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Norovirus is the predominant pathogen causing foodborne illnesses and acute gastroenteritis (AGE) outbreaks worldwide, imposing a significant disease burden. This study aimed to investigate the epidemiological characteristics and genotypic diversity of norovirus outbreaks in Hongshan District, Wuhan City. A total of 463 AGE cases from 39 AGE-related outbreaks in Hongshan District between January 1, 2021, and June 30, 2023, were included in the study. Reverse transcription-polymerase chain reaction (RT-PCR) was used to identify norovirus types GI and GII in anal swab samples from all cases. Norovirus-positive samples were sequenced and analyzed for the open reading frame (ORF) 1/ORF2 hinge region. 26 norovirus infectious outbreaks were reported among 39 acute diarrheal outbreaks, including 14 outbreaks in kindergartens, 8 in elementary schools, and 4 in universities. Based on clinical symptoms and epidemiological investigations, a total of 1295 individuals were identified as having been exposed to norovirus, yielding an attack rate of 35.75 %. A higher proportion of outbreaks was observed during the winter and spring seasons (38.46 %). Additionally, norovirus-positive samples were subjected to sequencing and analysis of the open reading frame (ORF) 1/ORF2 hinge region. Genotypic data for norovirus was successfully obtained from 18 (69.23 %) of the infectious outbreaks, revealing 10 distinct recombinant genotypes. GII.4 Sydney 2012 [P31] and GII.17[P17] were the predominant strains in 2021 and 2022, GII.3 [P12] emerged as the dominant strain in 2023. Norovirus outbreaks in Hongshan District predominantly occurred in crowded educational institutions, with peaks in the cold season and a high attack rate in universities. GII.3 [P12] has become the locally predominant strain. [ABSTRACT FROM AUTHOR]

Noise pollution has grown to be a major public health issue worldwide. We sought to profile serum metabolite expression changes related to occupational noise exposure by untargeted metabolomics, as well as to evaluate the potential roles of serum metabolites in occupational noise-associated arterial stiffness (AS). Our study involved 30 noise-exposed industrial personnel (Lipo group) and 30 noise-free controls (Blank group). The untargeted metabolomic analysis was performed by employing a UPLC-HRMS. The associations of occupational noise and significant differential metabolites (between Blank/Lipo groups) with AS were evaluated using multivariable-adjusted generalized linear models. We performed the least absolute shrinkage and selection operator regression analysis to further screen for AS's risk metabolites. We explored 177 metabolites across 21 categories significantly differentially expressed between Blank/Lipo groups, and these metabolites were enriched in 20 metabolic pathways. Moreover, 15 metabolites in 4 classes (including food, glycerophosphocholine, sphingomyelin [SM] and triacylglycerols [TAG]) were adversely associated with AS (all P < 0.05). Meanwhile, five metabolites (homostachydrine, phosphatidylcholine (PC) (32:1e), PC (38:6p), SM (d41:2) and TAG (45:1) have been proven to be useful predictors of AS prevalence. However, none of these 15 metabolites were found to have a mediating influence on occupational noise-induced AS. Our study reveals specific metabolic changes caused by occupational noise exposure, and several metabolites may have protective effects on AS. However, the roles of serum metabolites in noise-AS association remain to be validated in future studies. [Display omitted] • Serum metabolite expression changes were profiled by untargeted metabolomics. • Occupational noise exposure causes significant changes in serum metabolites. • Some metabolites were statistically significantly associated with both noise exposure and arterial stiffness. • Metabolites might be useful predictors of arterial stiffness prevalence. • The role of metabolites in noise-induced arterial stiffness needs to be confirmed. [ABSTRACT FROM AUTHOR]

