Association between Coronary Artery Spasm and the risk of incident Diabetes: A Nationwide population-based Cohort Study.

Non-diabetic coronary artery spasm (CAS) without obstructive coronary artery disease increases insulin resistance. We investigated the risk of incident type 2 diabetes (diabetes) associated with CAS. Patient records were retrospectively collected from the Taiwan National Health Insurance Research Database during the period 2000-2012.

Garcinol Attenuates Lipoprotein(a)-Induced Oxidative Stress and Inflammatory Cytokine Production in Ventricular Cardiomyocyte through α7-Nicotinic Acetylcholine Receptor-Mediated Inhibition of the p38 MAPK and NF-κB Signaling Pathways.

Garcinol, a nicotinic acetylcholine receptor (nAChR) antagonist, has recently been established as an anti-inflammation agent. However, the molecular mechanism by which garcinol suppresses inflammation in the context of acute myocardial infarction (AMI) remains unclear. We hypothesized that the administration of physiological doses of garcinol in mice with isoproterenol-induced AMI decreased the effect of lipoprotein(a) (Lp(a))-induced inflammation both in vivo and in vitro via the α7-nAChRs mediated p38 mitogen-activated protein kinase (MAPK)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signaling pathway.

Drug-eluting versus bare-metal stents for first myocardial infarction in patients with atrial fibrillation: A nationwide population-based cohort study.

Background: Acute myocardial infarction (AMI) complicates the clinical management of atrial fibrillation (AF) because coronary stenting may influence subsequent antithrombotic therapy. We investigated the use of a bare-metal stent (BMS) or a drug-eluting stent (DES) and associated outcomes in patients with pre-existing AF and first AMI undergoing percutaneous coronary intervention.

Methods And Results: Patient records in this population-based study were retrospectively collected from the Taiwan National Health Insurance Research Database.

Coronary Artery Spasm as Related to Anxiety and Depression: A Nationwide Population-Based Study.

Objective: Anxiety and depression are risk factors for obstructive coronary artery disease (CAD), but their effects on coronary artery spasm (CAS) remain unestablished.

Methods: Patient records in this population-based study were retrospectively collected from the Taiwan National Health Insurance Research Database. Using propensity score matching, we used 1:1:1 ratio stratification into a control group of 10,325 individuals without CAS or CAD, a CAS group comprising 10,473 patients, and a CAD group comprising 10,473 patients during 2000-2012.

Analysis of Titin in Red and White Muscles: Crucial Role on Muscle Contractions Using a Fish Model.

Several studies have compared molecular components between red and white skeletal muscles in mammals. However, mammalian skeletal muscles are composed of mixed types of muscle fibers. In the current study, we analyzed and compared the distributions of titin, lipid, phosphate ions, and fatty acid levels in red and white muscles using a fish model (), which is rich in red and white muscles, and these are well separated.

Effect of proton pump inhibitors on sympathetic hyperinnervation in infarcted rats: Role of magnesium.

The long-term use of proton pump inhibitors (PPIs) has been shown to increase the risk of cardiovascular mortality, however the molecular mechanisms are unknown. Superoxide has been implicated in the regulation of nerve growth factor (NGF), a mediator of sympathetic innervation. The purpose of this study was to determine whether PPIs increase ventricular arrhythmias through magnesium-mediated superoxide production in infarcted rats.

Inhibitory effect of PDGF-BB and serum-stimulated responses in vascular smooth muscle cell proliferation by hinokitiol via up-regulation of p21 and p53.

Introduction: Vascular smooth muscle cell (VSMC) proliferation plays a major role in the progression of vascular diseases. In the present study, we established the efficacy and the mechanisms of action of hinokitiol, a tropolone derivative found in , Cupressaceae, in relation to platelet-derived growth factor-BB (PDGF-BB) and serum-dependent VSMC proliferation.

Material And Methods: Primary cultured rat VSMCs were pre-treated with hinokitiol and then stimulated by PDGF-BB (10 ng/ml) or serum (10% fetal bovine serum).

Activation of the monocytic α7 nicotinic acetylcholine receptor modulates oxidative stress and inflammation-associated development of coronary artery spasm via a p38 MAP-kinase signaling-dependent pathway.

Objective: Smoking and high-sensitivity C-reactive protein (hs-CRP) are risk factors for coronary artery spasm (CAS), which is characterized by the increased interleukin-6 (IL-6) level and monocyte counts; however, limited data are available regarding the role of cigarette-embedded nicotine in the modulation of monocytic inflammatory activity in CAS.

