Serum Zinc Ion Concentration Associated with Coronary Heart Disease: A Systematic Review and Meta-Analysis.

Aim: Coronary heart disease is a major cause of mortality in developed and developing countries. Changes in the trace element concentration in the human body are one of the main reasons for the transition of the human body from a healthy to a diseased state. In this meta-analysis, we have studied the relationship between the reduction in serum zinc ion concentration and coronary heart disease.

Association of Low Expression of in Peripheral Blood with Acute Myocardial Infarction.

Objective: Our study's goal was to find out acute myocardial infarction (AMI) patients' gene expression patterns and to evaluate its role as a diagnostic marker for AMI detection.

Methods: Peripheral blood was drawn from 124 individuals who had an AMI and 115 patients who had stable coronary artery disease (SCAD). The real-time quantitative polymerase chain reaction was used to measure the mRNA expression level of the gene in peripheral blood.

Cardiovascular syphilis-associated acute myocardial infarction: A case report.

Rationale: In recent decades, the incidence of advanced syphilis has declined due to early recognition and the application of effective antibiotics. Advanced syphilis often manifests in the cardiovascular system as simple aortitis, aortic valve insufficiency, coronary artery stenosis or obstruction, Aortic aneurysm and mucinous myocarditis. In most case reports on the subject, acute myocardial infarction caused by syphilis was reported to be due to aortic valve insufficiency and coronary stenosis as a result of the involvement of the aorta.

A novel nonsense mutation in TNNT2 in a Chinese pedigree with hypertrophic cardiomyopathy: A case report.

Rationale: Hypertrophic cardiomyopathy (HCM) is an inherited myocardial disease and a common cause of sudden cardiac death, heart failure, atrial fibrillation and stroke. In families affected by HCM, genotyping is useful for identifying susceptible relatives. In the present study, we investigated the disease-causing mutations in a three-generation Chinese family with HCM using whole exome sequencing (WES).

MicroRNA-34c suppresses proliferation of vascular smooth muscle cell via modulating high mobility group box protein 1.

Background: Atherosclerosis is the most frequent pathological process that causes cardiovascular diseases.

Objective: The present study aimed to confirm miRNAs associated with atherosclerosis and explore the molecular mechanism of miR-34c and its target high mobility group box protein 1 (HMGB1) in the control of growth of smooth muscle cells in the development of atherosclerosis.

Methods: Real-time PCR was firstly performed to confirm miRNA correlation with atherosclerosis, and computational analysis and luciferase assay were performed to explore the target of miR-34c, Western blot, and real-time PCR were also utilized to reveal the effect of whether high glucose (HG) and miR-34c affect miR-34c, HMGB1 levels, NF-κB p65 and TNF-α levels, and the role of miR-34c on vascular smooth muscle cells (VSMCs) viability induced by HG.

Role of epigenetic in leukemia: From mechanism to therapy.

Epigenetic variations can play remarkable roles in different normal and abnormal situations. Such variations have been shown to have a direct role in the pathogenesis of various diseases either through inhibition of tumor suppressor genes or increasing the expression of oncogenes. Enzymes involving in epigenetic machinery are the main actors in tuning the epigenetic-based controls on gene expressions.

Vascular Risk Factors and Alzheimer's Disease: Blood-Brain Barrier Disruption, Metabolic Syndromes, and Molecular Links.

Alzheimer's disease (AD) is a neurodegenerative disorder, marked by cortical and hippocampal deposition of amyloid-β (Aβ) plaques and neurofibrillary tangles and cognitive impairment. Studies indicate a prominent link between cerebrovascular abnormalities and the onset and progression of AD, where blood-brain barrier (BBB) dysfunction and metabolic disorders play key risk factors. Pericyte degeneration, endothelial cell damage, astrocyte depolarization, diminished tight junction integrity, and basement membrane disarray trigger BBB damage.

Role of hydrogen sulfide in cognitive deficits: Evidences and mechanisms.

Hydrogen sulfide (HS) is a gaseous molecule and is endogenously produced in the brain by cystathionine beta-synthase, 3-mercaptopyruvate-sulfurtransferase, cysteine aminotransferase and cystathionine γ-lyase. Physiologically, HS acts as a neuromodulator and regulates synaptic activity of neurons and glia to promote the development of long-term potentiation. A decrease in HS levels in the brain and plasma has been directly correlated with the degree of severity of Alzheimer disease in patients.

l-Carnitine and heart disease.

Cardiovascular disease (CVD) is a key cause of deaths worldwide, comprising 15-17% of healthcare expenditure in developed countries. Current records estimate an annual global average of 30 million cardiac dysfunction cases, with a predicted escalation by two-three folds for the next 20-30years. Although β-blockers and angiotensin-converting-enzymes are commonly prescribed to control CVD risk, hepatotoxicity and hematological changes are frequent adverse events associated with these drugs.

An investigation of the levels of vitamins A, D, and E in the serum of Chinese pregnant women.

Background: Vitamins A, D (Vitamin D2 and vitamin D3) and E, play an important role during pregnancy.

Methods: Sera were collected from 1056 normal pregnant women, who were between 18 and 40 years old, at seven different hospitals in northeastern China. The levels of Vitamin A and E in the sera samples were detected using HPLC (High Performance Liquid Chromatography), and the level of vitamin D was measured by LC-MS (Liquid Chromatography-Mass Spectrometry).

Effects of the Activin A-Follistatin System on Myocardial Cell Apoptosis through the Endoplasmic Reticulum Stress Pathway in Heart Failure.

Background: A previous study suggested that activin A inhibited myocardial cell apoptosis. This study thus aimed to explore the effects of the activin A-follistatin system on myocardial cell apoptosis in heart failure (HF) rats in order to determine whether or not the mechanism operates through the endoplasmic reticulum stress (ERS) pathway.

Methods: Myocardial infarction (MI) by vascular deprivation was used to induce HF.

Overexpression of miR-203 sensitizes paclitaxel (Taxol)-resistant colorectal cancer cells through targeting the salt-inducible kinase 2 (SIK2).

MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression through the endogenous RNA interference machinery. Treatments with combination of chemotherapy with surgery are essential for advanced-stage colorectal cancer. However, the development of chemoresistance is a major obstacle for clinical application of anticancer drugs.

Levocarnitine protects H9c2 rat cardiomyocytes from H2O2-induced mitochondrial dysfunction and apoptosis.

Background: Although the protective effects of levocarnitine in patients with ischemic heart disease are related to the attenuation of oxidative stress injury, the exact mechanisms involved have yet to be fully understood. Our aim was to investigate the potential protective effects of levocarnitine pretreatment against oxidative stress in rat H9c2 cardiomyocytes.

Methods: Cardiomyocytes were exposed to H2O2 to create an oxidative stress model.

Glycyrrhizin improves p75NTR-associated sciatic nerve regeneration in a BALB/c mouse model.

Glycyrrhizin has a role in immune regulation in the central nervous system, but its impact on sciatic nerve injury had not previously been reported. In this study, a BALB/c mouse model of sciatic nerve injury was used to explore the role of glycyrrhizin in sciatic nerve repair and its underlying mechanism. Glycyrrhizin with intragastric gavage of 10 and 20 mg/kg weight per day (mid- and high-dose, respectively) inhibited p75 neurotrophin receptor (p75NTR) expression at the protein and mRNA levels versus the 5 mg/kg (low-dose) group and control (0.