid>        </item>
        <item>
            <title>Electrocardiographic Characterization of Rhesus Monkey Model of Ischemic Myocardial Infarction Induced by Left Anterior Descending Artery Ligation.</title>
            <link>http://www.medworm.com/index.php?rid=5106777&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21792668%26dopt%3DAbstract</link>
            <description>Authors: Yang P, Han P, Hou J, Zhang L, Song H, Xie Y, Chen Y, Xie H, Gao F, Kang YJ
    Myocardial infarction is a leading cause for morbidity and mortality in the modern society. Rhesus monkeys are excellent animal models for experimental and translational studies of cardiovascular diseases in humans. However, some detailed characterizations of cardiovascular disease, such as myocardial infarction, in Rhesus monkeys have not been available. The present study was undertaken to examine the progressive electrocardiographic changes in Rhesus monkeys after left anterior descending (LAD) artery ligation. Male Rhesus monkeys, aged 2-3 years and weighed 4.5-6.0 kg, were subjected to LAD ligation along with sham-operated controls. At 1 week, 1 month, and 6 months after the LAD ligation, ECG ...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106777</comments>
            <pubDate>Tue, 26 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5106777</guid>        </item>
        <item>
            <title>Carbon Monoxide Pollution Impairs Myocardial Perfusion Reserve: Implication of Coronary Endothelial Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=5106776&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21792669%26dopt%3DAbstract</link>
            <description>Authors: Meyer G, Boissiere J, Tanguy S, Rugale C, Gayrard S, Jover B, Obert P, Reboul C
    Chronic exposure to simulated urban CO pollution is reported to be associated with cardiac dysfunction. Despite the potential implication of myocardial perfusion alteration in the pathophysiology of CO pollution, the underlying mechanisms remain today still unknown. Therefore, the aim of this work was to evaluate the effects of prolonged exposure to simulated urban CO pollution on the regulation of myocardial perfusion. Cardiac hemodynamics and myocardial perfusion were assessed under basal conditions and during the infusion of a β-Adrenergic agonist. The effects of CO exposure on capillary density, coronary endothelium-dependent vasodilatation, eNOS expression and eNOS uncoupling were also evalua...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106776</comments>
            <pubDate>Tue, 26 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5106776</guid>        </item>
        <item>
            <title>Enapranil-Induced Angioedema in a 2-Year-Old Infant: Case Report.</title>
            <link>http://www.medworm.com/index.php?rid=5061972&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21779753%26dopt%3DAbstract</link>
            <description>Authors: El Koraichi A, Tadili J, Benjelloun MY, Benafitou R, El Kharraz H, Lahlou J, Chkoura M, El Haddoury M, Ech-Chérif El Kettani SS
    
    PMID: 21779753 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5061972</comments>
            <pubDate>Thu, 21 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5061972</guid>        </item>
        <item>
            <title>Erratum to: Isoproterenol Cytotoxicity is Dependent on the Differentiation State of the Cardiomyoblast H9c2 Cell Line.</title>
            <link>http://www.medworm.com/index.php?rid=5061973&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21779752%26dopt%3DAbstract</link>
            <description>Authors: Branco AF, Pereira SL, Moreira AC, Holy J, Sardão VA, Oliveira PJ
    
    PMID: 21779752 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5061973</comments>
            <pubDate>Wed, 20 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5061973</guid>        </item>
        <item>
            <title>Infrasound Exposure Induces Apoptosis of Rat Cardiac Myocytes by Regulating the Expression of Apoptosis-Related Proteins.</title>
            <link>http://www.medworm.com/index.php?rid=5061974&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21773807%26dopt%3DAbstract</link>
            <description>In conclusion, infrasound is an apoptotic inducer of cardiac myocytes.
    PMID: 21773807 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5061974</comments>
            <pubDate>Tue, 19 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5061974</guid>        </item>
        <item>
            <title>Curcumin Protects from Cardiac Reperfusion Damage by Attenuation of Oxidant Stress and Mitochondrial Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=5061976&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769543%26dopt%3DAbstract</link>
            <description>In conclusion, the protective effect of curcumin was associated with the attenuation of oxidant stress and mitochondrial dysfunction secondary to I/R injury.
    PMID: 21769543 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5061976</comments>
            <pubDate>Mon, 18 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5061976</guid>        </item>
        <item>
            <title>Cyclooxygenase-2-Derived Prostacyclin Protective Role on Endotoxin-Induced Mouse Cardiomyocyte Mortality.</title>
            <link>http://www.medworm.com/index.php?rid=5061975&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769544%26dopt%3DAbstract</link>
            <description>This study is focused on the links between these products of inflammation and cell loss of mouse cardiomyocytes during treatment by the Salmonella typhimurium lipopolysaccharide (LPS) in presence or in absence of NOS or COX inhibitors. LPS induced RelA/NF-κB p65 activation, iNOS and COX-2 up-regulations, resulting in NO and prostacyclin releases. These effects were reversed by the NO-synthase inhibitor and increased by the specific COX-2 inhibitor. Immunostainings with FITC-conjugated anti-Annexin-V and propidium iodide and caspase 3/7 activity assay showed that cardiomyocyte necrosis was inhibited by L-NA during LPS treatment challenge, while apoptosis was induced in presence of both LPS and NS-398. No effect on LPS cellular injury was observed using the specific cyclooxygenase-1 (COX-1)...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5061975</comments>
            <pubDate>Fri, 15 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5061975</guid>        </item>
        <item>
            <title>Emblica officinalis Exerts Antihypertensive Effect in a Rat Model of DOCA-Salt-Induced Hypertension: Role of (p) eNOS, NO and Oxidative Stress.</title>
            <link>http://www.medworm.com/index.php?rid=5061977&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21748534%26dopt%3DAbstract</link>
            <description>Authors: Bhatia J, Tabassum F, Sharma AK, Bharti S, Golechha M, Joshi S, Sayeed Akhatar M, Srivastava AK, Arya DS
    Emblica officinalis (EO) has antioxidant properties that could improve redox-sensitive vascular, cardiac and renal changes associated with deoxycorticosterone acetate/1% NaCl high salt (DOCA/HS)-induced hypertension. We determined whether hydroalcoholic lyophilized extract of EO may influence DOCA/HS-induced hypertension by modulating activity of (p) eNOS and endogenous antioxidants. Hypertension was induced in rats by DOCA-salt (20 mg/kg, s.c.) twice weekly for 5 weeks and replacing drinking water with 1% NaCl solution. These rats received cotreatment of different doses of EO (75, 150 and 300 mg/kg/day) for 5 weeks. EO significantly decreased arterial blood pressure an...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5061977</comments>
            <pubDate>Mon, 11 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5061977</guid>        </item>
        <item>
            <title>Leptin's regulation of obesity-induced cardiac extracellular matrix remodeling.</title>
            <link>http://www.medworm.com/index.php?rid=5061978&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21744298%26dopt%3DAbstract</link>
            <description>Authors: Zibadi S, Cordova F, Slack EH, Watson RR, Larson DF
    Obesity-induced remodeling of cardiac extracellular matrix (ECM) leads to myocardial fibrosis and ultimately diastolic dysfunction. Leptin, an adipocyte hormone, is emerging as a novel mechanistic link between obesity and heart diseases. Despite the known essential role of leptin in hepatic and renal fibrosis, the in vivo effects of leptin on cardiac ECM remodeling remain unclear. Our objective was to define the role of leptin as a key mediator of pro-fibrogenic responses in the heart. In vitro administration of leptin to primary cardiofibroblasts resulted in significant stimulation of pro-collagen Iα ( 1 ) and a decrease in pro-matrix metalloproteinase (MMP)-8, -9 and -13 gene expressions at 24 h. To study the in vivo pro-...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5061978</comments>
            <pubDate>Sat, 09 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5061978</guid>        </item>
        <item>
            <title>Isoproterenol-Induced Cardiomyopathy in Rats: Influence of Acorus calamus Linn. : A. calamus Attenuates Cardiomyopathy.</title>
            <link>http://www.medworm.com/index.php?rid=4965689&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21695526%26dopt%3DAbstract</link>
            <description>Authors: Singh BK, Pillai KK, Kohli K, Haque SE
    Acorus calamus has been used as a traditional remedy since ancient days but its cardioprotective effect is not yet well characterized. The aim of this study was to assess the effect of A. calamus rhizome extract in isoproterenol-induced cardiomyopathy in rats. Male Wistar rats were treated with normal saline (0.5 ml/kg, i.p.), isoproterenol (5 mg/kg, i.p.), A. calamus (100 and 200 mg/kg, respectively, by gavage) alone, amlodipine (9.0 mg/kg, by gavage) alone, A. calamus (100 and 200 mg/kg, respectively) + isoproterenol and amlodipine (9.0 mg/kg) + isoproterenol, single dose/day for 30 days, respectively. Isoproterenol-induced cardiomyopathy was characterized by a significant (P &amp;lt; 0.001) increase in heart weigh/body weight ...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4965689</comments>
            <pubDate>Tue, 21 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4965689</guid>        </item>
        <item>
            <title>Effect of Apoptosis-Inducing Antitumor Agents on Endocardial Endothelial Cells.</title>
            <link>http://www.medworm.com/index.php?rid=4965703&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21671064%26dopt%3DAbstract</link>
            <description>In this study, we investigated the cytotoxic effect of widely used antitumor agents doxorubicin, camptothecin, and thapsigargin on primary and immortalized porcine endocardial endothelial cells and compared with the effects of these agents on human umbilical vein endothelial cells, human aortic endothelial cells, and EA.hy926 cells. Our study revealed that endocardial endothelial cells are relatively resistant to apoptosis induced by these drugs. Interestingly, our study indicates that response to antitumor agents greatly differs depending on the site of origin of endothelial cells. Doxorubicin, camptothecin, and thapsigargin induce mitochondrial-dependent cell death following loss of mitochondrial membrane potential (MMP) in vascular endothelial cells, with subsequent increase in sub-G0 p...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4965703</comments>
            <pubDate>Mon, 13 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4965703</guid>        </item>
        <item>
            <title>Absence of Mutation at the 5'-Upstream Promoter Region of the TPM4 Gene From Cardiac Mutant Axolotl (Ambystoma mexicanum).</title>
            <link>http://www.medworm.com/index.php?rid=4921854&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21626230%26dopt%3DAbstract</link>
            <description>In this study, we amplified and sequenced the upstream regulatory region of the TPM4 gene from both normal and mutant axolotl hearts. To identify the cis-elements that are essential for the expression of the TPM4, we created various deletion mutants of the TPM4 promoter DNA, inserted the deleted segments into PGL3 vector, and performed promoter-reporter assay using luciferase as the reporter gene. Comparison of sequences of the promoter region of the TPM4 gene from normal and mutant axolotl revealed no mutations in the promoter sequence of the mutant TPM4 gene. CArG box elements that are generally involved in controlling the expression of several other muscle-specific gene promoters were not found in the upstream regulatory region of the TPM4 gene. In deletion experiments, loss of activity...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4921854</comments>
            <pubDate>Fri, 27 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4921854</guid>        </item>
        <item>
            <title>Perturbation of Rat Heart Plasma Membrane Fluidity Due to Metabolites of Permethrin Insecticide.</title>
            <link>http://www.medworm.com/index.php?rid=4872886&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21598078%26dopt%3DAbstract</link>
            <description>Authors: Vadhana D, Carloni M, Fedeli D, Nasuti C, Gabbianelli R
    Due to increased global use, acute and chronic exposures to pyrethroid insecticides in humans are of clinical concern. Pyrethroids have a primary mode of action that involves interference with the sodium and calcium channels in excitable cells, which may include cardiac myocytes. Here, we investigated the possible cardiac toxicity of permethrin metabolites (METP), 3-phenoxy-benzyl alcohol (3PBA), 3-phenoxy-benzaldehyde (3PBALD), and 3-phenoxybenzoic acid (3PBACID). Plasma membrane fluidity, polarity, lipid, and protein oxidation were studied in isolated rat heart cells. Laurdan was chosen as probe to detect the lateral mobility and polarity of its environment and thus water penetration into the hydrophobic part of the bil...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872886</comments>
            <pubDate>Thu, 19 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4872886</guid>        </item>
        <item>
            <title>A Scombroid Poisoning Causing a Life-Threatening Acute Pulmonary Edema and Coronary Syndrome in a Young Healthy Patient.</title>
            <link>http://www.medworm.com/index.php?rid=4872887&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21567294%26dopt%3DAbstract</link>
            <description>Authors: D'Aloia A, Vizzardi E, Della Pina P, Bugatti S, Del Magro F, Raddino R, Curnis A, Dei Cas L
    
    PMID: 21567294 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872887</comments>
            <pubDate>Thu, 12 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4872887</guid>        </item>
        <item>
            <title>Cardioprotective Effects of Hesperetin against Doxorubicin-Induced Oxidative Stress and DNA Damage in Rat.</title>
            <link>http://www.medworm.com/index.php?rid=4820260&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21553131%26dopt%3DAbstract</link>
            <description>This study was aimed to investigate the protective effect of hesperetin against doxorubicin-induced cardiotoxicity in rats. Doxorubicin was administered at the dosage of 4 mg/kg bw/week, ip for a period of 5 consecutive weeks. Hesperetin was administered at the dosages of 25, 50 and 100 mg/kg bw, po by gavage for 5 consecutive days in a week for 5 weeks. The animals were killed 1 week after the last injection of doxorubicin. Hesperetin at the doses of 50 and 100 mg/kg bw significantly reduced MDA and increased GSH levels in the doxorubicin-treated animals. Further, hesperetin significantly reduced doxorubicin-induced DNA damage as well as apoptosis at 25, 50, and 100 mg/kg bw as evident from the comet and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assays, r...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4820260</comments>
            <pubDate>Fri, 06 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4820260</guid>        </item>
        <item>
            <title>Trichloroethylene Induces Methylation of the Serca2 Promoter in H9c2 Cells and Embryonic Heart.</title>
            <link>http://www.medworm.com/index.php?rid=4765009&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21479763%26dopt%3DAbstract</link>
            <description>In this study, we investigated whether TCE reduced Serca2a expression by altering the methylation status of its proximal promoter region. Low doses of TCE exposure (10 ppb) induced DNA hyper methylation in the Serca2 promoter region in cardiac myoblast cells and rat embryonic cardiac tissue. TCE exposure induced DNA methylation in a region of the Serca2 promoter which is the target for SP1 binding site essential for regulation of Serca2a transcriptional activity. Chromatin immunoprecipitation data confirmed that TCE exposure reduced the binding of SP1 to the Serca2 promoter region adjacent to the methylated CpG dimer. Finally, low-dose TCE exposure reduced the concentration of S-adenosyl-methionine in exposed cells and embryos. These cumulative data indicate that epigenetic mechanisms, in...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4765009</comments>
            <pubDate>Fri, 08 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4765009</guid>        </item>
        <item>
            <title>Isoproterenol Cytotoxicity is Dependent on the Differentiation State of the Cardiomyoblast H9c2 Cell Line.</title>
            <link>http://www.medworm.com/index.php?rid=4765010&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455642%26dopt%3DAbstract</link>
            <description>Authors: Branco AF, Pereira SL, Moreira AC, Holy J, Sardão VA, Oliveira PJ
    H9c2 cells are used as a surrogate for cardiac cells in several toxicological studies, which are usually performed with cells in their undifferentiated state, raising questions on the applicability of the results to adult cardiomyocytes. Since H9c2 myoblasts have the capacity to differentiate into skeletal and cardiac muscle cells under different conditions, the hypothesis of the present work was that cells in different differentiation states differ in their susceptibility to toxicants. In order to test the hypothesis, the effects of the cardiotoxicant isoproterenol (ISO) were investigated. The present work demonstrates that differentiated H9c2 cells are more susceptible to ISO toxicity. Cellular content of bet...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4765010</comments>
            <pubDate>Wed, 30 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4765010</guid>        </item>
        <item>
            <title>Metabolic Remodeling During H9c2 Myoblast Differentiation: Relevance for In Vitro Toxicity Studies.</title>
            <link>http://www.medworm.com/index.php?rid=4658745&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21431998%26dopt%3DAbstract</link>
            <description>Authors: Pereira SL, Ramalho-Santos J, Branco AF, Sardão VA, Oliveira PJ, Carvalho RA
