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)

A 62-year-old woman developed neurologic deficits 7 months after pulmonary lobectomy for alveolar cell carcinoma of the lung. CT scan of the head demonstrated two metastases with marked peritumoral edema. Administration of Decadron, chemotherapy and 3,000 rad cranial radiation resulted in dramatic improvement of dysphasia and right hand paresis. Almost 2 months later, rhythmic, involuntary movements of the left hand developed. There was progression to multifocal seizures, grand mal seizures, postictal depression, status epilepticus, and coma, with death 9 days after onset of the movement disorder. Bronchoalveolar carcinoma was widely disseminated in lungs and bones, and as three metastases in brain. Bland "ischemic" necrosis in a pseudolaminar pattern was present in the neocortex. Innumerable Cowdry type A intranuclear inclusion bodies were seen in neurons, astrocytes, and oligodenodroglia. Immunofluorescence demonstrated Herpes simplex virus type 2 antigen and electron microscopy revealed virions with the morphology of the Herpes group. The case is significant for (1) the concurrence of intracranial metastases and Herpes simplex encephalitis, and (2) the causal agent, Herpes simplex virus type 2. The implication for the clinical neurocientist is the potential in a patient with systemic cancer, for the causation of neurologic complications by more than one factor or mechanism.
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PMID:Herpes simplex type 2 encephalitis concurrent with known cerebral metastases. 22 22

The effects of an 8-day intravenous infusion of dexamethasone (7.6 mg kg-0.75 body weight) on collagen biosynthesis and wool growth in skin were examined in four Merino wethers. Plasma dexamethasone concentrations reached their peaks during the first 24 h infusion, which were followed by relatively stable levels (c. 1 X 10(-7) M) for the next 4--5 days. Minor increases in plasma dexamethasone levels were recorded during the final 2 days of treatment. Dexamethasone concentrations quickly fell below the level of detection once infusion ceased. Marked decreases in the wet weight, thickness and protein content of skin were observed at the end of infusion. DNA content was reduced to 42.4 +/- 4.9% s.e.m. during the first 2 days of treatment, but in the next 4 days of infusion gradually increased to 85.0 +/0 12.5% of controls. The level of collagen (expressed as hydroxyproline content of its acid hydrolysate) was elevated throughout the infusion and then gradually declined in 3 weeks to about 60% of controls. The biosynthesis of collagen measured by the rate of [14C]hydroxyproline formation and the activity of proline, 2-oxoglutarate dioxygenase (EC 1.14.11.2. formerly prolyl hydroxylase) was reduced during the first half of treatment to a greater extent than the rate of [14C]proline incorporation into proteins. Wool growth was reduced by 80.4 +/- 11.6% in the post-infusion period which allowed three sheep out of four to be defleeced. Inhibition of collagen biosynthesis in sheep skin was due initially to a decrease in the activity of proline, 2-oxoglutarate dioxygenase and later to the reduced rate of proline incorporation into proteins. It was also evident that changes in biosynthetic rate of collagen were not reflected in the total level of skin collagen. The extent of wool growth depression in individual animals paralleled the changes in DNA content and the extent of collagen biosynthesis inhibition.
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PMID:Effect of intravenously infused dexamethasone on collagen metabolism in skin of merino sheep. 23 81

Dexamethasone acetate (100 microgram IP) protected male Holtzman rats (300-330 gm) against endotoxin shock due to Salmonella enteritidis lipopoly-saccharide B IV. Endotoxin (5.0 mg/rat) produced hypoglycemia within 180 minutes, ie, plasma glucose fell from 87 to 24 mg/dl; dexamethasone prevented the hypoglycemia, ie, plasma glucose levels were 129 mg/dl at 180 minutes after endotoxin. Dexamethasone antagonized both endotoxin-induced depression of hepatic gluconeogenesis and enhanced glucose oxidation as evaluated in vivo. Epididymal fat pads from endotoxic rats (100-110 gm) had increased rates of glucose oxidation as evaluated by the in vitro conversion of 14C-D-glucose to 14CO2. Dexamethasone both in vivo and in vitro antagonized endotoxin glucose hypercatabolism by isolated epididymal fat pads following administrated of endotoxin. Glucocorticoid protection against endotoxin shock is related to antagonism of glucose dyshomeostasis.
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PMID:Dexamethasone antagonism of glucose dyshomeostasis in endotoxin shock. 28 Apr 23

To investigate the sites of the negative feedback of corticoids in the regulation of ACTH secretion, the effect of 10 mug of dexamethasone on adrenocortical responses to ether stress was studied in intact and fornix-sectioned rats. Dexamethasone pretreatment in both groups depressed significantly both the basal and stress plasma corticosterone levels. However, in rats with fornix section the amount of depression of the adrenocortical response was much smaller than in intact animals, when compared to the non-treated group. These data would inicate that extrahypothalamic regions play a role in the action of glucocorticoids in the feedback control of pituitary-adrenal function and that the hippocampus participates in this mechaism.
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PMID:Feedback effects of dexamethasone on adrenocortical responses in rats with fornix section. 100 17

