N-Acetylcysteine Ameliorates Experimental Autoimmune Myocarditis in Rats via Nitric Oxide.

Background: Oxidative stress may play an important role in the development of myocarditis. We investigated the effects of N-acetylcysteine (NAC), a potent antioxidant, on experimental autoimmune myocarditis (EAM) in rats.

Methods And Results: A rat model of porcine myosin-induced EAM was used.

Nucleotide differences of coxsackievirus B3 and chronic myocarditis.

The in vivo mechanisms in chronic myocarditis remain unclear. The aim of the current study was to clarify the genomic difference of amyocarditic (CB3O) and myocarditic (CB3M) coxsackievirus B3 (CB3) and the pathogenesis of in vivo mechanisms in chronic myocarditis. We examined the histopathology of CB3-inoculated wild-type (WT) and severe combined immunodeficient (SCID) mice with and without adoptive transfer of lymphocytes.

Tall P waves associated with severe hypokalemia and combined electrolyte depletion.

A 32-year-old woman with anorexia nervosa showing tall P waves on electrocardiogram (ECG) was reported. Her ECG showed tall P waves (5.5mm in voltage, lead II) at 2.

Therapy with immunoglobulin in patients with acute myocarditis and cardiomyopathy: analysis of leukocyte balance.

Intravenous immunoglobulin (IVIG) therapy has been used to treat several autoimmune or inflammatory diseases. We conducted a clinical trial of immunoglobulin therapy for acute myocarditis. The study consisted of two projects: (1) a comparison of prognosis between patients treated with and those not treated with IVIG in a multi-center study; (2) analyses of inflammatory cytokines and blood cell profiles in a substudy.

Carvedilol reduces the severity of atherosclerosis in apolipoprotein E-deficient mice via reducing superoxide production.

It has been shown that oxidative stress may play an important role in the development of atherosclerosis, and carvedilol has the capacity of reducing oxidative stress. Accordingly, we assessed the hypothesis that carvedilol may reduce the severity of atherosclerosis in apolipoprotein E (apoE)-deficient mice in addition to its hemodynamic effects. Atherosclerosis was induced in apoE-deficient mice fed a high-fat diet containing 0.

Erythromycin treatment suppresses myocardial injury in autoimmune myocarditis in rats via suppression of superoxide production.

Background: Recent evidence suggests that erythromycin (EM), a major macrolide antibiotic, has many biological functions in addition to the anti-bacterial actions, including anti-inflammatory and free radical scavenging actions. However, the effects of the drug upon inflammatory myocardial diseases are unknown. We tested the hypothesis that EM ameliorates experimental autoimmune myocarditis in rats attributing to the suppression of superoxide production.

The role of Fcγ receptors in atherosclerosis.

Atherosclerosis is widely considered to be an immune-mediated process. Fcγ receptors (Fcγ Rs) contribute to the regulation of a multitude of immune and inflammatory responses and are implicated in human atherosclerotic lesions. Major cell types involved in the pathogenesis of atherosclerosis express Fcγ Rs and their proatherogenic ligands such as immune complexes and C-reactive protein, which act to activate Fcγ R signaling pathways.

Immunoglobulin treatment ameliorates myocardial injury in experimental autoimmune myocarditis associated with suppression of reactive oxygen species.

Aims: We tested the hypothesis that immunoglobulin ameliorated experimental autoimmune myocarditis (EAM) in mice attributing to the suppression of reactive oxygen species (ROS)-mediated myocardial injury.

Methods: We intraperitoneally administered intact type of human immunoglobulin (Ig) or F(ab')2 fragments of human immunoglobulin, 1g/kg/day daily for 3 weeks, to male BALB/c mice with heart failure due to EAM.

Results: The results showed that intact type of Ig, but not F(ab')2 type, reduced the severity of myocarditis by comparing the heart weight/body weight and lung weight/body weight ratios, pericardial effusion score, macroscopic and microscopic scores.