To quantify the association of polycyclic aromatic hydrocarbons (PAHs) and the polygenic risk score (PRS) with lung function decline, we developed a repeated-measures study with 4681 observations from baseline and 6-year follow-up of the Wuhan–Zhuhai cohort. Lung function and urinary monohydroxylated PAH metabolites (OH-PAHs) were measured for each observation. The PRS was derived from 246 lung function-associated genetic variants weighted by the effect size of the decreasing ratio of forced expiratory volume in 1 s by forced vital capacity (FEV1/FVC). Linear mixed models were used to estimate the longitudinal exposure–response relationships between OH-PAHs and lung function, and to evaluate the interactions between OH-PAHs and PRS on the longitudinal change of lung function. We found that each 1-unit increase in log-transformed values of 9-hydroxyfluorene, 2-hydroxyfluorene, 4-hydroxyphenanthrene, 9-hydroxyphenanthrene, 2-hydroxyphenanthrene, 1-hydroxyphenanthrene, 1-hydroxypyrene, low molecular weight OH-PAHs (ΣLMW–OH–PAHs), and total OH-PAHs (ΣOH-PAHs) was associated with an annual change in FEV1/FVC of −0.140, −0.112, −0.260, −0.300, −0.159, −0.220, −0.145, −0.156, and −0.177 %/year, respectively. Interactions on the annual decline of FEV1/FVC were detected between ΣLMW–OH–PAHs and PRS (−0.010 %/year, 95% confidence interval −0.018 to −0.001, P int = 0.0228), and between ΣOH-PAHs and PRS (−0.010 %/year, −0.018 to −0.001, P int = 0.0203). These results indicated that specific and total urinary OH-PAHs were associated with the longitudinal FEV1/FVC decline, and ΣLMW–OH–PAHs as well as ΣOH-PAHs interacted with PRS on the annual decline of FEV1/FVC. [Display omitted] • Positive longitudinal association between PAHs and lung function among general population. • The longitudinal lung function decline associated with PAHs enhanced across increased PRS. • Repeated-measures study was conducted to assess individual PAH exposure from varied sources over a long period. [ABSTRACT FROM AUTHOR]

Abstract The relations of polycyclic aromatic hydrocarbons (PAHs) exposure with platelet indices remain unclear. Based on the baseline data from the Wuhan-Zhuhai Cohort Study, we used generalized linear model, multivariate logistic regression analysis and restricted cubic splines (RCS) to assess linear and nonlinear relationship of PAHs exposure with platelet indices. The results showed that among Wuhan individuals, there were the non-linear relations between total hydroxynaphthalene (ΣOHNa) and mean platelet volume (MPV) or ratio of mean platelet volume to platelet count (MPVP), total hydrophenanthrene (ΣOHPh) and MPV or platelet distribution width (PDW), the sum concentration of urinary monohydroxylated metabolites of PAHs (ΣOH-PAHs) and ratio of platelet count to lymphocyte count (PLR) or MPVP, 1-hydropyrene (1-OHP) and PLR or PDW. But among Zhuhai individuals, neither linear nor non-linear relations were found between each of OH-PAHs or ΣOH-PAHs and platelet indices. The findings indicate that serum MPV and MPVP may be independent biomarkers of effects of exposing to environmental PAHs on human bodies. Graphical abstract Image 1 Highlights • Wuhan individuals had higher levels of 8 OH-PAHs and ΣOH-PAHs than Zhuhai ones. • Wuhan individuals with high OH-PAHs had longitudinal changes in platelet indices. • Wuhan individuals with high OH-PAHs were at high risk of increased MPV and MPVP. • Relations of certain OH-PAHs with platelet indices were non-linear in Wuhan ones. Serum MPV and MPVP may be independent biomarkers for affecting adverse effects of environmental PAHs exposure on human bodies. [ABSTRACT FROM AUTHOR]

Abstract Background Exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with metabolic diseases. However, relationships between PAH exposures and dyslipidemias have not been well addressed. Objectives To investigate associations between urinary PAH metabolite concentrations and dyslipidemias in the general population. Methods Twelve urinary PAH metabolites and four serum lipid profiles were measured in 3640 Chinese adults from the Wuhan-Zhuhai cohort. Dyslipidemias, including hyper-total cholesterol (HyperTC), hyper-triglyceride (HyperTG), hyper-low density lipoprotein cholesterol (HyperLDL-C), and hypo-high density lipoprotein cholesterol (HypoHDL-C) were classified according to the levels of serum lipids. Multiple logistic regression models were used to estimate the associations between urinary PAH metabolites and the prevalence of dyslipidemias. The effects of PAH exposure routes on dyslipidemias were further estimated by stratified analysis. Results We found positive exposure-response relationships between urinary PAH metabolites and the prevalence of dyslipidemias. Compared with the lowest tertile of urinary PAH metabolites, increased risk of HyperTC were observed in those in the highest tertiles; The odds ratios (ORs) and 95% confidence intervals were 1.23 (1.03, 1.47), 1.44 (1.21, 1.71), 1.19 (1.01, 1.42), and 1.43 (1.20, 1.71) for 1-OHNa, 9-OHFlu, 1-OHPh, and 4-OHPh, respectively. Participants in the highest tertiles of 1-OHNa and 2-OHFlu had higher risk for HyperLDL-C, and the ORs were 1.21 (1.01, 1.45) and 1.18 (0.98, 1.42), respectively. Among smokers, only urinary 1-OHNa was associated with increased risk of HyperTC (1.36, 1.08–1.73) and HyperLDL-C (1.33, 1.01–1.74). While the increasing urinary levels of 9-OHFlu, 1-OHPh, and 4-OHPh were significantly associated with increased risk of HyperTC among non-smokers. In addition, the associations between urinary PAH metabolites and dyslipidemias were more pronounced among non-smokers who are cooked for themselves and had long-term traffic exposure. Conclusion Elevated urinary PAH metabolites were associated with increased risks of HyperTC and HyperLDL-C. The source of PAH exposure could modify PAH species that affect dyslipidemias. Graphical abstract Image 1 Highlights • Urinary PAH metabolites were measured in general population of China. • Significant relationships were observed between the urinary PAH metabolites and the prevalence of dyslipidemias. • The source of PAH exposure could modify PAH species that affect dyslipidemias. [ABSTRACT FROM AUTHOR]

