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)

A kinetic analysis of cyclic 3',5'-adenosine monophosphate (cAMP) synthesis in an adenine auxotroph of Escherichia coli 3000 was made by assaying the incorporation of [3H]adenine into cAMP during exponential growth. The rate of increase in intracellular [3H]cAMP was very slow (0.1-0.2 pmol/min/DU660). The steady state level was attained at about 40-min incubation after the addition of [3H]adenine, and was estimated to be 5 to 7 pmol/DU660. The rate and level of intracellular cAMP were scarcely affected by growth conditions, such as change of carbon source, whereas the excretion of cAMP into the medium began immediately after the addition of [3H]adenine, and continued at a rate of 5 to 7 pmol/min/DU660 in the glycerol medium. The excretion rate decreased to 1.4 pmol/min/DU660 in the presence of glucose. These results are inconsistent with the view that the excretion rate is dependent on the intracellular concentration of cAMP. Although the decreased rate of cAMP synthesis in the presence of glucose accounts for the permanent catabolite repression of inducible enzyme systems, no immediate depression in cAMP synthesis, which might account for the transient repression, was found after the addition of glucose.
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PMID:Novel aspect of cyclic 3',5'-adenosine monophosphate synthesis in Escherichia coli 3000A1. 630 92

The production of extracellular 1,3-, 1,6-beta-glucanases and chitinase was studied during submerged cultivation of a Trichoderma viride strain 3/78 on various carbon sources: glycerol, glucose, lactose, sucrose, laminaran, starch, pustulan, chitin, and Agaricus bisporus fruit bodies. The synthesis of these enzymes and cellulase was studied also under the conditions of depression at low concentrations (10(-2) and 10(-3)M) of the first five aforementioned carbon sources as well as cellobiose, gentiobiose, N-acetyl-beta-D-glucosamine and 0.1% chitooligosaccharides and A. bisporus cell walls. The experiments were conducted with the washed mycelium of this strain grown for 2 days in a medium with glycerol as a carbon source. The results indicated that 1,3- and 1,6-beta-glucanases of the strain were of the constitutive nature and were repressed by such carbon sources as glycerol and glucose. Chitinase and cellulase were shown to be inducible enzymes. Chitinase was induced by N-acetyl-beta-D-glucosamine, chitooligosaccharides and A. bisporus cell walls as well as by lactose when the fungus was grown on this carbon source. Cellulase biosynthesis was induced by lactose, cellobiose and gentiobiose.
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PMID:[Beta-glucanase and chitinase biosynthesis in a culture of a mycophilic strain of Trichoderma viride]. 642 Jun 49

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

Following preincubation of isolated rat liver mitochondria in the absence of substrate, the carnitine-independent oxidation of octanoate or butyrate was markedly depressed when compared to rates observed with nonpreincubated mitochondria. Carnitine addition prevented the inhibition of octanoate oxidation but not that of butyrate. 2-Tetradecylglycidic acid or Zwittergent 3-08 (Z3-08) completely blocked the effect of carnitine. Replacement of ATP in the nonpreincubated incubation system with ADP mimicked the effect of preincubation by inhibiting octanoate and butyrate oxidation. This inhibition of octanoate oxidation was also prevented by carnitine addition. There was a direct and causal relationship between the ATP/ADP ratio of the total adenine nucleotide pool and the rate of carnitine-independent octanoate oxidation in mitochondria. The depression of octanoate oxidation was associated with a decrease in the intramitochondrial AMP content and intra- and extramitochondrial ATP/ADP ratios. In a cellular system, incubating isolated hepatocytes with fructose or glycerol to lower the ATP/ADP ratio resulted in greater inhibition of octanoate oxidation by 2-tetradecylglycidic acid. The data suggest that the ATP/ADP ratio may have a role in determining the site of octanoate activation and subsequent route of oxidation.
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PMID:Relationship of the ATP/ADP ratio to the site of octanoate activation. 671 56

