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)

Although numerous studies have provided indirect evidence for enhanced platelet activity in sickle cell anaemia, little attention has been directed to examination of platelet alpha and dense granule release in the sickling disorders. We simultaneously measured by radioimmunoassay plasma levels of the alpha granule constituents beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) in 43 children with sickle cell anaemia in steady state and 24 patients during severe vaso-occlusive crisis. beta-TG levels during steady state (50 +/- 3.6 ng/ml, mean +/- SEM) were greater (P less than 0.001) than in normal controls (36 +/- 1.6), but there was no additional significant rise during crisis (55 +/- 5.9). PF4 levels were similar (P = 0.12) in both steady state (10 +/- 1.2 ng/ml) and crisis (9.3 +/- 2.3) to those of normal controls (6.0 +/- 0.8). The similarity of beta-TG/PF4 ratios in normal and sickle cell anaemia patients as well as the positive correlation (P less than 0.05) between platelet count and beta-TG and PF4 suggested that an artefactual in vitro platelet activation was responsible for some of the observed increased beta-TG and PF4 levels. Further evidence against enhanced platelet activity in these sickle cell patients included normal intraplatelet content of the dense granule constituent 5-HT and a normal ATP/ADP ratio. From this data we conclude that platelet activation in children with sickle cell anaemia appears minimal.
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PMID:Evidence against enhanced platelet activity in sickle cell anaemia. 622 55

This study examined the effect of an aldose reductase inhibitor (Sorbinil, CP 45634, Pfizer, Sandwich, Kent, United Kingdom) on the metabolite profile of the lens during the first week after induction of diabetes with alloxan. The lens content of sorbitol, fructose, glycerol 3-phosphate, and glucose 6-phosphate was, respectively, 0.33 +/- 0.03, 0.55 +/- 0.05, 0.10 +/- 0.01, and 0.074 +/- 0.006 mumol/g (means +/- SEM) in the control group rising to 12.2 +/- 0.52, 3.20 +/- 0.10, 0.76 +/- 0.10, and 0.200 +/- 0.009 in lenses from alloxan-diabetic rats. Sorbinil treatment (40 mg/kg) decreased the lens content of sorbitol to 0.60 +/- 0.06, fructose to 0.85 +/- 0.08, and glycerol 3-phosphate to 0.36 +/- 0.03 mumol/g; glucose 6-phosphate remained unchanged. Significantly, the lens content of glutathione was decreased to 60% of the normal value in the diabetic group, but was sustained at normal levels with Sorbinil treatment. The ATP content of the lens was not altered by diabetes or Sorbinil treatment at this time interval. Sorbinil has no significant effect on the above metabolites in the normal rat lens. The effect of Sorbinil in restoring normal levels of glutathione and glycerol 3-phosphate may be a potentially important facet of the action of this drug. The interlocking of metabolic pathways by the redox state of NAD+/NADH and NADP+/NADPH, their derangement in diabetes, and the wider effects of Sorbinil on the network of reactions in the lens are discussed.
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PMID:The effect of an aldose reductase inhibitor (Sorbinil) on the level of metabolites in lenses of diabetic rats. 640 81

The lack of mucociliary transport causes chronic inflammations in the upper and lower respiratory tract and in the middle ear mucosa. The mucosa of 4 female patients with Kartagener's syndrome was studied by means of TEM (transmission electron microscopy) and SEM (scanning electron microscopy) and compared with the fine structure of normal cilia which were also found in these areas. All specimens studied showed, to a different extent, alterations in the fine structure of the axonemata, especially the absence or malformed ATP-ase dynein arms, the lack of spokes and/or the misarrangement of microtubuli within the cilia. The importance of this congenital anomaly - "immotile cilia" - is discussed with the trias of Kartagener's syndrome.
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PMID:[Ultrastructure of cilia in Kartagener syndrome]. 660 38

Intracranial pressure (ICP) was measured during induced hypotension with increasing doses of adenosine triphosphate (1-5 mg X kg-1 X min-1 ATP) in dogs without (group I) and with (group II) intracranial hypertension. After administration of 1 mg X kg-1 X min-1 ATP, ICP increased significantly from 11 +/- 4 mm Hg to 14 +/- 5 mm Hg (mean +/- SEM) (P less than 0.05; group I) and from 27 +/- 2 mm Hg to 38 +/- 6 mm Hg (P less than 0.05; group II), while mean arterial pressure (MAP) decreased from 103 +/- 10 mm Hg to 86 +/- 6 mm Hg (P less than 0.05; group I) and from 110 +/- 11 mm Hg to 90 +/- 11 mm Hg (P less than 0.05; group II). In both groups a slow decrease of ICP after the initial increase occurred with further lowering of MAP, but ICP remained significantly above control values even with a dose of 5 mg X kg-1 X min-1 ATP (P less than 0.05). Ventricular volume-pressure response curves (VPR) before and during intravenous infusion of 3 mg X kg-1 X min-1 ATP were constructed to determine changes in intracranial compliance (ICC). In both groups I and II ATP decreased ICC. On the basis of these results it is recommended that in the presence of intracranial mass lesions ATP should not be given to induce arterial hypotension before the dura is opened.
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PMID:Changes in intracranial pressure and compliance during adenosine triphosphate-induced hypotension in dogs. 670 64