Abstract Objective Association of oxidative DNA damage with gain in anthropometric indices has not been fully elucidated. Methods In this study, participants (n = 1151) were derived from the baseline visit of Wuhan residents in the Wuhan-Zhuhai Cohort Study. The participants finished the physical examinations at both baseline and 3-year follow up. Urinary levels of 8-hydroxydeoxyguanosine (8-OHdG) were measured by gradient-elution high performance liquid chromatography method and then calibrated by urinary creatinine (Cr) values. Results Generalized linear models showed that after adjusted for confounding factors, baseline central obesity individuals with a ≥2.5% hip circumference (HC) loss or >5% HC gain had a 0.290 μmol/mol Cr (95% confidence interval (CI): 0.108, 0.472) or 0.553 μmol/mol Cr (95% CI: 0.273, 0.833) increase in urinary 8-OHdG levels compared with those with a −2.5%–2.5% HC gain (both P < 0.05). Moreover, compared with non-central obesity at both baseline and 3-year follow-up, we observed that central obese men at both baseline and 3-year follow-up had a 0.46 μmol/mol Cr (95% CI: 0.16, 0.75) increased in urinary 8-OHdG levels. Conclusions HC gain showed dose-dependent associations with urinary 8-OHdG levels. Moreover, male central obesity at both baseline and 3-year follow-up had an increased risk for urinary 8-OHdG levels. Highlights • Adults with ≥2.5% HC loss increased urinary 8-OHdG levels. • Baseline central obesity with >5% HC gain was at higher risk of increasing 8-OHdG. • Developed central obesity during the 3-year follow-up had higher urinary 8-OHdG. [ABSTRACT FROM AUTHOR]

Abstract Polycyclic Aromatic Hydrocarbons (PAHs) exposure was related with metabolic syndrome (MetS) and heart rate variability (HRV) reduction, and HRV was also affected by cardiometabolic traits. However, the role of cardiometabolic traits in the associations from PAHs exposures to HRV was largely unknown. We conducted this study to investigate whether the relationship between PAHs exposure and HRV reduction was mediated by cardiometabolic traits. Levels of urinary polycyclic aromatic hydrocarbons metabolites (OH-PAHs), 10min-HRV, and metabolic traits were accurately measured for 2476 participants from Wuhan-Zhuhai (WHZH) cohort. Single mediator and multiple mediator models were used to evaluate the mediation effects of cadiometabolic traits. The concentrations of ΣOH-PAHs ranged from 4.20 to 8.63 mg/mmol Cr. When compared with the lowest tertile, ΣOH-PAHs in the highest tertile were significantly related with 20% (95% confidence interval [95%CI]:1%, 40%), 35% (95%CI: 14%, 56%), 22% (95%CI: 1%, 44%), and 38% (95%CI: 9%, 68%) decreases in very low frequency (VLF), low frequency (LF), high frequency (HF), and total power (TP) for participants with MetS, respectively. No statistically significant associations between ΣOH-PAHs and HRV indices were observed for participants without MetS. Similar results were found when we investigated the relationships between OH-PAHs and HRV indices by three groups of OH-PAHs (including total hydroxynaphthalene [ΣOHNa], total hydroxy fluorene [ΣOHFlu], and total hydroxyphenanthrene [ΣOHPh] metabolites). Further, mediation analysis suggested that cardiometabolic traits, including fasting glucose (GLU), high density lipoprotein (HDL), and blood pressure partially mediated the relationship from ΣOH-PAHs to HRV reduction. GLU was the strongest mediator, with mediation percentages of 15.70% for VLF, 14.70% for LF, 43.03% for HF, and 5.61% for TP. Our study found that the relationships between OH-PAHs and HRV reduction differed among participants with and without MetS, and these relationships were found to be partially mediated by cardiometabolic traits, especially fasting glucose. Further studies are encouraged to validate our findings and investigate potential mechanisms. Graphical abstract Image 1 Highlights • The relationships between OH-PAHs and HRV reduction differed among participants with and without MetS. • When grouped by parent PAH, total hydroxynaphthalene and hydroxyfluorene were significantly related with HRV reduction. • The relationship between OH-PAHs and HRV reduction were partially mediated by fasting glucose, HDL and blood pressure. • Our results highlighted cardiometabolic pathways in linking PAH exposure with cardiac autonomic dysfunction evaluating by HRV. The relationship between urinary polycyclic aromatic hydrocarbons metabolites (OH-PAHs) and HRV reduction was modified by metabolic status, and was partially mediated by fasting glucose, high density lipoprotein (HDL) and blood pressure. [ABSTRACT FROM AUTHOR]

