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)

Halothane (1.3 MAC) and ethanol (0.4%) depress albumin synthesis in isolated perfused rat livers (IPRLs). Addition of amino acids prevents depression by ethanol. We have examined the effects of amino acids on albumin synthesis by IPRLs exposed to halothane. Seventeen livers were perfused with a mixture of rat erythrocytes and rabbit plasma. Five were exposed to oxygen/carbon dioxide alone and 12 to oxygen/carbon dioxide with 1.5% halothane. A mixture of 10 essential amino acids was added to the perfusate of six of the halothane-exposed livers to a concentration approximately 10 times the normal rat plasma level. Perfusate concentrations of newly synthesized albumin were measured by radial immunodiffusion, and the rate of synthesis for the 4.25-h study period was calculated. The mean +/- SEM albumin synthetic rate (mg/h per 300-g rat) in the control group (12.13 +/- 1.36) was significantly greater than in the group receiving halothane alone (6.98 +/- 0.92). Amino acid treatment failed to prevent halothane depression of albumin synthesis (8.68 +/- 0.84). Thus, although amino acids block ethanol depression of albumin synthesis, we could show no such effect in rat livers exposed to halothane.
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PMID:Amino acids fail to prevent halothane depression of albumin synthesis: studies in the isolated perfused rat liver. 198 65

A spectrum of cholesterol oxidation derivatives (oxysterols) is generated in food products exposed to heat or radiation in the presence of oxygen. One of these derivatives (cholestan-3 beta,5 alpha,6 beta-triol) was shown to compromise the selective barrier function of cultured vascular endothelial cell monolayers, an action that may initiate atherosclerotic lesion formation. This study sought to investigate the relationship of cholesterol synthesis inhibition by several naturally occurring oxysterols to depression of vascular endothelial cell monolayer barrier function, determined as an increase in albumin transfer across cultured endothelial monolayers. All oxysterols tested caused a variable time- and dose-dependent elevation in trans-endothelial albumin transfer, and they were also able to inhibit cholesterol biosynthesis to varying degrees. Pure cholesterol was without effect on both counts. The correlation between the increase in albumin transfer related to oxysterol exposure and the ability of oxysterols to suppress cholesterol biosynthesis was, however, poor. Moreover, mevinolin, a water-soluble competitive inhibitor of cholesterol synthesis, reduced the rate of cholesterol synthesis to 0.9% of control but did not significantly increase albumin transfer. Cholestan-3 beta,5 alpha,6 beta-triol caused a 660% elevation in albumin transfer while cholesterol synthesis remained at 11% of control. We conclude that changes in endothelial barrier function caused by exposure to the oxysterols examined, but not pure cholesterol, are probably related to factors other than the well-known action of cholesterol biosynthesis inhibition. These findings may have implications in the development of atherosclerosis.
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PMID:Oxysterols, cholesterol biosynthesis, and vascular endothelial cell monolayer barrier function. 199 10

The ability of plasma to bind thyroxine (T4) was examined in the turtle, Pseudemys scripta, in relation to variations in thyroidal state associated with age, sex, environment, and surgical and chemical manipulations. Relative plasma binding activity was assessed by use of binding to [125I]T4 on minicolumns of Sephadex G-25 (fine). Hypothyroidism induced by surgical thyroidectomy (Tx) or goitrogen (Methimazole) treatment resulted in a marked depression of plasma binding (50- to 100-fold) in juveniles, and T4 treatment restored binding after 4-6 weeks in long-term Tx animals and increased levels in intact animals. Among intact turtles or those made slightly hypothyroid by partial thyroidectomy, binding was consistently correlated with plasma T4. For example, juvenile turtles kept under continuous light and constant temperature (28 degrees) for 4.5 months showed a pronounced depression of plasma T4 (2.6 +/- 1.1 ng/ml) and binding capacity compared to animals raised under variable conditions (T4 = 69.6 +/- 22 ng/ml) for the last 2 months. Plasma T3 was less than 1 ng/ml in all cases. Binding levels in adult turtles were similar to juveniles, but females had significantly higher binding levels than males which paralleled differences in their plasma T4 (137 +/- 17.4 vs 83.9 +/- 13.8 ng/ml). These variations in binding were independent of total plasma protein and albumin. Plasma T4 binding measured on Sephadex G-25 was reversible and reduced by addition of exogenous T4. The affinity for T3 was 10- to 100-fold less than for T4. When plasma preincubated with [125I]T4 was electrophoresed on polyacrylamide slab gels (7% nonreducing) only a small percentage of radiolabel was associated with albumin and the majority with a slower migrating protein(s). Addition of unlabeled T4 displaced binding from the slower migrating region to the albumin and dye front (unbound). In contrast, plasma from Tx turtles showed only minimal binding and radiolabel was associated primarily with the albumin fraction. Elution of proteins from gels confirmed that only the slower migrating components bound T4 when tested on Sephadex G-25, and Tx animals lacked this binding component. The protein(s) responsible for most of the T4 binding appears to exist in low concentration. Limited comparative studies with human blood showed a similar binding activity on Sephadex G-25, but electrophoretic mobilities of binding proteins were distinct from those in the turtle. Evidence suggests that this binding protein is not prealbumin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Relation of plasma thyroxine binding to thyroidal activity and determination of thyroxine binding proteins in a turtle, Pseudemys scripta. 212 5

