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)

Purified preparations of chitin synthetase (EC 2.4.1.16; UDP-2-acetamido-2-deoxy-D-glucose:chitin 4-beta-acetamidodeoxyglucosyltransferase), capable of forming microfibrils in vitro, were isolated from yeast cells of Mucor rouxii. Chitin synthetase was obtained either by substrate-induced liberation of bound enzyme (54,000 x g pellet) or by isolation of unbound enzyme present in the 54,000 x g supernatant of a cell-free extract. Both preparations contained ellipsoidal granules from about 350 to 1000 A diameter. Many granules exhibited a marked depression. No typical unit membrane profiles appeared in thin sections of glutaraldehyde/OsO4-fixed samples. Upon incubation with substrate and activators, chitin microfibrils were produced. The microfibrils were often found intimately associated with granules. The most common configurations were: a microfibril with a granule at one end, or two microfibrils "arising" from the same granule. These findings lend support to the granule hypothesis for the elaboration of cell wall microfibrils by end-synthesis.
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PMID:Microfibril assembly by granules of chitin synthetase. 105 85

The fine structure of isolated chitin synthetase (UDP-2-acetamido-2-deoxy-D-glucose:chitin 4-beta-acetamido-deoxyglucosyltransferase; EC 2-4-1-16) particles (chitosomes) from Mucor rouxii and the elaboration of chitin microfibrils were studied by electron microscopy. Chitosomes are spheroidal, but often polymorphic, structures, mostly 40-70 nm in diameter. Their appearance after negative staining varies. Some reveal internal granular structure enclosed by a shell measuring 6-12 nm thick; others do not show internal structure but have a pronounced depression of the external surface. In thin sections, isolated chitosomes appear as microvesicular structures with a tripartite shell 6.5-7.0 nm thick. Morphologically similar structures can be seen in intact cells of M. rouxii. Isolated chitosomes undergo a seemingly irreversible series of transformations when substrate and activators are added. The internal structure changes, and a coiled microfibril (fibroid) appears inside the chitosome. The shell of the chitosome is opened or shed, and an extended microfibril arises from the fibroid particle. During prolonged incubation, the fibroid coils become less common and extended microfibrils appear thicker. We regard the chitosome as the cytoplasmic container and conveyor of chitin synthetase en route to its destination at the cell surface. Isolated chitosomes are well suited for integrated ultrastructural-biochemical studies of microfibril biogenesis in vitro.
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PMID:Structure and transformation of chitin synthetase particles (chitosomes) during microfibril synthesis in vitro. 107 6

There was rapid efflux of L-leucine, L-phenylalanine, and alpha-methyl-D-glucoside after infection of Salmonella typhimurium with the clear plaque mutant C1 of phage P22. The efflux was similar to that observed with cyanide or arsenate treatment except that there was partial recovery in the case of phage infection and almost complete recovery under the condition of lysogeny. There was no efflux after infection with the temperature-sensitive mutant ts16C1 at nonpermissive temperature. Superinfection of superinfection exclusion negative lysogen (sie A minus sie B minus) with C1 led to efflux, whereas the efflux was much less on superinfection of sie A+ Sie B+ lysogen. These results indicate that an effective injection process is enough to cause depression in the cellular transport processes.
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PMID:Transport in bacteriophage P22-infected Salmonella typhimurium. 109 32

Although it is generally agreed that active sugar absorption in vitro is absolutely dependent on the presence of sodium ions on the luminal side of the mucosa, previous in vivo studies in the ileum of rat, dog and man have shown that active glucose absorption is almost as rapid from a sodium-free mannitol solution as from a sodium chloride solution. These experiments were performed in hopes of reconciling this discreptancy. Absorption of three actively transported sugars (glucose, galactose, and 3-O-methylglucose) having different apparent Km's, and of fructose (absorbed by a separate carrier-mediated process) were measured in the human ileum in vivo. The following observations were made: (1) Mannitol substitution for sodium results in only a slight reduction (23%) in the active absorption of glucose. (2) Magnesium substitution for sodium results in a greater depression (45%) of glucose absorption. (3) The apparent Km for glucose absorption is increased when sodium is replaced by magnesium, but the Vmax is not altered. (4) Magnesium does not depress glucose absorption or the apparent Km for glucose transport when sodium is present in the perfusing solution. (5) Neither sodium removal nor magnesium has any effect on fructose absorption. (6) Absorption of galactose and 3-O-methylglucose (low affinity sugars for the glucose carrier) is reduced by about 40 to 50% when mannitol replaces sodium, but magnesium substitution for mannitol in a sodium-free medium does not further depress absorption of these sugars. The following conclusions are suggested by these results: First, part of the discrepancy between previous in vitro and in vivo experiments was due to the type of test sugar (glucose versus glucose analogue) and the solute used to replace sodium in the luminal solution. Second, magnesium is more effective than mannitol in reducing sodium concentration at the glucose transport site on the brush border. Third, luminal sodium ions have an important effect on active sugar absorption in the human small intestine in vivo, as they do in vitro. And, fourth, there is a component of active sugar absorption (about one-half) which appears to be independent of luminal sodium ions in vivo.
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PMID:Effect of sodium, mannitol, and magnesium on glucose, galactose, 3-O-methylglucose, and fructose absorption in the human ileum. 111 66

