Carsim-based simulation study on the performances of raised speed deceleration facilities under different profiles.

Objective: Studying the optimal profile shape and size of deceleration facilities suitable for low-speed environment roads under different speed control intervals.

Methods: Simulation modeling of deceleration facilities with various profile shapes and sizes and for vehicles in different speed intervals was performed using the vehicle dynamics simulation software Carsim. The height jumped by a vehicle's wheels, the vertical force on the wheels, and the vertical acceleration of the vehicle were used as indicators of ride comfort and operational stability for the various deceleration facility profiles.

Arsenic is a potent co-mutagen of ultraviolet light.

Arsenic enhances the carcinogenicity of ultraviolet radiation (UVR). However, the mechanisms of arsenic-driven oncogenesis are not well understood. Here, we utilize experimental systems to investigate the carcinogenic and mutagenic properties of co-exposure to arsenic and UVR.

Arsenic and UVR co-exposure results in unique gene expression profile identifying key co-carcinogenic mechanisms.

Changes in gene expression underlie many pathogenic endpoints including carcinogenesis. Metals, like arsenic, alter gene expression; however, the consequences of co-exposures of metals with other stressors are less understood. Although arsenic acts as a co-carcinogen by enhancing the development of UVR skin cancers, changes in gene expression in arsenic UVR co-carcinogenesis have not been investigated.

Identification of Potential Biomarkers of Septic Shock Based on Pathway and Transcriptome Analyses of Immune-Related Genes.

Immunoregulation is crucial to septic shock (SS) but has not been clearly explained. Our aim was to explore potential biomarkers for SS by pathway and transcriptional analyses of immune-related genes to improve early detection. GSE57065 and GSE95233 microarray data were used to screen differentially expressed genes (DEGs) in SS.

Arsenite Methyltransferase Is an Important Mediator of Hematotoxicity Induced by Arsenic in Drinking Water.

Chronic arsenic exposures via the consumption of contaminated drinking water are clearly associated with many deleterious health outcomes, including anemia. Following exposure, trivalent inorganic arsenic (As) is methylated through a series of arsenic (+III oxidation state) methyltransferase (As3MT)-dependent reactions, resulting in the production of several intermediates with greater toxicity than the parent inorganic arsenicals. The extent to which inorganic vs.

Arsenic is a potent co-mutagen of ultraviolet light.

Environmental co-exposures are widespread and are major contributors to carcinogenic mechanisms. Two well-established environmental agents causing skin cancer are ultraviolet radiation (UVR) and arsenic. Arsenic is a known co-carcinogen that enhances UVR's carcinogenicity.

Distribution of polycyclic aromatic hydrocarbons in indoor/outdoor window films and the indoor film/air partition of northeastern Chinese college dormitories.

Indoor window films can represent short-term air pollution conditions of indoor environment through rapidly capturing organic contaminants as effective passive air samplers. To investigate the temporal variation, influence factors of polycyclic aromatic hydrocarbons (PAHs) in indoor window films, and the exchange behavior with gas phase in college dormitories, 42 pairs window films of interior and exterior window surfaces and corresponding indoor gas phase and dust samples were collected monthly in six selected dormitories, Harbin, China, from August to December 2019 and September 2020. The average concentration of ∑PAHs in indoor window films (398 ng/m) was significantly (p < 0.

Particulate arsenic trioxide induces higher DNA damage and reactive oxygen species than soluble arsenite in lung epithelial cells.

Environmental arsenic exposure is associated with lung cancer. Arsenic is the first substance known to cause lung cancer by two distinct routes, ingestion and inhalation, in the forms of soluble arsenite and particulate arsenic trioxide, respectively. In comparison to significant progresses in research on mechanisms for lung carcinogenesis of arsenic ingestion, inhalation arsenic exposure route in particulate form and its lung carcinogenic mechanisms are relatively under-investigated.

Arsenic impairs the lineage commitment of hematopoietic progenitor cells through the attenuation of GATA-2 DNA binding activity.

Arsenic exposure produces significant hematotoxicity in vitro and in vivo. Our previous work shows that arsenic (in the form of arsenite, AsIII) interacts with the zinc finger domains of GATA-1, inhibiting the function of this critical transcription factor, and resulting in the suppression of erythropoiesis. In addition to GATA-1, GATA-2 also plays a key role in the regulation of hematopoiesis.

Antibiotic resistance of Helicobacter pylori isolated from children in Chongqing, China.

The resistance of Helicobacter pylori (H. pylori) to antibiotics has been increasing worldwide and varies across different geographic areas and times. Limited studies reported the prevalence of antibiotic resistance and its related gene mutations in children in Chongqing, a city located in southwest China.

Arsenite exposure inhibits the erythroid differentiation of human hematopoietic progenitor CD34 cells and causes decreased levels of hemoglobin.

Arsenic exposure poses numerous threats to human health. Our previous work in mice has shown that arsenic causes anemia by inhibiting erythropoiesis. However, the impacts of arsenic exposure on human erythropoiesis remain largely unclear.

Isobaric Tags for Relative and Absolute Quantitation-Based Quantitative Serum Proteomics Analysis in Ischemic Stroke Patients With Hemorrhagic Transformation.

Hemorrhagic transformation (HT), which occurs with or without reperfusion treatments (thrombolysis and/or thrombectomy), deteriorates the outcomes of ischemic stroke patients. It is essential to find clinically reliable biomarkers that can predict HT. In this study, we screened for potential serum biomarkers from an existing blood bank and database with 243 suspected acute ischemic stroke (AIS) patients.

Arsenite and monomethylarsonous acid disrupt erythropoiesis through combined effects on differentiation and survival pathways in early erythroid progenitors.

Strong epidemiological evidence demonstrates an association between chronic arsenic exposure and anemia. We recently found that As impairs erythropoiesis by disrupting the function of GATA-1; however the downstream pathways impacted by the loss of GATA-1 function have not been evaluated. Additionally, our previous findings indicate that the predominant arsenical in the bone marrow of mice exposed to As in their drinking water for 30 days was MMA, but the impacts of this arsenical on erythorpoisis also remain largely unknown.

Endogenous zinc protoporphyrin formation critically contributes to hemorrhagic stroke-induced brain damage.

Hemorrhagic stroke is a leading cause of death. The causes of intracerebral hemorrhage (ICH)-induced brain damage are thought to include lysis of red blood cells, hemin release and iron overload. These mechanisms, however, have not proven very amenable to therapeutic intervention, and so other mechanistic targets are being sought.

Uranium directly interacts with the DNA repair protein poly (ADP-ribose) polymerase 1.

People living in southwest part of United States are exposed to uranium (U) through drinking water, air, and soil. U is radioactive, but independent of this radioactivity also has important toxicological considerations as an environmental metal. At environmentally relevant concentrations, U is both mutagenic and carcinogenic.

Modulation of PARP activity by Monomethylarsonous (MMA) acid and uranium in mouse thymus.

Arsenic exposure is well established to impair the function of zinc finger proteins, including PARP-1. Previous studies from our lab show that early developing T cells in the thymus are very sensitive to arsenite (As)-induced genotoxicity mediated through PARP-1 inhibition. Additionally, it has been shown that uranium (in the form of uranyl acetate, UA) also suppresses PARP-1 activity in HEK cells.

Inhibition of red blood cell development by arsenic-induced disruption of GATA-1.

Anemia is a hematological disorder that adversely affects the health of millions of people worldwide. Although many variables influence the development and exacerbation of anemia, one major contributing factor is the impairment of erythropoiesis. Normal erythropoiesis is highly regulated by the zinc finger transcription factor GATA-1.