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Background Although interleukin-10 (IL-10) is a potent inhibitor of allergic diseases, the association between promoter -1082/-819/-592 polymorphisms and asthma susceptibility remains inconclusive. We sought to determine if IL-10 promoter -1082/-819/-592 polymorphisms contribute to asthma susceptibility and are associated with phenotypes of atopic asthma. Methods Systematic computerized searches were performed. Pooled odds ratios (ORs) and 95 % confidence intervals (CIs) were estimated by using random-effect and fixed-effect models, based on between-study heterogeneity. Subgroup analyses were performed according to age, ethnicity, and atopy. Publication bias was detected by funnel plot using Egger's test. Results A total of 4,716 asthmatic patients and 5,093 controls were included. The asthma susceptibility correlated significantly with IL-10 promoter gene -1082 polymorphism [OR (95 % CI) 1.26 (1.02, 1.55) for AA vs. AG + GG] and -592 polymorphism [OR (95 % CI) 1.12 (1.07, 1.34) for AC + AA vs. CC] (both P < 0.05), but not with -819 polymorphism (P > 0.05). Subgroup analyzes suggested that the AA versus AG + GG genotype of -1082A/G polymorphism and AC + AA versus CC genotype of -592A/C polymorphism contributed significantly to increased asthma susceptibility in adults [OR (95 % CI) 1.39 (1.03, 1.87) for -1082A/G and 1.53 (1.25, 1.87) for -592A/C polymorphism]. The Asian population [OR (95 % CI) 1.35 (1.1, 1.7) for -1082A/G and 1.4 (1.12, 1.64) for -592A/C polymorphism] and subjects with atopic asthma [OR (95 % CI) 1.49 (1.18, 1.88) for -1082A/G and 1.23 (1.01, 1.48) for -592A/C polymorphism] also had an increased susceptibility of asthma. No publication bias was detected. Conclusions IL-10 promoter -1028A/G, -592A/C polymorphisms and their haplotypes, but not -819T/C polymorphism, correlate with asthma susceptibility. Electronic supplementary material The online version of this article (doi:10.1007/s00408-013-9519-8) contains supplementary material, which is available to authorized users., Author(s): Xue-yan Zheng[sup.1] , Wei-jie Guan[sup.2] , Chen Mao[sup.3] , Hui-fang Chen[sup.1] , Hong Ding[sup.1] , Jin-ping Zheng[sup.2] , Ting-ting Hu[sup.1] , Min-hong Luo[sup.1] , Yan-hui Huang[sup.1] , Qing Chen[sup.1] [...]

Background: We aimed to explore the association between long-term exposure to particulate matter ≤ 2.5 µm (PM2.5) and metabolic syndrome (MetS) and its components including fasting blood glucose (FBG), blood pressure, triglyceride (TG), high-density lipoprotein cholesterol (HDL-c) and waist circumference among adults and elderly in south China.Methods: We surveyed 6628 participants in the chronic disease and risk factors surveillance conducted in 14 districts of Guangdong province in 2015. MetS was defined based on the recommendation by the Joint Interim Societies' criteria. We used the spatiotemporal land-use regression (LUR) model to estimate the two-year average exposure of ambient air pollutants (PM2.5, PM10, SO2, NO2, and O3) at individual levels. We recorded other covariates by using a structured questionnaire. Generalized linear mixed model was used for analysis.Results: A 10-μg/m3 increase in the two-year mean PM2.5 exposure was associated with a higher risk of developing MetS [odd ratio (OR): 1.17, 95% confidence interval (CI): 1.01, 1.35], increased risk of fasting blood glucose level. (OR: 1.18, 95% CI: 1.02, 1.36), and hypertriglyceridemia (OR: 1.36, 95% CI: 1.18, 1.58) in the adjusted/unadjusted models (all P < 0.05). We found significant interaction between PM2.5 and the region, exercise on the high TG levels, and an interaction with the region, age, exercise and grain consumption on FBG (P interaction < 0.05).Conclusions: Long-term exposure to PM2.5 was associated with MetS, dyslipidemia and FBG impairment. Efforts should be made for environment improvement to reduce the burden of MetS-associated non-communicable disease. [ABSTRACT FROM AUTHOR]

