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Abstract Cardiovascular diseases (CVDs) and cerebrovascular diseases (CeVDs) are closely related vascular diseases, sharing common cardiometabolic risk factors (RFs). Although pleiotropic genetic variants of these two diseases have been reported, their underlying pathological mechanisms are still unclear. Leveraging GWAS summary data and using genetic correlation, pleiotropic variants identification, and colocalization analyses, we identified 11 colocalized loci for CVDs-CeVDs-BP (blood pressure), CVDs-CeVDs-LIP (lipid traits), and CVDs-CeVDs-cIMT (carotid intima-media thickness) triplets. No shared causal loci were found for CVDs-CeVDs-T2D (type 2 diabetes) or CVDs-CeVDs-BMI (body mass index) triplets. The 11 loci were mapped to 12 genes, namely CASZ1, CDKN1A, TWIST1, CDKN2B, ABO, SWAP70, SH2B3, LRCH1, FES, GOSR2, RPRML, and LDLR, where both GOSR2 and RPRML were mapped to one locus. They were enriched in pathways related to cellular response to external stimulus and regulation of the phosphate metabolic process and were highly expressed in endothelial cells, epithelial cells, and smooth muscle cells. Multi-omics analysis revealed methylation of two genes (CASZ1 and LRCH1) may play a causal role in the genetic pleiotropy. Notably, these pleiotropic loci are highly enriched in the targets of antihypertensive drugs, which further emphasizes the role of the blood pressure regulation pathway in the shared etiology of CVDs and CeVDs.

Abstract There is a growing interest in the health impacts of PM2.5 originating from landscape fires. We conducted a time-series study to investigate the association between daily exposure to landscape fire PM2.5 and hospital admissions for cardiovascular events in 184 major Chinese cities. We developed a machine learning model combining outputs from chemical transport models, meteorological information and observed air pollution data to determine daily concentrations of landscape fire PM2.5. Furthermore, we fitted quasi-Poisson regression to evaluate the link between landscape fire PM2.5 concentrations and cardiovascular hospitalizations in each city, and conducted random-effects meta-analysis to pool the city-specific estimates. Here we show that, on a national scale, a rise of 1-μg/m3 in landscape fire PM2.5 concentrations is positively related to a same-day 0.16% (95% confidence interval: 0.01%–0.32%) increase in hospital admissions for cardiovascular disease, 0.28% (0.12%–0.44%) for ischemic heart disease, and 0.25% (0.02%–0.47%) for ischemic stroke. The associations remain significant even after adjusting for other sources of PM2.5. Our findings indicate that transient elevation in landscape fire PM2.5 levels may increase risk of cardiovascular diseases.

Abstract Background Implementing training programs to educate patients on the prodromal symptoms of acute coronary syndrome (ACS) may assist patients in accurately recognizing these symptoms, and ultimately decrease their time delay in seeking emergency medical services (EMS). However, the effectiveness of this approach remains uncertain, particularly among the Chinese population. Methods A cross-sectional study was conducted within 22 communities in Beijing, China between 2015 and 2018, with a total of 1099 participants recruited. The study utilized a standardized questionnaire to evaluate the presence of intentional decision delay in turning to EMS under a hypothetical chest pain, the participants’ knowledge of ACS prodromal symptoms, and whether they had ever received any training programs aimed at increasing their symptom knowledge. Mediation analysis was performed with regression models and bootstrapping methods, and gender difference was further analyzed through moderated mediation analysis. Results A total of 1099 participants (58.2% female, median [IQR] age 34 [20]) were included in the study. The results of the mediation analysis indicated that training programs were associated with a decrease risk in decision delay, with increased knowledge playing a mediating role (mediation effect/total effect = 36.59%, P 0.05), even though they did improve women’s knowledge of ACS prodromal symptoms (β = 0.57, P = 0.012). Conclusion The results suggested a relationship between prior training programs and reduced decision delay, with increased knowledge of prodromal symptoms of ACS serving as a mediator. However, the effect was only observed in male participants and not in female participants. This highlights the notion that mere transfer of knowledge regarding ACS prodromal symptoms may not be sufficient to mitigate decision delay in the female population. Further research is needed to corroborate these results and to gain deeper insights into the gender-specific barriers encountered in this study.

Abstract Background Comorbidities of coronavirus disease 2019 (COVID-19)/coronary heart disease (CHD) pose great threats to disease outcomes, yet little is known about their shared pathology. The study aimed to examine whether comorbidities of COVID-19/CHD involved shared genetic pathology, as well as to clarify the shared genetic variants predisposing risks common to COVID-19 severity and CHD risks. Methods By leveraging publicly available summary statistics, we assessed the genetically determined causality between COVID-19 and CHD with bidirectional Mendelian randomization. To further quantify the causality contributed by shared genetic variants, we interrogated their genetic correlation with the linkage disequilibrium score regression method. Bayesian colocalization analysis coupled with conditional/conjunctional false discovery rate analysis was applied to decipher the shared causal single nucleotide polymorphisms (SNPs). Findings Briefly, we observed that the incident CHD risks post COVID-19 infection were partially determined by shared genetic variants. The shared genetic variants contributed to the causality at a proportion of 0.18 (95% CI 0.18–0.19) to 0.23 (95% CI 0.23–0.24). The SNP (rs10490770) located near LZTFL1 suggested direct causality (SNPs → COVID-19 → CHD), and SNPs in ABO (rs579459, rs495828), ILRUN(rs2744961), and CACFD1(rs4962153, rs3094379) may simultaneously influence COVID-19 severity and CHD risks. Interpretation Five SNPs located near LZTFL1 (rs10490770), ABO (rs579459, rs495828), ILRUN (rs2744961), and CACFD1 (rs4962153, rs3094379) may simultaneously influence their risks. The current study suggested that there may be shared mechanisms predisposing to both COVID-19 severity and CHD risks. Genetic predisposition to COVID-19 is a causal risk factor for CHD, supporting that reducing the COVID-19 infection risk or alleviating COVID-19 severity among those with specific genotypes might reduce their subsequent CHD adverse outcomes. Meanwhile, the shared genetic variants identified may be of clinical implications for identifying the target population who are more vulnerable to adverse CHD outcomes post COVID-19 and may also advance treatments of ‘Long COVID-19.’