The effects of triazine herbicides on glucose metabolism remain unclear. In this study, we aimed to assess the associations between serum triazine herbicides and glycemia-related risk indicators in general adults, and to evaluate the mediating role of natural immunoglobulin M antibodies (IgM) in the above associations among uninfected participants. We measured the concentrations of atrazine, cyanazine, and IgM in serum, as well as fasting plasma glucose (FPG), and fasting plasma insulin in 4423 adult participants from the Wuhan-Zhuhai cohort baseline population, enrolled in 2011–2012. Generalized linear models were used to evaluate the associations of serum triazine herbicides with glycemia-related risk indicators, and mediation analyses were performed to evaluate the mediating role of serum IgM in the above associations. The median levels of serum atrazine and cyanazine were 0.0237 μg/L and 0.0786 μg/L, respectively. Our study found significant positive associations of serum atrazine, cyanazine, and Σtriazine with FPG levels, risk of impaired fasting glucose (IFG), abnormal glucose regulation (AGR), and type 2 diabetes (T2D). Additionally, serum cyanazine and Σtriazine were found to be significant positive associated with the homeostatic model assessment of insulin resistance (HOMA-IR) levels. Significant negative linear relationships were observed in associations of serum IgM with serum triazine herbicides, FPG, HOMA-IR levels, the prevalence of T2D, and AGR (P < 0.05). Furthermore, we observed a significant mediating role by IgM in the associations of serum triazine herbicides with FPG, HOMA-IR, and AGR, with the proportions ranging from 2.96% to 7.71%. To ensure the stability of our findings, we conducted sensitivity analyses in normoglycemic participants and found that the association of serum IgM with FPG and the mediating role by IgM remained stable. Our results suggest that triazine herbicides exposure is positively associated with abnormal glucose metabolism, and decreasing serum IgM may partly mediate these associations. [Display omitted] • Serum samples were measured for atrazine and cyanazine among general urban adults. • Triazine herbicide exposure was associated with abnormal glucose metabolism. • Triazine herbicide exposure was negatively associated with serum IgM level. • Down-regulated serum IgM level was associated with abnormal glucose metabolism. • IgM mediated triazine herbicide exposure-associated abnormal glucose metabolism. [ABSTRACT FROM AUTHOR]

The adverse health effects of ozone pollution have been a globally concerned public health issue. Herein we aim to investigate the association between ozone exposure and glucose homeostasis, and to explore the potential role of systemic inflammation and oxidative stress in this association. A total of 6578 observations from the Wuhan-Zhuhai cohort (baseline and two follow-ups) were included in this study. Fasting plasma glucose (FPG) and insulin (FPI), plasma C-reactive protein (CRP, biomarker for systemic inflammation), urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG, biomarker for oxidative DNA damage), and urinary 8-isoprostane (biomarker for lipid peroxidation) were repeatedly measured. After adjusting for potential confounders, ozone exposure was positively associated with FPG, FPI, and homeostasis model assessment of insulin resistance (HOMA-IR), and negatively associated with HOMA of beta cell function (HOMA-β) in cross-sectional analyses. Each 10 ppb increase in cumulative 7-days moving average ozone was associated with a 13.19%, 8.31%, and 12.77% increase in FPG, FPI, and HOMA-IR, respectively, whereas a 6.63% decrease in HOMA-β (all P < 0.05). BMI modified the associations of 7-days ozone exposure with FPI and HOMA-IR, and the effects were stronger in subgroup whose BMI ≥24 kg/m2. Consistently high exposure to annual average ozone was associated with increased FPG and FPI in longitudinal analyses. Furthermore, ozone exposure was positively related to CRP, 8-OHdG, and 8-isoprostane in dose-response manner. Increased CRP, 8-OHdG, and 8-isoprostane could dose-dependently aggravate glucose homeostasis indices elevations related to ozone exposure. Increased CRP and 8-isoprostane mediated 2.11−14.96% of ozone-associated glucose homeostasis indices increment. Our findings suggested that ozone exposure could cause glucose homeostasis damage and obese people were more susceptible. Systemic inflammation and oxidative stress might be potential pathways in glucose homeostasis damage induced by ozone exposure. [Display omitted] • Ozone exposure could cause glucose homeostasis disorder. • Effects of ozone exposure on FPI and HOMA-IR were more susceptible in obese people. • Ozone exposure was positively associated with CRP, 8-OHdG, and 8-isoprostane. • CRP, 8-OHdG, and 8-isoprostane aggravated glucose homeostasis harm caused by ozone. • CRP and 8-isoprostane partly mediated ozone-associated glucose homeostasis disorder. [ABSTRACT FROM AUTHOR]

