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)

Both concentrations of total 3-methoxy-4-hydroxyphenylglycol (MHPG) and 3,4-dihydroxyphenylglycol (DHPG) in the human urine, plasma and CSF were determined with a high-pressure liquid chromatography with electrochemical detection in order to clarify the dynamic change in these noradrenaline metabolites. Three different biological fluids were collected simultaneously from 16 orthopedic patients who were regarded clinically as substitutes for normal subjects. In the urine, the MHPG concentrations were 1.67 +/- 0.65 micrograms/mg creatinine (mean +/- S.D.) and DHPG 0.39 microgram/mg creatinine +/- 0.21. The plasma levels were 21.16 ng/ml +/- 9.58 for MHPG, and 19.58 ng/ml +/- 8.13 for DHPG. The CSF levels of MHPG and DHPG were 24.08 ng/ml +/- 8.10 and 34.76 ng/ml +/- 11.46, respectively. The CSF levels of these metabolites were correlated significantly with those in the plasma (r = 0.852, p less than 0.001 for MHPG; r = 0.799, p less than 0.001 for DHPG), while no significant correlations were found between the urinary levels and either the plasma or CSF levels of these metabolites. In the urine, the MHPG levels were proportional to the DHPG levels, while the former were inversely proportional to the latter in the plasma or CSF. Neither the MHPG nor DHPG levels in the urine from depressed patients revealed to have any significant correlation with their clinical assessments using the Hamilton Rating Scale Score (HRS). The patients were treated with an antidepressant active selectively on the noradrenergic system, and no significant changes in urinary excretion of these metabolites were observed before and after the drug treatment. These findings suggest that in the case of psychiatric disorders such as depression, these compound levels in the plasma or CSF would provide more important information than those in the urine.
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PMID:Studies on 3-methoxy-4-hydroxyphenylglycol (MHPG) and 3,4-dihydroxyphenylglycol (DHPG) levels in human urine, plasma and cerebrospinal fluids, and their significance in studies of depression. 377 51

Findings from natural cases and experiments with cattle emphasise that flowering plants are the most important form of Bryophyllum (Kalanchoe) spp in poisonings in Australia. The main life-threatening lesion is myocardial. The effects on the alimentary tract are less important than was believed previously. B. tubiflorum, B. daigremontianum x B. tubiflorum, B. pinnatum and B. proliferum caused 41 recorded poisoning incidents affecting 379 cattle in Queensland between 1960 and 1984. Poisoning occurred between May and October--the flowering season of these plants. Experimental B. tubiflorum poisoning and natural poisonings produced anorexia, depression, ruminal atony, diarrhoea, heart rate and rhythm abnormalities, dyspnoea and death. Increased plasma concentrations of urea, creatinine and glucose and decreased chloride were measured experimentally. Both natural and experimental cases had myocardial degeneration and necrosis with haemorrhages of the heart and alimentary tract. Cattle with severe dyspnoea had atelectasis and emphysema of the lungs. Some cattle had mild nephrosis. The median lethal doses of B. tubiflorum flowers, roots and leaf plus stem were 0.7, 2.3 and 5.0 g dry matter/kg liveweight respectively (7, 7 and 40 g wet weight/kg). Bufadienolides have been isolated recently from B. tubiflorum flowers and the syndrome is consistent with cardiac glycoside poisoning.
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PMID:Hearts and flowers: Bryophyllum poisoning of cattle. 377 71

