Explore the vast range of titles available.

The lattice Boltzmann method (LBM) has experienced tremendous advances and has been well accepted as a useful method to simulate various fluid behaviors. For computational microfluidics, LBM may present some advantages, including the physical representation of microscopic interactions, the uniform algorithm for multiphase flows, and the easiness in dealing with complex boundary. In addition, LBM-like algorithms have been developed to solve microfluidics-related processes and phenomena, such as heat transfer, electric/magnetic field, and diffusion. This article provides a practical overview of these LBM models and implementation details for external force, initial condition, and boundary condition. Moreover, recent LBM applications in various microfluidic situations have been reviewed, including microscopic gaseous flows, surface wettability and solid–liquid interfacial slip, multiphase flows in microchannels, electrokinetic flows, interface deformation in electric/magnetic field, flows through porous structures, and biological microflows. These simulations show some examples of the capability and efficiency of LBM in computational microfluidics.

Oxides of nitrogen (NO ) and volatile organic compounds (VOCs) released into the atmosphere can react in the presence of solar irradiation, leading to ozone formation in the troposphere. Historically, before clean air regulations were implemented to control NO and VOCs, ozone concentrations were high enough to exert acute effects such as eye and nose irritation, respiratory disease emergencies, and lung function impairment. At or above current regulatory standards, day-to-day variations in ozone concentrations have been positively associated with asthma incidence and daily non-accidental mortality rate. Emerging evidence has shown that both short-term and long-term exposures to ozone, at concentrations below the current regulatory standards, were associated with increased mortality due to respiratory and cardiovascular diseases. The pathophysiology to support the epidemiologic associations between mortality and morbidity and ozone centers at the chemical and toxicological property of ozone as a strong oxidant, being able to induce oxidative damages to cells and the lining fluids of the airways, and immune-inflammatory responses within and beyond the lung. These new findings add substantially to the existing challenges in controlling ozone pollution. For example, in the United States in 2016, 90% of non-compliance to the national ambient air quality standards was due to ozone whereas only 10% was due to particulate matter and other regulated pollutants. Climate change, through creating atmospheric conditions favoring ozone formation, has been and will continue to increase ozone concentrations in many parts of world. Worldwide, ozone is responsible for several hundreds of thousands of premature deaths and tens of millions of asthma-related emergency room visits annually. To combat ozone pollution globally, more aggressive reductions in fossil fuel consumption are needed to cut NO and VOCs as well as greenhouse gas emissions. Meanwhile, preventive and therapeutic strategies are needed to alleviate the detrimental effects of ozone especially in more susceptible individuals. Interventional trials in humans are needed to evaluate the efficacy of antioxidants and ozone-scavenging compounds that have shown promising results in animal studies.

Background The roles of C-reactive protein (CRP) and cartilage oligomeric matrix protein (COMP) in knee osteoarthritis (KOA) remain controversial, thus the present study is aimed to explore the relationships between CRP, COMP, and the incidence/progression of KOA. Methods A systematic search was conducted on PubMed and Embase until September, 2016 for all the relevant studies. The pooled mean difference (MD) with its 95% confidence interval (95% CI) based on fixed effects model or random effects model was calculated to assess the potential role of CRP and COMP in the incidence or progression of KOA. Heterogeneity was evaluated by Cochran’s Q and I 2 tests. When P  < 0.05 or I 2  > 50%, a random effects model was chosen, otherwise, a fixed effects model was used. Moreover, the role of CRP in different degrees of pain was also analyzed. Sensitivity analysis was performed to evaluate the strength of the meta-analysis. Results Fourteen studies were enrolled in the meta-analysis. No difference was found between baseline CRP and CRP levels in the last follow-up period of KOA (MD = − 0.09, 95% CI: -0.30, 0.13). Pooled data showed higher CRP concentration in patients with incident KOA when compared with controls (MD = 0.33, 95% CI: 0.04, 0.63). Moreover, higher serum COMP levels were found in patients with incident KOA (MD = 1.69, 95% CI: 0.61, 2.76) Additionally, significant higher CRP concentration was observed in KOA patients with highest degree of pain (MD = 1.60, 95% CI: 0.52, 2.67). Conclusion CRP and COMP serum levels were both associated with the incidence of KOA. Patients with a higher CRP and COMP concentration might have an increased probability of developing KOA. However, higher CRP serum levels was not related with KOA progression. Furthermore, KOA patients with more pain had higher CRP concentrations.

