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Biomedical subjects

A F Almeida

Publications and source records attributed to A F Almeida.

At least 37 records · Page 2Linked to original sources
PubMed1989

Acute renal failure due to viperine snake bite as seen in tropical western India.

A wide spectrum of clinicopathological changes have been described in 50 cases of ARF following viperine snake bite studied prospectively over a 15-year period. Disseminated intravascular coagulation (DIC) was seen in 24/50 cases (Russel's viper bite in 62% and Ecchis carinatus bite in 42% of subjects). Histological examination of renal tissue obtained 1.5 days to 8 weeks after the bite revealed proliferative glomerular changes in 17 cases. These were characterized by ballooning of the capillaries, thickening and splitting of glomerular basement membrane (GMB), fibrin thrombi in the capillaries, and mesangial cell proliferation most prominently seen in Ecchis carinatus bites resulting in ARF.

Acute Kidney Injury↗
PubMed1989

Clinicopathological study of acute renal failure following viperine snake bite.

Fifty patients of acute renal failure following Viperine snake bite were studied. Oliguria (100%), local swelling (48%) and bleeding tendencies (42%) were the predominant clinical features encountered. Of the 25 patients in whom detailed coagulation studies were done, 24 patients had disseminated intravascular coagulation (DIC) and 1 had primary fibrinolysis. DIC was commoner with Russell's viper bite (62%) in comparison to Echis carinatus bites (40%). Renal histology obtained in 29 cases revealed tubular necrosis (35%), cortical necrosis (24%) tubular degeneration (17%) and glomerular changes (17%). Ballooning of glomerular capillaries (59%), splitting of glomerular basement membrane (40.7%), swelling of endothelial cells (29.6%), and focal proliferation of mesangial cells (17%) were the significant glomerular changes encountered. 20 (40%) patients succumbed, DIC (50%), irreversible shock (30%) and septicaemia (20%) being the immediate causes of death. Development of oliguria within 24 hours of snake bite and cortical necrosis were associated with higher mortality.

Acute Kidney Injury↗
PubMed1987

Regulation of the number of Na+,K+-pump sites after mitogenic activation of lymphocytes.

The early activation of Na+,K+-ATPase-mediated ion fluxes after concanavalin A (ConA) stimulation of pig lymphocytes is caused by an increase in intracellular Na+ concentration. A second mechanism of regulation of Na+,K+-ATPase activity becomes apparent between 3 and 5 h after mitogenic stimulation, but prior to onset of increase in cell volume; this consists of an increase (about 75%) in the number of ouabain-binding sites (from 35 X 10(3) +/- 12 X 10(3)/cell in resting to 60 X 10(3) +/- 27 X 10(3)/cell in activated lymphocytes). The increase in ouabain binding was attributed to an increase in the number of active Na+,K+-ATPase molecules, based on the following evidence: there was an increase in the Vmax of ouabain binding, without variation in the Km; the increase in ouabain binding was accompanied by a proportional increase in K+ influx, when the assay was performed in the presence of the Na+ ionophore monesin, which was used to eliminate the difference in intracellular Na+ concentration between resting and activated cells; there was proportionality between ouabain-inhibitable ATPase activity in permeabilized cells and the number of ouabain-binding sites in resting and activated lymphocytes. The ConA-induced increase in ouabain-binding sites was influenced neither by amiloride nor by incubation in low Na+ medium, under conditions which prevented both increase in intracellular Na+ concentration and K+ influx. Increase in intracellular Na+ concentration was ineffective in altering the number of active pump molecules in resting cells. During incubation with ConA, the presence of ouabain did not affect the increase in ouabain-binding sites; thus, regulation of the number of pump sites is independent of the regulation of their activity. The ConA-induced increase in number of ouabain-binding sites did not require protein synthesis; indeed, cycloheximide, anisomycin, and puromycin, under conditions in which they inhibited protein synthesis by by 95%, induced the increase to approximately the same extent as did ConA. This suggests the presence in resting lymphocytes of a rapidly turning over protein that either prevents the ATPase subunits from assembling or from integrating into the membrane.

