[Association between exposure to PM_(2.5) and chronic kidney disease in a population with metabolic syndrome].

OBJECTIVE: To investigate the association between long-term fine particulate matter(PM_(2.5)) exposure and the risk of chronic kidney disease(CKD) in people with abnormal metabolism syndrome(MS) components. METHODS: Based on health checkup data from a hospital in Beijing, a retrospective cohort study was used to collect annual checkup data from 2013-2019. A questionnaire was used to obtain information on demographic characteristics and lifestyle habits. We measured blood pressure, height, weight, waist circumference, concentrations of triglycerides(TG), fasting glucose, and high-density lipoprotein cholesterol(HDL-C). Longitude and latitude were also extracted from the addresses of the study subjects for pollutant exposure data estimation. Logistic regression models were used to explore the estimated effect of long-term PM_(2.5) exposure on the risk of CKD prevalence in people with abnormal MS components. Two-pollutant and multi-pollutant models were developed to test the stability of these result. Subgroup analysis was conducted based on age, the presence of MS, individual MS component abnormalities, and dual-component MS abnormalities. RESULTS: The study included 1540 study subjects with abnormal MS components at baseline, 206 with CKD during the study period. The association between long-term PM_(2.5) exposure and increased risk of CKD in people with abnormal MS fractions was statistically significant, with a 2.26-fold increase in risk of CKD for every 10 µg/m~3 increase in PM_(2.5) exposure(OR=3.26, 95% CI 2.72-3.90). The result in the dual-pollutant models and multi-pollutant models suggested that the association between long-term PM_(2.5) exposure and increased risk of CKD in people with abnormal MS fractions remained stable after controlling for contemporaneous confounding by other air pollutants. The result of subgroup analysis revealed that individuals aged 45 or older, without MS, with TG<1.7 mmol/L, HDL-C≥1.04 mmol/L, without hypertension, and with central obesity and high blood sugar had a stronger association between PM_(2.5) exposure and CKD-related health effects. CONCLUSION: Long-term exposure to PM_(2.5) may increase the risk of CKD in people with abnormal MS components. More attention should be paid to middle-aged and elderly people aged ≥45 years, people with central obesity and hyperglycemia.

Greater variability in HDL-C was associated with an increased risk of cognitive decline in the middle- and elderly Chinese: A cohort study.

BACKGROUND: Previous studies into relationship between high-density lipoprotein cholesterol (HDL-C) and cognitive decline were constrained to a single measurement, leaving the association between HDL-C variability and risk of cognitive decline unclear. METHODS: We identified 5930 participants from the China Health and Retirement Longitudinal Study (CHARLS) who were devoid for stroke, dementia, and memory-related diseases at baseline and underwent a minimum of 2 sequential health examinations during 2011-2015. Variability in HDL-C was defined as (1) variability independent of the mean (VIM), (2) average real variability (ARV), and (3) standard deviation (SD) of HDL-C change from baseline and follow-up visits. Cognitive function was evaluated in 2018 by Mini-mental state examination (MMSE) in the Chinese version. Logistic regression was employed to explore the association between HDL-C variability and cognitive decline. Odd ratios (OR) and 95 % confidence intervals (CI) were reported. RESULTS: The study included participants from CHARLS, mean age of 57.84±8.44 years and 44 % male. After adjustment for covariates, the highest quartile of VIM was associated with an increased risk of cognitive decline [OR:1.049, 95 %CI: 1.014-1.086] compared to the lowest quartile. For each SD increment of VIM, the OR was 1.015 (95 %CI:1.003-1.027). Strong dose-response relationships were identified (P for trend: 0.005). Consistent results were obtained for other measures of HDL-C variability (ARV and SD). Similar patterns were identified in different dimensions of cognition. CONCLUSIONS: Elevated HDL-C variability was associated with increased cognitive decline risk. Strategies to reducing HDL-C variability may lower the risks of cognitive decline among the general population.

Associations between sleep duration trajectories and cognitive decline: A longitudinal cohort study in China.

