Long-term Exposure Research Articles

A diffusion tensor imaging-based multidimensional study of brain structural changes after long-term high-altitude exposure and their relationships with cognitive function

BackgroundBrain structure changes after long-term adaptation to the high-altitude environment; however, related studies are few, results are in consistent, and long-term effects on cognitive function and pathophysiological mechanisms are unclear. Therefore, diffusion tensor imaging (DTI) was used to investigate the damage to white matter fiber tracts and correlations between brain structural abnormalities and cognitive function.MethodsForty healthy Han people living on the high-altitude and 40 healthy Han people living on the plains were enrolled in this study and underwent magnetic resonance imaging, emotional state assessment, and cognitive function tests. The sex, age, education level, and social status of the two groups were not different. The tract-based spatial statistics (TBSS) method was used to analyze the DTI parameters of the white matter fiber tracts of the two groups. Moreover, the partial correlation method (age and sex as covariates) was used to analyze the correlations between the intergroup differences in the DTI parameters and a series of clinical indicators of emotional state and cognitive function. Two-sample t tests, Mann-Whitney U test, generalized linear model, or chi-square tests were used for statistical analysis.ResultsCompared with those individuals in the plain group, the scores on the PSQI, SDS, SAS, PHQ-9, and GAD-7 of individuals in the high-altitude group were higher, while the scores on the DST-Backwards, MoCA, and MMSE in the high-altitude group were lower. The fractional anisotropy (FA) value of the body of the corpus callosum in the high-altitude group was lower than that in the plain group. The FA value of the body of the corpus callosum in the plain group was negatively correlated with the Logical Memory, while no significant correlation was found in the high-altitude group.ConclusionThis study revealed that long-term exposure to a high-altitude environment could lead to a series of changes in sleep, emotion, and cognitive function and irreversible damage to the white matter microstructure of the body of the corpus callosum, which is the related brain region responsible for logical memory. The absence of logical memory impairment in the healthy Han Chinese population living on the high-altitude in this study may be due to the existence of adaptive compensation after long-term high-altitude exposure.

Microgravity and Human Body: Unraveling the Potential Role of Heat-Shock Proteins in Spaceflight and Future Space Missions

In recent years, the increasing number of long-duration space missions has prompted the scientific community to undertake a more comprehensive examination of the impact of microgravity on the human body during spaceflight. This review aims to assess the current knowledge regarding the consequences of exposure to an extreme environment, like microgravity, on the human body, focusing on the role of heat-shock proteins (HSPs). Previous studies have demonstrated that long-term exposure to microgravity during spaceflight can cause various changes in the human body, such as muscle atrophy, changes in muscle fiber composition, cardiovascular function, bone density, and even immune system functions. It has been postulated that heat-shock proteins (HSPs) may play a role in mitigating the harmful effects of microgravity-induced stress. According to past studies, heat-shock proteins (HSPs) are upregulated under simulated microgravity conditions. This upregulation assists in the maintenance of the proper folding and function of other proteins during stressful conditions, thereby safeguarding the physiological systems of organisms from the detrimental effects of microgravity. HSPs could also be used as biomarkers to assess the level of cellular stress in tissues and cells exposed to microgravity. Therefore, modulation of HSPs by drugs and genetic or environmental techniques could prove to be a potential therapeutic strategy to reduce the negative physiological consequences of long-duration spaceflight in astronauts.

Short- and Long-Term Effects of Inhaled Ultrafine Particles on Blood Pressure: A Systematic Review and Meta-Analysis

Background: Air pollution contributes to up to 60% of premature mortality worldwide by worsening cardiovascular conditions. Ultrafine particles (UFPs) may negatively affect cardiovascular outcomes, and epidemiological studies have linked them to short- and long-term blood pressure (BP) imbalance. Methods: We conducted a systematic review and meta-analysis of the short- and long-term effects of UFP exposure on systolic (SBP) and diastolic (DBP) blood pressure. Eligibility criteria were established using the Population, Exposure, Comparator, Outcome, and Study Design (PECOS) model, and literature searches were conducted in Web of Science, PubMed, Embase, and Scopus for studies published between 1 January 2013 and 9 October 2024. Risk of Bias (RoB) was assessed following World Health Organization (WHO) instructions. Separate meta-analyses were performed for the short- and long-term effects of UFP exposure on SBP and DBP. Additionally, we analyzed SBP and DBP imbalances across different timespans following short-term exposure. Results: The results showed an increase in BP during short-term UFP exposure, which returned to baseline values after a few hours. Changes in SBP were greater than in DBP following both short- and long-term exposure. Prolonged exposure to UFPs is associated with increased SBP and concurrently low DBP values. Chronic exposure to UFPs may lead to a persistent increase in SBP, even without a concurrent increase in DBP. Conclusions: The findings presented here highlight that UFPs may contribute to worsening cardiovascular outcomes in vulnerable populations living in air-polluted areas.