Anaesthesia and surgery are known to depress granulocyte function in the early postoperative period, leading to deterioration of the immune defence against infection. Carbohydrate-lectin interactions may play an important role in the activities of phagocytic cells in that they facilitate initial host defence in the event of microbial antigenic challenge. A panel of biotinylated (neo)glycoproteins (chemically glycosilated carrier proteins) was used to detect endogenous carbohydrate-binding receptors /lectins/, on peripheral blood polymorphonuclear leukocytes of patients undergoing prolonged anaesthesia for replantation surgery. Four hours after induction of anaesthesia, a progressive decline of expression of endogenous sugar receptors on granulocytes was detected using the labelled (neo)glycoproteins lactose-BSA, N-acetyl-D-glucosamine-BSA, D-mannose-BSA, sialic-acid-BSA and D-xylose-BSA. Concomitant changes in peripheral white blood cell counts and the lack of depression in the absence of general anaesthetic agents suggested the existence of a possible relationship between reduced expression of (neo)glycoprotein receptors to impaired granulocyte function and anaesthetic-induced immunodepression.
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PMID:Changes of expression of endogenous sugar receptors by polymorphonuclear leukocytes after prolonged anaesthesia and surgery. 137 52

We measured regional cerebral glucose metabolism using 2-[18F]-fluoro-2-deoxy-D-glucose and positron emission tomography in depressed and nondepressed patients with early Huntington's disease (HD), compared with appropriately matched controls. Caudate, putamen, and cingulate metabolism was significantly lower in patients with HD than in control subjects, independent of mood state. Orbital frontal-inferior prefrontal cortex hypometabolism, however, differentiated depressed patients from both nondepressed patients and normal controls. These findings implicate selective dysfunction of the paralimbic regions of the frontal lobes in the mood disorder of HD. The metabolic pattern is similar to that in depression associated with Parkinson's disease, suggesting that the integrity of pathways linking paralimbic frontal cortex and the basal ganglia may be integral to the normal regulation of mood.
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PMID:Paralimbic frontal lobe hypometabolism in depression associated with Huntington's disease. 138 63

Although hepatocellular dysfunction occurs early in sepsis despite fluid resuscitation, it is unknown if an increased volume of resuscitation protects hepatocellular function. To study this, rats were subjected to sepsis by cecal ligation and puncture (CLP). These and sham-treated rats then received either 3 or 6 mL/100 g BW normal saline subcutaneously. Studies were performed at 5 hours (i.e., early sepsis) or 20 hours (late sepsis) after CLP. Hepatic blood flow was determined by radioactive microspheres, 3H-galactose clearance technique, and laser Doppler flowmetry in both groups. Active hepatocellular function (i.e., Vmax and Km) was assessed by an in vivo indocyanine green clearance technique. The results indicate that: (1) hepatic blood flow increased markedly in early sepsis; (2) Vmax and Km decreased significantly at 5 hours and 20 hours after CLP; and (3) the increased volume of fluid resuscitation did not improve the depressed active hepatocellular function 5 hours following CLP. Cardiac output and hepatic microcirculation, however, were significantly increased in early sepsis. These results confirm the notion that the depression in hepatocellular function in early sepsis is not the result of any reduction of hepatic perfusion. The dissociation of increased hepatic blood flow from depressed hepatocellular function remains despite the larger volume of resuscitation. The hepatocellular dysfunction that occurs even in early sepsis cannot be corrected simply by increasing the volume of crystalloid resuscitation.
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PMID:Hepatocellular dysfunction persists during early sepsis despite increased volume of crystalloid resuscitation. 154 29