The purpose of this study was to examine proximal and distal tubular function in rats with nonoliguric, myohemoglobinuric acute renal failure (ARF). ARF was induced with glycerol (50%, 10 ml/kg of body wt, i.m.), and renal function was studied 24 hours after glycerol or saline (controls) injection. Glycerol injection caused a 50 to 90% depression in GFR and a significant rise in blood urea nitrogen concentration. Animals with ARF exhibited glycosuria with normal blood sugar levels and a striking depression in tubular glucose reabsorption per milliliter of GFR. The capacity to reabsorb (mEq/liter GFR) was intact at normal blood bicarbonate levels, but was markedly depressed when blood bicarbonate was raised. The tubular maximum for para-aminohippurate (PAH) secretion and the renal extraction fraction of PAH were strikingly depressed in rats with ARF. Distal acidification as assessed by the urine-to-blood gradient of PCO2 (UB PCO2) was normal both during maximal alkalinization of the urine with bicarbonate (urine pH, approximately 7.8) or during neural phosphate infusion (urine pH, approximately 7.0). Net acid excretion per milliliter GFR and minimal urine pH (less than 5.5) following 3 days of ammonium chloride ingestion was similar in control and ARF animals. Potassium excretion was intact in maximal urinary osmolality were significantly altered in animals with ARF. Cortical and outer medullary Na-K-ATPase specific activities were significantly depressed in ARF rats. This occurred as a consequence of enzyme loss and not secondary to alterations in enzyme kinetics of absolute tubular sodium reabsorption. Light and electron microscopy showed diffuse proximal tubular damage, whereas glomeruli and distal tubules were intact. These data demonstrate that glycerol injection produces a diffuse proximal tubular transport defect associated with histologic and enzymatic alterations.
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PMID:Renal tubular function in glycerol-induced acute renal failure. 678 13

The freezing-tolerant gall fly larva, Eurosta solidaginis, provides an excellent model system for the study of metabolic adaptation and metabolic control for low-temperature survival during overwintering. Low-temperature acclimation of the larvae results in dramatic alterations in metabolic flux producing a sequential synthesis of two cryoprotectants, glycerol at warmer temperatures followed by sorbitol when larvae are exposed to 5 degrees C. Regulation of metabolism in the larvae appears to exploit temperature change, temperature effects on enzyme kinetics, and temperature/modulator interactions with enzymes producing the alterations in metabolic flux leading to differential polyol synthesis. For instance, temperature/modulator effects on phospho-fructokinase appear to be the major factor halting carbon flow into glycerol synthesis at low temperatures and diverting flux instead into the pathway of sorbitol synthesis. Alterations in the cellular content of bound water and the metabolic pools of free versus bound soluble metabolites may also have important regulatory consequences for low-temperature metabolism. Bound water content of the larvae increases with low-temperature acclimation and is attributable to changes in water binding by both low-molecular-weight (polyols) and high-molecular-weight (proteins, glycogen) subcellular components. A restrictive effect of high bound water content may be one factor causing the strong depression of metabolic activity seen in the larvae as a result of extracellular freezing. In addition, bound water may have a more subtle effect in determining the relative pool sizes of bound versus free metabolites in the cell. 31P-NMR studies of whole larvae show that the content of free phosphorylated intermediates in the cell diminishes with decreasing temperatures despite a measured constancy in the total pool size of these intermediates. An increase in the content of bound metabolites with low temperature may restrict metabolism by limiting the availability of substrates and effectors of enzyme reactions.
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PMID:Metabolism and bound water in overwintering insects. 688 77

The addition of many oxidizable substrates to the medium of incubating rat renal slices decreases ammoniagenesis from glutamine and glutamate. Interestingly, lactate and beta-hydroxybutyrate depress ammoniagenesis less in renal slices from acidotic rats compared with normal-control rats. In this study, the effects of an expanded panel of substrates on ammoniagenesis in kidney slices from control and acidotic rats were followed to discern patterns of inhibition. In addition to lactate and beta-hydroxybutyrate, acetate, pyruvate, and perhaps acetoacetate caused relatively less depression of ammoniagenesis in acidotic slices. Citrate, succinate, fumarate, octanoate, and alpha-ketoglutarate decreased ammoniagenesis to the same extent or more in acidotic slices compared with that in normal-control slices. Glycerol had little effect on ammoniagenesis under either condition. From the substrates tested, it can be generalized that those outside the TCA cycle (with exception of octanoate) depress ammoniagenesis less during acidosis, while those in the TCA cycle depress ammoniagenesis equally or even more during acidosis. We hypothesize from the pattern of our results that changes in renal intermediary metabolism at or before citrate formation occur during acidosis and are important regulatory mechanisms for ammoniagenesis.
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PMID:The regulation of renal ammoniagenesis in the rat by extracellular factors. III. Effects of various fuels on in vitro ammoniagenesis. 688 70