The effect of short-term dexamethasone administration (8 mg daily for 3 days) on thyroid hormone response to exogenous TSH (bovine TSH, 5 IU i.m.) was studied in 16 euthyroid volunteers. Serum T3 and T4 concentrations were measured by radio-immunoassay prior to and 2, 6, 12, 24, and 49 hr after bTSH injection, both under basal conditions and during dexamethasone treatment. In all subjects bTSH administration raised both T3 and T4 concentrations significantly. Dexamethasone treatment induced a slight depression of endogenous TSH (m +/- SEM = 2.0 +/- 0.4 versus 1.6 +/- 0.3 muU/ml) and T4 (6.8 +/- 0.4 versus 6.1 +/- 0.2 mug/100 ml) basal values and a significant decrease in T3 value (1.16 +/- 0.09 versus 0.64 +/- 0.06 ng/ml, p = 0.005). The mean increment of both T3 and T4 after bTSH injection was percentually unchanged during dexamethasone treatment but, due to lowered basal value, T3 levels at each time interval after TSH + dexamethasone were significantly lower than the corresponding values observed after TSH alone. The present data show that high dexamethasone doses decrease T3 serum levels significantly without inhibiting T3 response to TSH stimulation. Only a slight lowering was observed in T4 levels.
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PMID:Effect of dexamethasone on thyroid hormone response to TSH. 118 94

A41 304 at 400 mug/kg produced depression of body weight gains in the rat dams but did not increase the number of the fetuses with gross malformations. At 400 mug/kg of dexamethasone, body weight gains of the rat dams were markedly depressed and fetuses presented cleft palate and depression of the placental weight, body weight and crown-rump length. As for the influence of both drugs upon the fetal skeleton, ossification of the odontoid process and metatarsus was delayed and lumbar ribs increased. Dexamethasone at 400 mug/kg, in addition to these findings, caused prominently delayed ossification to the caudal vertebrae. When A41 304 at 1600 mug/kg and dexamethasone at 400 mug/kg were given to pregnant mice, cleft palate occurred with high incidences, but neither visceral abnormalities nor skeletal malformations attributable to the drug administration were observed. The critical period of cleft palate which was noted in the mice given A41 304 was day 11 through day 15 of pregnancy, mainly 11 approximately 13 of pregnancy. Cleft palate was seen in a dose-related manner in either A41 304-treated groups or dexamethasone-treated groups, but the incidence at the same dosage level was higher in dexamethasome-treated groups than in A41 304-treated groups.
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PMID:[Effects of 9-fluoro-11 beta, 21-dihydroxy-16 ampha-methylpregna-1, 4-diene-3, 20-dione (A41 304) and dexamethasone on the fetus of mice and rats]. 123 51

Dexamethasone Suppression Test was performed during an acute phase in 81 patients with endogenous depression and 105 schizophrenic patients. The lack of suppression of cortisol was found in 1/3 if those ill with depression and 1/3 of those ill with schizophrenia. A relationship between those results and age was shown in female schizophrenic patients. In both groups a yearly rhythm was observed, however female patients differed from male patients.
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PMID:[Dexamethasone suppression test in endogenous depression and schizophrenia in male and female patients]. 130 36

The influence of dexamethasone and cyclophosphamide on the goat immune system was investigated. Seven goats, with a previous contact with caprine herpesvirus type 1 (CHV-1), were used. All had been vaccinated with live Mycobacterium paratuberculosis vaccine. Six goats were injected intravenously (i.v.) with dexamethasone daily for 5 days (2.5-4 mg/kg BW per day). Three also received 25 mg/kg BW of cyclophosphamide on day 0. The seventh goat was not treated. Dexamethasone alone caused depression, slight lymphopenia and fall in tuberculin reaction. Dexamethasone plus cyclophosphamide caused a severe clinical reaction, marked leukopenia (lymphopenia and polymorphopenia), fall in tuberculin reaction and significant increase in CHV-1 neutralizing antibody titres. M. paratuberculosis antibody reaction was variable and thus difficult to be assessed. CHV-1 was not isolated.
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PMID:Immunosuppression in goats by dexamethasone and cyclophosphamide. 133 Apr 22

From 9 centres 293 patients took part in the WHO-collaborative study on Dexamethasone-Suppression-Test (DST) in depression to examine the relationship of psychopathological and psychiatric history information to cortisol-levels and suppression/non-suppression status. Differences between the centres were large and significant on nearly all of the measures. The predictor analyses generally suffered from numerically weak correlations with many variables correlating to sex and age. Therefore analyses of the data were adjusted for centre-, sex-, and age-influences. The best predicting features of cortisol were 'fitful, restless sleep', 'change of bodyweight' and 'affective disorders in blood relatives'. The last 2 items together with 'hypersomnia' and 'ideas of insufficiency' were the best predictors of suppression/nonsuppression status. However, statistical evidence did not seem to be strong enough to describe a typical symptom profile of a depressive cortisol suppressor or nonsuppressor.
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PMID:Clinical correlates of response to DST. The Dexamethasone Suppression test in depression: a World Health Organisation collaborative study. 143 Jun 64

Stress has been implicated as a major confounding factor in the interpretation of Dexamethasone Suppression Test (DST) results. This study was designed to examine the effects of stress on DST results. Fifty patients with high levels of acute, chronic, and environmental stress participated in the study. Each patient was given a comprehensive psychiatric and psychological assessment, a routine administration of dexamethasone, and blood tests of cortisol values. The results indicate that the three measures of stress do not appear to affect levels of cortisol suppression, however, all three measures of stress predicted depression. As expected, DST cortisol levels were related to depression. Results are discussed in terms of their implications for understanding the associations among stress, depression and DST results.
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PMID:The role of stress in interpreting the dexamethasone suppression test. 147 78


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