Antiatherogenic effect of pioglitazone on uremic apolipoprotein E knockout mice by modulation of the balance of regulatory and effector T cells.

Objective: Uremia markedly accelerates atherogenesis, but the pathogenesis remains to be elucidated and effective anti-atherogenic treatments are needed. The aim of this study was to investigate the relationship between accelerated atherosclerosis (AS) and the balance of regulatory/effector T cells (Treg/Teff) in uremic apolipoprotein E knockout (apoE-/-) mice, and the effect of pioglitazone on uremic AS and possible mechanisms.

Methods And Results: Uremia was induced surgically in 8-week-old male apoE-/- mice.

Plasma miR-124 as a biomarker for cerebral infarction.

MicroRNAs (miRNAs) are endogenous small RNAs that play an important role in various physiological processes by downregulating target genes. Recently, plasma miRNAs have been investigated as biomarkers for various diseases. In this study, miRNA array analysis in various tissues showed that miR-124 is almost exclusively expressed in the central nervous system and neuronal cells, suggesting that it might be useful as a potential biomarker for neurological diseases.

WIN55212-2 ameliorates atherosclerosis associated with suppression of pro-inflammatory responses in ApoE-knockout mice.

The role of inflammation in all stages of atherosclerosis has been actively investigated, with an emphasis on the discovery of novel and innovative drugs for treatment and prevention. The anti-inflammatory and immunomodulatory capacity of cannabinoids are well established, and these agents have a broad therapeutic potential in various inflammatory diseases, including cardiovascular diseases. The aim of this study was to investigate the effect of WIN55212-2, a synthetic cannabinoid, on atherosclerosis using the apolipoprotein E-knockout (ApoE(-/-)) mouse on a cholate-containing high-fat diet.

Atherosclerotic plaques induced by marble-burying behavior are stabilized by exercise training in experimental atherosclerosis.

Background: We assessed the hypothesis whether behavioral stress may affect the development of atherosclerosis and whether regular exercise training may influence the composition of atherosclerotic plaques in apolipoprotein (apo) E-deficient mice.

Methods: Atherosclerosis was induced in apo E-deficient mice fed a high fat diet. Exercise training (45 min swimming, 3 times/week) was conducted, and behavioral stress was provoked by glass marble-burying procedure.

Therapy with granulocyte colony-stimulating factor in the chronic stage, but not in the acute stage, improves experimental autoimmune myocarditis in rats via nitric oxide.

We systematically investigated serial efficacy of granulocyte colony-stimulating factor (G-CSF) therapy upon experimental autoimmune myocarditis (EAM) in rats treated with and without the inhibition of nitric oxide (NO) with the analyses of tissue regeneration. G-CSF could mobilize multipotent progenitor cells of bone marrow into the peripheral blood and may improve ventricular function. A rat model of porcine myosin-induced EAM was used.

High glucose promotes intracellular lipid accumulation in vascular smooth muscle cells by impairing cholesterol influx and efflux balance.

Aims: High glucose promotes macrophage-derived foam cell formation involved in increased influx or reduced efflux of lipids. The aim of this study is to investigate the influence of hyperglycaemia on foam cell transformation of vascular smooth muscle cells (VSMCs) and possible mechanisms contributing to these effects.

Methods And Results: The results showed that high glucose increased the expression of CD36, a regulator of lipid influx, and suppressed the expression and activity of the adenosine triphosphate-binding cassette (ABC) transporter ABCG1, a regulator of cholesterol efflux to high-density lipoprotein, in a dose- and time-dependent manner.

N-acetylcysteine reduces the severity of atherosclerosis in apolipoprotein E-deficient mice by reducing superoxide production.

Background: Oxidative stress may play an important role in the development of atherosclerosis. Because N-acetylcysteine (NAC) is able to reduce oxidative stress, the present study assessed the hypothesis that NAC may reduce the severity of atherosclerosis in apolipoprotein (apo) E-deficient mice.

