Terrelllocklear6102

Sleep disturbance is one of the neurobehavioral complications of lead neurotoxicity. Selleckchem CP-690550 The present study evaluated the impacts of chronic lead exposure on alteration of the sleep-wake cycle in association with changes of clock gene expression in the hypothalamus. Sprague-Dawley rats with chronic lead exposure consumed drinking water that contained 250 ppm of lead acetate for five weeks. Electroencephalography and electromyography were recorded for scoring the architecture of the sleep-wake cycle in animals. At six Zeitgeber time (ZT) points (ZT2, ZT6, ZT10, ZT14, ZT18, and ZT22), three clock genes, including rPer1, rPer2, and rBmal1b, were analyzed. The rats with chronic lead exposure showed decreased slow wave sleep and increased wakefulness in the whole light period (ZT1 to ZT12) and the early dark period (ZT13 to ZT15) that was followed with a rebound of rapid-eye-movement sleep at the end of the dark period (ZT22 to ZT24). The disturbance of the sleep-wake cycle was associated with changes in clock gene expression that was characterized by the upregulation of rPer1 and rPer2 and the feedback repression of rBmal1b. We concluded that chronic lead exposure has a negative impact on the sleep-wake cycle in rats that predominantly disrupts sleep homeostasis. link2 The disruption of sleep homeostasis was associated with a toxic effect of lead on the clock gene expression in the hypothalamus.The phthalate and semi-volatile organic compounds (SVOCs) are modern chemical substances and extensively existing in the indoor environment. The European Commission stipulated the "European Unified Test Criteria", since 2011, for the declared specifications of building products (CEN/TS 16516), based on the "lowest concentrations of interest (LCI)", the index pollutants, test method, and emission standard of "phthalate" and "SVOC" were specified in detail. The purpose of this study is to use six common indoor floor construction products in Taiwan (regenerated pseudoplastic rubber flooring, healthy pseudoplastic imitation wood floor, regenerated pseudoplastic rubber flooring, PVC floor tile/floor, plastic click floor, composite floor covered with carpet) to detect the changes in the concentration of phthalate emitted to the air. The ISO 16000-25 Indoor air-Part 25 Determination of the emission of semi-volatile organic compounds by building products-micro-chamber method is used to build a DS-BMEMC (glass micro-cage 2 (high temperature) emission concentration, meaning the phthalate SVOC of floor construction materials is unlikely to be volatilized or emitted at normal temperature. An interesting finding is that only S3 was detected DINP 72.6 (μg/m3) in stage 1. Others were detected DINP in stage 2. This might be because S3 has carpet on the surface. This implies that floor material with carpet may have an emission of DINP at normal temperature. The result of this study refers to the limited value evaluation of EU structural material standard emission TSVOC ≤ 0.1 ug/m3, the floor building material emissions are much higher than the evaluation criteria, increasing the health risk of users. The detection method and baseline can be used as the standard for controlling the emission of phthalate SVOC of Taiwan's green building material labeling system in the future.Di-2-ethylhexyl phthalate (DEHP) is a plasticizer commonly found in polyvinyl chloride, medical equipment, and food packaging. DEHP has been shown to target the reproductive system and alter the gut microbiome in humans and experimental animals. However, very little is known about the impact of DEHP-induced microbiome changes and its effects during pregnancy. Thus, the objective of this study was to investigate the effects of DEHP exposure during pregnancy on the cecal microbiome and pregnancy outcomes. Specifically, this study tested the hypothesis that subacute exposure to DEHP during pregnancy alters the cecal microbiome in pregnant mice, leading to changes in birth outcomes. To test this hypothesis, pregnant dams were orally exposed to corn oil vehicle or 20 µg/kg/day DEHP for 10 days and euthanized 21 days after their last dose. Cecal contents were collected for 16S Illumina and shotgun metagenomic sequencing. Fertility studies were also conducted to examine whether DEHP exposure impacted birth outcomes. Subacute exposure to environmentally relevant doses of DEHP in pregnant dams significantly increased alpha diversity and significantly altered beta diversity. Furthermore, DEHP exposure during pregnancy significantly increased the relative abundance of Bacteroidetes and decreased the relative abundance of Firmicutes and Deferribacteres compared with controls. The affected taxonomic families included Deferribacteraceae, Lachnospiraceae, and Mucisprillum. In addition to changes in the gut microbiota, DEHP exposure significantly altered 14 functional pathways compared with the control. Finally, DEHP exposure did not significantly impact the fertility and birth outcomes compared with the control. Collectively, these data indicate that DEHP exposure during pregnancy shifts the cecal microbiome, but the shifts do not impact fertility and birth outcomes.Bladder inflammation is associated with several lower urinary tract symptoms that greatly reduce quality of life, yet contributing factors are not completely understood. Environmental chemicals are plausible mediators of inflammatory reactions within the bladder. Here, we examine whether developmental exposure to polychlorinated biphenyls (PCBs) leads to changes in immune cells within the bladder of young mice. Female mice were exposed to an environmentally relevant mixture of PCBs through gestation and lactation, and bladders were collected from offspring at postnatal day (P) 28-31. We identify several dose- and sex-dependent PCB effects in the bladder. The lowest concentration of PCB (0.1 mg/kg/d) increased CD45+ hematolymphoid immune cells in both