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

---

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.
...
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.
...
PMID:Determination of total insulin (TIRI) in plasma of insulin-treated diabetics and newborn infants of insulin-treated diabetic mothers. 0 60

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.
...
PMID:The role of adrenergic mechanisms in the substrate and hormonal response to insulin-induced hypoglycemia in man. 0 91

Both a low pleural fluid glucose concentration and pleural fluid acidosis are markers of severe pleural inflammation, but the relationship between these phenomena has not been defined clearly. Therefore, we measured simultaneous pleural fluid glucose concentrations and pH in 25 consecutive parapneumonic pleural fluids. Seventeen effusions had a glucose concentration greater than 60 mg/dl (group 1, 126 +/- 7 mg/dl, mean +/- SEM), while eight had a pleural fluid glucose less than 60 mg/dl (group 2, 15 +/- 3 mg/dl, P less than .01). Pleural fluid pH was 7.35 +/- 0.03 in group 1 compared with 6.83 +/- 0.09 in group 2 (P less than .01). A significant correlation between pleural fluid glucose and pH was found (r = .81, P less than .01). Low-glucose, low-pH effusions were complicated (either loculated or empyemas). Uncomplicated effusions had glucose concentrations greater than 60 mg/dl and a pleural fluid pH greater than 7.30. The concomitant occurrence of low pleural fluid glucose and pH suggests that the mechanisms leading to these phenomena are interrelated.
...
PMID:The glucose-pH relationship in parapneumonic effusions. 2 7

A single oral dose of 0.15 mg/m2 of clonidine was given to eighteen healthy children and adolescents and to seven patients with hypopituitarism. In healthy subjects there was a pronounced increase in plasma growth hormone from 4.9 +/- 1.3 ng/ml (+/- SEM) to 34.4 +/- 4.5 ng/ml. In the patients with hypopituitarism there was no change in growth-hormone concentrations. Clonidine induced a slight increase in blood glucose in healthy subjects and a slight decrease in patients with hypopituitarism. During the test systolic blood-pressure decreased by a mean of 20 mm Hg in the healthy subjects and by 25 mm Hg in the patients with hypopituitarism. The only side-effect observed was drowsiness. Oral administration of clonidine, a well-tolerated drug, seems to be a simple test for of GH reserves in children and adolescents.
...
PMID:Oral clonidine as a growth hormone stimulation test. 8 10

Thirty-two episodes of diabetic ketoacidosis in 30 children treated with conventional repeated s.c. injections of insulin every 4 h are compared with 18 episodes in 14 children treated with continuous i.v. insulin infusion. Fluid therapy, bicarbonate and potassium supplementation were essentially the same for both groups. Recovery as reflected in serum glucose, bicarbonate and the rate of rehydration, was smoother and more rapid in the children receiving continuous i.v. insulin, though the difference just failed to attain statistical significance in this small series of cases. There was, however, a marked difference in insulin administered (0.58 U/kg +/- 0.05 SEM in the children treated with continuous i.v. insulin infusion vs 2.54 +/- 0.27 SEM in the children treated with repeated s.c. injections). Hypoglycemia was noted in 11 and hypokalemia in 10 children on conventional insulin therapy given every 4 h s.c. In contrast, there was no hypoglycemia and only one case of hypokalemia with the i.v. insulin infusion.
...
PMID:Continuous infusion of insulin vs repeated S.C. injections in the treatment of diabetic ketoacidosis in children. 10 98

The [14C]deoxyglucose method for quantitative determination of local cerebral glucose utilization was extended to the macaque monkey. The necessary constants required by its operational equation were evaluated. The lumped constant, measured in 7 normal conscious monkeys, was found to equal 0.344 (SEM, +/- 0.036). The rate constants were also estimated and found to be very similar to those obtained previously in the rat. With these essential constants evaluated, the method was applied to normal conscious monkeys. Local cerebral glucose utilization was found to vary marked throughout the brain but to fall within two distributions, a higher one in gray matter and lower one in white matter. In general, the values fell in a range to be expected from previous measurements of average energy metabolism in the brain as a whole. The values were considerably lower than those observed previously in the conscious rat. Marked heterogeneity of rates of glucose utilization were observed in a number of anatomical structures. In some cases the patterns of heterogeneity were consistent with known histological cytoarchitecture; in others the heterogeneity did not conform with known cytoarchitectural features but corresponded to patterns previously demonstrated by electrophysiological techniques. Many of the regions of the cerebral cortex showed columnar patterns of distribution of higher and lower rates of glucose utilization. These may be a metabolic reflection of the columnar organization of function within the cerebral cortex.
...
PMID:Local cerebral glucose utilization in the normal conscious macaque monkey. 10 88