OBJECT: The relationship between sleep duration trajectories and cognitive decline remains uncertain. This study aims to examine the connections between various patterns of sleep duration and cognitive function. METHODS: Group-based trajectory modeling (GBTM) was employed to identify longitudinal trajectories of sleep duration over four-year follow-up period, while considering age, sex and nap duration as adjustments. Logistic regression was utilized to analyze the association between sleep trajectories and cognition, with odds ratios (OR) and 95 % confidence intervals (CI) reported. Subgroup analyses based on various demographic characteristics were conducted to explore potential differences in sleep trajectories and cognitive decline across different population subgroups. RESULTS: A total of 5061 participants were followed for four years, and three sleep duration trajectories were identified: high increasing (n = 2101, 41.6 %), stable increasing (n = 2087, 40.7 %), and low decreasing (n = 873, 17.7 %). After adjustment for basic demographic information, health status, and baseline cognition, the high increasing trajectory was found to be associated with cognitive decline in terms of global cognition (OR:1.52,95 %CI:1.18-1.96), mental intactness (OR:1.36,95 %CI:1.07-1.73) and episodic memory (OR:1.33, 95 %CI:1.05-1.67), as compared to stable increasing trajectory. These associations were particularly prominent among the non-elderly population (≤65 years) and those without depressive symptoms. CONCLUSION: This study suggests that both high increasing and low decreasing sleep duration trajectories are linked to cognitive decline, as compared to the stable increasing trajectory. Long-term attention to changes in sleep duration facilitates early prevention of cognitive decline.

Association and pathways of baseline and longitudinal hemoglobin A1c with the risk of incident stroke: A nationwide prospective cohort study.

AIMS: To investigate the association of baseline and long-term mean hemoglobin A1c (HbA1c) with the risk of stroke. METHODS: A total of 11,220 participants aged over 45 years and without stroke at baseline were enrolled from the China Health and Retirement Longitudinal Study. Mean HbA1c was calculated as the mean of HbA1c at all previous visits before stroke occurred or the end of follow-up. Multivariable-adjusted Cox regressions and Bayesian network were used for the analysis. RESULTS: During a median follow-up of 7.50 years, a total of 626 cases of stroke occurred. The risk of stroke increased with quintiles of baseline and mean HbA1c, the hazard ratio (HR) in Q5 versus Q1 was 1.30 (95 % confidence interval [CI],1.03-1.64) and 1.79 (95 % CI, 1.38-2.34), respectively. Per 1 unit increase in baseline and mean HbA1c was associated with 10 % (HR, 1.10; 95 % CI, 1.02-1.18) an 12 % (HR, 1.12; 95 % CI, 1.05-1.19) higher risk of stroke. Bayesian network analysis showed that the pathway from HbA1c to stroke was through hypertension, dyslipidemia, obesity, and inflammation. CONCLUSIONS: Elevated levels of both baseline and long-term HbA1c were associated with increased risk of stroke, and hypertension and obesity played an important role in the pathway.

Temporary relationship between sleep duration and depression and its impact on future risk of cardiovascular disease.

BACKGROUND: Although sleep duration and depression were correlated, their temporal sequence and how the sequence influence on future risk of cardiovascular disease (CVD) remained undetermined. This study aimed to explore the temporal relationship between sleep duration and depression, and its association with future CVD risk. METHODS: We included 10,629 middle-aged and elderly participants with repeated measurements of sleep duration and depressive symptoms (measured by Center for Epidemiological Studies-Depression scale [CESD]) at the first two visits from the China Health and Retirement Longitudinal Study. Cross-lagged analysis and mediation analysis were used to examine the temporal relationship between sleep duration and depression and its impact on future risk of CVD. RESULTS: The adjusted cross-lagged path coefficient from baseline sleep duration to follow-up CES-D (ß1 = -0.191; 95 % confidence interval [CI], -0.239 to -0.142) was significantly greatly than that from baseline CES-D to follow-up sleep duration (ß2 = -0.031; 95 % CI, -0.031 to -0.024) (Pdifference < 0.0001). Similarly, the path coefficient from baseline sleep duration to annual changes in CES-D was significantly greater than that from baseline CES-D to annual changes in sleep duration (ß1 = -0.093 versus ß2 = -0.015, Pdifference < 0.0001). The path coefficient from baseline sleep duration to follow-up CES-D in CVD group was significantly greater than that in those without CVD (Pdifference of ß1 = 0.0378). Furthermore, 27.93 % of the total association of sleep duration with CVD was mediated by depression symptoms. CONCLUSIONS: The findings provide evidence that decrease in sleep duration probably precedes the increased in depressive symptoms, and depression partially mediated the pathway from sleep duration to incident CVD.