Environmental pyrethroids are concerning due to their widespread residues and potential implications on human health. We aimed to assess the association of pyrethroid exposure with glucose homeostasis and examine the interaction between obesity and pyrethroid exposure. A total of 4233 US general adults from the National Health and Nutrition Examination Survey with measured urinary pyrethroid metabolites, fasting plasma glucose (FPG), fasting insulin (FINS), and glycated hemoglobin A1c (HbA1c) were included in the study. The homeostasis model assessment (HOMA2) calculator was utilized to assess insulin resistance (HOMA2-IR), insulin sensitivity (HOMA2-IS), and beta-cell function (HOMA2-β). We estimated the associations of pyrethroid metabolites with glucose homeostasis parameters (FPG, FINS, HbA1c, HOMA2-IR, HOMA2-IS, and HOMA2-β) using multivariate linear regression models and restricted cubic spline models and further assessed the interaction between obesity and pyrethroid metabolites on glucose dyshomeostasis. Urinary 3-phenoxybenzoic acid (3-PBA) was the most detected pyrethroid metabolite (81%) with a median concentration of 0.43 (interquartile range 0.20–1.01) μg/g urinary creatinine. Compared with the participants in the lowest quartile, those in the highest quartile of 3-PBA had a 1.93% (95% confidence interval: 0.46%, 3.42%), 6.69% (1.96%, 11.64%), 1.60% (0.64%, 2.57%), 7.06% (2.33%, 12.01%), −6.59% (−10.72%, −2.28%), and 1.10% (−2.69%, 5.04%) alteration in FPG, FINS, HbA1c, HOMA2-IR, HOMA2-IS, and HOMA2-β, respectively. The restricted cubic spline model displayed a linear positive association between 3-PBA and FPG, FINS, HbA1c, and HOMA2-IR, and a negative association with HOMA2-IS (all P for overall <0.05 and P for non-linear >0.05). Additionally, the association between urinary 3-PBA and FPG was modified by general obesity (P for interaction <0.05), with a more pronounced association observed in obese participants than in non-obese participants. Our findings suggested that pyrethroid exposure was associated with glucose dyshomeostasis. General obesity significantly heightened the association between pyrethroid exposure and increased FPG level. [Display omitted] • We assessed the link with glucose homeostasis of pyrethroids in US general adults. • Urinary pyrethroid metabolite 3-PBA was associated with glucose dyshomeostasis. • The relationship of urinary 3-PBA with FPG was modified by general obesity. • Obesity exacerbated the increased FPG associated with urinary 3-PBA. [ABSTRACT FROM AUTHOR]

Abstract The relation between nonalcoholic fatty liver disease (NAFLD) and hypertension is not fully understood. To examine the effect of the change in NAFLD status on the risk of incident hypertension, and vice versa, 6704 eligible hypertension-free subjects and 9328 NAFLD-free subjects from the Dongfeng-Tongji cohort study at baseline were enrolled in the study. Among the hypertension-free subjects, development and persistence of NAFLD were associated with an increased odds ratio (OR) for incident hypertension (OR: 1.49, 95% confidence interval [CI]: 1.26–1.76, P <.0001; OR: 1.50, 95% CI: 1.27–1.78, P <.0001). However, the resolution of NAFLD was not a risk factor for incident hypertension. Among the NAFLD-free subjects, the risk of new-emerging NAFLD was robust for hypertension status both in no-yes (OR: 1.45, CI: 1.23–1.71) and yes-yes (OR: 1.61, CI: 1.35–1.92). Moreover, stratified analysis by diabetes and overweight/obese for the risk of incident NAFLD showed that incident hypertension (no-yes) and persistent hypertension (yes-yes) were associated with risk of incident NAFLD in subjects without diabetes or overweight/obesity. In the overweight/obese participants, persistent hypertension (yes-yes) was a risk factor for incident NAFLD (OR: 1.29, 95% CI: 1.01–1.64, P =.0387). Conclusively, incidence and persistence of NAFLD are associated with increased risk of hypertension, and vice versa. Highlights • There are bidirectional associations between nonalcoholic fatty liver disease (NAFLD) and hypertension. • Hypertension is associated with increased risk of NAFLD. • Incident hypertension and persistent hypertension were associated with risk of incident NAFLD in subjects without diabetes or overweight/obesity. [ABSTRACT FROM AUTHOR]

