Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cross-clamping of the ascending aorta in dogs for 15 min produced severe neurological deficit, observed for up to 20 h. Immediately after restoration of the circulation, the intracranial pressure in the cisterna magna increased transiently to a mean peak of 22.8 Torr (SD +/- 1.7) because of a compensatory increase in systemic arterial pressure, without a fall in cerebral perfusion pressure. The intracranial pressure returned to control values 15-30 min after ischaemia and showed no secondary rise during the 8 h of observation. The electroencephalogram became isoelectric 34 +/- 6.5 s (mean +/-SD) after circulatory occlusion, and was abnormal when it reappeared 5 h 36 min (SD +/- 2 h 4 min) after the circulation was restored. The electrical impedance of the brain increased immediately after ischaemia and returned rapidly towards pre-ischaemic values during re-perfusion. The cerebral water had not increased measurably 4 h after ischaemia. After ischaemia, the lactate concentration in the cerebrospinal fluid increased to 4.7 mequiv./1(SEM +/-0.1) and the pH decreased to 7.17 (SEM +/-0.02); both returned to control values after 3.5 h. The cerebral glucose uptake was decreased 35 min after ischaemia, cerebral oxygen uptake remained unchanged but cerebral blood flow decreased (P less than 0.05 at 90 min). Immediately after cardiac arrest, recovery was impaired more by the presence of focal abnormal brain perfusion than by intracranial hypertension.
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PMID:Total brain ischaemia in dogs: cerebral physiological and metabolic changes after 15 minutes of circulatory arrest. 0 Jul 50

Plasma of insulin-treated diabetics and of newborn infants of insulin-treated diabetic mothers contains insulin antibodies which invalidates the radioimmunoassay of insulin. Therefore, the endogenous insulin antibody complex must be splitted at a pH lower than 5 and the total IRI (TIRI) is separated by ethanol extraction. It was investigated the recovery rate in dependence upon plasma volume used for extraction. By reduction of used plasma volume from 500 to 200 mul per extraction the recovery rate was increased from 65.1 +/- 8.4 to 88.3 +/- 4.2% (mean +/- SEM). The low plasma volume of 200 mul for TIRI extraction made it possible to determine TIRI during glucose loads of newborn infants. To eliminate different conditions of incubation for standard and unknown plasma samples the TIRI levels were computed by means of so-called "extracted" standard curve, obtained with extracted insulin from standard insulin dilution in insulin-free pooled human plasma. Using the described method a temporary regeneration of insulin secretion of a newly diagnosed juvenile diabetic after insulin treatment could be shown. In contrast to newborn infants of healthy mothers a biphasic/insulin release was found during the intravenous glucose loads in newborn infants of insulin-treated diabetic mothers.
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PMID:Determination of total insulin (TIRI) in plasma of insulin-treated diabetics and newborn infants of insulin-treated diabetic mothers. 0 60

