Fine Particulate Matter Exposure, Genetic Susceptibility, and the Risk of Incident Stroke: A Prospective Cohort Study.

BACKGROUND: Both genetic factors and environmental air pollution contribute to the risk of stroke. However, it is unknown whether the association between air pollution and stroke risk is influenced by the genetic susceptibilities of stroke and its risk factors. METHODS: This prospective cohort study included 40 827 Chinese adults without stroke history. Satellite-based monthly fine particulate matter (PM2.5) estimation at 1-km resolution was used for exposure assessment. Based on 534 identified genetic variants from genome-wide association studies in East Asians, we constructed 6 polygenic risk scores for stroke and its risk factors, including atrial fibrillation, blood pressure, type 2 diabetes, body mass index, and triglyceride. The Cox proportional hazards model was applied to evaluate the hazard ratios and 95% CIs for the associations of PM2.5 and polygenic risk score with incident stroke and the potential effect modifications. RESULTS: Over a median follow-up of 12.06 years, 3147 incident stroke cases were documented. Compared with the lowest quartile of PM2.5 exposure, the hazard ratio (95% CI) for stroke in the highest quartile group was 2.72 (2.42-3.06). Among individuals at high genetic risk, the relative risk of stroke was 57% (1.57; 1.40-1.76) higher than those at low genetic risk. Although no statistically significant interaction was found, participants with both the highest PM2.5 and high genetic risk showed the highest risk of stroke, with ≈4× that of the lowest PM2.5 and low genetic risk group (hazard ratio, 3.55 [95% CI, 2.84-4.44]). Similar upward gradients were observed in the risk of stroke when assessing the joint effects of PM2.5 and genetic risks of blood pressure, type 2 diabetes, body mass index, atrial fibrillation, and triglyceride. CONCLUSIONS: Long-term exposure to PM2.5 was associated with a higher risk of incident stroke across different genetic susceptibilities. Our findings highlighted the great importance of comprehensive assessment of air pollution and genetic risk in the prevention of stroke.

Discordant High Remnant Cholesterol With LDL-C Increases the Risk of Stroke: A Chinese Prospective Cohort Study.

BACKGROUND: Previous studies focusing on assessing the effects of remnant cholesterol (RC) and low-density lipoprotein cholesterol (LDL-C) on stroke may not consider their mutual influence. We aimed to explore the associations of RC and discordant high RC with LDL-C with stroke, ischemic stroke (IS), and hemorrhagic stroke. METHODS: This prospective cohort study was conducted based on 3 cohorts of the China-PAR (Prediction for Atherosclerotic Cardiovascular Disease Risk in China) project. RC was calculated as non-high-density lipoprotein cholesterol minus LDL-C estimated by Martin/Hopkins equations. Concordant/discordant categories for RC versus LDL-C were determined based on cut-points of 130 mg/dL for LDL-C and equivalent percentile (32.50 mg/dL) for RC. Cox models were used to estimate adjusted hazard ratios and 95% CIs for incident stroke. RESULTS: Among 113 448 participants recruited at baseline, a total of 98 967 participants were eligible for the final analysis (mean age of 51.44 years; 40.45% were men). During 728 776.87 person-years of follow-up, 2859 stroke cases, 1811 IS cases, and 849 hemorrhagic stroke cases were observed. RC was positively associated with stroke and IS, but not hemorrhagic stroke, with adjusted hazard ratios (95% CIs) of 1.06 (1.02-1.10), 1.09 (1.04-1.13), and 0.95 (0.88-1.03) for per SD increase in RC. Compared with low LDL-C/low RC group, low LDL-C/high RC group had higher risks of stroke (adjusted hazard ratio, 1.15 [95% CI, 1.02-1.30]) and IS (1.19, 1.03-1.38), while high LDL-C/low RC group had no increased risk of stroke (1.07 [0.95-1.20]) and IS (1.09 [0.94-1.25]). CONCLUSIONS: Higher RC was associated with increased risks of stroke and IS but not hemorrhagic stroke. Discordantly high RC, not discordantly high LDL-C, conferred higher risks of stroke and IS. Our findings support further lowering RC by interventions to reduce residual IS risk.

