Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clotting parameter of a primigravida with factor XII deficiency was studied during her third trimester of pregnancy, labor and post-partum; and compared with those of her newborn male infant. Sharp increases in factors VII, VIII, IX, X and moderate increases in factors II and XI were documented during pregnancy and at labor. All factors had returned to normal or near normal levels 24 hours after delivery. Factor XII remained at 0.0 level throughout. In the infant the clotting factor levels reflected depression of vitamins K-dependent factors II, IX, and X and a factor XII level of 40.0%. No undue bleeding was noted in the mother at delivery or placental separation, and no bleeding manifestation was apparent in the infant. These findings suggest that factor XII does not play a major role in triggering or modulating the course of normal labor, nor is its absence necessarily associated with bleeding complications during parturition or placental separation.
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PMID:Effect of factor XII deficiency on pregnancy and parturition. 46 18

When rats were given single or multiple doses of warfarin, the levels of prothrombin and factors VII, IX, and X were depressed, as expected. However, modest reductions of factors V, VIII, XI, and XII, but not of fibrinogen, also occurred. The levels of all eight factors promptly returned to normal when vitamin K1 was given. Warfarin-resistant rats had no depression of any of the eight factors. When vitamin K deficiency was induced by internal or external biliary fistula, factors II-VII-IX-X decreased sharply and factors V-VIII-XI-XII decreased modestly. Again, all depression were promptly reversed by vitamin K1. Isolated livers from warfarinized rats did not generate the classic vitamin K-dependent factors during 5 h of perfusion but did generate small amounts of factors V, XI, and XII, although less than normal. The isolated rat liver apparently does not generate factor VIII.
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PMID:Rat coagulation factors V, VIII, XI, and XII: vitamin K dependent. 65 84

Twelve patients with acute, untreated inflammatory bowel disease (IBD) were followed prospectively for coagulation and platelet function. With no symptomatic coagulopathy, abnormalities were found in all patients. With acute diseases, elevations of fibrinogen (9/12), factor V (8/12), and factor VIII (6/12) were common. Depressions of antithrombin III levels were also observed acutely (8/12). Abnormalities of platelets were both quantitative and qualitative. Thrombocytosis was present (11/12), and abnormalities in the rate and percent platelet aggregation were seen (9/10). During therapy, factors V and VIII, antithrombin III levels, and the quantitative and qualitative platelet abnormalities returned towards normal in direct correlation with sedimentation rate and clinical disease activity.
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PMID:Hemostatic alterations in inflammatory bowel disease: response to therapy. 71 49

In the beginning objects and problems of clinical pharmacology were outlined. Results from experimental studies in animals with the metabolite VIII of bromhexine (N-[trans-4-hydroxy-cyclohexyl]=[2-amino-3,5-dibromo-benzyl]-amine, Ambroxol (NA 842)) are described in order to contribute to the understanding of this substance's mode of action. Hence NA 872 is an expectorant which fully meets all requirements expected from this category of druggs -- increase in sputum amount, easement in breathing, reducing the viscosity, and depression of coughing. The dose-effect rate of the substance was tested in 54 adults and 32 children. The average dose of 45.0 mg/kg for adults was determined as sufficient for the majority of patients. In the following test in 124 patients on dose tolerance and efficacy, the substance proved to be tolerated extremely well, to cause no adverse side effects while achieving good effects particularly with regard to improvement of expectoration. There was no casual relationship between some occurring changes in laboratory data and the application of the substance.
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PMID:[Results of some clinical-pharmacological studies on ambroxol (NA 872)]. 117 81