Concentrations of pregnenolone (delta5P), dehydroepiandrosterone (DHEA), 16alpha-hydroxydehydroepiandrosterone (16alpha-OH DHEA), pregnenolone sulfate (delta5P-S), and dehydroepiandrosterone sulfate (DHEA-S) were measured simultaneously by radioimmunoassay in individual, paired umbilical artery (UA) and vein (UV) sera from 18 normal term pregnancies, 6 in labor, 12 not in labor. Mean UA and UV levels +/- SEM (ng/ml) were for delta5P: 30.39 +/- 1.69, 35.55 +/- 3.06; DHEA: 12.31 +/- 2.34, 3.66 +/- 0.38; 16alpha-OH DHEA: 7.48 +/- 0.63, 10.59 +/- 0.78; delta5P-S: 1,652 +/- 154, 1,486 +/- 130; DHEA-S: 2,122 +/- 134, +/- 134, 1,906 +/- 134. Umbilical artery delta5P-S, DHEA-S, and DHEA levels were significantly higher than UV levels, whereas the reverse was true for delta5P and 16alpha-OH DHEA. The inverse arterio-venous (A-V) gradient for 16alpha-OH DHEA was contrary to previous published reports using pooled samples. Comparison by linear regression of paired UA and UV steroid concentrations of delta5P, delta5P-S, DHEA, and DHEA-S revealed a significant correlation (P less than 0.01) for each steroid. Labor was associated with a significant increase in UA levels of DHEA-S and a smaller, but not quite significant, increase in UA levels of delta5P-S, while similar changes for unconjugated delta5-3beta-hydroxysteroids were not observed. Mean A-V gradients between the group of patients in labor and those not in labor were not significantly different. These data demonstrate that: 1) a significant difference between UA and UV concentrations exists for delta5P, DHEA, 16alpha-OH DHEA, delta5P-S, and DHEA-S; 2) there is a significant correlation between UA and UV concentrations for delta5P, DHEA, delta5P-S, and DHEA-S, implying that each fetoplacental unit maintains an equilibrium relative to these steroid concentrations in the umbilical circulation; 3) labor is associated with a significant increase in UA levels of DHEA-S and probably of delta5P-S.
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PMID:Simultaneous comparison of delta 5-3beta-hydroxysteroid levels in the fetoplacental circulation of normal pregnancy in labor and not in labor. 0 67

This study was designed to determine the effect of acute hyperventilation on distal nephron hydrogen ion secretion. The blood PCO2 declined and stabilized rapidly when bicarbonate loaded rats were hyperventilated. In contrast, the urine PCO2 declined slowly, resulting in an early increase in the urine minus blood (U-B) PCO2 which could not be obliterated by carbonic anhydrase infusion. Within approximately 50 min, the U-B PCO2 in the hyperventilated and carbonic anhydrase infused rats approached zero. Consequently, equilibrium between collecting duct urine and arterial blood PCO2 was then presumed to exist. This provided the basis for the subsequent studies on a series of rats. The U-B PCO2 decreased from a control of 22+/-1 mm Hg (mean+/-SEM) to 11+/-2 mm Hg (mean+/-SEM) with hypocapnia, and rose again to its control value when the blood PCO2 returned to prehyperventilation values. This decline in U-B PCO2 with acute hyperventilation could not be attributed to changes in urine flow, phosphate, or bicarbonate excretion, suggesting, therefore, a decrease in distal nephron (probably collecting duct) hydrogen ion secretion with acute hyperventilation. Possible pitfalls in the interpretation of the UB PCO2 are illustrated.
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PMID:The effect of hyperventilation on distal nephron hydrogen ion secretion. 0 92

Sequential determinations of glucose outflow and inflow, and rates of gluconeogenesis from alanine, before, during and after insulin-induced hypoglycemia were obtained in relation to alterations in circulating epinephrine, norepinephrine, glucagon, cortisol, and growth hormone in six normal subjects. Insulin decreased the mean (+/-SEM) plasma glucose from 89+/-3 to 39+/-2 mg/dl 25 min after injection, but this decline ceased despite serum insulin levels of 153+/-22 mul/ml. Before insulin, glucose inflow and outflow were constant averaging 125.3+/-7.1 mg/kg per h. 15 min after insulin, mean glucose outflow increased threefold, but then decreased at 25 min, reaching a rate 15% less than the preinsulin rate. Glucose inflow decreased 80% 15 min after insulin, but increased at 25 min, reaching a maximum of twice the basal rate. Gluconeogenesis from alanine decreased 68% 15 min after insulin, but returned to preinsulin rates at 25 min, and remained constant for the next 25 min, after which it increased linearly. A fourfold increase in mean plasma epinephrine was found 20 min after insulin, with maximal levels 50 times basal. Plasma norepinephrine concentrations first increased significantly at 25 min after insulin, whereas significantly increased levels of cortisol and glucagon occurred at 30 min, and growth hormone at 40 min after insulin. Thus, insulin-induced hypoglycemia in man results from both a decrease in glucose production and an increase in glucose utilization. Accelerated glycogenolysis produced much of the initial, posthypoglycemic increment in glucose production. The contribution of glycogenolysis decreased with time, while that of gluconeogenesis from alanine increased. Of the hormones studied, only the increments in plasma catecholamines preceded or coincided with the measured increase in glucose production after hypoglycemia. It therefore seems probable that adrenergic mechanisms play a major role in the initiation of counter-regulatory responses to insulin-induced hypoglycemia in man.
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PMID:The role of adrenergic mechanisms in the substrate and hormonal response to insulin-induced hypoglycemia in man. 0 91