    H9c2 cells, derived from the ventricular part of an E13 BDIX rat heart, possess a proliferative and relatively undifferentiated phenotype but can be readily directed to differentiate under reduced serum conditions originating cells presenting muscle features. Skeletal or cardiac phenotypes can be originated depending on whether or not serum reduction is accompanied by a daily treatment with all-trans-retinoic acid. In the present study, we aimed to characterize and compare the metabolic profile of H9c2 cells at various differentiation states, correlating the differences between different populations with muscle-specific development. We determined that H9c2 myoblasts remodel their metabolism upon diff...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4658745</comments>
            <pubDate>Thu, 24 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4658745</guid>        </item>
        <item>
            <title>In Vitro Evidence for the Protective role of Sida rhomboidea. Roxb Extract Against LDL Oxidation and Oxidized LDL-Induced Apoptosis in Human Monocyte-Derived Macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=4599104&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21384160%26dopt%3DAbstract</link>
            <description>Authors: Thounaojam MC, Jadeja RN, Devkar RV, Ramachandran AV
    The present study was undertaken to evaluate protective role of S. rhomboidea. Roxb (SR) leaf extract against in vitro low-density lipoprotein (LDL) oxidation and oxidized LDL (Ox-LDL) induced macrophage apoptosis. Copper and cell-mediated LDL oxidation, Ox-LDL-induced peroxyl radical generation, mitochondrial activity, and apoptosis in human monocyte-derived macrophages (HMDMs) were assessed in presence of SR extract. Results clearly indicated that SR was capable of reducing LDL oxidation and formation of intermediary oxidation products. Also, SR successfully attenuated peroxyl radical formation, mitochondrial dysfunction, nuclear condensation, and apoptosis in Ox-LDL-exposed HMDMs. This scientific report is the first detai...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4599104</comments>
            <pubDate>Tue, 08 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4599104</guid>        </item>
        <item>
            <title>Valsartan, an Angiotensin II Receptor Blocker, Attenuates Cardiac Dysfunction and Oxidative Stress in Isoproterenol-Induced Cardiotoxicity.</title>
            <link>http://www.medworm.com/index.php?rid=4599107&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21380857%26dopt%3DAbstract</link>
            <description>Authors: Goyal S, Bharti S, Sahoo KC, Sharma AK, Arya DS
    Valsartan has significant blood pressure lowering effect via modulating renin-angiotensin system although its mechanism of action in isoproterenol (ISO)-induced myocardial injury is largely unknown. We therefore evaluated the effect of valsartan in ISO-induced oxidative stress and cardiotoxicity during β-adrenergic receptor stimulation in rats. ISO (85 mg/kg, s.c.) was administered on thirteenth and fourteenth day for induction of cardiotoxicity. ISO-treated rats showed significant decrease (P &amp;lt; 0.01) in mean arterial pressure (70.2 ± 9.11 vs. 104.86 ± 8.93), maximal positive (1601.3 ± 338.87 vs. 2789.16 ± 301.76), and negative (1495.76 ± 151.78 vs. 2039.6 ± 279.1) rate of developed left ventricular press...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4599107</comments>
            <pubDate>Sun, 06 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4599107</guid>        </item>
        <item>
            <title>Angiotensin II Infusion-Induced Inflammation, Monocytic Fibroblast Precursor Infiltration, and Cardiac Fibrosis are Pressure Dependent.</title>
            <link>http://www.medworm.com/index.php?rid=4599108&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373977%26dopt%3DAbstract</link>
            <description>Authors: Qi G, Jia L, Li Y, Bian Y, Cheng J, Li H, Xiao C, Du J
    The activated renin-angiotensin-aldosterone system increases blood pressure and intracellular signals, thus leading to cardiac fibrosis. Whether increased blood pressure or angiotensin II-activated signaling is responsible for elevated angiotensin II-induced cardiac remodeling is unknown. Here, we aimed to determine whether lowering blood pressure with hydralazine might prevent inflammation and cardiac fibrosis in response to angiotensin II. We used the C57/BL6 mouse model of angiotensin II infusion (1,500 ng/kg per minute) for 7 days; 40 male mice (6 weeks old) were randomly assigned to 4 groups for treatment: mice with angiotensin II or vehicle infusion were given hydralazine in drinking water (250 mg/l per day). Hea...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4599108</comments>
            <pubDate>Fri, 04 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4599108</guid>        </item>
        <item>
            <title>Doxycycline Ameliorates Vascular Endothelial and Contractile Dysfunction in the Thoracic Aorta of Diabetic Rats.</title>
            <link>http://www.medworm.com/index.php?rid=4599109&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21360312%26dopt%3DAbstract</link>
            <description>Authors: Zeydanli EN, Kandilci HB, Turan B
    Studies have shown that tetracycline class antibiotics exhibit an ameliorating action with its antioxidant property on increased oxidative stress in tissues, including heart. Since endothelial vascular dysfunction in diabetes is associated with increased oxidative stress and prevented with antioxidants, herein, we aimed to test a hypothesis whether a low-dose doxycycline treatment of diabetic rats for 4 weeks can ameliorate endothelial vascular dysfunction of thoracic aortas. Results of the present study shows that both direct and alpha receptor-mediated contractile responses as well as endothelium-dependent and endothelium-independent vasodilatory responses were preserved with low-dose doxycycline treatment (30 μmol/kg, daily; for 4 weeks...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4599109</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4599109</guid>        </item>
        <item>
            <title>A Prospective Study on Electrocardiographic Findings of Patients with Organophosphorus Poisoning.</title>
            <link>http://www.medworm.com/index.php?rid=4599110&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21336997%26dopt%3DAbstract</link>
            <description>In this study, we evaluated 20 patients who presented to our emergency department with organophosphorus (OP) poisoning and discussed their associated electrocardiographic (ECG) abnormalities. Over 3 months, 20 patients with OP poisoning were included in this prospective study. ECG analysis included the rate, ST-T abnormalities, conduction defects, and measurement of PR and &quot;QTc&quot; intervals. Our results show that 12 patients were having prolonged QTc interval i.e., &amp;gt;0.43 s. Eight patients were having mild elevated ST segment and low-amplitude &quot;T&quot; waves. Most of the patients have shown increased heart rate, where as some has shown decreased value. From this study, we conclude that acute organophosphorus poisoning is associated with ventricular arrhythmias, tachycardia and bradycardia, an...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4599110</comments>
            <pubDate>Sun, 20 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4599110</guid>        </item>
        <item>
            <title>Cardiac Arrhythmias Induced by Chloral Hydrate in Rhesus Monkeys.</title>
            <link>http://www.medworm.com/index.php?rid=4482629&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21318465%26dopt%3DAbstract</link>
            <description>This study thus suggests that cautions need to be taken when chloral hydrate is used above certain levels and beyond a certain period of anesthesia, and cardiac arrhythmias induced by chloral hydrate need to be closely monitored because compromised cardiac function may occur simultaneously. In addition, patients with cardiac arrhythmias induced by chloral hydrate should be monitored even after they are recovered from the anesthesia.
    PMID: 21318465 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4482629</comments>
            <pubDate>Sun, 13 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4482629</guid>        </item>
        <item>
            <title>High-Dose Testosterone Propionate Treatment Reverses the Effects of Endurance Training on Myocardial Antioxidant Defenses in Adolescent Male Rats.</title>
            <link>http://www.medworm.com/index.php?rid=4482630&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21312070%26dopt%3DAbstract</link>
            <description>This study was aimed at evaluation of changes in activities of selected antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) and contents of key nonenzymatic antioxidants (glutathione, protein thiol groups, and α- and γ-tocopherols) in the left heart ventricle of young male Wistar rats subjected to endurance training (treadmill running, 1 h daily, 5 days a week, for 6 weeks) or/and testosterone propionate treatment (8 or 80 mg/kg body weight, intramuscularly, once a week, for 6 weeks) during adolescence. The training alone increased the activities of key antioxidant enzymes, but lowered the pool of nonenzymatic antioxidants and enhanced myocardial oxidative stress as evidenced by elevation of the lipid peroxidation biomarker malondi...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4482630</comments>
            <pubDate>Sat, 12 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4482630</guid>        </item>
        <item>
            <title>Merits of Non-Invasive Rat Models of Left Ventricular Heart Failure.</title>
            <link>http://www.medworm.com/index.php?rid=4482631&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21279739%26dopt%3DAbstract</link>
            <description>Authors: Carll AP, Willis MS, Lust RM, Costa DL, Farraj AK
    Heart failure (HF) is characterized as a limitation to cardiac output that prevents the heart from supplying tissues with adequate oxygen and predisposes individuals to pulmonary edema. Impaired cardiac function is secondary to either decreased contractility reducing ejection (systolic failure), diminished ventricular compliance preventing filling (diastolic failure), or both. To study HF etiology, many different techniques have been developed to elicit this condition in experimental animals, with varying degrees of success. Among rats, surgically induced HF models are the most prevalent, but they bear several shortcomings, including high mortality rates and limited recapitulation of the pathophysiology, etiology, and progressi...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4482631</comments>
            <pubDate>Sun, 30 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4482631</guid>        </item>
        <item>
            <title>Values of Using QTc and N-Terminal Fragment of B-Type Natriuretic Peptide as Markers for Early Detection of Acute Antipsychotic Drugs-Induced Cardiotoxicity.</title>
            <link>http://www.medworm.com/index.php?rid=4352676&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21234705%26dopt%3DAbstract</link>
            <description>Authors: Khalaf MA, Abdelrahman TM, Abbas MF
    We aimed at studying the acute cardiotoxicity of the most commonly used antipsychotics in Egypt using QTc interval and NT-proBNP as markers for the early detection of such cases. Eighty-two admitted patients, at El-Minia PCC (period from 1-7-2005 to 30-6-2010), were classified into 3 groups: I: acute thioridazine overdose (n = 28), II: acute pimozide overdose (n = 23), and III: acute clozapine overdose (n = 31). Patients were investigated for NT-proBNP level and QTc on admission (day 0) and after 24 h (day 1). All the studied drugs had the ability to induce cardiotoxicity in the form of hypotension and dysrhythmias. Thioridazine and pimozide had potentially serious cardiotoxic effects than clozapine. NT-proBNP levels were elevated sig...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4352676</comments>
            <pubDate>Fri, 14 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4352676</guid>        </item>
        <item>
            <title>Grape Seed Extract Alleviates High-Fat Diet-Induced Obesity and Heart Dysfunction by Preventing Cardiac Siderosis.</title>
            <link>http://www.medworm.com/index.php?rid=4352675&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21234706%26dopt%3DAbstract</link>
            <description>Authors: Charradi K, Sebai H, Elkahoui S, Ben Hassine F, Limam F, Aouani E
    Obesity is a tremendous public health problem, characterized by ectopic accumulation of fat into non-adipose tissues, leading to oxidative stress and chronic inflammation, in which the heart is the most severely affected organ. We used an experimental model of high-fat-diet (HFD)-induced obesity to analyze the link between oxidative stress and heart dysfunction. We also studied the cardioprotective effect of a grape seed and skin extract (GSE). Exposure of rats to HFD during 45 days induced heart hypertrophy, inflammation as assessed by plasma CRP elevation and contractile dysfunction as revealed after ischemia/reperfusion of Langendorff-perfused hearts. HFD also induced cardiac steatosis and lipotoxicity, whic...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4352675</comments>
            <pubDate>Fri, 14 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4352675</guid>        </item>
        <item>
            <title>Gene Expression, Function and Ischemia Tolerance in Male and Female Rat Hearts After Sub-Toxic Levels of Angiotensin II.</title>
            <link>http://www.medworm.com/index.php?rid=4282950&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21170686%26dopt%3DAbstract</link>
            <description>Authors: Aljabri MB, Lund T, Höper AC, Andreasen TV, Al-Saad S, Lindal S, Ytrehus K
    To examine the response to chronic high-dose angiotensin II (Ang II) and a proposed milder response in female hearts with respect to gene expression and ischemic injury. Female and male litter-matched rats were treated with 400 ng kg(-1) min(-1) Ang II for 14 days. Hearts were isolated, subjected to 30-min ischemia and 30-min reperfusion in combination with functional monitoring and thereafter harvested for gene expression, WB and histology. Ang II-treated hearts showed signs of non-hypertrophic remodeling and had significantly higher end diastolic pressure after reperfusion, but no significant gender difference was detected. Ang II increased expression of genes related to heart function (ANF, β-M...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4282950</comments>
            <pubDate>Sun, 19 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4282950</guid>        </item>
        <item>
            <title>Preventive Effects of Vanillic Acid on Lipids, Bax, Bcl-2 and Myocardial Infarct Size on Isoproterenol-Induced Myocardial Infarcted Rats: A Biochemical and In Vitro Study.</title>
            <link>http://www.medworm.com/index.php?rid=4282951&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21161433%26dopt%3DAbstract</link>
            <description>This study may have a significant impact on myocardial infarcted patients.
    PMID: 21161433 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4282951</comments>
            <pubDate>Wed, 15 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4282951</guid>        </item>
        <item>
            <title>Glutathione-Related Antioxidant Defense System in Elderly Patients Treated for Hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=4254885&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21140238%26dopt%3DAbstract</link>
            <description>Authors: Rybka J, Kupczyk D, Kędziora-Kornatowska K, Motyl J, Czuczejko J, Szewczyk-Golec K, Kozakiewicz M, Pawluk H, Carvalho LA, Kędziora J
    The purpose of this study was to analyze glutathione antioxidant defense system in elderly patients treated for hypertension. Studies were carried out in the blood collected from 18 hypertensive and 15 age- and sex-matched controls, all subjects age over 60. Hypertensives were on their usual antihypertensive treatment at the time of blood collection. The concentration of glutathione (GSH) in whole blood and activities of glutathione peroxidase (GPx-1), glutathione transferase (GST), and glutathione reductase (GR) in erythrocytes were measured. The data from patients and controls were compared using independent-samples t test. P value of 0.05 an...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4254885</comments>
            <pubDate>Wed, 08 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4254885</guid>        </item>
        <item>
            <title>Mechanistic Clues in the Cardioprotective Effect of Terminalia Arjuna Bark Extract in Isoproterenol-Induced Chronic Heart Failure in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=4223094&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21116736%26dopt%3DAbstract</link>
            <description>Authors: Parveen A, Babbar R, Agarwal S, Kotwani A, Fahim M
    The present study demonstrated prophylactic and therapeutic potential of Terminalia arjuna bark extract in isoproterenol (ISO)-induced chronic heart failure (CHF). Fifteen days after injection of ISO (85 mg/kg twice at an interval of 24 h, s.c), rats showed decline in maximal rate of rise and fall of left ventricular pressure (LV (dP/dt)(max) and LV (dP/dt)(min)), cardiac contractility index (LV (dP/dt)(max)/LVP), cardiac output and rise in LV end-diastolic pressure. CHF rats showed a significant increase in serum creatine kinase isoenzyme-MB (CK-MB) and malondialdehyde levels, as well as fall in the activities of superoxide dismutase, reduced glutathione. Altered lipid profile and increased level of cytokine tumour necrosis...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4223094</comments>
            <pubDate>Tue, 30 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4223094</guid>        </item>
        <item>
            <title>Erratum to: A Combination of Melatonin and Alpha Lipoic Acid has Greater Cardioprotective Effect than Either of them Singly Against Cadmium-Induced Oxidative Damage.</title>
            <link>http://www.medworm.com/index.php?rid=4203845&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21080237%26dopt%3DAbstract</link>
            <description>Authors: Mukherjee R, Banerjee S, Joshi N, Singh PK, Baxi D, Ramachandran AV
    
    PMID: 21080237 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4203845</comments>
            <pubDate>Tue, 16 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4203845</guid>        </item>
        <item>
            <title>Fatal Pulmonary Oedema Following Oxytocin Administration in a Pregnant Woman with Acute Myocardial Infarction.</title>
            <link>http://www.medworm.com/index.php?rid=4171360&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21076981%26dopt%3DAbstract</link>
            <description>We present a 34-year-old pregnant woman who had mitral and aortic valve prosthesis. She developed resistant pulmonary oedema in the post-partum period after myocardial infarction. Oxytocin was used in this patient to induce midterm labour and prevent post-partum bleeding. Issues surrounding management of pulmonary oedema and use of oxytocin therapy during pregnancy are discussed. We emphasize the need for awareness of this condition and call attention to the risk of pulmonary oedema during labour.
