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)

Platelets eluted from nylon fiber filters after filtration leukapheresis have been studied. The platelet yield from 61 routine donations was 1.25 +/- 0.18 x 10(11), (mean +/- SEM) corresponding to 1.78 x 10(10) per 500 ml blood processed. Filtered platelets labeled with radiochromate demonstrated reduced recovery in vivo 15 minutes after infusion (38.5 +/- 1.7%) when compared to the control value (68.5 +/- 6.8, p less than 0.001). The survival of those platelets remaining in the circulation after 15 minutes did not however differ from the control value. ADP (10 micrometer, 1 mM), adrenaline (100 micrometer) and collagen (7.25 mg/ml) added in vitro induced less aggregation of filtered platelets than normal control platelets and electron microscopy revealed structural abnormalities. It is concluded that recipients of granulocyte transfusions obtained by filtration leukapheresis are unlikely to be benefited by the platelets contained in these transfusions.
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PMID:Studies on platelets contained in eluates following filtration leukapheresis. 43 22

The authors had previously found an inverse correlation between per sperm creatine phosphokinase activity and sperm concentrations in men. Because creatine phosphokinase is a key enzyme in sperm energy transport, the possible relationship of sperm creatine phosphokinase activity, sperm adenosine triphosphate (ATP) concentrations, sperm ATP/ADP (adenosine diphosphate) ratios, and computer-aided semen analysis sperm motility parameters were then studied. The ATP concentrations and ATP/ADP ratios, measured by high-pressure liquid chromatography in washed sperm, were similar in normospermic and oligospermic specimens (ATP: 123.1 +/- 21.6 vs. 90.0 +/- 24.5 pmol/10(6) sperm; ATP/ADP: 2.8 +/- 0.4 vs. 2.1 +/- 0.4, N = 32 and 17, mean +/- SEM), and in samples with normal and less than 40% sperm motility (ATP: 96.8 +/- 27.2 vs. 122.2 +/- 19.6 pmol/10(6) sperm; ATP/ADP: 2.4 +/- 0.5 vs. 2.8 +/- 0.4, n = 26 and 23). In the swim-up sperm fractions, which showed improved motility, the ATP concentrations, but not the ATP/ADP ratios, were lower than in the initial semen samples (ATP: 152.9 +/- 28.4 vs. 90.3 +/- 10.6 pmol/10(6) sperm, P less than 0.05; ATP/ADP: 3.3 +/- 0.5 vs. 3.9 +/- 0.7, N = 18 pairs of samples). This is consistent with our previous finding of a lower cytoplasmic content in sperm in swim-up fractions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adenosine triphosphate (ATP) concentrations and ATP/adenosine diphosphate ratios in human sperm of normospermic, oligospermic, and asthenospermic specimens and in their swim-up fractions: lack of correlation between ATP parameters and sperm creatine kinase concentrations. 139 31

Changes in energy metabolism after 70% partial hepatectomy were investigated in normal and carbon-tetrachloride-(CCl4)-induced-cirrhotic rats by evaluating hepatic mitochondrial ATP synthesizing activity as well as liver tissue levels of adenine nucleotides and lipid peroxide. Preoperative concentrations of ATP and total adenine nucleotides (TAN: ATP + ADP + AMP) in mumol/g dry weight (dw) and the energy charge potential (ECP) in the cirrhotic livers were 8.53 SEM 0.25, 14.73 SEM 0.54, and 0.74 SEM 0.01, respectively, and were significantly lower than those of normal livers (12.04 SEM 0.34, 15.75 SEM 0.12, and 0.86 SEM 0.01, P less than 0.01 in TAN). There was no difference in the preoperative mitochondrial phosphorylation rate (PR = x 10(-10) mol ATP/sec per mg mitochondrial protein) between normal and cirrhotic livers (21.01 SEM 0.95 and 21.55 SEM 1.03, respectively). After hepatectomy, in the normal livers these values decreased slightly after 12 h, remained low until 48 h, and returned to the preoperative value at 72 h. PR was remarkably enhanced and reached the maximum level of 32.54 SEM 2.07 at 24 h (P less than 0.001, compared to the sham-operated rats) and gradually returned to the preoperative value at 72 h. In the cirrhotic livers, ATP and ECP levels were drastically decreased at 12 h and recovered to the preoperative levels within 24 h, while TAN level remained unchanged. Enhancement of PR was not observed in any of the cirrhotic livers during the experiment. Lipid peroxidation was transiently increased postoperatively with no difference between normal and cirrhotic livers both in the sham-operated and the hepatectomized rats. These findings suggest that the energy status was more depressed in the cirrhotic livers than in normal livers both before and after hepatectomy. This depressed energy status might be attributed to the low preoperative tissue levels of adenine nucleotides and ECP level in the cirrhotic livers as well as to the absence of the enhancement of PR in the remnant livers.
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PMID:Absence of mitochondrial enhancement in the remnant liver after partial hepatectomy in cirrhotic rats. 152 68

