Arsenic activated GLUT1-mTORC1/HIF-1α-PKM2 positive feedback networks promote proliferation and migration of bladder epithelial cells.

Arsenic (As) is recognized as a potent environmental contaminant associated with bladder carcinogenesis. However, its molecular mechanism remains unclear. Metabolic reprogramming is one of the hallmarks of cancer and is as a central feature of malignancy.

Targeting mA mRNA demethylase FTO alleviates manganese-induced cognitive memory deficits in mice.

Manganese (Mn) induced learning and memory deficits through mechanisms that are not fully understood. In this study, we discovered that the demethylase FTO was significantly downregulated in hippocampal neurons in an experimental a mouse model of Mn exposure. This decreased expression of FTO was associated with Mn-induced learning and memory impairments, as well as the dysfunction in synaptic plasticity and damage to regional neurons.

The hippo-YAP1/HIF-1α pathway mediates arsenic-induced renal fibrosis.

Epidemiological evidence reveals that arsenic increases the risk of chronic kidney disease (CKD) in humans, but its mechanism of action has so far been unclear. Fibrosis is the manifestation of end-stage renal disease. Hypoxia is recognized as a vital event accompanying the progression of renal fibrosis.

SLC1A5 regulates cell proliferation and self-renewal through β-catenin pathway mediated by redox signaling in arsenic-treated uroepithelial cells.

Arsenic exposure increases the risk of bladder cancer in humans, but its underlying mechanisms remain elusive. The alanine, serine, cysteine-preferring transporter 2 (ASCT2, SLC1A5) is frequently overexpressed in cancer cells. The aim of this study was to evaluate the effects of arsenic on SLC1A5, and to determine the role of SLC1A5 in the proliferation and self-renewal of uroepithelial cells.

2, 2', 4, 4'-tetrabromodiphenyl ether induces placental toxicity via activation of p38 MAPK signaling pathway in vivo and in vitro.

2, 2', 4, 4'-tetrabromodiphenyl ether (BDE-47) is one of the most important polybrominated diphenyl ethers (PBDEs) congeners, and epidemiological studies have shown that it can cause adverse pregnancy outcomes. The aim of our study was to investigate the role of placental injury in BDE-47-induced adverse pregnancy outcomes through in vivo and in vitro models. From day 0.

Targeting SLC1A5 blocks cell proliferation through inhibition of mTORC1 in arsenite-treated human uroepithelial cells.

Arsenic is an environmental contaminant, which is widely distributed in soil, air, and water. There is sufficient evidence to indicate that arsenic increases the risk of bladder cancer in humans. However, its underlying mechanisms remain elusive.

Trends in global, regional and national incidence of pneumoconiosis caused by different aetiologies: an analysis from the Global Burden of Disease Study 2017.

Objectives: Pneumoconiosis remains a major global occupational health hazard and illness. Accurate data on the incidence of pneumoconiosis are critical for health resource planning and development of health policy.

Methods: We collected data for the period between 1990 and 2017 on the annual incident cases and the age-standardised incidence rates (ASIR) of pneumoconiosis aetiology from the Global Burden of Disease Study 2017.

The effects of heavy metals on human metabolism.

As technology continues to advance, heavy metals in drinking water have exceeded recommended limits from regulators around the world. The main source of human exposure to heavy metals is from contaminated drinking water. The effects of drinking water contaminated with heavy metals, such as arsenic, lead, nickel, cadmium and mercury, have gradually caught the attention of the relevant departments and personnel.