Association between ATG16L1 gene polymorphism and the risk of Crohn's disease.

Objective To perform a meta-analysis to evaluate studies investigating the association between ATG16L1 gene polymorphism and Crohn's disease. Methods PubMed, Embase and Web of Science databases were searched for all studies focusing on the association of ATG16L1 and Crohn's disease. Combined odds ratios with 95% confidence intervals were calculated for four genetic models (allelic model: G allele versus A allele; additive model: GG versus AA; dominant model: GA + GG versus AA; recessive model: GG versus GA + AA) using either a random effects or fixed effects model.

Intermittent cold stress enhances features of atherosclerotic plaque instability in apolipoprotein E‑deficient mice.

The cold weather is associated with an increased occurrence of acute coronary events. However, the mechanisms underlying cold‑induced myocardial infarctions have not yet been fully elucidated. In the present study, 20 male, eight week‑old, apolipoprotein E (ApoE)‑deficient mice were subjected to either control conditions or intermittent cold exposure for eight weeks.

Association between vacA genotypes and the risk of duodenal ulcer: a meta-analysis.

Epidemiological studies have reported the relationship between vacuolating cytotoxin A (vacA) s-/m- region genotypes and duodenal ulcer (DU), but the results remained inconclusive. We performed the present meta-analysis to investigate a more authentic association between vacA s-/m- region genotypes and DU. Literature search was performed by searching Embase, PubMed and ISI Web of Science databases as well as checking references from identified articles, reviews and the abstracts presented at related scientific societies meetings.

Expression of mammalian target of rapamycin in atherosclerotic plaques is decreased under diabetic conditions: a mechanism for rapamycin resistance.

Our previous study demonstrated that diabetes increases in-stent restenosis following rapamycin-eluting stent placement, which was defined as rapamycin resistance. However, the underlying mechanisms of rapamycin resistance remain to be determined. In the present study, male apolipoprotein E-deficient (ApoE-/-) mice were randomly divided into control and diabetic groups.

Antibiotic drug tigecycline inhibited cell proliferation and induced autophagy in gastric cancer cells.

Tigecycline acts as a glycylcycline class bacteriostatic agent, and actively resists a series of bacteria, specifically drug fast bacteria. However, accumulating evidence showed that tetracycline and their derivatives such as doxycycline and minocycline have anti-cancer properties, which are out of their broader antimicrobial activity. We found that tigecycline dramatically inhibited gastric cancer cell proliferation and provided an evidence that tigecycline induced autophagy but not apoptosis in human gastric cancer cells.

POU5F1 enhances the invasiveness of cancer stem-like cells in lung adenocarcinoma by upregulation of MMP-2 expression.

Lung cancer is the leading cause of cancer-related human deaths. Exploration of the mechanisms underlying the metastasis of cancer stem-like cells (CSLCs) will open new avenues in lung cancer diagnosis and therapy. Here, we demonstrated that CSLCs-derived from lung adenocarcinoma (LAC) cells displayed highly invasive and migratory capabilities via expressing high levels of POU5F1 and MMP-2.

Transgenic overexpression of uncoupling protein 2 attenuates salt-induced vascular dysfunction by inhibition of oxidative stress.

Background: Ablation of uncoupling protein 2 (UCP2) has been involved in the enhancement of salt sensitivity associated with increased superoxide level and decreased nitric oxide (NO) bioavailability. However, the role of overexpression of UCP2 in salt-induced vascular dysfunction remains elusive.

Methods: UCP2 transgenic (TG) and wild-type (WT) mice were placed on either a normal-salt (NS, 0.

Toll-like receptor 4 gene Asp299Gly polymorphism in myocardial infarction: a meta-analysis of 15,148 subjects.

It remains controversial regarding the association between toll-like receptor 4 (TLR4) gene Asp299Gly (+896 A/G) polymorphism and myocardial infarction (MI) risk. Thus, a large-scale meta-analysis evaluating the potential association between this gene variant and MI risk is required. PubMed, Embase, Web of Science, CBMdisc, CNKI, and Google Scholar were searched until February 6, 2013.

