BACKGROUND:Little is known about associations of metal/metalloids (the widespread environmental pollutants) with ovarian reserve, and the underlying mechanisms. METHODS:We conducted a longitudinal study of 897 women (20-49 years) with 1958 repeated observations from two infertility centers in Hubei, China, and measured 22 serum metal/metalloids, C-reactive protein, cell-based inflammatory biomarkers, and anti-müllerian hormone (AMH) at baseline and follow-up surveys. We examined associations of metal/metalloid exposures with AMH levels and diminished ovarian reserve (DOR, defined as AMH < 1.1 ng/mL) risk using single- and multiple-metal/metalloid models, and explored the mediating role of inflammatory biomarkers. RESULTS:Of all observations, the median (P25, P75) of AMH levels was 2.81 (1.56, 4.90) ng/mL. Each 1-unit increment in log-transformed cobalt was cross-sectionally associated with 23.68% (13.57%, 32.60%) decreased AMH levels and 118% (33%, 255%) higher risk of DOR. Joint exposure to 22 metal/metalloids reduced AMH levels, with cobalt contributing the largest weight (0.3150) and posterior inclusion probability (0.9990). In longitudinal analyses, we observed decreased AMH levels in association with cobalt (13.61% [5.84%, 20.98%]), molybdenum (12.10% [2.60%, 20.76%]), and antimony (7.28% [0.26%, 13.79%]), and increased risks of DOR in association with nickel (1.23 [1.04, 1.46]), antimony (2.62 [1.62, 4.23]), and lead (1.32 [1.04, 1.66]). Additionally, white blood cell count, lymphocyte count, and percentage of monocyte mediated 7.15%-15.79% of the associations of cobalt with AMH levels and DOR risk. CONCLUSIONS:Our findings revealed the potential hazards of metal/metalloids on ovarian reserve, identified the key metal/metalloid specie (cobalt), and provided novel insights on inflammatory mechanisms for metal/metalloid-associated DOR.

BACKGROUND:There exists long-lasting concern, but no substantive evidence, that exercise may cause compensatory eating and compromise its glycemic benefits. We performed a randomized controlled, three-period crossover trial of moderate- and vigorous-intensity endurance exercise (MOD-EX and VIG-EX) intervention to fill this knowledge gap, which was also externally validated in the UK Biobank (UKB) cohort. METHODS:In total, 54 healthy college students (aged 22.2 ± 2.5 years) completed the 5-day WHO-recommended doses of MOD-EX, VIG-EX, or control treatments. Outcomes included dietary responses, assessed by daily weighed dietary logs in ad libitum eating condition, and glycemic control status, assessed both at fasting state and during oral glucose tolerance test (OGTT). Cox proportional hazard models were fitted to estimate associations of the interaction between physical activity (PA) and dietary intake with the risk of type 2 diabetes (T2D). RESULTS:MOD-EX and VIG-EX did not induce significant increases in total energy intake, but 15.67% (-13.5 kcal/day) decreased vegetable intake and 10.92% ( + 31.1 kcal/day) increased intake of added oil in food for VIG-EX (p < 0.05). MOD-EX and VIG-EX both reduced postprandial glucose (HbA1c: -3.82% [-6.40% to -1.24%] and -2.18% [-4.67% to 0.32%]; 2 h total area under the glucose curve (tAUC) during OGTT: -11.92% [-24.48% to 0.64%] and -13.48%, [-25.34% to -1.63%]). The effect had been masked by 7.52% and 10.85% from diet, respectively, primarily attributing to decreased fiber and increased saturated fatty acid (SFA) intakes ( | factors loadings | >0.4), exactly matching to dietary responses to exercise. Interaction analysis supported that higher fiber (p-interaction=0.022) and lower SFA (p-interaction=0.009) intakes augmented exercise-induced glycemic benefit, which was confirmed in the UKB study (N = 50 162) that participants with higher fiber or lower SFA intake showed more pronounced association between PA and reduced risk of incident type 2 diabetes (p-interaction=0.035). CONCLUSIONS:We provide evidence to recommend dietary fiber supplementation and SFA restriction accompanying exercise training to achieve maximum glycemic improvement. TRIAL REGISTRATION CHINESE CLINICAL TRIAL REGISTRY:ChiCTR2100055095. 2021/12/31. https://www.chictr.org.cn/showproj.html?proj=139665.

