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)

Experiments were conducted with immature rats fed L-amino acid purified diets varying in total N and arginine. The experiments demonstrated that total N intake was the factor responsible for increased orotic acid excretion during arginine deficiency. Increased orotic acid excretion was accompanied by increased liver transaminase activities and increased liver concentrations of NH4-N and glutamine. Arginine requirements for growth and normal metabolite excretion increased as dietary N was increased. Accompanying elevated urinary citrate during N deprivation and arginine deficiency was a depression of liver isocitrate dehydrogenase activity. Citrate excretion was lower if arginine was fed as the HCl compared to the free base. During a partial or total arginine deficiency citrate excretion was elevated at varying dietary N concentrations. Urinary pH was not significantly changed by level of dietary N or arginine.
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PMID:Dietary protein intake and arginine requirements in the rat. 62 13

A partially purified enterotoxin was obtained from the growth medium of Escherichia coli strain 711 (P307), a derivative of E. coli K-12, by ultrafiltration, precipitation with ammonium sulfate, molecular sieving, and anion exchange column chromatography. The active moiety, which is heat-labile, behaved like a protein particle of 180,000 to 200,000 daltons during molecular sieving and ultracentrifugation. During polyacrylamide gel electrophoresis in sodium dodecyl sulfate (SDS-PAGE), it dissociated into two subunits with apparent molecular weights of 68,000 to 70,000 and 14,000 to 15,000. SDS-PAGE after heating in SDS changed the larger subunit to an apparent molecular weight of about 40,000; the smaller subunit did not change. The intact particle induced rounding of the cells in Y-1 mouse adrenal tumor cells used for assay. The detergent-dissociated molecules were not active. Proteolysis of the purified toxin by tolylsulfonyl phenylalanyl chloromethyl ketone-trypsin appeared to enhance its activity. The addition of serum to the assay medium resulted in partial depression of the activity. Activity was also abolished by preincubation of the toxin with either a rabbit antiserum to it or solutions containing GM1 ganglioside. The length of time needed to evoke a response in the assay system by fractions from different stages in the purification of the enterotoxin was a useful parameter in the evaluation of specific activity.
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PMID:Partial purification and characterization of a heat-labile enterotoxin of Escherichia coli. 78 81

Events underlying depression of the nitrogen fixation (nif) genes in Klebsiella pneumoniae M5A1 were analyzed in vivo by comparing the effects of selective inhibitors of transcription and translation on subsequent nitrogenase activity (rate of acetylene reduction). When batch cultures were induced for depression, an 87-min lag separated ammonium ion/oxygen removal and the appearance of activity.
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PMID:Arrangement and regulation of the nitrogen fixation genes in Klebsiella pneumoniae studied by depression kinetics. 81 85

In experiments on cats ammonium acetate (AA) injected intravenously (2--4 mM/kg body weight) depressed the process of primary afferent depolarization (PAD) which were thought to be responsible for presynaptic inhibition of spinal reflexes. PAD depression is reversible and proceeds in parallel to depression of postsynaptic inhibition of monosynaptic reflexes. The ammonium depression of PAD is not connected with the block of the negative postsynaptic potential recorded from the dorsal surface of the spinal cord or with the block of the reflex electrical discharges from the ventral roots. A conclusion was drawn that one of the possible mechanisms for convulsive action of AA consists in depression of presynaptic inhibition. It is supposed that the depression of PAD by AA results from the block of the chloride ion pump existing in primary afferent terminals. The block of the pump leads to abolition of the EMF for the outwardly directed transmembrane chloride current producing PAD.
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PMID:[Block of presynaptic inhibition of spinal cord reflexes by ammonium acetate]. 91 55

Substitution of ammonium ions for sodium ion initially potentiated and then depressed twitch tension of the frog sartorius muscle. The extent of potentiation and the rate of depression of the twitch were dependent upon the concentration of ammonium ions. Ammonium ion depolarized individual muscle fibers in proportion to concentration. Maximum depolarization (33 mV) occurred in muscles equilibrated in 120 mM ammonium-Ringer for 30 min. At the higher concentration of ammonium (72--120 mM), the potentiation was quickly reversed and the tension response was eliminated completely. The gradual loss of twitch tension was accompanied by progressive decrease in the electrical excitability of individual muscle fibers. Raising the extracellular calcium concentration fivefold reduced the twitch-depressant effect of ammonium ions by maintaining excitability of the muscle fibers. Caffeine contractures (3 and 10 mM) in muscles preequilibrated in 72 mM ammonium-Ringer developed similar tensions to paired controls muscles, but the onset of tension was more rapid in the ammonium-treated muscle. It was concluded that the depression of tension could be accounted for by the loss of membrane excitability and that the evidence did not support the hypothesis that ammonium ions acted at other sites in the excitation contraction coupling.
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PMID:Influence of ammonium ions on mechanical and electrophysiological responses of skeletal muscle. 108 37