Cholesterol, combined with albumin, induced rapid functional changes in the isolated perfused rat heart. Under constant perfusion pressure, the decline in contractile force and the rate of development of force due to cholesterol was accompanied by an increase in resting tension and a decrease in coronary flow. Such effects were not produced by albumin alone. Depression in contractile force and increase in resting tension were also evident when coronary flow was kept constant; these effect of cholesterol were dependent on time and dose. The findings support the view that cholesterol may affect cardiac function independently of the atherosclerotic lesion in the hypercholesterolemic state.
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PMID:Depression in cardiac contractile force induced by cholesterol. 215 60

Elevation of total protein is the most frequent pathologic finding in the cerebrospinal fluid (CSF) examination. It occurs in a variety of situations, such as inflammation or tumors of the central nervous system (CNS), degenerative disorders, and subarachnoid hemorrhage, or as a result of traumatic taps. It has also been reported, for unknown reasons, in patients with psychiatric disease. In a study of hormone changes in depression, 9 of 24 (38%) patients (13 male, 11 female) were found to have elevated CSF protein levels (greater than 45 mg/dl), whereas no elevations were found in healthy controls (8 male, 9 female). Eight of the patients with the elevated CSF protein levels were male (62%) and one was female (9%). Depressed patients had significantly higher CSF protein levels (44.7 +/- 18.0 mg/dl) than controls (31.5 +/- 6.0 mg/dl) (t = 3.32, df = 30.37, p = 0.002). No relationship was found between CSF protein levels and (1) the use of medication (tricyclic antidepressants, lithium carbonate, or monoamine oxidase inhibitors) or (2) post-dexamethasone suppression test cortisol levels. Female controls, however, tended to have lower protein levels than male controls, whereas female patients had significantly lower levels than male patients. Protein electrophoresis was performed on 21 of the 41 subjects (13 patients, 8 controls). Male patients had nonsignificantly higher absolute concentrations of CSF albumin and the globulin fractions when compared to male controls. These differences in CSF protein do not suggest monoclonal CSF protein production, nor are they the result of this elevated peripheral protein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevated CSF protein in male patients with depression. 222 29

The increased susceptibility to infections after surgery in jaundiced patients is considered to be caused by an impairment of cellular immunity and/or nutritional status. Endotoxins are suggested to play a role in the pathogenesis. However, the mechanism of action is unknown. Germ-free rats were used to study the effect of biliary obstruction in a model with negligible amounts of endotoxin. Cellular immunity, production of tumor necrosis factor (as a mediator of endotoxin toxicity) by peritoneal macrophages, and the nutritional status were assessed. Significant suppression of cellular immunity was found in conventional rats with obstructive jaundice. In contrast, cellular immunity was not suppressed in jaundiced germ-free rats. Large amounts of tumor necrosis factor were spontaneously secreted by peritoneal macrophages of jaundiced conventional rats, whereas macrophages from jaundiced germ-free rats did not. Moreover macrophage activation (expressed in tumor necrosis factor production) was significantly related to suppression of cellular immunity. Weight changes and depression of albumin levels were not different in germ-free and conventional rats after bile duct ligation. The data presented indicate that suppression of cellular immunity in obstructive jaundice is caused by endotoxins, whereas the impaired nutritional status seems to not be affected by the presence of endotoxins.
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PMID:Suppression of cellular immunity in obstructive jaundice is caused by endotoxins: a study with germ-free rats. 229 4

Plasma levels of the N-terminal peptide of proopiomelanocortin (NPP) were measured in rainbow trout, Salmo gairdneri, following treatment of handling stress with or without administration of dexamethasone, adaptation to white and black background, and maintenance on a constant light/dark cycle. Effects of exogenously administered NPP on plasma constituents were also examined to provide insight into the biological significance of NPP. Thirty minutes of handling stress in shallow water had no effect on plasma levels of NPP during and after the stress period, whereas significant increases in plasma cortisol and glucose were observed. Intraperitoneal administration of dexamethasone blocked the stress-induced elevation of plasma levels of cortisol and caused a depression of plasma NPP. No difference was observed in plasma levels of NPP between trout adapted to a white background and those adapted to a black background. No diurnal changes in NPP were observed under an artificial light/dark cycle (14L/10D light cycle, 0500-1900 hr light) in May and September. Thus, plasma levels of NPP were considerably constant under various physiological conditions, and no synchronism was observed between plasma NPP and cortisol, although NPP modifies the corticotropin-induced release of cortisol from the interrenal. Plasma constituents such as cortisol, total protein, albumin, plasma amino nitrogen, glucose, free fatty acid, ketone body, sodium, potassium, calcium, and magnesium were not altered by intraperitoneal injections of NPP (1 or 10 micrograms) once daily for 6 days (total of six injections) or once every other day for 28 days (14 injections). High concentrations of NPP were found in the plasma 24 hr after cessation of the serial injections of NPP (10 micrograms), suggesting slow metabolic clearance of the peptide.
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PMID:Plasma profiles of the N-terminal peptide of proopiomelanocortin in the rainbow trout with reference to stress. 229 28

