Endothelial progenitor cells are influenced by serum of patients with systemic inflammatory response syndrome or multiple organ dysfunction.

BACKGROUND AND AIM: To investigate the effects of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndromes (MODS) on human peripheral blood endothelial progenitor cells. PATIENTS AND METHODS: Twenty patients admitted to Changhai Hospital, Second Military Medical University, from February, 2011 to November, 2011 were recruited consecutively. The serum samples were collected from the twenty patients who were divided into four groups as following: normal group, post-traumatic group without SIRS, post-traumatic group with SIRS, and post-traumatic group with MODS. Endothelial progenitor cells (EPCs) were isolated from peripheral blood of healthy subjects by using density gradient centrifugation and the effect of the serum on EPCs was detected after stimulating by the serum samples for 0, 6, 12, 24, and 36 h. RESULTS: Compared with the normal group, the proliferation of EPCs was significantly increased in a time-independent manner in the other three groups, especially in the SIRS serum treated group. The expression of pro-inflammation cytokines was increased in the other three groups compared with the normal group, but the expression of IL-10 in the normal group was higher than the other groups. CONCLUSIONS: Oxidative stress balance was also broken as the disease progressed. Serum from patients with sepsis could influence proliferation and the inflammation and oxidative stress states of EPCs.

[Cause of leaf yellowing of Amomum villosum Lour. from Yunnan and its prevention].

The results of the experiment showed that manganese deficiency in soil is one of the main causes of leaf yellowing of Amomum villosum and applying trace element fertilizer can make up deficiency. Manganese sulphate can effectively prevent the leaf yellowing.

The visfatin gene is associated with glucose and lipid metabolism in a Chinese population.

AIMS: Visfatin is a newly discovered adipokine found in abundance in visceral fat. It lowers plasma glucose in humans and mice. In this study, we explored the relationships between the plasma level of visfatin and genetic single nucleotide polymorphisms (SNPs) and Type 2 diabetes mellitus (T2DM) and anthropometric and metabolic parameters in Chinese subjects. METHODS: Oral glucose tolerance tests (OGTT) and biochemical assays for plasma insulin, lipid profiles and serum visfatin were performed in 241 newly diagnosed T2DM patients, subjects with impaired glucose regulation (IGR), and normal glucose tolerant subjects more than 40 years of age. Genotyping for three SNP loci: -1535C/T, rs2058539 and rs10953502 were performed using the allele-specific real-time PCR method. RESULTS: Visfatin levels were similar in T2DM patients, IGR and normal glucose tolerant subjects. However, visfatin levels were significantly lower in obese than normal-weight subjects (13.66 +/- 0.87 vs. 15.46 +/- 0.47 ng/ml, P = 0.03). There was suggestively significant correlation between visfatin level and body mass index (r = -0.17 P = 0.07) and waist-hip ratio (r = 0.16 P = 0.08) in male subjects, but not in female subjects. Allele and common haplotype frequencies of the three SNP loci were similar in T2DM patients, IGR and normal glucose tolerant subjects. However, significant associations were found between these three SNP loci and plasma glucose concentration at 0 and 120 min during OGTT, the area under the response curve for plasma glucose, and triglyceride and total cholesterol levels. CONCLUSIONS: Serum visfatin levels may be related to visceral obesity in men, and the visfatin gene may account for variation of glucose and lipid parameters in Chinese subjects.

A genome-wide search for type II diabetes susceptibility genes in Chinese Hans.

AIMS/HYPOTHESIS: The aim of the study was to search for Type II (non-insulin-dependent) diabetes mellitus susceptibility genes in a Chinese population. METHODS: A genome-wide scan was carried out using non-parametric linkage analyses. We studied 102 families (478 family members) who were Chinese Hans residing in east and south-east China, including 282 diabetic patients, among them 142 independent affected sibpairs were available for genotyping. A total of 247 fluorescence labelled microsatellite markers, with an average resolution of 15 cM, were amplified. GENEHUNTER was used for the non-parametric linkage analyses. RESULTS: Two loci on chromosome 9 D9S171 and D9S175 showed suggestive evidence for linkage, with an NPL-score of 3.286 and 2.939 respectively, and a p value of 1.19 x 10(-4) and 4.47 x 10(-4). A locus on the long arm of chromosome 20, D20S196 showed a rise in the non-parametric-linkage score (from 1.517 to 2.922) and a corresponding decrease in the p value from 0.04 to 6.5 x 10(-4) when families with lower BMI were analysed alone. Other loci with weaker evidence for linkage were also observed. CONCLUSIONS: Our results suggest that chromosome 9 contains genes involved in the susceptibility to Type II diabetes in an eastern and southeastern Chinese Han population, and chromosome 20 could hide genes linked to Type II diabetes in families with a lower BMI. Other regions could also hide susceptibility genes with minor effects.