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)

Attempts were made to develop an animal model for phytosterolemia. Infusion of Intralipid containing 0.2% sitosterol in rats gave circulating levels of sitosterol of about 2.5 mmol/l, which is similar to or higher than those present in patients with untreated phytosterolemia. In addition, the infusions gave serum levels of cholesterol nearly twice those obtained in rats infused with Intralipid alone or Intralipid containing 0.2% cholesterol. The hepatic HMG-CoA reductase activity was unaffected or slightly increased by the sitosterol infusions (not statistically significant). The cholesterol 7 alpha-hydroxylase activity was slightly depressed (ca. 30%). In the case of 7 alpha-hydroxylation of endogenous cholesterol, the depression reached statistical significance (p less than 0.05). The microsomal content of sitosterol in the sitosterol-infused rats was about 30% of that of microsomal cholesterol. The effect of sitosterol on 7 alpha-hydroxylation of cholesterol was investigated by incubations of acetone powder of rat liver microsomes with mixtures of cholesterol and sitosterol. Sitosterol mixed with cholesterol to a composition similar to that found in the above microsomal fraction had a depressing effect on 7 alpha-hydroxylation of cholesterol. This degree of depression was of the same magnitude as that found in the sitosterol infusion experiments. The possibility is discussed that the hypercholesterolemia obtained in the beta-sitosterol-infused rats is due to the inhibitory effect of sitosterol on the cholesterol 7 alpha-hydroxylase.
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PMID:Effect of sitosterol on the rate-limiting enzymes in cholesterol synthesis and degradation. 274 37

The conventional "stepped-care" approach to the treatment of hypertension deserves revision. Rational therapy considers a variety of factors to obtain maximum efficacy, safety, tolerability, compliance, and neutralization of neural tone for the prevention of sudden death. The patient's age, gender, race, behavior profile, hemodynamic and neurohumoral status (plasma renin activity, norepinephrine/epinephrine ratio), and quality of life will help determine the choice of antihypertensive agent. Concomitant risk factors (smoking, obesity, diabetes, hypercholesterolemia), the presence of sequelae (left ventricular hypertrophy and/or failure, renal failure), and the existence of other disorders (mitral valve prolapse, depression, anxiety) must also be considered when initiating treatment. In addition, the cost of ancillary expenses (laboratory tests, hospitalizations, and emergency room visits) must be weighed against the potential benefits of therapy. Beta blockers are effective, well tolerated, and versatile for the treatment of concomitant cardiovascular disorders and as behavior modifiers. Calcium channel blockers and angiotensin converting enzyme inhibitors also show promise and merit consideration as therapy for specific groups of hypertensive patients.
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PMID:The 1980s: a patient-specific therapeutic approach in hypertension. 288 36

In a two years reinfarction study including all patients suffering from myocardial infarction in the district of Cottbus (900000 inhabitants) between the 1.1.1981 and 31.8.1983 (totally 701 patients) we found a statistically significant lower rate of reinfarctions, in patients over 60 years also of the total mortality treated with 30 mg aspirin per day compared with 1000 mg per day. A statistically significant superiority of the 30 mg aspirin dosage compared with the 1000 mg dosage was found in patients aged over 50 years, in male patients, in patients with angina pectoris in their anamnesis, in patients with ST-depression of greater than 0.5 mm 2 weeks after the cardiac event, in patients with all kinds of infarct localization except posterior myocardial infarction and in patients with hypercholesterolaemia (greater than = 7.3 mmol/l).
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PMID:Superior prevention of reinfarction by 30 mg/d aspirin compared with 1000 mg/d: results of a two years follow-up study in Cottbus. 307 65

An analysis of 1,600 consecutive treadmill exercise tests is made, with emphasis on those with an ischaemic response. An ischaemic response is defined as a horizontal or downsloping depression of the ST segment of 1 mm or more. A hypertensive response is recorded where the blood pressure exceeds 200 mm Hg systolic or 100 mm Hg diastolic during exercise. There were 150 (9%) ischaemic responses and 279 (17%) hypertensive responses. Cardiac arrhythmias were detected in 173 (11%) subjects. Among the 150 subjects with ischaemic responses, 69 (46%) of them presented with anginal symptoms while 64 (43%) of them had no precordial pain. Twenty-seven (18%) of them had definite previous myocardial infarction. Risk factors observed included hypertension in 54 (36%) subjects, diabetes mellitus in 33 (22%) subjects, hypercholesterolaemia in 41 (37%) out of 112 subjects and 44 (29%) cigarette smokers.
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PMID:Treadmill exercise testing in ischaemic heart disease. 368 10

