this meta-analysis reveals that older adults with diabetes mellitus are associated with greater risk of falls, and this association is more pronounced in insulin-treated patients.

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Objective: Xingnaojing injection (XNJ) is derived from An-Gong-Niu-Huang pill, a well-known traditional Chinese patent medicine, which is widely used for stroke. To evaluate the therapeutic effect of XNJ on cerebral infarction, an extensive meta-analysis was used.Methods: Six major electronic databases including the Chinese Biomedical Database (CBM), Wanfang, the VIP medicine information system (VMIS) and the China National Knowledge Infrastructure (CNKI), PubMed, Embase, and the Cochrane Library were examined to retrieve randomized controlled trials designed to evaluate the clinical efficacy of XNJ in treating CI before November 26, 2016.Results: There were 53 randomized controlled trials with 4915 participants in this study. The results reflected that compared with the conventional therapy (CT) alone, XNJ could significantly improve the overall response rate (OR = 3.56, 95% CI [2.94, 4.32], P < 0.00001), and clinical symptom (including increasing activities of daily living (ADL, MD = 10.23, 95% CI [9.47, 10.99], P < 0.00001), and reduce infarction size (MD = -1.83, 95% CI [-2.49, -1.16], P < 0.00001)). However, there was no significant difference between the XNJ treatment and conventional therapy in Glasgow Coma Scale (GCS, P = 0.32). Neurological deficit score demonstrated that XNJ could significantly reduce the score in two different evaluation criterions as National Institutes of Health Stroke Scale (NIHSS, MD = -3.44, 95% CI [-4.52, -2.36], P < 0.00001), and the Chinese Stroke Scale (CSS, MD = -5.72, 95% CI [-6.94, -4.50], P < 0.00001). Additionally, serum MMPs, including MMP-2 and MMP-9 were significantly reduced by XNJ treatment compared with conventional therapy (MD = -11.24, 95% CI [-20.83, -1.65], P = 0.02; MD = -25.08, 95% CI [-35.49, -14.67], P < 0.00001, respectively). Moreover, XNJ was able to improve hemorrheology in reducing whole blood viscosity, plasma viscosity, and hematocrit (MD = -1.44, 95% CI [-2.18, 0.70], P = 0.001; MD = -0.22, 95% CI [-0.37, -0.07], P = 0.003; MD = -3.63, 95% CI [-6.23, -1.03], P = 0.006, respectively). The therapeutic efficacy of XNJ was found associated with improving hemodynamics (increasing peak-flow rate, and average velocity) (MD = 12.66, 95% CI [10.50, 14.81], P < 0.00001; MD = 9.90, 95% CI [8.63, 11.17], P < 0.00001). XNJ was also related to reducing cholesterol and triglyceride (MD = -1.06, 95% CI [-1.21, -0.92], P < 0.00001; MD = -1.05, 95% CI [-1.12, -0.97], P < 0.00001).Conclusion: Despite the sample size and the poor quality of the included studies of this review, the results of the research showed that XNJ might be a beneficial therapeutic method for the treatment of cerebral infarction.

The T-cell immunoglobulin and mucin domain 3 (TIM-3) has been shown to be associated with susceptibility to rheumatoid arthritis (RA). In this study, we investigated the association of four single-nucleotide polymorphisms (SNPs) of the TIM-3 gene with RA susceptibility in Chinese Hui and Han groups. Using restriction fragment length or sequence-specific primer-polymerase chain reaction (PCR), patients with RA and nonarthritis control individuals from these two ethnicities were analysed for SNPs of -1541 C>T, -882 T>C, -574 T>G and +4259 G>T, in the TIM-3 gene. Our results demonstrated that the polymorphisms of +4259 G>T SNP of TIM-3 gene was associated with the RA susceptibility in both the Hui (P < 0.01) and Han populations (P < 0.05). However, the -1541 C>T and -574 T>G SNPs were distinctly associated with RA for the Hui and Han populations, respectively. In addition, haplotype analysis found no statistically differences in the distribution of nine detected haplotype frequency between patients with RA and controls in this study (P > 0.05). These findings suggest that polymorphism of +4259 G>T in TIM-3 gene may be one of the most important genetic factors associated with the RA susceptibility among different populations, and genetic variations of TIM-3 gene contribute to RA susceptibility among different populations.