Qian Wu

Hypertrophy of the ligamentum flavum (LF) contributes to lumbar spinal stenosis (LSS), and results mainly from fibrosis. Connective tissue growth factor (CTGF) is a profibrotic factor involved in the fibrotic process. This study aimed to evaluate CTGF expression in hypertrophied lumbar LF and the involvement of CTGF in LF hypertrophy. Ten patients with LSS were enrolled in this study. The control group included 10 patients with lumbar disc herniation. LF thickness was measured on the preoperative axial T1-weighted MRI. LF samples were collected during surgery. LF fibrosis was scored by Masson's trichrome staining. CTGF expression was determined by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry. Correlation between LF thickness and CTGF expression was analyzed. Human LF cells were cultured and treated with recombinant human (rh) CTGF. Expression of types I and III collagen was determined by real-time PCR and ELISA. The thickness and fibrosis scores of LF in the LSS group were higher than that in the control group (all P < 0.001). CTGF was expressed in the extracellular matrix of all ligament samples, and was significantly higher in the LSS group than that in the control group (P < 0.001). The increase of CTGF expression was positive correlation with the LF thickness (r = 0.969, P = 0.000). rhCTGF treatment increased the mRNA expression and protein synthesis of types I and III collagen of the LF cells (all P < 0.001). Our results suggest that the increased expression of CTGF is associated with hypertrophy of the LF in patients with LSS.

OBJECTIVE: To investigate the temporal trends in mortality and disease burden of injuries in Anhui province from 2008 to 2017, so as to provide reference for injury control and prevention. METHODS: Data of mortality were collected from 9 national surveillance points in Anhui province during 2008-2017 in the Information System for Death Cause Register and Management. The surveillance data were analyzed by using crude mortality, standardized mortality rate (SMR), potential year of life lost (PYLL), PYLL rate (PYLLR), and average of year life lost (AYLL). RESULTS: There were a total of 44855 people died from injury, accounted for 9.44% of the all-cause mortality, ranked as the fifth leading cause of deaths in the whole population, and denoted the first leading cause of deaths in the 0-44 year's group. The leading causes of injury deaths were road traffic accidents, suicide, accidental falls, drowning, and poisoning. Road traffic accidents was the primary cause of injury deaths among the male population, while suicide was the dominate cause of injury deaths among the female population. Drowning, traffic accidents, and suicide accounted for the most injury deaths among the population aged 0-14 years, 15-64 years, and above 60 years, respectively. The road traffic accidents accounted for the largest proportion of injury PYLL and PYLLR, and drowning caused the highest AYLL among injury deaths. CONCLUSION: In Anhui province, road traffic accidents, suicide, accidental falls, drowning, and poisoning were the top five causes of injury deaths that harm the health of local residents; corresponding injury prevention strategies should be formulated.

OBJECTIVES: Several studies have reported increased serum/plasma adiponectin levels in SLE patients. This study was performed to estimate the causal effects of circulating adiponectin levels on SLE. METHODS: We selected nine independent single-nucleotide polymorphisms that were associated with circulating adiponectin levels (P < 5 × 10-8) as instrumental variables from a published genome-wide association study (GWAS) meta-analysis. The corresponding effects between instrumental variables and outcome (SLE) were obtained from an SLE GWAS analysis, including 7219 cases with 15 991 controls of European ancestry. Two-sample Mendelian randomization (MR) analyses with inverse-variance weighted, MR-Egger regression, weighted median and weight mode methods were used to evaluate the causal effects. RESULTS: The results of inverse-variance weighted methods showed no significantly causal associations of genetically predicted circulating adiponectin levels and the risk for SLE, with an odds ratio (OR) of 1.38 (95% CI 0.91, 1.35; P = 0.130). MR-Egger [OR 1.62 (95% CI 0.85, 1.54), P = 0.195], weighted median [OR 1.37 (95% CI 0.82, 1.35), P = 0.235) and weighted mode methods [OR 1.39 (95% CI 0.86, 1.38), P = 0.219] also supported no significant associations of circulating adiponectin levels and the risk for SLE. Furthermore, MR analyses in using SLE-associated single-nucleotide polymorphisms as an instrumental variable showed no associations of genetically predicted risk of SLE with circulating adiponectin levels. CONCLUSION: Our study did not find evidence for a causal relationship between circulating adiponectin levels and the risk of SLE or of a causal effect of SLE on circulating adiponectin levels.