Exploring the relationship between infectious agents and autoimmune diseases: a review.

The relationship between infectious agents and autoimmune diseases is a complex issue. In recent years, increasing clinical cases have indicated that infectious agents play an important role in the development of autoimmune diseases. Molecular mimicry is currently widely regarded as the primary pathogenic mechanism of various autoimmune diseases in humans. Components of infectious agents can undergo molecular mimicry with components in patients' bodies, leading to the development of various autoimmune diseases. In this article, we provide a brief overview of current research of the current research status on the relationship between infectious agents and autoimmune diseases, and describe our current understanding of their mechanisms of action in order to better understand the pathogenesis, diagnosis, and treatment of autoimmune diseases.

The impact of sestrin2 on reactive oxygen species in diabetic retinopathy.

Diabetic retinopathy (DR) is a significant complication of diabetes that often leads to blindness, impacting Müller cells, the primary retinal macroglia involved in DR pathogenesis. Reactive oxygen species (ROS) play a crucial role in the development of DR. The objective of this study was to investigate the involvement of sestrin2 in DR using a high-glucose (HG)-induced Müller cell model and assessing cell proliferation with 5-ethynyl-2-deoxyuridine (EdU) labeling. Following this, sestrin2 was upregulated in Müller cells to investigate its effects on ROS, tube formation, and inflammation both in vitro and in vivo, as well as its interaction with the nuclear factor erythroid2-related factor 2 (Nrf2) signaling pathway. The findings demonstrated a gradual increase in the number of EdU-positive cells over time, with a subsequent decrease after 72 h of exposure to high glucose levels. Additionally, the expression of sestrin2 exhibited a progressive increase over time, followed by a decrease at 72 h. The rh-sestrin2 treatment suppressed the injury of Müller cells, decreased ROS level, and inhibited the tube formation. Rh-sestrin2 treatment enhanced the expression of sestrin2, Nrf2, heme oxygenase-1 (HO-1), and glutamine synthetase (GS); however, the ML385 treatment reversed the protective effect of rh-sestrin2. Finally, we evaluated the effect of sestrin2 in a DR rat model. Sestrin2 overexpression treatment improved the pathological injury of retina and attenuated the oxidative damage and inflammatory reaction. Our results highlighted the inhibitory effect of sestrin2 in the damage of retina, thus presenting a novel therapeutic sight for DR.

Multimorbidity, healthy lifestyle, and the risk of cognitive impairment in Chinese older adults: a longitudinal cohort study.

BACKGROUND: Evidence on the association between multimorbidity and cognitive impairment in Chinese older population is limited. In addition, whether a healthy lifestyle can protect cognitive function in multimorbid older population remains unknown. METHODS: A total of 6116 participants aged ≥ 65 years from the Chinese Longitudinal Healthy Longevity Survey were followed up repeatedly. The number of coexisting chronic diseases was used for assessing multimorbidity and cardiometabolic multimorbidity. Three lifestyle statuses (unhealthy, intermediate, and healthy) were defined based on a lifestyle score covering smoking, alcohol drinking, body mass index, outdoor activities, and dietary pattern. Cognitive impairment was defined as the Mini-Mental State Examination score < 24. A modified Poisson regression model with robust error variance was used to assess the associations between multimorbidity, healthy lifestyle, and cognitive impairment. RESULTS: During a median follow-up period of 5.8 years, 1621 incident cases of cognitive impairment were identified. The relative risk (RR) of cognitive impairment associated with heavy multimorbidity burden (≥ 3 conditions) was 1.39 (95% confidence interval: 1.22-1.59). This association declined with age, with RRs being 3.08 (1.78-5.31), 1.40 (1.04-1.87), and 1.19 (1.01-1.40) in subjects aged < 70 years, ≥ 70 and < 80 years, and ≥ 80 years, respectively (P for interaction = 0.001). Compared to unhealthy lifestyle, a healthy lifestyle was related to an approximately 40% reduced risk of cognitive impairment regardless of multimorbidity burden. Among the 5 lifestyle factors assessed, daily outdoor activities and a healthy dietary pattern showed convincing protective effects on cognitive function. CONCLUSIONS: The relationship between multimorbidity and cognitive impairment is age-dependent but remains significant in the population aged 80 years or older. A healthy lifestyle may protect cognitive function regardless of the multimorbidity burden. These findings highlight the importance of targeting individuals with heavy multimorbidity burden and promoting a heathy lifestyle to prevent cognitive impairment in Chinese older population.