    PMID: 21076981 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4171360</comments>
            <pubDate>Mon, 15 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4171360</guid>        </item>
        <item>
            <title>Protective Effect of FK506 on Myocardial Ischemia/Reperfusion Injury by Suppression of CaN and ASK1 Signaling Circuitry.</title>
            <link>http://www.medworm.com/index.php?rid=4171362&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21076890%26dopt%3DAbstract</link>
            <description>Authors: Feng X, Li J, Liu J, Jin M, Liu X, Du H, Zhang L, Sun Z, Li X
    We investigated protective effect of FK506 on rat hearts subjected to ischemia/reperfusion (I/R) injury by regulating CaN and ASK1. Wistar rats were divided into four groups: Ischemia/reperfusion group (I/R), FK506 + Ischemia/reperfusion group (FK506-I/R), sham group, and FK506 + sham group (FK506-sham). Ischemia/reperfusion was achieved by occluding left coronary artery for 30 min and subsequently reperfusing for 120 min. FK506 was administered 15 min before ischemia. Rats in sham group and FK506-sham group were operated only by placing a ligature around the coronary artery, and the blood supply was not blocked. I/R group showed a rapid increase in TUNEL-positive cells and high risks of histopathological cha...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4171362</comments>
            <pubDate>Sat, 13 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4171362</guid>        </item>
        <item>
            <title>Homocysteine Induces Oxidative-Nitrative Stress in Heart of Rats: Prevention by Folic Acid.</title>
            <link>http://www.medworm.com/index.php?rid=4171361&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21076891%26dopt%3DAbstract</link>
            <description>Authors: Kolling J, Scherer EB, da Cunha AA, da Cunha MJ, Wyse AT
    Hyperhomocysteinemia is a risk factor for cardiovascular disease, stroke, and thrombosis; however, the mechanisms by which homocysteine triggers these dysfunctions are not fully understood. In the present study, we investigated the effect of chronic hyperhomocysteinemia on some parameters of oxidative stress, namely thiobarbituric acid reactive substances, an index of lipid peroxidation, 2',7'-dichlorofluorescein (H(2)DCF) oxidation, activities of antioxidant enzymes named superoxide dismutase and catalase, as well as nitrite levels in heart of young rats. We also evaluated the effect of folic acid on biochemical alterations elicited by hyperhomocysteinemia. Wistar rats received daily subcutaneous injection of homocystei...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4171361</comments>
            <pubDate>Sat, 13 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4171361</guid>        </item>
        <item>
            <title>A Combination of Melatonin and Alpha Lipoic Acid has Greater Cardioprotective Effect than Either of them Singly Against Cadmium-Induced Oxidative Damage.</title>
            <link>http://www.medworm.com/index.php?rid=4140386&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21046280%26dopt%3DAbstract</link>
            <description>Authors: Mukherjee R, Banerjee S, Joshi N, Singh PK, Baxi D, Ramachandran AV
    Present study evaluates cardioprotective role of melatonin (Mel), alpha lipoic acid (ALA), a combination of melatonin and alpha lipoic acid (Mel + ALA) against cadmium (Cd)-induced oxidative damage. Female albino rats were subjected to 15-day exposure to Cd (5.12 mg/kg bw) alone or treated with ML (10 mg/kg bw) + ALA (25 mg/kg bw) simultaneously. Plasma markers of cardiac damage, cardiac free radical generation, lipid peroxidation, endogenous antioxidant status, cadmium load, metallothionein induction, and histopathology were evaluated in various experimental groups. Combination of Mel + ALA significantly prevented leakage of marker enzymes of cardiac damage, changes in cardiac free radical generation...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4140386</comments>
            <pubDate>Wed, 03 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4140386</guid>        </item>
        <item>
            <title>Evidence of Altered Cardiac Electrophysiology Following Prolonged Androgenic Anabolic Steroid Use.</title>
            <link>http://www.medworm.com/index.php?rid=4140387&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21038102%26dopt%3DAbstract</link>
            <description>In conclusion, the higher incidence of abnormal SAECG measurements immediately post-exercise in the AAS group places them at a greater risk of sudden death. The present study provides a strong contraindication to the use of AAS.
    PMID: 21038102 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4140387</comments>
            <pubDate>Sun, 31 Oct 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4140387</guid>        </item>
        <item>
            <title>Acute Cardioprotective and Cardiotoxic Effects of Bilberry Anthocyanins in Ischemia-Reperfusion Injury: Beyond Concentration-Dependent Antioxidant Activity.</title>
            <link>http://www.medworm.com/index.php?rid=4108657&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20978867%26dopt%3DAbstract</link>
            <description>This study reveals the biphasic concentration-dependent bioactivity of bilberry anthocyanins under I-R, which results in strong cardioprotective activity in low concentrations and cardiotoxic activity in high concentrations.
    PMID: 20978867 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4108657</comments>
            <pubDate>Tue, 26 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4108657</guid>        </item>
        <item>
            <title>Ramipril-Like Activity of Spondias Mombin Linn Against No-Flow Ischemia and Isoproterenol-Induced Cardiotoxicity in Rat Heart.</title>
            <link>http://www.medworm.com/index.php?rid=4013908&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20872093%26dopt%3DAbstract</link>
            <description>Authors: Akinmoladun AC, Obuotor EM, Barthwal MK, Dikshit M, Farombi EO
    The cardioprotective property of Spondias mombin (SM) was investigated and compared with that of the ACE inhibitor, ramipril. Alterations to markers of myocardial injury and indices of antioxidant capacity by isoproterenol (ISP) intoxication were significantly corrected in groups treated with SM. The inflammatory index was increased by 24% in ISP-intoxicated group compared with control (PÂ &amp;lt;Â 0.001) but reduced in the groups administered ISP and treated with 100 or 250Â mg/kg SM by 17% (PÂ &amp;lt;Â 0.001) and 11% (PÂ &amp;lt;Â 0.05) respectively. Serum lactate dehydrogenase activity and cholesterol level which were significantly increased in ISP-intoxicated group compared with control were reduced in grou...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4013908</comments>
            <pubDate>Fri, 24 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4013908</guid>        </item>
        <item>
            <title>Potential Cardiotoxic Reaction Involving Rivastigmine and Beta-Blockers: A Case Report and Review of the Literature.</title>
            <link>http://www.medworm.com/index.php?rid=4001274&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20865460%26dopt%3DAbstract</link>
            <description>We report a case of potential cardiovascular toxicity including syncope, bradycardia, and ECG pauses associated with the use of rivastigmine and atenolol. A 65-year-old African American female with a medical history of dementia, hypertension, seizure disorder, stroke, and peripheral vascular disease was admitted to the hospital with shortness of breath and syncope. She was witnessed to have experienced a presyncopal episode followed by a true syncopal episode in which she was unresponsive for 20-30Â s. On day two of hospital stay, the patient's ECG showed a sinus bradycardia with a heart rate in the 40Â s and sinus pauses greater than 2Â s in duration. Atenolol was immediately discontinued, with a continuance of the bradycardia despite one missed dose. The potentially toxic combinati...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4001274</comments>
            <pubDate>Fri, 24 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4001274</guid>        </item>
        <item>
            <title>Ethanol and Its Metabolites Induce Histone Lysine 9 Acetylation and an Alteration of the Expression of Heart Development-Related Genes in Cardiac Progenitor Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3935032&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20811785%26dopt%3DAbstract</link>
            <description>Authors: Zhong L, Zhu J, Lv T, Chen G, Sun H, Yang X, Huang X, Tian J
    Alcohol exposure during pregnancy may cause congenital heart disease (CHD), but the underlying mechanisms are not clear. Recent evidence suggests that ethanol and its metabolites can selectively increase histone H3 acetylation at lysine 9 (H3AcK9) residue in rat hepatocytes. This may be a mechanism by which ethanol alters gene expression. The goal of current study is to investigate the effect of ethanol and its metabolites on H3AcK9 acetylation and the mRNA expression of heart development-related genes (GATA4, Mef2c, and Tbx5) in cardiac progenitor cells. We used mitochondrial activity (MTT) assay to assess the viability of cardiac progenitor cells. Western blotting and real-time PCR were employed to determine H3AcK9...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3935032</comments>
            <pubDate>Wed, 01 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3935032</guid>        </item>
        <item>
            <title>Effects of the HIV-1 Protein Tat on Myocardial Function and Response to Endotoxin.</title>
            <link>http://www.medworm.com/index.php?rid=3886184&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20721641%26dopt%3DAbstract</link>
            <description>Authors: McDonough KH, Doumen C, Giaimo M, Prakash O
    HIV-1 infection has been associated with cardiomyopathy in a subset of patients. In order to determine whether HIV-1 alters myocardial function or the myocardial response to stress, transgenic mice that express the HIV-1 protein Tat were used. Heart function was assessed using the isolated working heart preparation. Response to infection was assessed by measuring heart function at various times after endotoxin administration. Since cytokines are implicated in myocardial dysfunction, plasma tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) and myocardial mRNA and protein levels of TNF-alpha and IL-6 were determined. Tat by itself did not cause myocardial dysfunction; however, 4 h after endotoxin, myocardial function was...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3886184</comments>
            <pubDate>Thu, 19 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3886184</guid>        </item>
        <item>
            <title>The Novel Role of Fenofibrate in Preventing Nicotine- and Sodium Arsenite-Induced Vascular Endothelial Dysfunction in the Rat.</title>
            <link>http://www.medworm.com/index.php?rid=3857071&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20694523%26dopt%3DAbstract</link>
            <description>Authors: Kaur J, Reddy K, Balakumar P
    The present study investigated the effect of fenofibrate, an agonist of PPAR-alpha, in nicotine- and sodium arsenite-induced vascular endothelial dysfunction (VED) in rats. Nicotine (2 mg/kg/day, i.p., 4 weeks) and sodium arsenite (1.5 mg/kg/day, i.p., 2 weeks) were administered to produce VED in rats. The scanning electron microscopy study in thoracic aorta revealed that administration of nicotine or sodium arsenite impaired the integrity of vascular endothelium. Further, administration of nicotine or sodium arsenite significantly decreased serum and aortic concentrations of nitrite/nitrate and subsequently reduced acetylcholine-induced endothelium-dependent relaxation. Moreover, nicotine or sodium arsenite produced oxidative stress by increasing ...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3857071</comments>
            <pubDate>Fri, 06 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3857071</guid>        </item>
        <item>
            <title>In Vivo Canine Model Comparison of Cardiovascular Effects of Antidepressants Milnacipran and Imipramine.</title>
            <link>http://www.medworm.com/index.php?rid=3827607&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20680703%26dopt%3DAbstract</link>
            <description>In this study, cardiovascular effects of milnacipran were assessed in comparison with those of a typical tricyclic antidepressant imipramine using the halothane-anesthetized dogs. Milnacipran (n = 6) or imipramine (n = 6) was intravenously administrated in three escalating doses of 0.1, 1 and 10 mg/kg over 10 min with a pause of 20 min between the doses. Clinically relevant plasma concentrations were obtained after 0.1-1 mg/kg of milnacipran in this study, whereas therapeutic dose and plasma concentration of imipramine were reported to be similar to those of milnacipran. The low and middle doses of milnacipran hardly affected cardiohemodynamic or electrophysiological variables except that they slightly increased vascular tone and ventricular contraction, whereas same doses of imipramine de...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3827607</comments>
            <pubDate>Sat, 31 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3827607</guid>        </item>
        <item>
            <title>Perinatal Tobacco Smoke Exposure Increases Vascular Oxidative Stress and Mitochondrial Damage in Non-Human Primates.</title>
            <link>http://www.medworm.com/index.php?rid=3806351&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20668962%26dopt%3DAbstract</link>
            <description>Authors: Westbrook DG, Anderson PG, Pinkerton KE, Ballinger SW
    Epidemiological studies suggest that events occurring during fetal and early childhood development influence disease susceptibility. Similarly, molecular studies in mice have shown that in utero exposure to cardiovascular disease (CVD) risk factors such as environmental tobacco smoke (ETS) increased adult atherogenic susceptibility and mitochondrial damage; however, the molecular effects of similar exposures in primates are not yet known. To determine whether perinatal ETS exposure increased mitochondrial damage, dysfunction and oxidant stress in primates, archived tissues from the non-human primate model Macaca mulatta (M. mulatta) were utilized. M. mulatta were exposed to low levels of ETS (1 mg/m(3) total suspended parti...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3806351</comments>
            <pubDate>Wed, 28 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3806351</guid>        </item>
        <item>
            <title>Glycolaldehyde Induces Oxidative Stress in the Heart: A Clue to Diabetic Cardiomyopathy?</title>
            <link>http://www.medworm.com/index.php?rid=3761975&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20632216%26dopt%3DAbstract</link>
            <description>Authors: Lorenzi R, Andrades ME, Bortolin RC, Nagai R, Dal-Pizzol F, Moreira JC
    Cardiovascular complications account for 80% of the mortality related to diabetes mellitus. Hyperglycemia is believed to be the major culprit of angiopathy and cardiomyopathy. High glucose levels and oxidative stress cause elevation of Advanced Glycation End-products that are known to contribute to diabetic complications and correlate with many diseases. However, there are few reports describing the effects of glycating agents other than glucose. Here, we aimed to evaluate the effects of glycolaldehyde (GA) on oxidative stress parameters in the heart of Wistar rats. Male Wistar rats received a single injection of GA (10, 50 or 100 mg/Kg) and were sacrificed 6, 12 or 24 h after injection. As indexes of oxida...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3761975</comments>
            <pubDate>Wed, 14 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3761975</guid>        </item>
        <item>
            <title>Differential Cardiopulmonary Effects of Size-Fractionated Ambient Particulate Matter in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3727120&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20602262%26dopt%3DAbstract</link>
            <description>This study was designed to evaluate the cardiopulmonary effects of ambient coarse, fine, and ultrafine particles collected in Chapel Hill, NC. Mice were exposed to each size fraction by oropharyngeal instillation. Twenty-four hours later, pulmonary inflammation was assessed by bronchoalveolar lavage and cardiac injury was measured using a Langendorff cardiac perfusion preparation. Recovery of post-ischemic left ventricular developed pressure and infarct size were measured as indeces of cardiac ischemia/reperfusion injury. Coronary flow rate was measured before, during, and after ischemia. We demonstrate that coarse PM caused the most significant pulmonary inflammatory responses. In contrast, hearts from ultrafine-exposed mice had significantly lower post-ischemic functional recovery and gr...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3727120</comments>
            <pubDate>Fri, 02 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3727120</guid>        </item>
        <item>
            <title>Cytochrome c Oxidase is Essential for Copper-Induced Regression of Cardiomyocyte Hypertrophy.</title>
            <link>http://www.medworm.com/index.php?rid=3711449&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20582486%26dopt%3DAbstract</link>
            <description>This study demonstrates that both Cu and VEGF can restore COX activity that is depressed in hypertrophic cardiomyocytes, and COX plays a determinant role in both Cu- and VEGF-induced regression of cardiomyocyte hypertrophy.