Thirteen patients suffering from acute malaria attack and thirteen apparently healthy human volunteers (control) were used for the study. Platelet aggregation was determined by platelet count ratio technique in which a reduction in platelet count ratio signified an increase in platelet aggregation. Platelet count ratio in acute malaria patients was 0.75 +/- 0.03 (SEM). Platelet count ratio in subjects used as control was 0.88 +/- 0.02. This value was significantly higher than the former (P less than 0.001). Platelet count ratio correlated negatively with the degree of parasitaemia (r = -0.71; P less than 0.01). ADP, a platelet aggregating drug, also reduced platelet count ratio in rats significantly. Acute malaria attack therefore enhances platelet aggregation in vivo.
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PMID:In vivo platelet aggregation in acute malaria. 168 3

This study compared new and traditional measures of platelet function in 16 patients with severe peripheral arterial occlusive disease and 15 age-matched controls. Circulating platelets were characterized by the use of fluorescence flow cytometry to assess platelet aggregate formation and expression of the secretion-dependent alpha granule membrane protein GMP-140, by measurement of plasma beta-thromboglobulin (beta-TG), and by performance of platelet-rich plasma aggregation studies. In addition, blood samples were treated with graded concentrations of adenosine diphosphate (ADP; 0 to 10 mumols/L) to characterize by fluorescence flow cytometry the secretory and aggregatory responses to mild stimulation. No differences were detected between the two groups with regard to platelet function in unstimulated circulating blood by use of these techniques. Values (mean +/- SEM) observed were: GMP-140-positive platelets, 11% +/- 3% versus 13% +/- 2%; platelet aggregates in circulating whole blood, 4% +/- 1% versus 9% +/- 3%; plasma beta-TG, 92 +/- 12 versus 94 +/- 22 ng/ml; and ED50 (concentration of ADP required to produce half maximal aggregation), 3.8 +/- 1.1 versus 3.1 +/- 0.5 mumol/L in the patients with peripheral arterial occlusive disease and controls, respectively. Treatment with ADP caused a dose-related increase in GMP-140 expression in both groups, without significant differences in this parameter between the groups at any given concentration. However, stimulation with ADP concentrations greater than 1 mumol/L resulted in more frequent aggregate formation in the control than in the peripheral arterial occlusive disease group (25% +/- 4% versus 11% +/- 2%, respectively at 5.0 mumols/L, p = 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Flow cytometric assessment of platelet function in patients with peripheral arterial occlusive disease. 172 Apr 68

The quantification of adenine nucleotides released from the heart is hampered by their rapid dephosphorylation to adenosine in the extracellular space catalyzed by highly active ectonucleotidases. To determine the total release of adenine nucleotides from isolated Langendorff-perfused guinea pig hearts, ecto 5'-nucleotidase was effectively blocked by infusion of alpha, beta-methylene-ADP (AOPCP, 50 microM). Adenine nucleotides were measured in the coronary venous effluent by the luciferin-luciferase method after enzymatic rephosphorylation to ATP. In hearts perfused at a constant flow rate (10 ml/min) with normoxic buffer (95% O2, 5% CO2) the release +/- SEM of adenine nucleotides and adenosine was 0.06 +/- 0.01 (n = 11) and 0.04 +/- 0.01 (n = 13) nmol/min. In the presence of AOPCP, the release of adenine nucleotides increased to 0.43 +/- 0.04 nmol/min (n = 9; p less than 0.05), whereas adenosine remained unchanged. Hypoxic perfusion (10% O2, 85% N2, 5% CO2) caused a threefold increase in adenine nucleotide release but a 40-fold increase in adenosine. In contrast, global ischemia (30 seconds) caused adenine nucleotide and adenosine release to rise to similar values of 1.06 +/- 0.10 and 0.80 +/- 0.14 nmol/min (n = 9). Stimulation of hearts with isoproterenol (4 nM) likewise increased the release of adenine nucleotides (0.50 +/- 0.04 nmol/min) and adenosine (0.87 +/- 0.21 nmol/min) (n = 6). To determine the cellular source of adenine nucleotides released from the heart, the coronary endothelial adenine nucleotide pool was selectively prelabeled by [3H]adenosine. Global ischemia increased the specific radioactivity of released adenine nucleotides by 57%. The findings indicate that 1) adenine nucleotides and adenosine are released at the same order of magnitude from the well-oxygenated heart; 2) beta-adrenergic stimulation and ischemia stimulate the release of adenine nucleotides and adenosine, both purines reaching vasoactive concentrations in the effluent perfusate; 3) during hypoxic perfusion only the release of adenosine is greatly enhanced; and 4) the coronary endothelium preferentially contributes to the ischemia-induced adenine nucleotide release.
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PMID:Adenine nucleotide release from isolated perfused guinea pig hearts and extracellular formation of adenosine. 174 67