No association between IL-1RN VNTR and the risk of duodenal ulcer: a meta-analysis.

The aim of this study was to perform a meta-analysis to investigate a more authentic association between interleukin-1 RN variable number of tandem repeats (IL-1RN VNTR) and duodenal ulcer (DU). Systematic searches of electronic databases Embase, PubMed and Web of Science were performed. Statistical analyses were conducted using software Stata 11.

Intermittent hypobaric hypoxia promotes atherosclerotic plaque instability in ApoE-deficient mice.

Aim: Sudden cardiac death is one of the most frequent causes of death at high altitude. It has been reported that the intermittent normobaric hypoxia experienced by patients with obstructive sleep apnea may enhance the development of atherosclerosis. However, the effect of hypobaric hypoxia, which mimics the ambient air at high altitude, in the development of atherosclerosis has not been investigated.

Association between TNF α gene polymorphisms and the risk of duodenal ulcer: a meta-analysis.

Background: Epidemiological studies have evaluated the association between tumor necrosis factor α (TNF-α) single nucleotide polymorphisms (SNPs) and duodenal ulcer (DU), but the results remain inconclusive. The aim of this study was to perform a meta-analysis to investigate a more authentic association between TNF-α SNPs and DU.

Methods: We performed the meta-analysis by searching PubMed, Embase, and Web of Science databases from the first available year to Sep.

Establishment of a conditional transgenic mouse model expressing human uncoupling protein 2 in vascular smooth muscle cells.

Increased oxidative stress is involved in the development of vascular dysfunction and remodeling. Uncoupling protein 2 (UCP2) regulates the production of reactive oxygen species in vascular smooth muscle cells (SMCs). To promote the study of the role of UCP2 in vascular diseases, a transgenic mouse model expressing human UCP2 (hUCP2) in vascular SMCs was established.

Inhibition of uncoupling protein 2 with genipin exacerbates palmitate-induced hepatic steatosis.

Background: Uncoupling protein 2 (UCP2) was reported to be involved in lipid metabolism through regulating the production of superoxide anion. However, the role of UCP2 in hepatocytes steatosis has not been determined. We hypothesized that UCP2 might regulate hepatic steatosis via suppressing oxidative stress.

Acipimox attenuates atherosclerosis and enhances plaque stability in ApoE-deficient mice fed a palmitate-rich diet.

Saturated fatty acids (FA) have been linked to an increased risk of cardiovascular disease. The effects of acipimox, a FA-lowering agent, on palmitate- (an important saturated fatty acid) stimulated atherosclerosis remains to be elucidated. We investigated the effects of acipimox on atherosclerosis in ApoE(-/-) mice fed a palmitate-rich diet.

No association between IL-1β -31 C/T polymorphism and the risk of duodenal ulcer: a meta-analysis of 3793 subjects.

The aim of this study was to perform a meta-analysis to investigate a more authentic association between IL-1β -31 C/T polymorphism and duodenal ulcer (DU). Systematic searches of electronic databases Embase, PubMed and Web of Science were performed. Study selection, data abstraction and study quality evaluation were independently conducted in duplicate.

No association between IL-1β -511 C/T polymorphism and the risk of duodenal ulcer: a meta-analysis of 4667 subjects.

Epidemiological studies have evaluated the association between IL-1β -511 C/T polymorphism and duodenal ulcer (DU) risk. However, the results remain conflicting. The aim of this study was to perform a meta-analysis to investigate a more authentic association between IL-1β -511 C/T polymorphism and DU.

Cryptotanshinone attenuates isoprenaline-induced cardiac fibrosis in mice associated with upregulation and activation of matrix metalloproteinase-2.

Cryptotanshinone is an active ingredient of Salvia miltiorrhiza that has been used in traditional Chinese medicine for treating cardiovascular disorders. Thus, we investigated the effects of cryptotanshinone on cardiac fibrosis induced by isoprenaline and examined whether cardiac matrix metalloproteinase (MMP)-2 is involved in this process. Male C57BL/6 mice received a daily injection of 0.