Association between heat exposure and diminished ovarian reserve (DOR) among women undergoing assisted reproductive technologies remains underexplored. We conducted a retrospective cohort study of 4296 women from a reproductive medicine center in Wuhan, China. Ambient temperature exposures were estimated based on the women's residential address and then averaged over short-term (1 month, 3 months, and 6 months) and long-term (1 year, 2 years, and 3 years) exposure windows. Heatwave exposure was defined using absolute (≥ 35°C) and relative (90th/95th percentiles) temperature thresholds over consecutive days (D2: >2 days; D3: >3 days), and was further categorized into high exposure (above median), low exposure (median and below) and no exposure. Multivariable logistic regression models were used to estimate odds ratios (ORs) for DOR (Anti-Müllerian hormone [AMH] < 1.1 ng/mL). Each standard deviation (SD) increase in mean, maximum, and apparent temperature over a 1-month period was associated with a 37 % (2 %-83 %), 36 % (2 %-80 %), and 55 % (4 %-131 %) higher odds of DOR. Compared to no exposure, 1-year heatwave exposure (35°C-D3) was associated with a 64 % (5 %-156 %) higher odds of DOR. Low-frequency heatwave exposure over 1 year (90th-D3: OR=1.33 [1.02-1.74]) and 3 years (95th-D2: OR=1.41 [1.08-1.70]) also showed significant associations, while high-frequency heat exposure did not exhibit such effects. Similarly, low-duration heatwave exposure over the 3-year period was associated with higher DOR risk. Higher temperatures and heatwaves exposure were associated with higher risk of DOR. Highlighting the needs to both short-term temperature variability and prolonged low-frequency heatwaves, rather than focusing solely on extreme high-intensity events.

The preservation of synaptic integrity and physiological activity is pivotal for post-traumatic auditory rehabilitation following acoustic overexposure. Neuritin, a neurotrophic factor that facilitates synapse formation, maturation, and enhanced synaptic transmission, is essential for synapse development. In this study, we established a noise-induced cochlear synaptopathy model in CBA/CaJ mice, revealing a temporal association between endogenous Neuritin expression and synaptic density. Furthermore, administration of recombinant Human Neuritin (rhNeuritin) effectively preserves synaptic density in the cochlear basal turn at 7 days and 14 days following noise exposure. Importantly, it preserves the density of functional synapses (represented by overlapping CtBP2 and GluA2 puncta) and synapse function (indicated by ABR I wave amplitudes), thus diminishing the impairment of auditory function. In addition, rhNeuritin reverses the decrease in phosphorylated extracellular signal-regulated protein kinase 1/2 (p-ERK1/2) levels resulting from noise exposure. By primarily preserving both the number and functionality of synapses in the basal turn, potentially via the induction of ERK1/2 phosphorylation, rhNeuritin mitigated hearing loss. These findings underscore the protective efficacy of rhNeuritin against noise-induced synaptic injury.

Little is known about the association of ambient ozone with ovarian reserve. Based on a retrospective cohort study of 6008 women who attended a fertility center in Hubei, China, during 2018-2021, we estimated ozone exposure levels by calculating averages during the development of follicles (2-month [W1], 4-month [W2], 6-month [W3]) and 1-year before measurement (W4) according to Tracking Air Pollution in China database. We used multivariate logistic regression and linear regression models to investigate association of ozone exposure with anti-mullerian hormone (AMH), the preferred indicator of ovarian reserve. Each 10 mu g/m(3) increases in ozone were associated with 2.34% (0.68%, 3.97%), 2.08% (0.10%, 4.01%), 4.20% (1.67%, 6.67%), and 8.91% (5.79%, 11.93%) decreased AMH levels during W1-W4; AMH levels decreased by 15.85%, 11.90%, 16.92% in the fourth quartile during W1, W3, and W4 when comparing the extreme quartile, with significant exposure response relationships during W4 (P < 0.05). Ozone exposure during W1 was positively associated with low AMH. Additionally, we detected significant effect modification by age, body mass index, and temperature in ozone-associated decreased AMH levels. Our findings highlight the potential adverse impact of ozone pollution on female ovarian reserve, especially during the secondary to small antral follicle stage and 1-year before measurement.

