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)

Overnight metabolic studies in 39 poorly controlled insulin-treated diabetic patients aged 9 to 66 years showed hypoglycaemia (blood-glucose less than 2 mmol/1) in 22 patients; it lasted 3 h or more in 17. Hypoglycaemic symptoms were very mild or absent, but 19 patients had other features of overtreatment with insulin. These included lethargy, depression, night sweats, morning headaches, fits (3 patients), glycogen-laden hepatomegaly (3), and acquired tolerance to high doses of insulin (mean 1 u/kg/24 h). The best clinical clue to recurrent nocturnal hypoglycaemia was the intermittent occurrence of symptoms, however "mild" and infrequent these appeared to be. Reduction of insulin by a mean of 25% in these patients (without change of species) did not result in loss of overall control; 1 patient with recurrent ketoacidosis was stablished on 40% of his initial dose. It is difficult, sometimes impossible, to achieve good overnight control with conventional once or twice daily insulin therapy. Since patients readily become tolerant of low blood-glucose levels, reliance on urine tests and symptoms of hypoglycaemia as a guide to dosage easily produces a spiral of overtreatment.
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PMID:Unrecognised nocturnal hypoglycaemia in insulin-treated diabetics. 8 75

Liver enlargement is frequently reported in studies on the short-term toxicity of chemicals. In many such studies no histological evidence of damage is present but biochemically there is often an increased microsomal enzyme activity (MEA) which is interpreted to represent a type of work hypertrophy. In a few instances, the MEA in the enlarged liver is either normal or less than normal. In such instances histochemical evidence of liver damage (depression of G-6-Pase and autophagy) is found. A compound which produced the latter changes is Ponceau MX. When administered for up to 21 months at a dose-level which produces biochemical and histochemical evidence of liver injury, a series of changes were observed consisting of progerssive diminution of MEA, areas of glycogen accumulation and centrilobular fatty change and these were followed first by nodular hyperplasia and then by frank carcinoma. The protective effect of increased MEA in carcinogenesis was shown by the reduction in tumour incidence on the administration of phenobarbitone simultaneously with acetylaminofluorene, 4-dimethyl aminoazo benzene and diethylnitrosamine. But no such protective effect is seen if the phenobarbitone is administered after treatment with these carcinogens. In fact the number of tumours is enhanced presumably due to preferential stimulation of the growth of malignant cells.
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PMID:Liver growth and tumorigenesis in rats. 28 28

Systemic lupus erythematosus (SLE) is poorly described among black children in Africa despite being more frequent among some black adult populations than their white counterparts. The first black South African child with SLE is documented. The patient was a 10-year-old girl who had fever, facial rash (with complement (C4) deposited at the dermo-epidermal junction of normal skin), weight loss, central nervous system involvement (depression, withdrawal, retinal exudates), renal involvement (glomerular filtration rate 54 ml/min/1.73 m2; membranous nephropathy with mild mesangial proliferation; World Health Organisation classification Vb), alopecia, lymphadenopathy, hepatomegaly, positive Coombs test, hypeocomplementaemia, anti-DNA antibodies and positive anti-nuclear factor.
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PMID:Systemic lupus erythematosus in a black South African child. First documented case report. 198 78

A 14-year-old girl was admitted with chief complaints of edema and chest pain. She had hepatomegaly, but did not have heart murmur and accentuation of the pulmonary component of the second heart sound. The electrocardiogram showed right axis deviation, negative T wave in V3,4 and ST depression in III, aVF. But right ventricular hypertrophy was not dominant. Chest radiography showed a cardiothoracic ratio of 54% and a slight prominence of proximal pulmonary arteries. The edema was soon diminished only by the diuretics, but it appeared again without the diuretics. At the cardiac catheterization 3 months after the onset of symptoms, the pulmonary arterial pressure was 150/85 mmHg and the pulmonary resistance was 3,232 dyn/sec/cm5. The right atrial pressure was 9.5 mmHg and oxygen saturation at the pulmonary artery was 31.0%. Prostaglandin E1 reduced the pulmonary artery pressure only a little, but raised the systemic pressure. The patient was treated with several vasodilators, but her condition deteriorated rapidly and she developed severe right ventricular failure. She died only 8 months after the onset of symptoms and 5 months after the catheterization. At autopsy, histological examination demonstrated intimal fibrotic thickening of the small-sized pulmonary arteries and organizing thrombus. But there was not plexiform lesion. Heart failure was easily improved when she was first admitted. But after 3 months the cardiac catheterization revealed that her condition was already severe. Several vasodilators was not effective to such a rapidly progressive primary pulmonary hypertension.
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PMID:[A case of rapidly progressive pulmonary pulmonary hypertension in a 14-year-old girl]. 259 31