Swiss-Webster mice fed a diet containing 0.5% cyclopropenoid fatty acids (CPFA) for 6 weeks showed depressed growth rates and developed hypercholesteremia and increased concentrations of serum phospholipid and free cholesterol compared to control mice. No depression of cytochromes P-450 and b5 or microsomal mixed-function oxidase activities occurred to indicate impaired oxidative catabolism of serum cholesterol. Elimination of intragastrically administered [3H]cholesterol from blood was biphasic; there was no significant difference in first-order rate constants for absorption, distribution, and elimination processes between control and CPFA-fed animals. However, the area under the blood clearance curve for CPFA-fed animals was significantly increased (p less than or equal to 0.01) by 29% over controls, demonstrating a net increase in clearance time for exogenous cholesterol in CPFA-fed animals, thus contributing to their hypercholesteremia. In the CPFA-fed mice, the percentage of saturated fatty acid residues increased at the expense of monounsaturates in the cholesterol ester, triglyceride, and phosphatidyl choline fractions of serum lipids. Total polyene content of serum lipid was not altered; however, CPFA-fed animals demonstrated increased linoleic acid at the expense of arachidonic acid in all serum lipid fractions. Excessively saturated serum lipids may impede clearance of serum cholesterol in CPFA-fed animals by inhibited plasma lecithin-cholesterol acyltransferase (LCAT) and hepatic cholesterol esterase activities.
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PMID:Altered lipid metabolism and impaired clearance of plasma cholesterol in mice fed cyclopropenoid fatty acids. 392 32

Using data from Lipid Research Clinics study participants at visit 2 (3972 and 2346 adult men and women), we examined the hypothesis that parental mortality from cardiovascular disease (CVD) or cancer before age 60 predicts their adult progeny's lipid and lipoprotein levels. Weighted regression analysis was used to control for the potential effect of progeny's other CVD risk factors (age, systolic blood pressure, Quetelet index, cigarette smoking, and alcohol consumption), and to assess for the effect of progeny's parental cause-specific mortality status on progeny's lipids and lipoproteins. Nearly all of the statistically significant parent-progeny predictions were for sons. Paternal death from CVD before age 60 years was associated with significantly higher plasma total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels in sons and (at marginal significance) in daughters, when compared with those in reference progeny with paternal survival over age 60 or over age 75. Maternal death from CVD before 60 was associated with lower levels of high-density lipoprotein cholesterol (HDL-C) in sons. Paternal and maternal death from cancer before age 60 years were associated with higher triglyceride levels in adult sons than in sons whose parents had lived beyond ages 60 and 75. Paternal all-cause mortality before age 60 was associated with higher cholesterol and triglycerides in sons; maternal all-cause mortality before age 60 was associated with depression of HDL-C in sons. Familial aggregation of lipids and lipoproteins may account, in part, for familial aggregation of CVD. Knowledge of family history facilitates identification of progeny at higher risk for CVD by virtue of elevated cholesterol or LDL-C, or reduced HDL-C.
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PMID:Progeny's lipid and lipoprotein levels by parental mortality. The Lipid Research Clinics Program Prevalence Study. 394 Jun 84

Since hypercholesterolemia sensitizes isolated rabbit coronary arteries to vasoconstrictor stimuli, we assessed the possibility of reproducing occlusive coronary spasm both in vitro and in vivo in atherosclerotic rabbits. In Langendorff-perfused hearts from nine atherosclerotic rabbits (2% cholesterol diet for 18 weeks), despite a threefold increase of cholesterol concentration in the coronary wall compared with nine control rabbits, ergonovine and serotonin did not produce any increase of coronary vascular resistances; the increase produced by pitressin was significantly less in atherosclerotic than in normal hearts (56 +/- 13% vs 138 +/- 28%, p less than 0.05, respectively), whereas that produced by phenylephrine was similar (10.1 +/- 1.8% vs 8.5 +/- 2.4%, p = n.s.). In eight other unanesthetized rabbits we recorded the ECG during ergonovine administration (0.05 mg/kg) and during hypothalamic stimulation before and at regular intervals during the 2% cholesterol diet; rabbits survived for periods ranging from 1 to 22 weeks (mean 9.6 weeks). Only one animal had ST depression during episodes of marked tachycardia; no ischemic ECG changes were ever observed in the other rabbits despite the diffuse subintimal coronary deposition of cholesterol found postmortem. Thus, in atherosclerotic rabbits with chronic marked hypercholesterolemia, coronary arteries do not develop occlusive coronary spasm as observed in patients with variant angina.
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PMID:Failure of experimental atherosclerosis to sensitize coronary arteries to spasm in hypercholesterolemic rabbits. 397 75

