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:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Initial transfusion needs aremet by type-specific rather than low titer O-negative blood. When the patient's problem approaches the magnitude of exchange transfusion (5 to 10 units) in less than 4 hours, platelet transfusion to treat dilutional thrombocytopenia is administered. Fresh frozen plasma is administered to provide clotting factors. When five units have been exceeded, platelet, pro-thrombin, and partial thromboplastin are measured. A blood clot is checked for clotting, retraction, and lysis. These tests screen platelet quantity and the intrinsic and extrinsic clotting system. Administered blood is warmed in a water bath or heating coil. Blood gas analysis (pH, pO2, and pCO2) is performed every five units to allow for precise administration of bicarbonate. The electrocardiogram is used to monitor potassium and calcium abnormalities. Hyperkalemia is seldom a problem. Hypocalcemia may be present transiently and is treated with calcium choride. Component therapy is the standard recommended practice. Fresh blood is recommended for the patient who has had an acute exchange transfusion and continues to require large quantities of blood. Fresh blood obviates the need for combining components and allows one transfusion unit to address itself to the multiple needs of the patient.
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PMID:The use of fresh blood in the treatment of critically injured patients. 23 51

The effects of three widely spaced levels of bacterial contamination of reagent water on several chemistry, radioimmunoassay, and coagulation procedures were studied. These included determinations of lactate dehydrogenase, creatine kinase, aspartate transaminase, alkaline phosphatase, blood urea nitrogen, total protein, thyroid-stimulating hormone, digoxin, thrombin time, activated partial thromboplastin time, and prothrombin time. Statistical analyses included calculations of means and coefficients of variation, and analysis of variance, as well as correlation coefficients for test results versus logarithm of bacterial contamination. Statistically and clinically significant differences occurred together only for an elevated level of creatine kinase.
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PMID:Effects of bacterial contamination of reagent water on selected laboratory tests. 43 36

Hematologic alterations after daily exposure to compression/decompression in open water are described. A standard dive to 100 fsw for 25 min was employed. Erythrocytes decreased postdive, reaching an apparent minimun 4 to 6 h after exposure and recovering to normal or supranormal value by 20 h postdive. Measurements of plasma volume after repeated dives showed a significant increase in volume at 4 h postdive. It is speculated that a phenomenon akin to cardiovascular deconditioning, caused by loss of the hydrostatic blood column in the lower extremities during immersion, results in a transitory fluid recruitment that may persist following several daily dives. Pre- and postdive partial thromboplastin times measured after repeated exposures failed to show a consistent response to compression/decompression.
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PMID:Hematologic changes after daily asymptomatic dives. 60 6

In order to determine whether asymtomatic gas phase separation causes hematologic abnormalities, studies were carried out following two dive series, one to 210 feet of sea water (FSW) for 50 min and the other to 132 FSW for 30 min. Studies included white and red cell count, red cell indices, platelet count, ESR, fibrinogen, fibrin split products, prothrombin time, partial thromboplastin time, coagulation factors II, V, VII, VIII, and X, clot retraction, platelet aggregation and adhesion, euglobulin lysis time, and platelet factor III. Changes were seen in platelet and white cell count, prothrombin time and partial thrombo-plastin time. White cell count was the only variable which correlated with total bubble score. The results are presented and implications of the findings discussed.
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PMID:Hematologic changes in man during decompression: relations to overt decompression sickness and bubble scores. 94 7

A 78-year-old woman, who had received steroid therapy for four years, had strikingly prolonged prothrombin time (PT) and partial thromboplastin time (PTT). The presumptive diagnosis was chronic hemolytic anemia. Platelet count and functions, fibrinogen, and factor XIII assays were all normal, but other factors assayed abnormally low; Sia water-dilution test was positive. When water-insoluble protein was removed by centrifugation, coagulation factors became normal. Dissolution of this precipitate in normal plasma caused marked prolongation of PT and PTT and lower factor assays. Serum electrophoresis showed a homogeneous M spike and an anomalous IgM, lambda-antigenic type in the gamma-globulin zone at point of origin. Ultracentrifugation of serum and of the precipitate showed 10% S17 and almost 100% S17 components, respectively. Five other patients with water-insoluble paraproteins were tested; two were clot-inhibitory.
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PMID:Water-insoluble paraproteins with anticoagulant properties. 115 70

This investigation was undertaken to standardize the determination of the one-stage prothrombin time for use with chickens. Homologous thromboplastin was essential and the most active thromboplastin was obtained from chickens four-weeks old or younger. Acetone-dried brain powder could be stored for at least 4 months at -15 degrees C. without loss of activity. Extraction of brain powder with 0.025 M CaCl2 at 42 degrees C. gave better thromboplastic activity than the standard extraction with physiological saline at room temperature. Thromboplastin solutions could be stored in ice water for only 6 hours without loss of activity. Citrate concentration had to be increased from the usual 0.10 M to 0.18 M to prevent premature clotting of plasma. Plasma donor age had no effect on the prothrombin times. Freezing and thawing as well as storage of plasma in the frozen state increased the prothrombin times. Using the best conditions, the mean prothrombin time for 1200 birds determined over a 6-month period was 9.4 sec. with an individual range of 7.18-11.4 sec. This represents a significantly lower prothrombin time with lower variability than that reported in the literature.
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PMID:Investigation and standardization of prothrombin times in chickens. 116 26

