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BACKGROUND Folate supplementation treatment is the first-line therapy in hyperhomocysteinaemia (HHcy). Up to 40% of HHcy patients do not benefit from folate therapy. Genetic and epigenetic factors of one-carbon metabolism (1-CM) might be identified as a predictor of folate supplementation treatment response. In the present study, we attempt to identify whether genetic and epigenetic factors might predict folate treatment response. METHODS A total of 230 patients with HHcy were involved in this prospective cohort study. Differences between baseline concentrations and concentrations obtained at 90 days of treatment were calculated to evaluate the treatment response. General linear models and Pearson correlation was used to explore associations among single-nucleotide polymorphisms (SNPs), DNA methylation, and folate treatment response. Finally, mediation analysis was performed to investigate whether DNA methylation of MTRR mediates the association between SNPs and treatment response. RESULTS MTHFD rs1950902 and MTRR rs162036, rs1801394 was associated with the folate treatment response (P = 0.000, 0.048, and 0.043, respectively). CBS and CBS_2 DNA methylation was significantly associated with folate treatment response (P = 0.0009 and less then 0.001). DNA methylation of MTHFR, MTR, and MTRR was also significantly associated with folate treatment response (P less then 0.001). DNA methylation of MTRR and MTRR_1 mediated 40.71% and 40.47% of the effect of rs1801394 on folate treatment response, respectively. CONCLUSIONS Our results indicated that the 1-CM gene SNPs and DNA methylation was associated with folate treatment response and can be further evaluated relationship between SNPs and DNA methylation in 1-CM with treatment response in a larger sample.An updated Cochrane Review showed that maternal supplementation with omega-3 fatty acids reduced preterm birth, offering a potential strategy for prevention. We hypothesised that pregnant women with obesity, at higher risk of preterm birth, would have low omega-3 fatty acid levels and may benefit from supplementation. Our study measured the omega-3 fatty acid levels of 142 participants from the Healthy Mums and Babies study, Counties Manukau, Auckland, New Zealand. Counties Manukau is a multi-ethnic community with high rates of socio-economic deprivation, obesity, and preterm birth. Red blood cell omega-3 fatty acid levels were measured from samples collected between 120 and 176 weeks' gestation. Contrary to our hypothesis, participants in our study had similar or higher levels of omega-3 fatty acids to those reported in pregnant populations in Australia, Norway, China, and Germany. Our findings emphasise the importance of testing omega-3 fatty acid status before supplementing groups at risk of preterm birth.BACKGROUND Dietary factors may play a role in bladder cancer etiology through modulation of inflammation. The purpose of this study was to examine the relationship between the inflammatory potential of diet, as estimated by the Dietary Inflammatory Index (DII®), and bladder cancer risk. METHODS Energy-adjusted DII (E-DIITM) scores were computed among 101,721 participants in the Prostate, Lung, Colorectal, and Ovarian (PLCO) study. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression analysis stratified by sex, with adjustment for smoking status and other confounding. RESULTS Over a median of 12.5 years of follow-up, 776 bladder cancer cases were diagnosed. E-DII scores were not associated with bladder cancer risk in the multivariable models. The HRs (95% CIs) in the highest compared with the lowest E-DII quintile were 0.90 (0.70-1.17) and 1.22 (0.72-2.06) for men and women, respectively. The associations did not differ when DII score was set as a continuous variable. The HRs (95% CIs) of one-unit increment in the E-DII for bladder cancer risk were 0.99 (0.96-1.02) and 1.01 (0.94-1.10) for men and women, respectively. CONCLUSIONS Our study does not support an association between inflammatory potential of diet, as estimated by the E-DII, and bladder cancer risk.We aimed to examine the association of weight gain during adulthood with the risk of cardiovascular disease (CVD) in the general population. We performed a systematic search of PubMed and Scopus, from inception to June 2019. Prospective cohort studies investigating the association of weight gain during adulthood with the risk of CVD were included. The relative risks (RRs) were calculated by using random-effect models. Twenty-three prospective cohort studies with 1,093,337 participants were included. The RRs for a 5-kg increment in body weight were 1.11 (95% CI 1.04, 1.19; I2 = 80%, n = 11) for CVD mortality, 1.18 (95% CI 1.04, 1.32; I2 = 90%, n = 8) for coronary heart disease (CHD), 1.08 (95% CI 1.04, 1.12; I2 = 0%, n = 3) for stroke, 1.18 (95% CI 1.12, 1.25; I2 = 0%, n = 2) for myocardial infarction and 1.05 (95% CI 0.86, 1.23; I2 = 80%, n = 2) for heart failure. A dose-response analysis demonstrated that the risk of CVD mortality was unchanged with weight gain of 0-5 kg, and then increased sharply and linearly (P for nonlinearity less then 0.001). The analysis of CHD indicated a sharp increase in risk from baseline up to weight gain equal to 25 kg (P for nonlinearity = 0.12). Ipatasertib mouse Adult weight gain may be associated with a higher risk of CVD. Measuring weight gain during adulthood may be better than static, cross-sectional assessment of weight because it considers trend over time, and thus, can be used as a supplementary approach to predict CVD.BACKGROUND Malnutrition is confirmed to be associated with poor outcomes in stroke patients. The present study aimed to confirm that being at risk of malnutrition assessed by Nutritional Risk Screening Tool 2002 (NRS-2002) and the Controlling Nutritional Status (CONUT) score predicts poor outcomes at 3 months in acute ischemic stroke (AIS) patients. METHODS In total, 682 patients with AIS were recruited within 7 days of stroke onset consecutively and 110 were dropped out. They were screened for risk of malnutrition using NRS-2002 and the CONUT score. The primary outcome is the follow-up modified Rankin Scale (mRS) score. Poor outcomes were defined as an (mRS) score ≥ 3 at 3 months post discharge. RESULTS There was a significant difference in the mRS score at 3 months between patients at risk of malnutrition compared to those not at risk assessed by NRS-2002(P less then 0.001) and CONUT (P = 0.011). The logistic regression model showed that the risk of malnourishment (according to NRS-2002), low risk of malnourishment (according to CONUT), and the moderate-to-severe risk of malnourishment (according to CONUT) were associated with higher risk of poor outcomes at 3 months (P less then 0.
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