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Biomedical subjects

A Sanchez

Publications and source records attributed to A Sanchez.

At least 253 records · Page 14Linked to original sources
PubMed1984

Stimulus-response coupling in human platelets. Changes evoked by platelet-activating factor in cytoplasmic free calcium monitored with the fluorescent calcium indicator quin2.

The role of changes in cytoplasmic free calcium, [Ca2+]i, in the responses to platelet-activating factor (PAF) was studied in human platelets loaded with the fluorescent calcium indicator, quin2. In the presence of 1 mM external calcium, PAF raised [Ca2+]i 8-10-fold in a few seconds to peak near 1 microM. [Ca2+]i then declined over several minutes towards the basal level. In the absence of external calcium there was a much smaller increase in [Ca2+]i of similar pattern. These findings suggest that PAF increases [Ca2+]i partly by discharge of internal Ca2+, but mainly by stimulated influx. Blockade of cyclo-oxygenase with aspirin only slightly reduced the [Ca2+]i changes, indicating that thromboxane A2 is not a major mediator of the calcium movements. In control conditions PAF could stimulate shape-change, aggregation and secretion. Aggregation and secretion were roughly halved by blockade of cyclo-oxygenase. Shape-change and secretion still occurred under conditions where the [Ca2+]i rise was small or suppressed, indicating a role for intracellular activators other than Ca2+. The possible involvement of products of phosphoinositide breakdown is discussed.

Aminoquinolines↗
PubMed1984

Selenium deficiency in cattle associated with Heinz bodies and anemia.

Cattle grazing St. Augustine grass growing on peaty muck soils in the Florida Everglades developed anemia associated with the presence of Heinz bodies and suboptimal concentrations of selenium in blood. Selenium supplementation corrected the anemia, prevented Heinz body formation, increased the body weight of cows and calves, and elevated blood selenium. This may be the first recorded example of widespread anemia in a population due to selenium deficiency.

Anemia, Hemolytic↗
PubMed1984

Rhizobium phaseoli symbiotic mutants with transposon Tn5 insertions.

Rhizobium phaseoli CFN42 DNA was mutated by random insertion of Tn5 from suicide plasmid pJB4JI to obtain independently arising strains that were defective in symbiosis with Phaseolus vulgaris but grew normally outside the plant. When these mutants were incubated with the plant, one did not initiate visible nodule tissue (Nod-), seven led to slow nodule development (Ndv), and two led to superficially normal early nodule development but lacked symbiotic nitrogenase activity (Sna-). The Nod- mutant lacked the large transmissible indigenous plasmid pCFN42d that has homology to Klebsiella pneumoniae nitrogenase (nif) genes. The other mutants had normal plasmid content. In the two Sna- mutants and one Ndv mutant, Tn5 had inserted into plasmid pCFN42d outside the region of nif homology. The insertions of the other Ndv mutants were apparently in the chromosome. They were not in plasmids detected on agarose gels, and, in contrast to insertions on indigenous plasmids, they were transmitted in crosses to wild-type strain CFN42 at the same frequency as auxotrophic markers and with the same enhancement of transmission by conjugation plasmid R68.45. In these Ndv mutants the Tn5 insertions were the same as or very closely linked to mutations causing the Ndv phenotype. However, in two mutants with Tn5 insertions on plasmid pCFN42d, an additional mutation on the same plasmid, rather than Tn5, was responsible for the Sna- or Ndv phenotype. When plasmid pJB4JI was transferred to two other R. phaseoli strains, analysis of symbiotic mutants was complicated by Tn5-containing deleted forms of pJB4JI that were stably maintained.

Bacterial Proteins↗
PubMed1983

Trifluoperazine and chlorpromazine block secretion from human platelets evoked at basal cytoplasmic free calcium by activators of C-kinase.

Trifluoperazine, chlorpromazine and other drugs known to inhibit calmodulin-dependent processes are also known to inhibit protein kinase C. The effect of these agents on secretion evoked by known activators of C-kinase has been studied in human platelets loaded with the fluorescent Ca indicator, quin2 and preincubated with aspirin. The secretory response stimulated by phorbol ester and exogenous diacylglycerol, at basal levels of cytoplasmic free Ca2+, [Ca2+]i, was suppressed by trifluoperazine, chlorpromazine and W-7, as was the secretion evoked by collagen that occurs without a change in [Ca2+]i. The response to thrombin, which is accompanied by elevated [Ca2+]i was barely affected. Modest elevation of [Ca2+]i by Ca ionophore was able to overcome the inhibitory effect of these drugs on the response to phorbol ester, diacylglycerol, and collagen.

Blood Platelets↗
PubMed1983

Volume restoration in osmotically swollen lymphocytes does not involve changes in free Ca2+ concentration.

An increase in cytoplasmic free [Ca2+], [Ca2+]i, has been suggested as the trigger for the permeability changes that bring about cell volume restoration following exposure to anisotonic media. This idea was directly tested in human peripheral lymphocytes undergoing regulatory volume decrease following a hypotonic dilution of the suspension. [Ca2+]i was measured with the intracellularly trapped fluorescent indicator, quin2, and showed no measureable change on hypotonic swelling or during the subsequent volume decrease. Moreover, even though the incorporated quin2 adds significant Ca-buffering to the cytoplasm, regulatory volume decrease occurred normally in the quin2-loaded cells. It appears that alterations in [Ca2+]i are not involved in these processes of volume regulation. An intracellularly trapped derivative of fluorescein, bis(carboxyethyl)carboxyfluorescein, was used to monitor cytoplasmic pH, which also showed no change during regulatory volume decrease.