    PMID: 20582486 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3711449</comments>
            <pubDate>Fri, 25 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3711449</guid>        </item>
        <item>
            <title>Purine Bases Oxidation and Repair Following Permethrin Insecticide Treatment in Rat Heart Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3695899&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20574784%26dopt%3DAbstract</link>
            <description>Authors: Dhivya Vadhana MS, Nasuti C, Gabbianelli R
    Pollutants including insecticides have been recently reported to be a risk factor involved in various diseases. Permethrin, a member of the family of synthetic pyrethroids, is widely used as insecticide in agriculture and other domestic applications. To investigate possible cardiotoxicity, we had examined different concentrations of permethrin on the freshly isolated rat heart cells using the alkaline comet assay. A significant difference in % tail DNA between all concentrations of permethrin (5, 10, 20 muM) and vehicle (control) without enzymes and with Fpg-treated cells were measured. The results indicated that permethrin induced oxidative damage to purine bases in the heart cells. Pyrimidines oxidation was evaluated using Endonucle...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3695899</comments>
            <pubDate>Wed, 23 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3695899</guid>        </item>
        <item>
            <title>T Lymphocyte Regulation of Lysyl Oxidase in Diet-Induced Cardiac Fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=3684243&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20556665%26dopt%3DAbstract</link>
            <description>Authors: Zibadi S, Vazquez R, Larson DF, Watson RR
    Left ventricular diastolic dysfunction is an important predictor of prognosis and mortality of heart failure. Increased left ventricular stiffness can be associated with excessive myocardial fibrosis and increased cross-linked collagen by the enzyme lysyl oxidase (LOX). These cardiac extracellular matrix (ECM) remodeling processes are affected by T-lymphocyte function and phenotype. We sought to examine the role of T lymphocytes in myocardial LOX regulation in diet-induced fibrotic hearts. Female SCID mice, devoid of functional T lymphocytes, and wild-type (WT) C57BL/6 were treated with a high-fat high-simple carbohydrate (HFHSC) diet for 12 months. HFHSC-fed WT mice demonstrated a significant increase in the catalytic activity of myoc...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3684243</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3684243</guid>        </item>
        <item>
            <title>Protective Effects of Rutin on Mitochondrial Damage in Isoproterenol-Induced Cardiotoxic Rats: An In Vivo and In Vitro Study.</title>
            <link>http://www.medworm.com/index.php?rid=3684244&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20532835%26dopt%3DAbstract</link>
            <description>This study may have a significant impact on myocardial infarcted patients.
    PMID: 20532835 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3684244</comments>
            <pubDate>Mon, 07 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3684244</guid>        </item>
        <item>
            <title>Pomegranate (Punica granatum L.) Juice Supplementation Attenuates Isoproterenol-Induced Cardiac Necrosis in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3610772&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20509006%26dopt%3DAbstract</link>
            <description>Authors: Jadeja RN, Thounaojam MC, Patel DK, Devkar RV, Ramachandran AV
    The aim of the present study was to evaluate the efficacy of pre-supplementation with pomegranate (Punica granatum L.) juice (PJ) on heart weight, infarct size, plasma marker enzymes of cardiac damage, lipid peroxidation, endogenous enzymatic and non-enzymatic antioxidants, cardiac ATPases and histopathology of isoproterenol (IP)-induced cardiac necrosis (CN) in rats. Rats treated with IP (85 mg/kg, s.c.) for 2 days at an interval of 24 h caused significant (P &amp;lt; 0.05) infarct in myocardium and increase in heart weight, lipid peroxidation (LPO), activity levels of Ca(+2) ATPase and plasma marker enzymes, while there was significant (P &amp;lt; 0.05) decrease in endogenous enzymatic and non-enzymatic antioxidants and ...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3610772</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3610772</guid>        </item>
        <item>
            <title>Epigallocatechin-3-Gallate Protects Na(+) Channels in Rat Ventricular Myocytes Against Sulfite.</title>
            <link>http://www.medworm.com/index.php?rid=3571014&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20473584%26dopt%3DAbstract</link>
            <description>In conclusion, EGCG could protect Na(+) channels in rat ventricular myocytes against the oxidative damage induced by sulfite as a scavenger of the ROS.
    PMID: 20473584 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3571014</comments>
            <pubDate>Fri, 14 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3571014</guid>        </item>
        <item>
            <title>Arsenic Induces Apoptosis of Human Umbilical Vein Endothelial Cells Through Mitochondrial Pathways.</title>
            <link>http://www.medworm.com/index.php?rid=3571013&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20473585%26dopt%3DAbstract</link>
            <description>Authors: Shi Y, Wei Y, Qu S, Wang Y, Li Y, Li R
    To clarify the molecular mechanisms through which arsenic causes injuries to blood vessels, we analyzed the effects of sodium arsenite (NaAsO(2)) on the apoptosis of human umbilical vein endothelial cells (HUVECs), mitochondrial membrane potential (DeltaPsim), intracellular reactive oxygen species (ROS), and the expression of the related genes. HUVECs apoptosis increased and DeltaPsim decreased in a dose-dependent manner following arsenic treatment. Intracellular ROS showed 2 phase alterations: a slight decrease with low levels of arsenic (5 and 10 muM) treatment; but a sharp increase at higher concentrations (&amp;gt;==20 muM). The arsenic-induced cell apoptosis and intracellular ROS were blocked by the addition of the antioxidant N-acetyl-L...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3571013</comments>
            <pubDate>Fri, 14 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3571013</guid>        </item>
        <item>
            <title>Comparison of the Effects of Methadone and Heroin on Human ether-Ã -go-go-Related Gene Channels.</title>
            <link>http://www.medworm.com/index.php?rid=3566941&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20467834%26dopt%3DAbstract</link>
            <description>In conclusion, the potency for block of hERG currents is about 100-fold lower for heroin when compared to methadone.
    PMID: 20467834 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3566941</comments>
            <pubDate>Thu, 13 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3566941</guid>        </item>
        <item>
            <title>Protective Role of Antioxidants in Diabetes-Induced Cardiac Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=3557159&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20458637%26dopt%3DAbstract</link>
            <description>Authors: Vassort G, Turan B
    Cardiac dysfunction occurs during type 1 and type 2 diabetes and results from multiple parameters including glucotoxicity, lipotoxicity, fibrosis and mitochondrial uncoupling. Oxidative stress arises from an imbalance between the production of ROS and the biological system's ability to readily detoxify the reactive intermediates. It is involved in the etiology of diabetes-induced downregulation of heart function. Several studies have reported beneficial effects of a therapy with antioxidant agents, including trace elements and other antioxidants, against the cardiovascular system consequences of diabetes. Antioxidants act through one of three mechanisms to prevent oxidant-induced cell damages. They can reduce the generation of ROS, scavenge ROS, or interfere...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3557159</comments>
            <pubDate>Mon, 10 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3557159</guid>        </item>
        <item>
            <title>The Role of Lipophilic Bile Acids in the Development of Cirrhotic Cardiomyopathy.</title>
            <link>http://www.medworm.com/index.php?rid=3499763&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20414815%26dopt%3DAbstract</link>
            <description>Authors: Zavecz JH, Battarbee HD
    Marked hemodynamic changes occur in humans and experimental animals with cirrhotic liver disease. In the heart, basal contractility, responsiveness to beta-adrenoceptor activation, and excitation-contraction coupling (ECC) are negatively affected in models of cirrhosis and portal hypertension with portosystemic shunting (PVS), and comprise what has been called cirrhotic cardiomyopathy. These effects are accompanied by elevated circulating levels of bile acids. We investigated whether elevated bile acids act as a myocardial toxicant by exposing cardiac muscle in vitro to bile acids and compared these results with two models of cirrhotic cardiomyopathy with elevated bile acids: CCl(4)-induced cirrhosis and PVS. Cholic acid, a lipophilic bile acid, produce...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3499763</comments>
            <pubDate>Thu, 22 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3499763</guid>        </item>
        <item>
            <title>Protective Effect of Sulforaphane on Human Vascular Endothelial Cells Against Lipopolysaccharide-Induced Inflammatory Damage.</title>
            <link>http://www.medworm.com/index.php?rid=3493712&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20405237%26dopt%3DAbstract</link>
            <description>In this study, human vascular endothelial cell, a barrier of blood, was used as an in vitro model to investigate the protective effect of sulforaphane on inflammatory damage induced by lipopolysaccharide (LPS). The results showed that sulforaphane inhibited the expression of COX-2 and iNOS stimulated by lipopolysaccharide in a dose- and time-dependent manner. Moreover, sulforaphane suppressed the phosphorylation of ERK1/2, JNK, and p38 activated by lipopolysaccharide. Pretreatment with SB202190, the specific inhibitor of p38, abolished the expression of COX-2 induced by LPS. Likewise, SP600125, inhibitor of JNK, abrogated iNOS expression stimulated by LPS. Moreover, pretreatment with anisomycin (AM), an activator of p38 and JNK, instead of LPS, the expression of COX-2 and iNOS is still inh...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3493712</comments>
            <pubDate>Mon, 19 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3493712</guid>        </item>
        <item>
            <title>Mitochondrial Dysfunction Induced by Statin Contributes to Endothelial Dysfunction in Patients with Coronary Artery Disease.</title>
            <link>http://www.medworm.com/index.php?rid=3468542&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20383667%26dopt%3DAbstract</link>
            <description>In conclusion, a significant proportion of patients with CAD on statin developed MD, which was associated with high-dose statin and with impaired FMD, suggesting that increased statin dosage may induce MD and contribute to endothelial dysfunction in patients with CAD.
    PMID: 20383667 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3468542</comments>
            <pubDate>Fri, 09 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3468542</guid>        </item>
        <item>
            <title>Absence of Mitochondrial Toxicity in Hearts of Transgenic Mice Treated with Abacavir.</title>
            <link>http://www.medworm.com/index.php?rid=3457346&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20379802%26dopt%3DAbstract</link>
            <description>Authors: Kohler JJ, Hosseini SH, Green E, Fields E, Abuin A, Ludaway T, Russ R, Lewis W
    Abacavir (ABC) is a guanosine nucleoside reverse transcriptase inhibitor (NRTI) with potent antiretroviral activity. Since NRTIs exhibit tissue-specific inhibition of mitochondrial DNA (mtDNA) synthesis, the ability of ABC to inhibit mtDNA synthesis in vivo was evaluated. Inbred wild-type (WT) and transgenic mice (TG) treated with ABC (3.125 mg/d p. o., 35 days) were used to define mitochondrial oxidative stress and cardiac function. Chosen TGs exhibited overexpression of HIV-1 viral proteins (NL4-3Deltagag/pol, non-replication competent), hemizygous depletion or overexpression of mitochondrial superoxide dismutase (SOD2(+/-) knock-out (KO) or MnSOD OX, respectively), overexpression of mitochondrial...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3457346</comments>
            <pubDate>Thu, 08 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3457346</guid>        </item>
        <item>
            <title>Deferasirox Decreases Age-Associated Iron Accumulation in the Aging F344XBN Rat Heart and Liver.</title>
            <link>http://www.medworm.com/index.php?rid=3374776&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20229123%26dopt%3DAbstract</link>
            <description>Authors: Arvapalli RK, Paturi S, Laurino JP, Katta A, Kakarla SK, Gadde MK, Wu M, Rice KM, Walker EM, Wehner P, Blough ER
    It is thought that aging in rats and humans is associated with increases in iron accumulation and cell apoptosis. Here, we examine the relationship between cardiac iron levels and apoptosis in aged F344XBN rats that had been treated with an oral iron chelator (Deferasirox; 100 mg/kg body weight) on alternate days for 6 months. Compared to adult animals (6 month), cardiac iron (+72%), liver iron (+87%), ferritin light chain (+59%), divalent metal transporter-1 (+56%) and the number of TdT-mediated dUTP nick end labeling (TUNEL) positive cells (4.3 fold increase) were higher in 33-month-old animals (P &amp;lt; 0.05). Deferasirox treatment decreased cardiac iron levels by ...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3374776</comments>
            <pubDate>Sat, 13 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3374776</guid>        </item>
        <item>
            <title>Erratum to: Nitrogen Compounds Prevent H9c2 Myoblast Oxidative Stress-Induced Mitochondrial Dysfunction and Cell Death.</title>
            <link>http://www.medworm.com/index.php?rid=3331866&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20195793%26dopt%3DAbstract</link>
            <description>Authors: Silva JP, Sard&amp;#xE3;o VA, Coutinho OP, Oliveira PJ
    
    PMID: 20195793 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331866</comments>
            <pubDate>Tue, 02 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3331866</guid>        </item>
        <item>
            <title>Exposure to Low-Dose Trichloroethylene Alters Shear Stress Gene Expression and Function in the Developing Chick Heart.</title>
            <link>http://www.medworm.com/index.php?rid=3316473&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20186580%26dopt%3DAbstract</link>
            <description>Authors: Makwana O, King NM, Ahles L, Selmin O, Granzier HL, Runyan RB
    Trichloroethylene is an organic solvent used as an industrial degreasing agent. Due to its widespread use and volatile nature, TCE is a common environmental contaminant. Trichloroethylene exposure has been implicated in the etiology of heart defects in human populations and animal models. Recent data suggest misregulation of Ca(2+) homeostasis in H9c2 cardiomyocyte cell line after TCE exposure. We hypothesized that misregulation of Ca(2+) homeostasis alters myocyte function and leads to changes in embryonic blood flow. In turn, changes in cardiac flow are known to cause cardiac malformations. To investigate this hypothesis, we dosed developing chick embryos in ovo with environmentally relevant doses of TCE (8 and 80...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3316473</comments>
            <pubDate>Fri, 26 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3316473</guid>        </item>
        <item>
            <title>In Utero Exposure of Female CD-1 Mice to AZT and/or 3TC: II. Persistence of Functional Alterations in Cardiac Tissue.</title>
            <link>http://www.medworm.com/index.php?rid=3280478&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20155331%26dopt%3DAbstract</link>
            <description>Authors: Torres SM, Divi RL, Walker DM, McCash CL, Carter MM, Campen MJ, Einem TL, Chu Y, Seilkop SK, Kang H, Poirier MC, Walker VE
    To delineate temporal changes in the integrity and function of mitochondria/cardiomyocytes in hearts from mice exposed in utero to commonly used nucleoside analogs (NRTIs), CD-1 mice were exposed in utero to 80 mg AZT/kg, 40 mg 3TC/kg, 80 mg AZT/kg plus 40 mg 3TC/kg, or vehicle alone during days 12-18 of gestation and hearts from female mouse offspring were examined at 13 and 26 weeks postpartum. Alterations in cardiac mitochondrial DNA (mtDNA) content, oxidative phosphorylation (OXPHOS) enzyme activities, mtDNA mutations, and echocardiography of NRTI-exposed mice were assessed and compared with findings in vehicle-exposed control mice. A hybrid capture-ch...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3280478</comments>
            <pubDate>Sat, 13 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3280478</guid>        </item>
        <item>
            <title>The Effect of Saffron Consumption on Biochemical and Histopathological Heart Indices of Rats with Myocardial Infarction.</title>
            <link>http://www.medworm.com/index.php?rid=3232146&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20119744%26dopt%3DAbstract</link>
            <description>This study was designed to assess the effects of saffron (Crocus sativus) on rats' heart with isoproterenol-induced myocardial injury. Animals were divided randomly into four groups: vehicle-control group (CTL); ISO group, administrated with Isoproterenol 85 mg/kg s.c.; saffron group; and finally combined Saffron + ISO group. Basal and final serum levels of heart troponin I, heart tissue antioxidants and histopathological indices were assessed in all groups. Isoproterenol administration significantly increased serum level of troponin I when compared to control group (3.46 +/- 0.77 vs. 0.53 +/- 0.35 ml in ng/ml, P &amp;lt; 0.001) and reduced significantly the glutathione peroxidase activity of heart muscle (1.63 +/- 0.21 vs. 4.01 +/- 0.64 nmol/mg protein, P &amp;lt; 0.05). The grade of heart muscle...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3232146</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3232146</guid>        </item>