The effects of metoprolol, a selective beta adrenergic receptor antagonist, on blood pressure, beta receptor blockade (antagoinst of isoproterenol and exercise tachycardia), and plasma renin activity (PRA) have been compared with those of placebo in 16 patients with essential hypertension. The dose of metroprolol was 25 mg three times daily for 1 wk and thereafter 100 mg three times daily for 5 wk. The mean decrease in blood pressure during treatment with metoprolol was 24 +/- 3.8 (SEM)/10 +/- 2.1 mm Hg in the lying position and 23 +/- 4.4/9 +/- 3.1 mm Hg after 1 min in the standing position. At a dose of 2.9 to 5.4 mg/kg, steady-state plasma concentrations of metoprolol varied 17-fold (from 20 to 341 ng/ml) between patients and correlated with the interindividual variability in isoproterenol antagonism (r = 0.58, p less than 0.05) and decrease in exercise tachycardia (r = 0.65, p less than 0.01). By contrast, neither of these variables correlated with the dose of metoprolol in mg/kg. Metoprolol decreased PRA by 67 +/- 1.9 and 71 +/- 1.2% in the lying and standing positions, respectively. The decrease in the mean arterial blood pressure in the lying position was significantly correlated to the PRA during the placebo period (r = 0.61, p less than 0.05) but not to the plasma steady-state levels of metoprolol, the degree of beta receptor blockade, and the decrease in PRA.
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PMID:Plasma levels and effects of metoprolol on blood pressure, adrenergic beta receptor blockade, and plasma renin activity in essential hypertension. 0 73

The composition and structure were studied in the cast and in the solder of bridges which had failed clinically. Both materials were gold alloys but with different contents of Pt, Ag and Zn. The metallographic investigation revealed defects mostly in the solder, situated in the subsurface layer. SEM studied of the fracture surface revealed large porosites and a structure of dense parallel lines--striations--, indicating that the material had failed from fatigue. The materials in the fractured bridges were identified by micro-probe measurements. It was stated that cast material and solder material used together, were of different composition.
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PMID:Microstructure of the solder-casting zone in bridges of dental gold alloys. 1 May 39

The effects of uranyl ion (UO22+; at low concentrations binds specifically to phosphate groups) and the cationic dye methylene blue (MB+; binds strongly to carboxyl groups) on saxitoxin (STX) potency in crayfish axon has been studied by means of intracellular microelectrodes. At pH 6.00 +/- 0.05 and 13.5 mM Ca2+, addition of 10.0 muM UO22+ + 5.0 nM STX had only slightly, if any, less effect on the spike's maximum rate of rise [0.79 +/- 0.04 (viz., mean +/- SEM) of control value] than did addition of 5.0 nM STX alone (0.72 +/- 0.05). Under the same conditions of pH and Ca2+ concentration, 1.0 mM MB+ had approximately the same effect: 1.0 mM MB+ + 5.0 nM STX, 0.76 +/- 0.03; 5.0 nM STX alone, 0.70 +/- 0.04. However, at pH 7.00 +/- 0.05 and lower Ca2+ concentrations, 1.0 mM MB+ significantly reduced STX potency. Using 6.0 mM Ca2+: 1.0 mM MB+ + 5.0 nM STX, 0.92 +/- 0.01; 5.0 nM STX alone, 0.68 +/- 0.08. Using 3.0 mM Ca2+, the corresponding values were 0.94 +/- 0.03 and 0.67 +/- 0.04. It is concluded that: (1) In accord with previous suggestions, the ionized acidic group known to exist in the Na channel (and to which a guanidinium group of STX appears to bind) is very likely a carboxyl group and not a phosphate group. (2) The accessible part of the Na channel mouth serving as the saxitoxin receptor probably does not include phospholipid in its structure proper.
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PMID:Structural characteristics of the saxitoxin receptor on nerve. 1 48