Outdoor fine particulate matter exposure and telomere length in humans: A systematic review and meta-analysis.

Although the association between changes in human telomere length (TL) and ambient fine particulate matter (PM2.5) has been documented, there remains disagreement among the related literature. Our study conducted a systematic review and meta-analysis of epidemiological studies to investigate the health effects of outdoor PM2.5 exposure on human TL after a thorough database search. To quantify the overall effect estimates of TL changes associated with every 10 µg/m3 increase in PM2.5 exposure, we focused on two main topics, which were outdoor long-term exposure and prenatal exposure of PM2.5. Additionally, we included a summary of short-term PM2.5 exposure and its impact on TL due to limited data availability. Our qualitative analysis included 20 studies with 483,600 participants. The meta-analysis showed a statistically significant association between outdoor PM2.5 exposure and shorter human TL, with pooled impact estimates (ß) of -0.12 (95% CI: -0.20, -0.03, I2= 95.4%) for general long-term exposure and -0.07 (95% CI: -0.15, 0.00, I2= 74.3%) for prenatal exposure. In conclusion, our findings suggest that outdoor PM2.5 exposure may contribute to TL shortening, and noteworthy associations were observed in specific subgroups, suggesting the impact of various research variables. Larger, high-quality studies using standardized methodologies are necessary to strengthen these conclusions further.

Family Resilience and Its Influencing Factors in Patients With Cancer and Their Family Members: A Systematic Review.

AIMS: This review aims to explore factors influencing family resilience in families providing care for patients with cancer and to provide suggestions for future research directions. METHODS: Six electronic databases were searched including Web of Science, CINAHL, EMBASE, PsycINFO, PubMed and CNKI from their inception to December 2023. The article reference lists were also manually searched. The Mixed Method Appraisal Tool was used to assess the included studies in this review. The 27-item checklist Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement was followed to report this review. RESULTS: Twenty-one studies from six online databases reported that either individual or family factors have effects on family resilience and were described into five clusters on the basis of the Walsh model of family resilience, including demographic and clinical factors, personal strengths and resources, family stressors, family resilient coping processes and family resilient adaptation outcomes. CONCLUSION: Family resilience in cancer families plays a pivotal role in coping with family stressors and facilitating positive outcomes through domains of coping. Future researches need to explore factors related to family resilience from dyadic perspectives and to establish multidisciplinary intervention strategies for developing levels of family resilience in cancer families. TRIAL REGISTRATION: PROSPERO: CRD42024535349.

Research progress on the application of single-cell sequencing in autoimmune diseases.

Autoimmune diseases (AIDs) are caused by immune tolerance deficiency or abnormal immune regulation, leading to damage to host organs. The complicated pathogenesis and varied clinical symptoms of AIDs pose great challenges in diagnosing and monitoring this disease. Regrettably, the etiological factors and pathogenesis of AIDs are still not completely understood. It is noteworthy that the development of single-cell RNA sequencing (scRNA-seq) technology provides a new tool for analyzing the transcriptome of AIDs. In this essay, we have summarized the development of scRNA-seq technology, and made a relatively systematic review of the current research progress of scRNA-seq technology in the field of AIDs, providing a reference to preferably understand the pathogenesis, diagnosis, and treatment of AIDs.

Characterisation of T and B cell receptor repertoire in patients with systemic lupus erythematosus.