Long-Term Air Pollution Exposure and Severity of Idiopathic Pulmonary Fibrosis: Data from the IPF-PRO Registry

Long-Term Air Pollution Exposure and Severity of Idiopathic Pulmonary Fibrosis: Data from the IPF-PRO Registry

Air pollution and skin aging

Air pollution is a leading environmental health risk worldwide, with detrimental effects not only on human health but also on skin aging. This review explores the link between air pollution and skin aging, focusing on the harmful effects of particulate matter (PM) and other pollutants such as polycyclic aromatic hydrocarbons (PAHs), nitrogen oxides (NO2), and ozone (O3). These pollutants penetrate the skin, inducing oxidative stress and inflammation, which accelerates the degradation of collagen and elastin in the extracellular matrix. This contributes to premature aging, wrinkles, hyperpigmentation, and inflammatory skin conditions. The smallest fractions of PM, particularly PM2.5, are the most harmful, causing significant cellular damage. Long-term exposure to these pollutants also disrupts the skin's microbiome, leading to dysbiosis and further weakening the skin's protective barrier. Current therapeutic strategies focus on protecting the skin using antioxidants, such as Vitamin C and Vitamin E, as well as probiotics and moisturizers that support the skin's natural defenses. Sunscreens also play a vital role in protecting the skin from UV-induced oxidative stress, further mitigating pollution-related damage. This review highlights the importance of developing comprehensive skincare regimens that target both pollution-induced oxidative stress and the maintenance of a healthy skin barrier. It also emphasizes the need for further research into personalized approaches to counteract the aging effects of air pollution on the skin.

Abstract 4118766: Lower Winter and Higher Summer Temperatures Increase the Risk of Hospitalization With Aortic Aneurysm or Aortic Dissection

Background: Seasonal variation in aortic dissection incidence are well-documented. This study utilized a high-resolution surface temperature model and state-specific administrative medical data to investigate the relationship between long-term exposure to winter and summer temperature averages and hospitalization rates for aortic aneurysm or dissection. Methods: Using data from the 2000-2016 State Inpatient Databases (SID), 265,795 hospitalizations with a principal diagnosis of aortic aneurysm or dissection for residents of 19 U.S. states were identified via ICD-9 and 10 codes. Daily surface temperature data, extracted from Oak Ridge National Laboratory’s Daymet weather model on a 1-km grid, were aggregated to zip codes to match SID's spatial resolution. Linear regressions, adjusted for demographics, comorbidities (including hypertension, hyperlipidemia, atherosclerosis, smoking, and genetic disorders), air pollution, and neighborhood socioeconomic status, estimated absolute changes in annual hospitalization rates associated with variations in winter and summer temperature averages. Nonlinear exposure-effect relationships were assessed using penalized cubic splines with at most nine degrees of freedom. Results: Each Celsius degree decrease in winter and increase in summer was associated with 19.0 (95% CI: 17.5, 20.8, p<0.001) and 10.4 (95% CI: 8.0, 12.7, p<0.001) additional hospitalizations per one million person-years, respectively. These statistically significant associations were consistent across subgroups, including thoracic vs. abdominal and aneurysm vs. dissection. Further analysis revealed that cooler-than-average winter temperatures consistently correlated with increased hospitalization rates for overall aortic aneurysms or dissections and their subtypes. Conclusion: Colder winter and hotter summer temperatures significantly increase the risk of hospitalization for aortic aneurysm or dissection. This emphasizes the importance of understanding how environmental factors contribute to aortic disease.