Exposure to ambient fine particulate matter (PM2.5) has a great impact on human body's immune system, but the correlation between PM2.5 and ankylosing spondylitis has not yet been clarified. We extracted 58,600 outpatient visits for ankylosing spondylitis from the Beijing Medical Claim Data for Employees database from 2010 to 2017. The percentage of outpatient visits following PM2.5 concentrations was estimated using generalized additive models with Poisson connections. Increase by 10 μ g/m3, PM2.5 is associated with daily outpatient visits for ankylosing spondylitis. In this test, the average concentration of PM2.5 was 86.8 ± 74.3 μ g/m3. For every 10 μg/m3 increase in PM2.5 concentration, there was a 0.34% (95% CI, 0.26–0.42%) increase in the risk of patients who visited the doctor on the same day. Females and younger patients were most susceptible to the impact of PM2.5 exposure (P＜0.05). This study revealed the relationship between exposure to PM2.5 and ankylosing spondylitis, and future research can further confirm this finding and explore the potential mechanisms.

Harmine is a naturally occurring β-carboline alkaloid originally isolated from Peganum harmala. As a major active component, harmine exhibits a broad spectrum of pharmacological properties, particularly remarkable antitumor effects. Recent mechanistic studies have shown that harmine can inhibit cancer cell proliferation and metastasis through epithelial-to-mesenchymal transition, cell cycle regulation, angiogenesis, and the induction of tumor cell apoptosis. Furthermore, harmine reduces drug resistance when used in combination with chemotherapeutic drugs. Despite its remarkable antitumor activity, the application of harmine is limited by its poor solubility and toxic side effects, particularly neurotoxicity. Novel harmine derivatives have demonstrated strong clinical application prospects, but further validation based on drug activity, acute toxicity, and other aspects is necessary. Here, we present a review of recent research on the action mechanism of harmine in cancer treatment and the development of its derivatives, providing new insights into its potential clinical applications and strategies for mitigating its toxicity while enhancing its efficacy.

Background Cardiovascular risk burden is associated with dementia risk and neurodegeneration-related brain structure, while the role of genetics and incident cardiovascular disease (CVD) remains unclear.Aims To examine the association of overall cardiovascular risk burden with the risk of major dementia subtypes and volumes of related brain regions in a large sample, and to explore the role of genetics and CVD onset.Methods A prospective study among 354 654 participants free of CVD and dementia (2006–2010, mean age 56.4 years) was conducted within the UK Biobank, with brain magnetic resonance imaging (MRI) measurement available for 15 104 participants since 2014. CVD risk burden was evaluated by the Framingham General Cardiovascular Risk Score (FGCRS). Dementia diagnosis was ascertained from inpatient and death register data.Results Over a median 12.0-year follow-up, 3998 all-cause dementia cases were identified. Higher FGCRS was associated with increased all-cause dementia risk after adjusting for demographic, major lifestyle, clinical factors and the polygenic risk score (PRS) of Alzheimer’s disease. Comparing the high versus low tertile of FGCRS, the odds ratios (ORs) and 95% confidence intervals (CIs) were 1.26 (1.12 to 1.41) for all-cause dementia, 1.67 (1.33 to 2.09) for Alzheimer’s disease and 1.53 (1.07 to 2.16) for vascular dementia (all ptrend

Abstract Background Polypharmacy is one of the most important health issues for its potential impacts on disease burden and healthcare costs. The aim of this study was to update a comprehensive picture of prevalence and trends in polypharmacy over 20 years in U.S. adults. Methods Participants included 55,081 adults aged ≥ 20 from the National Health and Nutrition Examination Survey, January 1, 1999, through December 31, 2018. The simultaneously use of ≥ 5 drugs in one individual was defined as polypharmacy. National prevalence and trends in polypharmacy were evaluated among U.S. adults within different demo-socioeconomic status and pre-existing diseases. Results From 1999–2000 to 2017–2018, the overall percentages of adults with polypharmacy remained on the rise, increasing from 8.2% (7.2–9.2%) to 17.1% (15.7–18.5%) (average annual percentage change [AAPC] = 2.9%, P = .001). The polypharmacy prevalence was considerably higher in the elderly (from 23.5% to 44.1%), in adults with heart disease (from 40.6% to 61.7%), and in adults with diabetes (from 36.3% to 57.7%). Also, we observed a greater increase rate of polypharmacy in men (AAPC = 4.1%, P

Abstract Background The associations of multimorbidity patterns with transitions between frailty states remain unclear in older individuals. Methods We used data from the National Health and Aging Trends Study 2011–2019. Frailty was measured annually using the Fried frailty phenotype. Multimorbidity patterns at baseline were identified using latent class analysis based on 14 chronic conditions. We used the semi‐Markov multi‐state model to investigate the influences of multimorbidity characterized by condition counts and patterns on subsequent frailty transitions over follow‐ups. Results Among 9450 participants aged ≥65 years at baseline, 34.8% were non‐frail, 48.1% were pre‐frail and 17.0% were frail. Over a median follow‐up of 4.0 years, 16 880 frailty transitions were observed, with 10 527 worsening and 6353 improving. For 7675 participants with multimorbidity, four multimorbidity patterns were identified: osteoarticular pattern (62.4%), neuropsychiatric–sensory pattern (17.2%), cardiometabolic pattern (10.3%) and complex multimorbidity pattern (10.1%). Compared with no disease, multimorbidity was significantly associated with an increased risk of worsening transitions, including from non‐frail to pre‐frail (hazard ratio [HR] = 1.35; 95% confidence interval [CI] = 1.21–1.52), from non‐frail to frail (HR = 1.68; 95% CI = 1.04–2.73), from pre‐frail to frail (HR = 2.19; 95% CI = 1.66–2.90) and from pre‐frail to death (HR = 1.64; 95% CI = 1.11–2.41). Compared with the osteoarticular pattern, neuropsychiatric–sensory, cardiometabolic and complex multimorbidity patterns had a significantly higher risk of worsening frailty (all P