        <item>
            <title>Nitrogen Compounds Prevent H9c2 Myoblast Oxidative Stress-Induced Mitochondrial Dysfunction and Cell Death.</title>
            <link>http://www.medworm.com/index.php?rid=3232145&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20119745%26dopt%3DAbstract</link>
            <description>Authors: Silva JP, Sard&amp;#xE3;o VA, Coutinho OP, Olveira PJ
    Oxidative stress has been connected to various forms of cardiovascular diseases. Previously, we have been investigating the potential of new nitrogen-containing synthetic compounds using a neuronal cell model and different oxidative stress conditions in order to elucidate their potential to ameliorate neurodegenerative diseases. Here, we intended to extend these initial studies and investigate the protective role of four of those new synthetic compounds (FMA4, FMA7, FMA762 and FMA796) against oxidative damage induced to H9c2 cardiomyoblasts by tert-butylhydroperoxide (t-BHP). The data indicates that FMA762 and FMA796 decrease t-BHP-induced cell death, as measured by both sulforhodamine B assay and nuclear chromatin condensation...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3232145</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3232145</guid>        </item>
        <item>
            <title>In Utero Exposure of Female CD-1 Mice to AZT and/or 3TC: I. Persistence of Microscopic Lesions in Cardiac Tissue.</title>
            <link>http://www.medworm.com/index.php?rid=3213339&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20101476%26dopt%3DAbstract</link>
            <description>Authors: Torres SM, March TH, Carter MM, McCash CL, Seilkop SK, Poirier MC, Walker DM, Walker VE
    The current study was designed to delineate temporal changes in cardiomyocytes and mitochondria at the light and electron microscopic levels in hearts of mice exposed transplacentally to commonly used nucleoside analogs (NRTIs). Pregnant CD-1 mice were given 80 mg AZT/kg, 40 mg 3TC/kg, 80 mg AZT/kg plus 40 mg 3TC/kg, or vehicle alone during the last 7 days of gestation, and hearts from female mouse pups were examined at 13 and 26 weeks postpartum for histopathological or ultrastructural changes in cross-sections of both the ventricles and the interventricular septum. Using light microscopy and special staining techniques, transplacental exposure to AZT, 3TC, or AZT/3TC was shown to induce s...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3213339</comments>
            <pubDate>Wed, 27 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3213339</guid>        </item>
        <item>
            <title>Nanoparticle Inhalation Impairs Coronary Microvascular Reactivity via a Local Reactive Oxygen Species-Dependent Mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=3120835&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20033351%26dopt%3DAbstract</link>
            <description>Authors: Leblanc AJ, Moseley AM, Chen BT, Frazer D, Castranova V, Nurkiewicz TR
    We have shown that nanoparticle inhalation impairs endothelium-dependent vasodilation in coronary arterioles. It is unknown whether local reactive oxygen species (ROS) contribute to this effect. Rats were exposed to TiO(2) nanoparticles via inhalation to produce a pulmonary deposition of 10 mug. Coronary arterioles were isolated from the left anterior descending artery distribution, and responses to acetylcholine, arachidonic acid, and U46619 were assessed. Contributions of nitric oxide synthase and prostaglandin were assessed via competitive inhibition with N(G)-Monomethyl-L-Arginine (L-NMMA) and indomethacin. Microvascular wall ROS were quantified via dihydroethidium (DHE) fluorescence. Coronary arteriole...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120835</comments>
            <pubDate>Tue, 22 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120835</guid>        </item>
        <item>
            <title>Arsenic-Induced QT Dispersion is Associated with Atherosclerotic Diseases and Predicts Long-Term Cardiovascular Mortality in Subjects with Previous Exposure to Arsenic: A 17-Year Follow-Up Study.</title>
            <link>http://www.medworm.com/index.php?rid=3058207&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19957052%26dopt%3DAbstract</link>
            <description>Authors: Wang CH, Chen CL, Hsiao CK, Chiang FT, Hsu LI, Chiou HY, Hsueh YM, Wu MM, Chen CJ
    Chronic arsenic poisoning is a major worldwide public health problem. Recently, we had reported chronic arsenic poisoning was dose-dependently associated with ventricular abnormalities quantified by electrocardiographic QT prolongation linking to atherosclerotic diseases. An association of chronic arsenic poisoning with ventricular repolarization inhomogeneity quantified by QT dispersion (QTD) is of particular interest from a theoretical and practical perspective. We aimed to further elucidate (1) the association of chronic arsenic exposure with ventricular abnormalities quantified by QTD, (2) the association of QTD with atherosclerotic diseases and (3) the predictability of QTD for long-term mor...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3058207</comments>
            <pubDate>Thu, 03 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3058207</guid>        </item>
        <item>
            <title>Amelioration of Cardiac Remodeling in Congestive Heart Failure by beta-Adrenoceptor Blockade is Associated with Depression in Sympathetic Activity.</title>
            <link>http://www.medworm.com/index.php?rid=3052539&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19949891%26dopt%3DAbstract</link>
            <description>This study investigated whether improvement in cardiac function and attenuation of cardiac remodeling by some beta-adrenoceptor (beta-AR) antagonists were associated with a depression in sympathetic activity in congestive heart failure (CHF) due to myocardial infarction (MI). Although cardiac dysfunction, hypertrophy and dilatation as well as increased plasma level of catecholamines are known to occur in CHF, the relationship between these parameters is poorly understood. Three weeks after occlusion of the coronary artery, rats were treated daily with 20 and 75 mg/kg of either atenolol or propranolol for 5 weeks. Sham-operated rats served as controls. Both atenolol and propranolol at 20 and 75 mg/kg doses attenuated the MI-induced cardiac hypertrophy, increases in left ventricular (LV) end...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3052539</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3052539</guid>        </item>
        <item>
            <title>Erratum to: Antiarrhythmic Effects of Some Antioxidant Vitamins in Rats Injected with Epinephrine.</title>
            <link>http://www.medworm.com/index.php?rid=3012906&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19924570%26dopt%3DAbstract</link>
            <description>Authors: Sethi R, Rehsia NS, Jindal K, Dhalla KS, Elimban V, Dhalla NS
    
    PMID: 19924570 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3012906</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3012906</guid>        </item>
        <item>
            <title>Mechanisms of Myocyte Cytotoxicity Induced by the Multikinase Inhibitor Sorafenib.</title>
            <link>http://www.medworm.com/index.php?rid=3004469&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19915982%26dopt%3DAbstract</link>
            <description>In conclusion, given the extreme lack of kinase selectivity that sorafenib exhibits, it is likely that inhibition of kinases other than RAF, or combinations of kinases, contributes to the cardiotoxic effects of sorafenib.
    PMID: 19915982 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3004469</comments>
            <pubDate>Sat, 14 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3004469</guid>        </item>
        <item>
            <title>Erythropoietin Promotes Deleterious Cardiovascular Effects and Mortality Risk in a Rat Model of Chronic Sports Doping.</title>
            <link>http://www.medworm.com/index.php?rid=2935937&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19859831%26dopt%3DAbstract</link>
            <description>In conclusion, rhEPO doping in rats under chronic exercise promotes not only the expected RBC count increment, suggesting hyperviscosity, but also other serious deleterious cardiovascular and thromboembolic modifications, including mortality risk, which might be known and assumed by all sports authorities, including athletes and their physicians.
    PMID: 19859831 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2935937</comments>
            <pubDate>Tue, 27 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2935937</guid>        </item>
        <item>
            <title>Mitochondrial Involvement in Cardiac Apoptosis During Ischemia and Reperfusion: Can We Close the Box?</title>
            <link>http://www.medworm.com/index.php?rid=2931302&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19855945%26dopt%3DAbstract</link>
            <description>Authors: Machado NG, Alves MG, Carvalho RA, Oliveira PJ
    Myocardial ischemia is the main cause of death in the Western societies. Therapeutic strategies aimed to protect the ischemic myocardium have been extensively studied. Reperfusion is the definitive treatment for acute coronary syndromes, especially acute myocardial infarction; however, reperfusion has the potential to exacerbate tissue injury, a process termed reperfusion injury. Ischemia/reperfusion (I/R) injury may lead to cardiac arrhythmias and contractile dysfunction that involve apoptosis and necrosis in the heart. The present review describes the mitochondrial role on cardiomyocyte death and some potential pharmacological strategies aimed at preventing the opening of the box, i.e., mitochondrial dysfunction and membrane per...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2931302</comments>
            <pubDate>Sat, 24 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2931302</guid>        </item>
        <item>
            <title>Arsenic Exposure and Cardiovascular Disorders: An Overview.</title>
            <link>http://www.medworm.com/index.php?rid=2848237&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19787300%26dopt%3DAbstract</link>
            <description>Authors: Balakumar P, Kaur J
    The incidence of arsenic toxicity has been observed in various countries including Taiwan, Bangladesh, India, Argentina, Australia, Chile, China, Hungary, Peru, Thailand, Mexico and United States of America. Arsenic is a ubiquitous element present in drinking water, and its exposure is associated with various cardiovascular disorders. Arsenic exposure plays a key role in the pathogenesis of vascular endothelial dysfunction as it inactivates endothelial nitric oxide synthase, leading to reduction in the generation and bioavailability of nitric oxide. In addition, the chronic arsenic exposure induces high oxidative stress, which may affect the structure and function of cardiovascular system. Further, the arsenic exposure has been noted to induce atheroscleros...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2848237</comments>
            <pubDate>Mon, 28 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2848237</guid>        </item>
        <item>
            <title>An Elementary Framework for Judging the Cardiovascular Toxicity of Carbon Soot: Experiences from an Occupational Health Survey of Diamond Industry Workers.</title>
            <link>http://www.medworm.com/index.php?rid=2832736&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19777380%26dopt%3DAbstract</link>
            <description>The objective of this study is to assess the cardiovascular effects consequent to chronic respiratory exposure of carbon soot. A cross-sectional occupational health survey was conducted in all consenting workers who employed in the production wing of diamond-processing industries. Blood pressure, ECGs, height, weight, and blood counts were measured and evaluated. Blood pressure measurements revealed a high prevalence of hypertension in young workers. Left atrial abnormality (LAA) was the major finding in the electrocardiograms. We found a high prevalence of hypertension in young diamond workers. The LASER saw operators had highest prevalence of LAA. White cell count and prevalence of hypertension was highest for the workers in grinder operations.
    PMID: 19777380 [PubMed - as supplied by...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832736</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832736</guid>        </item>
        <item>
            <title>Mitochondrial Preservation in Celsior Versus Histidine Buffer Solution During Cardiac Ischemia and Reperfusion.</title>
            <link>http://www.medworm.com/index.php?rid=2807967&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19757201%26dopt%3DAbstract</link>
            <description>Authors: Alves MG, Oliveira PJ, Carvalho RA
    Various stressful conditions such as ischemia in cold cardioplegic solutions and reperfusion occur during heart transplantation. Since ATP production is essential for the maintenance of contractile activity, mitochondrial function may be a mediator of ischemia and ischemia/reperfusion (I/R) injury. We aimed at testing the ability of two distinct cardioplegic solutions, Celsior (Cs) and Histidine Buffer (HBS), to protect rat heart mitochondria (HM) function during ischemia alone or ischemia followed by reperfusion. A standard Krebs-Henseleit solution (KH) was used as &quot;negative&quot; control. Male and Female Wistar rats were divided into control (Ctrl), reperfusion control (Ctrl_R), ischemia and I/R groups. Ischemia and I/R were divided into three s...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2807967</comments>
            <pubDate>Mon, 14 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2807967</guid>        </item>
        <item>
            <title>Preventive Effect of Amiodarone During Acute Period in Isoproterenol-Induced Myocardial Injury in Wistar Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2744360&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19714493%26dopt%3DAbstract</link>
            <description>Authors: Albayrak F, Bayir Y, Halici Z, Kabalar E, Bayram E, Ozturk C, Suleyman H, Keles MS, Kurt M, Bakan E
    The ability of amiodarone to prevent pathological changes and oxidative stress after isoproterenol (ISO)-induced myocardial injury was investigated in rats. A better understanding of the processes involved in the pathophysiology of myocardial infarction has led to the search for drugs that can limit the extent of myocardial injury. Amiodarone was administered to groups of rats groups once per day for 30 days. On days 29 and 30, the rats of the ISO control and drug treatment groups were administered 180 mg/kg ISO subcutaneously at an interval of 24 h for two consecutive days. In the control groups, clinical indicators, such as creatine kinase-isoenzymes and troponin-I, were found...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2744360</comments>
            <pubDate>Thu, 27 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2744360</guid>        </item>
        <item>
            <title>P38 MAP Kinase Inhibitor Prevents Diastolic Dysfunction in Rats Following HIV gp120 Injection In vivo.</title>
            <link>http://www.medworm.com/index.php?rid=2661164&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19644660%26dopt%3DAbstract</link>
            <description>Authors: Berzingi C, Chen F, Finkel MS
    HIV infection in patients is associated with a surprisingly high frequency of diastolic dysfunction followed by the development of a dilated cardiomyopathy. Potential mechanisms include direct effects of HIV proteins, including gp120. We have previously reported direct inotropic and p38 MAP kinase signaling effects of HIV gp120 on isolated cardiac myocytes in vitro. We now report effects of a single injection of HIV gp120 on cardiac hemodynamics in vivo. HIV gp120 (50 mug/kg) was injected intravenously and hemodynamics assessed at 1, 24, 48 and 72 h in freely ambulatory, awake rats. Rats injected with gp120 demonstrated a blunted diastolic response to increasing intravenous (IV) injections of the beta-adrenergic agonist, isoproterenol (ISO), compa...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2661164</comments>
            <pubDate>Thu, 30 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2661164</guid>        </item>
        <item>
            <title>Zinc Antagonizes Homocysteine-Induced Fetal Heart Defects in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2661165&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19641857%26dopt%3DAbstract</link>
            <description>Authors: He X, Hong X, Zeng F, Kang F, Li L, Sun Q
    It has been suggested that zinc may have a protective role against heart defects during fetal development. We investigated the effects of zinc on the development of fetal cardiac malformations induced by homocysteine. Pregnant Sprague-Dawley rats were randomized into one of five groups: control (C), homocysteine (H), homocysteine + zinc (Z), homocysteine + folic acid (F), or homocysteine + zinc + folic acid (ZF) (each n = 8). Homocysteine (8 nmol/day) was administered intraperitoneally in the H, Z, F, and ZF groups on gestation days (GD) 8, 9, and 10. Zinc (30 mg/kg day), folic acid (30 mg/kg day), or both (30 mg/kg day each) were administered intragastrically daily in the Z, F, and ZF groups, respectively, throughout the pregnancy. In...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2661165</comments>
            <pubDate>Wed, 29 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2661165</guid>        </item>
        <item>
            <title>Dose Dependency and Reversibility of Serotonin-Induced Valvular Heart Disease in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2615760&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19609730%26dopt%3DAbstract</link>
            <description>In conclusion, this study provides evidence for a dose-dependent valvular toxicity of serotonergic drugs, which appears to be reversible after drug withdrawal.
