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)

Luminescence temperature antiquenching (LTAQ) is observed for water-soluble CdTe quantum dots (QDs) capped with aminoethanethiol (AET). The efficient exciton emission (quantum efficiency of approximately 40% at 300 K) is quenched almost completely as the QD solutions are cooled to below 230 K and is fully recovered around 270 K upon warming up to room temperature (LTAQ). Temperature-dependent lifetime measurements show that the quenching rate is high, resulting in an on/off behavior. No LTAQ is observed for CdTe QDs capped with aminoundecanethiol (AUT). The LTAQ is explained by the influence of solvent freezing on the surface of the QD core. Freezing of the solvation water molecules surrounding the QD will induce strain in the capping shell, due to the interaction between water and the charged heads of the capping molecules. Short carbon chains (AET) will propagate the strain to the QD surface, creating surface quenching states, whereas long and flexible chains (AUT) will dissipate the strain, thus avoiding surface distortion. Freezing-point depression by the addition of methanol results in a lowering of the transition temperature. Additional support is provided by the size dependence of the LTAQ: smaller particles, with higher local ionic strength due to a higher density of charged NH(3)(+) surface groups, experience a lower transition temperature due to stronger local freezing-point depression.
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PMID:Luminescence temperature antiquenching of water-soluble CdTe quantum dots: role of the solvent. 1531 55

Potentially carcinogenic bromate forms during the ozonation of bromide-containing waters. Some water treatment facilities have had to use ammonia addition and pH depression to minimize bromate formation, but these processes may prove to be insufficient to comply with upcoming regulations. The chlorine-ammonia process (Cl2-NH3), consisting of prechlorination followed by ammonia addition priorto ozonation is shown to cause a 4-fold decrease in bromate formed when compared to the ammonia-only process. Experiments revealed three key mechanisms: (i) oxidation by HOCl of Br- to HOBr and its subsequent masking by NH3 as NH2Br; (ii) decrease of HO- exposure through halogenation of Dissolved Natural Organic Matter (DNOM) by HOCI and scavenging of HO by NH2Cl; and (iii) DNOM acting as a bromine sink after oxidation of Br- to HOBr. At an ozone exposure of 6 mg/L x min and pH 8, conventional ozonation of Lake Zurich water spiked with 560 microg/L Br- formed 35 microg/L BrO3-, whereas the application of the Cl2-NH3 process resulted in 5 microg/L BrO3-. Additional pH depression to pH 6 further decreased bromate formation by a factor of 4. Trihalomethanes (THM) and cyanogen chloride (CNCl), that mayform during prechlorination and monochloramination, respectively, were well below regulatory limits. The chlorine-ammonia process holds strong promise for water treatment facilities struggling with a bromate formation problem during ozonation.
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PMID:Enhanced bromate control during ozonation: the chlorine-ammonia process. 1550 16

The clinical features, complications, and pharmacokinetics of intentional acute valproic acid (VPA) overdoses are described. Alteration in fatty acid metabolism is evaluated and therapy-induced changes are discussed. Central nervous system features were the predominant clinical manifestations (6/6), followed by respiratory failure (5/6) and multiorgan failure (2/6). Mechanical ventilation was required in 5 of 6 patients because of respiratory depression or deep coma. Hemodialysis was applied in 4/6 of the cases due to hyperammonemia, worsening neurologic condition, or organ dysfunction. Cerebral edema and hemorrhagic pancreatitis ensued in 2/6 of the patients and ICU mortality was 2/6. VPA peak levels ranged from 520 to 1700 mg/L with a mean of 1127 mg/L. Ammonia was elevated in all cases with a mean of 550 microg/dL. All patients showed signs of impaired mitochondrial beta-oxidation with increase of medium- and long-chain acylcarnitines in serum. Severe VPA overdose is associated with a high mortality rate requiring early medical interventions. Beside supportive intensive care, hemodialysis can be considered as an adjunctive measure.
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PMID:Acute valproate poisoning: pharmacokinetics, alteration in fatty acid metabolism, and changes during therapy. 1601 83

The effect of tea saponins (TS) on rumen fermentation and methane emission was examined using an in vitro gas production technique named Reading Pressure Technique. Three levels of TS addition (0, 0.2, 0.4 mg/ml) were evaluated in the faunated and defaunated rumen fluid. Compared to the control, TS addition decreased the 24 h gas production in the faunated rumen fluid, but had a minor effect on gas yield in the defaunated rumen fluid. The TS significantly reduced methane production in vitro. In the faunated rumen fluid, 0.2 or 0.4 mg/ml TS decreased the 24 h methane emission by 12.7% or 14.0%, respectively. Rumen fluid pH value was affected neither by TS addition nor by defaunation. The TS addition had only minor effects on volatile fatty acids, but the yield and pattern of volatile fatty acids were greatly affected by defaunation. While the molar proportion of acetate was not affected by defaunation, the propionate was significantly increased and the butyrate significantly decreased. Ammonia-N concentration and microbial protein yield were influenced by TS inclusion and defaunation. Inclusion of 0.4 mg/ml TS increased the microbial protein mass by 18.4% and 13.8% and decreased the ammonia-N concentration by 8.3% and 19.6% in the faunated and defaunated rumen fluid, respectively. Protozoa counts were significantly reduced by TS inclusion. The current study demonstrated the beneficial effect of TS on methane production and rumen fermentation, and indicated that this may be due to the effect of the associated depression on protozoa counts.
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PMID:Tea saponins affect in vitro fermentation and methanogenesis in faunated and defaunated rumen fluid. 1605 12