OBJECTIVES: Systemic lupus erythematosus (SLE) is an autoimmune disease with extreme heterogeneity, marked clinically by multi-systemic inflammatory involvement. However, the molecular mechanism of breakdown of self-tolerance is still unclear. T cell/B cell-mediated immune disorders may play a vital role in the pathogenesis of SLE. METHODS: In this context, we used a combination of multiplex-PCR, Illumina sequencing and IMGT/HighV-QUEST for a standardised analysis of the T cell receptor ß-chain (TCRß) and B cell receptor H-chain (BCR-H) repertoire of peripheral blood mononuclear cells in SLE patients compared with healthy volunteers. RESULTS: The results showed that there was an obvious reduction in BCR-H repertoire diversity and BCR-H CDR3 length in SLE patients. Notably, the pre-selection BCR-H CDR3s in SLE patients also displayed abnormal shortening, which suggests that early events in bone marrow B cell development and repertoire generation were abnormal in SLE patients. However, there was no obvious change of T cell repertoire in SLE patients, including repertoire diversity and CDR3 length. In addition, there was skewed usage of V genes and CDR3 sequences in SLE patients, which might be the result of physiological responses to environmental antigens or pathogens. CONCLUSIONS: In conclusion, our data revealed the specific changes of the TCR and BCR repertoires in SLE patients, which may provide new ideas for its prevention and treatment.

Association of Long-Term Exposure to Ambient Fine Particulate Matter with Atherosclerotic Cardiovascular Disease Incidence Varies across Populations with Different Predicted Risks: The China-PAR Project.

Previous studies have established a significant link between ambient fine particulate matter (PM2.5) exposure and atherosclerotic cardiovascular disease (ASCVD) incidence, but whether this association varies across populations with different predicted ASCVD risks was uncertain previously. We included 109,374 Chinese adults without ASCVD at baseline from the Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR) project. We obtained PM2.5 data of participants' residential address from 2000 to 2015 using a satellite-based spatiotemporal model. Participants were classified into low-to-medium and high-risk groups according to the ASCVD 10-year and lifetime risk prediction scores. Hazard ratios (HRs) and 95% confidence intervals (CIs) for PM2.5 exposure-related incident ASCVD, as well as the multiplication and additive interaction, were calculated using stratified Cox proportional hazard models. The additive interaction between risk stratification and PM2.5 exposure was estimated by the synergy index (SI), the attributable proportion due to the interaction (API), and the relative excess risk due to interaction (RERI). Over the follow-up of 833,067 person-years, a total of 4230 incident ASCVD cases were identified. Each 10 µg/m3 increment of PM2.5 concentration was associated with 18% (HR: 1.18; 95% CI: 1.14-1.23) increased risk of ASCVD in the total population, and the association was more pronounced among individuals having a high predicted ASCVD risk than those having a low-to-medium risk, with the HR (95% CI) of 1.24 (1.19-1.30) and 1.11 (1.02-1.20) per 10 µg/m3 increment in PM2.5 concentration, respectively. The RERI, API, and SI were 1.22 (95% CI: 0.62-1.81), 0.22 (95% CI: 0.12-0.32), and 1.37 (95% CI: 1.16-1.63), respectively. Our findings demonstrate a significant synergistic effect on ASCVD between ASCVD risk stratification and PM2.5 exposure and highlight the potential health benefits of reducing PM2.5 exposure in Chinese, especially among those with high ASCVD risk.

Shift work and nonalcoholic fatty liver disease incidence among Chinese rail workers: a 4-year longitudinal cohort study.