Acclimated normal rainbow trout were exposed to 130 ppb hexachlorocyclopentadiene (HEX) in a flow-through well water circuit which was designed to permit measurements of oxygen consumption by the fish. Compared to preHEX values, HEX increased oxygen consumption rates by 186 +/- 24% (means +/- SEM), with maximum oxygen consumption rates being reached in approximately 84 min after HEX exposure. Oxygen consumption subsequently decreased, and all HEX-exposed fish died within 6.5 hr of exposure. Fish exposed to HEX-free vehicle (acetone) showed no changes of oxygen consumption. When added to normal isolated trout heart mitochondria, HEX appeared to uncouple oxidative phosphorylation, with calculated respiratory control ratios being decreased 50% from control values at a HEX concentration of 0.41 microM. We postulate that one important mechanism of HEX intoxication in the intact animal may be due to increased oxygen consumption and impaired oxidative ATP synthesis due to the mitochondrial uncoupling action of the toxicant.
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PMID:Respiratory effects of hexachlorocyclopentadiene on intact rainbow trout (Salmo gairdneri) and on oxidative phosphorylation of isolated trout heart mitochondria. 683 75

Changes in myocardial purine metabolism were studied after temporary coronary artery occlusion and subsequent reperfusion in the dog. Sequential myocardial biopsies were performed to allow for measurements of ATP, adenine nucleotide, nucleoside, and base concentrations after 15 min of ischemia, and after 90 min and 72 hr of reperfusion following this period of ischemia. Control, nonischemic sites were also sampled. After 15 min of coronary occlusion, subendocardial ATP concentrations (reported in nmol/mg of protein; mean +/- SEM) were depressed in the ischemic zone at 19.9 +/- 3.5 compared to 38.1 +/- 2.8 in the nonischemic zone (P < 0.001). Subepicardial ATP concentrations also were depressed at 27.0 +/- 2.2 in ischemic sites compared to subepicardial nonischemic sites (40.0 +/- 4.0, P < 0.005). After 90 min of reperfusion ATP concentrations remained depressed in the previously ischemic subendocardium 26.8 +/- 4.2 (P < 0.025 vs. nonischemic sites). After 72 hr of reperfusion, ATP was still depressed in the previously ischemic subendocardium at 29.2 +/- 2.5 (P < 0.025 vs. nonischemic) and subepicardium (27.9 +/- 3.3, P < 0.05 vs. nonischemic). Total purines were determined as the sum of ATP, ADP, AMP, adenosine, inosine, and hypoxanthine. After 15 min of occlusion, the total purine pool in the ischemic subendocardium tended towards being lower than in the nonischemic zone (42.0 +/- 5.9 vs. 53.8 +/- 5.2, not significant) but in the ischemic subepicardium the total purine pool was similar to that in the nonischemic zone. After 90 min of reperfusion the previously ischemic subendocardial purine pool was reduced compared to the nonischemic zone (39.0 +/- 4.8, P < 0.025). Total purines were also depleted in both the subendocardium and subepicardium of previously ischemic zones after 72 hr of reperfusion (44.5 +/- 2.9 and 40.0 +/- 4.4, respectively, P < 0.05). Histologic analysis of the previously ischemic tissue revealed no evidence of necrosis. Therefore, brief temporary coronary artery occlusions not associated with anatomic evidence of necrosis may result in prolonged abnormalities of ATP concentration and significant depletion of the total purine pool.
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PMID:Prolonged derangements of canine myocardial purine metabolism after a brief coronary artery occlusion not associated with anatomic evidence of necrosis. 693 66