OBJECTIVE:Growing evidence suggests that alcohol consumption is a risk factor for hearing loss; however, the evidence has been inconsistent. This systematic review and meta-analysis aimed to evaluate the effect of alcohol consumption on hearing loss. METHODS:We searched several databases up to November 2021, for published articles using the keywords "alcohol drinking" and "hearing loss". Two investigators independently conducted the study selection and data extraction. Based on the results of the heterogeneity analysis (Q statistic and I2 statistic), a fixed- or random-effects model was used to calculate the pooled odds ratios (ORs). Subgroup and sensitivity analyses were performed to assess the potential sources of heterogeneity and robustness of the pooled estimation. Publication bias in the literature was evaluated using Egger's test. RESULTS:In total, 18 (9 cross-sectional, 5 case-control, and 4 cohort) observational studies were identified in this search; 27,849 participants were included. Compared with non-drinkers, the pooled OR of drinkers was 1.22 (95% confidence interval: 1.09-1.35). CONCLUSION:Evidence suggests a positive association between alcohol consumption and hearing loss. Drinkers were at a higher risk than non-drinkers. Drinking limitations may be useful for preventing hearing loss.

OBJECTIVES:Occupational noise-induced hearing loss (NIHL) is one of the most prevalent occupational diseases worldwide. Few studies have been reported on applying kurtosis-adjusted noise energy (e.g., kurtosis-adjusted cumulative noise exposure, CNE-K) as a joint indicator for assessing NIHL. This study aimed to analyze the effectiveness of CNE-K in assessing occupational hearing loss associated with complex noise in typical manufacturing industries. DESIGN:A cross-sectional survey of 1404 Chinese manufacturing workers from typical manufacturing industries was conducted. General demographic characteristics, noise exposure data, and noise-induced permanent threshold shifts (NIPTS) at 3, 4, and 6 kHz (NIPTS 346 ) were collected and analyzed. The role of kurtosis in high-frequency noise-induced hearing loss (HFNIHL) was also analyzed. The degree of overlap of the two logistic curves (i.e., between complex noise CNE-K and HFNIHL%, and between Gaussian noise CNE and HFNIHL%) was used to evaluate the effectiveness of CNE-K, using a stratified analysis based on age, sex, industry, or job type. RESULTS:The binary logistic regression analysis showed that in addition to age, sex, exposure duration, and Eight-hour Continuous Equivalent A-weighted Sound Pressure Level (L Aeq,8h ), kurtosis was a key factor influencing HFNIHL% in workers (odds ratio = 1.18, p < 0.05), and its odds ratio increased with an increase in kurtosis value. Multiple linear regression analysis demonstrated that the contribution of kurtosis to NIPTS 346 was second to L Aeq,8h . Complex noise led to a higher risk of NIHL than Gaussian noise at frequencies of 3, 4, 6, and 8 kHz after adjusting for age, sex, and CNE ( p < 0.05). As kurtosis increased, the notch in the audiogram became deeper, and the frequency at which the notch began to deepen shifted from 3 to 1 kHz. The logistic curve between complex noise CNE-K and HFNIHL% nearly overlapped with that between Gaussian noise CNE and HFNIHL%, and the average difference in HFNIHL% between the two curves decreased from 8.1 to 0.4%. Moreover, the decrease of average difference in HFNIHL% between the two logistic curves was evident in several subgroups, such as male workers, aged <30 and 30 to 50 years, furniture and woodworking industries and gunning and nailing job types with relatively high kurtosis values. CONCLUSIONS:Kurtosis, as an indirect metric of noise temporal structure, was an important risk factor for occupational NIHL. Kurtosis-adjusted CNE metric could be more effective than CNE alone in assessing occupational hearing loss risk associated with complex noise.

