Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.10.2 (focal adhesion kinase)
44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous investigations have documented a reduced activity of the sodium-potassium-stimulated adenosine triphosphatase enzyme (Na+,K+ ATPase) in platelet membranes of allergic subjects. The purpose of this study was to determine if the reduced Na+,K+ ATPase activity was due to an enzyme inhibitor. Na+,K+ ATPase activity of a particulate fraction of sonicated platelets was determined by spectrophotometry in asymptomatic adults with and without allergy. The Na+,K+ ATPase level (mean, nanomoles per microgram of protein per minute; +/- STD) of allergic subjects (0.9 +/- 1.3) was lower (p less than 0.001) than that of nonallergic subjects (3.9 +/- 1.6). In contrast, when the same platelet fractions were frozen before assay, Na+,K+ ATPase was higher (p less than 0.005) in allergic subjects (6.0 +/- 1.4) than in nonallergic subjects (3.6 +/- 2.0). An inhibitor of canine kidney Na+,K+ ATPase was detected in the buffer in which these platelet fractions were frozen, allergic subjects (0.5% +/- 0.4% inhibition per microgram of protein) compared to nonallergic subjects (0.04% +/- 0.08%; p less than 0.005). The level of inhibition correlated positively with the postfreezing increase in platelet membrane Na+,K+ ATPase, suggesting a freezing-induced displacement of an inhibitor from the membrane. Plasma from these same subjects inhibited Na+,K+ ATPase activity of normal platelets, allergic subjects (70% +/- 31% inhibition) compared to nonallergic subjects (13% +/- 16%; p less than 0.001). These data suggest that the transport-enzyme defect observed in platelets from allergic subjects was due to a circulating Na+,K+ ATPase inhibitor. In vivo Na+,K+ ATPase inhibition in allergy could have profound effects on intracellular cation concentrations and broad implications for pathogenesis.
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PMID:A circulating inhibitor of the platelet Na+,K+ adenosine triphosphatase (ATPase) enzyme in allergy. 184 56

To determine the effects of food deprivation on the physical, physiological, and metabolic responses to exercise in the heat, adult, male rats (330-360g, N = 16/group) were food-deprived for 24, 48, or 72 h. They were then exercised (9.14m X min-1) in the heat (35.5 degrees C) to hyperthermic exhaustion (Tco approximately 43 degrees C). Food deprivation had no effects on endurance, but ad lib fed controls manifested significantly (p less than 0.05) increased Tco and Tsk during the latter portion of the treadmill interval. While plasma osmolality was significantly (p less than 0.01) increased in all groups as a result of the heat/exercise contingency, hematocrit ratios were elevated (p less than 0.01) as a result of 48 and 72 h of food deprivation. Food deprivation resulted in severe hypoglycemia following exercise (p less than 0.01), and these decrements were accompanied by marked (p less than 0.01) reductions in circulating insulin levels. Prolonged food deprivation (48 and 72 h) resulted in significant (p less than 0.01) hypertriglyceridemia and hyperlactacidemia subsequent to exercise. Levels of sodium, potassium, urea nitrogen, and creatine phosphokinase were unaffected by the food deprivation intervals. We have concluded from these studies that while several thermoregulatory and metabolic responses to exercise in the heat can be significantly affected by food deprivation, short-term endurance capacity was unaltered.
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PMID:Food deprivation and exercise in the heat: thermoregulatory and metabolic effects. 389 96

The role of calcium in initiating smooth muscle contraction is widely accepted. The sources of this calcium are thought to be located both intracellularly and extracellularly. We have recently developed a method by which the cellular localization of calcium in smooth muscle can be determined. This method involves exposing the tissue to 45Ca, rapidly freezing and vacuum dehydrating the tissue, and preparing the tissue for electron microscopic autoradiography (EM ARG). In the present study the distribution of calcium in control and potassium-contracted tissue of the rabbit vas deferens was compared. No significant differences in distribution were observed in the two treatments. This finding provides morphological support for the hypothesis that the calcium used in potassium-induced contraction is primarily of extracellular origin. In addition, significant sequestration by intracellular organelles does not occur during a potassium contraction. In other experiments, the effect of rinsing tissue in cold calcium prior to freezing was investigated. From these data is appears that calcium is removed from the cytoplasmic matrix, plasma membrane, and organelles in a nonuniform manner. Further investigation into these findings should enable us to characterize more precisely the intracellular redistribution of calcium that occurs as a result of a variety of physiological manipulations.
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PMID:The cellular distribution of calcium in freeze-dried rabbit vas deferens using EM autoradiography. 397 81