Cutaneous pectoris muscles of Rana pipiens were transected distal to the innervated region. Within 10 min, membrane potentials (Em's) of -33 +/- 2.5 mV and end-plate potentials (3-15 mV) were recorded unaccompanied by muscle action potentials or twitch. The fall in Em was associated with a net loss of [K+]i and a net gain of [Na+]i. Although input resistance fell by 50% and the space constant was slightly reduced in the transected muscle fibers, end-plates could be adequately voltage-clamped with two microelectrodes. End-plate currents (e.p.c.s) with rise times of 350 to 700 musec were recorded as a function of holding potential (Vm). The current-voltage relationship of peak e.p.c.s over the range of -70 to +20 mV was linear and the reversal potential (-6.6 +/- 2.2 mV) was the same as that found for intact muscle fibers. The decay phase of e.p.c.s could be described as a single exponential at all Vm's and had a voltage and temperature dependence similar to that described for e.p.c.s of glycerol-treated muscles. Tubocurarine (0.3 microM) caused a significant decrease in the time constant (tau) of e.p.c. decay and e.p.c. amplitude. The depression of e.p.c. amplitude by tubocurarine was reversed by 4-aminopyridine while the decrease of tau was not. Atropine (10(-4) M) caused a monotonic shortening of e.p.c.s at a Vm of -90 mV but e.p.c.s recorded at +50 mV were biphasic. Lidocaine, a quaternary nitrogen analog of lidocaine (QX314), lobeline and hexafluorenium were studied also in transected muscle and their effects on the parameters of e.p.c. are described. Both lobeline (50 microM) and hexafluorenium caused a decrease of tau and eliminated the voltage dependence of tau at negative Vm's. The transected muscle can be used for the study of conductance kinetics of end-plate and for the study of drug action uncomplicated by the presence of other drugs of Mg++ to eliminate contraction.
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PMID:Characterization of end-plate conductance in transected frog muscle: modification by drugs. 696 98

To assess the influence of fasting on the lipolytic effect of catecholamines in vivo noradrenaline (NA) was infused to 15 obese subjects before and after 7 days of fasting. The infusion of 7.5 microgram/min NA for 10 min was associated with a greater lipolytic response during than before fasting, as judged from changes in the plasma FFA and glycerol levels. The hemodynamic effects of NA were similar in both conditions. NA sensitivity was tested by infusing the hormone at an increasing rate from 0.05-2 microgram/min. During fasting, there was a 10-fold increase in the sensitivity to the lipolytic effect of NA, and the NA infusion significantly reduced the mean serum insulin level. Before fasting, the insulin level was constant during NA infusion. The increments in the plasma NA concentration were similar in both conditions. When insulin was infused at a constant rate, and graded NA doses were infused simultaneously, no lipolytic effect of NA at rates of 1 and 2 microgram/min significantly increased the plasma glycerol level. Thus, fasting enhances the lipolytic effect of NA in vivo, and this effect is due to increased sensitivity to NA and also to NA-induced depression of the circulating insulin level.
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PMID:In vivo observations on the lipolytic effect of noradrenaline during therapeutic fasting. 702 75

Mycobacteria have the ability to enhance or depress immune responses. This paper describes experiments designed to investigate the parameters determining the direction of modulation. It has been shown previously that 10(8) liver Mycobacterium bovis BCG depress the ability of mouse spleen cells to produce a primary antibody response in vitro to SRBC 2-3 weeks after i.v. injection, whereas the same number of dead organisms enhance this response. Using the same growth medium for the BCG (Glaxo glycerol-free medium), we now find that decreasing the BCG dose to mice from 10(8) to 10 (6) liver organisms results in enhanced responses and increasing the dose to more than 10(8) dead organisms results in depressed responses. It thus appears that bacterial load is the important factor determining whether depression or enhancement of the primary antibody response will occur, rather than the viability of the organisms per se. However, when the BCG was grown in Middlebrook 7H9 broth, doses as high as 4 X 10(9) dead BCG/mouse failed to depress although depressed responses were found if sufficient live organisms (7 X 10(8)) were injected. In view of the known growth characteristics of BCG in these 2 bacteriological media, it is suggested that the degree of aggregation of the injected suspension may also be of importance in determining whether or not depression will occur. A comparison of the effects of BCG injected untreated or after dispersion of bacterial aggregates supports this idea. Some degree of splenomegaly was always found in mice with depressed splenic responses but a large spleen did not necessarily yield cell suspensions with depressed responses.
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PMID:Mycobacterium bovis, BCG, modulation of murine antibody responses: influence of dose and degree of aggregation of live or dead organisms. 704 44


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