ABSTRACT To explore the functions of Txnip and its mechanism in adipocyte differentiation, the preadipocytes were isolated from subcutaneous adipose tissue of three-day-old piglets and induced into adipogenic differentiation. The expression of Txnip and ChREBP was silenced, and the Txnip overexpression was achieved in the cells with transfection of the recombinant lentivirus strategies. Txnip silencing promoted the differentiation of porcine preadipocytes and PPARγ expression, and a PPARγ inhibitor reduced this facilitation. Instead, Txnip overexpression exerted a suppressive effect on the cell differentiation and PPARγ expression, and the PPARγ agonist offset this inhibition. High glucose stimulated the preadipocyte differentiation and expressions of ChREBP and Txnip. In contrast, Txnip expression was reduced by ChREBP silencing, suggesting glucose-regulated Txnip expression through the mediation of ChREBP. Moreover, the expressions of ChREBP and Glut4 induced by high glucose and glucose uptake of the cells were reduced by Txnip-overexpression, but increased by Txnip silencing, while these changes of Txnip did not alter their expressions under low glucose. Collectively, Txnip could be an inhibitor of porcine preadipocyte differentiation, which attenuated the adipogenesis through the negative feedback regulation on PPARγ. Txnip impaired the induction of glucose on the preadipocyte differentiation through decreasing Glut4 expression and glucose uptake and subsequent decrease of the expression and transcriptional activity of ChREBP. threedayold three day old silenced strategies facilitation Instead inhibition contrast glucoseregulated regulated Moreover Glut Txnipoverexpression, Txnipoverexpression overexpression, Txnip-overexpression Collectively

OBJECTIVE: To evaluate the correlation between the severity of intervertebral disc injury and the anteroposterior type of thoracolumbar vertebral fractures. METHODS: Fifty-six cases of thoracolumbar vertebral fractures treated in our trauma center from October 2012 to October 2013 were included in this study. The fractures were classified by the anteroposterior classification, whereas the severity of intervertebral disc injury was evaluated using magnetic resonance imaging. The Spearman correlation coefficient was used to analyze the correlation between the severity of intervertebral disc injury and the anteroposterior type of thoracolumbar fractures, whereas a χ2 test was adopted to measure the variability between different fracture types and upper and lower adjacent disc injuries. RESULTS: The Spearman correlation coefficients between fracture types and the severity of the upper and lower adjacent disc injuries were 0.739 (PU<0.001) and 0.368 (PL=0.005), respectively. It means that the more complex Arbeitsgemeinschaft für Osteosynthesefragen (AO) classifications are the disc injury is more severe. There was also a significant difference in the severity of injury between the upper and lower adjacent discs near the fractured vertebrae (p<0.001). CONCLUSIONS: In thoracolumbar spinal fractures, the severity of the adjacent intervertebral disc injury is positively correlated with the anteroposterior fracture type. The injury primarily involves intervertebral discs near the fractured end plate, with more frequent and severe injuries observed in the upper than in the lower discs. The presence of intervertebral disc injury, along with its severity, may provide useful information during the clinical decision-making process.

OBJECTIVE:The goal of the present study was to compare the prognoses of patients with non-ST-elevation acute coronary syndromes who were treated with invasive or conservative treatment strategies.METHODS:We performed a meta-analysis of studies of patients with non-ST-elevation acute coronary syndromes to assess the benefits of an invasive strategy vs. a conservative strategy for short- and long-term survival. We searched PubMed for studies published from 1990 to November 2012 that investigated the effects of an invasive vs. conservative strategy in patients with non-ST-elevation acute coronary syndromes. The following search terms were used: “non-ST-elevation myocardial infarction”, “unstable angina”, “acute coronary syndromes”, “invasive strategy”, and “conservative strategy”. The primary endpoints were all-cause mortality at 30 days and 1 year.RESULTS:Seven published studies were included in the present meta-analysis. The pooled analyses show that an invasive strategy decreased the risk of death (risk ratio [0.839] [95% confidence interval {0.648-1.086}; I2, 86.46%] compared to a conservative strategy over a 30-day-period. Furthermore, invasive treatment also decreased patient mortality (risk ratio [0.276] [95% confidence interval {0.259-0.294}; I2, 94.58%]) compared to a conservative strategy for one year.CONCLUSION:In non-ST-elevation acute coronary syndromes, an invasive strategy is comparable to a conservative strategy for decreasing short- and long-term mortality rates.

