Publications by authors named "Adela Rendon-Ramirez"

The mechanisms of Pb(II) toxicity have been studied in human red blood cells using confocal microscopy, immunolabeling, fluorescence-activated cell sorting and atomic force microscopy. The process follows a sequence of events, starting with calcium entry, followed by potassium release, morphological change, generation of ceramide, lipid flip-flop and finally cell lysis. Clotrimazole blocks potassium channels and the whole process is inhibited.

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The excessive intake of alcohol is a serious public health problem, especially given the severe damage provoked by chronic or prenatal exposure to alcohol that affects many physiological processes, such as memory, motor function, and cognitive abilities. This damage is related to the ethanol oxidation in the brain. The metabolism of ethanol to acetaldehyde and then to acetate is associated with the production of reactive oxygen species that accentuate the oxidative state of cells.

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Background: Oxidative damage (OD) biomarkers have been used to evaluate metabolic stress undergone by alcoholic individuals. In alcoholic patients, these biomarkers are usually measured at late stages, i.e.

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Proteolytic enzymes have evolved several mechanisms to cleave peptide bonds. These distinct types have been systematically categorized in the MEROPS database. While a BLAST search on these proteases identifies homologous proteins, sequence alignment methods often fail to identify relationships arising from convergent evolution, exon shuffling, and modular reuse of catalytic units.

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Rat erythrocytes, or erythrocyte membrane ghosts, have been subjected to either chronic (drinking water containing 15 mM lead acetate for 3 months) or acute (10(-9)-10(-2 )M lead acetate for 1 h) Pb(2+) treatments and subsequent changes in membrane properties have been measured. Pb(2+) concentration in chronically treated rat plasma was 1.8 μM, which is one order of magnitude above normal values.

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The long term side effects of any newly introduced drug is a subject of intense research, and often raging controversies. One such example is the dipeptidyl peptidase-IV (DPP4) inhibitor used for treating type 2 diabetes, which is inconclusively implicated in increased susceptibility to acute pancreatitis. Previously, based on a computational analysis of the spatial and electrostatic properties of active site residues, we have demonstrated that phosphoinositide-specific phospholipase C (PI-PLC) from Bacillus cereus is a prolyl peptidase using in vivo experiments.

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