UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study concerned 69 depressed patients (26 men, 43 women). The antidepressant drug was prescribed in accordance with perturbations of tyrosine and tryptophan membrane transports (MT) across the red cell, measured in vitro after a wash-out period of ten days. After two to four months of treatment, the clinical results were divided into two groups: normal mood (AMDP - Depression Scale less than 6) and no recovery (AMDP - Depression Scale greater than 6). The initial criteria (e.g. MT) was completed by using plasma tyrosine, tryptophan and the product MT by plasma level. Indeed, the success of this treatment was corresponding to precise abnormalities of variable: (i) tyrosine and tryptophan values for imipramine, (ii) tyrosine values, plasma tryptophan and tryptophan product for desipramine, (iii) tryptophan variables and plasma tyrosine for fluvoxamine (and indalpine). The analysis of clinical failures permitted to complete our previous choice of antidepressant drug.
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PMID:[Efficacy of antidepressants selected as a function of erythrocyte membrane transport and plasma levels of L-tyrosine and L-tryptophan]. 327 98

1. Antitussive, antinociceptive and respiratory depressant effects of codeine, morphine and H.Tyr.D-Arg.Gly.Phe(4-NO2) Pro.NH2 (compound BW443C) were investigated in unanaesthetized guinea-pigs. Antagonism of the antitussive and antinociceptive effects was investigated by the use of nalorphine and N-methylnalorphine. Naloxone was used to antagonize respiratory depression. 2. Antitussive ED50s (with 95% confidence limits) for inhibition of cough induced by citric acid vapour were for codeine, morphine and BW443C respectively, 9.1(5.8-15), 1.3(0.7-2.4) and 1.2(0.6-2.6) mg kg-1 s.c. and 8.7(4.2-12), 1.6(1.2-1.9) and 0.67(0.002-3.3) mg kg-1, i.v. The antitussive effects of subcutaneous codeine (25 mg kg-1) morphine (8.1 mg kg-1) and BW443C (2.5 mg kg-1) were significantly antagonized by subcutaneous nalorphine (3.0 mg kg-1) and N-methylnalorphine (3.0 mg kg-1). 3. In the multiple toe-pinch test, the antinociceptive ED50s (with 95% confidence limits) of codeine and morphine were 18(16-22) and 2.3(0.4-4.3) mg kg-1, s.c., respectively. Compound BW443C was ineffective in doses of 2.5 and 10 mg kg-1 s.c., a result consistent with its lacking penetration into the CNS. Subcutaneous nalorphine (3.0 mg kg-1) antagonized the antinociceptive action of codeine (25 mg kg-1) and morphine (8.1 mg kg-1). In contrast, N-methylnalorphine (3.0 mg kg-1) had no significant effect on the antinociceptive action of codeine and morphine, suggesting lack of penetration of the CNS by N-methylnalorphine. 4. At doses near to the i.v. ED50 values for the antitussive activity, morphine (1.5mg kg- ', i.v.) and codeine (10mg kg-', i.v.) caused small but significant depressions of ventilation (7.0 +/- 2.3% and 16.5 +/- 8.4% respectively). Higher doses of morphine (10, 30 and 60mg kg- ', i.v.) caused further doserelated depression of ventilation (9.6 +/- 5.3%, 22.4 +/- 6.2% and 36.2 +/- 9.6% respectively) whereas codeine (30 and 60mg kg-' i.v.) caused stimulation of ventilation which was marked (191.3 +/- 43.9%) at 60 mg kg-'. 5. Compound BW443C in doses of 1 or 10mgkg-',i.v. (approximately equal to, and 10 times the EDo for antitussive activity) did not cause significant depression of ventilation. Only at higher doses of 30 and 60mg kg-', i.v. was there a significant decrease in minute volume (13.1 +/- 6.8% and 15.9 +/- 1.89% respectively). The depression of ventilation caused by either BW443C (60mg kg-', i.v.) or morphine (60mg kg-', i.v.) was prevented by pretreatment with naloxone (3mg kg-', i.v.) administered 15 min before morphine or BW443C. 6. These results in the guinea-pig support the hypothesis that the antitussive action of the opiates codeine and morphine and the opioid pentapeptide BW443C do not require penetration of these drugs into the CNS.
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PMID:Effects of codeine, morphine and a novel opioid pentapeptide BW443C, on cough, nociception and ventilation in the unanaesthetized guinea-pig. 334 36