Abstract 4124226: Long-term exposure to air pollutants and incidence of cardiovascular disease events and mortality in The Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air)

Introduction: Exposure to ambient air pollution may increase the risk of cardiovascular disease events and mortality, but prior publications have primarily included administrative cohorts with outcomes that have not been individually reviewed and with air pollution estimates created without cohort-specific exposure monitoring. Multi-Ethnic Study of Atherosclerosis (MESA) is a multi-site cohort study designed specifically to prospectively collect and adjudicate cardiovascular disease (CVD) events. MESA Air recruited additional participants into sub-cohorts for enhanced air pollution variation and sample size. Research Question: The aim of this analysis was to characterize the relationship between long-term exposure to nitrogen dioxide (NO 2 ) and fine particulate matter (PM 2.5 ) and all-cause mortality and CVD events. Methods: Air pollution exposure was assessed using address history with a purpose-built exposure model incorporating cohort-specific monitoring including measurement and validation at participant homes. We used Cox models to assess the risk of rolling 2-year average exposures on all cause-mortality and on a composite CVD endpoint (definite angina, probable angina with revascularization, myocardial infarction, atherosclerosis or other CVD death, resuscitated cardiac arrest, and stroke). Models were stratified for baseline hazard by age, sub-cohort, and recruitment year and were additionally adjusted for age, sex, race/ethnicity, field center, smoking/second-hand smoke, pack-years, physical activity, education, income, neighborhood socioeconomic status, and statin use. Results: MESA Air participants were aged 44-87 years at enrollment between 2000 and 2007; follow-up averaged 14 years. 6,915 participants had follow-up for events, NO 2 exposure, and covariate information. We observed 1,442 deaths and 985 CVD events. The interquartile range over all 2-year averages was 10.5-23.1 ppb for NO 2 and 10.1-14.9 µ/m 3 for PM 2.5 . The adjusted hazard ratio (aHR) for a 10 ppb increment in NO 2 was 1.38 (95% CI: 1.17, 1.64) for all-cause mortality and 1.16 (95% CI: 0.95, 1.42) for incident CVD events. The aHR for a 5 µg/m 3 increment in PM 2.5 was 1.20 (95% CI: 0.99, 1.46) for all-cause mortality and 1.15 (95% CI: 0.95, 1.39) for incident CVD events Conclusions: These results add to growing literature demonstrating an association between air pollution exposure, mortality, and CVD in a cohort with well-characterized clinical endpoints and cohort-specific exposure assessment.

Accelerated Hydrothermal Aging and Degradation Mechanism of PE100 Butt-Fusion Welded Joint

High-density polyethylene (HDPE) pipelines are extensively utilized in energy transportation in the ocean. However, long-term exposure to water can alter the performance of HDPE, potentially leading to pipeline accidents. This study focuses on simulating the aging characteristics of PE100 polyethylene pipeline butt-fusion welded joints (B-FWJs) in water using hydrothermal accelerated aging experiments at various temperature gradients. The performance of the B-FWJ after hydrothermal aging was characterized using scanning electron microscopy (SEM), oxidation induction time (OIT), attenuated total reflectance Fourier transform infrared (ATR FT-IR) spectroscopy, and mechanical testing. Furthermore, this study analyzed the performance characteristics and changes in the micro-molecular chains of an HDPE B-FWJ pipeline following hydrothermal aging. An investigation was conducted into the effects of hydrothermal aging temperature and duration on the physical and chemical characteristics of HDPE B-FWJ, and the aging mechanism under hydrothermal aging conditions was explored. The results indicate that increasing hydrothermal aging temperature leads to a more significant decrease in the mechanical properties of the B-FWJ. These findings contribute to understanding the aging behavior of PE100 pipelines in the joint section and offer insights to mitigate the risks associated with the aging of and damage to B-FWJ pipelines in the ocean.