Ticlopidine (T) and aspirin (ASA) are two antiplatelet drugs both capable of prolonging bleeding time (BT), with a different mechanism of action. A synergism in BT prolongation has been reported and is currently considered an argument for not recommending their combination. However, a profound suppression of platelet function might be a desirable counterpart of a marked prolongation of BT, with a possible use in selected clinical situations. We therefore studied ex vivo platelet function (aggregation by ADP 0.5-1-2.5 microM; adrenaline 0.75-2.5 microM; collagen 1.5-150 micrograms/ml; arachidonic acid 1 mM; PAF 1 microM; adrenaline 0.17 microM + ADP 0.62 microM; serum thromboxane [( TX]B2 generation) and BT (Mielke) in 6 patients with stable coronary artery disease receiving such combination. Patients underwent sequential laboratory evaluations at baseline, after 7 days of T 250 mg b.i.d., before and after the intravenous administration of ASA 500 mg, respectively, and, finally, after a minimum of 7 days of sole ASA oral administration (50 mg/day). The experimental design, therefore, allowed a comparison of T and ASA effects (2nd and 4th evaluation), and an assessment of the combination effect (3rd evaluation). Platelet aggregation in response to all doses of ADP was depressed more by T than by ASA. Conversely, responses to adrenaline, and arachidonate were affected more by ASA than by T. For all other agents, differences were not significant. T + ASA combination was more effective (p less than 0.05) than either treatment alone in depressing responses to high-dose collagen (% over control, mean +/- SEM: T: 95 +/- 3; ASA: 96 +/- 5; T + ASA: 89 +/- 4).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Benefit/risk profile of combined antiplatelet therapy with ticlopidine and aspirin. 187 11

The exchange of intramitochondrial ATP (ATP(in)) for extramitochondrial ATP (ATP(out)) was measured by using 31P NMR spectroscopy over a range of temperatures in isolated rat liver mitochondria oxidizing glutamate and succinate in the presence of external ATP but no added ADP (state 4). The rate of this exchange is more than an order of magnitude faster than rates reported previously that were determined by using isotopic techniques in the presence of oligomycin, the potent ATPase inhibitor. Differences are ascribed in part to the low levels of matrix ATP present in oligomycin-treated mitochondria. The addition of oligomycin to mitochondrial suspensions decreases intramitochondrial ATP levels from 17 +/- 3 (SEM) nmol/mg of protein in state 4 to 1.51 +/- 0.1 nmol/mg of protein in the presence of inhibitor at 8 degrees C. Simultaneously, transporter flux falls from 960 +/- 55 nmol/min.mg to undetectable levels (less than 300 nmol/min.mg). Although transport rates are much faster when measured by saturation-transfer than by conventional isotopic methods, the enthalpy values obtained by determining the effect of temperature on flux are very similar to those reported in the past that were determined by using isotopic techniques. Intramitochondrial ATP content regulates the rate of the ATP(in)/ATP(out) exchange. At 18 degrees C, the concentration of internal ATP that produces half-maximal transport rate is 6.6 +/- 0.12 nmol/mg of mitochondrial protein. The relationship between substrate concentration and flux is sigmoidal and is 90% saturated at 11.3 +/- 0.18 nmol/mg of mitochondrial protein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:31P NMR saturation-transfer study of the in situ kinetics of the mitochondrial adenine nucleotide translocase. 188 22

