Ozone exposure induced kidney damage in diabetic mice: The key role of lipid metabolism and water-electrolyte homeostasis.

Ozone (O) is an important environmental pollutant that has garnered growing public concern. Epidemiological studies indicate that exposure to O is associated with an elevated risk of kidney disease, a common complication of diabetes. However, the harmful effects of O on the kidneys remain unconfirmed.

-Mediated Insulin Signaling Pathway Was Involved in O-Induced Multigenerational Effects of Shortened Lifespan in .

As a long-standing atmospheric pollutant, ozone (O) exerts enduring effects on biological health. However, experimental research on its impact on organism lifespan and generational effects is limited. This study exposed three generations of fruit flies () to O, revealing a shortened lifespan across generations.

Experimental Investigation of Dispersant on Dynamics of Impact of AlO Nanofluid Droplet.

Spray cooling, of which the essence is droplet impacting, is an efficient thermal management technique for dense electronic components in unmanned aerial vehicles (UAVs). Nanofluids are pointed as promising cooling dispersions. Since the nanofluids are unstable, a dispersant could be added to the fluid.

Ozone induced multigenerational glucose and lipid metabolism disorders in Drosophila.

Ozone (O), a persistent pollutant, poses a significant health threat. However, research on its multigenerational toxicity remains limited. Leveraging the Drosophila model with its short lifespan and advanced genetic tools, we explored the effects of O exposure across three generations of fruit flies.

YTHDC2 mediated RNA mA modification contributes to PM-induced hepatic steatosis.

Exposure to fine particulate matter (PM) is a significant risk factor for hepatic steatosis. The N-methyladenosine (mA) is implicated in metabolic disturbances triggered by exogenous environmental factors. However, the role of mA in mediating PM-induced hepatic steatosis remains unclear.

Screening Organic Components and Toxicogenic Structures from Regional Fine Particulate Matters Responsible for Myocardial Fibrosis in Male Mice.

Numerous studies indicate that fine particulate matters (PM) and its organic components are urgent risk factors for cardiovascular diseases (CVDs). Combining toxicological experiments, effect-directed analyses, and nontarget identification, this study aims to explore whether PM exposure in coal-combustion areas induces myocardial fibrosis and how to identify the effective organic components and their toxic structures to support regional risk control. First, we constructed an animal model of real-world PM exposure during the heating season and found that the exposure impaired cardiac systolic function and caused myocardial fibrosis, with chemokine Ccl2-mediated inflammatory response being the key cause of collagen deposition.

Fetal Origin of Abnormal Glucose Tolerance in Adult Offspring Induced by Maternal Bisphenol A Analogs Exposure.

With the widespread use of bisphenol A (BPA) analogs, their health risks have attracted attention. The effects of maternal BPA analogs exposure on glucose homeostasis in adult offspring and the underlying fetal origins require further exploration. Herein, we exposed pregnant mice to two types of BPA analogs─BPB and BPAF; we evaluated glucose homeostasis in adult offspring and maternal-fetal glucose transport by testing intraperitoneal glucose tolerance, determining glucose and glycogen contents, conducting positron emission tomography (PET)/computed tomography (CT), detecting expression of placental nutrient transport factors, and assessing placental barrier status.

Multilevel Screening Strategy to Identify the Hydrophobic Organic Components of Ambient PM Associated with Hepatocellular Steatosis.

Hepatic steatosis is the first step in a series of events that drives hepatic disease and has been considerably associated with exposure to fine particulate matter (PM). Although the chemical constituents of particles matter in the negative health effects, the specific components of PM that trigger hepatic steatosis remain unclear. New strategies prioritizing the identification of the key components with the highest potential to cause adverse effects among the numerous components of PM are needed.

Circadian rhythm disturbances involved in ozone-induced glucose metabolism disorder in mouse liver.

Ozone (O) is a key environmental factor for developing diabetes. Nevertheless, the underlying mechanisms remain unclear. This study aimed to investigate alterations of glycometabolism in mice after O exposure and the role of circadian rhythms in this process.

The Flow Stress Behavior and Physical-Based Constitutive Model for As-Quenched Al-Zn-Mg-Cu Alloy.

Although heat-treatable Al-Zn-Mg-Cu alloys are widely used in aerospace industries, distortion and cracks exist due to the residual stress during quenching. Understanding the flow stress behavior and numerically modeling the process is the key to predicting the residual stress. This paper investigated the flow stress behavior of the as-quenched 7050 alloy at strain rates from 0.

Overview of PM and health outcomes: Focusing on components, sources, and pollutant mixture co-exposure.

PM varies in source and composition over time and space as a complicated mixture. Consequently, the health effects caused by PM varies significantly over time and generally exhibit significant regional variations. According to numerous studies, a notable relationship exists between PM and the occurrence of many diseases, such as respiratory, cardiovascular, and nervous system diseases, as well as cancer.

Effects of differential regional PM induced hepatic steatosis and underlying mechanism.

Emerging evidence suggests that exposure to PM is associated with a high risk of nonalcoholic fatty liver disease (NAFLD). NAFLD is typically characterised by hepatic steatosis. However, the underlying mechanisms and critical components of PM-induced hepatic steatosis remain to be elucidated.

Biochemical evidence of PM critical components for inducing myocardial fibrosis in vivo and in vitro.

PM constituents are tightly linked to the initiation of many cardiovascular diseases (CVDs). Little is known, however, about the events which critical components of PM can induce the initiating events in CVDs. C57BL/6 female mice were exposed to PM (3 mg/kg b.