Fine particle (PM 2.5 )-related lung damage has been reported in most studies regarding environmental or personal PM 2.5 concentrations. To assess effects of personal PM 2.5 exposures on lung function, we recruited 20 postgraduate students and estimated the individual doses of inhaled PM 2.5 based on their microenvironmetal PM 2.5 concentrations, time-activity patterns and refereed inhalation rates. During the period of seven consecutive days in each of the four seasons, we repeatedly measured the daily lung function parameters and airway inflammation makers such as fractional exhaled nitric oxide (FeNO) as well as systemic inflammation markers including interleukin-1β on the final day. The high individual dose (median (IQR)) of inhaled PM 2.5 was 957 (948) μg/day. We observed a maximum FeNO increase (9.1% (95%CI: 2.2–15.5)) at lag 0 day, a maximum decrease of maximum voluntary ventilation (11.8% (95% CI: 4.6–19.0)) at lag 5 day and a maximum interleukin-1β increase (103% (95% CI: 47–159)) at lag 2 day for an interquartile range increase in the individual dose of inhaled PM 2.5 during the four seasons. Short-term exposure to PM 2.5 assessed by the individual dose of inhaled PM 2.5 was associated with higher airway and systemic inflammation and reduced lung function. Further studies are needed to understand better underlying mechanisms of lung damage following acute exposure to PM 2.5. [ABSTRACT FROM AUTHOR]

The future Internet of Things (IoT) will enable Internet connectivity for a vast amount of battery-powered devices, which usually need to wirelessly communicate with each other or to some remote gateways through multi-hop communications. Although ZigBee has become a widely used communication technology in IoT, Wi-Fi, on the other hand, has its unique advantages such as high throughput and native IP compatibility, despite its potentially higher energy consumption. With the development of IoT, more and more IoT devices are equipped with multiple radio interfaces, such as both Wi-Fi and ZigBee. Inspired by this, we propose a cross-interface power saving management (CPSM) scheme, which leverages the existing low-power ZigBee interfaces to wake up the high-power Wi-Fi interfaces on demand towards enabling multi-hop communications in IoT. The objective is to minimize the network energy consumption while satisfying certain end-to-end delay requirements. The results of extensive simulations and prototype-based experiments have demonstrated that the energy consumption of our proposed CPSM is 79.2% and 68.9% lower than those of the IEEE 802.11’s standard power saving scheme and a state-of-the-art scheme in moderate traffic scenarios, respectively. [ABSTRACT FROM AUTHOR]

Background Inflammation may play an important role in the association between exposure to polycyclic aromatic hydrocarbons (PAHs) and atherosclerotic cardiovascular disease (ASCVD) risk. However, the underlying mechanisms remain unclear. Objectives To investigate the association of PAHs exposure with ASCVD risk and effects of mean platelet volume (MPV) or Club cell secretory protein (CC16) on the association. Methods A total of 2022 subjects (689 men and 1333 women) were drawn from the baseline Wuhan residents of the Wuhan-Zhuhai Cohort study. Data on demography and the physical examination were obtained from each participant. Urinary monohydroxy PAH metabolites (OH-PAHs) levels were measured by a gas chromatography-mass spectrometry. We estimated the association between each OH-PAHs and the 10-year ASCVD risk or coronary heart disease (CHD) risk using logistic regression models, and further analyze the mediating effect of MPV or plasma CC16 on the association by using structural equation modeling. Results The results of multiple logistic regression models showed that some OH-PAHs were positively associated with ASCVD risk but not CHD risk, including 2-hydroxyfluoren (β = 1.761; 95% CI: 1.194–2.597), 9-hydroxyfluoren (β = 1.470; 95% CI: 1.139–1.898), 1-hydroxyphenanthrene (β = 1.480; 95% CI: 1.008–2.175) and ΣOH-PAHs levels (β = 1.699; 95% CI: 1.151–2.507). The analysis of structural equation modeling shows that increased MPV and increased plasma CC16 levels contributed 13.6% and 15.1%, respectively, to the association between PAHs exposure and the 10-year ASCVD risk (p < 0.05). Conclusions Exposure to PAHs may increase the risk of atherosclerosis, which was partially mediated by MPV or CC16. [ABSTRACT FROM AUTHOR]