Methods And Results: Atherosclerosis was induced in apoE-deficient mice fed a high-fat diet containing 0.

Naloxone, an opiate receptor antagonist, ameliorates acute experimental autoimmune myocarditis by reducing cytotoxic activities.

Little is known about effects of naloxone, an opiate receptor antagonist, upon experimental autoimmune myocarditis (EAM) in mice. The aim of the present study was to test the effects of naloxone upon EAM in mice. Four-week-old C57BL/6 mice were injected with porcine cardiac myosin.

L-arginine ameliorates experimental autoimmune myocarditis by maintaining extracellular matrix and reducing cytotoxic activity of lymphocytes.

It was previously shown that administration of the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) aggravated murine viral myocarditis by increasing myocardial virus titres. Experimental autoimmune myocarditis in mice and rats mimics human fulminant myocarditis. The effects of L-arginine, a precursor of nitric oxide, upon heart failure in experimental autoimmune myocarditis were evaluated.

Effects of exercise on the development of atherosclerosis in apolipoprotein E-deficient mice.

It has already been shown that mild to moderate exercise training may protect against the development of atherosclerosis. However, the precise mechanisms behind this protection are still unknown. The hypothesis that exercise training reduces the severity of experimental atherosclerosis in apolipoprotein (apo) E-deficient mice was assessed.

Carotid intima-media thickness is increased in subjects with ischemic heart disease having a familial incidence.

Objectives: A family history of ischemic heart disease (IHD) is an independent risk factor for cardiovascular events. However, the mechanisms underlying this susceptibility have not been fully elucidated. The authors hypothesized that an important mediator of the familial incidence of IHD is subclinical atherosclerosis, which is detectable by noninvasive imaging.

QRS voltages are transiently increased at the superacute stage of experimental myocarditis.

Background: There are few reports on the precise electrocardiographic characteristics of acute myocarditis. The present study was focused on QRS voltage changes at the superacute stage of murine myocarditis.

Methods: Serial electrocardiograms were recorded during the acute stage of viral myocarditis in mice, and then the cardiac pathology was examined.

PPARgamma gene C161T substitution is associated with reduced risk of coronary artery disease and decreased proinflammatory cytokine expression.

Background: Peroxisome proliferator-activated receptor gamma (PPARgamma) is a transcription factor implicated in the expression of proinflammatory cytokines in atheroma-associated cells, and the expression of proinflammatory cytokines, such as tumor necrosis factor alpha (TNF-alpha) and matrix metalloproteinases (MMPs), represents a critical step in atherogenesis and atherosclerosis. In this study, we test the hypothesis of whether a polymorphism corresponding to C161T substitution in exon 6 of the PPARgamma gene may affect the expression of proinflammatory cytokines and the onset of coronary artery diseases (CADs) in a Chinese population.

Methods: We have studied distribution of the PPARgamma C161T substitution at exon 6 in 247 patients with CAD and 214 patients with chest pain syndrome.

Exercise training reduces severity of atherosclerosis in apolipoprotein E knockout mice via nitric oxide.

Background: Exercise training may protect against the development of atherosclerosis, although the precise mechanisms are still unknown. The present study assessed the hypothesis that exercise training would reduce the severity of experimental atherosclerosis in apolipoprotein-E (apoE)-deficient mice via nitric oxide (NO).

Methods And Results: ApoE-deficient mice fed a high-fat diet underwent exercise training (30 min swimming) 3 times per week for 8 weeks.

Swimming reduces the severity of atherosclerosis in apolipoprotein E deficient mice by antioxidant effects.

Objective: It was shown that aerobic exercise training may protect against the development of atherosclerosis. However, the precise mechanisms are still unknown. We assessed the hypothesis that exercise training reduced the severity of experimental atherosclerosis in apolipoprotein (apo) E-deficient mice by antioxidant effects.