Background Mitochondrial damage leading to oxidant stress may play an important role in the pathogenesis of airflow obstruction and emphysema. NLPR3 inflammasome can be activated by mitochondrial ROS (mtROS) and other stimuli. We examined the importance of mtROS and NLRP3 inflammasome and their interactions in multiple ozone-induced lung inflammation and emphysema. Methods C57/BL6 mice were exposed to ozone (2.5 ppm, 3 h) or filtered air twice a week over 6 weeks. MitoTEMPO (20 mg/kg), an inhibitor of mtROS, and VX765 (100 mg/kg), an inhibitor of caspase-1 activity, were administered by intraperitoneal or intragastric injection respectively 1 h prior to each ozone exposure for 6 weeks. Results Ozone-exposed mice had increased bronchoalveolar lavage (BAL) total cells and levels of IL-1β, KC and IL-6, augmented lung tissue inflammation scores, enhanced oxidative stress with higher serum 8-OHdG concentrations, emphysema with greater mean linear intercept (Lm), airway remodeling with increased airway smooth muscle mass and airflow limitation as indicated by a reduction in the ratio of forced expiratory volume at 25 and 50 milliseconds to forced vital capacity (FEV 25 /FVC, FEV 50 /FVC). Both MitoTEMPO and VX765 reduced lung inflammation scores, cytokine levels, oxidative stress and increased mitochondrial fission proteins. VX765 also attenuated emphysema, airway remodeling and airflow limitation. MitoTEMPO inhibited the increased expression of mitochondrial complex II and IV and of NLPR3 while VX765 inhibited the expression and activity of NLRP3 and caspase-1 pathway in the lung. Conclusions Both mtROS and NLRP3 inflammasome play a role in ozone-induced lung inflammation while only NLRP3 is involved in ozone-induced emphysema.

Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD. We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults. In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers. Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases. All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study. Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park). Baseline measurements of participants were taken before the walk in the hospital laboratory. During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured. Between October, 2012, and June, 2014, we screened 135 participants, of whom 40 healthy volunteers, 40 individuals with COPD, and 39 with ischaemic heart disease were recruited. Concentrations of black carbon, NO2, PM10, PM2.5, and ultrafine particles were higher on Oxford Street than in Hyde Park. Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96–3·95; p<0·1), sputum (3·15, 1·39–7·13; p<0·05), shortness of breath (1·86, 0·97–3·57; p<0·1), and wheeze (4·00, 1·52–10·50; p<0·05) after walking down Oxford Street compared with Hyde Park. In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk. By contrast, these beneficial responses were attenuated after walking on Oxford Street. In participants with COPD, a reduction in FEV1 and FVC, and an increase in R5–20 were associated with an increase in during-walk exposure to NO2, ultrafine particles and PM2.5, and an increase in PWV and augmentation index with NO2 and ultrafine particles. In healthy volunteers, PWV and augmentation index were associated both with black carbon and ultrafine particles. Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD, ischaemic heart disease, and those free from chronic cardiopulmonary diseases. Medication use might reduce the adverse effects of air pollution in individuals with ischaemic heart disease. Policies should aim to control ambient levels of air pollution along busy streets in view of these negative health effects. British Heart Foundation.

