Accuracy of breath tests for colorectal neoplasms diagnosis: a meta-analysis.

Early noninvasive and rapid screening for colorectal cancer critically influences treatment outcomes. Breath testing, as an emerging screening technology, allows for noninvasive and convenient screening for different biomarkers and is a reliable screening method for various diseases. In this study, a meta-analysis of the accuracy and current status of volatile organic compounds present in exhaled breath for colorectal cancer detection was performed.

Prenatal exposure on nanoplastics: A study of spatial transcriptomics in hippocampal offspring.

Nanoplastics, as environmental contaminants, are thought to have irreversible impacts on the developing brains of infants and early children; however, the degree of the effects and the mechanisms of damage are unknown. In this study, spatial transcriptomics was used to investigate changes in the hippocampal region of rats descended from maternal exposure to polystyrene nanoplastics (PS-NPs), and the transcriptomes of each spot were sequenced, allowing us to visualize the hippocampus's transcriptional landscape as well as clarify the gene expression profiles of each cell type. Spatial transcriptomics was used to explore changes in the hippocampus region of rats exposed to PS-NPs during brain formation and maturation.

Oil mist particulate matter induces myocardial tissue injury by impairing fatty acid metabolism and mitochondrial bioenergetics function via inhibiting the PPAR alpha signaling pathway in rats.

Air pollution is a significant concern for human health, particularly in relation to cardiovascular damage. Currently, the precise mechanisms underlying myocardial tissue injury induced by air pollution remain to be fully elucidated. Oil mist particulate matter (OMPM) is a key environmental factor that has been linked to increased mortality from cardiovascular diseases.

Exercise in ozone-polluted air evokes pathological cardiac hypertrophy via up-regulation of nuclear lncRNA EYA4-au1 and recruiting Med11 to activating EYA4/p27kip1/CK2α/HDAC2 cascade.

Engaging in exercise in an ozone (O)-polluted environment can lead to lung damage, respiratory inflammation, and deterioration in performance, however, the effects on the heart are undefined. Herein, we report that rats performing moderate-intensity exercise under O-polluted air evoked pathological myocardial hypertrophy (MH). O exposure increased serum levels of MH-promoting factors (angiotensin II [AngII], endothelin-1 [ET-1], and cyclophilin A [CyPA]), and decreased expression of MH-inhibiting factors (adiponectin [ADPN], follistatin-like protein 1 [FSTL1], and apelin).

Effects of nanoplastic exposure during pregnancy and lactation on neurodevelopment of rat offspring.

Microplastics have emerged as a prominent global environmental contaminant, and they have been found in both human placenta and breast milk. However, the potential effects and mechanisms of maternal exposure to microplastics at various gestational stages on offspring neurodevelopment remain poorly understood. This investigation delves into the potential neurodevelopmental ramifications of maternal exposure to polystyrene nanoplastics (PS-NPs) during distinct phases of pregnancy and lactation.

Selective bioaccumulation of polystyrene nanoplastics in fetal rat brain and damage to myelin development.

Micro(nano)plastic, as a new type of environmental pollutant, have become a potential threat to the life and health of various stages of biology. However, it is not yet clear whether they will affect brain development in the fetal stage. Therefore, this study aims to explore the potential effects of nanoplastics on the development of fetal rat brains.

Early-life exposure to PM2.5 leads to ASD-like phenotype in male offspring rats through activation of PI3K-AKT signaling pathway.

Previous studies have shown that early-life exposure to fine particulate matter (PM2.5) is associated with an increasing risk of autism spectrum disorder (ASD), however, the specific sensitive period of ASD is unknown. Here, a model of dynamic whole-body concentrated PM2.

One-Step Fast Fabrication of Electrospun Fiber Membranes for Efficient Particulate Matter Removal.

Rapid social and industrial development has resulted in an increasing demand for fossil fuel energy, which increases particulate matter (PM) pollution. In this study, we employed a simple one-step electrospinning technique to fabricate polysulfone (PSF) fiber membranes for PM filtration. A 0.

Molecular mechanisms underlying mitochondrial damage, endoplasmic reticulum stress, and oxidative stress induced by environmental pollutants.

Mitochondria and endoplasmic reticulum (ER) are essential organelles playing pivotal roles in the regulation of cellular metabolism, energy production, and protein synthesis. In addition, these organelles are important targets susceptible to external stimuli, such as environmental pollutants. Exposure to environmental pollutants can cause the mitochondrial damage, endoplasmic reticulum stress (ERS), and oxidative stress, leading to cellular dysfunction and death.

Identification of potential glioma drug resistance target proteins based on ultra-performance liquid chromatography-mass spectrometry differential proteomics.