The paper overviews experimental evidence suggestive of the engagement of three endogenous metabolites: taurine, kynurenic acid, and glutathione (GSH) in the protection of central nervous system (CNS) cells against ammonia toxicity. Intrastriatal administration of taurine via microdialysis probe attenuates ammonia-induced accumulation of extracellular cyclic guanosine monophosphate (cGMP) resulting from over-activation of the N-methyl-D: -aspartate/nitric oxide (NMDA/NO) pathway, and this effect involves agonistic effect of taurine on the GABA-A and glycine receptors. Taurine also counteracts generation of free radicals, increased release of dopamine, and its metabolism to dihydroxyphenylacetic acid (DOPAC). Taurine reduces ammonia-induced increase of cell volume (edema) in cerebrocortical slices by a mechanism involving GABA-A receptors. Massive release of radiolabeled or endogenous taurine from CNS tissues by ammonia in vivo and in vitro is thought to promote its neuroprotective action, by making the amino acid available for interaction with cell membranes and/or by driving excess water out of the CNS cells (astrocytes) that underwent ammonia-induced swelling. Ammonia in vivo and in vitro affects in variable ways the synthesis of kynurenic acid (KYNA). Since KYNA is an endogenous NMDA receptor antagonist with a high affinity towards its glycine site, changes in its content may counter over-activation or depression of glutaminergic transmission observed at the different stages of hyperammonemia. GSH is a major antioxidant in the CNS whose synthesis is partly compartmented between neurons and astrocytes: astrocytic GSH is a source of precursors for the synthesis of neuronal GSH. Ammonia in vitro stimulates GSH synthesis in cultured astrocytes, which may compensate for increased GSH consumption (decreased GSH/GSSG ratio) in neurons.
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PMID:Endogenous neuro-protectants in ammonia toxicity in the central nervous system: facts and hypotheses. 1638 36

Routine monitoring of an 81-year-old man receiving treatment with nortriptyline for generalized anxiety disorder and depression revealed plasma concentrations of both amitriptyline and nortriptyline. In humans, the tricyclic antidepressant (TCA) tertiary amines imipramine and amitriptyline are typically metabolized by demethylation to the secondary active metabolites desipramine and nortriptyline, respectively. However, to our knowledge, methylation of secondary amine TCAs has been reported in only one case report of nortriptyline overdose and in two studies involving desipramine. In a retrospective analysis of patients from five Veterans Affairs medical centers, the rate of methylation of desipramine and nortriptyline was 8.9 % (five of 56 patients) and 14.6% (36 of 247), respectively. Possible explanations for methylation include genetic polymorphisms in cytochrome P450 metabolizing enzymes, polymorphism of amine N-methyltransferase enzyme, drug-drug interactions, smoking, and alcohol consumption. However, the mechanism by which methylation occurs is unclear and warrants further investigation. Awareness of the phenomenon could help in discouraging repeated laboratory tests and unnecessary adjustments of drug therapies, resulting in cost savings and better patient outcomes.
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PMID:Rates of in vivo methylation of desipramine and nortriptyline. 1655 9

Nitrogen nutrition strongly affected the growth rate of young sunflower (Helianthus annuus L.) leaves. When plants were grown from seed on either of two levels of N availability, a 33% decrease in tissue N of expanding leaves was associated with a 75% overall inhibition of leaf growth. Almost all of the growth inhibition resulted from a depression of the daytime growth rate. Measurements of pressure-induced water flux through roots showed that N deficiency decreased root hydraulic conductivity by about half. Thus, N deficiency lowered the steady-state water potential of expanding leaves during the daytime when transpiration was occurring. As a result, N-deficient leaves were unable to maintain adequate turgor for growth in the daytime. N deficiency also decreased the hydraulic conductivity for water movement into expanding leaf cells in the absence of transpiration, but growth inhibition at night was much less than in the daytime. N nutrition had no detectable effects on plastic extensibility or the threshold turgor for growth.
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PMID:Control of Leaf Expansion by Nitrogen Nutrition in Sunflower Plants : ROLE OF HYDRAULIC CONDUCTIVITY AND TURGOR. 1666 94