Association of obesity with cardiovascular disease in the absence of traditional risk factors.

BACKGROUND: The association between obesity and cardiovascular disease (CVD) in people without traditional CVD risk factors is unclear. This study aimed to investigate the association of obesity with CVD and its subtypes in people without traditional CVD risk factors. METHODS: Based on the Kailuan cohort study, the included participants were divided into different groups according to levels of body mass index (BMI) and waist height ratio (WHtR), respectively. Multivariate Cox proportional hazard models were used to evaluate the associations. RESULTS: This study included 31,955 participants [men 63.99%; mean age (48.14 ± 3.33) years]. During a median follow-up period of 12.97 (interquartile range: 12.68-13.17) years, 1298 cases of CVD were observed. Compared with the normal BMI group, the hazard ratios (HRs) for CVD, stroke, and myocardial infarction (MI) in the BMI obese group were 1.31 (95% confidence interval [CI] 1.11-1.55), 1.21 (95%CI 1.01-1.46), 1.62 (95%CI 1.13-2.33), respectively. Compared with the WHtR non-obese group, the HRs for CVD, stroke, and MI in the obese group were 1.25(95%CI 1.11-1.41), 1.18 (95%CI 1.03-1.34), 1.57 (95%CI 1.18-2.09), respectively. There was an interaction between age and WHtR (P for interaction was 0.043). The association between WHtR and CVD was stronger in people under 60 years old, with a HR of 1.44 (95%CI 1.24-1.67). CONCLUSION: We found that obesity increased the risk of CVD in people without traditional CVD risk factors. The association of WHtR with CVD was stronger in people under 60 years old.

Association of cumulative blood glucose load with cardiovascular risk and all-cause mortality.

BACKGROUND: Incorporation both the magnitude and duration of exposure to elevated fasting blood glucose (FBG) into a single risk parameter (cumulative FBG load) for future diseases is intuitively appealing, although a data-based demonstration of the utility of this metric is not available. This study aimed to investigate the associations with cumulative FBG load with the risk of cardiovascular diseases (CVD) and all-cause mortality in the general population. METHODS: This prospective cohort study included 41,728 participants who were free of CVD and underwent four health examinations from 2006 to 2012. Cumulative FBG load during 2006-2012 was calculated as the area under curve for FBG values ≥ 5.6 mmol/L divided by the total area curve. We also compared the predicting value cumulative FBG load with other FBG metrics. RESULTS: During a median follow-up of 6.75 years, we identified 2323 cases of CVD and 1724 cases of all-cause mortality. Per 1-standard deviation increase in cumulative FBG load was associated with a 16 % higher risk of CVD (hazard ratio [HR]: 1.16; 95 % confidence interval [CI], 1.13-1.20) and 20 % higher risk of all-cause mortality (HR, 1.20; 95 % CI, 1.16-1.25). For the prediction of cardiovascular outcomes and all-cause mortality, cumulative FBG load outperformed FBG time-in-target, visit-to-visit FBG variability, and mean FBG in terms of C-statistics and reclassification indexes. CONCLUSIONS: Cumulative FBG load may provide a better prediction of cardiovascular outcomes compared with other FBG metrics in the general population. These findings emphasized the important role of cumulative FBG load in assessing cardiovascular and mortality risk.

Electrospun Nanofiber Materials for Photothermal Interfacial Evaporation.

Photothermal interfacial evaporation with low cost and environmental friendliness has attracted much attention. However, there are still many problems with this technology, such as heat loss and salt accumulation. Due to their different structures and adjustable chemical composition, electrospun nanofiber materials generally exhibit some unique properties that provide new approaches to address the aforementioned issues. In this review, the rational design principles for improving the total efficiency of solar evaporation are described for thermal/water management systems and salt-resistance strategies. And we review the state-of-the-art advancements in photothermal evaporation based on nanofiber materials and discuss their derivative applications in desalination, water purification, and power generation. Finally, we highlight key challenges and opportunities in both fundamental research and practical applications to inform further developments in the field of interfacial evaporation.

The impact of serum acid, arterial stiffness, and hypertension as a mediating factor: A cohort study.