    PMID: 19609730 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2615760</comments>
            <pubDate>Wed, 15 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2615760</guid>        </item>
        <item>
            <title>Report and Recommendations of the Workshop of the European Centre for the Validation of Alternative Methods for Drug-Induced Cardiotoxicity.</title>
            <link>http://www.medworm.com/index.php?rid=2573793&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19572114%26dopt%3DAbstract</link>
            <description>Authors: Stummann TC, Beilmann M, Duker G, Dumotier B, Fredriksson JM, Jones RL, Hasiwa M, Kang YJ, Mandenius CF, Meyer T, Minotti G, Valentin YJ, Z&amp;#xFC;nkler BJ, Bremer S
    Cardiotoxicity is among the leading reasons for drug attrition and is therefore a core subject in non-clinical and clinical safety testing of new drugs. European Centre for the Validation of Alternative Methods held in March 2008 a workshop on &quot;Alternative Methods for Drug-induced Cardiotoxicity&quot; in order to promote acceptance of alternative methods reducing, refining or replacing the use of laboratory animals in this field. This review reports the outcome of the workshop. The participants identified the major clinical manifestations, which are sensitive to conventional drugs, to be arrhythmias, contractility toxici...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2573793</comments>
            <pubDate>Wed, 01 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2573793</guid>        </item>
        <item>
            <title>Comparison of the Cardiac Electrophysiology and General Toxicology of Two Formulations of Intravenous Amiodarone in Dogs.</title>
            <link>http://www.medworm.com/index.php?rid=2530045&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19554478%26dopt%3DAbstract</link>
            <description>Authors: Cushing DJ, Cooper WD, Gralinski MR, Lipicky RJ, Kudenchuk PJ, Kowey PR
    Intravenous amiodarone (AIV) must be administered slowly after dilution to avoid hypotension, which is due to the cosolvents polysorbate 80 and benzyl alcohol used in its formulation. PM101 is a formulation of amiodarone devoid of these cosolvents, which enables bolus administration. We evaluated any potential toxicity or exaggerated adverse cardiac electrophysiologic effects of PM101 compared with AIV and control. Beagle dogs were treated with the human-equivalent amiodarone loading dose (2.14 mg/kg) with PM101 (bolus push) or AIV (10 min infusion in the toxicology study and bolus push in the electrophysiology study) followed by maintenance infusion (0.014 mg kg(-1) min(-1) through 6 h followed by 0.007 m...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2530045</comments>
            <pubDate>Wed, 24 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2530045</guid>        </item>
        <item>
            <title>ST elevation myocardial infarction presenting after use of pseudoephedrine.</title>
            <link>http://www.medworm.com/index.php?rid=2530060&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19381878%26dopt%3DAbstract</link>
            <description>Authors: Celik A
    
    PMID: 19381878 [PubMed - in process] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2530060</comments>
            <pubDate>Sun, 31 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2530060</guid>        </item>
        <item>
            <title>Influence of infrasound exposure on the whole L-type calcium currents in rat ventricular myocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2530059&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19387569%26dopt%3DAbstract</link>
            <description>This study was designed to examine the effect of infrasound exposure (5 Hz at 130 dB) on whole-cell L-type Ca2+ currents (WLCC) in rat ventricular myocytes and the underlying mechanism(s) involved. Thirty-two adult Sprague-Dawley rats were randomly assigned to infrasound exposure and control groups. [Ca2+](i), WLCC, mRNA expression of the a(1c) subunit of L-type Ca2+ channels (LCC), and SERCA2 protein were examined on day 1, 7, and 14 after initiation of infrasound exposure. Fluo-3/AM fluorescence and the laser scanning confocal microscope techniques were used to measure [Ca2+](i) in freshly isolated ventricular myocytes. The Ca2+ fluorescence intensity (FI), denoting [Ca2+](i) in cardiomyocytes, was significantly elevated in a time-dependent manner in the exposure groups. There was a sign...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2530059</comments>
            <pubDate>Sun, 31 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2530059</guid>        </item>
        <item>
            <title>The cardiac effects of prolonged vitamin B12 and folate deficiency in rats.</title>
            <link>http://www.medworm.com/index.php?rid=2530057&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19399644%26dopt%3DAbstract</link>
            <description>Authors: Taban-Shomal O, Kilter H, Wagner A, Schorr H, Umanskaya N, H&amp;#xFC;bner U, B&amp;#xF6;hm M, Herrmann W, Herrmann M
    In the recent past, hyperhomocysteinemia (HHCY) has been linked to chronic heart failure. Folate and vitamin B12 deficiencies are the common causes of HHCY. The impact of these vitamins on cardiac function and morphology has scarcely been investigated. The aim of this study was to conduct an analysis of the cardiac effect of folate and vitamin B12 deficiency in vivo. Two groups of rats, a control (Co, n = 10) and a vitamin-deficient group (VitDef, n = 10), were fed for 12 weeks with a folate and vitamin B12-free diet or an equicaloric control diet. Plasma and tissue concentrations of HCY, S-adenosyl-homocysteine (SAH), S-adenosyl-methionine (SAM), and brain natriuretic...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2530057</comments>
            <pubDate>Sun, 31 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2530057</guid>        </item>
        <item>
            <title>Commentary on &quot;A case of acute cardiomyopathy and pericarditis associated with methylphenidate&quot;; Cardiovasc Toxicol, DOI 10.1007/s12012-009-9033-7.</title>
            <link>http://www.medworm.com/index.php?rid=2530055&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19415530%26dopt%3DAbstract</link>
            <description>Commentary on &quot;A case of acute cardiomyopathy and pericarditis associated with methylphenidate&quot;; Cardiovasc Toxicol, DOI 10.1007/s12012-009-9033-7.
    Cardiovasc Toxicol. 2009 Jun;9(2):105
    Authors: Ghanizadeh A
    
    PMID: 19415530 [PubMed - in process] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2530055</comments>
            <pubDate>Sun, 31 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2530055</guid>        </item>
        <item>
            <title>Quo vadis: whither homocysteine research?</title>
            <link>http://www.medworm.com/index.php?rid=2530053&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19484390%26dopt%3DAbstract</link>
            <description>Authors: Joseph J, Handy DE, Loscalzo J
    Four decades of research on the link between hyperhomocysteinemia and cardiovascular disease has led to a crossroads. Several negative studies on the role of homocysteine-lowering B-vitamin therapy in reducing the risk of atherothrombotic cardiovascular disease have dampened enthusiasm for this important field of research. In this review, we assess the present state of homocysteine research and suggest potential avenues that would help to clarify the purported link between the plasma homocysteine level and cardiovascular risk. We address several questions raised by the findings of various basic, epidemiological and clinical studies and attempt to construct a framework that we believe will allow us to address the fundamental unresolved issues in t...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2530053</comments>
            <pubDate>Sun, 31 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2530053</guid>        </item>
        <item>
            <title>Cardiac lesions induced by testosterone: protective effects of dexrazoxane and trimetazidine.</title>
            <link>http://www.medworm.com/index.php?rid=2530051&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19484391%26dopt%3DAbstract</link>
            <description>Authors: Belhani D, Fanton L, Vaillant F, Descotes J, Manati W, Tabib A, Bui-Xuan B, Timour Q
    Further to our previous observation of post-mortem cardiac lesions after sudden death in several athletes with a history of anabolic steroid abuse, this study was intended to reproduce these lesions in rabbits administered testosterone oenanthate, a prototypic anabolic steroid abused by athletes, and to provide evidence for the protective effects of trimetazidine and dexrazoxane that are used as antianginal and cardioprotective drugs, respectively. Groups of six rabbits each were administered saline, testosterone, or a combination of testosterone and either trimetazidine or dexrazoxane for 3 months. Histologic cardiac lesions including necrosis, misshapen cell nuclei, interstitial and endocard...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2530051</comments>
            <pubDate>Sun, 31 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2530051</guid>        </item>
        <item>
            <title>AZT-induced oxidative cardiovascular toxicity: attenuation by Mg-supplementation.</title>
            <link>http://www.medworm.com/index.php?rid=2530049&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19484392%26dopt%3DAbstract</link>
            <description>Authors: Mak IT, Chmielinska JJ, Kramer JH, Weglicki WB
    Cardiovascular effects of chronic AZT treatment on SD male rats (185 g) fed either a normal Mg diet (0.1% MgO) or a high Mg diet (0.6% MgO) were examined. AZT treatment (1 mg/ml drinking water) for 3 weeks led to a 5.5-fold (0.88 +/- 0.11 nmol/min/10(6) cells, P &amp;lt; 0.05) elevation in neutrophil basal activity of O2(-) production versus controls (0.16 +/- 0.03 nmol/min, assayed ex vivo as SOD-inhibitable cytochrome c reduction). Concomitantly, plasma 8-isoprostane and PGE(2) levels rose 2.1-fold and 3-fold (both P &amp;lt; 0.05), respectively, compared to control; however, RBC GSH decreased 28% (P &amp;lt; 0.02) with GSSG content increased 3-fold, indicative of systemic oxidative stress. High Mg diet substantially attenuated the AZT-indu...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2530049</comments>
            <pubDate>Sun, 31 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2530049</guid>        </item>
        <item>
            <title>Zinc- and copper-induced interleukin-6 release in primary cell cultures from rat heart.</title>
            <link>http://www.medworm.com/index.php?rid=2530047&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19517273%26dopt%3DAbstract</link>
            <description>In conclusion, Zn2+ and Cu2+ increased IL-6 release and MAP-kinase activation in primary cardiac cells, processes known to be involved in cardiac inflammation and hypertrophy.
    PMID: 19517273 [PubMed - in process] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2530047</comments>
            <pubDate>Sun, 31 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2530047</guid>        </item>
        <item>
            <title>Dilated Cardiomyopathy in Transgenic Mice Expressing HIV Tat.</title>
            <link>http://www.medworm.com/index.php?rid=2304364&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19337863%26dopt%3DAbstract</link>
            <description>Authors: Fang Q, Kan H, Lewis W, Chen F, Sharma P, Finkel MS
    Mechanisms responsible for HIV cardiomyopathy are unknown, but may include direct effects of HIV proteins on the heart. Transgenic mice (TG) expressing HIV Tat protein targeted to the myocardium, +/- Tat TG, have revealed anatomical and biochemical defects in the heart. The present studies were conducted to clarify the effect of Tat on cardiac function. In vivo hemodynamics was measured in awake mice after inserting a catheter tip in the left ventricle under general anesthesia. Under the age of 3 months, the heart rate (HR) was significantly lower in TG (591 +/- 47 vs. 716 +/- 45 bpm, TG versus FVB control (FVB), respectively (P &amp;lt; 0.05; n = 8-12). Other hemodynamic indexes, including left ventricular systolic pressure (LVS...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2304364</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2304364</guid>        </item>
        <item>
            <title>Metabolites of MDMA Induce Oxidative Stress and Contractile Dysfunction in Adult Rat Left Ventricular Myocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2304370&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19333788%26dopt%3DAbstract</link>
            <description>In this study, we demonstrated that metabolites of MDMA induce oxidative stress and contractile dysfunction in adult rat left ventricular myocytes. Metabolites of MDMA used in this study included alpha-methyl dopamine, N-methyl alpha-methyl dopamine and 2,5-bis(glutathion-S-yl)-alpha-MeDA. Dihydroethidium was used to detect drug-induced increases in reactive oxygen species (ROS) production in ventricular myocytes. Contractile function and changes in intracellular calcium transients were measured in paced (1 Hz), Fura-2 AM loaded, myocytes using the IonOptix system. Production of ROS in ventricular myocytes treated with MDMA was not different from control. In contrast, all three metabolites of MDMA exhibited time- and concentration-dependent increases in ROS that were prevented by N-acetyl-...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2304370</comments>
            <pubDate>Tue, 31 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2304370</guid>        </item>
        <item>
            <title>A Case of Acute Cardiomyopathy and Pericarditis Associated with Methylphenidate.</title>
            <link>http://www.medworm.com/index.php?rid=2286654&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19296063%26dopt%3DAbstract</link>
            <description>We report the case of a 17-year-old male who developed chest pain, elevated cardiac biomarkers, and acute left ventricular dysfunction following a single dose of methylphenidate. The risk of cardiomyopathy in the setting of methylphenidate treatment should prompt further study on the safety of this drug, and lead to ways of identifying those at risk of developing these complications.
    PMID: 19296063 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2286654</comments>
            <pubDate>Thu, 19 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2286654</guid>        </item>
        <item>
            <title>Acute Myocardial Infarction Following Oral Methyl-Ergometrine Intake.</title>
            <link>http://www.medworm.com/index.php?rid=2191761&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19219407%26dopt%3DAbstract</link>
            <description>We report the case of a 38-year-old woman with a ST elevation myocardial infarction (STEMI) few days after artificially induced abortion by oral prescription of methylergometrine. Coronary angiography performed 2 days after onset of chest pain did not reveal any abnormalities of the coronary arteries but a provocative test using intravenous methylergometrine was positive with reproduction of chest pain, ECG changes and with a significant narrowing localized on the second segment of the left anterior descending artery at the angiogram. Thus, since methylergometrin may clearly induce coronary spasm when prescribed orally, chest pain occurring under oral treatment should require immediate attention even if atypical or in the absence of cardiovascular risk factors.
    PMID: 19219407 [PubMed -...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2191761</comments>
            <pubDate>Sat, 14 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2191761</guid>        </item>
        <item>
            <title>Expression of Nkx2.5 in Wild Type, Cardiac Mutant, and Thyroxine-Induced Metamorphosed Hearts of the Mexican Axolotl.</title>
            <link>http://www.medworm.com/index.php?rid=2164297&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19191032%26dopt%3DAbstract</link>
            <description>In this study, we cloned and sequenced the as yet uncharacterized Nkx2.5 cDNA from normal and cardiac mutant axolotl heart RNA. Comparison of cDNA sequences of Nkx2.5 from normal and mutant axolotl hearts did not show differences suggesting that loss of function mutation in Nkx2.5 is not responsible for the mutant phenotype. However, quantitative studies show higher expression of Nkx2.5 in mutant hearts raising the possibility that increased expression of Nkx2.5 may contribute to the mutant phenotype. We also evaluated quantitative changes in expression of Nkx2.5 in axolotl hearts during embryonic and postembryonic heart development induced by exogenous thyroid hormone. There is an apparent increase in Nkx2.5 transcript levels in metamorphosed hearts.