Spontaneous improvement of active juvenile rheumatoid arthritis (JRA) occurred after T lymphocytosis in an 8-year-old boy. He had prominent lymphocytosis, the count reaching 59,000/mm3, followed by spontaneous disappearance of fever, arthralgia, lymphadenopathy, hepatomegaly, and C-reactive protein. The serum immunoglobulin levels were gradually decreased. The surface marker analysis, using two color flow cytometry, showed that the lymphocytes were activated suppressor T lymphocytes, expressing CD3, CD8, HLA-DR, and CD8 plus CD11. When studied in vitro with pokeweed mitogen stimulation, the T lymphocytes significantly suppressed the immunoglobulin production by autologous B lymphocytes as compared with the T lymphocytes at remission (p less than 0.01). Based on the widely believed notion that depression of suppressor T lymphocyte functions is one of the important mechanisms underlying systemic JRA, the activated T lymphocytosis with the suppressor phenotype and suppressive function on the immunoglobulin production may have been related to the improvement of active JRA in the patient.
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PMID:Spontaneous improvement of juvenile rheumatoid arthritis after T lymphocytosis with suppressor phenotype and function. 297 87

Although butylated hydroxytoluene (BHT) is non-mutagenic, at high doses it has recently been associated with an increased incidence of liver tumours in laboratory rodents. To establish whether chronic liver cell injury may be involved in the genesis of these tumours, BHT was administered to rats by orogastric gavage at doses of 0, 25, 250 or 500 mg/kg/day for up to 28 days and also at daily doses of 1000 and 1250 mg BHT/kg for up to 4 days (sublethal doses). The sublethal doses induced centrilobular necrosis within 48 hr, whereas administration of BHT for 7 or 28 days caused dose-related hepatomegaly and at the highest dose level induced progressive periportal hepatocyte necrosis. The periportal lesions were associated with proliferation of bile ducts, persistent fibrous and inflammatory cell reactions, hepatocyte hyperplasia and hepatocellular and nuclear hypertrophy. Biochemical changes consisted of dose-related induction of epoxide hydrolase, dose-related changes in the ratio of cytochrome P-450 isoenzymes and depression of glucose-6-phosphatase. Measurement of BHT demonstrated a dose-related accumulation in fat but not in the liver. Changes in hepatic activating and detoxifying enzyme profiles are implicated both in the mechanism of periportal hepatocyte damage and in the change of site of damage according to the dose and duration of the treatment. The persistent and active nature of the lesions in rats dosed with 500 mg BHT/kg for 28 days, combined with evidence of cell damage at doses equivalent to those associated with hepatic tumours (250 mg BHT/kg), suggests that chronic liver cell damage may be involved in their aetiology. In this and several other studies, there was no evidence that BHT causes liver damage at a dose level of 25 mg/kg/day. As this is several hundred times higher than the normal human intake, it is considered unlikely that BHT poses a threat to human health.
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PMID:Hepatic responses to the administration of high doses of BHT to the rat: their relevance to hepatocarcinogenicity. 302 37

Two cases of Yersinia enterocolitica septicemia occurred in a breeding group of 22 adult patas monkeys (Erythrocebus patas). Affected animals had acute clinical signs of depression, weakness, dehydration, hypothermia, hepatomegaly and pronounced leukopenia. Both animals died a few hours after treatment was initiated. Gross necropsy findings included jaundice, fluid in body cavities, hepatomegaly, splenomegaly, multiple white foci within the liver and spleen, generalized lymph node enlargement and numerous mucosal ulcerations in the colon. Primary histopathological lesions were multifocal hepatic necrosis, splenic necrosis, chronic ulcerative enteritis and diaphragmatic myositis with necrosis and edema. Yersinia enterocolitica was cultured from the liver, spleen, lung, jejunum and rectum. Wild rodents, particularly mice, may have been a source of infection for these animals, as the monkeys were housed in a rural, indoor-outdoor facility. A preliminary culture survey showed that some clinically normal patas monkeys harbored the organism in their intestinal tracts.
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PMID:Naturally occurring Yersinia enterocolitica septicemia in patas monkeys (Erythrocebus patas). 405 42

