Biomarkers of methylmercury neurotoxicity and neurodevelopmental features: A systematic review.

The issue of MeHg contamination is a significant concern due to its detrimental impact on the environment. This study aimed to thoroughly investigate the effects of MeHg on neurodevelopmental biomarkers, as there is a lack of systematic reviews in this area. We conducted a comprehensive search of three databases (PubMed, Scopus, and Web of Science) and found 522 records, which were then meticulously reviewed by two independent reviewers.

Lipocalin-2 induces mitochondrial dysfunction in renal tubular cells via mTOR pathway activation.

Mitochondrial dysfunction is a critical process in renal epithelial cells upon kidney injury. While its implication in kidney disease progression is established, the mechanisms modulating it remain unclear. Here, we describe the role of Lipocalin-2 (LCN2), a protein expressed in injured tubular cells, in mitochondrial dysfunction.

Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice.

Sarcopenia, the decline in muscle mass and functionality during aging, might arise from age-associated endocrine dysfunction. Ghrelin is a hormone circulating in both acylated (AG) and unacylated (UnAG) forms with anti-atrophic activity on skeletal muscle. Here, we show that not only lifelong overexpression of UnAG (Tg) in mice, but also the deletion of ghrelin gene ( KO) attenuated the age-associated muscle atrophy and functionality decline, as well as systemic inflammation.

Hepatic and neurobiological effects of foetal and breastfeeding and adulthood exposure to methylmercury in Wistar rats.

Methylmercury (MeHg) is an organic bioaccumulated mercury derivative that strongly affects the environment and represents a public health problem primarily to riparian communities in South America. Our objective was to investigate the hepatic and neurological effects of MeHg exposure during the phases foetal and breast-feeding and adult in Wistar rats. Wistar rats (n = 10) were divided into 3 groups.

Opposing effects of 25-hydroxy- and 1α,25-dihydroxy-vitamin D on pro-cachectic cytokine-and cancer conditioned medium-induced atrophy in C2C12 myotubes.

Aim: Loss of skeletal muscle is one of the main features of cancer cachexia. Vitamin D (VD) deficiency is associated with impairment of muscle mass and performance and is highly prevalent in cachectic patients; therefore, VD supplementation has been proposed to counteract cancer cachexia-associated muscle loss. However, in both cachectic cancer patients and tumour-bearing animals, VD supplementation led to disappointing results, urging the need for a better understanding of VD activity on skeletal muscle.

Blood pressure and phosphate level in diabetic and non-diabetic kidney disease: Results of the cross-sectional "Low Clearance Consultation" study.

Highlights: A statistically significant and moderate positive correlation was verified between systolic blood pressure and plasma phosphate concentration in the whole sample (diabetic and non-diabetic), due to the diabetic chronic kidney disease group.A statistically significant and moderate positive correlation was verified between the diastolic blood pressure and plasma phosphate concentration in the whole sample (diabetic and non-diabetic), due to the diabetic chronic kidney disease group.A statistically significant and strong negative correlation was found between diastolic blood pressure and estimated glomerular filtration rate in the diabetic chronic kidney disease group, but there was no statistically significant correlation in the whole sample (diabetic and non-diabetic).

[Rhabdomyolysis].

Rhabdomyolysis is a common entity that often has a multifactorial etiology. It usually affects healthy individuals, following trauma, excessive physical activity, convulsive crisis, alcohol and other drugs consumption or infections. Accumulation of intracellular calcium, activation of proteases and lipases, production of free radicals and the infiltration by inflammatory cells, are some of the mechanisms responsible for muscular necrosis.