    PMID: 19191032 [PubMed - as suppli...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2164297</comments>
            <pubDate>Wed, 04 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2164297</guid>        </item>
        <item>
            <title>Long-Term Exposure to AZT, but not d4T, Increases Endothelial Cell Oxidative Stress and Mitochondrial Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=2028843&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19067249%26dopt%3DAbstract</link>
            <description>Authors: Kline ER, Bassit L, Hernandez-Santiago BI, Detorio MA, Liang B, Kleinhenz DJ, Walp ER, Dikalov S, Jones DP, Schinazi RF, Sutliff RL
    Nucleoside reverse transcriptase inhibitors (NRTIs), such as zidovudine (AZT) and stavudine (d4T), cause toxicities to numerous tissues, including the liver and vasculature. While much is known about hepatic NRTI toxicity, the mechanism of toxicity in endothelial cells is incompletely understood. Human aortic endothelial and HepG2 liver cells were exposed to 1 muM AZT or d4T for up to 5 weeks. Markers of oxidative stress, mitochondrial function, NRTI phosphorylation, mitochondrial DNA (mtDNA) levels, and cytotoxicity were monitored over time. In endothelial cells, AZT significantly oxidized glutathione redox potential, increased total cellular and...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2028843</comments>
            <pubDate>Tue, 09 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2028843</guid>        </item>
        <item>
            <title>A Hyperlipidemic Rabbit Model Provides New Insights into Pulmonary Zinc Exposure Effects on Cardiovascular Health.</title>
            <link>http://www.medworm.com/index.php?rid=1912196&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18953671%26dopt%3DAbstract</link>
            <description>This study ascertains the effects of zinc, a major component of particulate matter, on pulmonary and systemic endpoints using hyperlipidemic rabbits to model diet-induced human atherosclerosis. New Zealand White rabbits were fed a normal or cholesterol-enriched diet and then were intratracheally instilled 1x/week for 4 weeks with saline or 16 microg/kg of zinc, equal parts sulfate and oxide. Physiologic responses, blood after each exposure, and terminal bronchoalveolar lavage (BAL) were assessed. Rabbits fed a cholesterol-rich diet developed hyperlipidemia and had consistently higher circulating leukocyte counts than rabbits fed normal chow. Within minutes after zinc instillation, saturation of peripheral oxygen was decreased in hyperlipidemic rabbits and heart rate was increased in hyperl...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1912196</comments>
            <pubDate>Sat, 25 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1912196</guid>        </item>
        <item>
            <title>Hypertension, Cardiac Hypertrophy, and Impaired Vascular Relaxation Induced by 2,3,7,8-Tetrachlorodibenzo-p-Dioxin are Associated with Increased Superoxide.</title>
            <link>http://www.medworm.com/index.php?rid=1873551&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18850075%26dopt%3DAbstract</link>
            <description>Authors: Kopf PG, Huwe JK, Walker MK
    The mechanisms by which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increases the incidence of human cardiovascular disease are not known. We investigated the degree to which cardiovascular disease develops in mice following subchronic TCDD exposure. Adult male C57BL/6 mice were dosed with vehicle or 300 ng TCDD/kg by oral gavage three times per week for 60 days. Blood pressure was recorded by radiotelemetry and aortic endothelial function was assessed by acetylcholine-induced vasorelaxation. Mean arterial pressure of TCDD-exposed mice was increased significantly by day 4 and between days 7-10, 25-35, and 45-60 with two periods of normalization on days 11-24 and days 36-39. Consistent with a prolonged period of systemic hypertension, heart weight was...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1873551</comments>
            <pubDate>Sat, 11 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1873551</guid>        </item>
        <item>
            <title>CXCR4 Receptor Antagonist Blocks Cardiac Myocyte P38 MAP Kinase Phosphorylation by HIV gp120.</title>
            <link>http://www.medworm.com/index.php?rid=1873550&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18850076%26dopt%3DAbstract</link>
            <description>Authors: Yuan Y, Kan H, Fang Q, Chen F, Finkel MS
    The prognosis for patients with human immunodeficiency virus (HIV) infection has improved remarkably as a result of effective antiretroviral therapy. This has resulted in an increased awareness of cardiac complications from HIV infection, including cardiomyopathy and overt heart failure. Mechanisms responsible for HIV cardiomyopathy and heart failure are unknown, but may include direct effects of HIV proteins on the heart. We have previously reported that the HIV envelope glycoprotein, gp120, has a p38 MAP kinase-dependent negative inotropic effect on adult rat ventricular myocytes (ARVM). This signaling pathway presumably results from the binding of gp120 to a specific receptor on the surface of cardiac myocytes. HIV gp120 has been sho...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1873550</comments>
            <pubDate>Sat, 11 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1873550</guid>        </item>
        <item>
            <title>Molecular Analysis of Cocaine-Induced Endothelial Dysfunction: Role of Endothelin-1 and Nitric Oxide.</title>
            <link>http://www.medworm.com/index.php?rid=1830029&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18813882%26dopt%3DAbstract</link>
            <description>Authors: Pradhan L, Mondal D, Chandra S, Ali M, Agrawal KC
    Cocaine remains the most frequently used illicit substance. Although cocaine-induced atherosclerosis is well documented, its mechanism of action on human vascular endothelial cells has not been determined. Nitric oxide (NO) and endothelin-1 (ET-1) are involved in endothelial cell activation and leukocyte recruitment. The present study monitored the effects of cocaine on NO and ET-1 production in human aortic endothelial cells (HAECs) and the effects of sodium nitroprusside (SNP) and BQ-123 on leukocyte adhesion to HAECs. Acute exposure to cocaine (1 and 3 muM) significantly increased ET-1 production (2-fold) and ET-1 receptor type-A (ET(A)R) protein expression, within 6-12 h. Cocaine exposure for a longer duration (24-72 h) sho...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1830029</comments>
            <pubDate>Wed, 24 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1830029</guid>        </item>
        <item>
            <title>The Prevalence of Type 2 Diabetes and Hypertension in Uygur and Kazak Populations.</title>
            <link>http://www.medworm.com/index.php?rid=1776223&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18777166%26dopt%3DAbstract</link>
            <description>This study was designed to evaluate the epidemiology of type 2 diabetes and hypertension in Uygur and Kazak ethnic populations. A three-step stratified sampling method was used. Questionnaires, blood pressure, anthropometric measurement, and fasting blood glucose were monitored. In total, 1,571 Uygur and 2,913 Kazak subjects were randomly enrolled. The prevalence of type 2 diabetes and glucose intolerance was 5.55- and 1.90-fold higher, respectively, in Uygur than in the Kazak population (8.16 vs. 1.47%, P &amp;lt; 0.001 and 3.29 vs. 1.73%, P &amp;lt; 0.001). However, the prevalence of hypertension and obesity was significantly higher in the Kazak than in the Uygur population (hypertension: 43.52 vs. 31.98%, P &amp;lt; 0.001; obesity: 25.0 vs. 14.5%, P &amp;lt; 0.001, respectively). Our data suggest a sig...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1776223</comments>
            <pubDate>Sat, 06 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1776223</guid>        </item>
        <item>
            <title>Antiplatelet Agents Sarpogrelate and Cilostazol Affect Experimentally-induced Ventricular Arrhythmias and Mortality.</title>
            <link>http://www.medworm.com/index.php?rid=1743225&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18751928%26dopt%3DAbstract</link>
            <description>Authors: Barta J, Sanganalmath SK, Kumamoto H, Takeda N, Edes I, Dhalla NS
    Antiplatelet agents, sarpogrelate (SAR), a 5-hydroxy tryptamine 2A receptor antagonist and cilostazol (CIL), a phosphodiesterase-III inhibitor, were observed to be beneficial in attenuating cardiac remodeling and improving cardiac function in congestive heart failure due to myocardial infarction in rats; however, CIL increased ventricular tachycardia and mortality. In order to study the effects of these antiplatelet agents on arrhythmias, Sprague-Dawley rats were pretreated with either SAR or CIL (5 mg/kg/day) for 2 weeks and were then either injected cumulative doses of epinephrine (Epi) or subjected to coronary occlusion. Saline-treated animals served as controls. Electrocardiographic analysis revealed that SA...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1743225</comments>
            <pubDate>Wed, 27 Aug 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1743225</guid>        </item>
        <item>
            <title>Estrogen-Mediated Protection in Myocardial Ischemia-Reperfusion Injury.</title>
            <link>http://www.medworm.com/index.php?rid=1689568&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18683081%26dopt%3DAbstract</link>
            <description>Authors: Booth EA, Lucchesi BR
    Before menopause, a woman has a relatively low risk for developing cardiovascular disease. After menopause, however, the risk increases nearly twofold and cardiovascular disease remains the number one cause of death among women. Observational trials and studies in animal models of cardiovascular disease suggested that females have reduced injury after myocardial ischemia and reperfusion injury. However, two large clinical trials, the women's health initiative (WHI) and the heart estrogen and progestin replacement study (HERS), found an increase in cardiovascular incidences in women taking hormone replacement therapy. The discrepancy between these data highlights the need for further research on the mechanism of estrogen in the cardiovascular system. Anima...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1689568</comments>
            <pubDate>Wed, 06 Aug 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1689568</guid>        </item>
        <item>
            <title>Role of Copper and Homocysteine in Pressure Overload Heart Failure.</title>
            <link>http://www.medworm.com/index.php?rid=1683973&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18679830%26dopt%3DAbstract</link>
            <description>In conclusion, our data suggest that copper supplement helps improve cardiac function in a pressure overload dilated cardiomyopathic heart.
    PMID: 18679830 [PubMed - as supplied by publisher] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1683973</comments>
            <pubDate>Tue, 05 Aug 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1683973</guid>        </item>
        <item>
            <title>Perinatal 2,3,7,8-Tetrachlorodibenzo-p-dioxin Exposure Sensitizes Offspring to Angiotensin II-induced Hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=1675665&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18670907%26dopt%3DAbstract</link>
            <description>Authors: Aragon AC, Goens MB, Carbett E, Walker MK
    In utero and lactational exposure of mice to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to cardiac hypertrophy and hydronephrosis in adulthood. We tested the hypothesis that perinatal TCDD exposure increases the susceptibility to cardiovascular disease when offspring are exposed to a common cardiovascular disease risk factor, angiotensin II (Ang II). Pregnant C57BL/6N mice were exposed to corn oil (control) or 6.0 mug/kg TCDD on gestation day 14.5. Male offspring were then exposed to a subpressor (0.1 mg/kg/day) or pressor (0.7 mg/kg/day) dose of Ang II at 3.5 months and cardiac morphology and blood pressure analyzed, respectively. Perinatal TCDD exposure increased left ventricular cavity dilation during diastole, and wall thickn...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1675665</comments>
            <pubDate>Fri, 01 Aug 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1675665</guid>        </item>
        <item>
            <title>QT Prolongation: A Case of Arsenical Pericardial and Pleural Effusion.</title>
            <link>http://www.medworm.com/index.php?rid=1626280&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18084726%26dopt%3DAbstract</link>
            <description>We describe a case of a man, 76 years old, who was admitted to our department for dyspnoea in APL in treatment with arsenic trioxide. Chest radiograph illustrated an enlarged cardiac silhouette and bilateral pleuric effusion and the ECG evidenced QT prolongation. The patient was also submitted to transthoracic echocardiography that revealed moderate pericardial effusion without signs of cardiac tamponade and a normal biventricular function. This condition was considered to be associated with arsenic trioxide polyserosit and the drug therapy was immediately discontinued and steroid drugs started. After 2 weeks of arsenic trioxide therapy suspension there was evidence of complete resolution of pericardial and pleuric effusion and the ECG showed normal QT interval.
    PMID: 18084726 [PubMed ...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626280</comments>
            <pubDate>Wed, 16 Jul 2008 14:52:47 +0100</pubDate>
            <guid isPermaLink="false">1626280</guid>        </item>
        <item>
            <title>Severe Impairment of Endothelial Function with the HIV-1 Protease Inhibitor Indinavir is not Mediated by Insulin Resistance in Healthy Subjects.</title>
            <link>http://www.medworm.com/index.php?rid=1626279&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18172783%26dopt%3DAbstract</link>
            <description>Authors: Dub&amp;#xE9; MP, Gorski JC, Shen C
    Endothelial dysfunction may contribute to increased cardiovascular events among HIV-1-infected patients receiving antiretroviral therapy. The HIV-1 protease inhibitor indinavir causes both vascular dysfunction and insulin resistance, but the relationship between the two disturbances is not established. Endothelium-dependent vasodilation (EDV), insulin-mediated vasodilation (IMV), and whole body and leg glucose uptake during a euglycemic hyperinsulinemic clamp (40 mU/m(2)/min) were measured before and after four weeks of indinavir in nine healthy men. EDV fell from 270 +/- 67% above basal to 124 +/- 30% (P = 0.04) and IMV from 56 +/- 14% above basal to 8 +/- 8% (P = 0.001) with indinavir. During the clamp, arteriovenous glucose difference and leg...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626279</comments>
            <pubDate>Wed, 16 Jul 2008 14:52:47 +0100</pubDate>
            <guid isPermaLink="false">1626279</guid>        </item>
        <item>
            <title>Adhesion proteins, stem cells, and arrhythmogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=1626278&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18176845%26dopt%3DAbstract</link>
            <description>Authors: Gillum N, Sarvazyan N
    Cell-transplantation therapy is a promising treatment option that is being actively explored as a way to repair cardiac muscle. The ultimate goal is to reconstitute the architecture of the cardiac muscle and to reestablish electrical propagation, while avoiding hypertrophy and scar formation. In this review, we focus on recent advances in the field as well as the difficulties encountered when the engraftment of cells into the host tissue is to be confirmed and functionally characterized. This is critical since incomplete or partial engraftment of transplanted cells within the host cardiac network exacerbates the heterogeneity already present in the injured myocardium and increases its propensity to arrhythmia. We conclude with a brief discussion of how th...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626278</comments>
            <pubDate>Wed, 16 Jul 2008 14:52:47 +0100</pubDate>
            <guid isPermaLink="false">1626278</guid>        </item>
        <item>
            <title>An Unusual CO-conspirator in a Case of Acute Coronary Syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=1626277&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18273709%26dopt%3DAbstract</link>
            <description>We present the case of a young man with CO poisoning who had elevated cardiac biomarkers, a regional wall motion abnormality, and was found to have obstructive coronary disease. Evidence of myocardial necrosis in the setting of CO toxicity should prompt consideration of an evaluation for coronary artery disease, particularly among those with risk factors.
    PMID: 18273709 [PubMed - in process] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626277</comments>
            <pubDate>Wed, 16 Jul 2008 14:52:47 +0100</pubDate>
            <guid isPermaLink="false">1626277</guid>        </item>
        <item>
            <title>Differential Phosphorylation of Translation Initiation Regulators 4EBP1, S6k1, and Erk 1/2 Following Inhibition of Alcohol Metabolism in Mouse Heart.</title>
            <link>http://www.medworm.com/index.php?rid=1626276&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18317950%26dopt%3DAbstract</link>
            <description>Authors: Vary TC, Lang CH
    Acute alcohol intoxication leads to an inhibition of protein synthesis in heart that results in part through altered phosphorylation of protein factors controlling mRNA translation initiation. The purpose of the present set of experiments was designed to examine the effects of inhibitors of ethanol metabolism on the phosphorylation of 4E-binding protein (4EBP1) and S6k1(Thr(389)), two factors regulating mRNA translation initiation. Phosphorylation of 4E-BP1, S6k1(Thr(389)), and Erk 1/2 was reduced 2 h following IP injection of alcohol. Pretreatment with 4-methylpyrazole (4-MP), an inhibitor of alcohol dehydrogenase (ADH), did not attenuate the ethanol-induced decrease in phosphorylation of 4EBP1 and S6k1(Thr(389)). In contrast, 4-MP prevented the decrease in E...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626276</comments>
            <pubDate>Wed, 16 Jul 2008 14:52:47 +0100</pubDate>
            <guid isPermaLink="false">1626276</guid>        </item>
        <item>
            <title>Trichloroethylene and trichloroacetic Acid regulate calcium signaling pathways in murine embryonal carcinoma cells p19.</title>
            <link>http://www.medworm.com/index.php?rid=1626274&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18437584%26dopt%3DAbstract</link>
            <description>In this study, we investigated the global changes in gene expression caused by exposure of P19 embryonal carcinoma cells to TCE and TCA, and whether or not TCE and/or TCA influence the expression levels of genes encoding for proteins that regulate calcium fluxes in cardiac cells. We report that TCE and TCA disrupt the expression of genes involved in processes important during embryonic development suggesting that exposure to environmentally significant concentrations of TCE may have deleterious effects on specific stages of cardiac differentiation.