PURPOSE: Occupational harmful factors, such as shift work, are attracting increasing attention as a potential cause of nonalcoholic fatty liver disease (NAFLD). In this study, we aimed to identify the association between shift work and NAFLD incidence in Chinese rail population. METHODS: A cohort study was conducted among 14,112 rail workers for 4-year follow-up. Shift work frequency and other potential variables were recorded by questionnaires, including demographic, lifestyle, and occupation information. Besides, body mass index, blood pressure, fasting blood glucose, total cholesterol, triglyceride, alanine aminotransferase, and aspartate aminotransferase were measured by anthropometric measurement and blood test. Diagnosis of new NAFLD case was based on abdominal ultrasonography. Cox proportional hazards regression model was used to determine whether shift work has effect on occurrence of NAFLD. RESULTS: The incidence of NAFLD was 30.43% in total subjects. After adjustment for possible confounders, the RRs of NAFLD were 1.069 (95% CI 0.998-1.146) and 1.179 (95% CI 1.059-1.312) in occasionally shift work group and frequently shift work group respectively, compared to the seldom shift work group. In stratified analyses, the RRs of NAFLD incidence linked to shift work exposure seems increase among female and elder. The results of three sensitivity analyses were similar with main analysis. CONCLUSIONS: This research provided further evidence of positive harmful effect of shift work on NAFLD incidence in Chinese rail workers, particularly in frequently shift work population. The risk estimate of shift work on NAFLD was higher in female and elder.

The 17-y spatiotemporal trend of PM2.5 and its mortality burden in China.

Investigations on the chronic health effects of fine particulate matter (PM2.5) exposure in China are limited due to the lack of long-term exposure data. Using satellite-driven models to generate spatiotemporally resolved PM2.5 levels, we aimed to estimate high-resolution, long-term PM2.5 and associated mortality burden in China. The multiangle implementation of atmospheric correction (MAIAC) aerosol optical depth (AOD) at 1-km resolution was employed as a primary predictor to estimate PM2.5 concentrations. Imputation techniques were adopted to fill in the missing AOD retrievals and provide accurate long-term AOD aggregations. Monthly PM2.5 concentrations in China from 2000 to 2016 were estimated using machine-learning approaches and used to analyze spatiotemporal trends of adult mortality attributable to PM2.5 exposure. Mean coverage of AOD increased from 56 to 100% over the 17-y period, with the accuracy of long-term averages enhanced after gap filling. Machine-learning models performed well with a random cross-validation R2 of 0.93 at the monthly level. For the time period outside the model training window, prediction R2 values were estimated to be 0.67 and 0.80 at the monthly and annual levels. Across the adult population in China, long-term PM2.5 exposures accounted for a total number of 30.8 (95% confidence interval [CI]: 28.6, 33.2) million premature deaths over the 17-y period, with an annual burden ranging from 1.5 (95% CI: 1.3, 1.6) to 2.2 (95% CI: 2.1, 2.4) million. Our satellite-based techniques provide reliable long-term PM2.5 estimates at a high spatial resolution, enhancing the assessment of adverse health effects and disease burden in China.

Effects of PM2.5 and high-fat diet interaction on blood glucose metabolism in adolescent male Wistar rats: A serum metabolomics analysis based on ultra-high performance liquid chromatography/mass spectrometry.

Fine particulate matter (PM2.5) and high-fat diet (HFD) are known to contribute to blood glucose metabolic disorders. However, limited research has investigated the combined impact of PM2.5 and HFD on blood glucose metabolism. This study aimed to explore the joint effects of PM2.5 and HFD on blood glucose metabolism in rats using serum metabolomics and to identify involved metabolites and metabolic pathways. The 32 male Wistar rats were exposed to filtered air (FA) or PM2.5 (real-world inhaled, concentrated PM2.5, 8 times the ambient level, ranging from 131.42 to 773.44 µg/m3) and fed normal diet (ND) or HFD for 8 weeks. The rats were divided into four groups (n = 8/group): ND-FA, ND-PM2.5, HFD-FA and HFD-PM2.5 groups. Blood samples were collected to determine fasting glucose (FBG), plasma insulin and glucose tolerance test and HOMA Insulin Resistance (HOMA-IR) index was calculated. Finally, the serum metabolism of rats was analyzed by ultra-high performance liquid chromatography/mass spectrometry (UHPLC-MS). Then we constructed the partial least squares discriminant analysis (PLS-DA) model to screen the differential metabolites, and performed pathway analysis to screen the main metabolic pathways. Results showed that combined effect of PM2.5 and HFD caused changes in glucose tolerance, increased FBG levels and HOMA-IR in rats and there were interactions between PM2.5 and HFD in FBG and insulin. By metabonomic analysis, the serum differential metabolites pregnenolone and progesterone, which involved in steroid hormone biosynthesis, were two different metabolites in the ND groups. In the HFD groups, the serum differential metabolites were L-tyrosine and phosphorylcholine, which involved in glycerophospholipid metabolism, and phenylalanine, tyrosine, and tryptophan biosynthesis. When PM2.5 and HFD coexist, they may lead to more severe and complex effects on glucose metabolism by affecting lipid metabolism and amino acid metabolism. Therefore, reducing PM2.5 exposure and controlling dietary structure are important measures for preventing and reducing glucose metabolism disorders.