BACKGROUND: Serum uric acid (SUA) has been associated with arterial stiffness. However, previous studies were limited to contradicting cross-sectional studies. This study aimed to examine the longitudinal association between SUA and the progression of arterial stiffness and the potential mechanisms. METHODS: Based on the Kailuan study, arterial stiffness progression was assessed by the annual growth rate of repeatedly measured brachial-ankle pulse wave velocity (baPWV). Generalized linear regression models were used to estimate the association of SUA with baseline arterial stiffness (n = 37,659) and arterial stiffness progression (n = 16,506), and Cox regressions were used to investigate the risk of incident arterial stiffness (n = 13,843). Mediation analysis was used to explore the potential mediators of the associations. RESULTS: Per standard deviation increase in SUA was associated with an 11.89 cm/s increment (95% confidence interval [CI], 8.60-15.17) in baseline baPWV and a 2.67 cm/s/yr increment in the annual growth rate of baPWV. During the 5.77-year follow-up, there were 1953 cases of incident arterial stiffness. Participants in the highest quartile of SUA had a 39% higher risk of arterial stiffness (HR, 1.39; 95% CI, 1.21-1.60), as compared with those in the lowest quartile of SUA. Furthermore, the observed associations were more pronounced in women than in men (Pint<0.05). The pathological pathway from high SUA to arterial stiffness was mainly mediated through hypertension (mediated proportion: 24.74%). CONCLUSIONS: Our study indicates that SUA was positively associated with the risk of arterial stiffness and its progression, especially in women. The association was mainly mediated through hypertension.

Cumulative Serum Uric Acid Exposure and Its Time Course With the Risk of Incident Stroke.

BACKGROUND: Evidence on the longitudinal associations between serum uric acid (SUA) and stroke was limited and yielded inconsistent conclusions. We aimed to investigate the associations of cumulative SUA (cumSUA), incorporating the time course of cumSUA accumulation, with the risk of stroke. METHODS: The prospective cohort study enrolled 50 871 participants from Kailuan, China. CumSUA from 2006 to 2010 was derived by calculating the means of SUA values between consecutive examinations and multiplying by time intervals between visits. Time course of cumSUA accumulation was categorized as the slope of SUA versus time or by splitting the overall accumulation into an early (cumSUA06-08) and late accumulation (cumSUA08-10). Participants were classified by cumSUA quartiles, SUA slope (negative versus positive), and the combined median cumSUA (1105.21 µmol/L×year) with SUA slope, respectively. The associations with incident stroke between 2010 and 2019 were evaluated with competing risk model. RESULTS: During a median follow-up of 9.02 years, 2217 cases of incident stroke were identified. In the multivariable-adjusted model, a higher risk of stroke was observed in participants with the highest quartile versus the lowest quartile of cumSUA (subdistribution hazard ratio, 1.15 [95% CI, 1.01-1.31]), and those with a negative versus positive SUA slope (subdistribution hazard ratio, 1.09 [95% CI, 1.01-1.19]). Consistently, a later accumulation of SUA was not associated with the risk of stroke after adjustment for an early accumulation, indicating early accumulation may contribute more to the risk of stroke than later accumulation. When cumSUA was incorporated with its time course, those with changes in cumSUA suggesting early accumulation had elevated risk of stroke (subdistribution hazard ratio, 1.17 [95% CI, 1.03-1.33]). Similar results were observed for ischemic stroke. CONCLUSIONS: Incident stroke risk was associated with cumulative exposure to SUA and its accumulation time course. Early SUA accumulation resulted in a greater risk compared with later accumulation, underscoring the importance of early control of SUA to an optimal level.

Association of Normal Serum Uric Acid Level and Cardiovascular Disease in People Without Risk Factors for Cardiac Diseases in China.

Background Healthy individuals with normal level of serum uric acid (SUA) may not be truly at the lowest risk of cardiovascular disease (CVD). This study aimed to assess the association of SUA levels with CVD and its subtypes in people without CVD risk factors and determine a suitable target of SUA to prevent CVD. Methods and Results We enrolled 25 284 participants who were free of CVD, absent of CVD risk factors, and with an SUA level between 180 and 359 µmol/L (3-6 mg/dL) at baseline from the Kailuan study. Cox proportional hazards models were applied to calculated adjusted hazard ratio (HR) and 95% CI for the risk of CVD and its subtypes. During a median follow-up of 12.97 years (interquartile range, 12.68-13.16 years), we identified 1007 cases of CVD. There was an increase in the risk of incident CVD with increasing SUA levels (Ptrend=0.0011). Compared with participants with SUA levels of 180 to 239 µmol/L (3-4 mg/dL), the HR of CVD was 1.12 (95% CI, 0.96-1.31) and 1.28 (95% CI, 1.08-1.52) for SUA levels of 240 to 299 µmol/L (4-5 mg/dL) and 300 to 359 µmol/L (5-6 mg/dL), respectively. A multivariable-adjusted spline regression model showed a J-shaped association between SUA and the risk of CVD. Similar results were observed for stroke and myocardial infarction. Conclusions The risk of incident CVD increased with elevating SUA levels among individuals without hyperuricemia or other traditional CVD risk factors. These findings highlighted the importance of primordial prevention for SUA level increase along with other traditional CVD risk factors.