The effects of water temperature (6 degrees, 22 degrees, 46 degrees C) and chlorination on voluntary dehydration (D), sweat electrolyte losses (SEL), and total body electrolyte losses (BEL) were studied in 12 healthy males during 6 h of intermittent treadmill exercise (1.34 m X s-1, 5% grade) in a climatic chamber (40.6 degrees C DB, 25.5 degrees C WB). Body weight (BW), rectal temperature (Tre), mean weighted skin temperature (Tsk), heart rate (HR), plasma osmolality (PO), sweat rate (SR), sweat sodium (Na+), chloride (Cl-), potassium (K+), and magnesium (MG++), urine volume, Na+, and K+ were measured. No differences were found between chlorinated and non-chlorinated treatments except SEL of Mg++. Subjects (Ss) who drank 46 degrees C (-2.1% BW) consumed approximately 50% less water (p less than 0.001), and had D which was 1.050 kg larger (p less than 0.001) than subjects who consumed 6 degrees C (-0.5 %BW). There were no significant between-group PO differences, but Tre and Tsk differed between 46 degrees and 6 degrees C (p less than 0.01), and the HR of 22 degrees and 46 degrees C were both different from 6 degrees C (p less than 0.05). SR of all groups were essentially equal, although differences in total sweat Na+ (p less than 0.02) and Cl- (p less than 0.04) losses were observed between 46 degrees and 6 degrees C. SEL of sweat K+ and Mg++ were not affected by the experimental design. Based on 24 h projections of BEL, it was concluded that K+ depletion is more likely than Na+ depletion because food is often supplemented with sodium chloride.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Voluntary dehydration and electrolyte losses during prolonged exercise in the heat. 403 32

Bacterial contamination and the effects of time, temperature, and preservative on bacterial growth in enteral nutrient solutions were studied. Bacteria were counted after 24-hour incubation of five samples of frozen Travasorb STD (Travenol Laboratories) from the pharmacy and five samples freshly reconstituted in the dietary department. Growth in samples of Travasorb STD prepared in the pharmacy was studied after (1) fresh mixing, 24-hour refrigeration, and 12 hours at room temperature, (2) freezing, thawing, and 12 hours at room temperature, and (3) freezing, thawing, 24-hour refrigeration, and 12 hours at room temperature. Duplicate samples of five products [Ensure (Ross Laboratories), Precision LR (Doyle Pharmaceuticals), Travasorb STD, Vital (Ross Laboratories), and Vivonex STD ( Norwich -Eaton)] were inoculated with Enterobacter cloacae, and growth curves for 24 hours were plotted. This challenge study was repeated using Travasorb STD as a control and Travasorb STD with potassium sorbate added. Bacterial contamination following reconstitution was not significantly different between pharmacy and dietary department samples. Growth after 12 hours at room temperature was not significantly different for the three sets of storage conditions. Logarithmic growth occurred only at room temperature. All products supported growth of E. cloacae, but growth was significantly lower in Vivonex STD (which contains potassium sorbate) and Precision LR. Growth was reduced by 70% versus control at 12 hours in Travasorb STD containing 0.036% potassium sorbate and by 90% with 0.2% potassium sorbate. Microbial growth in enteral nutrient solutions was dependent on the initial inoculum and the storage time at room temperature. Addition of potassium sorbate to these solutions may greatly reduce bacterial growth.
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PMID:Effects of time, temperature, and preservative on bacterial growth in enteral nutrient solutions. 643 69

To determine the effects of low-dosage organophosphate administration on exercise in a hot environment, malathion (7.5 mg/day, 4 days) was administered IP to rats, and effected a 35% (p less than 0.01) reduction in plasma cholinesterase levels. Treadmill endurance (9.14 m/min, no incline, 35 degrees C ambient) was unaffected when the animals were exercised to hyperthermic exhaustion (Tre approximately 43 degrees C). While rates of heat gain were similar between groups, malathion-treated rats displayed higher Tsk (p less than 0.05) at a number of sampling times during the treadmill run. While creatine phosphokinase levels were unaffected by either cholinesterase inhibition or exercise in the heat, lactate dehydrogenase activities were increased (p less than 0.01) in both groups following hyperthermic exhaustion. Although plasma levels of lactate, potassium, urea nitrogen, and creatinine were all significantly (p less than 0.01) increased as a result of exercise in the heat, these increments were not exacerbated by cholinesterase inhibition. Results generally indicated that at this moderate level cholinesterase inhibition, malathion administration did not adversely affect physiological, physical, or thermoregulatory efficacy.
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PMID:Malathion administration: effects on physiological and physical performance in the heat. 665 21