Abstract 4129036: Air pollution and Cardiovascular Disease Incidence in a Pooled Analysis of 6 U.S. Cohorts

Introduction/Background: Long term air pollution is associated with cardiovascular disease (CVD) incidence, however the effects at low levels in the US are unknown. Research Questions/Hypothesis: To assess the effect of long-term exposure to ambient air pollution CVD incidence (myocardial infarction [MI], stroke, and all CVD) in a pooled analysis of epidemiological cohorts. Materials and Methods: We harmonized data from six cohorts (Cardiovascular Health Study, Nurses’ Health Study II, Multi-Ethnic Study of Atherosclerosis, and Reasons for Geographic And Racial Differences in Stroke Study, Sister Study, and Women’s Health Initiative) with both CVD incidence data and extensive covariate information. We predicted time-varying two-year average concentrations of particulate matter <2.5 microns (PM 2.5 ) and nitrogen dioxide (NO 2 ) from 1990-2019 at participant residential addresses using validated regionalized spatio-temporal models, combining spatio-temporal universal kriging and partial least squares regression with inputs from monitoring data from regulatory and researcher-deployed networks, satellite remote-sensing data and chemical transport modeling. Cox proportional hazards regression models adjusted for individual and area-level information, including smoking status, socio-economic factors, anthropometry, blood pressure, cholesterol, and other clinical variables. Results: Our analysis included over 300,000 participants and 10,229 incident CVD events. The median residential concentration of PM 2.5 was 10.1 µg/m 3 and NO 2 was 9.3 ppb. A 5 µg/m 3 increase in PM 2.5 was not significantly associated with a higher hazard ratio for all outcomes: 1.03 (95%CI: 0.96, 1.10) for CVD incidence, 1.03 (95%CI 0.93, 1.15) for MI, and 1.00 (95%CI 0.90, 1.10) for stroke. We found that a 10ppb increase in NO 2 was associated with a 1.06 (95%CI: 1.01, 1.11) higher hazard ratio for CVD, 1.07 (95%CI: 1.01, 1.11) for MI, and 1.02 (95%CI 0.96, 1.09) for stroke. Conclusions: In this analysis of a large, pooled cohort with excellent exposure, outcome, and covariate information, we found an association of NO 2 exposure—considered a surrogate for traffic-related air pollution—with CVD incidence and MI. Associations with particulate matter were not statistically significant, but could not exclude a small increased risk. We are extending this analysis to include 6 additional cohorts and an additional 700,000 participants to allow for generation of a highly resolved concentration-response function.

SERCA Modulators Reveal Distinct Signaling and Functional Roles of T Lymphocyte Ca2+ Stores

The allosteric SERCA (Sarcoplasmic/Endoplasmic Reticulum Ca2+-ATPase) activator CDN1163 has been recently added to the group of pharmacological tools for probing SERCA function. We chose to investigate the effects of the compound on T lymphocyte Ca2+ stores, using the well-described Jurkat T lymphocyte as a reliable cell system for Ca2+ signaling pathways. Our study identified the lowest concentrations of the SERCA inhibitors thapsigargin (TG) and 2,5-di-(tert butyl)-1,4-benzohydroquinone (tBHQ) capable of releasing Ca2+, permitting the differentiation of the TG-sensitive SERCA 2b Ca2+ store from the tBHQ-sensitive SERCA 3 Ca2+ store. We proceeded to test the effects of CDN1163 on Ca2+ stores, examining specific actions on the SERCA 2b and SERCA 3 Ca2+ pools using our low-dose SERCA blocker regimen. In contrast to previous work, we find CDN1163 exerts complex time-sensitive and SERCA isoform-specific actions on Ca2+ stores. Surprisingly, short-term exposure (0–30 min) to CDN1163 perturbs T cell Ca2+ stores by suppressing Ca2+ uptake with diminished Ca2+ release from the SERCA 2b-controlled store. Concomitantly, we find evidence for a SERCA-activating effect of CDN1163 on the SERCA-3 regulated store, given the observation of increased Ca2+ release inducible by low-dose tBHQ. Intriguingly, longer-term (>12 h) CDN1163 exposure reversed this pattern, with increased Ca2+ release from SERCA 2b-regulated pools yet decreased Ca2+ release responses from the tBHQ-sensitive SERCA 3 pool. Indeed, this remodeling of SERCA 2b Ca2+ stores with longer-term CDN1163 exposure also translated into the compound’s ability to protect Jurkat T lymphocytes from TG but not tBHQ-induced growth suppression.

