[Effect of Arg188Gln (G/A) mutation on enzymatic activity of kynureninase].

To verify whether the enzymatic activity of kynureninase (KYNU) could be changed by the Arg188Gln (G/A) mutation. The total RNA of human hepatic tissue was extracted and the gene cDNA was amplified by RT-PCR. Primers were designed according to the sequences around the site Arg188Gln of gene and the Arg188Gln (G/A) mutant cDNA was generated by site-directed mutagenesis.

Osteoglycin attenuates cardiac fibrosis by suppressing cardiac myofibroblast proliferation and migration through antagonizing lysophosphatidic acid 3/matrix metalloproteinase 2/epidermal growth factor receptor signalling.

Aims: Cardiac myofibroblasts (CMFs) play a crucial role in the progression of pathological fibrotic cardiac remodelling. The expression of osteoglycin (OGN) is increased in diseased hearts; however, the role of OGN in pathological cardiac remodelling is not understood. Here, we sought to determine the effect of OGN on cardiac interstitial fibrosis and investigate the molecular mechanisms of OGN in CMF activation and matrix production.

Preoperative Metabolic Syndrome Is Predictive of Significant Gastric Cancer Mortality after Gastrectomy: The Fujian Prospective Investigation of Cancer (FIESTA) Study.

Metabolic syndrome (MetS) has been shown to be associated with an increased risk of gastric cancer. However, the impact of MetS on gastric cancer mortality remains largely unknown. Here, we prospectively examined the prediction of preoperative MetS for gastric cancer mortality by analyzing a subset of data from the ongoing Fujian prospective investigation of cancer (FIESTA) study.

Preoperative blood-routine markers and prognosis of esophageal squamous cell carcinoma: The Fujian prospective investigation of cancer (FIESTA) study.

This prospective study was designed to investigate the prognosis of preoperative blood-routine markers for esophageal cancer mortality by using data from the ongoing Fujian prospective investigation of cancer (FIESTA) study. Patients who received three-field lymphadenectomy for esophageal cancer between 2000 and 2010 were enrolled. Of 2535 patients with complete survival data, esophageal squamous cell carcinoma (ESCC) accounted for 94.

Endothelial‑like cells differentiated from mesenchymal stem cells attenuate neointimal hyperplasia after vascular injury.

The present study investigated the contribution of bone marrow-derived mesenchymal stem cells (BM‑MSCs) to neointimal formation, and whether endothelial‑like cells (ELCs) differentiated from BM‑MSCs could attenuate intimal hyperplasia following vascular injury. BM‑MSCs were isolated from rat femurs and tibias and expanded ex vivo. Differentiation into ELCs was induced by cultivation in the presence of 50 ng/ml vascular endothelial growth factor (VEGF).

Preoperative metabolic syndrome and prognosis after radical resection for colorectal cancer: The Fujian prospective investigation of cancer (FIESTA) study.

This prospective study sought to investigate the prediction of preoperative metabolic syndrome and its components for the risk of colorectal cancer (CRC) mortality by analyzing a subset of data from the ongoing Fujian prospective investigation of cancer (FIESTA) study. In total, 1,318 CRC patients who received radical resection were consecutively enrolled between January 2000 and December 2008. The median follow-up time was 58.

Silencing of osterix expression by siRNA inhibits aldosterone‑induced calcification of vascular smooth muscle cells in mice.

The process of vascular calcification shares numerous similarities with that of skeletal mineralization and involves the deposition of hydroxyapatite crystals in arteries and cardiac valves. However, the underlying cellular mechanism remains to be fully elucidated. Microarray analysis in the present study demonstrated that greater than 2,000 genes were upregulated during the calcification of murine vascular smooth muscle cells (VSMCs), of which osterix (OSX) and integrin‑binding sialoprotein (IBSP) were the most significantly differentially expressed genes.

Association of a SNP in SLC35F3 Gene with the Risk of Hypertension in a Chinese Han Population.

A recent study suggested that SLC35F3 which encoded a thiamine transporter was a new candidate gene for hypertension. The goal of this study was to investigate the association between the single-nucleotide polymorphisms (SNPs) in the SLC35F3 gene and hypertension in a Chinese population. Sanger sequencing was performed in 93 samples to find SNPs in coding regions and intron-exon boundaries in the SLC35F3 gene.

Complement-mediated macrophage polarization in perivascular adipose tissue contributes to vascular injury in deoxycorticosterone acetate-salt mice.

Objective: We have previously shown an increased expression of complement 3 (C3) in the perivascular adipose tissue (PVAT) in the deoxycorticosterone acetate (DOCA)-salt hypertensive model. This study aims to examine the role and underlying mechanism of C3 in PVAT for understanding the pathogenesis of hypertensive vascular remodeling further.