Maternal smoking during pregnancy is related to altered DNA methylation in infant umbilical cord blood. The extent to which low levels of smoke exposure among nonsmoking pregnant women relates to offspring DNA methylation is unknown. This study sought to evaluate relationships between maternal prenatal plasma cotinine levels and DNA methylation in umbilical cord blood in newborns using the Infinium HumanMethylation 450K BeadChip. Participants from the Newborn Epigenetics Study cohort who reported not smoking during pregnancy had verified low levels of cotinine from maternal prenatal plasma (0 to ), and offspring epigenetic data from umbilical cord blood were included in this study ( ). Multivariable linear regression models were fit to the data, controlling for cell proportions, age, race, education, and parity. Estimates represent changes in response to any unit increase in exposure. Multivariable linear regression models yielded 29,049 CpGs that were differentially methylated in relation to increases in cotinine at a 5% false discovery rate. Top CpGs were within or near genes involved in neuronal functioning ( , , ), carcinogenesis ( , ) and inflammation ( ). Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses suggest cotinine was related to methylation of gene pathways controlling neuronal signaling, metabolic regulation, cell signaling and regulation, and cancer. Further, enhancers associated with transcription start sites were enriched in altered CpGs. Using an independent sample from the same study population ( ), bisulfite pyrosequencing was performed with infant cord blood DNA for two genes within our top 20 hits ( and ). Results from pyrosequencing replicated epigenome results for (cg17079497, , , ) but not for AGER (cg09199225; , , ). Secondhand smoke exposure among nonsmoking women may alter DNA methylation in regions involved in development, carcinogenesis, and neuronal functioning. These novel findings suggest that even low levels of smoke exposure during pregnancy may be sufficient to alter DNA methylation in distinct sites of mixed umbilical cord blood leukocytes in pathways that are known to be altered in cord blood from pregnant active smokers. https://doi.org/10.1289/EHP8099.

Background There is a discourse on whether air pollution mixture or air pollutant components are causally linked to increased mortality. In particular, there is uncertainty on whether the association of NO 2  with mortality is independent of fine particulate matter (PM 2.5 ). Furthermore, effect modification by temperature on air pollution-related mortality also needs more evidence. Methods We used the Chinese Longitudinal Healthy Longevity Study (CLHLS), a prospective cohort with geographical and socio-economic diversity in China. The participants were enrolled in 2008 or 2009 and followed up in 2011-2012, 2014, and 2017-2018. We used remote sensing and ground monitors to measure nitrogen dioxide (NO 2 ), fine particulate matter (PM 2.5 ) , and temperature. We used the Cox-proportional hazards model to examine the association between component and composite air pollution and all-cause mortality, adjusted for demographic characteristics, lifestyle, geographical attributes, and temperature. We used the restricted cubic spline to visualize the concentration–response curve. Results Our study included 11 835 individuals with an average age of 86.9 (SD: 11.4) at baseline. Over 55 606 person-years of follow-up, we observed 8 216 mortality events. The average NO 2 exposure was 19.1 μg/m 3 (SD: 14.1); the average PM 2.5 exposure was 52.8 μg/m 3 (SD: 15.9). In the single pollutant models, the mortality HRs (95% CI) for 10 μg/m 3 increase in annual average NO 2 or PM 2.5 was 1.114 (1.085, 1.143) and 1.244 (1.221, 1.268), respectively. In the multi-pollutant model co-adjusting for NO 2 and PM 2.5 , the HR for NO 2 turned insignificant: 0.978 (0.950, 1.008), but HR for PM 2.5 was not altered: 1.252 (1.227, 1.279). PM 2.5 and higher mortality association was robust, regardless of NO 2 . When acccounting for particulate matter, NO 2 exposure appeared to be harmful in places of colder climates and higher seasonal temperature variation. Conclusions We see a robust relationship of PM 2.5  exposure and premature mortality in advance aged individuals, however, NO 2 exposure and mortality was only harmful in places of colder climate such as northeast China, indicating evidence of effect modification by temperature. Analysis of NO 2 without accounting for its collinearity with PM 2.5, may lead to overestimation.