The causal association between circulating beta-carotene concentrations and cardiovascular disease (CVD) remains controversial. We conducted a Mendelian randomization study to explore the effects of beta-carotene on various cardiovascular diseases, including myocardial infarction, atrial fibrillation, heart failure, and stroke. Three single nucleotide polymorphisms (SNPs) associated with the beta-carotene levels were obtained by searching published data and used as instrumental variables. Genetic association estimates for 4 CVDs (including myocardial infarction, atrial fibrillation, heart failure, and stroke) in the primary analysis, blood pressure and serum lipids (high-density lipoprotein [HDL] cholesterol, LDL cholesterol, and triglycerides) in the secondary analysis were obtained from large-scale genome-wide association studies (GWASs). We applied inverse variance-weighted as the primary analysis method, and 3 others were used to verify as sensitivity analysis. Genetically predicted circulating beta-carotene levels (natural log-transformed, mu g/L) were positively associated with myocardial infarction (odds ratio [OR] 1.10, 95% confidence interval [CI] 1.02-1.18, P = .011) after Bonferroni correction. No evidence supported the causal effect of beta-carotene on atrial fibrillation (OR 1.02, 95% CI 0.96-1.09, P = .464), heart failure (OR 1.07, 95% CI 0.97-1.19, P = .187), stroke (OR 1.03, 95% CI 0.93-1.15, P = .540), blood pressure (P > .372) and serum lipids (P > .239). Sensitivity analysis produced consistent results. This study provides evidence for a causal relationship between circulating beta-carotene and myocardial infarction. These findings have important implications for understanding the role of beta-carotene in CVD and may inform dietary recommendations and intervention strategies for preventing myocardial infarction.

Background Noise energy has been well-established to increase the risk of occupational noise-induced hearing loss (NIHL). However, the role of noise temporal structure (expressed by kurtosis) or its combination with energy metrics (e.g., kurtosis-adjusted cumulative noise exposure, adj-CNE) in occupational NIHL was still unclear. Methods A cross-sectional survey of 867 Chinese workers, including 678 metal manufacturing workers and 189 workers exposed to Gaussian noise, was conducted. Noise energy metrics, including L Aeq,8h and CNE, kurtosis (β), and adj-CNE were used to quantify noise exposure levels. Noise-induced permanent threshold shift at frequencies 3, 4, and 6 kHz (NIPTS 346 ) and the prevalence of high-frequency NIHL (HFNIHL%) were calculated for each participant. The dose–response relationship between kurtosis or adj-CNE and occupational NIHL was observed. Results Among 867 workers, different types of work had specific and independent noise energy and kurtosis values ( p > 0.05). HFNIHL% increased with an increase in exposure duration (ED), L Aeq,8h , CNE, or kurtosis ( p < 0.01), and there were strong linear relationships between HFNIHL% and ED (coefficient of determination [ R 2 ] = 0.963), CNE ( R 2 = 0.976), or kurtosis ( R 2 = 0.938, when CNE < 100 dB(A)∙year). The “V” shape notching extent in NIPTS became deeper with increasing kurtosis when CNE < 100 dB(A)∙year and reached the notching bottom at the frequency of 4 or 6 kHz. The workers exposed to complex noise (β ≥ 10) had a higher risk of NIHL than those exposed to Gaussian noise (β < 10) at the frequencies of 3, 4, 6, and 8 kHz (OR > 2, p < 0.01). Moreover, HFNIHL% increased with adj-CNE ( p < 0.001). There were strong linear relationships between NIHL and adj-CNE or CNE when β ≥ 10 ( R 2 adj-CNE > R 2 CNE ). After CNE was adjusted by kurtosis, average differences in NIPTS 346 or HFNIHL% between the complex and Gaussian noise group were significantly reduced ( p < 0.05). Conclusion Kurtosis was a key factor influencing occupational NIHL among metal manufacturing workers, and its combination with energy metrics could assess the risk of NIHL more effectively than CNE alone.