Abstract Background Evidence linking air pollution to major depressive disorder (MDD) remains sparse and results are heterogeneous. In addition, the evidence about the interaction and joint associations of genetic risk and lifestyle with air pollution on incident MDD risk remains unclear. We aimed to examine the association of various air pollutants with the risk of incident MDD and assessed whether genetic susceptibility and lifestyle influence the associations. Methods This population-based prospective cohort study analyzed data collected between March 2006 and October 2010 from 354,897 participants aged 37 to 73 years from the UK Biobank. Annual average concentrations of PM2.5, PM10, NO2, and NOx were estimated using a Land Use Regression model. A lifestyle score was determined based on a combination of smoking, alcohol drinking, physical activity, television viewing time, sleep duration, and diet. A polygenic risk score (PRS) was defined using 17 MDD-associated genetic loci. Results During a median follow-up of 9.7 years (3,427,084 person-years), 14,710 incident MDD events were ascertained. PM2.5 (HR: 1.16, 95% CI: 1.07–1.26; per 5 μg/m3) and NOx (HR: 1.02, 95% CI: 1.01–1.05; per 20 μg/m3) were associated with increased risk of MDD. There was a significant interaction between the genetic susceptibility and air pollution for MDD (P-interaction < 0.05). Compared with participants with low genetic risk and low air pollution, those with high genetic risk and high PM2.5 exposure had the highest risk of incident MDD (PM2.5: HR: 1.34, 95% CI: 1.23–1.46). We also observed an interaction between PM2.5 exposure and unhealthy lifestyle (P-interaction < 0.05). Participants with the least healthy lifestyle and high air pollution exposures had the highest MDD risk when compared to those with the most healthy lifestyle and low air pollution (PM2.5: HR: 2.22, 95% CI: 1.92–2.58; PM10: HR: 2.09, 95% CI: 1.78–2.45; NO2: HR: 2.11, 95% CI: 1.82–2.46; NOx: HR: 2.28, 95% CI: 1.97–2.64). Conclusions Long-term exposure to air pollution is associated with MDD risk. Identifying individuals with high genetic risk and developing healthy lifestyle for reducing the harm of air pollution to public mental health.

Evidence for the health effects of ambient PM1 (particulate matter with an aerodynamic diameter ≤ 1 µm) pollution is limited, and it remains unclear whether a smaller particulate matter has a greater impact on human health. We conducted a time-series study in 184 major cities by extracting daily hospital data on admissions for ischemic heart disease, heart failure, heart rhythm disturbances, and stroke between 2014 and 2017 from a medical insurance claims database of 0.28 billion beneficiaries. City-specific associations were estimated with over-dispersed generalized additive models. A random-effects meta-analysis was used to estimate regional and national average associations. We conducted stratified and meta-regression analyses to explore potential effect modifiers of the association. We recorded 8.83 million cardiovascular admissions during the study period. At the national-average level, a 10-μg/m3 increase in same-day PM1, PM2.5(particulate matter with an aerodynamic diameter ≤ 2.5 µm) and PM10(particulate matter with an aerodynamic diameter ≤ 10 µm) concentrations corresponded to a 1.14% (95% confidence interval 0.88–1.41%), 0.55% (0.40–0.70%), and 0.45% (0.36–0.55%) increase in cardiovascular admissions, respectively. PM1 exposure was also positively associated with all cardiovascular disease subtypes, including ischemic heart disease (1.28% change; 0.99–1.56%), heart failure (1.30% change; 0.70–1.91%), heart rhythm disturbances (1.11% change; 0.65–1.58%), and ischemic stroke (1.29% change; 0.88–1.71%). The associations between PM1 and cardiovascular admissions were stronger in cities with lower PM1 levels, higher air temperatures and relative humidity, as well as in subgroups with elder age (all P

In recent years, the potential of Traditional Chinese Medicine in preventing and treating gastric cancer has gained clear recognition. However, there is a lack of comprehensive analysis of the data on the involvement of Traditional Chinese Medicine in the prevention, diagnosis, and treatment of gastric cancer. Therefore, this article aims to organize and analyze relevant information to provide a reference for the use of Traditional Chinese Medicine in the prevention and treatment of gastric cancer. [ABSTRACT FROM AUTHOR]

Edwardsiella piscicida is an important fish pathogen with a broad host that causes substantial economic losses in the aquaculture industry. Ferric uptake regulator (Fur) is a global transcriptional regulator and contains two typical domains, the DNA-binding domain and dimerization domain. In a previous study, we obtained a mutant strain of full-length fur of E. piscicida, TX01Δfur, which displayed increased siderophore production and stress resistance factors and decreased pathogenicity. To further reveal the regulatory mechanism of Fur, the DNA-binding domain (N-terminal) of Fur was knocked out in this study and the mutant was named TX01Δfur2. We found that TX01Δfur2 displayed increased siderophore production and enhanced adversity tolerance, including a low pH, manganese, and high temperature stress, which was consistent with the phenotype of TX01Δfur. Contrary to TX01Δfur, whose virulence was weakened, TX01Δfur2 displayed an ascended invasion of nonphagocytic cells and enhanced destruction of phagocytes via inducing overpowering or uncontrollable pyroptosis, which was confirmed by the fact that TX01Δfur2 induced higher levels of cytotoxicity, IL-1β, and p10 in macrophages than TX01. More importantly, TX01Δfur2 displayed an increased global virulence to the host, which was confirmed by the result that TX01Δfur2 caused higher lethality outcomes for healthy tilapias than TX01. These results demonstrate that the mutation of the Fur N-terminal domain augments the resistance level against the stress and pathogenicity of E. piscicida, which is not dependent on the bacterial number in host cells or host tissues, although the capabilities of biofilm formation and the motility of TX01Δfur2 decline. These interesting findings provide a new insight into the functional analysis of Fur concerning the regulation of virulence in E. piscicida and prompt us to explore the subtle regulation mechanism of Fur in the future.

In this study, antibacterial PVA-SS-LJ-AgNPs composite films were made by using polyvinyl alcohol (PVA) and soluble starch (SS) as ingredients, glycerol as plasticizer, and lemon juice (LJ) as reducing agent to in situ reduced AgNPs from AgNO3. After single factor and orthogonal experiments, the optimum films preparation process was PVA 3 g, SS 0.5 g, glycerol 3 g, LJ 7 mL, AgNO3 130 mmol/L. Under the optimal process, the tensile strength, elongation at break, water vapor permeability coefficient, moisture absorption rate, and light transmittance of the membrane were 12.16 MPa, 1111.59%, 0.09 g/0.01 h·m2, 12.56%, 48.05%, respectively. Through the analysis of physical properties and structure of the films, lemon juice could successfully restore AgNPs in situ to films. Compared with the PVA-SS films, the tensile strength and elongation at break of the composite films were improved up to 11.51 MPa and 1470.20%, respectively. Compared with PVA-SS-LJ films, the water vapor penetration and moisture absorption were effectively balanced, AgNPs evenly dispersed in the composite films, the compound films had good inhibition effect for E. coli, Salmonella, Bacillus subtilis, S. aureus, P. aeruginosa. In summary, PVA-SS-LJ-AgNPs composite films met the current new requirements of food packaging materials, and had its potential application prospects.

