Alberto Lázaro

TL;DR: Pt turned out to accumulate in the kidney cortex and corticomedullary junction, corresponding to areas where the proximal tubule S3 segments (the most sensitive cells to cisplatin nephrotoxicity) are located, demonstrating the connection between platinum accumulation and renal damage proved by histological examination of HE-stained sections.

TL;DR: The more complicated the lesion, the higher the number of secreted proteins, suggesting the production of specific proteins relating to the complexity of the atherosclerotic lesion.

TL;DR: It is concluded that Fc&ggr;R deficiency limits development and progression of atherosclerosis and support the use of immunotherapy in the treatment of this disease.

TL;DR: Specific focus will be placed on the generation specific uremic toxins with nephrotoxic potential, the decreased availability of bacteria-derived metabolites withNephroprotective potential, such as vitamin K and butyrate and the cellular and molecular mechanisms linking these toxins and protective factors to kidney diseases.

TL;DR: Cilastatin, a small molecule inhibitor of renal dehydropeptidase I, prevents proximal tubular cells from undergoing cisplatin-induced apoptosis in vitro as mentioned in this paper.