The purpose of this study was to determine whether or not the biochemical, functional, and ultrastructural abnormalities produced by brief temporary coronary occlusions (unassociated with necrosis) ever resolve and, if so, when they do. Anesthetized open-chest dogs were subjected to 15 min of coronary artery occlusion followed by 72 hr, 7 days, or 14 days of reperfusion. Serial in vivo myocardial biopsies were performed for measurement of ATP and for ultrastructural analysis. Regional function was evaluated by sonomicrometry. Mean (+/- SEM) myocardial ATP concentration was 36.6 +/- 1.2 nmol/mg of cardiac protein in nonischemic subendocardium and 18.9 +/- 1.5 in ischemic subendocardium after 15 min of ischemia. ATP remainede performed for measurement of ATP and for ultrastructural analysis. Regional function was evaluated by sonomicrometry. Mean (+/- SEM) myocardial ATP concentration was 36.6 +/- 1.2 nmol/mg of cardiac protein in nonischemic subendocardium and 18.9 +/- 1.5 in ischemic subendocardium after 15 min of ischemia. ATP remainede performed for measurement of ATP and for ultrastructural analysis. Regional function was evaluated by sonomicrometry. Mean (+/- SEM) myocardial ATP concentration was 36.6 +/- 1.2 nmol/mg of cardiac protein in nonischemic subendocardium and 18.9 +/- 1.5 in ischemic subendocardium after 15 min of ischemia. ATP remained depressed in the reperfused previously ischemic subendocardium at both 90 min (68% of nonischemic value) and 72 hr (78% of nonischemic value) but returned to normal at 7 days. Regional systolic function and cardiac ultrastructural abnormalities required 7 days for full recovery. Histologic and histochemical analysis did not reveal necrosis at any time. Therefore, biochemical, functional, and ultrastructural abnormalities induced by brief periods of transient coronary occlusion not associated with necrosis do resolve completely but the recovery period is prolonged.
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PMID:Recovery from prolonged abnormalities of canine myocardium salvaged from ischemic necrosis by coronary reperfusion. 676 71

A cell-free system prepared from rat liver containing cytosol and mitochondria as well as a number of cofactors at near physiological concentrations was shown to form glucose 6-phosphate from malate + 3-phosphoglycerate at a rate of 1.11 +/- 0.09 mumol . min-1 . g liver-1 (mean +/- SEM, n = 9, 30 degrees C). At least 70% of glucose 6-phosphate formed was derived from malate as calculated from experiments with [U-14C]malate. The indicated rates were measured between 10 min and 30 min incubation time when the system was near steady state with respect to the lactate/pyruvate ratio and to most of the gluconeogenic intermediates. In the absence of mitochondria, the rate of formation of glucose 6-phosphate from malate was about seven times lower than in their presence. A comparison between incubations carried out in presence or absence of mitochondria revealed that mitochondria decreased the lactate/pyruvate ratio and increased the ratio of (ATP + ITP)/(ADP + IDP). It could be shown that under the present incubation conditions, formation of glucose 6-phosphate was closely linked to the ratio of (ATP + ITP)/(ADP + IDP) whereas changing redox ratios had little influence on the gluconeogenic rate.
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PMID:Gluconeogenesis in vitro. Formation of glucose 6-phosphate from malate by a cell-free rat-liver system consisting of cytosol and mitochondria. 710 24

The protective effect of vinpocetine on experimental brain ischemia was studied in stroke-prone spontaneously hypertensive rats (SHRSP) with bilateral carotid artery occlusion (BCAO) and in Wistar-Kyoto rats (WKY) subjected to BCAO and hemorrhage (1% of body weight). In SHRSP with BCAO, intraperitoneal (i.p.) injection of vinpocetine (1 mg/kg) 10 min before BCAO significantly prolonged the time required for the onset of ischemic seizure from 65 +/- 13 min (mean +/- SEM) to 117 +/- 19 min. In WKY with BCAO and hemorrhage, vinpocetine (5 mg/kg, i.p.) reduced the lactate level in the cerebral cortex from 11.6 +/- 2.7 mmol/g to 5.9 +/- 1.2 mmol/g and elevated the concentration of ATP from 2.05 +/- 0.09 mmol/g to 2.25 +/- 0.03 mmol/g. These results suggest a protective effect of vinpocetine against brain ischemia.
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PMID:[Protective effect of vinpocetine on experimental brain ischemia]. 715 92

Rabbit anti-human platelet antiserum (RPA) has been shown to mediate human platelet aggregation and 14C-serotonin release. This effect is not inhibited by aspirin. However, it is not known whether antibody induces platelet prostaglandin synthesis. We, therefore, investigated the effect of RPA on human platelets by measuring malondialdehyde (MDA) production as a reflection of prostaglandin synthesis and comparing it with 14C-serotonin release. Independently, ATP release was also measured as a further measure of platelet secretion. Normal rabbit serum did produce a small amount of MDA (0.54 +/- 0.09 SEM nmole/10(9) platelets). However, RPA produced a much larger amount of MDA (1.43 +/- 0.18 nmole/10(9) platelets) and pre-incubation with aspirin significantly decreased MDA production (0.16 +/- 0.07 nmole/10(9) platelets) (p less than .001). Aspirin did not significantly impair the capacity of RPA to release 14C-serotonin or ATP. These results demonstrate that prostaglandin synthesis occurs when heterologous antibody is added to human platelets. However, prostaglandin formation must be a secondary event in this process since the inhibition of prostaglandin synthesis by aspirin had little effect on the ability of RPA to induce 14C-serotonin release or ATP release.
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PMID:Effect of heterologous antibody on human platelet prostaglandin synthesis. 736 55


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