Previous studies have reported an association of exposure to polycyclic aromatic hydrocarbons (PAHs) with lung function decline or cardiovascular diseases, or reduced lung function with 10-year cardiovascular (CV) risk. We analyzed risk factors for the 10-year Framingham CV risk using multiple logistic regression, and examined the mediational effect of reduced lung function on the association between exposure to PAHs and FRS using the post-exploratory structural equation modeling. Participants (n = 2268) were drawn from the Wuhan residents at baseline from the Wuhan-Zhuhai Cohort Study. They completed the physical examination, measurements of lung function and urinary monohydroxylated-PAHs (OH-PAHs). In all individuals, we found a dose-response relationship of PAHs exposure, forced expiratory volume in 1 s (FEV1) or forced vital capacity (FVC) with the 10-year CV risk. The proportions of FEV1 and FVC mediation effects in association of PAH exposure with the10-year CV risk were 35% and 24%, respectively. The findings indicated that PAHs exposure or reduced lung function increased the 10-year CV risk. Impaired lung function may partly contribute to increase in the 10-year CV risk regarding exposure to PAHs. [ABSTRACT FROM AUTHOR]

The effect of PM 2.5 exposure on lung function reduction has been well-documented, but the underlying mechanism remains unclear. MiR-4301 may be involved in regulating pathways related to lung injury/repairment, and this study aimed to explore the potential role of miR-4301 in PM 2.5 exposure-associated lung function reduction. A total of 167 Wuhan community nonsmokers were included in this study. Lung function was measured and personal PM 2.5 exposure moving averages were evaluated for each participant. Plasma miRNA was determined by real-time polymerase chain reaction. A generalized linear model was conducted to assess the relationships among personal PM 2.5 moving average concentrations, lung function, and plasma miRNA. The mediation effect of miRNA on the association of personal PM 2.5 exposure with lung function reduction was estimated. Finally, we performed pathway enrichment analysis to predict the underlying pathways of miRNA in lung function reduction from PM 2.5 exposure. We found that each 10 μg/m3 increase in the 7-day personal PM 2.5 moving average concentration (Lag0-7) was related to a 46.71 mL, 1.15%, 157.06 mL/s, and 188.13 mL/s reductions in FEV 1 , FEV 1 /FVC, PEF, and MMF, respectively. PM 2.5 exposure was negatively associated with plasma miR-4301 expression levels in a dose‒response manner. Additionally, each 1% increase in miR-4301 expression level was significantly associated with a 0.36 mL, 0.01%, 1.14 mL/s, and 1.28 mL/s increases in FEV 1 , FEV 1 /FVC, MMF, and PEF, respectively. Mediation analysis further revealed that decreased miR-4301 mediated 15.6% and 16.8% of PM 2.5 exposure-associated reductions in FEV 1 /FVC and MMF, respectively. Pathway enrichment analyses suggested that the wingless related-integration site (Wnt) signaling pathway might be one of the pathways regulated by miR-4301 in the reduction of lung function from PM 2.5 exposure. In brief, personal PM 2.5 exposure was negatively associated with plasma miR-4301 or lung function in a dose‒response manner. Moreover, miR-4301 partially mediated the lung function reduction associated with PM 2.5 exposure. [Display omitted] • MiR-4301 may play a role in PM 2.5 exposure-related lung function reduction. • PM 2.5 exposure was negatively associated with miR-4301 or lung function. • Pathway regulated by miR-4301 in PM 2.5 -related lung injury was predicted. [ABSTRACT FROM AUTHOR]

We aimed to explore the association between occupational noise exposure duration and heart rate variability (HRV) and the underlying mechanism. A total of 449 subjects in a manufacturing company in Wuhan, China were included in our study and six candidate miRNAs (miR-200a-3p, miR-200b-3p, miR-200c-3p, miR-1-3p, miR-92a-3p and miR-21–5p) were tested among 200 individuals. Information combining the work histories and the occupational noise monitoring records were used to calculate the exposure of occupational noise, HRV indices were measured by using 3-channel digital Holter monitors, including the standard deviation of all normal R-R intervals (SDNN), the root mean of the square of successive differences between adjacent normal NN intervals (r-MSSD), SDNN index, low-frequency power (LF), high-frequency power (HF) and TP (total power). We found a significant linear negative dose-response relationship between occupational noise exposure duration and HRV indices (P for overall <0.05, P for nonlinear >0.05), including SDNN, r-MSSD, SDNN index, LF and HF. In the continuous models, the β (95% CIs) for each 1-year occupational noise exposure were −0.002 (−0.004, −0.001) for SDNN, −0.002 (−0.004, −0.001) for r-MSSD, −0.002 (−0.004, −0.001) for SDNN index, and −0.006 (−0.012, −0.001) for HF. Meanwhile, we also found that occupational noise exposure duration was significantly associated with lower expression of five miRNAs, when adjusting for other covariates. The β (95% CIs) were −0.039 (−0.067, −0.011) for miRNA-200c-3p, −0.053 (−0.083, −0.022) for miRNA-200a-3p, −0.044 (−0.070, −0.019) for miRNA-200b-3p, −0.032 (−0.048, −0.017) for miRNA-92a-3p, and −0.063 (−0.089, −0.038) for miRNA-21–5p in the continuous models. In addition, we found a positive association between miRNA-1-3p and LF (β = 0.039, 95% CI = 0.002, 0.080). Our study suggests that occupational noise exposure duration is associated with cardiac autonomic dysfunction, and the role of miRNAs in noise induced HRV reduction needs to be confirmed in future studies. [Display omitted] • Occupational noise exposure duration is associated with reduced SDNN, SDNN index, and HF. • Occupational noise exposure duration is associated with lower miR-200c-3p, miR-200a-3p, miR-200b-3p, miR-92a-3p, and miR-21–5p. • The role of miRNAs in noise induced HRV reduction needs to be confirmed. [ABSTRACT FROM AUTHOR]