Approach: We investigated and elucidated the putative roles and associations of nicotine, monocytic IL-6, α7 nicotinic acetylcholine receptor (α7-nAChR), and CRP in CAS development.

Results: We demonstrated that a significantly increased α7-nAChR (p = 0.

Norcantharidin, a clinical used chemotherapeutic agent, acts as a powerful inhibitor by interfering with fibrinogen-integrin α β binding in human platelets.

During platelet activation, fibrinogen binds to its specific platelet receptor, integrin α β , thus completing the final common pathway for platelet aggregation. Norcantharidin (NCTD) is a promising anticancer agent in China from medicinal insect blister beetle. In this study, we provided the evidence to demonstrate NCTD (0.

Nicorandil regulates the macrophage skewing and ameliorates myofibroblasts by inhibition of RhoA/Rho-kinase signalling in infarcted rats.

We have demonstrated that ATP-sensitive potassium (K ) channel agonists attenuated fibrosis; however, the mechanism remained unclear. Since RhoA has been identified as a mediator of cardiac fibrosis, we sought to determine whether the anti-fibrotic effects of K channel agonists were mediated via regulating macrophage phenotype and fibroblast differentiation by a RhoA/RhoA-kinase-dependent pathway. Wistar male rats after induction of myocardial infarction were randomized to either vehicle, nicorandil, an antagonist of K channel glibenclamide, an antagonist of ROCK fasudil, or a combination of nicorandil and glibenclamide or fasudil and glibenclamide starting 24 hrs after infarction.

Anti-embolic effect of Taorenchengqi Tang in rats with embolic stroke induced by occluding middle cerebral artery.

Objective: To investigate the anti-embolic effect of Taorenchengqi Tang (TRCQT), a formulas from Traditional Chinese Medicine, plus aspirin in rats with embolic stroke induced by selective occlusion of the middle cerebral artery (MCA). Possible side effects of hemorrhagic incident and other bleeding events and anti-platelet effect were also explored.

Methods: Ninety rats were randomly separated into 9 groups (n = 10): group 1 a sham-operated group (n = 10); groups 2 and 3 orally treated with an isovolumetric solvent (distilled water) for 1 and 3 months, followed by thromboembolic occlusion (n = 10); groups 4 and 5 orally treated with aspirin (5 mg/kg) alone for 1 and 3 months, followed by thromboembolic occlusion (n = 10); groups 6 and 7 orally treated with TRCQT (0.

The neuroprotective effects of --- against embolic stroke in rats.

Background: Combinations of the traditional Chinese and Western medicines have been used to treat numerous diseases throughout the world, and there is a growing body of evidence showing that some of the herbs used in traditional Chinese medicine elicit significant pharmacological effects. The aim of this study was to demonstrate the neuroprotective effects of --- (TRCQT) in combination with aspirin following middle cerebral artery occlusion (MCAO)-induced embolic stroke in rats.

Methods: A blood clot was embolized into the middle cerebral artery of rats to induce focal ischemic brain injury.

Dapagliflozin, a selective SGLT2 Inhibitor, attenuated cardiac fibrosis by regulating the macrophage polarization via STAT3 signaling in infarcted rat hearts.

During myocardial infarction, infiltrated macrophages have pivotal roles in cardiac remodeling and delayed M1 toward M2 macrophage phenotype transition is considered one of the major factors for adverse ventricular remodeling. We investigated whether dapagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor, attenuates cardiac fibrosis via regulating macrophage phenotype by a reactive oxygen and nitrogen species (RONS)/STAT3-dependent pathway in postinfarcted rats. Normoglycemic male Wistar rats were subjected to coronary ligation and then randomized to either saline, dapagliflozin (a specific SGLT2 inhibitor), phlorizin (a nonspecific SGLT1/2 inhibitor), dapagliflozin + S3I-201 (a STAT3 inhibitor), or phlorizin + S3I-201 for 4 weeks.

Effect of lithium on ventricular remodelling in infarcted rats via the Akt/mTOR signalling pathways.

Activation of phosphoinositide 3-kinase (PI3K)/Akt signalling is the molecular pathway driving physiological hypertrophy. As lithium, a PI3K agonist, is highly toxic at regular doses, we assessed the effect of lithium at a lower dose on ventricular hypertrophy after myocardial infarction (MI). Male Wistar rats after induction of MI were randomized to either vehicle or lithium (1 mmol/kg per day) for 4 weeks.

Inhibition of infarction-induced sympathetic innervation with endothelin receptor antagonism via a PI3K/GSK-3β-dependent pathway.