Abstract Purpose To describe the objective and design of the Fujian Eye Study and to introduce the general characteristics and vision condition of this study. Methods The Fujian Eye Study (FJES) is a population-based cross-sectional survey on the public eye health status of residents over 50 years old in the entire Fujian Province of Southern China, which contains both urban and rural areas and coastal and inland regions. 10,044 participants were enrolled using a two-stage cluster sampling design and underwent a questionnaire and a series of standard examinations both physical and ocular. The main subgroups of data collection included age, sex, region, refractive error, education background, income, eating habits, smartphone usage in the dark, complaints of eye discomfort, history of chronic diseases, consumption of tobacco, alcohol, or tea. Results 8211 (81.8%) participants were finally included and were divided into urban populations (4678 subjects) and rural populations (3533 subjects) and coastal residents (6434 subjects) and inland residents (1777 subjects); 4836 participants were female. The mean age was 64.39 (SD 8.87) years (median 64 years; range 50–98 years). 227 (3.33%) had vision impairment (VI), 195 (2.87%) had low vision and 14 (0.21%) were blind. The mean presenting near visual acuity (PNVA) was 0.28 (0.17), the mean presenting distance visual acuity (PDVA) was 0.61 (0.30), and the mean best corrected visual acuity (BCVA) was 0.82 (0.28). Conclusions The FJES collected detailed questionnaire information and overall ocular and physical examinations, which provide the opportunity to identify risk factors and images of VI and eye diseases and to evaluate their associations with chronic diseases and basic personal information.

IntroductionPolypharmacy might contribute to a range of adverse outcomes, which could get worse in the elderly with chronic kidney disease (CKD). Evidence on polypharmacy, CKD, and mortality is scarce. We aimed to investigate the prospective association between polypharmacy, CKD and all-cause and cause-specific mortality in adults aged ≥65 years.MethodsA total of 13,513 adults from the National Health and Nutrition Examination Surveys were included, following up from 1999 to 2018 until December 31, 2019. The simultaneous use of ≥5 medications by one individual was defined as polypharmacy. Survey-weighted Cox proportional hazard models were used to estimate the hazard ratio (HRs) for mortality from all-cause, cardiovascular diseases (CVD), and cancer after adjusting for potential confounding factors.ResultsAmong the elderly with CKD, we identified 3,825 total deaths (1,325 CVD and 714 cancer) during a median follow-up of 7.7 years. Participants with polypharmacy had a 27% (HR = 1.27 [1.15, 1.39]) and 39% (HR = 1.39 [1.19, 1.62]) higher risk of all-cause and CVD mortality, respectively, but not for cancer mortality. Compared with the elderly with no polypharmacy and no CKD, the corresponding HRs (95%CIs) for all-cause mortality were 1.04 (0.96, 1.14) for those with no polypharmacy but CKD, 1.24 (1.11, 1.39) for with polypharmacy but no CKD, and 1.34 (1.21, 1.49) for those with both polypharmacy and CKD. A similar pattern was detected for CVD mortality.DiscussionPolypharmacy was associated with elevated risks of all-cause and CVD mortality among the elderly CKD patients. More evidence-based approaches should be promoted for the appropriate deprescribing in the older adults with CKD.

Objectives: To examine the prospective association between art engagement and the risk of type 2 diabetes.Methods: Adults aged ≥50 from the English Longitudinal Study of Ageing were asked about the frequency of art engagement, including going to the cinema, the art gallery or museum, and the theatre, a concert, or the opera. Cox proportional hazards regression models were used to examine the risk of type 2 diabetes associated with art engagement.Results: During a median follow-up of 12.2 years, we identified 350 cases of type 2 diabetes from 4,064 participants through interviews. After multivariable adjustment, compared with people who never went to the cinema, those going to the cinema frequently had a significantly lower risk of developing type 2 diabetes (HR = 0.61, 95% CI: 0.44–0.86). After further adjustment for socioeconomic factors, the association was slightly attenuated but remained statistically significant (HR = 0.65, 95% CI: 0.46–0.92). Similar results were found for going to the theatre, a concert, or the opera.Conclusion: Frequent art engagement may be associated with a lower risk of type 2 diabetes, which was independent of individuals’ socioeconomic factors.

BackgroundMetformin treatment is associated with vitamin B12 deficiency, which is a risk factor for neuropathy. However, few studies have examined the relationship between metformin treatment and diabetic peripheral neuropathy (DPN), and the available findings are contradictory. We aimed to assess whether metformin treatment is associated with DPN in patients with type 2 diabetes mellitus (T2DM) in Beijing, China.MethodsAll patients with newly diagnosed T2DM between January 2010 and September 2012 in the Medical Claim Data for Employees database were included. Metformin treatment was defined as any record of metformin prescription. The average daily dose of metformin during follow-up was calculated. DPN was defined as DPN admissions occurring after a diagnosis of T2DM in the database. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazards models.ResultsAmong 49,705 T2DM patients, 1,933 DPN events were recorded during a median follow-up of 6.36 years. The crude incidence rates were 7.12 and 3.91 per 1000 person-years for patients treated with metformin (N=37,052) versus those not treated (N=12,653). Patients treated with metformin had an 84% increased risk of DPN compared with patients not using metformin (HR, 1.84; 95% CI, 1.62, 2.10). The daily dose was positively associated with DPN risk (HR, 1.48; 95% CI, 1.46, 1.51; P for trend 2.0 g, respectively, than in patients who did not receive treatment. Patients aged less than 60 years had a higher risk of DPN (P

Background. Aspiration pneumonia (AP) is difficult to diagnose and has poor outcomes. This case-control study aimed to explore the risk factors and delineate the antibiotic usage for AP. Methods. Inpatients diagnosed with community-acquired pneumonia (CAP) from 2013 to 2017, enrolled in the urban employee basic medical insurance program in Beijing, were included and classified into the AP (N = 2,885) and non-AP (N = 53,825) groups. Risk factors were identified by logistic regression. Results. Older age (compared to 18–64 years, OR for 65–79 years: 4.3, 95% CI: 3.8–4.9; OR for >80 years: 6.3, 95% CI: 5.6–7.2), male (OR: 1.4, 95% CI: 1.3–1.5), cerebrovascular disease (OR: 3.1, 95% CI: 2.8–3.5), dementia (OR: 2.0, 95% CI: 1.8–2.1), vomiting (OR: 1.4, 95% CI: 1.2–1.7), Parkinson’s disease (OR: 2.1, 95% CI: 1.8–2.4), and epilepsy (OR: 3.2, 95% CI: 2.8–3.7) were associated with an increased risk of AP. 92.8% of the AP patients received antibiotic therapy. Among them, patients treated with broad-spectrum antibiotics, antibiotics for injection, and combined antibiotics accounted for 93.3%, 97.9%, and 81.7%, respectively. Conclusions. Older age, male, and several comorbidities were independent risk factors for AP, and combined antibiotics treatments are common, which merits attention in accurate detection of AP in a high-risk population.

