The objective of this study was to investigate associations between carbohydrate intake/glycemic index (GI)/glycemic load (GL) and stroke risk. A literature search of MEDLINE, Embase, Web of Science, and CBM databases was performed to retrieve eligible studies published up to March 2014. Pooled relative risks (RRs) with 95% confidence intervals (CIs) were used to evaluate the strength of this association. Publication bias was assessed by the Egger's regression asymmetry test and Begg's rank correlation test with Begg's funnel plot. All analyses were conducted using software STATA 12.0 (StataCorp LP, College Station, TX) and SAS version 9.1 (SAS Institute Inc, Cary, NC). We identified 7 prospective studies that met the inclusion criteria and processed data from cohort studies to update available evidence. There were 25 independent estimates and 225 000 participants free of diabetes from 6 different countries; 3046 stroke events were included; and the follow-up range was 5 to 18 years. High GI was not associated with risk of stroke events (pooled RR = 1.10; 95% CI: 0.99-1.21); GL was a risk factor for stroke (pooled RR = 1.19; 95% CI: 1.05-1.36). There was no significant association between high carbohydrate intake and stroke risk (RR = 1.12; 95% CI: 0.93-1.35). A daily high GL diet is the risk factor of stroke event, and further researches need to verify the meta-analyses results and study associated mechanisms.
Purpose5-Fluorouracil (5-Fu) is used as a conventional chemotherapy drug in chemotherapy for patients with advanced colorectal cancer, but many patients still suffer from treatment failure due to 5-Fu resistance. Emerging observations revealed the important role of chemokine (C-X-C motif) ligand 13 (CXCL-13) in tumor microenvironment and its relationship with prognosis in patients with colorectal cancer. This study is designed to reveal the important role of CXCL-13 in causing colorectal cancer resistance to 5-Fu.Materials and MethodsCXCL-13 levels of patient's serum or cell culture supernatants were measured separately by enzyme-linked immunosorbent assay. In cell assays, cell viability is detected by Cell Counting Kit-8. Therefore, the recombinant human CXCL-13 was used to simulate its high expression in cells while its antibody and siRNA were used to reduce CXCL-13 expression in cells.ResultsIn this study, we demonstrated that CXCL-13 is associated with 5-Fu resistance by culture medium exchange experiments and cytokine arrays of colorectal cancer resistant and nonresistant cells. Clinical studies showed that CXCL-13 is highly expressed in the serum of 5-Fu–resistant patients. High levels of serum CXCL-13 also predict a worse clinical outcome. The addition of recombinant CXCL-13 cytokine resulted in 5-Fu resistance, while its antibody overcame 5-Fu resistance, and knockdown of CXCL-13 expression by siRNA also reduced 5-Fu resistance, which can be saved by added recombination CXCL-13.ConclusionThese results not only identify a CXCL-13 mediated 5-Fu resistance mechanism but also provide a novel target for 5-Fu–resistant colorectal cancer in prevention and treatment strategies.
ObjectiveOsteoporosis is a common disease in postmenopausal women. Several studies have analysed the associations between dietary supplementation with probiotics and bone health in postmenopausal women, but the results are still controversial. We conducted this meta-analysis to assess the effects of probiotics supplement on bone mineral density (BMD) and bone turnover markers for postmenopausal women.DesignSystematic review and meta-analysis.MethodsWe systematically searched PubMed, EMBASE and the Cochrane Library from their inception to November 2020 for randomised controlled trials (RCTs) assessing probiotic supplements and osteoporosis in postmenopausal women. Study-specific risk estimates were combined using random-effect models.ResultsFive RCTs (n=497) were included. Probiotic supplements were associated with a significantly higher BMD in the lumbar spine (standardised mean difference, SMD=0.27, 95% CI 0.09 to 0.44) than in control. There was no difference between probiotic supplements and BMD in hips (SMD=0.22, 95% CI −0.07 to 0.52). Collagen type 1 cross-linked C-telopeptide levels in the treatment groups were significantly lower than those of the placebo group (SMD=−0.34, 95% CI −0.60 to −0.09). In subgroup meta-analysis, levels of bone-specific alkaline phosphatase, osteoprotegerin, osteocalcin and tumour necrosis factor did not differ between the probiotic and placebo groups.ConclusionsWe conclude cautiously that supplementation with probiotics could increase lumbar BMD. More RCTs are recommended to validate or update these results.
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