The impact of urban irrigation on the temperature-carbon feedback in U.S. cities.

Urban areas experience numerous environmental challenges, among which the anthropogenic emissions of heat and carbon are two major contributors, the former is responsible for the notorious urban heat effect, the latter longterm climate changes. Moreover, the exchange of heat and carbon dioxide are closely interlinked in the built environment, and can form positive feedback loops that accelerate the degradation of urban environmental quality. Among a handful countermeasures for heat and carbon mitigation, urban irrigation is believed to be effective in cooling, yet the understanding of its impact on the co-evolution of heat and carbon emission remains obscure. In this study, we conducted multiphysics urban climate modeling for all urban areas in the contiguous United States, and evaluated the irrigation-induced cooling and carbon mitigation. Furthermore, we assessed the impact of urban irrigation on the potential heat-carbon feedback loop, with their strength of coupling quantified by an advanced causal inference method using the convergent cross mapping algorithms. It is found that the impact of urban irrigation varies vastly in geographically different cities, with its local and non-local effect unraveling distinct pathways of heat-carbon feedback mechanism.

Early prenatal exposure to air pollutants and congenital heart disease: a nested case-control study.

BACKGROUND: Congenital heart disease (CHD) is one of the most common congenital malformations in humans. Inconsistent results emerged in the existed studies on associations between air pollution and congenital heart disease. The purpose of this study was to evaluate the association of gestational exposure to air pollutants with congenital heart disease, and to explore the critical exposure windows for congenital heart disease. METHODS: The nested case-control study collected birth records and the following health data in Tianjin Women and Children's Health Center, China. All of the cases of congenital heart disease from 2013 to 2015 were selected matching five healthy controls for each case. Inverse distance weighting was used to estimate individual exposure based on daily air pollution data. Furthermore, the conditional logistic regression with distributed lag non-linear model was performed to identify the association between gestational exposure to air pollution and congenital heart disease. RESULTS: A total of 8,748 mother-infant pairs were entered into the analysis, of which 1,458 infants suffered from congenital heart disease. For each 10 µg/m3 increase of gestational exposure to PM2.5, the ORs (95% confidence interval, 95%CI) ranged from 1.008 (1.001-1.016) to 1.013 (1.001-1.024) during the 1st-2nd gestation weeks. Similar weak but increased risks of congenital heart disease were associated with O3 exposure during the 1st week and SO2 exposure during 6th-7th weeks in the first trimester, while no significant findings for other air pollutants. CONCLUSIONS: This study highlighted that gestational exposure to PM2.5, O3, and SO2 had lag effects on congenital heart disease. Our results support potential benefits for pregnancy women to the mitigation of air pollution exposure in the early stage, especially when a critical exposure time window of air pollutants may precede heart development.

Joint effects of meteorological factors and PM2.5 on age-related macular degeneration: a national cross-sectional study in China.