Body Fluids↗
PubMed1982

Dietary sodium and renal alpha 2-adrenergic receptors in Dahl hypertensive rats.

Dahl sodium-sensitive and resistant rats were fed low and high sodium diets. Renal plasma membrane alpha 2-adrenergic receptor concentrations were greater (p less than .05) in sensitive than in resistant rats while ingesting a low sodium diet. On a high sodium diet the alpha 2 receptor concentration increased (p less than .01) in sensitive but not in resistant rats. Since alpha 2 receptors are located in proximal tubules at sites where norepinephrine induces sodium reabsorption, we postulate that this genetically determined abnormal receptor regulation could lead to exaggerated sodium retention and possibly high blood pressure.

Animals↗
PubMed1982

Asian karyotype (2n = 42) in the black rat (Rattus rattus) in Mexico.

A cytogenetic survey in 10 black rats (Rattus rattus), captured in Guadalajara, Jalisco, Mexico, revealed a 42 chromosomal complement (Asian type) in all of them. Polymorphism due to pericentric inversions of chromosomes 9, 11 and 13, as well as a homomorphic subtelocentric pair 1, permitted further karyotypic distinction. An Asian origin of this rat with a subsequent isolated evolution in Mexico is concluded.

Animals↗
PubMed1981

A hypothesis on the etiological role of diet on age of menarche.

Body size and body composition have been suggested as the best explanation for the temporal trend toward early menarche over the last 100 years. There is evidence from human and animal studies that indicates that body size is not the primary factor in influencing the occurrence of menarche. The data actually show that diet may be a primary environmental control mechanism of menarche especially since it alters hormone levels. We see diet as an etiological factor in both the long term and immediate control of menarche. In the long term it influences body size and development leading to menarche. In the short term it acts at a critical state to precipitate the onset of menarche and related physiological changes. This hypothesis does not exclude other less important factors associated with menarche. Our data shows that the present trend toward early menarche can be reversed when a balanced vegetarian diet is selected in place of the ordinary American diet.

Adolescent↗
PubMed1981

Glucose-induced hyperkalemia in diabetic subjects.

Four insulin-deprived patients with diabetes mellitus and normal baseline potassium and aldosterone levels became hyperkalemic when given 100 g of glucose orally. The increases in plasma potassium concentrations averaged 1.3 mEq/L (range, 0.7 to 1.8 mEq/L) and were accompanied by increases in plasma aldosterone level. Four other insulin-deprived diabetics had normal plasma potassium and aldosterone responses when given 50 mEq of potassium chloride orally. These findings suggest that glucose-induced hyperkalemia is not infrequent in diabetics and that it is not usually associated with hypoaldosteronism. The acute suppression of aldosterone biosynthesis with aminoglutethimide did not lead to increased plasma potassium levels following oral potassium loads. This suggests that the acute responses of aldosterone to potassium loads may not be important in preventing postprandial hyperkalemia.

Adult↗
PubMed1980

Effect of amphetamine and dopamine on oxygen uptake of rat brain slices in vitro.

Effects of d-amphetamine and dopamine on rat brain cortical slices respiration were estimated to assess whether these drugs might modify membrane (Na+ + K+)-ATPase activity in intact cells as they do in isolate enzyme systems. d-Amphetamine, 10(-5) M (140%), 10(-6) M (123%) 10(-7) M (131%) and 10(-7) M (129%). These results may be related to estimates of (Na+ + K+)-ATPase activity in subcellular systems. In an incubation medium containing calcium, 10(-4) M ouabain does not modify brain slices respiration, but fully antagonizes oxygen consumption increases induced by d-amphetamine or dopamine, which might thus be mediated by membrane ATPase activity. Either phenoxybenzamine, oxprenolol or halo-peridol, nullify those metabolic effects of d-amphetamine and dopamine, by means of unspecific mechanisms rather than by a specific interaction at drug receptor sites. It is suggested that cell respiratory control is the final resultant of mechanisms which might be separately, and oppositely, modified by drugs.

Amphetamine↗
PubMed1979

Stimulation of monovalent cation fluxes by electron donors in the human red cell membrane.

When human red cells are incubated at 37 degrees C with the artificial electron donor system ascorbate + phenazine methosulphate the fluxes of Rb+ (K+) through the cell membrane are increased. The effect of this donor system is much stronger in energy-depleted than in normal cells. The same effects are produced by HS-glutathione, NADH or NADPH loaded into resealed ghosts, but these electron donors were ineffective when added to the incubation medium. The Rb+ (K+) fluxes induced by electron donors resemble closely those induced by an increase of intracellular Ca2+ (Gardos effect). The electron donors require the presence of intracellular Ca2+ to be effective, but at levels that do not stimulate by themselves the fluxes of K+. Flavoenzyme inhibitors (atebrin and chlorpromazine), oligomycin and quinine prevented the effects of both electron donors and Ca2+ alone; antimycin, upcouplers and ethacrynic acid inhibited them partially; ouabain, furosemide, and rotenone had no effect. The results could be explained if the effect of electron donors is to bring about a change in the redox state of some membrane component(s) that makes intracellular Ca2+ more effective to elicit rapid K+ movements. Plasma membrane oxidoreductase activities could be engaged in this change.

Ascorbic Acid↗