BACKGROUND:Little is known about the associations of exposure to fine particulate matter (PM2.5) and its constituents with ovarian reserve, and the potential susceptible window of exposure remains unclear. METHODS:We performed a retrospective cohort study of 5189 women who attended a fertility center in Hubei, China, during 2019-2022, and estimated concentrations of PM2.5 and its major constituents during the development of follicles (4th-6th month [W1], 0-4th month [W2], 0-6th month [W3]) and 1-year before measurement (W4) based on Tracking Air Pollution in China database. We used multivariable linear regression and logistic regression models to examine the associations of PM2.5 and its constituent exposures with anti-Müllerian hormone (AMH), the preferred indicator of ovarian reserve. RESULTS:We observed significantly decreased AMH levels associated with increasing PM2.5 concentrations, with the percent changes (95 % confidence intervals [CIs]) of 1.99 % (0.24 %-3.71 %) during W1 and 3.99 % (0.74 %-7.15 %) during W4 for per 10 μg/m3 increases in PM2.5.When PM2.5 exposure levels were equal to 50th percentile (32.6-42.3 μg/m3) or more, monotonically decreased AMH levels and increased risks of low AMH were seen with increasing PM2.5 concentrations during W1 and W4 (P < 0.05). Black carbon (BC), ammonium (NH4+), nitrate (NO3-), and organic matter (OM) during W1, and NH4+, NO3-, as well as sulfate (SO42-) during W4 were significantly associated with decreased AMH. Moreover, PM2.5 and SO42- exposures during W4 were positively associated with low AMH. Additionally, the associations were stronger among women aged <35 years, lived in urban regions, or measured AMH in cold-season (P for interaction <0.05). CONCLUSION:PM2.5 and specific chemical components (particularly NH4+, NO3-, and SO42-) exposure during the secondary to antral follicle stage and 1-year before measurement were associated with diminished ovarian reserve (DOR), indicating the adverse impact of PM2.5 and its constituent exposures on female reproductive potential.

目的 运用Meta分析的方法评价CDH23基因rs1227049、rs1227051、rs3802711和Exon7多态性与噪声性听力损失(noise-induced hearing lose,NIHL)的相关性.方法 检索PubMed、Embase、Web of Science、中国知网、维普、万方数据库,收集有关CDH23基因rs1227049、rs1227051、rs3802711和Exon7多态性与NIHL相关性的研究,检索时限均为建库至2020年5月13日,采用RevMan5.3软件进行Meta分析.结果 共纳入6篇病例对照研究,病例组合计798例,对照组1112例.Meta分析结果表明,CDH23-rs3802711多态性与NIHL具有相关性(等位基因模型:OR=0.75,95％CI:0.55～1.01,P=0.06;显性模型:OR=1.08,95％CI:1.38,P=0.52;隐性模型:OR=2.94,95％CI:1.12～7.71,P=0.03;加性基因模型:OR=2.24,95％CI.0.97～5.14,P=0.06);CDH23-Exon7多态性与NIHL具有相关性(等位基因模型:OR =3.38,95％CI.1.84～6.22,P＜0.01;显性模型:OR=1.77,95％CI:0.79～3.97,P=0.17;隐性模型:OR =9.59,95％CI:28.20,P＜0.01;加性基因模型:OR=6.95,95％CI:2.86～16.86,P＜0.01);CDH23-rs1227049和rs1227051多态性与NIHL无相关性(P＞0.05).结论 CDH23-rs380271和Exon7多态性与NIHL的发病风险有显著相关性,但未发现rs1227049和rs1227051多态性与NIHL易感性有关.

目的 比较两种不同防护服脱卸方法对操作者造成二次污染的部位及各部位的污染情况.方法 将64名新入职或未接受过防护服穿脱培训的护士随机分为传统方法组和改良方法组,两组分别采用传统方法和改良方法进行个人防护服穿脱培训.培训结束进行操作考核,用荧光剂均匀喷洒在防护服特定部位的表面,并采用紫外荧光检测技术对不同防护服脱卸方法脱卸后二次污染部位及各部位的污染情况进行分析和比较.结果 两组脱卸防护服后的主要二次污染部位为鞋面、颈部、左前臂等;左半侧身体部位荧光剂污染率高于右半侧身体.改良方法组脱卸防护服的荧光剂污染部位数明显低于传统方法组,差异有统计学意义(P<0.05).结论 改良防护服脱卸法能较传统方法降低操作者二次污染的机会.