Activation of δ-opioid Receptors in Anterior Cingulate Cortex Alleviates Affective Pain in Rats.

The negative emotions caused by persistent pain, called affective pain, are known to seriously affect human physical and mental health. The anterior cingulate cortex (ACC), especially the rostral ACC (rACC) plays a key role in the development of this affective pain. N-methyl-d-aspartate (NMDA) receptors, which are widely distributed in the ACC, are involved in the regulation of emotional behavior.

Suppression of NADPH oxidase 4 inhibits PM-induced cardiac fibrosis through ROS-P38 MAPK pathway.

Fine particulate matter (PM) has been consistently linked to cardiovascular diseases, and cardiac fibrosis plays a crucial role in the occurrence and development of heart diseases. It is reported that NOX4-dependent redox signaling are responsible for TGFβ-mediated profibrotic responses. The current study was designed to explore the possible mechanisms of cardiac fibrosis by PM both in vitro and in vivo.

Association of exposure to ambient air pollution with ovarian reserve among women in Shanxi province of north China.

Air pollution has been an important risk factor for female reproductive health. However, epidemiological evidence of ambient air pollution on the predictor for ovarian reserve (antral follicle count, AFC) is deficient. We aim to comprehensively evaluate the association of long-term exposure to ambient air pollution with AFC among women of reproductive age in Shanxi of north China.

Comparative studies on regional variations in PM in the induction of myocardial hypertrophy in mice.

Exposure to fine particulate matter (PM) has been indicated to be related to an increased risk of cardiovascular diseases (CVDs) in sensitive people. However, the underlying mechanisms of PM-induced CVDs are poorly understood. In the present study, PM samples were collected during winter from four cities (Taiyuan, Beijing, Hangzhou, and Guangzhou) in China.

Complex to simple: In vitro exposure of particulate matter simulated at the air-liquid interface discloses the health impacts of major air pollutants.

Particulate matter (PM) exposure poses many adverse effects on human health. However, it is challenging to clearly differentiate between the contributions of individual pollutants on toxicity from complex mixtures of ambient air pollutants. The aim of this study is to generate aerosols constituted by silica nanoparticles (NPs) and bisulfate to serve as simulators of particle-associated high-sulfur air pollution.

Sulfur dioxide induces apoptosis via reactive oxygen species generation in rat cardiomyocytes.

Epidemiological evidence suggests that the incidence and mortality of cardiovascular diseases are closely related to sulfur dioxide (SO). In the present study, H9C2 cells were incubated with 100 μM NaHSO with or without pretreatment of an antioxidant, N-acetyl-L-cysteine (NAC). The changes of apoptosis rate, mitochondrial membrane potential (MMP), ATP content, caspase-3 activity, and reactive oxygen species (ROS) were detected.

The Martensitic Transformation and Mechanical Properties of Ti6Al4V Prepared via Selective Laser Melting.

This article investigated the microstructure of Ti6Al4V that was fabricated via selective laser melting; specifically, the mechanism of martensitic transformation and relationship among parent β phase, martensite (α') and newly generated β phase that formed in the present experiments were elucidated. The primary X-ray diffraction (XRD), transmission electron microscopy (TEM) and tensile test were combined to discuss the relationship between α', β phase and mechanical properties. The average width of each coarse β columnar grain is 80⁻160 μm, which is in agreement with the width of a laser scanning track.

Synergistic effects of sulfur dioxide and polycyclic aromatic hydrocarbons on pulmonary pro-fibrosis via mir-30c-1-3p/ transforming growth factor β type II receptor axis.

SO and PAHs are well-known pollutants of coal burning and significant contributors to haze episodes. The purpose of the study is to determine whether the combined effects of SO and BaP are synergetic and to investigate the pro-fibrotic influences and possible mechanism from the aspect of microRNAs. In the present study cellular metabolic activity of BEAS-2B was assessed using MTT probe.

Ambient fine particulate matter exposure induces reversible cardiac dysfunction and fibrosis in juvenile and older female mice.

Background: Cardiovascular disease is the leading cause of mortality in the advanced world, and age is an important determinant of cardiac function. The purpose of the study is to determine whether the PM-induced cardiac dysfunction is age-dependent and whether the adverse effects can be restored after PM exposure withdrawal.

Methods: Female C57BL/6 mice at different ages (4-week-old, 4-month-old, and 10-month-old) received oropharyngeal aspiration of 3 mg/kg b.

Cadmium exposure on tissue-specific cadmium accumulation and alteration of hemoglobin expression in the 4th-instar larvae of Propsilocerus akamusi (Tokunaga) under laboratory conditions.

The expression of hemoglobin (Hb) genes has considerable potential as a biomarker for environmental monitoring in Chironomus. However, no sequence information is available regarding Hb genes in Propsilocerus akamusi (Tokunaga), thus the change in Hb mRNA gene expression caused by environmental pollutants remains unknown. In this study, we cloned two Hb gene fragments (PaHbV and PaHbVII) from P.

Sulfur dioxide inhibits expression of mitochondrial oxidative phosphorylation genes encoded by both nuclear DNA and mitochondrial DNA in rat lungs.

Epidemiological studies show that sulfur dioxide (SO), a major air pollutant, is associated with the morbidity and mortality of respiratory tract diseases. The aim of the present study was to determine the effects of SO on mitochondria and the corresponding molecular characterization in the lung. Male Wistar rats were exposed to 0, 3.