Single nucleotide polymorphisms in the promoter region ofinterleukin-18 (IL-18), an inflammatory cytokine, have been linked to susceptibility to many diseases, including cancer and immune dysfunction. Here, we explored the potential association between theIL-18 -607C/A (rs1946518) promoter region polymorphism and susceptibility to ischemic stroke (IS). This locus was amplified from peripheral blood samples of 386 IS patients (cases) and 364 healthy individuals (controls) by the polymerase chain reaction with sequence-specific primers. Significant differences were observed by the χ2 test in the -607C/A (rs1946518) genotype and allele frequencies between cases and controls (P < 0.05). Furthermore, after excluding for age, gender, smoking status, and hypertension, logistic regression indicated that IS susceptibility of -607C carriers increased 1.6 times (OR = 1.601, 95%CI = 1.148-2.233, P = 0.006) compared to -607A carriers. Additionally, similar increases in IS risk were noted for male patients or patients less than 65 years old. In conclusion,IL-18 -607C/A (rs1946518) promoter polymorphism is associated with IS susceptibility, and the C allele may confer increased IS risk.

YKL-40 has been identified as a growth factor in connective tissue cells and also a migration factor in vascular smooth muscle cells. To a large extent, the increase of serum YKL-40 is attributed to liver fibrosis and asthma. However, the relationship of the expression and clinical/prognostic significance of YKL-40 to the splenomegaly of patients with portal hypertension is unclear. In the present study, the expression of YKL-40 was studied by immunohistochemistry in 48 splenomegaly tissue samples from patients with portal hypertension and in 14 normal spleen specimens. All specimens were quickly stored at -80°C after resection. Primary antibodies YKL-40 (1:150 dilution, rabbit polyclonal IgG) and MMP-9 (1:200 dilution, rabbit monoclonal IgG) and antirabbit immunoglobulins (HRP K4010) were used in this study. The relationship of clinicopathologic features with YKL-40 is presented. The expression of YKL-40 indicated by increased immunochemical reactivity was significantly up-regulated in splenomegaly tissues compared to normal spleen tissues. Overexpression of YKL-40 was found in 68.8% of splenomegaly tissues and was significantly associated with Child-Pugh classification (P = 0.000), free portal pressure (correlation coefficient = 0.499, P < 0.01) and spleen fibrosis (correlation coefficient = 0.857, P < 0.01). Further study showed a significant correlation between YKL-40 and MMP-9 (correlation coefficient = -0.839, P < 0.01), indicating that YKL-40 might be an accelerator of spleen tissue remodeling by inhibiting the expression of MMP-9. In conclusion, YKL-40 is an important factor involved in the remodeling of spleen tissue of portal hypertension patients and can be used as a therapeutic target for splenomegaly.

Tetrodotoxin (TTX) is a highly potent neurotoxin that blocks the action potential by selectively binding to voltage-gated sodium channels (Na v). The skeletal muscle Na v (Na v1.4) channels in most pufferfish species and certain North American garter snakes are resistant to TTX, whereas in most mammals they are TTX-sensitive. It still remains unclear as to whether the difference in this sensitivity among the various vertebrate species can be associated with adaptive evolution. In this study, we investigated the adaptive evolution of the vertebrate Na v1.4 channels. By means of the CODEML program of the PAML 4.3 package, the lineages of both garter snakes and pufferfishes were denoted to be under positive selection. The positively selected sites identified in the p-loop regions indicated their involvement in Na v1.4 channel sensitivity to TTX. Most of these sites were located in the intracellular regions of the Na v1.4 channel, thereby implying the possible association of these regions with the regulation of voltage-sensor movement.