Approach And Results: The role of C3 in macrophage polarization was investigated using peritoneal macrophages from wild-type and C3-deficient (C3KO) mice because we found that C3 was primarily expressed in macrophages in PVAT of blood vessels from DOCA-salt mice, and results showed a decreased expression of M1 phenotypic marker in contrast to an increased level of M2 marker in the C3KO macrophages.

Confirmation of top polymorphisms in hypertension genome wide association study among Han Chinese.

Background: Confirmation of genome wide association (GWA) results in independent samples has recently become new research tendency.

Methods: We focused on 8 positive top polymorphisms identified in the to-date largest hypertension GWA study and determined whether these polymorphisms were associated with hypertension among Han Chinese. Genotyping was performed among 548 patients diagnosed with essential hypertension and 560 age- and gender-matched controls using ligase detection reactions method.

Validation of genetic association in apelin-AGTRL1 system with hypertension in a larger Han Chinese population.

Background And Objective: We have recently resequenced apelin and AGTRL1 genes to identify candidate polymorphisms in family-based association with hypertension and related phenotypes. In this study, we aimed to determine and replicate these polymorphisms via a larger, independent case-control study in Shanghai Han Chinese.

Methods: Two polymorphisms [rs3761581 (A/C) and T-1860C] in apelin gene and two [rs7119375 (G/A), rs10501367 (G/A)] in AGTRL1 gene were genotyped using the TaqMan assay among 969 patients diagnosed with essential hypertension and 980 age and sex-matched controls.

Perivascular gene transfer of dominant-negative N19RhoA attenuates neointimal formation via inhibition of TGF-beta1-Smad2 signaling in rats after carotid artery balloon injury.

Phenotypic differentiation of adventitial fibroblasts to myofibroblasts is an essential feature of vascular remodeling. Here, we carried out perivascular gene transfer of dominant-negative N19RhoA to investigate whether antagonism of RhoA signaling attenuates neointimal formation following rat carotid artery balloon injury and alters TGF-beta1-Smad2-induced differentiation of adventitial fibroblasts to myofibroblasts. Perivascular delivery of an adenovirus coexpressing dominant-negative N19RhoA and humanized Renilla green fluorescent protein (hrGFP) (Ad-N19RhoA-hrGFP), as demonstrated by hrGFP staining, suppressed neointimal formation at 7 and 14days post-injury.

Circulating endothelial progenitor cells in Chinese patients with acute stroke.

To test the hypothesis that a mobilization of endothelial progenitor cells (EPCs) occurs after acute cerebrovascular diseases, we evaluated the number of EPCs in the process of acute stroke. A total of 203 individuals were examined, including 100 patients with ischemic strokes, 36 patients with hemorrhagic strokes and 67 healthy controls. Ninety-eight patients were observed at days 1, 7, 14 and 28 after acute stroke.

Circulating endothelial progenitor cells, C-reactive protein and severity of coronary stenosis in Chinese patients with coronary artery disease.

We sought to investigate whether numbers and activity of circulating endothelial progenitor cells (EPCs) correlate with severity of coronary stenosis as well as cardiovascular risk factors in patients with stable coronary artery disease (CAD). Number of circulating EPCs was analyzed in 104 consecutive patients with proven or clinically suspected CAD. Adhesive and migratory activity was also determined.

NAD(P)H oxidase-derived reactive oxygen species regulate angiotensin-II induced adventitial fibroblast phenotypic differentiation.

Phenotypic differentiation of adventitial fibroblasts into myofibroblasts is an essential feature of vascular remodeling. The present study was undertaken to test the hypothesis that reactive oxygen species (ROS) are involved in rat adventitial fibroblast differentiation to myofibroblast. Activation of alpha-smooth muscle actin (alpha-SMA) was used as a marker of myofibroblast.

[Number of circulating endothelial progenitor cells inversely correlate with the severity of coronary artery disease in patients with stable coronary artery disease].

Objective: To investigate whether the number of circulating endothelial progenitor cells (EPCs) correlate with the severity of coronary stenosis in patients with stable coronary artery disease (CAD).

Methods: 80 consecutive patients who underwent coronary angiography (exclusion of acute coronary syndrome and myocardial infarction) were enrolled. Physical examination and blood tests were performed to assess the disease severity and cardiovascular risk factors.

[Osteopontin enhances migratory ability of cultured aortic adventitial fibroblasts from spontaneously hypertensive rats].

Migration of adventitial fibroblasts (AF) is involved in the neointimal formation which is one of the common pathological processes in several vascular diseases. The observation of whether the migratory response of AF from hypertensive animal is different from that of controls may provide an explanation of vascular remodeling in hypertension. We examined whether there is any difference between the migratory activity of AF derived from spontaneously hypertensive rat (SHR) and that from their normotensive counterpart Wistar-Kyoto rats (WKY).