In the unicellular green alga Chlamydomonas reinhardi (strain y-1), synthesis of the enzymes required for urea hydrolysis is under substrate induction control by urea and under end product repression control by ammonia. Hydrolysis of urea if effected by the sequential action of the discrete enzymes urea carboxylase and allophanate lyase, collectively called urea amidolyase. The carboxylase converts urea to allophanate in a reaction requiring biotin, adenosine 5'-triphosphate, and Mg2+. The lyase hydrolzyes allophanate to ammonium ions and bicarbonate. Neither activity is present in more than trace amounts when cultures are grown with ammonia or urea plus ammonia, or when they are starved for nitrogen for 8 h. Urea in the absence of ammonia induces both activities 10 to 100 times the basal levels. Addition of ammonia to an induced culture causes complete cessation of carboxylase accumulation and an 80% depression of lyase accumulation. Ammonia does not reduce urea uptake by repressed cells, so it does not prevent induction by the mechanism of inducer exclusion. The unicellular green alga Chlorella pyrenoidosa (strain 3 Emerson) also has discrete carboxylase and lyase enzymes, but only the carboxylase exhibits metabolic control.
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PMID:Metabolic control of urea catabolism in Chlamydomonas reinhardi and Chlorella pyrenoidosa. 111 94

The covalent modification of receptor proteins via phosphorylation and dephosphorylation is one of the principal mechanisms controlling carbohydrate metabolism and is known to be regulated by various protein kinases. Recent studies indicated that many hormones may exert their effects on cellular metabolism by regulating intracellular c-AMP levels and by activating a c-AMP dependent protein kinase, i.e., protein kinase A. The metabolic disturbances during sepsis are characterized by an initial hyperglycemia followed by a progressive hypoglycemia and a depletion of hepatic glycogen content. The latter is coupled with a slowdown in glycogenesis, an accelerated glycogenolysis, and a depression in gluconeogenesis in the liver. Since the liver is the major organ that regulates the homeostatic level of blood glucose, it is conceivable that the sepsis-induced glucose dyshomeostasis might be mediated by changes in protein kinase activity and the kinetic characteristics of enzymes. The present experiment was designed to study the correlation between protein kinase A and the pathophysiology of hepatic glucose dyshomeostasis during sepsis. Sepsis was induced in rats by cecal ligation and puncture (CLP). Late sepsis occurred 18 hours after CLP. Protein kinase A was extracted from the rat livers by acid precipitation and ammonium sulfate fractionation, and then partially purified by DEAE-cellulose. The results show that in the late sepsis, type-I protein kinase A (eluted at low ionic strength) activity was significantly decreased by 34-52% (P < 0.01). The kinetic parameters such as Vmax's for ATP, histone, and c-AMP were also significantly decreased from the control values of 6.1 +/- 0.9, 5.4 +/- 0.8, and 5.1 +/- 1.9 nmoles/mg.min. to 3.6 +/- 0.5, 2.8 +/- 0.3, and 2.5 +/- 0.5 nmoles/mg.min., respectively. Analysis using Hill's equation indicates that the S0.5 and n (Hill coefficient) values of the various substrates and activators for type-I protein kinase A remained unchanged. In the case of type-II protein kinase A (eluted at high ionic strength), the Vmax, S0.5, and n values for ATP, histone, and c-AMP were unchanged during late sepsis. The results of the present study indicate that the activities and kinetic characteristics of type I protein kinase A in rat liver are modified during late sepsis. Since protein kinase A is known to regulate glucose metabolism through adrenergic receptor mediation, these findings may have a pathophysiological significance in the understanding of hepatic glucose dyshomeostasis during sepsis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Kinetic studies of protein kinase A in rat liver during late sepsis]. 129 61