Antibiotic Residues in Milk and Milk-Based Products Served in Kuwait Hospitals: Multi-Hazard Risk Assessment

Antimicrobial resistance (AMR) poses a significant global health challenge affecting food safety and development. Residues of antibiotics in food from animal sources, particularly milk, contribute to the development and spread of AMR, alter intestinal microbiota, and potentially lead to allergies, serious health conditions, and environmental and technological problems within the dairy industry. Therefore, this study investigated the residue levels of veterinary drugs from β-lactam antibiotics and tetracyclines in milk and milk products and assessed human health risks. Two hundred milk and milk product samples (pasteurized milk, sterile milk, soft white cheese, and processed cheese, 50 each) were collected from different hospitals in the State of Kuwait and screened for antibiotic residues using a microbial inhibition assay (Delvotest SP-NT) and high-performance liquid chromatography (HPLC). Delvotest SP-NT and HPLC analyses showed that 30, 28, 26, and 24% of the pasteurized milk, sterilized milk, white soft cheese, and processed cheese samples tested positive for antibiotic residues. Forty-eight milk and cheese samples were confirmed as positive by both methods, and six samples initially found to be negative by Delvotest SP-NT were confirmed as positive by HPLC. Multi-antibiotic residues were detected in five samples by using HPLC. The kappa coefficient (0.921; p < 0.0001) revealed complete concordance between the HPLC and Delvotest SP-NT results. Ampicillin was the most abundant residue in the positive samples (31.48%), ranging from 2.44 to 3.89 μg/L, with an overall mean concentration of 3.492 ± 0.094 μg/L, followed by tetracycline and oxytetracycline (27.78% each), ranging from 54.13 to 220.3 μg/L and from 41.55 to 160.7 μg/L, with mean concentrations of 129.477 ± 14.22 and 91.86 ± 9.92 μg/L, respectively. The amoxicillin levels in the samples (12/54; 22.22%) ranged from 3.11 to 5.5 μg/L, with an overall mean concentration of 3.685 ± 0.186 μg/L. The maximum concentrations of ampicillin, amoxicillin, and tetracycline were detected in processed cheese with mean concentrations of 3.89 ± 0.28 µg/L, 3.95 ± 0.15 µg/L, and 170.3 ± 0.27 µg/L, respectively. Pasteurized milk contained the maximum concentrations of oxytetracycline, with a mean concentration of 120.45 ± 0.25 µg/L. The tetracycline residues exceeded the standard maximum residue limits (MRLs; 100 µg/L) in 6% of both pasteurized and sterilized milk samples, and in 4% of processed cheese. Additionally, the oxytetracycline levels in pasteurized milk (6%) and amoxicillin levels in processed cheese (2%) were higher than the permitted MRLs (100 µg/L and 4 µg/L, respectively). Furthermore, the antibiotic residues detected in 12.5% (25/200) of the samples were close to standard permissible MRL limits for ampicillin (5%), amoxicillin and oxytetracycline (3% each), and tetracycline (1.5%). Hazard quotients, which compare the standard acceptable daily intake (ADI) to the estimated daily exposure (EDI), indicated that the overall risk associated with antibiotic residues in these dairy products is low. The EDI was lower than the ADI for the tested antibiotics, indicating an elevated safety margin. While the overall hazard quotients are low, the potential for the development of antibiotic resistance due to long-term exposure to low levels of antibiotics should be considered. Hence, strict regulations and enforcement are necessary to prevent excessive residue levels and to promote responsible antibiotic use in dairy production. Regular monitoring of antibiotic residues in dairy products is essential for ensuring consumer safety.

Lavender and Black Pine Waste as Additives Enhancing Selected Mechanical and Hygrothermal Properties of Cement Mortars

The paper presents the mechanical and hygrothermal properties of cement mortars containing bio-powders made from lavender waste and black pine wood. The wastes were mechanically ground with a hammer mill to a fraction not exceeding 0.5 mm and then dried in air-dry conditions. The influence of bio-additives in amounts of 1.5% and 2.5% of the overall mortar volume was tested. The aim of the paper was to determine the impact of bio-additives on the mechanical and hygrothermal properties of the tested cement mortars. This publication included tests of compressive and flexural strength, elastic modulus, water absorption, absorption due to capillary rise, sorption and desorption properties, thermal properties, microstructural tests using mercury intrusion porosimetry and SEM, and EDS. The main conclusions of the research indicate that mortars with both 1.5% and 2.5% bio-powders are characterized by strong bactericidal properties, lower sorption properties at high air humidity, lower thermal conductivity, reduced compressive strength by 22–27%, no significant effect on the flexural strength, and significant reduction in capillary action of mortars both with short-term and long-term water exposure.