This study attempts to determine if fibers that project from the guinea pig red nucleus to the spinal cord use L-glutamate and/or L-aspartate as transmitters. Unilateral injections of kainic acid were placed stereotaxically in the red nucleus to destroy the cells of origin of the rubrospinal tract. Six days after the injection, Nissl-stained sections through the lesion site showed that the majority of neurons in the red nucleus ipsilateral to the kainic acid injection were destroyed. In addition, the lesioned area included parts of the surrounding midbrain reticular formation. Silver-impregnated, transverse sections of the cervical spinal cord revealed the presence of degenerating fibers contralaterally in laminae IV-VII of the gray matter. Ipsilaterally, very sparse degeneration was evident in laminae VII and VIII of the gray matter. Two to six days after surgery, the electrically evoked, Ca2(+)-dependent release of both D-[3H]aspartate, a marker for glutamatergic/aspartatergic neurons, and gamma-amino[14C]-butyric acid ([14C]GABA) was measured in dissected quadrants of the spinal cervical enlargement. Lesions centered on the red nucleus depressed the release of D-[3H]aspartate by 25-45% in dorsal and ventral quadrants of the cervical enlargement contralaterally. The release of [14C]GABA was depressed by 27% in contralateral ventral quadrants. To assess the contribution of rubro- versus reticulospinal fibers to the deficits in amino acid release, unilateral injections of kainic acid were placed stereotaxically in the midbrain reticular formation lateral to the red nucleus. Nissl-stained sections through the midbrain revealed the presence of extensive neuronal loss in the midbrain and rostral pontine reticular formation, whereas neurons in the red nucleus remained undamaged. In the spinal cord, degenerating axons were present ipsilaterally in laminae VII and VIII of the gray matter. Some fiber degeneration was also evident contralaterally in laminae V and VI of the gray matter. This lesion did not affect the release of either D-[3H]aspartate or [14C]GABA in the spinal cord. The substantial decrements in D-[3H]aspartate release following red nucleus lesions suggests that the synaptic endings of rubrospinal fibers mediate the release of D-[3H]aspartate in the spinal cord. Therefore, these fibers may be glutamatergic and/or aspartatergic. Because other evidence suggests that rubrospinal neurons are probably not GABAergic, the depression of [14C]GABA release probably reflects changes in the activity of spinal interneurons following the loss of rubrospinal input.
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PMID:Decreased release of D-aspartate in the guinea pig spinal cord after lesions of the red nucleus. 200 35

Disturbances of blood coagulation were studied in 32 consecutive patients with typhoid fever on their admission to hospital. Estimations of prothrombin time, activated partial thromboplastin time, fibrinogen, fibrin degradation products (FDPs), factors VII, VIII and XII, alpha I antitrypsin, plasminogen, CI esterase inhibitor, and platelet counts were performed as well as liver function tests and blood counts. Five patients had laboratory evidence of disseminated intravascular coagulation (DIC) and two had a generalised bleeding disorder which in the other three was inapparent. The platelet count in the group as a whole was low (P less than 0.05) and the FDPs in most cases were mildly elevated. The pre-kallikrein values were depressed in three of the five with DIC, whereas factor XII was not reduced. These results indicate that bleeding disorders in typhoid fever are uncommon. The depression of pre-kallikrein indicates that the DIC is probably triggered by activation of the intrinsic coagulation pathway. Most patients had lymphopenia and monocytopenia but only two had neutropenia.
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PMID:Disturbances of blood coagulation associated with Salmonella typhi infections. 335 16

The author studied in conscious rats the local spinal blood flow (SCBF) and metabolic effects of intrathecally administered bupivacaine. Fourteen rats received 0.75% bupivacaine, 15 microliters, through a chronically implanted lumbar subarachnoid catheter. Twelve control animals were treated identically, except that they received only an equal volume of saline intrathecally. Ten minutes after intrathecal drug injection, either local SCBF or glucose utilization was measured in the lumbar spinal cord of seven experimental and six control animals with the quantitative autoradiographic iodo-[14C]antipyrine or 2-[14C]deoxyglucose methods, respectively. Intrathecal bupivacaine produced a limp tail, absent hindlimb withdrawal to pinch, and 25-30 min of analgesia on the tail-flick test. Mean arterial blood pressure decreased 14% (P less than 0.01) after bupivacaine was administered, but there was no change in arterial blood gases, pH, or rectal temperature. Subarachnoid bupivacaine reduced both local SCBF and glucose utilization, but the SCBF effect was larger. Local SCBF decreased 27-34% (P less than 0.01) in all five spinal gray and three white matter areas measured, and there was little regional variability in the response. The reduction in spinal glucose utilization was regionally selective and less marked. For example, glucose utilization decreased 15% (P less than 0.05) and 21% (P less than 0.05) in lateral and anterior spinal white matter, respectively, but only decreased approximately 3% in laminae I-III and dorsal white matter (P greater than 0.1). A trend toward metabolic depression was also evident in laminae VIII (-15%, P = 0.06), VII (-13%, P = 0.09), and IV-VI (-11%, P greater than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Local spinal cord blood flow and glucose utilization during spinal anesthesia with bupivacaine in conscious rats. 401 71