Background The associations of the proportion of vigorous physical activity (VPA) to moderate to vigorous physical activity (MVPA) with incident cardiovascular disease (CVD) and all-cause mortality are unclear. Methods The present study included 366,566 participants (aged 40–69 years) without baseline CVD from the UK biobank during 2006 to 2010. Cox regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for risks of outcomes. Results During a median 11.8 years of follow-up, among 366,566 participants (mean age [SD]: 56.0 [8.1]), 31,894 incident CVD and 19,823 total deaths were documented. Compared with no VPA, 0%-30% of VPA to MVPA was associated with 12% and 19% lower risks of incident CVD (HR, 0.88 [95% CI, 0.86–0.91]) and all-cause mortality (HR, 0.81 [95% CI, 0.78–0.84]), respectively. Furthermore, we found that the maximum reduction of risks of incident CVD and all-cause mortality occurred at performing approximately 30% of VPA to MVPA ( P < 0.001). Compared with participants reporting the lowest levels of MVPA (moderate physical activity [MPA], 0–150 min/week; VPA, 0–75 min/week), those performing 150–300 min/week of MPA and ≥ 150 min/week of VPA experienced the lowest risk of incident CVD (HR, 0.87 [95% CI, 0.79–0.95]) and all-cause mortality (HR, 0.71 [95% CI, 0.63–0.80]). Interestingly, we found that smokers yielded more cardiovascular benefits than non-smokers by performing a higher volume of VPA. Conclusions Comparing with UK adults reporting no VPA, engaging in 30% of VPA was associated with the lowest risk of incident CVD and all-cause mortality.

Background: Observational studies have suggested that there may be an association between telomere length (TL) and hearing loss (HL). However, inferring causality from observational studies is subject to residual confounding effects, reverse causation, and bias. This study adopted a two-sample Mendelian randomization (MR) approach to evaluate the causal relationship between TL and increased risk of HL. Methods: A total of 16 single nucleotide polymorphisms (SNPs) associated with TL were identified from a genome-wide association study (GWAS) meta-analysis of 78,592 European participants and applied to our modeling as instrumental variables. Summary-level data for hearing loss (HL), age-related hearing loss (ARHL), and noise-induced hearing loss (NIHL) were obtained from the recent largest available GWAS and five MR analyses were used to investigate the potential causal association of genetically predicted TL with increased risk for HL, including the inverse-variance-weighted (IVW), weighted median, MR-Egger regression, simple mode, and weighted mode. In addition, sensitivity analysis, pleiotropy, and heterogeneity tests were also used to evaluate the robustness of our findings. Results: There was no causal association between genetically predicted TL and HL or its subtypes (by the IVW method, HL: odds ratio (OR) = 1.216, p = 0.382; ARHL: OR = 0.934, p = 0.928; NIHL: OR = 1.003, p = 0.776). Although heterogenous sites rs2736176, rs3219104, rs8105767, and rs2302588 were excluded for NIHL, the second MR analysis was consistent with the first analysis (OR = 1.003, p = 0.572). Conclusion: There was no clear causal relationship between shorter TLs and increased risk of HL or its subtypes in this dataset.