To evaluate the effect of various anesthetic agents on hyperosmolar blood-brain barrier disruption (BBBD), Sprague-Dawley rats were given pentobarbital (PB), ketamine-xylazine (KX), isoflurane (IF), methoxyflurane (MF), or fentanyl-droperidol (FD) before intracarotid infusion of mannitol or saline. Physiological monitoring showed that the effects of mannitol infusion differed significantly from those of saline infusion and were associated with transient bradycardia, hypotension, metabolic acidosis, and electroencephalographic depression. With PB, KX, or IF anesthesia, we obtained excellent BBBD as evidence by 3+ Evans blue staining of the mannitol-infused cerebral hemisphere. FD anesthesia was associated with tachycardia and MF anesthesia resulted in hypotension; both showed poor Evans blue staining. Radioisotope delivery to the disrupted hemisphere averaged 0.80% of the administered 125I-albumin compared to 0.03% in the contralateral and 0.06% in control (saline-infused) hemispheres. 99mTc-glucoheptonate delivery measured 0.49% of the administered dose after BBBD, 0.03% contralaterally, and 0.05% in control hemispheres. Pharmacological manipulation to normalize the cardiac index in the FD and MF groups resulted in 3+ Evans blue staining and significantly increased delivery of albumin and glucoheptonate. This study suggests that the cardiovascular changes of these specific anesthetic agents are important in obtaining optimal hyperosmolar BBBD.
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PMID:The effects of anesthesia on osmotic blood-brain barrier disruption. 230 75

Treatment of mice with interferon and interferon inducers causes down regulation of a number of hepatic proteins. In a previous publication it was demonstrated that these treatments depress hepatic protein synthesis and increase protein degradation, particularly of the endoplasmic reticulum Gooderham NJ and Mannering GJ, Arch Biochem Biophys 250: 418-425, 1986. In the present study the effects of polyriboinosinic acid.polyribocytidylic acid (poly IC) treatment on mouse hepatic RNA levels and the translation of this RNA in a cell-free system were examined. Poly IC treatment of mice increased hepatic poly (A+) RNA levels. The translation of isolated poly(A+)RNA was evaluated at various intervals after the administration of poly IC. Translation was marginally increased at 3-6 hr after treatment and depressed after 12-18 hr. Antibodies were employed to examine the effects of poly IC treatment on specific polypeptides in order to evaluate the in vitro translation of mRNAs for tyrosine aminotransferase and albumin; translation of these proteins was biphasic with pronounced depression. These studies indicate that in vivo interferon may regulate gene expression by altering levels of hepatic proteins via increased transcription and decreased translation.
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PMID:In vitro translational activity of messenger-RNA isolated from mice treated with the interferon inducer, polyriboinosinic acid.polyribocytidylic acid. 231 Apr 11

To examine how fat might influence the metabolic effects of tumour necrosis factor alpha (TNF alpha), human recombinant TNF alpha was given intravenously to rats that had been fed for 12 weeks on diets containing (g/kg) 200 maize oil or 190 coconut oil + 10 maize oil. Rectal temperature and tissue composition measurements were made 8 and 24 h after injection. Ambient temperatures of 20 degrees and 25 degrees were employed to accentuate rectal temperature changes. Doses of 30 and 300 micrograms TNF alpha/kg body-weight were given, and brought about depression of serum zinc and albumin and elevation of copper. Muscle protein content was decreased and liver protein and Zn content enhanced by TNF alpha. Serum Zn and liver Zn content were negatively correlated 8 h after injections. Hypothermia developed within 1 h of injection. All responses except the rise in serum Cu and gain in liver Zn were more intense at the higher than at the lower dose of TNF alpha. Hypothermia was exacerbated by an environmental temperature of 20 degrees. The coconut-oil diet blunted the hypothermia and likewise the changes in serum albumin and Cu content 8 h after injections and in muscle and liver protein after 24 h. Changes in eicosanoid metabolism may be involved in the modulatory effects of the coconut-oil-enriched diet.
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PMID:Dietary fat modifies some metabolic actions of human recombinant tumour necrosis factor alpha in rats. 238 39


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