Abstract Edwardsiella tarda is a facultative intracellular pathogen in humans and animals. The Gram-negative bacterium is widely considered a potentially important bacterial pathogen. Adaptation to acid stress is important for the transmission of intestinal microbes, so the acid-resistance (AR) system is essential. However, the AR systems of E. tarda are totally unknown. In this study, a lysine-dependent acid resistance (LDAR) system in E. tarda, CadBA, was characterized and identified. CadB is a membrane protein and shares high homology with the lysine/cadaverine antiporter. CadA contains a PLP-binding core domain and a pyridoxal phosphate-binding motif. It shares high homology with lysine decarboxylase. cadB and cadA are co-transcribed under one operon. To study the function of the cadBA operon, isogenic cadA, cadB and cadBA deletion mutant strains TX01ΔcadA, TX01ΔcadB and TX01ΔcadBA were constructed. When cultured under normal conditions, the wild type strain and three mutants exhibited the same growth performance. However, when cultured under acid conditions, the growth of three mutants, especially TX01ΔcadA, were obviously retarded, compared to the wild strain TX01, which indicates the important involvement of the cadBA operon in acid resistance. The deletion of cadB or cadA, especially cadBA, significantly attenuated bacterial activity of lysine decarboxylase, suggesting the vital participation of cadBA operon in lysine metabolism, which is closely related to acid resistance. The mutations of cadBA operon enhanced bacterial biofilm formation, especially under acid conditions. The deletions of the cadBA operon reduced bacterial adhesion and invasion to Hela cells. Consistently, the deficiency of cadBA operon abated bacterial survival and replication in macrophages, and decreased bacterial dissemination in fish tissues. Our results also show that the expression of cadBA operon and regulator cadC were up-regulated upon acid stress, and CadC rigorously regulated the expression of cadBA operon, especially under acid conditions. These findings demonstrate that the AR CadBA system was a requisite for the resistance of E. tarda against acid stress, and played a critical role in bacterial infection of host cells and in host tissues. This is the first study about the acid resistance system of E. tarda and provides new insights into the acid-resistance mechanism and pathogenesis of E. tarda.

BackgroundAmbient fine particulate matter (PM2.5) adversely affects human health and has been linked to a variety of skin disorders. However, little is known about the effects of PM2.5 on psoriasis.MethodsThe Beijing Medical Claim Data for Employees database recorded 500,266 outpatient visits for psoriasis during 2010–2017. A generalized additive quasi-Poisson model was used to examine the relationship between daily PM2.5 concentrations and outpatient visits for psoriasis with stratification by sex, age, and season.ResultsShort-term exposure to PM2.5 was associated with outpatient visits for psoriasis-related health concerns. A same-day increase of 10 μg/m3 in PM2.5 concentrations was associated with a 0.29% (95% confidence interval: 0.26–0.32%) increase in daily outpatient visits for psoriasis. Female and older patients appeared to be more sensitive to the effects of PM2.5 (P < 0.05).ConclusionsShort-term elevations in PM2.5 concentrations may be associated with exacerbations in psoriasis. Further work is warranted to confirm the findings and elucidate the underlying biological mechanisms.

Abstract CD9 is a glycoprotein of the transmembrane 4 superfamily that is involved in various cellular processes. Studies related to the immune functions and activities of CD9 in teleost fish are limited. In this study, we characterized two CD9 homologs, PoCD9.1 and PoCD9.3, from Japanese flounder (Paralichthys olivaceus). Sequence analysis showed that PoCD9.1 and PoCD9.3 possess characteristic transmembrane 4 superfamily (TM4SF) structures. PoCD9.1 shares 70.61% sequence identity with PoCD9.3. The expression of PoCD9.1 and PoCD9.3 in the three main immune tissues was significantly induced in a time-dependent manner by extracellular and intracellular pathogen infection, which indicates that the two CD9 homologs play an important role in the response to pathogenic infection. Following infection with the extracellular pathogen Vibrio anguillarum, the expression profiles of both PoCD9.1 and PoCD9.3 were similar. After infection with the intracellular pathogen Edwardsiella piscicida, the expression levels of PoCD9.1 and PoCD9.3 were different at different stages of infection, especially in the spleen. The spleen was the most important tissue for the PoCD9.1 and PoCD9.3 responses to pathogen infection among the three examined immune tissues. Knockdown of PoCD9.1 and PoCD9.3 attenuated the ability of host cells to eliminate pathogenic bacteria, and PoCD9.1 knockdown was more lethal than PoCD9.3 knockdown for host cells with E. piscicida infection. Overexpression of PoCD9.1 and PoCD9.3 promoted host or host cell defence against E. piscicida infection. These findings suggest that PoCD9.1 and PoCD9.3 serve as immune-related factors, play an important role in the immune defence system of Japanese flounder, and display different functions in response to different pathogens at different stages of infection.

Abstract Tissue factor pathway inhibitors (TFPI), including TFPI-1 and TFPI-2, are Kunitz-type serine protease inhibitors that mainly inhibit the blood coagulation induced by tissue factors. Previous reports on teleost proved TFPI play important roles in innate immunity. In this study, two TFPI (PoTFPI-1 and PoTFPI-2) molecules from Japanese flounder (Paralichthys olivaceus) were analyzed and characterized for their expression patterns, antibacterial and anticancer activities of the C-terminal derived peptides. Quantitative real time RT-PCR analysis shows that constitutive PoTFPI-1 expression occurred, in increasing order, in the brain, muscle, spleen, gills, head kidney, blood, intestine, heart, and liver; PoTFPI-2 was expressed, in increasing order, in the brain, gills, head kidney, muscle, intestine, spleen, liver, heart, and blood. Under the stimulation of fish pathogens, both PoTFPI-1 and PoTFPI-2 expressions increased significantly in a manner that depended on the pathogens, tissue type, and infection stage. Furthermore, C-terminal peptides TP25 and TP26, derived from PoTFPI-1 and PoTFPI-2, respectively, were synthesized and proved to be active against Micrococcus luteus (for TP25 and TP26) and Staphylococcus aureus (for TP25) via retardation effects on bacterial nucleic acids. In addition, TP25 and TP26 also displayed significant inhibitory effects on human colon cancer cell line HT-29. These results reveal that both PoTFPI-1 and PoTFPI-2 play important roles in host innate immunity. The antibacterial activity and anticancer cells function of TP25 and TP26 will add new insights into the roles of teleost TFPI.