RC-12 [1,2-dimethoxy-4-(bis-diethylaminoethyl)-amino-5-bromobenzene] was evaluated for prophylactic, radical curative, and suppressive activities against infections with Plasmodium cynomolgi and subacute toxicity in rhesus monkeys. Applied as a prophylactic agent, RC-12, administered in doses of 6.25 to 25.0 mg/kg daily throughout the incubation period, provided near-complete to complete protection against 10(5) to 10(6) times the minimum infective dose of sporozoites. Applied as a suppressive agent, daily doses of 100.0 mg of RC-12 per kg did not eradicate blood schizonts regularly; hence, the need for concomitant administration of a blood schizonticide, such as chloroquine, in assessments of radical curative activity. In such appraisals, daily doses of 6.25 to 25.0 mg of RC-12 per kg for 14 days, in combination with 2.5 mg of chloroquine per kg daily for 7 days, effected cure of 69 and 93% of established infections, respectively. The curative activity of RC-12 was related to the total dose and could be achieved with a regimen as brief as 4 days. With respect to outward expressions of toxicity, daily doses of 50.0 mg/kg or lower for 15 to 225 days evoked no reactions. Doses of 100.0 or 200.0 mg/kg, scheduled for 15 days, evoked convulsions and depression and were, respectively, lethal to 4 of 17 and 7 of 7 recipients. Doses of 25.0 mg/kg or lower evoked no discrete reactions. Doses of 50.0 mg/kg and higher evoked hepatomegaly, vacuolation of hepatocytes, and elevations of glutamic oxalacetic and glutamic pyruvic transferase activities in serum, reactions related in intensity to dose but not duration of dosage.
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PMID:Antimalarial activities and subacute toxicity of RC-12, a 4-amino-substituted pyrocatechol. 409 27

The effect of the nonsteroidal estrogenic compound, diethylstilbestrol (DES) on cell-mediated immunocompetence in the mouse has been assessed. Adult female B6C3F1 mice were injected (s.c.) with 0.2, 1.0 and 4.0 mg/kg of DES daily for 14 days. All immunological tests and toxicological parameters were determined at least 24 hr after the last exposure. Thymic involution and hepatomegaly were noted at the lowest dose of DES. The most sensitive indicator of immunosuppression by DES was the delayed hypersensitivity response (DHR) to keyhole limpet hemocyanin in mice sensitized without adjuvant. The lowest dose of DES produced a 93% decrease, compared with a 39% decrease for the same DHR model in mice sensitized to keyhole limpet hemocyanin plus adjuvant and a 63% decrease for the DHR to sheep erythrocytes. A 35% decrease of the acute inflammatory response to carrageenin was produced by the lowest dose of DES. Day 2 proliferative responses to both concanavalin A and phytohemagglutinin (T-cell mitogens) were depressed by the lowest dose of DES, whereas significant suppression of the response to lipopolysaccharide (B-cell mitogen) was only noted at the highest dose of DES. The effects of DES on Day 3 proliferative responses were less dramatic. The mixed lymphocyte response was significantly suppressed by 1.0 and 4.0 mg/kg of DES on all days in culture. The reversibility of the DES effects was studied by resting the mice for 30 days between exposure and measuring a given parameter. All effects on organ weights and the depression of both the sheep erythrocytes DHR and the carrageenin inflammatory response were reversed.
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PMID:Suppression of cell-mediated immunocompetence after subchronic exposure to diethylstilbestrol in female B6C3F1 mice. 622 65

Chloral hydrate has been found in our drinking water supplies at levels up to 5 micrograms/1. The purpose of this study was to evalute the acute and subchronic toxicology of chloral hydrate in the random-bred CD-1 mouse, to provide data for risk assessment. The acute oral LD50 of this compound was 1442 and 1265 mg/kg in male and female mice, respectively. Acute toxicity appeared to be related to depression of the central nervous system. Fourteen-day exposure by gavage in male mice at doses 1/10 and 1/100 the LD50 caused an increase in liver weight and a decrease in spleen weight at the highest dose level. Based on the data derived from 14 days of exposure, a 90-day study was performed. The compound was delivered via the drinking water; levels of the compound delivered per day were equivalent to those dosed in the 14-day study. The target organ in both sexes appeared to be the liver, with the males most affected. Male mice demonstrated a dose-related hepatomegaly accompanied by significant changes in serum chemistries and hepatic microsomal parameters. The females did not demonstrate the hepatomegaly observed in males, but did show alterations in hepatic microsomal parameters. No other significant toxicological changes were observed in either sex following 90 days of exposure.
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PMID:Toxicology of chloral hydrate in the mouse. 708 46


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