Capillary-flow driven microfluidic sensor based on tyrosinase for fast user-friendly assessment of pesticide exposures.

Pesticides are primarily used in agriculture to protect crops and extend their longevity. However, pesticide exposure has been linked to various acute and chronic health effects, raising significant environmental concerns. Current detection methods are often expensive and time-consuming, relying on complex instruments.

Citizen-Based Water Quality Monitoring: Field Testing a User-Friendly Sensor for Phosphate Detection in Global Surface Waters.

Widespread concern over surface water pollution has led to interest in developing easy-to-use accurate tools for citizen-based measurements that provide high spatial and temporal resolution while maintaining accuracy. Excessive anthropogenic phosphate significantly contributes to global eutrophication and necessitates regular on-site phosphate monitoring in surface waters. Traditional instrumentation for quantifying phosphate is labor-intensive, expensive, and performed in laboratories.

Microfluidics in environmental analysis: advancements, challenges, and future prospects for rapid and efficient monitoring.

Microfluidic devices have emerged as advantageous tools for detecting environmental contaminants due to their portability, ease of use, cost-effectiveness, and rapid response capabilities. These devices have wide-ranging applications in environmental monitoring of air, water, and soil matrices, and have also been applied to agricultural monitoring. Although several previous reviews have explored microfluidic devices' utility, this paper presents an up-to-date account of the latest advancements in this field for environmental monitoring, looking back at the past five years.

Intracellular pH reduction prevents excitotoxic and ischemic neuronal death by inhibiting NADPH oxidase.

Sustained activation of N-methyl-d-aspartate (NMDA) -type glutamate receptors leads to excitotoxic neuronal death in stroke, brain trauma, and neurodegenerative disorders. Superoxide production by NADPH oxidase is a requisite event in the process leading from NMDA receptor activation to excitotoxic death. NADPH oxidase generates intracellular H(+) along with extracellular superoxide, and the intracellular H(+) must be released or neutralized to permit continued NADPH oxidase function.

Impaired dexamethasone-mediated induction of tryptophan 2,3-dioxygenase in heme-deficient rat hepatocytes: translational control by a hepatic eIF2alpha kinase, the heme-regulated inhibitor.

Tryptophan 2,3-dioxygenase (TDO), a liver-specific cytosolic hemoprotein, is the rate-limiting enzyme in L-tryptophan catabolism and thus a key serotonergic determinant. Glucocorticoids transcriptionally activate the TDO gene with marked enzyme induction. TDO is also regulated by heme, its prosthetic moiety, as its expression and function are significantly reduced after acute hepatic heme depletion.