Sex-dependent effects of heat exposure on the middle ear health in mice.

Recent epidemiological studies have shown that emergency department discharge diagnoses of otitis media are associated with extreme heat or heat waves. However, little is known about the relationship between heat exposure and middle ear health, and the underlying mechanism remains to be uncovered. In this study, 8-week-old female and male C57BL/6 mice were randomly assigned to either a control group maintained at 22 ± 2 °C or a heat group exposed to 39.

Lead exposure in relation to gut homeostasis, microbiota, and metabolites.

Lead (Pb) is a hazardous heavy metal with no known safe threshold for exposure or consumption, posing significant risks to human health. Pb exposure can cause multiple system damage, depending on exposure levels, duration, and its high bioavailability and bioaccumulative potential. Gastrointestinal tract serves as a primary site for Pb absorption, making it particularly vulnerable to Pb-induced damage, including disruption of gut microbiota composition and metabolic function.

PPARα activation attenuated heat-induced myocardial injury in mice.

With climate change and global warming, extreme heatwaves occurred with more intense and higher frequency, significantly increasing the mortality rate associated with cardiovascular diseases. Using a mouse model of heat stress, the study aimed to clarify the adverse effects on heart, elucidate the underlying mechanism and explore the potential preventative strategies. Firstly, heat stress induced significant myocardial injury, which was further exacerbated even after termination of heat exposure.

Effects of extreme heat exposure on heatstroke and liver injury in mice: The role of PPARα.

Background: Liver injury is a frequent complication of heatstroke and constitutes a direct cause of death. However, only a few studies examined the mechanism underlying heatstroke-induced liver injury.

Objective: We aimed to evaluate the role of peroxisome proliferator-activated receptor α (PPARα) in heatstroke-induced liver injury and explore the potential mechanisms.

Air Toxicity Surveillance across Thirteen Cities Using Rats.

Current monitoring methods fail to assess air toxicity in real time, which is yet badly desired to better estimate the health impact. Here, we developed and deployed an automated, low-cost, and time-resolved system for noninvasive monitoring of air toxicity by detecting eight breath-borne biomarkers from rats, including VOCs, CO, CO, NO, HS, HO, O, and NH. Using this system, two large-scale monitoring campaigns were conducted across 13 cities in China during the 2023 winter and 2024 spring continuously on a 24-h-a-day basis.

Developmental Toxicity of Micro(Nano)Plastics (MNPs) Exposure in Mammals: A Mini-Review.

Micro(nano)plastics (MNPs) pose a significant threat to both ecological environments and human health. This review systematically examines the developmental toxicity of MNPs in mammals, with a particular focus on the impact of maternal and paternal exposure on offspring. Evidence indicates that MNPs can cross placental barriers, inducing abnormal development of embryos, fetuses, and placentas.

Insights From m6A RNA Methylation: Biomarkers for Diagnosis of Acute Myocardial Infarction.

Purpose: Acute myocardial infarction (AMI) is a major contributor to death. The purpose of this study is to explore circulating biomarkers for AMI diagnosis from the perspectives of immunological microenvironment and N6-methyladenosine (m6A) RNA methylation regulation.

Patients And Methods: The GSE59867 dataset was used to download platform and probe data for conducting differential analysis of m6A regulators.

AMPK agonist AICAR ameliorates maternal hepatic lipid metabolism disorder, inflammation, and fibrosis caused by PM exposure during pregnancy.

Liver is an important target organ of ambient fine particulate matter (PM). Numerous studies have shown that PM exposure can cause liver lipid metabolism disorders and other liver damage in mammals. However, the impact of PM on liver health during pregnancy, a sensitive life stage, remains understudied, and the underlying mechanisms are also unknown.

Gestational exposure to nanoplastics disrupts fetal development by promoting the placental aging via ferroptosis of syncytiotrophoblast.

Micro(nano)plastics (MNPs), are emerging environmental pollutants that have garnered widespread attention. Epidemiological and animal studies have shown that MNPs exposure during pregnancy is associated with adverse pregnancy outcomes, such as intrauterine growth restriction (IUGR) and miscarriage. However, the underlying mechanisms remain poorly understood.

Targeted Lipidomics and Transcriptomics Unveil Aberrant Lipid Metabolic Remodeling in Visceral and Subcutaneous Adipose Tissue under ER Stress.

Endoplasmic reticulum (ER) stress is known to impair the function of visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT), disrupting lipid metabolism. Despite the crucial role lipid plays in regulating adipose tissue function, the specific lipidomic alterations in VAT and SAT under ER stress remain unclear. In this study, ER stress was induced in VAT and SAT, and targeted lipidomic and transcriptomic approaches were used to analyze lipid metabolism and gene expression profiles.

β3 adrenergic receptor activation alleviated PM-induced hepatic lipid deposition in mice.

Increasing energy expenditure through activation of hepatocytes is a potential approach to treat fine particulate matter (PM) induced metabolic-associated fatty liver disease (MAFLD). Beta-3 adrenergic receptor (β3-AR) agonists could stimulate brown adipose tissue (BAT) energy expenditure, but it has never been investigated in MAFLD. The objective of this study is to explore the therapeutic effects of administering CL-316,243, a selective agonist of β3-AR, on hepatic lipid metabolism disturbances induced by PM.

Extreme Heat Exposure Induced Acute Kidney Injury through NLRP3 Inflammasome Activation in Mice.

Climate change has resulted in a marked increase in heat extremes that carry a severe risk for morbidity and mortality. Kidney is sensitive to heat stimulation, and acute kidney injury (AKI) is the early event. In this study, we investigated the adverse effects of heat extremes and their underlying mechanism.