Serum cholecystokinin (CCK) levels were measured in 10 patients with chronic duodenal ulcers, fasting and at intervals after two standard tests meals (300 ml of 40 mmol/1 phenylalanine solution), one given before and one during H2-receptor blockade with metiamide (200 mg four times a day). Fasting serum CCK levels were lower in all patients during treatment with metiamide (the mean level falling from 306-0 +/- 102-0 (SEM) to 82-1 +/- 23-6 pg/ml after treatment (p less than 0-01)). In contrast, peak serum CCK levels after the meal were not significantly different (7400 +/- 1141 pg/ml before treatment and 7569 +/- 1293 pg/ml on metiamide). We conclude that in duodenal ulcer patients CCK secretion under basal condtions may be in part dependent on stimulation of the small intestinal mucosa by gastric acid, but that, after an amino acid meal, gastric acid secretion is less important in determining the amount of CCK released.
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PMID:Effect of metiamide on basal and stimulated serum cholecystokinin levels in duodenal ulcer patients. 1 69

Carcass analysis data show that weanling rats fed high-fat (HF) and low-fat (LF) diets until the day of first estrus had similar body compositions at estrus, although the HF rats had estrus significantly earlier and at a lighter body weight (P less than 0.01) than the LF-diet rats. Total water as percent of wet weight, protein as percent of wet weight, and the water/protein ratios of the HF- and LF-diet rats did not differ significantly, whereas the absolute amounts of body water and protein of the two diet groups differed significantly (P less than 0.01), in accord with means (+/- SEM) of total body water as percent of wet weight were 66.2 +/- 0.3% for the HF rats and 66.4 +/- 0.3% for the LF-diet rats, whereas the mean absolute total body water for the two diet groups was 69.7 +/- 2.2 g and 81.1 +/- 2.4 g, respectively (P less than 0.01). Carcass fat of the HF rats, 15.6 +/- 1.0 g, was identical with that of the LF-diet rats, 15.6 +/- 0.9 g. The HF rats were therefore relatively fatter, 14.6 +/- 0.6 wet weight %, than the LF-diet rats, 12.6 +/- 0.4 wet weight % (0.05 greater than P greater than 0.01). The percentage of water in the fat-free wet weight of the HF rats, 77.5 +/- 0.3%, was significantly (P less than 0.01) greater than that of the LF-diet rats, 76.1 +/- 0.3%. These data and the high percentages of total water of body weight show that at first estrus the HF- and LF-diet rats had not as yet attained an adult body composition, similar to the human female at menarche. Within each diet group, the percentages of total water/body weight, protein/wet weight and fat/wet weight, or fat/dry weight, did not change significantly with increasing age of estrus, whereas each absolute carcass component--body water, protein, and fat--increased significantly with increasing age of estrus. The carcass data support G.C. Kennedy's hypothesis that a metabolic signal, related to fat stores, is a signal for puberty in the rat and are in accord with the hypothesis that a critical body composition of fatness is necessary for estrus in the rat, as in the human female. The greater relative fatness of the HF-diet rats may be associated with higher levels of estrogen in the HF rats than in the LF-diet rats.
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PMID:Carcass components at first estrus of rats on high-fat and low-fat diets: body water, protein, and fat. 1 68


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