Dietary calcium (CA++) supplementation attenuates gentamicin nephrotoxicity in rats. It has been proposed that this protective effect results from the ability of Ca++ to interfere with gentamicin binding to renal cell membranes. However, calcium supplementation also suppresses parathyroid hormone (PTH) activity, which may affect gentamicin nephrotoxicity by altering renal brush border phospholipid composition or renal calcium handling. We therefore compared gentamicin nephrotoxicity in PTH-stimulated control rats and parathyroidectomized (PTX) rats. Although their pretreatment serum ionized calcium concentration was significantly higher (1.27 +/- 0.01 vs. 0.88 +/- 0.06 mmol/L; P less than 0.001), PTH-stimulated rats had higher peak renal cortical gentamicin concentrations (543 +/- 20 vs. 395 +/- 49 micrograms/gm; P less than 0.025) and serum creatinine concentrations (3.0 +/- 0.8 vs. 0.9 +/- 0.3 mg/dl; P less than 0.05). Structural injury and depression of renal cortical slice uptake of p-aminohippurate were also less severe in PTX rats. Gentamicin treatment also caused increased urinary Ca++ excretion in control rats (from 2.12 +/- 0.64 mumol/mg creatinine per day [pretreatment] to 16.86 +/- 2.07 mumol/mg creatinine per day; P less than 0.001) but not in PTX rats. Control rats ingesting chow containing a standard Ca++ content (1.2%) resembled PTX rats. These results indicate that PTH stimulation exacerbates gentamicin nephrotoxicity. Increased peak renal cortical gentamicin concentrations in PTH-stimulated rats may be caused by increased gentamicin transport across the brush border as a consequence of PTH-mediated alteration of plasma membrane phospholipid composition, turnover, or both.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of parathyroid hormone activity on gentamicin nephrotoxicity. 379 14

The clinical, pathomorphological and serological features of acute canine leptospirosis are evaluated and the IgM- and IgG-specific ELISA for leptospirosis serology in dogs is assessed. The clinical syndrome of acute canine leptospirosis was characterized by depression, anorexia, vomiting and often haemorrhagic diarrhoea. In addition, jaundice, uraemia, elevated creatinine and alkaline phosphatase were observed in the majority of the dogs. In pups invagination of the intestines was a noteworthy finding. The clinical signs and the post-mortem findings were rather non-specific so that the clinical and post-mortem diagnosis had to be confirmed serologically. In acute clinical cases of canine leptospirosis a high anti-leptospiral IgM titre, ranging from 160 in pups to 10240 in adults, was always present, whereas the anti-leptospiral IgG titre and the agglutination titre usually were negative or low. Dogs died from leptospirosis in spite of a high anti-leptospiral IgM titre. Only two dogs having, at the first examination, a high IgM titre in conjunction with a high IgG titre survived an acute infection. The possible role of IgM and IgG in the pathogenesis of an acute leptospiral infection is discussed. Different serological patterns in reference dogs, which were not suffering from acute leptospirosis, are presented.
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PMID:Clinical, pathological and serological features of spontaneous canine leptospirosis. An evaluation of the IgM- and IgG-specific ELISA. 379 34

The effect of high levels of dietary magnesium (1.4%) alone or in combination with elevated calcium (1.8%) or phosphorus (1.6%) on growth and health of male calves was evaluated during a nine week feeding trial after weaning. Twenty calves were randomly divided into 4 feeding groups consisting of controls, high magnesium, high magnesium and calcium or high magnesium and phosphorus. Elevated dietary minerals caused decreased feed intake and growth rate. Blood urea nitrogen and serum creatinine levels were greatly elevated in calves fed high magnesium or magnesium and phosphorus and serum urea nitrogen was moderately elevated in calves fed high magnesium and calcium. These elevations suggested the occurrence of renal damage as a result of microcrystalline obstruction of renal tubules. Serum magnesium levels were three times normal in calves fed high magnesium or magnesium and phosphorus, but only twice normal in calves fed high magnesium and calcium. High dietary magnesium resulted in a significant depression in blood calcium level. This effect was somewhat overcome by additional dietary calcium Three calves fed the high magnesium diet and two calves fed the high magnesium and phosphorus diet developed urinary tract obstruction. The chemical composition of uroliths recovered from these calves was calcium apatite. Elevated dietary magnesium has been shown to be a cause of urolithiasis in growing male calves. Additional dietary calcium, but not phosphorus, appears to protect calves against urolithiasis induced by elevated dietary magnesium.
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PMID:Dietary magnesium and urolithiasis in growing calves. 380 29