Comparison of restenosis rate with sirolimus-eluting stent in STEMI patients with and without diabetes at 6-month angiographic follow-up.

Objective: Patients with diabetes mellitus (DM) are at high risk for restenosis after coronary stenting. However, whether drug-eluting stents are effective in diabetic patients presenting with ST-segment elevation myocardial infarction (STEMI) is uncertain. We report on a series of patients with or without DM followed up for 6 months after sirolimus-eluting stent implantation.

Cardiac extracellular matrix tenascin-C deposition during fibronectin degradation.

Tenascin-C (TN-C) might aggravate left ventricular remodeling after myocardial infarction (MI). Our previous study demonstrated that ventricular remodeling after MI is linked with the degradation of fibronectin (FN). The aim of the present study was to determine whether cardiac extracellular matrix TN-C deposition after MI requires FN degradation.

Oleic acid induces smooth muscle foam cell formation and enhances atherosclerotic lesion development via CD36.

Background: Elevated plasma free fatty acid (FFA) levels have been linked to the development of atherosclerosis. However, how FFA causes atherosclerosis has not been determined. Because fatty acid translocase (FAT/CD36) is responsible for the uptake of FFA, we hypothesized that the atherogenic effects of FFA may be mediated via CD36.

Adrenergic receptor blockade-induced regression of pressure-overload cardiac hypertrophy is associated with inhibition of the calcineurin/NFAT3/GATA4 pathway.

Calcineurin and its downstream effectors nuclear factor of activated T-cells 3 (NFAT3) and zinc finger-containing transcription factor (GATA4) have been implicated in the development of cardiac hypertrophy. The aims of the present study were to investigate alterations in the calcineurin/NFAT3/GATA4 pathway in pressure-overload hypertrophy, and to determine whether adrenergic receptor blockade affects this signaling pathway. In aorta-banded rats compared with sham-operated rats, a significant increase in the phosphorylation levels of calcineurin and GATA4 was observed (both p<0.

BTEB2 knockdown suppresses neointimal hyperplasia in a rat artery balloon injury model.

Basic transcription element-binding protein 2 (BTEB2) is a regulator of the proliferation and phenotypic changes of vascular smooth muscle cells (SMCs). The aim of the present study was to determine whether or not BTEB2 knockdown inhibits balloon injury-induced neointimal hyperplasia attributed to the proliferation and phenotypic changes of vascular SMCs. We found that the knockdown of BTEB2 with antisense oligonucleotides (Ad-As-BTEB2) significantly reduced the intima/media ratio compared to uninjured arteries and vessels treated with Ad-LacZ.

Overexpression of angiotensin II type 2 receptor suppresses neointimal hyperplasia in a rat carotid arterial balloon injury model.

Angiotensin II (ANG II) type 2 receptor (AT2R) has been recognized to suppress the proliferation of vascular smooth muscle cells (VSMCs). The aim of the present study was to determine whether AT2R overexpression inhibits neointimal hyperplasia in a rat carotid arterial balloon injury model and to examine the underlying mechanisms of its activity. Balloon-injured rats receiving Ad-AT2R showed significant diminutions in neointimal area and intima/media ratio compared to non-treated rats or rats receiving adenovirus containing green fluorescent protein (Ad-GFP).

Imbalance of matrix metalloproteinases/tissue inhibitor of metalloproteinase-1 and loss of fibronectin expression in patients with congestive heart failure.

Objective: Previous studies have demonstrated that an imbalance of matrix metalloproteinases (MMPs)/tissue inhibitors of metalloproteinase-1 (TIMP-1) and a loss of fibronectin are associated with postmyocardial infarction remodeling in rats. The present study was designed to examine this issue in patients with congestive heart failure (CHF).

Methods: We measured plasma levels and the cardiac protein expression of MMPs/TIMP-1 and fibronectin in 39 patients with CHF and 38 controls.