BACKGROUND: Weather conditions are a possible contributing factor to age-related macular degeneration (AMD), a leading cause of irreversible loss of vision. The present study evaluated the joint effects of meteorological factors and fine particulate matter (PM2.5) on AMD. METHODS: Data was extracted from a national cross-sectional survey conducted across 10 provinces in rural China. A total of 36,081 participants aged 40 and older were recruited. AMD was diagnosed clinically by slit-lamp ophthalmoscopy, fundus photography, and spectral domain optical coherence tomography (OCT). Meteorological data were calculated by European Centre for Medium-Range Weather Forecasts (ECMWF) reanalysis and were matched to participants' home addresses by latitude and longitude. Participants' individual PM2.5 exposure concentrations were calculated by a satellite-based model at a 1-km resolution level. Multivariable-adjusted logistic regression models paired with interaction analysis were performed to investigate the joint effects of meteorological factors and PM2.5 on AMD. RESULTS: The prevalence of AMD in the study population was 2.6% (95% CI 2.42-2.76%). The average annual PM2.5 level during the study period was 63.1 ± 15.3 µg/m3. A significant positive association was detected between AMD and PM2.5 level, temperature (T), and relative humidity (RH), in both the independent and the combined effect models. For PM2.5, compared with the lowest quartile, the odds ratios (ORs) with 95% confidence intervals (CIs) across increasing quartiles were 0.828 (0.674,1.018), 1.105 (0.799,1.528), and 2.602 (1.516,4.468). Positive associations were observed between AMD and temperature, with ORs (95% CI) of 1.625 (1.059,2.494), 1.619 (1.026,2.553), and 3.276 (1.841,5.830), across increasing quartiles. In the interaction analysis, the estimated relative excess risk due to interaction (RERI) and the attributable proportion (AP) for combined atmospheric pressure and PM2.5 was 0.864 (0.586,1.141) and 1.180 (0.768,1.592), respectively, indicating a synergistic effect between PM2.5 and atmospheric pressure. CONCLUSIONS: This study is among the first to characterize the coordinated effects of meteorological factors and PM2.5 on AMD. The findings warrant further investigation to elucidate the relationship between ambient environment and AMD.

Comprehensive analysis of B and T cell receptor repertoire in patients after kidney transplantation by high-throughput sequencing.

PURPOSE: The dynamic immunity of kidney transplant patients has not been fully elucidated. In this study, we explored the repertoire features of B/T cell receptor (BCR/TCR) of kidney transplant patients. METHODS: Using combined multiplex PCR amplification and high-throughput sequencing technique, we analyzed the uremic patients' BCR H chain and TCR beta chain repertoire which obtained 1 day before kidney transplantation (PRE-1), 1 day and 7 day after kidney transplantation (POST-1 and POST-7). RESULTS: Our analysis results showed the diversity of TCRß CDR3 in POST-7 group was highest. In addition, there were specific skewed usage of TRBV gene subfamilies, and V-J combinations in different time points during kidney transplantation. Moreover, the overlap degrees of BCR-H (TCR-ß) CDR3 repertoire among each group were identified. Notably, the abundance of some TCR-ß CDR3 sequences changed regularly in the time point of kidney transplantation. CONCLUSIONS: The BCR-H (TCR-ß) CDR3 repertoire of kidney transplant patients changed dynamically.

AuPd nanoparticles functionalized core-shell Co3O4/ZnO@ZnO for ultra-sensitive toluene detection.

In this work, core-shell AuPd nanoparticles (NPs) sensitized Co3O4/ZnO@ZnO ellipsoid nanoparticles was successfully synthesized via a simple liquid phase synthesis method. SEM and TEM characterization results showed that the as-prepared samples have core-shell ellipsoid morphology and the size of the nanoparticles were uniform. Systematic gas sensing characterization was carried out to obtain the gas sensing property of AuPd NPs decorated Co3O4/ZnO@ZnO. It was found that the gas sensing property could be significantly enhanced after noble metal decoration with Au, Pd and AuPd NPs, respectively. The optimal gas sensing performance was achieved by AuPd NPs functionalized Co3O4/ZnO@ZnO based gas sensor. The maximum response reached 256-100 ppm toluene at 250 °C, which is 50 °C lower than pure ZnO. The detection limit of AuPd functionalized Co3O4/ZnO@ZnO was as low as 100 ppb. The enhanced sensing mechanism was mainly attributed to the synergistic effect of Au and Pd, which was detailly discussed in gas sensing mechanism part.