    PMID: 18437584 [PubMed - in process] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626274</comments>
            <pubDate>Wed, 16 Jul 2008 14:52:47 +0100</pubDate>
            <guid isPermaLink="false">1626274</guid>        </item>
        <item>
            <title>Cardiac-Targeted Transgenic Mutant Mitochondrial Enzymes: mtDNA Defects, Antiretroviral Toxicity and Cardiomyopathy.</title>
            <link>http://www.medworm.com/index.php?rid=1626273&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18446447%26dopt%3DAbstract</link>
            <description>Authors: Kohler JJ, Hosseini SH, Green E, Hoying-Brandt A, Cucoranu I, Haase CP, Russ R, Srivastava J, Ivey K, Ludaway T, Kapoor V, Abuin A, Shapoval A, Santoianni R, Saada A, Elpeleg O, Lewis W
    Mitochondrial (mt) DNA biogenesis is critical to cardiac contractility. DNA polymerase gamma (Pol gamma) replicates mtDNA, whereas thymidine kinase 2 (TK2) monophosphorylates pyrimidines intramitochondrially. Point mutations in POLG and TK2 result in clinical diseases associated with mtDNA depletion and organ dysfunction. Pyrimidine analogs (NRTIs) inhibit Pol gamma and mtDNA replication. Cardiac &quot;dominant negative&quot; murine transgenes (TGs; Pol gamma Y955C, and TK2 H121N or I212N) defined the role of each in the heart. mtDNA abundance, histopathological features, histochemistry, mitochondrial pr...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626273</comments>
            <pubDate>Wed, 16 Jul 2008 14:52:47 +0100</pubDate>
            <guid isPermaLink="false">1626273</guid>        </item>
        <item>
            <title>Nuclear factor e2-related factor 2-dependent myocardiac cytoprotection against oxidative and electrophilic stress.</title>
            <link>http://www.medworm.com/index.php?rid=1626272&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18463988%26dopt%3DAbstract</link>
            <description>This study was undertaken to investigate if Nrf2 signaling could control the constitutive and inducible expression of antioxidants and phase 2 enzymes in primary cardiomyocytes as well as the susceptibility of these cells to oxidative and electrophilic injury. The basal expression of a series of antioxidants and phase 2 enzymes was significantly lower in cardiomyocytes from Nrf2(-/-) mice than those from wild-type littermates. Incubation of wild-type cardiomyocytes with 3H-1,2-dithiole-3-thione (D3T) led to significant induction of various antioxidants and phase 2 enzymes, including catalase, glutathione, glutathione peroxidase (GPx), glutathione reductase, glutathione S-transferase, NAD(P)H:quinone oxidoreductase 1, and heme oxygenase-1. The inducibility of the above cellular defenses exc...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626272</comments>
            <pubDate>Wed, 16 Jul 2008 14:52:47 +0100</pubDate>
            <guid isPermaLink="false">1626272</guid>        </item>
        <item>
            <title>Analysis of prevalence and risk factors of hypertension among uygur adults in tushala and hetian xinjiang uygur autonomous region.</title>
            <link>http://www.medworm.com/index.php?rid=1626271&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18483876%26dopt%3DAbstract</link>
            <description>In conclusion, our results indicated that high caloric food intake may trigger hyperlipidemia and subsequently elevated blood pressure, with elevated BMI and cholesterol levels being the major risk factors for hypertension.
    PMID: 18483876 [PubMed - in process] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626271</comments>
            <pubDate>Wed, 16 Jul 2008 14:52:47 +0100</pubDate>
            <guid isPermaLink="false">1626271</guid>        </item>
        <item>
            <title>Inhibitors of GSK-3 Prevent Corticosterone from Inducing COX-1 Expression in Cardiomyocytes.</title>
            <link>http://www.medworm.com/index.php?rid=1626270&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18584335%26dopt%3DAbstract</link>
            <description>Authors: Sun H, Chen QM
    Our recent study has demonstrated that glucocorticoids (GCs) induce cyclooxygenase-1 (COX-1) gene expression in rat cardiomyocytes. While investigating the mechanism underlying corticosterone (CT) induced COX-1, we found that three structurally and mechanistically distinct GSK-3 inhibitors, LiCl, SB216763, and (2'Z,3'E)-6-Bromoindirubin-3'-oxime (BIO), inhibited COX-1 transcription and protein induction. A genetic approach of expressing wild type GSK-3beta increased COX-1 promoter activity, which was abolished by LiCl. LiCl increased inhibitory GSK-3alpha/beta phosphorylation at Ser21/Ser9, while BIO or SB216763 prevented stimulatory phosphorylation at Tyr279/Tyr216 of GSK-3alpha/beta. GSK inhibitors failed to block nuclear translocation of glucocorticoid recept...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626270</comments>
            <pubDate>Wed, 16 Jul 2008 14:52:47 +0100</pubDate>
            <guid isPermaLink="false">1626270</guid>        </item>
        <item>
            <title>Potent Induction of Total Cellular and Mitochondrial Antioxidants and Phase 2 Enzymes by Cruciferous Sulforaphane in Rat Aortic Smooth Muscle Cells: Cytoprotection Against Oxidative and Electrophilic Stress.</title>
            <link>http://www.medworm.com/index.php?rid=1626269&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18607771%26dopt%3DAbstract</link>
            <description>Authors: Zhu H, Jia Z, Strobl JS, Ehrich M, Misra HP, Li Y
    Sulforaphane, a cruciferous isothiocyanate compound, upregulates cytoprotective genes in liver, but its effects on antioxidants and phase 2 defenses in vascular cells are unknown. Here we report that incubation of rat aortic smooth muscle A10 cells with sulforaphane (0.25-5 muM) resulted in concentration-dependent induction of a spectrum of important cellular antioxidants and phase 2 enzymes, including superoxide dismutase (SOD), catalase, the reduced form of glutathione (GSH), glutathione peroxidase, glutathione reductase (GR), glutathione S-transferase (GST), and NAD(P)H:quinone oxidoreductase 1 (NQO1). Sulforaphane also increased levels/activities of SOD, catalase, GSH and GST in isolated mitochondria of aortic smooth muscle...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626269</comments>
            <pubDate>Tue, 08 Jul 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1626269</guid>        </item>
        <item>
            <title>Chronic Contamination of Rats with (137)Cesium Radionuclide: Impact on the Cardiovascular System.</title>
            <link>http://www.medworm.com/index.php?rid=1626275&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18327657%26dopt%3DAbstract</link>
            <description>Authors: Gu&amp;#xE9;guen Y, Lestaevel P, Grandcolas L, Baudelin C, Grison S, Jourdain JR, Gourmelon P, Souidi M
    Cardiovascular system impairment has been observed in children and in liquidators exposed to the Chernobyl nuclear power plant accident. No experimental studies of animals have analyzed whether these disorders might be attributed to chronic ingestion of low levels of cesium 137 ((137)Cs). Biochemical, physiological, and molecular markers of the cardiovascular system were analyzed in rats exposed through drinking water to (137)Cs at a dose of 500 Bq kg(-1) (6500 Bq l(-1)). Plasma concentrations of CK and CK-MB were higher (+52%, P &amp;lt; 0.05) in contaminated rats. No histological alteration of the heart was observed, but gene expression was modified in the atria. Specifically, lev...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626275</comments>
            <pubDate>Sat, 01 Mar 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1626275</guid>        </item>
        <item>
            <title>Reduction of protein synthesis and statin-induced cardiomyocyte cell death.</title>
            <link>http://www.medworm.com/index.php?rid=1626317&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17646677%26dopt%3DAbstract</link>
            <description>The objective of this study was to determine whether an HMG Co A reductase inhibitor (statin) reduces protein synthesis in cardiomyocytes and whether this action maybe an underlying mechanism for statin-induced cell death. Cardiomyocytes from embryonic chick heart were maintained in culture. Cells exposed to lovastatin for 4 h showed a concentration dependent reduction in protein synthesis as assessed by [3H] leucine incorporation and [35S] methionine incorporation. Compared to control, lovastatin 100 microM, which produced a 25% increase in cell death, induced a three-fold reduction in methionine incorporation. [35S] methionine autoradiography showed little (new) protein synthesis at concentrations of lovastatin of 70 microM or higher; an effect that was not limited to specific proteins. ...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626317</comments>
            <pubDate>Mon, 01 Jan 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1626317</guid>        </item>
        <item>
            <title>Impact of Pycnogenol on cardiac extracellular matrix remodeling induced by L-NAME administration to old mice.</title>
            <link>http://www.medworm.com/index.php?rid=1626316&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17646678%26dopt%3DAbstract</link>
            <description>Authors: Zibadi S, Yu Q, Rohdewald PJ, Larson DF, Watson RR
    Cardiac remodeling is a determinant of the clinical progression of heart failure and now slowing or reversing remodeling is considered as a potential therapeutic target in heart failure. Pycnogenol has been reported to mediate a number of beneficial effects in the cardiovascular system but its effects on hemodynamic and functional cardiovascular changes following cardiac remodeling have not been elucidated. Therefore, we investigated the influence of Pycnogenol supplementation (30 mg/kg) on left ventricular function and myocardial extracellular matrix composition in old C57BL/6N mice following induction of cardiac remodeling by chronic nitric oxide synthase blockade by NG-nitro-L-arginine methyl ester (L-NAME) administration. ...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626316</comments>
            <pubDate>Mon, 01 Jan 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1626316</guid>        </item>
        <item>
            <title>The cytotoxicity of celecoxib towards cardiac myocytes is cyclooxygenase-2 independent.</title>
            <link>http://www.medworm.com/index.php?rid=1626315&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17646679%26dopt%3DAbstract</link>
            <description>Authors: Hasinoff BB, Patel D, Wu X
    The cyclooxygenase (COX)-2 inhibitors celecoxib and rofecoxib were studied for their effects on neonatal rat cardiac myocytes as a possible model for the adverse cardiovascular effects that this class of compounds have shown in their clinical use. Celecoxib, but not rofecoxib, as measured by lactate dehydrogenase release was toxic to myocytes in the low micromolar concentration range. This toxicity shown by celecoxib was also associated with a high degree of myofibrillar disruption similar to that caused by doxorubicin. As measured by induction of caspase-3/7 activity and by changes in nuclear morphology, neither celecoxib nor rofecoxib strongly induced apoptosis in myocytes. The stable prostacyclin analog iloprost was unable to reduce celecoxib-indu...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626315</comments>
            <pubDate>Mon, 01 Jan 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1626315</guid>        </item>
        <item>
            <title>Heart rate variability in rodents: uses and caveats in toxicological studies.</title>
            <link>http://www.medworm.com/index.php?rid=1626314&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17646680%26dopt%3DAbstract</link>
            <description>Authors: Rowan WH, Campen MJ, Wichers LB, Watkinson WP
    Heart rate variability (HRV) is a measure of cardiac pacing dynamics that has recently garnered a great deal of interest in environmental health studies. While the use of these measures has become popular, much uncertainty remains in the interpretation of results, both in terms of human and animal research. In humans, HRV endpoints, specifically chronic alterations in baseline HRV patterns, have been reasonably well characterized as prognostic indicators of adverse outcomes for a variety of diseases. However, such information is lacking for reversible HRV changes that may be induced by short-term exposures to environmental toxicants. Furthermore, there are minimal substantive data, either acute or chronic, regarding the pathologica...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626314</comments>
            <pubDate>Mon, 01 Jan 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1626314</guid>        </item>
        <item>
            <title>The anthracyclines: when good things go bad.</title>
            <link>http://www.medworm.com/index.php?rid=1626313&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17652803%26dopt%3DAbstract</link>
            <description>Authors: Minotti G, Sarvazyan N
    In the era of targeted therapy the anthracyclines, which were discovered almost half-century ago, may appear to be too old to be good. While it is certainly true that the prototypic anthracyclines have been around for many years, there are robust clinical facts to confute that their time is over. These drugs continue to play an undisputed role in the treatment of many forms of cancer, including hematological malignancies and solid tumors. Unfortunately, however, their main side-effect remains: a life-threatening cardiotoxicity which became apparent at the beginning of anthracyclines' clinical use. In addition to this long-standing problem, we are now discovering that new combination therapies often cause a higher than expected incidence of cardiotoxicity...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1626313</comments>
            <pubDate>Mon, 01 Jan 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1626313</guid>        </item>
        <item>
            <title>Role of anthracyclines in the era of targeted therapy.</title>
            <link>http://www.medworm.com/index.php?rid=1626312&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17652804%26dopt%3DAbstract</link>
            <description>Authors: Cort&amp;#xE9;s-Funes H, Coronado C
    Anthracyclines such as doxorubicin, epirubicin, and daunorubicin are among the most active cytoxic agents for treatment of a wide variety of solid tumors and hematological malignancies. The downside associated with chronic administration of anthracyclines is the induction of cardiomyopathy and congestive heart failure, usually refractory to common treatments. Anthracycline liposomal formulations are currently the best-known alternatives to improve the index and spectrum of anticancer activity of these drugs and decrease their cardiotoxicity. In the current target therapy era in oncology, anthracyclines increase the antitumor effects in more than additive fashion, being excellent partners for other active agents like taxanes and trastuzumab. It i...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
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            <pubDate>Mon, 01 Jan 2007 05:00:00 +0100</pubDate>
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            <title>Pathophysiology and diagnosis of cancer drug induced cardiomyopathy.</title>
            <link>http://www.medworm.com/index.php?rid=1626311&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17652805%26dopt%3DAbstract</link>
            <description>Authors: Zuppinger C, Timolati F, Suter TM
    The clinical manifestations of anti-cancer drug associated cardiac side effects are diverse and can range from acutely induced cardiac arrhythmias to Q-T interval prolongation, changes in coronary vasomotion with consecutive myocardial ischemia, myocarditis, pericarditis, severe contractile dysfunction, and potentially fatal heart failure. The pathophysiology of these adverse effects is similarly heterogeneous and the identification of potential mechanisms is frequently difficult since the majority of cancer patients is not only treated with a multitude of cancer drugs but might also be exposed to potentially cardiotoxic radiation therapy. Some of the targets inhibited by new anti-cancer drugs also appear to be important for the maintenance of...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
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            <pubDate>Mon, 01 Jan 2007 05:00:00 +0100</pubDate>
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            <title>Anthracycline cardiotoxicity in breast cancer patients: synergism with trastuzumab and taxanes.</title>
            <link>http://www.medworm.com/index.php?rid=1626310&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17652806%26dopt%3DAbstract</link>
            <description>Authors: Gianni L, Salvatorelli E, Minotti G
    Doxorubicin is known to cause cardiomyopathy and congestive heart failure (CHF) upon chronic administration. A major obstacle to doxorubicin-containing multiagent therapies pertains to the possible development of cardiomyopathy and CHF at lower than expected cumulative doses of doxorubicin. For example, the cardiac toxicity of doxorubicin is aggravated by the anti-HER2 antibody Trastuzumab or by the tubulin-active taxane paclitaxel; however, the mechanisms by which Trastuzumab and paclitaxel aggravate doxorubicin-induced cardiotoxicity are mechanistically distinct: Trastuzumab interferes with cardiac-specific survival factors that help the heart to withstand stressor agents like anthracyclines, while paclitaxel acts by stimulating the format...</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
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            <pubDate>Mon, 01 Jan 2007 05:00:00 +0100</pubDate>
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            <title>Cardiac safety of liposomal anthracyclines.</title>
            <link>http://www.medworm.com/index.php?rid=1626309&amp;cid=s_37758_7_f&amp;fid=37758&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17652807%26dopt%3DAbstract</link>
            <description>Authors: Batist G
    Anthracyclines remain amongst the most active therapeutic agents for breast cancer treatment. Rather than being supplanted by novel targeted agents, they are being combined with them in various schedules. Furthermore, anthracyclines themselves are still being studied, with increasing biological understanding of their biological activity and molecular targets. A cardiac safe formulation of doxorubicin opens a number of interesting therapeutic opportunities. Liposomal doxorubicins appear to provide this opportunity.
    PMID: 17652807 [PubMed - indexed for MEDLINE] (Source: Cardiovascular Toxicology)</description>
            <author>Cardiovascular Toxicology</author>
            <type>journals</type>
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            <pubDate>Mon, 01 Jan 2007 05:00:00 +0100</pubDate>
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