Identification and validation of IgG N-glycosylation biomarkers of esophageal carcinoma.

Introduction: Altered Immunoglobulin G (IgG) N-glycosylation is associated with aging, inflammation, and diseases status, while its effect on esophageal squamous cell carcinoma (ESCC) remains unknown. As far as we know, this is the first study to explore and validate the association of IgG N-glycosylation and the carcinogenesis progression of ESCC, providing innovative biomarkers for the predictive identification and targeted prevention of ESCC. Methods: In total, 496 individuals of ESCC (n=114), precancerosis (n=187) and controls (n=195) from the discovery population (n=348) and validation population (n=148) were recruited in the study. IgG N-glycosylation profile was analyzed and an ESCC-related glycan score was composed by a stepwise ordinal logistic model in the discovery population. The receiver operating characteristic (ROC) curve with the bootstrapping procedure was used to assess the performance of the glycan score. Results: In the discovery population, the adjusted OR of GP20 (digalactosylated monosialylated biantennary with core and antennary fucose), IGP33 (the ratio of all fucosylated monosyalilated and disialylated structures), IGP44 (the proportion of high mannose glycan structures in total neutral IgG glycans), IGP58 (the percentage of all fucosylated structures in total neutral IgG glycans), IGP75 (the incidence of bisecting GlcNAc in all fucosylated digalactosylated structures in total neutral IgG glycans), and the glycan score are 4.03 (95% CI: 3.03-5.36, P<0.001), 0.69 (95% CI: 0.55-0.87, P<0.001), 0.56 (95% CI: 0.45-0.69, P<0.001), 0.52 (95% CI: 0.41-0.65, P<0.001), 7.17 (95% CI: 4.77-10.79, P<0.001), and 2.86 (95% CI: 2.33-3.53, P<0.001), respectively. Individuals in the highest tertile of the glycan score own an increased risk (OR: 11.41), compared with those in the lowest. The average multi-class AUC are 0.822 (95% CI: 0.786-0.849). Findings are verified in the validation population, with an average AUC of 0.807 (95% CI: 0.758-0.864). Discussion: Our study demonstrated that IgG N-glycans and the proposed glycan score appear to be promising predictive markers for ESCC, contributing to the early prevention of esophageal cancer. From the perspective of biological mechanism, IgG fucosylation and mannosylation might involve in the carcinogenesis progression of ESCC, and provide potential therapeutic targets for personalized interventions of cancer progression.

Temporal relationship between hyperuricemia and hypertension and its impact on future risk of cardiovascular disease.

BACKGROUND: Although hyperuricemia and hypertension are significantly correlated, their temporal relationship and whether this relationship is associated with risk of cardiovascular disease (CVD) are largely unknown. This study aimed to examine temporal relationship between hyperuricemia and hypertension, and its association with future risk of CVD. METHODS: This study included 60,285 participants from the Kailuan study. Measurement of serum uric acid (SUA), systolic and diastolic blood pressure (SBP and DBP) were obtained twice at 2006 (baseline) and 2010. Cross-lagged and mediation analysis were used to examine the temporal relationship between hyperuricemia and hypertension, and the association of this temporal relationship with CVD events risk after 2010. RESULTS: After adjusting for covariates, the cross-lagged path coefficients (ß1) from baseline SUA to follow-up SBP and DBP were significantly greatly than path coefficients (ß2) from baseline SBP and DBP to follow-up SUA (ß1=0.041 versus ß2=0.003; Pdifference<0.0001 for SBP; ß1=0.040 versus ß2=0.000; Pdifference<0.0001 for DBP). The path coefficients from baseline SUA to follow-up SBP and DBP in group with incident CVD were significantly greatly than that in group without incident CVD (Pdifference of ß1 in the two groups was 0.0018 for SBP and 0.0340 for DBP). Furthermore, SBP and DBP partially mediated the effect of SUA on incident CVD, the mediation effect was 57.64% for SBP and 46.27% for DBP. Similar mediated results were observed for stroke and myocardial infarction. CONCLUSION: Increased SUA levels probably precede elevated BP, and BP partially mediates the pathway from SUA to incident CVD.