Association of Respiratory Morbidities with Particulate Air Pollution in Delhi, India- A Prospective Study

Abstract Background: Elevated levels of air pollution and long-term exposure can lead to detrimental health conditions, mainly affecting cardiorespiratory systems. Materials and Methods: A prospective observational study was conducted in five sampled hospitals in Delhi. A pre-designed, pre-tested, semi-structured questionnaire was filled out for each patient with data from hospital records. The admission rates were recorded daily over the study period along with the air quality with reference to particulate matter (PM). The trends of the hospital admissions for respiratory morbidity were corroborated with PM 2.5. Descriptive statistics and correlation amongst emergency admissions and air pollutants were analysed using Microsoft Excel. The impact of air quality on the rate of hospitalisation due to respiratory conditions was projected by mathematical modelling. Results: The rate of hospitalisation due to bronchial asthma, chronic obstructive pulmonary disease, bronchitis and lower respiratory tract infections was found to be directly proportional to an increase in PM2.5. Conclusion: The healthcare system is increasingly strained and thus, the additional burden due to rising air pollution needs to be prevented by making people aware about the methods of reducing air pollution.

Long-Term Ozone Exposure, COPD, and Asthma Mortality: A Retrospective Cohort Study in the Republic of Korea

Ozone concentrations have increased in recent decades, and several studies have reported that long-term exposure to ozone increases the mortality risk induced by respiratory conditions. However, research on cause-specific mortality related to ozone exposure and respiratory diseases remains scarce. We constructed a retrospective cohort of 5,360,032 adults aged ≥ 65 years from the National Health Insurance Service of Republic of Korea, and death certificates were obtained from Statistics Republic of Korea to determine the cause of death between 2010 and 2019. The daily maximum 8 h average levels of ozone during the warm season annually (May–September) and other air pollutants were determined for the residential district. We analyzed the data using a time-varying Cox proportional hazards model with individual- and district-level covariates, incorporating a competing risk framework to address deaths from causes other than chronic obstructive pulmonary disease (COPD) and asthma. In our single-pollutant model with a 3-year moving average, a 1 ppb increase in ozone exposure was associated with a hazard ratio (HR) of 1.011 (95% confidence interval [CI]: 1.008–1.013) for COPD mortality and an HR of 1.016 (95% CI: 1.011–1.022) for asthma mortality. In our model adjusted for the presence of underlying diseases and district-level variables, the HRs were 1.009 (95% CI: 1.008–1.014) for COPD and 1.017 (95% CI: 1.011–1.023) for asthma, respectively. These associations remained robust in our two-pollutant model, except for NO2 and COPD. A linear concentration–response relationship was identified between ozone concentration, COPD, and asthma mortality. In this large nationwide cohort study, long-term exposure to ozone was associated with an increased risk of death from COPD and asthma in older Korean adults.

Decomposing social groups differential in stunting among children under five in India using nationally representative sample data