Summary: Background: The effect of long-term exposure to air pollution on the development of chronic obstructive pulmonary disease (COPD) is still controversial, and the role of the interactions of air pollution with genetic risk and lifestyle in COPD risk is unclear. Methods: We included 452762 participants derived from the UK Biobank. Annual concentrations of air pollutions, including particle matter (PM2.5, PM10), nitrogen oxides (NOx), and nitrogen dioxide (NO2), were assessed using land-use regression model. We applied Cox proportional hazard model to evaluate the associations between air pollution and COPD risk. In addition, we constructed a polygenic risk score and a lifestyle score, and assessed whether genetic susceptibility and lifestyle modified the effect of air pollution on the COPD risk. Findings: Each interquartile range (IQR) increase in annual concentrations of PM2.5, PM10, NOx, and NO2 was associated with 1.17 (95% CI: 1.15,1.19), 1.05 (95% CI: 1.03,1.06), 1.13 (95% CI: 1.11,1.14), and 1.19 (95% CI: 1.16,1.21) times the risk of COPD, respectively. We observed an additive interaction between PM2.5 and genetic risk (P-interact=0.095), and a negative interaction between PM2.5 and lifestyle (P-interact=0.062). The HRs for each IQR increase in PM2.5 were 1.21, (95% CI: 1.16-1.25) and 1.24, (95% CI: 1.21-1.26) in individuals with healthy and unfavourable lifestyle, respectively; and 1.16, (95% CI: 1.13-1.19) and 1.19, (95% CI: 1.16-1.22) in those with low genetic risk and high genetic risk, respectively. Participants with high air pollution exposure, high genetic risk and unfavourable lifestyle showed the highest risk of COPD. Interpretation: Long-term exposure to air pollution was associated with increased risk of COPD, especially in those with high genetic risk and unfavourable lifestyle. Funding: None.

Abstract Background Early and accurate identification of sepsis patients with high risk of in-hospital death can help physicians in intensive care units (ICUs) make optimal clinical decisions. This study aimed to develop machine learning-based tools to predict the risk of hospital death of patients with sepsis in ICUs. Methods The source database used for model development and validation is the medical information mart for intensive care (MIMIC) III. We identified adult sepsis patients using the new sepsis definition Sepsis-3. A total of 86 predictor variables consisting of demographics, laboratory tests and comorbidities were used. We employed the least absolute shrinkage and selection operator (LASSO), random forest (RF), gradient boosting machine (GBM) and the traditional logistic regression (LR) method to develop prediction models. In addition, the prediction performance of the four developed models was evaluated and compared with that of an existent scoring tool – simplified acute physiology score (SAPS) II – using five different performance measures: the area under the receiver operating characteristic curve (AUROC), Brier score, sensitivity, specificity and calibration plot. Results The records of 16,688 sepsis patients in MIMIC III were used for model training and test. Amongst them, 2949 (17.7%) patients had in-hospital death. The average AUROCs of the LASSO, RF, GBM, LR and SAPS II models were 0.829, 0.829, 0.845, 0.833 and 0.77, respectively. The Brier scores of the LASSO, RF, GBM, LR and SAPS II models were 0.108, 0.109, 0.104, 0.107 and 0.146, respectively. The calibration plots showed that the GBM, LASSO and LR models had good calibration; the RF model underestimated high-risk patients; and SAPS II had the poorest calibration. Conclusion The machine learning-based models developed in this study had good prediction performance. Amongst them, the GBM model showed the best performance in predicting the risk of in-hospital death. It has the potential to assist physicians in the ICU to perform appropriate clinical interventions for critically ill sepsis patients and thus may help improve the prognoses of sepsis patients in the ICU.

Background: Little evidence is available about the association between diabetes and respiratory disease mortality among Japanese populations. We aimed to explore the association between diabetes and the risk of respiratory diseases mortality through a nationwide prospective study in Japan. Methods: We followed 95,056 participants (39,925 men and 55,131 women) for a median 17.1 years. The information about diabetes status, sociodemographic characteristics, and lifestyles was collected at baseline. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) of mortality from respiratory diseases associated with baseline diabetes status. Results: We identified 2,838 deaths from total respiratory diseases (1,759 respiratory infection, 432 chronic obstructive pulmonary disease, and 647 other respiratory diseases). The association between diabetes and total respiratory disease mortality was statistically significant among women (HR 1.81; 95% CI, 1.39–2.37) but of borderline statistical significance in men (P for interaction

ObjectiveThis study aimed to develop and validate a multimorbidity index using self-reported chronic conditions for predicting 5-year mortality risk.MethodsWe analyzed data from the Chinese Longitudinal Healthy Longevity Survey (CLHLS) and included 11,853 community-dwelling older adults aged 65–84 years. Restrictive association rule mining (ARM) was used to identify disease combinations associated with mortality based on 13 chronic conditions. Data were randomly split into the training (N = 8,298) and validation (N = 3,555) sets. Two multimorbidity indices with individual diseases only (MI) and disease combinations (MIDC) were developed using hazard ratios (HRs) for 5-year morality in the training set. We compared the predictive performance in the validation set between the models using condition count, MI, and MIDC by the concordance (C) statistic, the Integrated Discrimination Improvement (IDI), and the Net Reclassification Index (NRI).ResultsA total of 13 disease combinations were identified. Compared with condition count (C-statistic: 0.710), MIDC (C-statistic: 0.713) showed significantly better discriminative ability (C-statistic: p = 0.016; IDI: 0.005, p < 0.001; NRI: 0.038, p = 0.478). Compared with MI (C-statistic: 0.711), the C-statistic of the model using MIDC was significantly higher (p = 0.031), while the IDI was more than 0 but not statistically significant (IDI: 0.003, p = 0.090).ConclusionAlthough current multimorbidity status is commonly defined by individual chronic conditions, this study found that the multimorbidity index incorporating disease combinations showed supreme performance in predicting mortality among community-dwelling older adults. These findings suggest a need to consider significant disease combinations when measuring multimorbidity in medical research and clinical practice.

Edwardsiella piscicida is an important fish pathogen that causes substantial economic losses. In order to understand its pathogenic mechanism, additional new virulence factors need to be identified. The bacterial thioredoxin system is a major disulfide reductase system, but its function is largely unknown in E. piscicida. In this study, we investigated the roles of the thioredoxin system in E. piscicida (named TrxBEp, TrxAEp, and TrxCEp, respectively) by constructing a correspondingly markerless in-frame mutant strain: ΔtrxB, ΔtrxA, and ΔtrxC, respectively. We found that (i) TrxBEp is confirmed as an intracellular protein, which is different from the prediction made by the Protter illustration; (ii) compared to the wild-type strain, ΔtrxB exhibits resistance against H2O2 stress but high sensitivity to thiol-specific diamide stress, while ΔtrxA and ΔtrxC are moderately sensitive to both H2O2 and diamide conditions; (iii) the deletions of trxBEp, trxAEp, and trxCEp damage E. piscicida’s flagella formation and motility, and trxBEp plays a decisive role; (iv) deletions of trxBEp, trxAEp, and trxCEp substantially abate bacterial resistance against host serum, especially trxBEp deletion; (v) trxAEp and trxCEp, but not trxBEp, are involved in bacterial survival and replication in phagocytes; (vi) the thioredoxin system participates in bacterial dissemination in host immune tissues. These findings indicate that the thioredoxin system of E. piscicida plays an important role in stress resistance and virulence, which provides insight into the pathogenic mechanism of E. piscicida.