Distinct hyperuricemia trajectories are associated with different risks of incident diabetes: A prospective cohort study.

BACKGROUND AND AIM: Conflicting results suggest a link between serum uric acid and diabetes and previous studies ignored the effect of continuous exposure of serum uric acid on diabetes risk. This study aims to characterize hyperuricemia trajectories in middle-aged adults and to examine its potential impact on diabetes risk, considering the role of obesity, dyslipidemia, and hypertension. METHODS AND RESULTS: The cohort included 9192 participants who were free of diabetes before 2013. The hyperuricemia trajectories during 2009-2013 were identified by latent class growth models. Incident diabetes during 2014-2018 was used as the outcome. Modified Poisson regression models were used to assess the association of trajectories with diabetes. Furthermore, marginal structural models were used to estimate the mediating effects of the relationship between hyperuricemia trajectories and diabetes. We identified three discrete hyperuricemia trajectories: high-increasing (n = 5794), moderate-stable (n = 2049), and low-stable (n = 1349). During 5 years of follow-up, we documented 379 incident diabetes cases. Compared with the low-stable pattern, the high-increasing pattern had a higher risk of developing diabetes (RR, 1.42; 95% CI: 1.09-1.84). In addition, the percentages of total effect between the high-increasing hyperuricemia pattern and diabetes mediated by obesity, dyslipidemia, and hypertension were 24.41%, 18.26%, and 6.29%. However, the moderate-stable pattern was not associated with an increased risk of diabetes. CONCLUSIONS: These results indicate that the high-increasing hyperuricemia trajectory is significantly associated with an increased risk of diabetes. Furthermore, obesity, dyslipidemia, and hypertension play mediating roles in the relationship between the high-increasing hyperuricemia pattern and increased diabetes risk.

Serum uric acid variation and the risk of cardiovascular disease: A prospective cohort study.

BACKGROUND: The association of serum uric acid (SUA) with cardiovascular disease (CVD) is inconsistent and limited by a single measurement of SUA. This study aimed to investigate the association of SUA variation, considering its magnitude and direction, with the risk of CVD. METHODS: This study included 41,578 participants with four biennial measurements of SUA during 2006-2012 from the Kailuan study. SUA variation was measured using the coefficient of variation (primary index), standard deviation, average real variability, and variability independent of mean, and the direction of variation was also assessed. Multivariate-adjusted Cox regressions were used to assess the associations, and Bayesian network was utilized to find the most important pathway from SUA variation to CVD. RESULTS: During a median follow-up of 6.74 (interquartile range: 6.45-7.03) years, we identified 1,852 (4.45%) cases of incident CVD. A large SUA variation (top vs. bottom tertiles) was associated with a higher risk of CVD (hazard ratio [HR], 1.24; 95% confidence interval [CI], 1.11-1.40), especially in older adults than that in young adults (Pint=0.0137). The higher risk of CVD was observed with both large rises (HR, 1.24; 95% CI, 1.10-1.39) and falls (HR, 1.19; 95% CI, 1.03-1.38) in SUA variation. The hazardous effect of SUA variation on CVD was mainly induced by excessive inflammation and elevated blood pressure. Similar results were observed for CVD subtypes. CONCLUSIONS: Elevated SUA variation was associated with a higher risk of CVD, irrespective of the direction of SUA variation, and inflammation played an important role in the pathway.

Cumulative burden of abnormal visceral adiposity index and its components on the risk of hyperuricemia.

