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Surface modification by ion implantation-deposition is well established in materials science and can be an effective way to improve biocompatibility. The aim of this study is to evaluate the chemical composition of a modified titanium (Ti) surface after zinc (Zn) ion implantation and deposition and examine the effect of the modification on the formation of cellular focal adhesion plaques in vitro.cp-Ti discs were modified with Zn ion implantation and deposition via PIIID. The chemical composition of the surface modification was characterized by X-ray photoelectron spectroscopy (XPS). The formation of focal adhesion plaques on the modified Ti was investigated with human osteoblast-like MG-63 cells that were seeded onto the Ti surfaces and quantified by morphometric analysis under a confocal microscope.XPS data revealed that the modified Zn-Ti surface consisted of Ti, oxygen, Zn, and carbon. In addition, Gaussian fitting of the spectra indicated that the modified surface contained titanium dioxide and zinc oxide. After 6 hours of MG-63 cell culture, there were significantly more focal adhesion plaques on the modified surfaces than observed on the nonmodified Ti (P0.05).Zn ion implantation and deposition greatly improved the biocompatibility of Ti for the growth of MG-63 cells.

Adiponectin is an adipokine with insulin-sensitising and anti-atherogenic properties. The aim of this study was to investigate whether low adiponectin levels predict the impairment of endothelial function in newly diagnosed type 2 diabetic patients in an 8-year prospective study.In the prospective study, we enrolled 133 newly diagnosed type 2 diabetic patients without subclinical atherosclerosis and gave them intensive therapy; the mean treatment period was 8 years. Intensive treatment was a stepwise implementation of behavior modification and pharmacological therapy targeting hyperglycaemia, hypertension, dyslipidaemia and obesity. We measured baseline circulating adiponectin with an enzyme-linked immunosorbent assay, endothelium-dependent and -independent vasodilation by high-resolution vascular ultrasound. At year 8, 102 patients were reexamined for endothelium-dependent and -independent vasodilation.Sex-adjusted adiponectin level was positively correlated with endothelium-independent vasodilation both at baseline (r = 0.150, P = 0.043) and at year 8 (r = 0.339, P = 0.001), whereas no association was found between adiponectin and endothelium-dependent vasodilation. In a stepwise multivariate linear regression model, adiponectin was an independent predictor for impaired endothelium-independent vasodilation at year 8 (P = 0.001).Plasma adiponectin concentration was associated with endothelium-independent vasodilation and hypoadiponectinemia predicted the impairment of endothelium-independent vasodilation in newly diagnosed type 2 diabetic patients under multifactorial intervention. These data support the causative link of impairment of endothelium-independent vasodilation with hypoadiponectinemia.

Angelman syndrome (AS) is a neurogenetic disorder caused by an expression defect of the maternally inherited copy of ubiquitin protein ligase E3A (UBE3A) gene from chromosome 15. Although the most common genetic defects include maternal deletions of chromosome 15q11-13, paternal uniparental disomy and imprinting defect, mutations in the UBE3A gene have been identified in approximately 10% of AS patients.A Chinese girl of 28 months presented clinical manifestation of AS. Genetic diagnosis and molecular genetic defects were studied by methylation-specific PCR (MS-PCR) and linkage analysis by short tandem repeat (STR). We further performed sequence analysis of all the coding exons and flanking sequences of the UBE3A gene. The novel mutation screening was also performed in 100 unrelated healthy individuals to exclude the possibility of identifying a polymorphism variation.The MS-PCR analysis of the patient showed biparental inheritance of chromosome 15 with a normal methylation pattern in the 15q11-q13 region. And STR analysis revealed that the patient also inherited biparental alleles for six microsatellites. A novel mutation, cDNA1199 CA (p.P400H), in exon 9 of the maternal UBE3A gene, was identified in the patient. Meanwhile, the mutation was observed in the patient's mother who had a normal phenotype.It is necessary to perform the UBE3A gene mutation analysis in non-deletion/non-UPD/non-ID patients with AS. The clinical picture of the patient is concordant with that observed in previously reported AS patients with UBE3A mutation.

The severity of hypoalbuminemia has been shown to be related to morbidity and mortality in some critical illnesses, illustrating the need for better understanding of molecular mechanism of hypoalbuminemia. Lipopolysaccharide (LPS) is a key mediator inducing hypoalbuminemia in sepsis and septic shock. The present study was designed to identify if the reduction of albumin expression is directly induced by LPS and modulated by activated extracellular signal-regulated protein kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) in rat hepatocytes.Primary rat hepatocytes were divided into five groups. In two of them, hepatocytes were treated with normal saline or 1 microg/ml LPS, then albumin mRNA expression was observed at 0, 2, 8, 12 and 24 hours after treatment. In another group, hepatocytes were pretreated with 100, 40 or 20 micromol/L of cycloheximide (CHX, an inhibitor of protein synthesis) for 30 minutes followed by 1 microg/ml LPS for 24 hours. Then the RNA was extracted from the cells for RT-PCR to detect the expression of albumin. The other two groups were administered 1 micromol/L, 10 micromol/L and 50 micromol/L of SB203580 (p38 MAPK inhibitor) or PD98059 (ERK inhibitor) 30 minutes prior to 1 microg/ml LPS treatment. After 24 hours of LPS treatment, the supernatant was collected and assayed for albumin concentrations. Data were analyzed by one-way analysis of variance, followed by the Newman-Keul test; a P0.05 was considered significant.There was no marked change in albumin mRNA expression in the control group during 24-hours treatment with normal saline. The reduction did not occur until 24 hours after LPS treatment, and albumin mRNA decreased by 30% approximately compared to the control group at 24 hours (0.587 vs 0.832, P=0.007). CHX could inhibit the decline of albumin mRNA induced by LPS and the effect was correlated with the dose of CHX. The ERK inhibitor PD98059 caused a significant increase in LPS-induced albumin production at the three concentrations (119.7, 111.4 and 80.0 ng/ml vs 44.4 ng/ml, P=0.0013, 0.0025 and 0.009, respectively), whereas SB203580 obviously blocked albumin reduction in LPS-treated cells at the concentrations of 10 and 50 micromol/L (87.5 and 93.6 ng/ml vs 44.4 ng/ml, P=0.0076 and 0.0049, respectively).LPS can induce the reduction of albumin expression by new synthesized proteins indirectly, and the process may be related to the signal proteins of ERK and p38 kinase. The ERK and p38 kinase are critical signaling pathways in LPS-induced hypoalbuminemia which is worthwhile to understand in studying the molecular mechanism of hypoalbuminemia in sepsis and septic shock.