Objective: Nearly all China's rural residents and a shrinking fraction of urban residents use solid fuels (biomass and coal) for household cooking and/or heating. Consequently, global meta-analyses of epidemiologic studies indicate that indoor air pollution from solid fuel use in China is responsible for approximately 420,000 premature deaths annually, more than the approximately 300,000 attributed to urban outdoor air pollution in the country. Our objective in this review was to help elucidate the extent of this indoor air pollution health hazard. Data Sources: We reviewed approximately 200 publications in both Chinese- and English-language journals that reported health effects, exposure characteristics, and fuel/stove intervention options. Conclusions: Observed health effects include respiratory illnesses, lung cancer, chronic obstructive pulmonary disease, weakening of the immune system, and reduction in lung function. Arsenic poisoning and fluorosis resulting from the use of \"poisonous\" coal have been observed in certain regions of China. Although attempts have been made in a few studies to identify specific coal smoke constituents responsible for specific adverse health effects, the majority of indoor air measurements include those of only particulate matter, carbon monoxide, sulfur dioxide, and/or nitrogen dioxide. These measurements indicate that pollution levels in households using solid fuel generally exceed China's indoor air quality standards. Intervention technologies ranging from simply adding a chimney to the more complex modernized bioenergy program are available, but they can be viable only with coordinated support from the government and the commercial sector.

ObjectivesA decreased ability to repair oxidative DNA damage, due to melatonin suppression, is a compelling mechanism by which night shift workers are at an increased risk of cancer. We sought to determine if melatonin supplementation would improve oxidative DNA damage repair among night shift workers.MethodsWe conducted a parallel-arm randomised placebo-controlled trial of melatonin supplementation among 40 night shift workers. Supplements were consumed before engaging in day sleep over a 4-week period. All urine excreted during a representative day sleep and night work period before and during the intervention period was collected for measurement of creatinine-adjusted 8-hydroxy-2′-deoxyguanosine (8-OH-dG) as an indicator of oxidative DNA damage repair capacity, with higher concentrations indicating better repair. Linear regression models were used to analyse the association between ln-transformed 8-OH-dG concentration and intervention status during day sleep and night work.ResultsThe melatonin intervention was associated with a borderline statistically significant 1.8-fold increase in urinary 8-OH-dG excretion during day sleep (95% CI 1.0, 3.2, p=0.06). No statistically significant difference in 8-OH-dG excretion was observed during the subsequent night shift (melatonin vs placebo excretion ratio=0.9; 95% CI 0.6, 1.5; p=0.7).ConclusionsOur results suggest that melatonin supplementation improves oxidative DNA damage repair capacity among night shift workers. Future larger-scale trials are needed to evaluate the impact of varying doses of melatonin supplements and examine the impacts of longer-term use of melatonin supplements by night shift workers.

Objective To investigate the effect of glucocorticoids (GCs) on the risk of readmission in menopausal women with knee osteoarthritis (OA). Information and methods The study cohort comprised 80 menopausal women with knee OA treated at a tertiary hospital affiliated with Shanxi Medical University and who underwent follow-up between September 2018 and September 2023. Then the collected longitudinal monitoring data were used to construct a semi-variable coefficient shared Gamma frailty model (VCSGF). Based on the results of this model, we explored the impact of GCs on menopausal women with knee OA and made risk predictions. Results The mean patient age at study entry was 64.7 ± 9.3 (range 50–82 years). And during the research, patients were admitted to the hospital a mean of 2.4 ± 1.8 times (range 1–11 times). Compared to patients who have not used the drug, the risk of early readmission in patients who have used GCs was reduced by 96% (HR = 0.04, 95% CI : 0.006 ~ 0.284, ). This protective effect diminished over time ( ). In addition, the risk of hospital admission with recurrent symptoms was roughly 3.35-fold higher in patients who drink alcohol than in patients who do not (95% CI : 1.661~6.794, ). Conclusion GC use reduced the risk of readmission in menopausal women with knee OA, although this effect diminished over time. Therefore, in patients without further contraindications, GCs may be used in moderation to reduce the readmission risk. In clinical practice, additional research is needed to investigate the timing and appropriate use of GC in the treatment of menopausal women with knee OA, and to develop a more rational program for GC use.