Although endothelin (ET)-1 has been shown to upregulate nerve growth factor (NGF) expression, the molecular mechanisms are largely unknown. Phosphatidylinositol 3-kinase (PI3K)/Akt/glycogen synthase kinase (GSK)-3β signal has been implicated in the regulation of NGF. We investigated whether selective ET receptor blockers attenuated cardiac sympathetic reinnervation through restoring PI3K/Akt/GSK-3β activity.

Effects of urate-lowering agents on arrhythmia vulnerability in post-infarcted rat hearts.

Hyperuricemia has been shown to be associated with ventricular arrhythmias. However, the mechanisms remained unknown. We assessed whether different urate-lowering agents can attenuate arrhythmias through lowering urate itself or inhibiting xanthenes oxidize (XO) activity in infarcted rats.

Sitagliptin decreases ventricular arrhythmias by attenuated glucose-dependent insulinotropic polypeptide (GIP)-dependent resistin signalling in infarcted rats.

Myocardial infarction (MI) was associated with insulin resistance, in which resistin acts as a critical mediator. We aimed to determine whether sitagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, can attenuate arrhythmias by regulating resistin-dependent nerve growth factor (NGF) expression in postinfarcted rats. Normoglycaemic male Wistar rats after ligating coronary artery were randomized to either vehicle or sitagliptin for 4 weeks starting 24 h after operation.

Dipeptidyl peptidase-4 inhibition attenuates arrhythmias via a protein kinase A-dependent pathway in infarcted hearts.

Background: The effect of dipeptidyl peptidase-4 (DPP-4) inhibitors on arrhythmias remains unknown. The aim of this study was to investigate whether sitagliptin attenuates arrhythmias through inhibiting nerve growth factor (NGF) expression, focusing on cyclic adenosine monophosphate (cAMP) downstream signaling such as protein kinase A (PKA) and exchange protein directly activated by cAMP (Epac).

Methods and results: Male Wistar rats were randomized to either vehicle or sitagliptin for 4 weeks starting 24 h after ligating the coronary artery.

Comparative decline of the protein profiles of nebulin in response to denervation in skeletal muscle.

The sliding filament model of the sarcomere was developed more than half a century ago. This model, consisting only of thin and thick filaments, has been efficacious in elucidating many, but not all, features of skeletal muscle. Work during the 1980s revealed the existence of two additional filaments: the giant filamentous proteins titin and nebulin.

Effect of Feedback Signal on Blood Pressure Self-regulation Capability in Individuals With Prehypertension or Stage I Hypertension: A Randomized Controlled Study.

Objectives: We aimed to determine the efficacy of an 8-week direct blood pressure (BP) biofeedback training program for prehypertensive or stage I hypertensive patients with a particular focus on the impact of the authenticity of feedback signals on the efficacy of BP regulation.

Designs: This study has a randomized, double-blind, parallel-group design.

Participants And Methods: Fifty-nine individuals with ages from 18 to 64 years and who met the criteria for the diagnosis of prehypertenion or stage 1 hypertension participated in this study.

Synergistic Impact of Nicotine and Shear Stress Induces Cytoskeleton Collapse and Apoptosis in Endothelial Cells.

Nicotine is the major component in cigarette smoke and has been recognized as a risk factor for various cardiovascular diseases such as atherosclerosis. However, the definite pathogenesis of nicotine-mediated endothelial dysfunction remains unclear because hemodynamic factor in most of prior in vitro studies was excluded. To understand how nicotine affects endothelium in the dynamic environment, human umbilical vein endothelial cells were treated by different laminar shear stresses (LSS; 0, 6, 8, and 12 dynes cm(-2)) with and without 10(-4) M nicotine for 12 h in a parallel plate flow system, following detections of cellular morphology and apoptotic level.

Inhibition of glycogen synthase kinase-3β prevents sympathetic hyperinnervation in infarcted rats.

We have demonstrated that nerve growth factor (NGF) expression in the myocardium is selectively increased during chronic stage of myocardial infarction, resulting in sympathetic hyperinnervation. Glycogen synthase kinase-3 (GSK-3) signal has been shown to play key roles in the regulation of cytoskeletal assembly during axon regeneration. We assessed whether lithium, a GSK-3 inhibitor, attenuates cardiac sympathetic reinnervation after myocardial infarction through attenuated NGF expression and Tau expression.

Arterial Stiffness Index and Coronary Artery Plaques in Patients with Subclinical Coronary Atherosclerosis.

Background: Arterial stiffness is a physiologic quantitative value used to measure arterial compliance. It is predictive of coronary atherosclerosis in patients with intermediate to high cardiovascular risk. However, a correlation between arterial stiffness and subclinical coronary atherosclerosis has yet to be established.