Objectives: To analyse the patterns of transition of health burden for 110 causes of death by stratification of age, sex and geographic regions in Guangdong between 2005 and 2015.Methods: We analysed the age-specific, sex-specific, region-specific mortality in Guangdong based on assembled databases. County-level surveillance data were calculated to inform city-level changes.Results: The age-standardised mortality of all causes, non-communicable diseases (NCDs), communicable diseases, maternal diseases, neonatal diseases, malnutrition and injury declined progressively. Despite declining mortality of NCDs, the overall burden of disease was dominated by NCDs (ie, cerebrovascular disease, chronic obstructive pulmonary disease) that still accounted for 86.93% and 88.12% of death in 2005 and 2015, respectively. Considerable variations across geographic regions were observed (lowest in Pearl River Delta and highest in west Guangdong). There was a modest shift to transport injuries at younger ages and unintentional injuries in the elderly.Conclusions: We have documented a dramatic change in the overall mortality and age-specific, sex-specific and cause-specific mortality in Guangdong province between 2005 and 2015. The significant burden of NCDs remains a major healthcare issue despite the notable progress in reducing mortality in Guangdong, China. Our findings highlight important unmet needs to refine healthcare services by taking into account the inequity of age, sex and geographic regions. Identification of the 'treatable' risk factors and improved disease surveillance should be continuously improved to minimised the overall and cause-specific mortality. [ABSTRACT FROM AUTHOR]

We hypothesized that exposure to polluting fuels for cooking was associated with abnormality of glucose metabolism and diabetes mellitus (DM) in south urban China. 3414 residents were surveyed in 14 urban areas of Guangdong Province in 2018. We recorded polluting fuels for cooking exposure, different DM status (DM, prediabetes), fasting blood glucose (FBG), oral glucose tolerance test (OGTT), glycated hemoglobin (HbA1c), and other covariates by using a structured questionnaire. We conducted logistic regression model and multivariate linear regression model based on propensity‐score method (inverse probability of weighting) to examine the effect of polluting fuels for cooking exposure on DM and glucose metabolism. Exposure to polluting fuels for cooking was associated with DM (odds ratio: 2.57, 95% confidence interval: 1.71 to 3.86) and prediabetes (odds ratio: 1.98, 95% confidence interval: 1.52 to 2.58) in both the adjusted and unadjusted models (all p < 0.05). Exposure to polluting fuels for cooking was significantly associated with an increase of FBG (β: 0.30 mmol/L, 95% confidence interval: 0.22 to 0.38 mmol/L). Sensitivity analysis showed that the results were not substantially changed. There was an increased risk of DM, prediabetes and high levels of FBG, OGTT, and HbA1c among participants aged ≥ 40 years with exposure to polluting fuels for cooking. We demonstrated that exposure to polluting fuels for cooking was associated with higher levels of FBG, which contributed to the increased risk of DM and prediabetes in middle‐aged elderly Chinese population living in urban areas. [ABSTRACT FROM AUTHOR]

Background: Although interleukin-10 (IL-10) is a potent inhibitor of allergic diseases, the association between promoter −1082/−819/−592 polymorphisms and asthma susceptibility remains inconclusive. We sought to determine if IL-10 promoter −1082/−819/−592 polymorphisms contribute to asthma susceptibility and are associated with phenotypes of atopic asthma. Methods: Systematic computerized searches were performed. Pooled odds ratios (ORs) and 95 % confidence intervals (CIs) were estimated by using random-effect and fixed-effect models, based on between-study heterogeneity. Subgroup analyses were performed according to age, ethnicity, and atopy. Publication bias was detected by funnel plot using Egger's test. Results: A total of 4,716 asthmatic patients and 5,093 controls were included. The asthma susceptibility correlated significantly with IL-10 promoter gene −1082 polymorphism [OR (95 % CI) 1.26 (1.02, 1.55) for AA vs. AG + GG] and −592 polymorphism [OR (95 % CI) 1.12 (1.07, 1.34) for AC + AA vs. CC] (both P < 0.05), but not with −819 polymorphism ( P > 0.05). Subgroup analyzes suggested that the AA versus AG + GG genotype of −1082A/G polymorphism and AC + AA versus CC genotype of −592A/C polymorphism contributed significantly to increased asthma susceptibility in adults [OR (95 % CI) 1.39 (1.03, 1.87) for −1082A/G and 1.53 (1.25, 1.87) for −592A/C polymorphism]. The Asian population [OR (95 % CI) 1.35 (1.1, 1.7) for −1082A/G and 1.4 (1.12, 1.64) for −592A/C polymorphism] and subjects with atopic asthma [OR (95 % CI) 1.49 (1.18, 1.88) for −1082A/G and 1.23 (1.01, 1.48) for −592A/C polymorphism] also had an increased susceptibility of asthma. No publication bias was detected. Conclusions: IL-10 promoter −1028A/G, −592A/C polymorphisms and their haplotypes, but not −819T/C polymorphism, correlate with asthma susceptibility. [ABSTRACT FROM AUTHOR]