In this study, to screen for candidate markers of temozolomide (TMZ) resistance in glioblastoma, we artificially established TMZ drug-resistant glioblastoma (GBM) cell lines, U251-TMZ and U87-TMZ. In the U251-TMZ and U87-TMZ cell lines, we screened and analyzed differentially expressed proteins using ultra-performance liquid chromatography-mass spectrometry (UPLC-MS) differential proteomics. Compared with the U251 and U87 control cell lines, 95 differential proteins were screened in the U251-TMZ and U87-TMZ cell lines, of which 28 proteins were upregulated and 67 proteins were down-regulated.

PM triggers autophagic degradation of Caveolin-1 via endoplasmic reticulum stress (ERS) to enhance the TGF-β1/Smad3 axis promoting pulmonary fibrosis.

Air pollution is highly associated with respiratory diseases. However, the influence and mechanism of particulate matter with aerodynamic equal to or less than 2.5 μm (PM) in lung homeostasis remain unclear.

Short-term PM exposure induces transient lung injury and repair.

Exposure to fine atmospheric particulate matter (PM) is known to induce lung inflammation and injury; however, the way in which sophisticated endogenous lung repair and regenerative programs respond to this exposure remains unknown. In this study, we established a whole-body mouse exposure model to mimic real scenarios. Exposure to fine PM (PM with an aerodynamic diameter ≤ 2.

[Effect of epithelial-mesenchymal transition on cardiac fibrosis induced by oil mist particulate matter].

To investigate the effects of oil-mist particulate matter (OMPM) on cardiac tissue structure fibrosis in rats and the role of epithelial-mesenchymal transition (EMT). Six-week-old Wistar rats (half male and half female) were randomly divided into 3 groups: control group (without OMPM exposure), low-dose exposure group (50 mg/m) and high-dose exposure group (100 mg/m), 18 rats in each group, with 6.5 hours per day of dynamic inhalation exposure.

Role of SHANK3 in concentrated ambient PM2. 5 exposure induced autism-like phenotype.

Perinatal air pollution plays an important role in the development of autism. However, research on the pathogenic mechanism remains limited. In this study, the model of systemic inhalation of concentrated approximately 8-fold the level (mean concentration was 224 μg/m) reported in ambient outdoor air of PM2.

The impact of subchronic ozone exposure on serum metabolome and the mechanisms of abnormal bile acid and arachidonic acid metabolisms in the liver.

Ambient ozone (O) pollution can induce respiratory and cardiovascular toxicity. However, its impact on the metabolome and the underlying mechanisms remain unclear. This study first investigated the serum metabolite changes in rats exposed to 0.

Effects of Different Concentrations of Oil Mist Particulate Matter on Pulmonary Fibrosis In Vivo and In Vitro.

Oil-mist particulate matter (OMPM) refers to oily particles with a small aerodynamic equivalent diameter in ambient air. Since the pathogenesis of pulmonary fibrosis (PF) has not been fully elucidated, this study aims to explore the potential molecular mechanisms of the adverse effects of exposure to OMPM at different concentrations in vivo and in vitro on PF. In this study, rats and cell lines were treated with different concentrations of OMPM in vivo and in vitro.

Different exposure modes of PM induces bronchial asthma and fibrosis in male rats through macrophage activation and immune imbalance induced by TIPE2 methylation.

Exposure to PM can aggravate the occurrence and development of bronchial asthma and fibrosis. Here, we investigated the differences in bronchial injury caused by different exposure modes of PM (high concentration intermittent exposure and low concentration continuous exposure), and the mechanism of macrophage activation and respiratory immune imbalance induced by PM, leading to bronchial asthma and airway fibrosis using animal and cell models. A "PM real-time online concentrated animal whole-body exposure system" was used to conduct PM respiratory exposure of Wistar rats for 12 weeks, which can enhance oxidative stress in rat bronchus, activate epithelial cells and macrophages, release chemokines, recruit inflammatory cells, release inflammatory factors and extracellular matrix, promote bronchial mucus hypersecretion, inhibit the expression of epithelial cytoskeletal proteins, destroy airway barrier, and induce asthma.

Superconductivity Induced by Lifshitz Transition in Pristine SnS under High Pressure.

The importance of electronic structure evolutions and reconstitutions is widely acknowledged for strongly correlated systems. The precise effect of pressurized Fermi surface topology on metallization and superconductivity is a much-debated topic. In this work, an evolution from insulating to metallic behavior, followed by a superconducting transition, is systematically investigated in SnS under high pressure.

PM exposure at different concentrations and modes induces reproductive toxicity in male rats mediated by oxidative and endoplasmic reticulum stress.

The molecular mechanisms of PM exposure in the male reproductive system, have scarcely been studied. Here, we demonstrate the possible relationship and molecular mechanisms between endoplasmic reticulum stress (ERS), oxidative stress, and reproductive toxicity caused by PM. A "PM real-time online concentrated animal whole-body exposure system" was employed to expose male Wistar rats to PM for 12 weeks, which could induce sperm quality decline, apoptosis, inflammation, oxidative stress, ERS, and histopathological damage in the testis.