The mediating effect of TyG-related indicators between long-term exposure to particulate matter and cardiovascular disease: evidence from a national longitudinal cohort study.

Background: Ambient particulate matter (PM) exposure is recognized as a risk factor for cardiovascular disease (CVD). However, the extent to which PM exposure is associated with CVD via triglyceride glucose (TyG)-related indicators remains unknown. This study examines the relationship between long-term PM exposure and CVD events, further assessing whether TyG-related indicators mediate this association.

Kidney Injury Evoked by Fine Particulate Matter: Risk Factor, Causation, Mechanism and Intervention Study.

Fine particulate matter (PM) is suggested to pose a severe risk to the kidneys by inducing functional degradation and chronic kidney diseases (CKD). This study aims to explore the nephrotoxicity of PM exposure and the underlying mechanism. Herein, based on the UK Biobank, it is found that per interquartile range (IQR) increase in PM is associated with a 6% (95% CI: 1%-11%), 7% (95% CI: 3%-11%), 9% (95% CI: 4%-13%), 11% (95% CI: 9%-13%), and 10% (95% CI: 8%-12%) increase in the risk of nephritis, hydronephrosis, kidney stone, acute renal failure, and CKD, respectively.

Fine particulate matter and osteoporosis: evidence, mechanisms, and emerging perspectives.

Air pollution, particularly fine particulate matter with an aerodynamic diameter of ≤2.5 μm (PM2.5), has been recognized for its adverse effects on multiple organs beyond the lungs.

Pan-cancer analysis identifies venous thromboembolism-related genes F3, PLAT, and C1S as potential prognostic biomarkers for glioblastoma and lower grade glioma.

Venous thromboembolism (VTE) is a prevalent complication among patients with cancer, contributing significantly to morbidity and mortality. However, the relationship between VTE-related genes (VRGs) and their potential impact on prognosis, immune response, and therapeutic targets in various cancer types remains unclear. Based on the coagulation and complement pathways, we identified hub VRGs that play a role in regulating the immune response in cancer.

Metabolic Profile and Lipid Metabolism Phenotype in Mice with Conditional Deletion of Hepatic BMAL1.

The disruption of circadian rhythms (CRs) has been linked to metabolic disorders, yet the role of hepatic BMAL1, a key circadian regulator, in the whole-body metabolism and the associated lipid metabolic phenotype in the liver remains unclear. floxed () and hepatocyte-specific knockout () C57BL/6J mice underwent a regular feeding regimen. Hepatic CR, lipid content, mitochondrial function, and systemic metabolism were assessed at zeitgeber time (ZT) 0 and ZT12.

Lung function benefits of traditional Chinese medicine Qiju granules against fine particulate air pollution exposure: a randomized controlled trial.

Introduction: Multiple targets are considered as the causes of ambient fine particulate matter [aerodynamic diameters of < 2.5 μm (PM)] induced lung function injury. Qiju granules are derived from the traditional Chinese medicine (TCM) formula known as Qi-Ju-Di-Huang-Wan (Lycium, Chrysanthemum, and Rehmannia Formula, QJDHW), which has been traditionally used to treat symptoms such as cough with phlegm, dry mouth and throat, and liver heat.

PM-induced cellular senescence drives brown adipose tissue impairment in middle-aged mice.

Airborne fine particulate matter (PM) exposure is closely associated with metabolic disturbance, in which brown adipose tissue (BAT) is one of the main contributing organs. However, knowledge of the phenotype and mechanism of PM exposure-impaired BAT is quite limited. In the study, male C57BL/6 mice at three different life phases (young, adult, and middle-aged) were simultaneously exposed to concentrated ambient PM or filtered air for 8 weeks using a whole-body inhalational exposure system.

Early Pulmonary Fibrosis-like Changes in the Setting of Heat Exposure: DNA Damage and Cell Senescence.

It is well known that extreme heat events happen frequently due to climate change. However, studies examining the direct health impacts of increased temperature and heat waves are lacking. Previous reports revealed that heatstroke induced acute lung injury and pulmonary dysfunction.

LRRK2 is involved in heat exposure-induced acute lung injury and alveolar type II epithelial cell dysfunction.

Heat exposure induces excessive hyperthermia associated with systemic inflammatory response that leads to multiple organ dysfunction including acute lung injury. However, how heat impairs the lung remains elusive so far. We aimed to explore the underlying mechanism by focusing on leucine-rich repeat kinase 2 (LRRK2), which was associated with lung homeostasis.

Gestational exposure to PM disrupts fetal development by suppressing placental trophoblast syncytialization via progranulin/mTOR signaling.

Recent epidemiological and animal studies have indicated that ambient fine particulate matter (PM) exposure during pregnancy is closely associated with intrauterine growth restriction (IUGR). However, the underlying mechanisms remain to be revealed. In this study, we found that gestational exposure to PM significantly decreased fetal weight and crown-rump length in mice, accompanied by insufficient placental trophoblast syncytialization and increased expression of progranulin (PGRN) in mice placenta.

Desipramine ameliorates fine particulate matter-induced hepatic insulin resistance by modulating the ceramide metabolism in mice.

Recent research has highlighted a correlation between exposure to ambient fine particulate matter (PM) and the development of systemic insulin resistance (IR) along with an elevated risk of diabetes. Ceramide has emerged as one of the pathogenic mechanisms contributing to IR. The inhibition of acid sphingomyelinase (ASMase) activity by desipramine (DES) has been shown to effectively reduce ceramide levels.