Animals↗
PubMed1986

Acute renal failure--a complication of new multidrug regimen for treatment of leprosy.

A leprosy patient who developed acute renal failure on multidrug therapy is reported. The patient had initially received a once-weekly dose of rifampin and after he had stopped taking the drug for a time, was given rifampin on a once-monthly dose schedule. He recovered completely from his acute renal failure. Kidney biopsy showed interstitial nephritis with mononuclear and eosinophilic cellular infiltrates.

Acute Kidney Injury↗
PubMed1985

Effects of mammalian brain extracts and chlormadinone acetate on neuronal Na+,K+-ATPase and electrogenic Na+,K+-pump activity in vitro.

Acid-acetone extracts of brain (from beef and guinea pig) and chlormadinone acetate (CMA) were compared with ouabain for their ability to inhibit the electrogenic Na+,K+-pump and the Na+,K+-ATPase of neuronal tissues. The membrane potential of neurones in the paravertebral sympathetic ganglion of the bullfrog was recorded in K+-free Ringer's solution by means of the sucrose gap technique. The potassium activated hyperpolarization (K+H), induced by the re-introduction of potassium, was used as an index of electrogenic Na+, K+-pumping. The K+H was blocked by 1 microM ouabain. Na+,K+-ATPase activity was measured in microsomal membrane preparations of frog and beef brain using a continuous spectrophotometric assay. Although ouabain consistently inhibited beef brain Na+,K+-ATPase (IC50 = 2.2 microM), acid-acetone extracts prepared from guinea pig and beef brain produced only partial inhibition. Neither of the extracts significantly reduced the K+H of the frog ganglion. CMA inhibited Na+,K+-ATPase prepared from bullfrog brain and spinal cord with slightly greater potency (IC50 = 4.5 microM) than did ouabain (IC50 = 10 microM). In contrast, electrogenic Na+,K+-pumping (i.e. the K+H) in the frog ganglion was not affected by this steroid. It is concluded that although both the extracts and CMA inhibited Na+,K+-ATPase, neither can be considered ouabain-like due to their failure to affect the electrogenic Na+,K+-pump in situ.

Animals↗
PubMed1985

Transmembrane transport of iron from extracellular transferrin by lymphoma cells.

Transferrin is essential for the entry of iron into cells, but whether the entire iron-transferrin complex or only the iron enters is not known. Separation of the cellular from the interparticulate radioactivity is a common problem with such studies. By pelleting cells under oil, we have made precise measurements of the uptake capacity for 59Fe of mouse lymphoma RI cells. At 37 degrees C an 18-fold concentration of iron was observed within 30 min; at 0 degrees C this value was about 3-fold. At 37 degrees C a maximum of 18,000 molecules of 125I-labelled Fe-transferrin were bound to each cell; this was reduced by about half at 0 degrees C. At 37 degrees C about 10,000-12,000 binding sites for 125I-apotransferrin were detected on each cell. From our data we conclude that although essential for the transport of iron, it is unlikely that transferrin enters RI cells. It is possible that iron is actively transported and that the receptor population is heterogeneous.

Animals↗
PubMed1985

Heterogeneous uptake of 9-beta-D-arabinofuranosyladenine by mouse spleen lymphocytes.

Spleens of mice treated with 9-beta-D-[2,8-3H]arabinofuranosyladenine (araA), 0.5-30.0 mg/kg showed rapid dose-dependent accumulation of 3H, which peaked at 2.5 mg/kg. Lymphocytes from spleens showed linear uptake when incubated with 0.68, 1.36, and 5.03 microM araA over 120 s. With 1.0 mM araA, uptake was reduced in rate but was not saturated. Tritiated metabolites identified from these lymphocytes were araA which predominated after brief incubations, its deaminated form (araH), and some phosphorylated product in small amount. Inhibition of deaminase increased intracellular araA. Although potent inhibitors of nucleoside transport inhibited araA uptake marginally, adenosine competed with araA for about 50% of the uptake capacity. The data suggest that the uptake of araA by mouse lymphocytes, which is not simple diffusion, occurs by a mechanism distinct from typical nucleoside transport.

Animals↗