Four hours of complete normothermic ischemia in the rat hindlimb has been thought to produce extensive and irreversible damage and no possibility of salvage by reperfusion. This study tests the hypothesis that, in contrast to conventional wisdom, the cellular integrity is preserved after 4 hours of complete warm ischemia and control of the initial reperfusion can restore immediate contractility in these limbs. Ninety-two rat hindlimbs were isolated and 26 of the 92 did not undergo ischemia or reperfusion and served as controls. Sixty-six limbs were subjected to 4 hours of complete warm ischemia; of those 34 were assessed after the ischemic period without reperfusion and 32 were reperfused after the ischemic period. Nineteen hindlimbs were reperfused with Krebs-Henseleit buffer at a pressure of 100 mmHg to simulate embolectomy (uncontrolled reperfusion). In 13 legs a modified reperfusate at a pressure of 60 mmHg was used during the initial 30 minutes followed by an additional 30 minutes of reperfusion with 100 mmHg using Krebs-Henseleit buffer (controlled reperfusion). At the end of each experimental protocol, limbs were assessed by the following methods: muscle contraction, water content, volume, high energy phosphate content, muscle pH, effluent pH, mitochondrial function, ultrastructure, flow, and creatinkinase activity in the effluent. Data are expressed as mean +/- SEM. Significant differences were defined as probabilities for each test of p less than 0.05. Four hours of complete warm ischemia resulted in a severe reduction of adenosine triphosphate (4.0 +/- 0.8 vs 27.1 +/- 6.7 mumol/gm protein, p less than 0.001) and no contractions could be stimulated (0.0 +/- 0.0% CC). Muscle pH fell to 6.3 +/- 0.1 (p less than 0.001), and ultrastructural damage occurred (score 3.3 +/- 0.4 vs 0.8 +/- 0.1, p less than 0.002). However, there was only a slight increase in water content of the soleus muscle (78.7 +/- 0.2% vs 74.8 +/- 1.1%, p less than 0.05) without increase in limb volume (103.6 +/- 0.6% CV). In addition mitochondrial function was preserved well: mitochondrial oxidative phosphorylation capacity remained at 94% of control levels, ST3 at 93%, and ADP/O at 100% of control. Most importantly, controlled reperfusion restored immediate contractility in all limbs and was superior in all parameters investigated compared to uncontrolled reperfusion. These data support our inference that necrosis of skeletal muscle does not invariably occur after four hours of complete warm ischemia and suggest that muscle salvage by controlled reperfusion is possible after at least 4 hours of warm ischemia.
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PMID:Studies of reperfusion injury in skeletal muscle: preserved cellular viability after extended periods of warm ischemia. 193 31

After ingestion of 220 mg zinc sulfate, platelet aggregation was evaluated at various time intervals (i.e., T = 0, 1, and 3 hr) and the autologous plasma analyzed by atomic absorption analysis. The zinc levels increased maximally some 0.4 +/- 0.2 microgram/ml within 3 hr after ingestion, which for the entire blood pool corresponds to only 5% of the ingested zinc. Aggregation responses of platelet rich plasma (PRP), instigated with suboptimal levels of thrombin (less than 0.2 U/ml), ADP (less than 2 microM), epinephrine (less than 2 microM), collagen (less than 2 micrograms/ml), or PAF (less than 50 ng/ml), show significant improvement to at least one aggregant. Mean +/- SEM values for delta % aggregation increase are as follows: thrombin, 51 +/- 10%; epinephrine, 21 +/- 6%; ADP, 31 +/- 6%; collagen 23 +/- 6%; and platelet aggregating factor (PAF), 56 +/- 6%. For controls, the platelets from one individual with Glanzmann thrombasthenia as well as four undosed volunteers exhibited no significant changes in platelet responsiveness. Increased platelet responsiveness to agonists after zinc sulfate ingestion was observed in PRP from blood collected in either citrate or heparin. We demonstrate that within a relatively short time period, single bolus of nutritional zinc intake can significantly increase platelet reactivity. These findings show that nutritional zinc availability is relevant to hemostasis and may pertain to the viability of platelet concentrates in blood banks.
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PMID:Nutritional zinc increases platelet reactivity. 195 15


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