Lens myo-inositol (MI) content is regulated by a pump-leak system consisting of an active Na-dependent MI transport and its passive permeability through the membrane. We measured the active MI uptake and membrane permeability in lenses of rats maintained on a 50% galactose diet for 1, 3 and 7 days. After only 1 day of galactose feeding, active MI uptake in the lens was reduced dramatically by 74% compared to age-matched control lenses; by day 3, active MI transport was decreased by 89% and it was undetectable by day 7. The passive membrane permeability was determined by measuring (a) the passive MI influx and (b) the 3H-sorbitol flux. After 1 day of galactose feeding, the membrane permeability increased such that within 3 days it increased to 5-6 fold. Galactose feeding also led to a rapid increase in lens polyol content. After 1 day, lens polyol increased to 53 mumol/g wet wt compared to a control value of 0.35 mumol/g wet wt and increased further to 65 and 72 mumol/g wet wt after 3 and 7 days of galactose feeding respectively. Lens galactose accumulation was low (3 mumol/g wet wt) up to 7 days; however, it was rapidly increased after 7 days. Our results indicate that galactose feeding rapidly interfered with MI homeostasis by a severe depression of active MI transport and a rapid increase in membrane permeability. These interferences of MI homeostasis correlate with the appearance of high polyol levels.
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PMID:Myo-inositol transport in the lens of galactose-maintained rats. 155 89

In this study, whole body insulin action on glucose uptake and muscle glucose transporter number of rats subjected to 14 days of physical inactivity conditions was examined. Unlike other suspension and denervation models of muscle disuse, this physical inactivity model allows voluntary contractile activity with minimal stress. Minimal depression of body weight gain and significant depression of gastrocnemius muscle growth were observed compared with that of control rats after 14 days of physical inactivity. The whole body insulin sensitivity and responsiveness were determined by the euglycemic clamp technique, with 1.4, 3.6, and 14 mU insulin.kg-1.min-1 perfusion and 2-deoxy-D-[3H]glucose incorporation. The rates of glucose disposal were the same in the restrained rats as in the controls with the 1.4 and 3.6 mU insulin perfusion; however, glucose disposal significantly decreased with 14 mU insulin perfusion. 2-Deoxy-D-[3H]glucose uptake into the gastrocnemius muscle was higher in the control rats than in the physically inactive rats. Glucose transporters in the gastrocnemius and quadriceps muscles, measured by means of the D-glucose-inhibitable cytochalasin B binding assay, were significantly decreased in number in the physically inactive rats. These findings suggest that the decrease in whole body glucose uptake might in part be explained by the decreases in the total glucose transporter number in muscles.
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PMID:Decrease in muscle glucose transporter number in chronic physical inactivity in rats. 167 41

The rapid infusion of vancomycin produces histamine release resulting in rash ("red-man's" syndrome) and hypotension. Because this phenomenon has been described primarily in healthy subjects, we prospectively studied the rapid infusion of vancomycin in 16 critically ill patients after open heart surgery in an attempt to document histamine release with resulting hemodynamic changes, and to see if there is any correlation with vancomycin levels. After establishing baseline hemodynamic stability and histamine levels, 1 g vancomycin diluted in 50 mL of 5% dextrose was infused over 30 min. Cardiac index, heart rate, blood pressure, pulmonary venous pressures, and systemic and pulmonary vascular resistances remained unchanged during the infusion. Although the mean plasma vancomycin level increased to a peak of 69 +/- 20 micrograms/mL after 20 min of the infusion before declining, mean plasma histamine levels in 15 of the 16 patients remained within the normal range during the infusion. In one patient a baseline histamine level (2.8 ng/mL) more than three times the normal before the vancomycin infusion increased further during the infusion (3.0, 4.9, and 5.0 ng/mL at t = 10, 20, and 30 min, respectively), and remained elevated (2.9 ng/mL) 30 min after the infusion. This patient developed the red-man's syndrome, although there were no hemodynamic changes. There was no evidence of myocardial depression in any of the patients. In conclusion, we safely infused a concentrated solution of vancomycin into critically ill patients over 30 min without any adverse hemodynamic changes. One patient developed the red-man's syndrome. There was no correlation between peak vancomycin levels and the release of histamine in this patient population.
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PMID:Hemodynamic effects of rapid vancomycin infusion in critically ill patients. 169 40


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