The cardiovascular effects of adenosine-induced hypotension were studied in 47 patients undergoing intracranial vascular surgery under neurolept anesthesia. Adenosine infusion (214 +/- 18 micrograms X kg-1 X min-1) decreased mean arterial pressure (MAP) by 42 +/- 1% from 80 +/- 1 to 46 +/- 1 mm Hg for an average of 29 +/- 5 min of hypotension. Hypotension was associated with a minor increase in heart rate (13 +/- 2%) and with prolongation of the PR interval (9 +/- 2%). ST-T depression did not occur except in one patient with a previous history of myocardial infarction. The adenosine-induced increase in cardiac index (42 +/- 9%, n = 7) was associated with a 63 +/- 10% decrease in systemic vascular resistance index (n = 7) while the pulmonary capillary wedge pressure remained unchanged. Adenosine metabolism was limited and there was no accumulation of the end metabolite, uric acid. Serum creatinine levels were normal in all patients postoperatively. We conclude that adenosine rapidly induces a stable and easily controlled hypotension in man without tachyphylaxis or rebound hypertension. There were no signs of renal or myocardial dysfunction except for dysrhythmias that occurred in two patients with a history of myocardial infarction.
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PMID:Clinical experience with adenosine for controlled hypotension during cerebral aneurysm surgery. 382 65

Drug-induced nephrotoxicity (NT) has become an increasingly significant clinical problem. An in vitro model of drug-induced NT was therefore developed using gentamicin and the effects of ATP-MgCl2 on reduction or prevention of NT were determined. To study this, non-pulsatile perfusion in isolated rat kidneys was maintained at 100 mm Hg during 2 hr of perfusion at 37 degrees C. The oxygenated Krebs-HCO3 perfusate contained 7.5 g/dl albumin as colloid, glucose, creatinine, amino acids, trace amounts of [3H]inulin and 125I-lysozyme, and either 0, 0.4, 0.8, or 1.2 mg/ml of gentamicin. In some studies, 2 mM ATP-MgCl2 was added with 0.8 mg/ml of gentamicin at 0 and 60 min of perfusion. During each 10-min clearance period, glomerular filtration rates, sodium absorption, water absorption, and fractional clearance of TCA-precipitable lysozyme were measured. The results indicate that renal perfusate flow, glomerular filtration rate, urinary flow and tubular absorption of protein (a sensitive indicator of tubular function), sodium, and water were affected by gentamicin in a dose-dependent manner. An isolated kidney preparation can therefore be used to study gentamicin-induced NT. Higher in vitro perfusate concentrations of the drug were needed, however, to acutely mimic the in vivo cumulative effects. Nonetheless, renal perfusate flow, glomerular filtration rate, and the depression in protein reabsorption which occurred with gentamicin treatment were markedly improved by simultaneous treatment with ATP-MgCl2. Thus, ATP-MgCl2 may be useful in reducing drug-induced nephrotoxicity.
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PMID:Reduction of the drug-induced nephrotoxicity by ATP-MgCl2. II. Effects on gentamicin-treated isolated perfused kidneys. 387 64

The effects of 2 days of oral dosing with sulindac (200 mg twice a day) or indomethacin (75 mg twice a day) on glomerular filtration rate, urinary excretion of prostaglandin E2, sodium homeostasis, and other renal function parameters were investigated in eight patients with chronic stable impaired renal function. Indomethacin reduced creatinine clearance (from 41.0 +/- 7.9 to 30.3 +/- 6.3 ml/min) and increased serum levels of creatinine and beta 2-microglobulin. Sulindac had no effect on any of these parameters. Both drugs induced depression of urinary prostaglandin E2 excretion; this depression was greater after indomethacin. Urinary sodium excretion fell from 144.4 +/- 18.7 to 85.5 +/- 9.7 mmol/24 hr after indomethacin and from 131.7 +/- 11.6 to 103.4 +/- 13.3 mmol/24 hr after sulindac. Body weight increased 1.2 kg after indomethacin but was not changed by sulindac. Plasma renin activity was reduced from 2.3 +/- 0.8 to 1.7 +/- 0.6 nmol/L/hr by sulindac and from 2.8 +/- 0.8 to 1.5 +/- 0.5 nmol/L/hr by indomethacin. Urinary N-acetyl-beta-glucosaminidase and kallikrein excretion was not changed by either drug. Our data suggest that sulindac affects renal prostaglandin E2 synthesis and sodium excretion in patients with severe renal failure to a lesser extent than does indomethacin. Sulindac still seems to be the drug of choice in this group of patients, but glomerular filtration rate, body weight, and electrolyte balance should be carefully monitored.
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PMID:Acute renal effects of sulindac and indomethacin in chronic renal failure. 388 24