Disseminated intravascular coagulation was induced in kittens by intraperitoneal inoculation of feline infectious peritonitis virus (FIPV). Kittens seronegative to FIPV survived significantly (P less than 0.05) longer than those seropositive to FIPV. Pyrexia, anemia, icterus, hyperbilirubinemia, and elevated concentrations of liver-specific enzymes were detected in the inoculated cats. Lesions induced included disseminated fibrinonecrotic and pyogranulomatous inflammation, hepatic necrosis, and widespread phlebitis and thrombosis. Localization of FIP viral antigen and immunoglobulin G was demonstrated in foci of heptic necrosis by immunofluorescence miroscopy. Lymphopenia, thrombocytopenia, hyperfibrinogenemia, and increased quantities of fibrin-fibrinogen degradation products were present in cats after the onset of clinical illness. Depression of factor VII, VIII, IX, X, XI, and XII plasma activities and prolongation of prothrombin and partial thromboplastin times also developed in infected cats. The accelerated onset of clinical disease and mortality in seropositive kittens vs seronegative kittens and the association of virus and antibody in multiple foci of hepatic necrosis suggest an immune-mediated component is involved in the pathogenesis of this disease.
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PMID:Disseminated intravascular coagulation in experimentally induced feline infectious peritonitis. 625 Apr 26

Plasma factor VIII coagulant activity is decreased in hypothyroid patients and increased in hyperthyroid patients. We studied 21 untreated hypothyroid patients. Factor VIII coagulant activity was mildly decreased in association with significant depression of factor-VIII-related antigen and ristocetin cofactor activity in five patients. Factor-VIII-related properties significantly increased with oral thyroid replacement therapy in seven of 10 patients. Twenty-two untreated hyperthyroid patients were similarly evaluated. In 21 of these patients significant increases were noted in factor VIII coagulant activity, factor-VIII-related antigens, and ristocetin cofactor activity. Elevated factor-VIII-related properties returned to normal in all of 10 patients treated with radioactive iodine or propylthiouracil. We discuss the relation between thyroid function and factor-VIII-related properties in both hypothyroid and hyperthyroid patients.
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PMID:Factor VIII activity and thyroid function. 681 17

The study includes 119 patients with minor ischemic cerebrovascular lesions before the age of 55 during 1976-78. Atherosclerotic signs were found in 65% at aortocranial angiography and/or exercise test (ST depression). Abnormalities in hemostasis (defective fibrinolytic response in 50%, high Factor VIII activity in 45% of those investigated, and high Factor VIII related antigen (VIII R:Ag) in 20%) could not be explained by accumulation of atherosclerotic risk factors as most often no significant independent correlations were found at stepwise multiple regression. Significant correlations with aortocranial atherosclerosis was found for age, VIII R:Ag and blood pressure reaction at exercise test. Only E-SR showed significant correlation to ST depression at exercise test. These results indicate different determinants and risk indicators for atherosclerosis with different locations. An early evaluation of the longitudinal study (mean 42 months' follow up) showed that 16 patients had suffered new occlusive vascular incidents. The malign prognostic subgroup (cerebral or myocardial infarction or death; n = 10) showed significantly higher levels of VIII R:Ag (p less than 0.005) and triglycerides (p less than 0.05) than the benign group (new TIA, n = 6). This indicates that VIII R:Ag may be a useful marker for development of atherosclerosis and predictor for the outcome of ICD.
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PMID:A study of hemostasis in ischemic cerebrovascular disease. V. A multivariate evaluation of risk indicators and predictors. Early results of a longitudinal study. 681 52


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