Aberrant mitochondrial DNA methylation and declined pulmonary function in a population with polycyclic aromatic hydrocarbon composition in particulate matter.

Air pollution exposure has been found to be associated with epigenetic modification of the mitochondrial genome, which could subsequently induce adverse health outcomes. However, very limited studies exist regarding the association between fine particulate matter (PM2.5) exposure and pulmonary function at the molecular level of mitochondrial epigenetic changes. This study aimed to investigate the association of platelet mitochondrial DNA (mtDNA) methylation with occupational PM2.5 exposure and pulmonary function. First, 768 participants were occupationally exposed to polycyclic aromatic hydrocarbon (PAH)-enriched PM2.5 in a coke-oven plant in East China. The levels of PM2.5, PAH components bound to PM2.5, and urinary PAH metabolites in the workplace environment were measured as an internal dose, respectively. mtDNA methylation was measured by bisulfite pyrosequencing of two genes of ATP synthase (MT-ATP6 and MT-ATP8). Mediation analysis was conducted to evaluate the role of mtDNA methylation in pulmonary alteration induced by PAH. A decreasing trend of platelet mtDNA methylation was observed with increase in PM2.5 exposure across all participants. As an important PAH metabolite in urine, 1-hydroxypyrene (1-OHP) was significantly negatively associated with FEV1/FVC (Forced Expiratory Volume in 1s/Forced Vital Capacity) ratio. The participants with high serum folate levels (≥10 nmol/L) showed positive association between MT-ATP6 methylation and FEV1/FVC ratio. Mediation analysis suggested that MT-ATP6 methylation mediated the significant association of urinary 1-OHP with FEV1/FVC. Our findings suggested the methylation of platelet mitochondrial gene MT-ATP6 and FEV1/FVC to be negatively associated with PM exposure. Platelet mtDNA methylation acted as an intermediary between PAH exposure and lung function decline. The mitochondrial epigenetic regulation in platelets, in response to PM exposure, might be involved in subsequent progress of abnormal pulmonary function.

Long-term PM2.5 exposure in association with chronic respiratory diseases morbidity: A cohort study in Northern China.

Several literatures have examined the risk of chronic respiratory diseases in association with short-term ambient PM2.5 exposure in China. However, little evidence has examined the chronic impacts of PM2.5 exposure on morbidity of chronic respiratory diseases in cohorts from high pollution countries. Our study aims to investigate the associations. Based on a retrospective cohort among adults in northern China, a Cox regression model with time-varying PM2.5 exposure and a concentration-response (C-R) curve model were performed to access the relationships between incidence of chronic respiratory diseases and long-term PM2.5 exposure during a mean follow-up time of 9.8 years. Individual annual average PM2.5 estimates were obtained from a satellite-based model with high resolution. The incident date of a chronic respiratory disease was identified according to self-reported physician diagnosis time and/or intake of medication for treatment. Among 38,047 urban subjects analyzed in all-cause chronic respiratory disease cohort, 482 developed new cases. In CB (38,369), asthma (38,783), and COPD (38,921) cohorts, the onsets were 276, 89, and 14, respectively. After multivariable adjustment, hazard ratio and 95% confidence interval for morbidity of all-cause chronic respiratory disease, CB, asthma, and COPD were 1.15 (1.01, 1.31), 1.20 (1.00, 1.42), 0.76 (0.55, 1.04), and 0.66 (0.29, 1.47) with each 10 µg/m3 increment in PM2.5, respectively. Stronger effect estimates were suggested in alcohol drinkers across stratified analyses. Additionally, the shape of C-R curve showed an increasing linear relationship before 75.00 µg/m3 concentrations of PM2.5 for new-onset all-cause chronic respiratory disease, and leveled off at higher levels. These findings indicated that long-term exposure to high-level PM2.5 increased the risks of incident chronic respiratory diseases in China. Further evidence of C-R curves is warranted to clarify the associations of adverse chronic respiratory outcomes involving air pollution.