Human health risks of heavy metals in water and vegetables: a deterministic and probabilistic study in Gilgit-Baltistan, Pakistan.

There is a growing global concern about the presence of heavy metals in the environment due to their detrimental effects on human health. These metals are eminent poisons with carcinogenic features that can harm organs such as brain, kidney, lungs, etc. This study investigated the human health risks associated with toxic metals such as lead (Pb), nickel (Ni), cadmium (Cd), chromium (Cr), and copper (Cu) in drinking water and vegetable sources from Northern Areas, Gilgit-Baltistan, Pakistan.

Evaluating the Carcinogenic and Non-Carcinogenic Health Risks of Heavy Metals Contamination in Drinking Water, Vegetables, and Soil from Gilgit-Baltistan, Pakistan.

Environmental pollutants significantly impact health and quality of life. High levels of harmful metals in drinking water, vegetables, and soil can accumulate in the body, leading to serious health issues. In Gilgit-Baltistan, Pakistan, the prevalence of cancer is notably high, and heavy metals are considered among the possible risk factors.

Repeat modules and N-linked glycans define structure and antigenicity of a critical enterotoxigenic E. coli adhesin.

Enterotoxigenic Escherichia coli (ETEC) cause hundreds of millions of cases of infectious diarrhea annually, predominantly in children from low-middle income regions. Notably, in children, as well as volunteers challenged with ETEC, diarrheal severity is significantly increased in blood group A (bgA) individuals. EtpA, is a secreted glycoprotein adhesin that functions as a blood group A lectin to promote critical interactions between ETEC and blood group A glycans on intestinal epithelia for effective bacterial adhesion and toxin delivery.

Host-derived CEACAM-laden vesicles engage enterotoxigenic for elimination and toxin neutralization.

Enterotoxigenic (ETEC) cause hundreds of millions of diarrheal illnesses annually ranging from mildly symptomatic cases to severe, life-threatening cholera-like diarrhea. Although ETEC are associated with long-term sequelae including malnutrition, the acute diarrheal illness is largely self-limited. Recent studies indicate that in addition to causing diarrhea, the ETEC heat-labile toxin (LT) modulates the expression of many genes in intestinal epithelia, including carcinoembryonic cell adhesion molecules (CEACAMs) which ETEC exploit as receptors, enabling toxin delivery.