The proximal tubule model of this laboratory [Am. J. Physiol. 250 (Renal Fluid Electrolyte Physiol. 19): F860-F873, 1986] has been updated to examine proposed pathways for Cl- transport. Two additional buffer pairs have been added, i.e., HCO2-/H2CO2 and NH3/NH4+. At the luminal cell membrane Cl-/HCO2- and Cl-/HCO3- exchange are considered as pathways for Cl- entry, whereas at the peritubular membrane, Cl- exit occurs by either Na(+)-2HCO3-/Cl- exchange or K(+)-Cl- cotransport. Calculations with this model indicate that absolute proximal reabsorption of both Na+ and Cl- are critically dependent on the rate of luminal Na+/H+ exchange. In contrast, increases in the coefficient for Cl-/HCO2- exchange have little impact on overall Cl- flux, but, by enhancing base secretion, limit the depression of end-proximal HCO3-. Model calculations confirm those of Preisig and Alpern (J. Clin. Invest. 83: 1859-1867, 1989) showing that their measured value of luminal membrane H2CO2 permeability is inadequate to sustain the transcellular Cl- flux as Cl-/HCO2- exchange. Conversely, with sufficiently high H2CO2 permeability, luminal Cl- uptake is enhanced along the tubule, as HCO2- secretion and luminal acidification increase luminal H2CO2 to values severalfold greater than in glomerular filtrate. At the basolateral membrane, the thermodynamic driving force across the Na(+)-2HCO3-/Cl- exchanger is small. Although its contribution to steady-state Cl- exit may be less than the K(+)-Cl- cotransporter, the Na(+)-2HCO3-/Cl- exchanger can be a mechanism by which cytosolic acidification enhances peritubular Cl- transport, when luminal acidification enhances luminal Cl- uptake. A simulation is presented in which impermeant replacement of luminal Na+ leads to enhanced convective Cl- flux across the tight junction and alkalinization of the lateral interspace. In this setting, cytosolic Cl- depletion via the Na(+)-2HCO3-/Cl- exchanger may mimic luminal membrane Na(+)-Cl- cotransport.
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PMID:Chloride transport in a mathematical model of the rat proximal tubule. 144 69

Resident peritoneal macrophages (PEM) harvested from female B6C3F1 mice given an intraperitoneal injection of ammonium metavanadate (2.5 or 10 mg V/kg), an equivalent amount of ammonium in the form of ammonium chloride, or sodium phosphate buffer (0.1 M, pH 7.2) every third day for 6 weeks, were subjected to flow cytometric analysis of Fc tau 2a and Fc tau 2b receptor expression, and photometric microassay to measure receptor mediated binding and phagocytosis of sheep red blood cells (SRBC). The NH4Cl and 10V groups showed 21.7 and 17.2% lower mean fluorescence channel (MFC) values and 7.1 and 5.9% lower values in percentage fluorescence-positive cells than the phosphate buffer control with respect to Fc tau 2a expression. For Fc tau 2b expression, the 10V group showed significantly (P less than 0.05) lower MFC (31.2%) and percentage fluorescence-positive cells (15.7%) than the phosphate buffer control. Though the four groups did not show a significant difference in Fc tau 2a mediated binding and phagocytosis of SRBC, the 10V group showed a significantly lower Fc tau 2b mediated binding and phagocytosis. The results indicate that the reduction in Fc tau 2b expression and function could contribute toward the previously observed depression in phagocytosis, NADPH-oxidase and superoxide generation in peritoneal macrophages obtained from vanadate-treated animals.
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PMID:Modulation of Fc tau receptor expression and function in mouse peritoneal macrophages by ammonium metavanadate. 166 52

A simple RNA isolation method was developed to purify bacterial RNAs from a large number of samples simultaneously in an hour. The method is based on boiling the cells in the presence of Triton X-100 and lysozyme, and then preferential RNA precipitation with ammonium acetate. There is no CsCl centrifugation required. For the nitrogen-fixing bacterium Klebsiella pneumoniae, the depression condition can be maintained during the cell-harvesting process. The intact isolated RNAs appeared to be free of protein, with a yield of 100 micrograms RNA from a 4-ml cell culture of 100 Klett units (10(9) cells/ml). Any DNA present was in a form that did not react with a nifH probe following Northern blotting to nitrocellulose (i.e., was not single-stranded).
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PMID:Two-step isolation of bacterial ribonucleic acid without using a chaotropic agent or cesium chloride centrifugation. 169 54


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