Background Cardiovascular health (CVH) status is associated with cardiovascular diseases (CVD). However, evidence for association of CVH change with risk of CVD is scarce. Methods and Results Seven metrics (smoking status, body mass index, physical activity, diet, total cholesterol, blood pressure, and fasting blood glucose) were used to evaluate the CVH status. Having 0 to 2, 3 to 4, and 5 to 7 ideal cardiovascular metrics were categorized as low, moderate, and high CVH status, respectively. Change in CVH status was assessed from 2006/2007 to 2010/2011. We calculated lifetime risk of CVD using a modified Kaplan–Meier method, and life expectancy was evaluated via the multistate lifetable method. There were 82 349 participants included in our analysis. At 35 years index age, the age‐adjusted incident rate and lifetime risk of CVD were increased with decreasing number of ideal CVH metrics. The direction of change in status of CVH was consistently associated with age‐adjusted incident rate and lifetime risk of CVD. At 35 years index age, improvement from low to moderate (37.6% [95% CI, 32.8%–42.4%]) or to high status (24.4% [95% CI, 12.7%–36.0%]) had lower lifetime risk of CVD compared with consistently low status (44.6% [95% CI, 40.8%–48.5%]). The improvement in CVH could prolong the years of life free from CVD. The pattern of incident rate and lifetime risk across change in CVH status was similar at 45 and 55 years index age. Conclusions Higher number of CVH metrics was associated with lower lifetime risk of CVD. The improvement of CVH status could reduce the lifetime risk of CVD and prolonged the year of life free from CVD.

The single nucleotide polymorphism (SNP) rs4148727 in ABCB1 (encoding p-glycoprotein) is associated with lipid levels; however, its association with type 2 diabetes (T2DM) and its the genetic correlation with lipid profiles and T2DM are unclear. We included 2300 participants from 593 families. A generalized estimating equations (GEE) model and Cox regression models were used to estimate the SNP’s effects on T2DM and lipid profiles. The participation of the SNP in T2DM pathogenesis through lipid-associated pathways was tested using mediation analysis. The G allele of the SNP was related to a 32% (6–64%, p = 0.015) increase in T2DM risk. It was also associated with a 10% (1–20%, p = 0.029), 17% (3–32%, p = 0.015), and 4% (1–7%, p = 0.015) increment in total cholesterol (TC), triglyceride (TG), and apolipoprotein A (Apo-A) concentrations, respectively. According to the mediation analysis, only TG (6.9%) and Apo-B (4.0%) had slight but significant mediation effects on the total impact of the SNP on T2DM. The pleiotropic effects of the ABCB1 variant on T2DM and lipids likely act via different pathways. The biological mechanisms should be verified in a future study.

Environmental factors play an important role in the development of ulcerative colitis (UC). However, only few studies have examined the effects of air pollution on UC occurrence. We conducted a time–series analysis to explore the association between short-term exposure to fine particulate matter (PM2.5) and outpatient visits for UC in Beijing, China. In total, 84,000 outpatient visits for UC were retrieved from the Beijing Medical Claim Data for Employees between January 1, 2010 and June 30, 2012. Measurements of daily PM2.5 concentrations were obtained from the United States Embassy air-monitoring station. A generalized additive model with quasi-Poisson link was applied to examine the association between PM2.5 concentrations and outpatient visits for UC stratified by sex, age, and season. We found that short-term exposure to PM2.5 was significantly associated with increased daily outpatient visits for UC at lag 0 day. A 10 μg/m3 increase in PM2.5 concentration at lag 0 day corresponded to a 0.32% increase in outpatient visits for UC (95% confidence interval (CI), 0.05–0.58%; P = 0.019). There was a clear concentration–response association between daily outpatient visits for UC and PM2.5 concentrations. The PM2.5 effects were significant across all sex and season subgroups, without evidence of effect modification by sex (P = 0.942) or season (P = 0.399). The association was positive in patients younger than 65 years old but negative in those 65 years old or older, although the difference was not significant (P = 0.883). In conclusion, our study demonstrated that short-term exposure to ambient PM2.5 was significantly associated with an increased risk of daily outpatient visits for UC, especially in younger people. Additional studies are warranted to confirm our findings.

The emergence of drug resistant bacteria is a tricky and confronted problem in modern medicine, and one of important reasons is the widespread of toxin-antitoxin (TA) systems in pathogenic bacteria. Edwardsiella piscicida (also known as E. tarda) is the leading pathogen threatening worldwide fresh and seawater aquaculture industries and has been considered as a model organism for studying intracellular and systemic infections. However, the role of type II TA systems are completely unknown in aquatic pathogenic bacteria. In this study, we identified and characterized a type II TA system, YefM-YoeB, of E. piscicida, where YefM is the antitoxin and YoeB is the toxin. yefM and yoeB are co-expressed in a bicistronic operon. When expressed in E. coli, YoeB cause bacterial growth arrest, which was restored by the addition of YefM. To investigate the biological role of the TA system, two markerless yoeB and yefM-yoeB in-frame mutant strains, TX01ΔyoeB and TX01ΔyefM-yoeB, were constructed, respectively. Compared to the wild strain TX01, TX01ΔyefM-yoeB exhibited markedly reduced resistance against oxidative stress and antibiotic, and markedly reduced ability to form persistent bacteria. The deletion of yefM-yoeB enhanced the bacterial ability of high temperature tolerance, biofilm formation, and host serum resistance, which is the first study about the relationship between type II TA system and serum resistance. In vitro infection experiment showed that the inactivation of yefM-yoeB greatly enhanced bacterial capability of adhesion in host cells. Consistently, in vivo experiment suggested that the yefM-yoeB mutation had an obvious positive effect on bacteria dissemination of fish tissues and general virulence. Introduction of a trans-expressed yefM-yoeB restored the virulence of TX01ΔyefM-yoeB. These findings suggest that YefM-YoeB is involved in responding adverse circumstance and pathogenicity of E. piscicida. In addition, we found that YefM-YoeB negatively autoregulated the expression of yefM-yoeB and YefM could directly bind with own promoter. This study provides first insights into the biological activity of type II TA system YefM-YoeB in aquatic pathogenic bacteria and contributes to understand the pathogenesis of E. piscicida.