Background and Objectives To investigate the association of change in leisure-time physical activity (LTPA) occurring during the postretirement period with incident stroke. Methods The current study enrolled 12,644 retired workers from the Dongfeng-Tongji cohort from April to October 2013. The change in LTPA was categorized as follows, according to whether the LTPA time met the WHO recommended minimum (at least 150 minutes per week): (1) stayed inactive at both surveys; (2) stayed inactive at the 2008 survey but became active at the 2013 survey; (3) stayed active at the 2008 survey but became inactive at the 2013 survey; (4) stayed active at both surveys. We used multivariable-adjusted Cox proportional hazards regression models to examine the association between change in LTPA and the risk of incident stroke. Results During 70,437 person-years of follow-up, we documented 549 incident stroke cases, including 434 incident ischemic stroke cases and 115 incident hemorrhagic stroke (HS) cases. Compared with participants who stayed active at both the 2008 and 2013 surveys, those who were active at the 2008 survey but became inactive at the 2013 survey had significantly higher risks of incident total stroke (hazard ratio [HR] 1.30, 95% CI 1.03, 1.65) and HS (HR 2.34, 95% CI 1.51, 3.63). When stratified by body mass index (BMI) categories, a significant elevated risk of total stroke was seen among overweight participants who stayed active at the 2008 survey but became inactive at the 2013 survey (HR 1.65, 95% CI 1.20, 2.27). The risk of incident stroke decreased with increasing LTPA levels between the 2 surveys (HR of per 150 min/wk increase of LTPA: HR 0.97, 95% CI 0.94, 1.00). In addition, we found that compared with participants who maintained their BMI and stayed active at both the 2008 and 2013 surveys, those who were inactive at both points or who became inactive had higher risks of stroke (HR 2.13, 95% CI 1.09, 4.15; HR 1.50, 95% CI 1.07, 2.08, respectively). Discussion Among Chinese older adults, increasing LTPA levels during the postretirement period was associated with a lower risk of incident stroke. Retired individuals should be encouraged to participate in LTPA more frequently to lessen future risk of incident stroke.

目的 探讨制造业工人噪声暴露特征与高频听力损失的关系.方法 采用典型抽样法,选择浙江省5家制造业工厂755名噪声作业工人为研究对象,测量其接触的8 h等效声级(LEX,8h)并记录噪声波形,计算累积噪声暴露量(CNE)和峰度;测试双耳纯音气导听阈.结果 研究对象的高频听力损失患病率(HFHL％)为19.3％(146/755),且HFHL％均随着CNE和峰度的增加而升高(P值均＜0.01).研究对象高频噪声诱发永久性听阈位移中位数为23.0 dB,其与CNE、LEX.8h和峰度均呈正相关(相关系数分别为0.24、0.19、0.17,P值均＜0.01).多因素Logistic回归分析结果显示,在排除性别和年龄等混杂因素的影响后,CNE、峰度均可导致罹患高频听力损失的风险增加[比值比及其95％可信区间分别为2.59(1.84～3.65)、1.53(1.20～1.95),P值均＜0.01].结论 制造业工人噪声暴露特征与其高频听力损失呈剂量-反应关系;除能量指标LEX,8h和CNE外,峰度也是影响高频听力损失的关键因素.

OBJECTIVE: In the present study, we evaluated the efficacy and safety of different stem cell types for spinal cord injury (SCI) therapy to determine the superior treatment of SCI. METHODS: A systematic literature search was performed using PubMed, Embase, the Cochrane Library, Web of Science, VIP, Chinese National Knowledge Infrastructure, and Wan Fang databases from initiation to January 30, 2021. A Bayesian network meta-analysis was performed using ADDIS (Aggregate Data Drug Information System) software. The PROSPERO registration number was CRD42020129635. RESULTS: We included 12 studies with 642 patients in the present study. A network meta-analysis revealed that bone mesenchymal stem cells (BMSCs) combined with rehabilitation training were significantly more effective than rehabilitation training alone in improving the American Spinal Injury Association (ASIA) impairment scale grade (odds ratio, 94.25; 95% confidence interval [CI], 6.71-9321.95), ASIA motor score (weighted mean difference [WMD], 6.67; 95% CI, 0.83-12.73), ASIA sensory functional score (WMD, 12.41; 95% CI, 3.42-21.72), and Barthel index (WMD, 7.24; 95% CI, 0.21-14.30). However, no statistically significant differences were observed between bone marrow mononuclear cells (MNCs) combined with rehabilitation training, umbilical cord-derived mesenchymal stem cells (UCMSCs) combined with rehabilitation training, or UCMSCs alone and rehabilitation alone for all indicators. In terms of safety, there were no serious and permanent adverse effects after transplantation of BMSCs, MNCs, or UCMSCs. CONCLUSIONS: BMSCs plus rehabilitation might be superior to other stem cell treatments of SCI in improving the ASIA impairment scale grade, ASIA motor score, ASIA sensory functional score, and Barthel index. The therapeutic effects of UCMSCs and MNCs remain to be confirmed.