sexes. While PCBs had no effect on CD79b+ B cells or CD3+ T cells, PCBs (0.1 mg/kg/d) did increase F4/80+ macrophages particularly in female bladder. link3 Collagen density was also examined to determine whether inflammatory events coincide with changes in the stromal extracellular matrix. PCBs (0.1 mg/kg/d) decreased collagen density in female bladder compared to control. PCBs also increased the number of cells undergoing cell division predominantly in male bladder. These results implicate perturbations to the immune system in relation to PCB effects on the bladder. Future study to define the underlying mechanisms could help understand how environmental factors can be risk factors for lower urinary tract symptoms.The complementary construction of polychlorinated biphenyl (PCB) phytotoxicity and the biotoxicity 3D-QSAR model, combined with the constructed PCB environmental risk characterization model, was carried out to evaluate the persistent organic pollutant (POP) properties (toxicity (phytotoxicity and biotoxicity), bioconcentration, migration, and persistence) of PCBs and their corresponding transformation products (phytodegradation, microbial degradation, biometabolism, and photodegradation). The transformation path with a significant increase in environmental risks was analyzed. Some environmentally friendly PCB derivatives, exhibiting a good modification effect, and their parent molecules were selected as precursor molecules. Their transformation processes were simulated and evaluated for assessing the environmental risks. Some transformation products displayed increased environmental risks. The environmental risks of plant degradation products of the PCBs in the environmental media showed the maximum risk, indicating that the potential risks of the transformation products of the PCBs and their environmentally friendly derivatives could not be neglected. It is essential to further improve the ability of plants to degrade their transformation products. The improvement of some degradation products for environmentally friendly PCB derivatives indicates that the theoretical modification of a single environmental feature cannot completely control the potential environmental risks of molecules. In addition, this method can be used to analyze and evaluate environmentally friendly PCB derivatives to avoid and reduce the potential environmental and human health risks caused by environmentally friendly PCB derivatives.Aluminum is in our water and food, and is used as an adjuvant in vaccines. About 40% of the ingested dose accumulates within the intestinal mucosa, making the gut the main target of inflammation and autoimmunity; about 1% accumulates in the skeletal system and brain, inducing the cross-linking of amyloid-β-42 peptide and the formation of amyloid aggregates associated with Alzheimer's disease. To examine whether the accumulation of aluminum in the gut and brain tissues results in neoantigen formation, we bound aluminum compounds to human serum albumin. We used ELISA to measure IgG antibody in 94 different sera from healthy controls and 47 sera from each group of patients anti-Saccharomyces cerevisiae antibody-positive (Crohn's), and positive for deamidated α-gliadin and transglutaminase-2 IgA antibodies (celiac disease), autoimmune disorders associated with intestinal tissue antigens. Because earlier studies have shown that aluminum exposure is linked to Alzheimer's disease etiology, and high aluminum content is detected in Alzheimer's patients' brain tissue, we also measured aluminum antibody in the blood of these patients. Additionally, we measured aluminum antibody in the sera of mixed connective tissue disease patients who were positive for antinuclear antibodies, and used them as disease controls. We found significant IgG antibody elevation against all three aluminum compounds in the sera of patients with Crohn's, celiac and Alzheimer's disease, but not in patients with mixed connective tissue disease. We concluded that aluminum ingestion and absorption from the GI tract and brain may contribute to Crohn's, celiac and Alzheimer's disease, but not to mixed connective tissue disease.Uranium (U) is a heavy metal used in military and industrial settings, with a large portion being mined from the Southwest region of the United States. Uranium has uses in energy and military weaponry, but the mining process has released U into soil and surface waters that may pose threats to human and environmental health. The majority of literature regarding U's human health concern focuses on outcomes based on unintentional ingestion or inhalation, and limited data are available about its influence via cutaneous contact. Utilizing skin dermis cells, we evaluated U's topical chemotoxicity. Employing soluble depleted uranium (DU) in the form of uranyl nitrate (UN), we hypothesized that in vitro exposure of UN will have cytotoxic effects on primary dermal fibroblasts by affecting cell viability and metabolic activity and, further, may delay wound healing aspects via altering cell proliferation and migration. Using environmentally relevant levels of U found in water (0.1 μM to 100 μM [UN]; 23.8-23,800 ppb [U]), we quantified cellular mitosis and migration through growth curves and in vitro scratch assays. Cells were exposed from 24 h to 144 h for a time-course evaluation of UN chemical toxicity. The effects of UN were observed at concentrations above and below the Environmental Protection Agency threshold for safe exposure limits. UN exposure resulted in a dose-dependent decrease in the viable cell count; however, it produced an increase in metabolism when corrected for the viable cells present. Furthermore, cellular proliferation, population doubling, and percent closure was hindered at levels ≥10 μM UN. Therefore, inadvertent exposure may exacerbate pre-existing skin diseases in at-risk demographics, and additionally, it may substantially interfere in cutaneous tissue repair processes.