Carbohydrate-active enzymes (CAZymes) are an important characteristic of bacteria in marine systems. We herein describe the CAZymes of Paenibacillus algicola HB172198T, a novel type species isolated from brown algae in Qishui Bay, Hainan, China. The genome of strain HB172198T is a 4,475,055 bp circular chromosome with an average GC content of 51.2%. Analysis of the nucleotide sequences of the predicted genes shows that strain HB172198T encodes 191 CAZymes. Abundant putative enzymes involved in the degradation of polysaccharides were identified, such as alginate lyase, agarase, carrageenase, xanthanase, xylanase, amylases, cellulase, chitinase, fucosidase and glucanase. Four of the putative polysaccharide lyases from families 7, 15 and 38 were involved in alginate degradation. The alginate lyases of strain HB172198T exhibited the maximum activity 152 U/mL at 50 °C and pH 8.0, and were relatively stable at pH 7.0 and temperatures lower than 40 °C. The average degree of polymerization (DP) of the sodium alginate oligosaccharide (AOS) degraded by the partially purified alginate lyases remained around 14.2, and the thin layer chromatography (TCL) analysis indicated that it contained DP2-DP8 oligosaccharides. The complete genome sequence of P. algicola HB172198T will enrich our knowledge of the mechanism of polysaccharide lyase production and provide insights into its potential applications in the degradation of polysaccharides such as alginate.

Few large multicity studies have assessed acute effect of tropospheric ozone pollution on pneumonia risk. We aimed to examine the relation between day-to-day changes in ozone concentrations and hospital admissions for pneumonia in China. We conducted a national time-series study in 184 major Chinese cities from 2014 to 2017. City-specific relation between ozone concentrations and pneumonia admissions was evaluated using an over-dispersed generalized additive model. Random-effects meta-analysis was conducted to pool the city-specific estimates. Two-pollutant models were fitted to test the robustness of the relations. We also investigated potential effect modifiers. Overall, we observed increased admissions for pneumonia associated with ozone exposure. The national-average estimates per 10-μg/m3 increase in ozone were 0.14% (95% CI: 0.03%–0.25%) at lag 0 day in the whole year, 0.30% (95% CI: 0.17%–0.43%) at lag 0 day in the warm season, and 0.20% (95% CI: 0.05%–0.34%) at lag 1 day in the cool season. Two-pollutant models indicated that the ozone effects were not confounded by PM2.5, SO2, NO2 or CO. The association between ozone and pneumonia was stronger in the elderly. Ozone levels and gross domestic product per capita reduced the effects of ozone, and smoking enhanced the effects of ozone. In conclusion, we estimated an increase in daily pneumonia admissions associated with ozone exposure in China. As the first national study in China to report acute effect of ozone on pneumonia hospitalizations, our findings are incredibly meaningful in terms of both ozone pollution related policy development and pneumonia prevention. Keywords: Air pollution, Pneumonia, Ozone, Time-series study

Near medium intense (NMI) fringe is a kind of intense fringe which can be formed near Kerr medium in high-power laser beam propagation. The formation properties of NMI fringe and the relations between NMI fringe and related important parameters are systematically investigated. It is found that it is the co-existence of two wirelike phase-typed scatterers in the incident beam spot which is mainly responsible for the high intensity of NMI fringe. From the viewpoint of coherent superposition, the formation process of NMI fringe is analyzed, and the mechanism that NMI fringe is formed by the coherent superposition of the localized bright fringes in the exit field of Kerr medium slab is demonstrated. The fluctuations of NMI fringe properties with beam wavelength, scatterer spacing and object distance are studied, the coherence of NMI fringe are revealed, and the approximate periodicity of the appearance of remarkable NMI fringe for these parameters are obtained. Especially, it is found that the intensity of NMI fringe is very sensitive to scatterer spacing. Besides, the laws about how NMI fringe properties will be changed by the modulation properties of scatterers and the medium thickness are demonstrated. Keywords: High-power laser beam, Nonlinear propagation, Kerr medium, Small-scale scatterer, Nonlinear imaging

Abstract Background Little is known about the effect of ambient fine particulate matter (PM2.5) on chronic obstructive pulmonary disease (COPD) in China. The objective of this study was to explore the short-term effects of PM2.5 on outpatient and inpatient visits for COPD in Beijing, China. Methods A total of 3,503,313 outpatient visits and 126,982 inpatient visits for COPD between January 1, 2010, and June 30, 2012, were identified from the Beijing Medical Claim Data for Employees. A generalized additive Poisson model was applied to estimate the percentage change with 95% confidence interval (CI) in hospital visits for COPD in relation to an interquartile range (IQR) (90.8 μg/m3) increase in PM2.5 concentrations. Results Short-term exposure to PM2.5 was significantly associated with increased use of COPD-related health services. There were clear exposure–response associations of PM2.5 with COPD outpatient and inpatient visits. An IQR increase in the concurrent day PM2.5 concentrations was significantly associated with a 2.38% (95% CI, 2.22%–2.53%) and 6.03% (95% CI, 5.19%–6.87%) increase in daily outpatient visits and inpatient visits, respectively. Elderly people were more sensitive to the adverse effects. The estimated risk was higher during the warm season compared to the cool season. Conclusions Short-term exposure to PM2.5 was associated with increased risk of hospital visits for COPD. Our findings contributed to the limited evidence concerning the effects of ambient PM2.5 on COPD morbidity in developing countries.

Abstract Little is known about the acute effects of ozone on morbidity risk in China. We conducted a time-series study to examine the association between ozone and daily emergency room visits (ERVs) in Beijing, China. We identified 7,088,309 ERVs between January 1, 2014 and December 31, 2015. A generalized additive model with Poisson regression incorporating penalized spline functions was employed to analyze ERVs in association with daily 8-h maximum ozone concentrations. An increase of 10 μg/m3 of same-day ozone concentration was significantly associated with a 0.24% (95% CI, 0.21%–0.26%), 0.31% (95% CI, 0.27%–0.35%), and 0.43% (95% CI, 0.36%–0.50%) increase in daily ERVs for the whole study period, days when the daily 8-h maximum ozone met the Chinese Ambient Air Quality Standards (CAAQS) Grade II standard, and days that met the CAAQS Grade I standard, respectively. These results were robust when considering the potential confounding effects of PM2.5, PM10, NO2, SO2, and CO. In conclusion, our findings suggested significant effects of ozone exposure on daily ERVs in Beijing. Improving air quality with even lower ozone level than the current CAAQS could yield important public health.