Previous studies have suggested that short-term exposure to ambient air pollution was associated with pediatric hospital admissions and emergency room visits for certain respiratory diseases; however, there is limited evidence on the association between short-term air pollution exposure and pediatric outpatient visits. Our aim was to quantitatively assess the short-term effects of ambient air pollution on pediatric outpatient visits for respiratory diseases. We conducted a time-series study in Yichang city, China between Jan 1, 2014 and Dec 31, 2015. Daily counts of pediatric respiratory outpatient visits were collected from 3 large hospitals, and then linked with air pollution data from 5 air quality monitoring stations by date. We used generalized additive Poisson models to conduct linear and nonlinear exposure-response analyses between air pollutant exposures and pediatric respiratory outpatient visits, adjusting for seasonality, day of week, public holiday, temperature, and relative humidity. Each interquartile range (IQR) increase in PM 2.5 (lag 0), PM 10 (lag 0), NO 2 (lag 0), CO (lag 0), and O 3 (lag 4) concentrations was significantly associated with a 1.91% (95% CI: 0.60%, 3.23%), 2.46% (1.09%, 3.85%), 1.88% (0.49%, 3.29%), 2.00% (0.43%, 3.59%), and 1.91% (0.45%, 3.39%) increase of pediatric respiratory outpatient visits, respectively. Similarly, the nonlinear exposure-response analyses showed monotonic increases of pediatric respiratory outpatient visits by increasing air pollutant exposures, though the associations for NO 2 and CO attenuated at higher concentrations. These associations were unlikely modified by season. We did not observe significant association for SO 2 exposure. Our results suggest that short-term exposures to PM 2.5 , PM 10 , NO 2 , CO, and O 3 may account for increased risk of pediatric outpatient visits for respiratory diseases, and emphasize the needs for reduction of air pollutant exposures for children. [ABSTRACT FROM AUTHOR]

PM 2.5 exposure leads to lung function alteration. The potential pathway underlying above association, especially the role of DNA methylation is unclear. The objectives of this study are to evaluate the associations of personal PM 2.5 concentrations with DNA methylation at the epigenome-wide level, and investigate how PM 2.5 -related DNA methylation affects lung function. A total of 402 observations of non-smokers were selected from the Wuhan-Zhuhai cohort. PM 2.5 exposure was estimated through a model established in the same population. Blood DNA methylation levels were determined through Illumina Infinium MethylationEPIC BeadChips. Lung function was tested through spirometry on the day of blood sampling. The associations of PM 2.5 exposure with DNA methylation and DNA methylation with lung function were determined through linear mixed models. Ten PM 2.5 -related CpG sites (mapped to 7 different genes) were observed with false discovery rate <0.05. Methylation levels of cg24821877, cg24862131, cg23530876, cg11149743 and cg10781276 were positively associated with PM 2.5 concentrations. While methylation levels of cg10314909, cg08968107, cg18362281, cg24663971 and cg17834632 were negatively associated with PM 2.5 concentrations. The top CpG was cg24663971 (P = 1.51✕10−9). Among the above 10 sites, significantly positive associations of methylation levels of cg24663971 with FVC%pred and FEV 1 %pred, and cg10314909 with FVC, FVC%pred, and FEV 1 %pred were observed. Age had modification effect on the associations between cg24663971 methylation and FVC%pred, and the associations were more obvious among participants with age ≥58 years. In conclusion, PM 2.5 exposure was associated with DNA methylation, and PM 2.5 -related DNA methylation was associated with lung function among Wuhan urban non-smokers. [Display omitted] • Ten CpGs were linked to PM 2.5 exposure with false discovery rate <0.05. • Cg24663971 and cg10314909 methylation was positively associated with lung function. • PM 2.5 exposure concentrations at the individual level were estimated. • Blood DNA methylation at the epigenome level were determined. [ABSTRACT FROM AUTHOR]