BackgroundObservational studies suggest that frailty is associated with hearing loss (HL) but with inconsistent results. This study aims to examine such association and to assess its causality.Materials and methodsThe cross-sectional data from the National Health and Nutrition Examination Survey (NHANES). Multivariate logistic regression models were used to assess the association between HL and frailty index (FI). Genetic variants associated with the FI and HL were obtained from a large genome-wide association study (GWAS) meta-analysis and UK Biobank GWAS. The inverse variance weighting (IVW) method was used to estimate causal effects. Sensitivity analyses were performed to further validate the robustness of results.ResultsIn this cross-sectional analysis, results support the possibility that frailty may be associated with a higher risk of developing HL, with self-reported [odds ratio (OR) = 2.813; 95% CI, 2.386, 3.317; p < 0.001], speech frequency HL (OR = 1.975; 95% CI, 1.679–2.323; p < 0.001), and high frequency HL (OR = 1.748; 95% CI, 1.459–2.094; p < 0.001). In the adjusted model, frail participants remained at high risk of HL. Mendelian randomization (MR) studies showed a bidirectional causal association between genetically predicted FI and risk of HL (FI for exposure: OR = 1.051; 95% CI, 1.020–1.083; p = 0.001; HL for exposure: OR = 1.527; 95% CI, 1.227–1.901; p < 0.001).ConclusionOur observational study found that inter-individual differences in frailty were associated with the risk of developing HL. Genetic evidence suggests a potential bidirectional causal association between FI and HL. Furthermore, the potential mechanisms of this association require investigation.

OBJECTIVE:The effects of interactions between genetic and environmental factors on the noise-induced hearing loss (NIHL) are still unclear. This study aimed to assess interactions among gene polymorphisms, noise metrics, and lifestyles on the risk of NIHL.METHODS:A case-control study was conducted using 307 patients with NIHL and 307 matched healthy individuals from five manufacturing industries. General demographic data, lifestyle details, and noise exposure levels were recorded. The Kompetitive allele-specific polymerase chain reaction (KASP) was used to analyze the genotypes of 18 SNPs.RESULTS:GMDR model demonstrated a relevant interaction between NRN1 rs3805789 and CAT rs7943316 (P = 0.0107). Subjects with T allele of rs3805789 or T allele of rs7943316 had higher risks of NIHL than those with the SNP pair of rs3805789-CC and rs7943316-AA (P < 0.05). There was an interaction among rs3805789, rs7943316, and kurtosis (P = 0.0010). Subjects exposed to complex noise and carrying both rs3805789-CT and rs7943316-TT or rs3805789-CT/TT and rs7943316-AA had higher risks of NIHL than those exposed to steady noise and carrying both rs3805789-CC and rs7943316-AA (P < 0.05). The best six-locus model involving NRN1 rs3805789, CAT rs7943316, smoking, video volume, physical exercise, and working pressure for the risk of NIHL was found to be the interaction (P = 0.0010). An interaction was also found among smoking, video volume, physical exercise, working pressure, and kurtosis (P = 0.0107).CONCLUSION:Concurrence of NRN1 and CAT constitutes a genetic risk factor for NIHL. Complex noise exposure significantly increases the risk of NIHL in subjects with a high genetic risk score. Interactions between genes and lifestyles as well as noise metrics and lifestyles affect the risk of NIHL.

近年来,大量研究致力于鉴定可能与噪声性听力损失(noise-induced hearing loss,NIHL)易感性相关的候选基因单核苷酸多态性(single nucleotide polymorphisms,SNPs)的探讨,但尚未见对该领域研究成果的归纳总结.通过全面系统的检索,本文汇总了与NIHL相关的SNPs,并对NIHL易感基因多态性的研究现状进行综述,以期为该领域的研究方向提供科学的指导.