Mitogen-activated protein kinase (MAPK) cascade is essential for synaptic plasticity and learning. In the hippocampus, three different MAPK subfamilies, extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAPK and c-Jun NH2-terminal protein kinase (JNK), selectively regulate activity-dependent glutamate receptor trafficking during long-term potentiation (LTP), long-term depression (LTD), and depotentiation after LTP, respectively. Although LTP and LTD at cerebellar parallel fibre (PF)-Purkinje cell synapses are thought to be controlled by glutamate receptor trafficking, the involvement of MAPK subfamilies has not been systemically studied in cerebellar slice preparations. To clarify the role of the MAPK cascade in cerebellar LTD, we performed biochemical and electrophysiological analyses using ICR mouse cerebellar slices. Immunoblot analyses using phosphorylation-specific antibodies for MAPKs revealed that among the three MAPKs, ERK1/2 was specifically activated by phorbol ester, which could induce LTD in cerebellar slices. In addition, U0126, a specific inhibitor of the MAPK kinase-ERK1/2 pathway, abrogated the induction of LTD in cerebellar slices, whereas SB203580 and SP600125, specific inhibitors of p38 MAPK and JNK, respectively, had no effect. Although metabotropic glutamate receptor 1 (mGluR1) has been suggested as a possible downstream target of ERK1/2 in cell-culture preparations, mGluR1-activated slow excitatory postsynaptic currents (EPSCs) were not affected by U0126 treatment in slices. These findings indicate that unlike hippocampal LTD mediated by p38 MAPK, glutamate receptor trafficking during cerebellar LTD was regulated by a distinct mechanism involving ERK1/2 in slice preparations.
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PMID:ERK1/2 but not p38 MAP kinase is essential for the long-term depression in mouse cerebellar slices. 1700 25

Trace amines have been implicated in a number of neuropsychiatric disorders including depression and schizophrenia. Although long known to modulate neurotransmission indirectly through the release of catecholamines, the identification of the Trace Amine 1 receptor (TA1) offers a mechanism by which trace amines can influence synaptic activity directly. TA1 binds and is activated by trace amines such as beta-phenylethylamine and tyramine. Our pharmacological characterization of mouse TA1 showed that, as in rat and primate, amphetamine is an agonist at this receptor but with surprisingly high potency. Without selective ligands for TA1 that do not also possess catecholamine-releasing properties, however, it has not been possible to study its physiological role in the central nervous system. To that end, a line of mice lacking the TA1 receptor was generated to characterize its contribution to the regulation of behavior. Compared with wild-type littermates, TA1 knockout (KO) mice displayed a deficit in prepulse inhibition. Knockout animals, in which the TA1-agonist influence of amphetamine was absent, showed enhanced sensitivity to the psychomotor-stimulating effect of this drug, which was temporally correlated with significantly larger increases in the release of both dopamine and norepinephrine in the dorsal striatum and associated with a 262% increase in the proportion of striatal high-affinity D2 receptors. TA1 therefore appears to play a modulatory role in catecholaminergic function and represents a potentially novel mechanism for the treatment of neuropsychiatric disorders. Furthermore, the TA1 KO mouse may provide a useful model for the development of treatments for some positive symptoms of schizophrenia.
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PMID:The Trace Amine 1 receptor knockout mouse: an animal model with relevance to schizophrenia. 1721 50

This in vitro study was designed to investigate the effects of calcium addition to substrates differing in source and level of oil on fermentation, gas production, and digestibility parameters. Substrates were made from basal mixtures containing three levels of calcium salt (0, 1, and 2% CaCl2) to contain three levels (3, 6, and 9%) of two types (sunflower and soy) of oil. After collecting from two Holstein bulls and mixing with buffer, rumen fluid was used to incubate the resulting 18 mixtures in duplicate. Ionizable calcium, pH and NH3-N concentration were measured during incubation. Gas production was measured at 6, 12, 24, and 48 h after incubation. Kinetics parameters of gas production and in vitro dry matter digestibility (IVDMD) were calculated from regression coefficients of an exponential equation and a linear equation, respectively. Data were analysed using 3-way ANOVA with repeated measure option in which the parameter time was a subplot. Oil type did not affect pH and ionizable calcium concentration. There were linear increases and decreases in pH and ionizable calcium concentration in response to increasing oil and calcium levels, respectively. However, with increasing oil levels there were no interactions between calcium addition and oil level on pH and ionizable calcium concentration. None of the treatments affected NH3-N concentration. The amount of gas produced from substrates containing sunflower oil was greater than soy oil (41.7 vs. 40.5 ml). Cumulative gas production and amount of gas production from insoluble but slowly fermentable portion of the supplemental mixtures linearly decreased and linearly increased as oil and calcium levels increased in the substrates, respectively. However, interactions of calcium addition and oil level on gas production and kinetics of gas production were lacking. Oil type did not affect IVDMD. Despite lacking main effects, interaction of calcium addition and oil level indicated that increasing calcium level alleviated depression in IVDMD resulting from increasing oil level. In conclusion, increasing oil level depressed, whereas calcium addition stimulated ruminal fermentation. Improvement in IVDMD may partially support that calcium addition alleviates the adverse effects of oil and that more calcium is needed when diets are supplemented with increasing amounts of oil.
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PMID:Impacts of calcium addition and different oil types and levels on in vitro rumen fermentation and digestibility. 1723 4


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