Background: Few studies have compared the associations between long-term exposures to particulate matters (aerodynamic diameter ≤1, ≤2.5 and ≤10 µm: PM 1 , PM 2.5 and PM 10 , respectively) and asthma and asthma-related respiratory symptoms. The objective of the present study was to compare the strength of the aforementioned associations in middle-aged and elderly adults., Methods: We calculated the mean 722-day personal exposure estimates of PM 1 , PM 2.5 and PM 10 at 1 km×1 km spatial resolution between 2013 and 2019 at individual levels from China High Air Pollutants (CHAP) datasets. Using logistic regression models, we presented the associations as odds ratios and 95% confidence intervals, for each interquartile range (IQR) increase in PM 1 /PM 2.5 /PM 10 concentration. Asthma denoted a self-reported history of physician-diagnosed asthma or wheezing in the preceding 12 months., Results: We included 7371 participants in COPD surveillance from Guangdong, China. Each IQR increase in PM 1 , PM 2.5 and PM 10 was associated with a greater odds (OR (95% CI)) of asthma (PM 1 : 1.22 (1.02-1.45); PM 2.5 : 1.24 (1.04-1.48); PM 10 : 1.30 (1.07-1.57)), wheeze (PM 1 : 1.27 (1.11-1.44); PM 2.5 : 1.30 (1.14-1.48); PM 10 : 1.34 (1.17-1.55)), persistent cough (PM 1 : 1.33 (1.06-1.66); PM 2.5 : 1.36 (1.09-1.71); PM 10 : 1.31 (1.02-1.68)) and dyspnoea (PM 1 : 2.10 (1.84-2.41); PM 2.5 : 2.17 (1.90-2.48); PM 10 : 2.29 (1.96-2.66)). Sensitivity analysis results were robust after excluding individuals with a family history of allergy. Associations of PM 1 , PM 2.5 and PM 10 with asthma and asthma-related respiratory symptoms were slightly stronger in males., Conclusion: Long-term exposure to PM is associated with increased risks of asthma and asthma-related respiratory symptoms., Competing Interests: Conflict of interest: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. Wei-jie Guan is an Associate Editor of ERJ Open Research., (Copyright ©The authors 2024.)

Competing Interests: Dr. Guan reports grants from Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme 2017, during the conduct of the study.

Background: Japanese encephalitis caused by Japanese encephalitis virus (JEV) is an endemic zoonotic disease of high public health importance in the Asian Pacific region. The aim of this study was to investigate the presence of JEV infection in commensal and field rodents in South China., Materials and Methods: RNA copies of JEV were detected in brain samples of rodents using real-time RT-PCR. Detection of serum against JEV-reactive antibodies was performed using indirect enzyme-linked immunosorbent assay and microneutralization test., Results: In total, 198 rodents were collected from Guangzhou City and Xiamen City between November 2013 and May 2014. JEV RNA was not detected in 188 brain samples. Forty-four in 96 serum samples (45.8%) were positive for JEV-reactive IgG antibodies. The prevalence of neutralizing antibodies to against JEV-reactive in these serum samples was 61.5% (24/39), with titers ranging from 1:10 to 1:56., Conclusion: Rodents are not known to play a role in transmission of JEV in Asia, nor is there an evidence to support a role for rodents in transmission of other related flaviviruses in China. However, in the current study, we detected evidence of JEV-reactive antibodies in large numbers of Rattus norvegicus and Rattus losea Swinhoe. Further studies of rodents as potential hosts of JEV or other related flaviviruses are warranted.

Herpesviruses (HVs) can cause asymptomatic, benign, or fatal infections in a variety of animal species. However, the prevalence and phylogenetic characteristics of HVs in rodents and shrews in China are poorly understood. We thus performed a molecular detection and phylogenetic analysis of rat and shrew HVs in southern China between 2012 and 2014. Seventeen (6.7%) of 255 rectal swab specimens from rats and six (6.7%) of 90 rectal swab specimens from shrews tested positive for HVs. Phylogenetic analysis revealed that rodent and shrew HVs detected in this study were species specific, clustering in the Betaherpesvirinae and Gammaherpesvirinae clade. Novel Macavirus was detected in Rattus norvegicus (RN/13YX52/24 and RN/14HC50) and gammaherpesviruses in Suncus murinus (SM/14BY7/16/20/97/99/106).These findings have contributed to our understanding of the taxonomy, phylogeny, and biology of HVs.