Stunting among children is a reflection of the chronic malnutrition caused by a complex set of behavioural, demographic, and socioeconomic factors. This long-term detrimental exposure to chronic malnutrition is disproportionately higher among social and economically deprived groups, leading to significant differentials in the prevalence of stunting across various social strata. Therefore, this study investigates the inequality of social groups in terms of the prevalence of stunting across Schedule Caste (SC)-Scheduled Tribe (ST) and non-SC-ST. The study used 1,93,886 children’s data aged 0–59 months from the recent round of the National Family Health Survey. Descriptive statistics, multivariable logistic regression, F-test, t-test and chi-squared (χ²) test were applied to understand the prevalence, determinants, and associations, respectively. The Fairlie decomposition model was applied to quantify the factors contributing to the inequality of stunting across social groups. The results revealed that the prevalence of stunting was higher among SC-ST (39.60%) children compared to non-SC-ST (33.27%). In addition, children aged 15–30 months (AOR: 1.895, 95% CI: 1.843–1.949), and male (AOR: 1.074, 95% CI: 1.053–1.095), mothers had lower BMI (AOR: 1.543, 95% CI: 1.492–1.595), mothers who had no education (AOR: 1.595, 95% CI: 11.532–1.662), belongs to poorest wealth index (AOR: 1.857, 95% CI: 1.766–1.952), and the children belong to the household with unhygienic satiation practices (AOR: 1.097, 95% CI: 1.070–1.123) were more likely to be stunted. The decomposition results revealed that the variables included in the study could explain 68.9% of the stunting inequality between SC-ST and non-SC-ST groups. The household’s wealth index is found to be a leading factor, which contributed nearly 41.3% of total stunting inequality exists between these two groups, followed by mothers’ education (12.86%) and mothers’ BMI (11.02%), sanitation facilities (4.26%), children’s birth order (3.32%) and mother’s type of delivery (1.49%). These findings emphasize the importance of targeted interventions. Prioritizing policies that address household economic enhancement, women’s education and empowerment can be instrumental in reducing social group inequality and lowering the overall prevalence of stunting. Ensuring access to improved hygienic sanitation facilities in the household is equally important for achieving better health outcomes for the children.

Molecular identification of methane-consuming bacteria in the Persian Gulf: a study for microbial gas exploration

The seepage of gaseous compounds from underground reservoirs towards the surface causes abnormalities in the population of microbial communities that consume light hydrocarbons on the surface of the reservoir. This microbial population can serve as indicators for determining the location of gas reservoirs prior to drilling operations. In this study, the simulation of methane gas leakage in the sediments of the Persian Gulf was conducted using a laboratory model. The objective of this simulation was to identify the microbial population consuming methane within the sediments of the Persian Gulf, aiding in the exploration of gas reserves. Continuous injection of methane gas into the system was performed for a period of 3 months to enrich the microbial consortia consuming methane. Subsequently, the microbial population was identified using next-generation sequencing (NGS) analysis. The results indicated that, based on the 16S rRNA sequencing dataset, aerobic methanotrophs, including genera Methylobacter, Methylomarinum, Methylomicrobium, Methylomonas, and Methylophage, were the dominant microbial group on the surface of the sediments. Additionally, anaerobic methane oxidation archaea in sediments were performed by ANME-2 and ANME-3 clades. The findings demonstrate that these microbial communities are capable of coexistence and thrive in long-term exposure to methane in the sediments of the Persian Gulf. Identifying this microbial pattern, alongside other geophysical and geological data, can increase the success rate of gas reservoir exploration.

Current trend in air pollution exposure and stroke.

Stroke is the second leading cause of death worldwide, and exposure to particulate air pollution is now recognized as one of the major modifiable risk factors. However, air pollution can vary in terms of physicochemical composition and exposition specificities. Therefore, its relationships with stroke outcomes remain under intense investigation. This review highlights, alongside particles, that short-term and long-term exposure to nitrogen dioxide (NO2) and ozone is likely to be also linked to stroke-related morbidity and mortality. Moreover, air pollution may increase the risk of transitioning from a healthy status to incident stroke and morbimortality after stroke. Additionally, relationships may vary depending on the air pollution mixture (e.g., particle-related components, pollutant interactions), pollutant sources (e.g., traffic-related or not), stroke etiology (ischemic or hemorrhagic), or exposed individual's characteristics (e.g., age, sex, genetic predisposition, weight status). Nonlinear dose-response functions and short-term effect lags have been reported, but these features need further refinement. The relationship between stroke and air pollution is now well established. Nonetheless, future research should further consider the physicochemical properties of air pollutants, multiple exposures, and individual vulnerabilities. Moreover, advanced statistical methods should be more commonly used to better describe the relationship shapes.