Cultured endothelial cells can be induced by tumor necrosis factor/cachectin (TNF) and other cytokines to synthesize the procoagulant cofactor tissue factor (TF). Intact monolayers of TNF-treated endothelial cells showed only minimal TF activity. In contrast, after permeabilization of these monolayers with detergent (saponin, 0.02%), there was approximately 10- to 20-fold increase in TF-mediated, factor VIIa-dependent factor Xa formation. Extracellular matrix derived from TNF-treated endothelium, prepared after removing the cells by hypotonic lysis or ammonium hydroxide (0.1 N), also had similarly enhanced TF activity. Incubation with a blocking monoclonal antibody to TF inhibited the procoagulant activity of both TNF-stimulated endothelial cells, whether they were intact or permeabilized, and of their matrices. However, when the apical cell surface was pretreated with anti-TF antibody, washed, and then cells were lysed with water or permeabilized with saponin, similar augmentation of TF activity was still observed, suggesting the presence of a pool of TF to which the antibody did not initially gain access. Consistent with this concept, the presence of TF in the matrix of TNF-treated endothelial cells was shown by immunoblotting and morphologic studies; cultured endothelial monolayers and the native endothelium of aortic segments after exposure to TNF showed TF in extracellular matrix, associated with vesicles. In contrast, TF was virtually undetectable on the apical endothelial surface. Taken together, these findings suggest that endothelial TF can be present in a cryptic pool that only gains access to the blood after alteration in the integrity of the endothelial monolayer.
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PMID:Tumor necrosis factor-induced endothelial tissue factor is associated with subendothelial matrix vesicles but is not expressed on the apical surface. 149 37

Heparin and dextran sulfates 8000 are separated from citrated plasma by absorption on epichlorohydrin triethanolamine cellulose columns followed by elution with 1.1 and 1.4 mol/L NaCl in 0.05 mol/L glycine-HCl buffer. The eluate is desalted with Sephadex G25-40, dried, and dissolved in water. A 1 microliters sample is applied to an agarose gel slide. After electrophoresis, the slide is fixed and stained with toluidine blue. The sulfated polysaccharide band(s) is identified by relative electrophoretic migration. The total amount of drug is estimated by matching its optical density with that of a band on one of a set of slides with graded amounts of heparin or dextran sulfate. The reaction with toluidine blue measures the total polyelectrolyte, not just the small proportion of the drug with anticoagulant activity. Pooled normal plasma showed a trace of chondroitin and no heparin. Recovery of heparin and hydrogenated dextran sulfate that was added to pooled normal plasma was complete (lowest concentration tested was 10 micrograms/ml); however, recovery for unhydrogenated dextran sulfate declined consistently by 9 micrograms/ml for concentrations below 50 micrograms/ml, setting a limit for its recovery. Plasma samples taken from patients for coagulation tests were examined by this procedure, and in so doing, steps were ascertained to improve the procedure for routine use. Results were compared with values for prothrombin time and activated partial thromboplastin times obtained on the same samples by the clinical laboratory. Because the procedure provides an independent parameter for measurement in patients who have received heparin therapy, insight into different patient responses to the drug is therefore possible. With minor modifications, the procedure can be used for heparans, dermatans, and chondroitins, because it allows identification and microscale quantitation on the basis of charge, molecular weight, and carbohydrate structure.
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PMID:Determination of absolute amounts of heparin and of dextran sulfate in plasma in microgram quantities. 169 Dec 56

We have expressed human alpha-globin to a high level in Escherichia coli as a fusion protein, purified it and removed the N-terminal leader sequence by site-specific proteolysis with blood coagulation factor Xa. The apo globin has been refolded and reconstituted with haem and native beta-globin to form fully functional haemoglobin (Hb) with properties identical to those of native human Hb. By site-directed mutagenesis we have altered the distal residues of the alpha subunits and compared the functional properties of these mutant proteins. The rates of various ligands binding to these proteins in the R-state have been reported by Mathews et al. Here, we present the oxygen equilibrium curves of three E11 alpha mutants and the crystal structures of two of these mutants in the deoxy form. Replacing the distal valine residue of alpha-globin with alanine, leucine or isoleucine has no effect on the oxygen affinity of the protein in either quaternary state, in contrast to the equivalent mutations of beta subunits. The crystal structure of the valine E11 alpha----isoleucine mutant shows that the larger E11 residue excludes water from the haem pocket, but causes no significant movement of other amino acid residues. We conclude that the distal valine residue of alpha-globin does not control the oxygen affinity of the protein by sterically hindering ligand binding.
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PMID:Functional role of the distal valine (E11) residue of alpha subunits in human haemoglobin. 202 47

Four patients with primary pulmonary hypertension, microangiopathic hemolysis, and thrombocytopenia were seen at the Charleston (WVa) Area Medical Center between 1983 and 1988. Characteristic laboratory and clinical features of these patients were the following: mild anemia, reticulocytosis, low serum haptoglobin value, microangiopathic red blood cell changes on peripheral blood smear, mild to moderate thrombocytopenia, normal clotting studies (ie, prothrombin time, partial thromboplastin time, fibrinogen), negative direct Coombs' test, negative glucose water test, normal serum urea nitrogen and creatinine levels, lack of improvement of hemolysis and thrombocytopenia in response to vasodilators or calcium channel blockers, and severe plexiform lesions in the pulmonary vasculature with fibrin deposition at autopsy. The hemolysis and thrombocytopenia probably developed as a result of flow through the fibrin deposition in the plexiform lesions in the pulmonary circulation and subsequent shearing of red blood cells and platelets.
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PMID:Primary pulmonary hypertension. Its association with microangiopathic hemolytic anemia and thrombocytopenia. 204 24


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