The systematic review and meta-analysis of X-ray detective rate of Kashin-Beck disease from 1992 to 2016.

BACKGROUND: Kashin-Beck disease (KBD) is a serious human endemic chronic osteochondral disease. However, quantitative syntheses of X-ray detective rate studies for KBD are rare. We performed an initial systematic review and meta-analysis to assess the X-ray detective rate of KBD in China. METHODS: For this systematic review and meta-analysis, we searched five databases (PubMed, Web of Science, Chinese National Knowledge Infrastructure (CNKI), WanFang Data and the China Science and Technology Journal Database (VIP))using a comprehensive search strategy to identify studies of KBD X-ray detective rate in China that were published from database inception to January 13, 2018. The X-ray detective rate of KBD was determined via an analysis of published studies using a random effect meta-analysis with the proportions approach. Subgroup analysis and meta-regression were used to explore heterogeneity, and study quality was assessed using the risk of bias tool. RESULTS: A total of 53 studies involving 14,039 samples with X-ray detective rate in 163,340 observations in total were included in this meta-analysis. These studies were geographically diverse (3 endemic areas). The pooled overall X-ray detective rate for KBD was 11% (95%CI,8-15%;Z = 13.14; p < 0.001). The pooled X-ray detective rate estimates were 11% (95%CI, 6-17%; Z = 7.06; p < 0.001) for northeast endemic areas, 13% (95%CI, 7-20%; Z = 7.45; p < 0.001) for northwest endemic areas, and 8% (95%CI, 5-12%; Z = 7.90; p < 0.001) for southwest endemic areas. There was a significant relationship between the survey year and the X-ray detective rate of KBD. CONCLUSIONS: Our systematic review found that the summary estimate of the X-ray detective rate of KBD was 11% and, that KBD X-ray positive rate ranged from 8.00 to 15.00% depending on the study. Further research is required to identify effective strategies for preventing and treating KBD.

Dietary exosome-miR-23b may be a novel therapeutic measure for preventing Kashin-Beck disease.

Previous studies have identified a close association between diet and the prevalence of Kashin-Beck disease (KBD); however, the mechanisms via which the diet protects against KBD-associated cartilage injury has remained elusive. Recent international research studies have revealed a therapeutic role of dietary exosome micro (mi)RNAs in repairing chondrocyte lesions by regulating genes and proteins associated with cellular apoptosis and extracellular matrix. Vital molecules affecting bio-functions of chondrocytes, including miR-23b and protein kinase cyclic AMP-activated catalytic subunit ß, were preliminarily identified to be dysregulated in cells and cartilage tissue of KBD patients. The function of dietary exosome in the repair of chondrocyte lesions in KBD is a novel topic in this field. It is worth exploring the protective role of dietary exosome-miR-23b against chondrocyte damage through the regulation of the protein kinase A (PKA) signaling pathway. The following aims are significant in future studies: i) To verify the association between exosome and cartilage damage in KBD patients; ii) to identify whether the protective mechanism of miR-23b in cartilage damage proceeds through regulating the PKA pathway; and iii) to explore the therapeutic role of dietary exosome-miR-23b in repairing chondrocyte lesions induced by environmental risk factors. These ideas may help establish the therapeutic role and mechanisms of dietary exosome-miR-23b in repairing chondrocyte lesions at the molecular, cellular and organismal level. These studies may simultaneously elucidate the disease pathogenesis and provide evidence for novel biomarkers and therapeutic methods for KBD.

Risk of severe pulmonary embolism in cancer patients receiving bevacizumab: Results from a meta-analysis of published and unpublished data.

To evaluate the association between severe pulmonary embolism events and bevacizumab, we conducted the first meta-analysis evaluating the incidence and risk of pulmonary embolism associated with bevacizumab-based therapy. We searched PubMed, EMBASE, Cochrane Library, and ClinicalTrials.gov up to September 2016 for randomized controlled trials comparing bevacizumab with no bevacizumab on cancer patients. Incidence rates, relative risks, and 95% confidence intervals were calculated using fixed- or random-effects models. The primary end point was the association of bevacizumab with pulmonary embolism. Subgroup analyses were performed according to tumor type, dose, and publication status. In total, 23 randomized controlled trials were included. For patients receiving bevacizumab, the overall incidence of severe pulmonary embolism events was 1.76% (95% confidence interval = 1.25%-2.27%). Cancer patients treated with bevacizumab did not increase the risk of pulmonary embolism events (relative risk = 1.00, 95% confidence interval = 0.80-1.25). No significant differences in pulmonary embolism incidence or risk among subgroup analyses were observed. No evidence of publication bias was observed. This study suggested that bevacizumab may not increase the risk of pulmonary embolism in cancer patients.