Cyclosporine A (CyA) is known to cause hyperkalemia by impairing renal potassium excretion. However, the observation of transient and severe hyperkalemia occurring within 3 to 5 hours of CyA ingestion in several organ transplant patients led us to postulate that it might also cause a potassium efflux from the intracellular to the extracellular fluid space. We tested this hypothesis by studying 22 nondiabetic, renal transplant patients with stable renal function (serum creatine < 2.25 mg/dL) who were treated with CyA (CyA group; n = 14) or imuran and prednisone (STD group; n = 8). Eight CyA and four STD patients also were treated with a beta-blocker (BB). While at rest, fasting plasma potassium levels were sampled hourly in all patients from 8:00 am to 1:00 pm. All medications (including CyA and BBs) were given after the 8:00 am blood sampling. Venous pH, osmolality, insulin, aldosterone, epinephrine, norepinephrine, and CyA levels also were determined at 8:00 am, 11:00 am, and 1:00 pm. Urine was collected from 11:00 pm to 8:00 am prior to the study (period I) and from 8:00 am to 1:00 pm during the study (period II) for measurement of potassium excretion (standardized to a 5-hour period). A significant increase in serial plasma potassium levels was noted in the CyA + BB group only (P = 0.0006 by repeated measures analysis of variance).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Extrarenal effect of cyclosporine A on potassium homeostasis in renal transplant recipients. 835 59

We evaluated a new analyzer designed for point-of-care testing of blood gases, sodium, potassium, ionized calcium, and hematocrit. The Gem Premier (Mallinckrodt) system has two components: the analyzer and a disposable cartridge. Analysis takes place in the cartridge, which contains the electrochemical sensors, the calibrants, the reagents, the sampling stylus, and the waste container. The system was evaluated for imprecision and accuracy. With aqueous control materials, total imprecision (CV) was: pH, 0.10-0.18%; PCO2, 3.16-5.78%; PO2, 2.92-4.85%; sodium, 0.82-1.44%; potassium, 1.35-1.48%; ionized calcium, 0.75-1.45%; and hematocrit, 1.13-1.83%. Accuracy of the system was assessed by split-sample comparison with the Radiometer ABL 330 blood gas analyzer for pH and blood gases, the Nova Stat Profile 5 for whole-blood electrolyte and hematocrit analysis, and the IL Phoenix for plasma electrolyte analysis. After outlier correction, regression statistics were excellent for all analytes except sodium, which demonstrated Sy[x values between 1.80 and 2.30 mmol/L and 0.85 < or = r < 0.90.
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PMID:Performance of Gem Premier blood gas/electrolyte analyzer evaluated. 837 66

There is now considerable evidence that nitric oxide (NO) is an important neuroregulatory agent, but there has been very little investigation of the possible role of NO in neuroendocrine mechanisms. We have previously shown that acute rat hypothalamic explants can be used to study the regulation of hypothalamic neuropeptide release, and we have now utilised this experimental approach to investigate the putative involvement of NO in the control of the principal corticotropin-releasing hormone, CRH. We studied the direct effects of the NO precursor L-arginine (L-ARG), as well as the NO donors molsidomine and sodium nitroprusside, on both the basal and stimulated release of CRH; the stimuli used were non-specific depolarisation with potassium chloride (KCl) and the specific cytokine, interleukin-1 beta (IL-1 beta; 100 U/ml). L-ARG was tested in each experimental condition with and without contemporaneous addition of its competitive antagonist NG-monomethyl-L-arginine (L-NMMA). IL-1 beta-induced CRH release was also investigated in the presence of D-arginine (D-ARG), which is not active as a precursor to NO, and ferrous hemoglobin (Hb), a substance which is a potent inactivator of NO. None of the NO precursors (L-ARG, molsidomine, sodium nitroprusside) or antagonists (L-NMMA or Hb) was able to affect basal CRH release. However, L-ARG 10 and 100 microM were found to significantly inhibit the release of CRH induced by 40 mM KCl; CRH fell to 45% of its stimulated level at the higher dose of L-ARG. This effect was attenuated in the presence of L-NMMA at a ten-fold higher dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitric oxide modulates the release of corticotropin-releasing hormone from the rat hypothalamus in vitro. 848 68

An automated gas chromatographic method for the simultaneous determination of cholesterol, alpha-tocopherol and alpha-tocopheryl acetate in edible oils and fats without derivatization is reported. Interferences from lipid material are avoided by using a continuous system to transesterify triglycerides with potassium methylate in methanol. The precision of the method is 1.9, 2.2 and 3.1% for cholesterol, alpha-tocopherol and alpha-tocopheryl acetate, respectively. The proposed methods was validated by analysing a standard reference material of coconut oil (SRM 1563-2) with good results. The method features a high throughput, minimal sample handling and analyte specificity (lipid material does not interfere).
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PMID:Gas chromatographic determination of cholesterol and tocopherols in edible oils and fats with automatic removal of interfering triglycerides. 858 31


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