BACKGROUND AND AIMS: The visceral adiposity index (VAI), a gender-specific surrogate maker of adipose tissue distribution and function, is associated with risk of hyperuricemia. However, the impact of time-burden of abnormal VAI and its components on the risk of hyperuricemia remains unknown. METHODS AND RESULTS: We included 56,537 participants without hyperuricemia and underwent two health examinations during 2006-2008 from the Kailuan study. Abnormal VAI burdens were evaluated as follows: (1) cumulative number of abnormal VAI presented at each examination (0-2 times); (2) cumulative number of each abnormal VAI component presented at each examination (0-2 times per component); (3) cumulative number of total abnormal VAI components presented at each examination (0-8 times). During a median follow-up of 8.81 years, 10,762 participants were diagnosed with hyperuricemia. The risk of hyperuricemia showed a positive association with cumulative number of abnormal VAI, the adjusted hazard ratio (HR) with 95% confidence interval (CI) of 2 times compared to 0 times was 1.69 (1.58-1.81). All four components of abnormal VAI, when diagnosed repeatedly, were independently associated with an increased risk of hyperuricemia, adjusted HR (95% CI) from 1.15 (1.02-1.28) for low high-density lipoprotein to 1.68 (1.58-1.79) for elevated triglyceride. The risk of hyperuricemia also gradually as abnormal components was accumulated from 0 to 8 counts, reaching an adjusted HR (95% CI) of 3.72 (2.64-5.23). Furthermore, the effect of cumulative abnormal VAI was more pronounced in females than males (P-interaction < 0.0001). CONCLUSIONS: Cumulative abnormal VAI burdens were positively associated with the risk of hyperuricemia, especially in females.

Association of serum uric acid to lymphocyte ratio, a novel inflammatory biomarker, with risk of stroke: A prospective cohort study.

MAIN PROBLEM: Inflammation plays an important role in the pathological progress associated with stroke. Serum uric acid (SUA) to lymphocyte ratio (ULR), a novel inflammatory biomarker, has been considered as a better risk stratification tool of adverse outcomes than SUA or lymphocyte alone. This study aimed to investigate whether ULR produced more predictive value for stroke and explore the potential mediators of the associations. METHODS: This study enrolled 93,023 Chinese participants without stroke and myocardial infarction at baseline. Cox proportional hazard models were used to analyze the associations of ULR with stroke and subtypes. Mediation analyses were conducted to explore potential mediators of the associations. RESULTS: During a median follow-up of 13.00 years, 6081 cases of incident stroke occurred, including 5048 cases of ischemic stroke (IS) and 900 cases of hemorrhagic stroke (HS). After adjustment for confounders, the Q4 group was associated with a higher risk of HS (HR, 1.25; 95% CI, 1.03-1.50), but not with total stroke (HR, 1.07; 95% CI, 1.03-1.13) or IS (HR, 1.04; 95% CI, 0.97-1.12). No significant associations were found between SUA or lymphocyte and any stroke. ULR outperformed SUA or lymphocytes alone in predicting stroke. Additionally, the significant association between ULR and HS was partially mediated by systolic blood pressure (20.32%), diastolic blood pressure (11.18%) and estimated glomerular filtration rate (9.19%). CONCLUSIONS: ULR was significantly associated with the risk of HS, but not with IS. Systolic blood pressure, diastolic blood pressure and estimated glomerular filtration rate were potential mediators for the association.

Long-term effects of PM2.5 components on hypertension: A national analysis in China.

BACKGROUND: Evidence is less about the associations between fine particulate matter (PM2.5) components and hypertension. We aimed to examine the long-term effects of PM2.5 components on prevalence of hypertension, diastolic blood pressure (DBP) and systolic blood pressure (SBP). METHODS: We included participants between March 1, and July 31, 2021, from 13 provinces in China. Geocoded residential address was used for exposure assignment. Mixed-effect regression was used to assess 3-year average concentrations of PM2.5 and its components (black carbon, organic matter, nitrate, ammonium, and sulfate) on prevalence of hypertension, DBP and SBP with covariate-adjusted. SHapley Additive exPlanation was used to compare the contribution of PM2.5 components to hypertension, DBP, and SBP. Sex and age subgroup were also analyzed. RESULTS: We enrolled a total of 113,159 participants aged ≥18 years. Long-term exposure to PM2.5 and its components (black carbon, organic matter, nitrate, ammonium, and sulfate) had associations with prevalence of hypertension, with the Odds Ratios and 95% confidence interval (CI) of 1.06 (95%CI: 1.03-1.09), 1.07 (95%CI: 1.04-1.09), 1.07 (95%CI: 1.04-1.10), 1.05 (95%CI: 1.01-1.08), 1.03 (95%CI: 1.00-1.06), and 1.03 (95%CI: 1.00-1.04), respectively. Effects of that except for black carbon on DBP with per interquartile upticks of concentration were 0.23 (95%CI: 0.11-0.35), 0.17 (95%CI: 0.04-0.29), 0.35 (95%CI: 0.21-0.48), 0.40 (95%CI: 0.28-0.52), and 0.25 (95%CI: 0.13-0.26), respectively. Ammonium was associated with SBP, corresponding to an increase of 0.18 (95%CI: 0.01-0.35). Males had higher risks of DBP (Z = 2.54-6.08, P < 0.001). Older people were substantially more affected by PM2.5 and its components. Nitrate showed the highest contribution to hypertension, DBP and SBP compared with other components. CONCLUSIONS: Long-term exposure to PM2.5 and its components had adverse consequences on prevalence of hypertension, DBP and SBP, especially for males and older people. Nitrate contributed the highest to hypertension, DBP and SBP. Findings may have implications for pollution and hypertension control.