Naturally-occurring hyperadrenocorticism was diagnosed in an 11-year-old female Dachshund with signs of polydipsia, polyuria, pendulous abdomen, weakness, depression and lethargy, and laboratory test abnormalities comprising lymphocytopaenia, eosinopaenia, hypercholesterolaemia and increased plasma alkaline phosphatase concentration. While awaiting hormonal test results, an adrenocorticolytic drug (o,p'-DDD) was administered for 14 days, during which the patient deteriorated. Hormonal assays suggested a functioning adrenocortical tumour, but the poor condition of the patient precluded adrenalectomy. An adrenocortical carcinoma with hepatic metastases was found at necropsy.
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PMID:Functioning adrenocortical tumour in a dog. 628 91

Feeding diets with 4% L-lysine to the chick produces an elevation of plasma lipids which does not occur when feeding an excess of any other amino acid. Experiments were conducted to determine whether lysine-induced hyperlipidemia is secondary to the antagonistic effect of lysine on arginine or to the anorexia which accompanies lysine feeding, and in addition, whether the lysine-induced hypercholesterolemia is affected by chick age. In all experiments gain and food intake were reduced by feeding chicks 4% lysine. Plasma cholesterol and triglyceride were elevated, but high-density-lipoprotein cholesterol, as a percentage of total, was reduced. Addition of dietary arginine up to 4% failed to reverse the depression in performance and elevation of plasma lipids. Pair-feeding the control diet to the amount consumed by lysine-fed chicks did not elevate plasma lipids above control levels. Thus, lysine-induced hyperlipidemia is not mediated by the antagonistic effect of lysine on arginine nor by the effect of lysine on food intake. The high-lysine diet prevented the normal decline in plasma cholesterol expected with advancing age of chicks. Preliminary results suggested that excess lysine stimulated cholesterol biosynthesis.
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PMID:Effect of excess dietary lysine on plasma lipids of the chick. 641 75

Male weanling rats were made copper deficient with a purified diet containing all known essential dietary nutrients except copper. Copper deficiency was verified by indirect (anemia, growth retardation, hypercholesterolemia, gross pathology, and abnormal electrocardiograms) and direct (tissue copper analysis) criteria. His bundle electrographic and electrocardiographic changes detected in the copper-deficient group consisted most notably of depressed His-Purkinje system conductivity and S-T segment depression. Phosphorus-31 nuclear magnetic resonance spectroscopic analysis of cardiac, renal, and hepatic tissue perchloric acid extracts revealed significant metabolic changes associated with the dietary copper deficiency, including a generalized marked decrease in ATP and phosphocreatine levels and a corresponding increase in inorganic orthophosphate and ADP levels in the various tissues. Tissue-specific changes consisting of elevated ribose 5-phosphate (heart), phosphocholine (heart), and inosine monophosphate (kidney) and decreased glycerol 3-phosphorylethanolamine (liver) and glycerol 3-phosphorylcholine (liver) levels were detected in copper-deficient rats. Microscopic examination of heart tissue from copper-deficient rats revealed extensive disruption of mitochondrial fine structure, including fragmentation of cristae and inner and outer mitochondrial membranes, which resulted in pronounced vacuolization throughout the tissue. Although the physiological and metabolic disturbances manifested in hearts from copper-deficient animals generally mimic myocardial responses to chronic ischemia, the observed changes are interpreted in a broader context to represent the appearance of a copper-dependent cardiomyopathy.
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PMID:Physiological and metabolic characterization of a cardiomyopathy induced by chronic copper deficiency. 663 5


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