The factors influencing the development of impaired sciatic motor nerve conduction velocity (MNCV) in acute experimental diabetes were examined. Decreased MNCV developed by the 14th day after streptozotocin administration but only in rats which became hyperglycemic. Insulin treatment, begun on day 3, failed to prevent imparied MNCV in diabetic rats in which improved or normal weight gain and a decreased degree of hyperglycemia was induced. However, insulin treatment prevented the development of impaired MNCV in a group of diabetic rats in which the tail vein plasma glucose concentration was never found to exceed 160 mg/dl during days 6 through 14, andin which the mean plus or minus SEM of the average plasma glucose concentration for each animal during the same period was 75 plus or minus 18 mg/dl. In normal rats fed diets containing 0.011% or 0.069% free myoinositol (a presumably normal range), sciatic nerve free myoinositol concentrations were 90- and 60-fold higher than those in plasma. On these diets the development of impaired MNCV in the diabetics was associated with a decrease in nerve free myoinositol as compared with nerves from normals fed the same diet, despite similar plasma levels in the normals and diabetics. Plasma and nerve free myoinositol increased with increasing dietary myoinositol content in both normals and diabetics, and nerve myoinositol content could be acutely increased by an i.p. myoinositol load. By supplementing the diets with 1.0% myoinositol, the difference in nerve myoinositol in normal and diabetic rats on day 14 was abolished; on this diet the development of impaired MNCV in the diabetics was moderated or totally prevented, despite persistent hyperglycemia and elevated nerve sorbitol and fructose concentrations. Insulin treatment that prevented impaired MNCV prevented a decrease in nerve myoinositol in diabetics. These studies suggest that insulin deficiency, and possibly hyperglycemia, are primary factors in the development of imparied MNCV in acute experimental diabetes. However, the development of impaired MNCV appears to be related in some manner to a derangement in the regulation of nerve free myoinositol content, which appears to be subject to modification by increases in plasma myoinositol concentration over a critical range.
...
PMID:Effects of insulin and dietary myoinositol on impaired peripheral motor nerve conduction velocity in acute streptozotocin diabetes. 12 20

Juvenile rats fed a diet containing 1% lead acetate for 7 weeks, in addition to an impaired growth rate and renal function derangements, suffered malabsorption of glucose and certain amino acids, as assessed by an in vivo perfusion technique. The reduction in glucose absorption ranged between 10% and 31% when the carbohydrate was pumped in concentrations of 2-80 mM. This alteration was compatible with a noncompetitive type of transport inhibition. The intestinal absorption of glycine, lysine, and phenylalanine were, respectively, decreased 22, 18, and 15% when these amino acids were present at 1 mM levels. Sodium transport was severely reduced (57.6 +/- 17.9 (SEM) vs. 124.2 +/- 17.4 muEq/min-cm) and intestinal mucosa (Na+-K+)-ATPase was concomitantly lower in the lead-intoxicated rats (186.4 +/- 19.0 vs 268.4 +/- 29.8 nmol P/min-mg protein). However, this enzyme was not altered in liver and kidney. Furthermore, intestinal mucosa fructose-1,6-diphosphatase, succinic dehydrogenase, pyruvate kinase, and tryptophan hydroxylase were not different in experimental and control animals. These studies substantiate the presence of functional and biochemical abnormalities in the intestinal mucosa of young rats when fed substantial amounts of a soluble lead salt. It is, therefore, reasonable to accept the possibility that physiologic damage occurs in tissues directly subjected to high and persistent levels of a toxic agents, as it occurs in other organs, underscoring the parallelism between transport mechanisms at the renal and intestinal levels.
...
PMID:Experimental lead poisoning and intestinal transport of glucose, amino acids, and sodium. 13 38

The importance of the hepatic portal circulation in the response to insulin was assessed in streptozotocin-diabetic rats transplanted with syngeneic fetal pancreases. Partial reversal of diabetes was accomplished by transplantation of two or three fetal pancreases beneath the capsule of the kidney; complete reversal followed shunting of the venous drainage from the transplants to the liver. Plasma glucose after streptozotocin of 509+/-31 mg/dl (mean+/-SEM) fell after transplantation to 395+/-23 and after the shunt to 143+/-5 mg/dl. Urine volume fell from 84+/-4 to 50+/-5 ml/d and then to normal (17+/-1 ml/d) after the shunt. Glucose excretion which was 8.1+/-0.3 g/d after streptozotocin fell after transplantation to 4.8+/-0.3 g/d and after the shunt completely disappeared from the urine. The disappearance rate of glucose injected into the circulation, which was 0.50+/-0.07%/min in untreated diabetes, increased to 1.39+/-0.38%/min after transplantation and to 2.52+/-0.31%/min after the shunt, not different from normal controls (2.79+/-0.25). Plasma immunoreactive insulin (IRI) was below normal (25-35 muU/ml) and unresponsive to glucose in untreated diabetic rats. After transplantation IRI levels ranged from 73-223 muU/ml and there was no rise after glucose injection. After the shunt both the basal IRI (36+/-5 muU/ml) and the peak response to glucose at 10 min (58+/-7 muU/ml) were the same as in normal controls (42+/-4 and 62+/-7 muU/ml, respectively). The fall in IRI after the shunt is explained by increased extraction of insulin passing into the liver and also diminished secretion. After removal of the transplants plasma glucose and urine values returned almost to pretransplant levels. Secretion of insulin by transplanted pancreases into the liver enhances the effectiveness probably by increased extraction and action and reveals the importance of the normal route for insulin delivery.
...
PMID:Importance of hepatic portal circulation for insulin action in streptozotocin-diabetic rats transplanted with fetal pancreases. 15 16


1 2 3 4 5 6 7 8 9 10 Next >>

---