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For 4Mn steel, the deterioration of austenite stability caused by insufficient Mn content and the neglect of strength in intercritical annealing (IA) process are the main reasons limiting its application. In this study, based on the IA and quenching + partitioning (Q&P) process, a more suitable intercritically annealed quenching and partitioning (IQ&P) process for 4Mn steel was proposed. It is found that the IQ&P process can combine the advantages of IA and Q&P, and can obtain more austenite with sufficient stability by using quenching + partitioning process while maintaining ultra-fine grain size. While maintaining high plasticity (total elongation: 23.4%), the ultimate tensile strength of 4Mn steel is increased to more than 1200 MPa with the Lüders effect eliminated.

Our study aimed to investigate the association between the transition of the TXNIPgene methylation level and the risk of incident type 2 diabetes mellitus (T2DM). This study included 263 incident cases of T2DM and 263 matched non-T2DM participants. According to the methylation levels of five loci (CpG1–5; chr1:145441102-145442001) on the TXNIPgene, the participants were classified into four transition groups: maintained low, low to high, high to low, and maintained high methylation levels. Compared with individuals whose methylation level of CpG2–5 at the TXNIPgene was maintained low, individuals with maintained high methylation levels showed a 61–87% reduction in T2DM risk (66% for CpG2 [OR: 0.34, 95% CI: 0.14, 0.80]; 77% for CpG3 [OR: 0.23, 95% CI: 0.07, 0.78]; 87% for CpG4 [OR: 0.13, 95% CI: 0.03, 0.56]; and 61% for CpG5 [OR: 0.39, 95% CI: 0.16, 0.92]). Maintained high methylation levels of four loci of the TXNIPgene are associated with a reduction of T2DM incident risk in the current study. Our study suggests that preserving hypermethylation levels of the TXNIPgene may hold promise as a potential preventive measure against the onset of T2DM.

Aim: Noise exposure during pregnancy may be correlated with a higher risk of pregnancy complications, such as hypertensive disorders of pregnancy (HDP), gestational diabetes mellitus (GDM), and pre-eclampsia (PE). The link between noise and pregnancy complications, however, has been inconsistently reported. The objective of our study is to summarize the association of noise exposure throughout pregnancy with the risk of pregnancy complications. Subject and methods: PubMed, EMBASE, and Web of Science were comprehensively searched up to 5 March 2024 for published articles investigating the relationship between noise pollution and pregnancy complications (HDP, GDM, and PE). Random and fixed-effects models were used to aggregate relative risks (RRs) and 95% confidence intervals (95% CIs). Eligible studies were assessed for quality using the Newcastle Ottawa Scale and the Agency for Healthcare Research and Quality scale. Results: A total of 12 articles (16 studies) with 1,349,210 participants and 76,438 cases (30,569 with HDP, 20,192 with GDM, and 25,677 with PE) were incorporated into our study. The pooled RRs showed a positive association of noise with HDP (RR: 1.11, 95% CI: 1.01–1.21, I2= 27.2%) and GDM (RR: 1.24, 95% CI: 1.01–1.52, I2= 86.0%). The pooled RRs and 95% CI of PE risk with noise were 1.10 (95% CI: 0.99–1.22, I2= 16.5%). Conclusions: This meta-analysis demonstrated a strong correlation between noise exposure and a higher risk of HDP and GDM. It may therefore be advisable for women to restrict their exposure to noise during pregnancy in order to reduce the risk of pregnancy complications from that source.

Alcohol consumption remains inconsistently correlated with fracture risk, and a dose–response meta-analysis for specific outcomes is lacking. The objective of this study was to quantitatively integrate the data on the relationship between alcohol consumption and fracture risk. Pertinent articles were identified in PubMed, Web of Science, and Embase databases up to 20 February 2022. Combined RRs and 95% CIs were estimated by random- or fixed-effects models. Restricted cubic splines were used to model linear or nonlinear relationships. Forty-four articles covering 6,069,770 participants and 205,284 cases of fracture were included. The combined RRs and 95% CIs for highest compared with lowest alcohol consumption were 1.26 (1.17–1.37), 1.24 (1.13–1.35), and 1.20 (1.03–1.40) for total, osteoporotic, and hip fractures, respectively. A linear positive relationship between alcohol consumption and total fracture risk was detected (Pnonlinearity= 0.057); the risk was correlated with a 6% increase (RR, 1.06; 95% CI: 1.02, 1.10) per 14 g/d increment of alcohol consumption. J-shaped relationships of alcohol consumption with risk of osteoporotic fractures (Pnonlinearity< 0.001) and hip fractures (Pnonlinearity< 0.001) were found. Alcohol consumption of 0 to 22 g/d was linked to a reduced risk of osteoporotic fractures and hip fractures. Our findings show that any level of alcohol consumption is a risk factor for total fractures. Moreover, this dose–response meta-analysis shows that an alcohol consumption level of 0 to 22 g/d is related to a reduction in the risk of osteoporotic and hip fractures.

Although the association of dietary inflammatory potential, evaluated by the dietary inflammatory index (DII), with all-cause and cause-specific mortality has been reported, evidence remains equivocal, with no relevant dose–response meta-analysis having been conducted. To examine the dose–response association of dietary inflammatory potential with risk of all-cause, cancer, and cardiovascular disease (CVD) mortality, PubMed, Embase, and Web of Science were systematically searched up to August 9, 2021. Cohort studies were included if DII was reported as ≥3 levels or per incremental increase, and if the associations of DII with all-cause, cancer, and CVD mortality were assessed. Generalized least squares regression was used to estimate study-specific dose–response associations, and the random effect model was used to pool the RRs and 95% CIs of all-cause, cancer, and CVD mortality per 1-unit increase in DII. Restricted cubic splines were used to intuitively display the dose–response association between dietary inflammatory potential and mortality. Of the 1415 studies retrieved, 15 articles (17 cohort studies involving 397,641 participants) were included in this meta-analysis. With per 1-unit increase in DII, the risks were significantly increased for all-cause mortality (RR: 1.04; 95% CI: 1.03, 1.05, I2= 51.8%; P-heterogeneity = 0.009), cancer mortality (RR: 1.02; 95% CI: 1.00, 1.04, I2= 58.6%; P-heterogeneity = 0.013), and CVD mortality (RR: 1.04; 95% CI: 1.02, 1.06, I2= 85.7%; P-heterogeneity <0.001), respectively. Restricted cubic splines showed significant positive linear associations between DII and the above 3 outcomes. Our study indicated that proinflammatory diets can increase the risk of all-cause, cancer, and CVD mortality in a linear manner.