We measured total and free plasma cortisol, 24-hour urinary cortisol excretion, and corticosteroid-binding globulin in 21 normal subjects, 25 patients with depressive illness, and 6 patients with Cushing's disease. Patients with depression had mean 24-hour plasma (8.3 +/- 2.7 micrograms/dl) and urinary (36 +/- 33.55 micrograms/g creatinine) cortisol levels that did not differ from those of normal subjects (6.6 +/- 1.7 microgram/dl; 24.6 +/- 15.4 micrograms/g creatinine), but were significantly lower than those of patients with Cushing's disease (14.4 +/- 2.4 micrograms/dl; 215 +/- 101 micrograms/g creatinine). Not all patients with depression had hypercortisolemia, and the 1-mg dexamethasone suppression test identified some of those with adrenal hyperfunction. 17 of 25 patients had normal 8 a.m. and/or 4 p.m. plasma cortisol after dexamethasone (suppressors), while 8 patients had values greater than 5 micrograms/dl (nonsuppressor). Suppressors had normal total 24-hour plasma and urinary cortisol, while nonsuppressors had levels that were in the range seen in Cushing's disease. Patients with depression showed the expected circadian variation in total and free cortisol, but nonsuppressors had elevated levels in evening and early a.m. hours when levels in normal subjects were low. Patients with Cushing's disease had elevated levels throughout the day. The mean binding capacity of corticosteroid-binding globulin was not different in normal and depressed subjects (23.9 +/- 3.2 vs. 22.2 +/- 3.4 micrograms/dl), but was significantly decreased in patients with Cushing's disease (15.7 +/- 3.5 micrograms/dl). Although total cortisol levels were similar, nonsuppressors had significantly lower mean 24-hour plasma free cortisol (1.01 +/- 0.27 microgram/dl) than patients with Cushing's disease (2.4 +/- 0.54 microgram/dl).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of adrenal cortical function in patients with depressive illness and Cushing's disease. 394 Sep 37

After surgical placement of end-to-side portacaval shunts (PCS), 4 adult mongrel dogs (11.8 to 18.2 kg) were fed purified diets and monitored for approximately 50 weeks for changes in body weight, neurologic status, and an array of clinically important biochemical variables. Two healthy dogs, fed the same diets and maintained in the same environment, were also observed (controls). Body weights were relatively stable over the period of observation. The branched-chain ratio ([valine] + [leucine] + [isoleucine]/[phenylalanine] + [tyrosine]), an index of the degree of change in plasma amino acid concentrations, was significantly lower in dogs with PCS than in controls. Despite this depression in branched-chain ratio, the principals (dogs with PCS) were essentially free of neurologic symptoms. Statistically significant decreases due to portacaval shunting were seen in the serum concentrations of glucose, calcium, urea nitrogen, creatinine, cholesterol, and albumin. Total protein, globulin, and triglyceride concentrations tended to be lower in the serum of principals than in serum of controls, but the differences were not statistically significant. Statistically significant increases due to portacaval shunting were seen in plasma concentrations of total conjugated bile acids and sulfobromophthalein retention. Concentrations of the following compounds tended to be higher in serum of principals than in serum of controls: phosphorus, chloride, uric acid, total bilirubin, lactate dehydrogenase, aspartate transaminase, alanine transaminase, and alkaline phosphatase. Liver biopsy at 7 months after operation showed mild-to-extensive atrophy of hepatocytes, mild-to-extensive fibrosis, and collapsed portal veins in all principals examined.
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PMID:Long-term biochemical and physiologic effects of surgically placed portacaval shunts in dogs. 395 18


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