The effect of excesses of the branched-chain amino acids (BCAA), particularly leucine, on growth, food intake and plasma amino acid concentrations were investigated in kittens. Effects of excess leucine were tested in kittens fed five basal diets that varied in their nitrogen and amino acid contents. Compared to rats, kittens were much less sensitive to excesses of the BCAA. Addition of 10% leucine to basal diets that provided nitrogen just at or below the minimal requirement of kittens resulted in no change or increased growth and food intake of kittens when the isoleucine and valine concentrations in the basal diet were just at or slightly in excess of the kitten's minimal requirements for those amino acids. An adverse effect of leucine added to low nitrogen basal diets was observed only when isoleucine and valine were provided below the kitten's requirement (80% of requirement). When basal diets containing adequate nitrogen (24% amino acids) were tested, the addition of leucine (10%) resulted in an adverse effect when isoleucine and valine were provided at 80% of the kitten's requirement and in mild growth depressions when isoleucine and valine were provided at 1.1 times the requirement. Leucine-induced growth depression was alleviated by the addition of isoleucine and valine at 0.5%, indicating that excess leucine caused a BCAA antagonism or an amino acid imbalance. With the addition of leucine to the basal diets, there were consistent decreases in concentrations of alanine and tyrosine in plasma but no consistent depressions in the concentrations of isoleucine and valine.
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PMID:Effects of dietary excesses of the branched-chain amino acids on growth, food intake and plasma amino acid concentrations of kittens. 335 31

Organotypic cultures of fetal mouse spinal cord-ganglion explants (2-4 weeks in vitro) contain forskolin-stimulated adenylate cyclase (AC) activity that is inhibited by levorphanol and other opioid agonists in a dose-dependent manner. Inhibition by levorphanol no longer occurs if sodium is omitted from the incubation and the levorphanol inhibition is blocked by the opioid antagonist, naloxone. These findings together with the ineffectiveness of dextrorphan indicate that the opioid inhibition of forskolin-stimulated AC is receptor mediated. Both the delta- and kappa-receptor subtypes appear to be involved since the selective delta-opioid agonist, [D-Pen2, D-Pen5]enkephalin, and the selective kappa-opioid agonist, t-3,4-dichloro-N-methyl-N[2-(1-pyrrolidinyl)cyclohexyl]-benzene acetamide (U-50,488H) are both effective at nanomolar concentrations. In contrast, the selective mu-opioid agonist, Tyr-D-Ala-Gly-N-MePhe-Gly-ol, has no significant effect even at micromolar concentrations. Both cord and ganglion components of the explants contain opioid-sensitive AC. Forskolin-stimulated AC of the explants is also inhibited by serotonin and carbachol. The serotonin effect appears to be mediated by 5-HT1A receptors, based on relative agonist and antagonist selectivity. Chronic exposure of cultures to morphine results in enhanced basal and forskolin-stimulated AC as well as attenuation of opioid-inhibition of AC assayed in the presence of forskolin; treatment of explants with pertussis toxin causes similar changes in the AC system. The inhibitory effect of serotonin is also attenuated by the pertussis toxin treatment. Basal AC activity of the explants (assayed without forskolin present) is stimulated to a small but significant extent by opioids and by serotonin. The opioid stimulatory effect is markedly enhanced following either morphine or pertussis toxin treatment of the explants. The attenuation of opioid- and serotonin-inhibition of AC produced by chronic exposure to pertussis toxin and the attenuation of opioid inhibition produced by exposure to morphine are consonant with the attenuation of opioid and monoaminergic depression of sensory evoked dorsal horn network responses after similar chronic treatments. It is proposed that the inhibitory effects of opioids and serotonin on these neurons are mediated by receptors that are negatively coupled via a pertussis toxin sensitive Gi protein to AC. Furthermore, alterations of AC with chronic morphine treatment may be involved in the development of physiologic tolerance to opioids.
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PMID:Modulation of adenylate cyclase activity of mouse spinal cord-ganglion explants by opioids, serotonin and pertussis toxin. 337 Apr 65

Two 12-day experiments were conducted with Large White turkeys to determine which amino acids are deficient in a diet containing dehulled soybean meal as the sole source of protein. A 22% protein basal diet composed of 43.3% glucose monohydrate, 45.4% dehulled soybean meal, .5% DL-methionine, 6% stabilized fat, and added minerals and vitamins served as the negative control. Two positive control diets were formed by substituting either 16.5% dehulled soybean meal or a mixture containing amounts of essential amino acids equivalent to those in the added dehulled soybean meal in place of an equal amount of glucose monohydrate in the basal diet. Nine additional diets were formed by removing one or more amino acids from the mixture. Each of the 12 diets in a block design was fed to two pens of males and two pens of females with 8 birds per pen from 7 to 19 days of age in each experiment. Average body weight gain of poults fed the 22% protein diet with added amino acids approached that of poults fed the 30% protein diet (288 vs. 300 g, respectively). Removal of the amino acid mixture from the 22% protein diet depressed body weight gain by 19.0%. Depressions of 19, 16, 11, 7, and 6% in body weight gains resulted from the removal of valine, threonine, lysine, phenylalanine (or tyrosine or glycine), and isoleucine, respectively. A decrease of 5% was required for significance (P less than or equal to .05). When evaluated by this deletion technique, effects of valine and threonine deficiency were more pronounced than effects of lysine deficiency in dehulled soybean meal for young turkeys.
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PMID:Deficient amino acids in protein of dehulled soybean meal for young turkeys. 344 40