Chronic corticosterone exposure causes anxiety- and depression-related behaviors with altered gut microbial and brain metabolomic profiles in adult male C57BL/6J mice

Chronic exposure to glucocorticoids in response to long-term stress is thought to be a risk factor for major depression. Depression is associated with disturbances in the gut microbiota composition and peripheral and central energy metabolism. However, the relationship between chronic glucocorticoid exposure, the gut microbiota, and brain metabolism remains largely unknown. In this study, we first investigated the effects of chronic corticosterone exposure on various domains of behavior in adult male C57BL/6J mice treated with the glucocorticoid corticosterone to evaluate them as an animal model of depression. We then examined the gut microbial composition and brain and plasma metabolome in corticosterone-treated mice. Chronic corticosterone treatment resulted in reduced locomotor activity, increased anxiety-like and depression-related behaviors, decreased rotarod latency, reduced acoustic startle response, decreased social behavior, working memory deficits, impaired contextual fear memory, and enhanced cued fear memory. Chronic corticosterone treatment also altered the composition of gut microbiota, which has been reported to be associated with depression, such as increased abundance of Bifidobacterium, Turicibacter, and Corynebacterium and decreased abundance of Barnesiella. Metabolomic data revealed that long-term exposure to corticosterone led to a decrease in brain neurotransmitter metabolites, such as serotonin, 5-hydroxyindoleacetic acid, acetylcholine, and gamma-aminobutyric acid, as well as changes in betaine and methionine metabolism, as indicated by decreased levels of adenosine, dimethylglycine, choline, and methionine in the brain. These results indicate that mice treated with corticosterone have good face and construct validity as an animal model for studying anxiety and depression with altered gut microbial composition and brain metabolism, offering new insights into the neurobiological basis of depression arising from gut-brain axis dysfunction caused by prolonged exposure to excessive glucocorticoids.

GLUT1 and prorenin receptor mediate differential regulation of TGF-β and CTGF in renal inner medullary collecting duct cells during high glucose conditions

BackgroundDuring diabetes, prorenin is highly produced by the renal collecting ducts. The binding of prorenin to (pro)renin receptor (PRR) on the apical plasma membrane triggers intracellular profibrotic genes, including TGF-β and CTGF. However, the underlying mechanisms contributing to the stimulation of these pathways remain unclear. Hence, we hypothesize that the glucose transporter-1 (GLUT1) favors the PRR-dependent stimulation of TGF-β and CTGF in the distal nephron segments during high glucose (HG) conditions.MethodsTo test this hypothesis, primary cultured renal inner medullary collecting duct (IMCD) cells were treated with normal glucose (NG, 5 mM) or high glucose (HG, 25 mM) for 48 h in the presence or absence of the GLUT1-specific inhibitor BAY 876 (2 nM). Additionally, IMCD cells were treated with the PRR antagonist PRO20. The expression of TGF-β and CTGF was quantified by immunoblot and qRT-PCR.ResultsHG increased GLUT1 mRNA and protein abundance, while BAY 876 inhibited these responses. HG treatment upregulated PRR, but the concomitant treatment with BAY 876 partially prevented this effect. TGF-β and CTGF expressions were augmented in IMCD cells treated with HG. However, PRO20 prevented the increases in TGF-β but not those of CTGF. GLUT1 inhibition partially prevented the increases in reactive oxygen species (ROS) during HG while PRO20 did not. ROS scavenging impaired CTGF upregulation during HG conditions. Additionally, long-term exposure to HG increases lipid peroxidation and reduced cell viability.ConclusionsThe data indicate that glucose transportation via GLUT1 is implicated in the PRR-dependent upregulation of TGF-β while CTGF is mediated mainly via a mechanism depending on ROS formation in renal medullary collecting duct cells.

Cyanide and Cyanogenic Compounds—Toxicity, Molecular Targets, and Therapeutic Agents

Cyanide (CN) is a well-known mitochondrial poison. CN poisoning may result from acute or long-term exposure to a number of CN compounds. Recent insight into the chemical affinities of the CN anion has increased our understanding of its toxicity and the mechanisms of antidotal actions, which, together with information on various exposure sources, are reviewed in the present article. A literature search in Scopus, Embase, Web of Science, PubMed, and Google Scholar for the period 2001–2024 revealed that the CN anion after exposure or degradation of CN compounds is distributed to vulnerable copper and iron-containing targets, especially in mitochondria, thus blocking the electron transport chain. Intake of cyanogenic compounds may exert subacute or chronic toxic effects, also because of the interaction with cobalt in vitamin B12. Antidotal agents exert their effects through the affinity of CN for cobalt- or iron-containing compounds. Research on CN interactions with metalloproteins may increase our insight into CN toxicity and efficient antidotal regimens.