Long-term exposure to PM2.5 and PM10 and chronic kidney disease: the Beijing Health Management Cohort, from 2013 to 2018.

Long-term exposure to ambient particulate pollutants (PM2.5 and PM10) may increase the risk of chronic kidney disease (CKD), but the results of previous research were limited and inconsistent. The purpose of this study was to assess the relationships of PM2.5 and PM10 with CKD. This study was a cohort study based on the physical examination data of 2082 Beijing residents from 2013 to 2018 in the Beijing Health Management Cohort (BHMC). A land-use regression model was used to estimate the individual exposure concentration of air pollution based on the address provided by each participant. CKD events were identified based on self-report or medical evaluation (estimated glomerular filtration rate, eGFR less than 60 ml/min/1.73 m2). Finally, the associations of PM2.5 and PM10 with CKD were calculated using univariate and multivariate logistic regression models. During the research period, we collected potentially confounding information. After adjusting for confounders, each 10 µg/m3 increase in PM2.5 and PM10 exposure was associated with an 84% (OR: 1.84; 95% CI: 1.45, 2.33) and 37% (OR: 1.37; 95% CI: 1.15, 1.63) increased risk of CKD. Adjusting for the four common gaseous air pollutants (CO, NO2, SO2, O3), the effect of PM2.5 and PM10 on CKD was significantly enhanced, but the effect of PM10 was no longer significant in the multi-pollutant model. The results of the stratified analysis showed that PM2.5 and PM10 were more significant in males, middle-aged and elderly people over 45 years old, smokers, drinkers, BMI ≥ 24 kg/m2, and abnormal metabolic components. In conclusion, long-term exposure to ambient PM2.5 and PM10 was associated with an increased risk of CKD.

Insulin resistance mediates obesity-related risk of cardiovascular disease: a prospective cohort study.

BACKGROUND: The mechanisms linking obesity to cardiovascular disease (CVD) are still not clearly defined. Individuals who are overweight or obese often develop insulin resistance, mediation of the association between obesity and CVD through the insulin resistance seems plausible and has not been investigated. This study aimed to evaluate whether and to what extend the effect of general and central obesity on cardiovascular disease (CVD) is mediated by insulin resistance. METHODS: A total of 94,136 participants without CVD at baseline were recruited from the Kailuan study. Insulin resistance was evaluated by the triglyceride-glucose (TyG) index, calculating as ln [fasting triglyceride (mg/dL) × fasting glucose (mg/dL)/2]. Mediation analysis using a new 2-stage regression method for survival data proposed by Valeri and VanderWeele was to explore the mediating effects of the TyG index on the association between obesity and CVD. RESULTS: During a median follow-up of 13.01 years, we identified 7327 cases of CVD. Mediation analyses showed that 47.81% of the total association (hazard ratio [HR], 1.18; 95% confidence interval [CI], 1.12-1.24) between overweight and CVD was mediated through the TyG index (HR [indirect association], 1.07; 95% CI, 1.07-1.09), and the proportion mediated was 37.94% for general obesity. For central obesity, analysis by waist circumference, waist/hip, and waist/height categories yielded an attenuated proportion mediated of 32.01, 35.02, and 31.06% for obesity, taken normal weight as reference. CONCLUSIONS: The association between obesity and CVD was mediated by TyG index, suggesting proper control of insulin resistance can be effective to reduce the effects of obesity on CVD.