Binding of the histone (H2A, H2B) dimer with chicken erythrocyte DNA has been studied by salt-titration spectroscopy in equilibrium conditions. The circular dichroism of DNA near 275 nm is depressed by the interaction with (H2A, H2B) at low concentrations of salt. The depression increases with increasing amounts of (H2A, H2B), and reaches a plateau at an (H2A, H2B) to DNA ratio of 1.5 (w/w), at which one (H2A, H2B) dimer occupies 28 base-pairs of DNA. The fluorescence emission intensity of the tyrosine residues in (H2A, H2B) is depressed by the H2A, H2B)-DNA interaction. When the DNA-(H2A, H2B) complex is titrated with NaCl, these two signals show transitions with increasing ionic strength of the buffer, whose normalized transition curves agree well. The midpoint of the transition is about 0.42 M-NaCl for a sample with a DNA concentration of 0.05 mg/ml and an (H2A, H2B) to DNA ratio of 0.4 (w/w). The fluorescence titration curves have been analyzed to obtain the binding constant for the (H2A, H2B) dimer with DNA. The sample concentration dependence of the titration profiles is consistent with the model of non-cooperative binding of (H2A, H2B) dimer to DNA. The titration profiles are reversible. The obtained binding constant for the (H2A, H2B) dimer with chicken erythrocyte DNA at 20 degrees C (pH 7.6), as a function of the ionic strength, I, is as follows: log10K = -14.9 log10(I)-1.2. The change of enthalpy delta H accompanied by the binding of the (H2A, H2B) dimer is nearly equal to zero, within an error of +/- 1.4 kcal/mol (1 cal = 4.184 J). DNA sequence dependence of the stability of DNA-(H2A, H2B) interactions is observed using reconstituted materials of synthetic DNAs. A decreasing stability of the interaction is observed following the order: the duplex of poly[(dA)-(dT)] greater than chicken erythrocyte DNA or the copolymer duplex of poly(dA).poly(dT) greater than the duplex of poly[(dG)-(dC)]. The difference in free energy of the association of the (H2A,H2B) dimer between the two copolymers is 0.8 kcal/mol.
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PMID:Spectroscopic studies on histone-DNA interactions. I. The interaction of histone (H2A, H2B) dimer with DNA: DNA sequence dependence. 365 50

A method has been established for studying the dynamic metabolism of tyrosine to its metabolites in humans using a deuterium-labelled amino acid. Phenylalanine-d5 was administered orally to human subjects (5 mg/kg) and the levels of p-hydroxyphenylacetic acid-d4, 4-hydroxy-3-methoxyphenylacetic acid-d3, and 4-hydroxy-3-methoxymandelic acid-d3 excreted into urine every hour were determined by gas chromatography-negative-ion chemical-ionization mass spectrometry. This method was also applied to some patients with depression and it was possible to detect a slight alteration in the excretion of some compounds compared with the control.
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PMID:Sensitive determination of tyrosine metabolites, p-hydroxyphenylacetic acid, 4-hydroxy-3-methoxyphenyl-acetic acid and 4-hydroxy-3-methoxymandelic acid, by gas chromatography-negative-ion chemical-ionization mass spectrometry. Application to a stable isotope-labelled tracer experiment to investigate their metabolism in man. 375 83

We studied the direct cardiac effects of arginine vasopressin (AVP) by use of an isolated working rat heart model perfused with Krebs-Henseleit medium. At a concentration of 878 +/- 15 pg/ml, AVP produced significant (P less than 0.05) decreases in coronary flow (-31 +/- 2%); myocardial O2 consumption (-12 +/- 2%); left ventricular peak systolic pressure (-5 +/- 1%); dP/dtmax (-7 +/- 1%); -dP/dtmax (-6 +/- 3%); peak aortic flow rate (-5 +/- 1%); stroke work (-3 +/- 1%); peak power (-8 +/- 1%); and total output (-3 +/- 1%). Aortic output increased significantly (+7 +/- 1%) as did arteriovenous O2 difference (+108 +/- 14 mmHg); left ventricular end-diastolic pressure (+0.4 +/- 0.1 mmHg); efficiency (+1.5 +/- 0.4%); and rate of lactate release (+1.27 +/- 0.21 nmol/ml perfusate/min). Dose-response relationships were studied at 9 +/- 1, 25 +/- 1, 75 +/- 3, 303 +/- 15, and 817 +/- 42 pg AVP/ml. Significant dose-dependent depression of coronary flow occurred at the three highest AVP concentrations; cardiac function was significantly depressed at the highest dose. The AVP analogue d(CH2)5[Tyr(Me)]AVP (20 ng/ml) completely reversed the cardiac effects attributed to AVP. The data indicate that AVP is a potent direct coronary constrictor that produces myocardial ischemia and decreased contractile function at AVP concentrations that are observed in some pathophysiologic states.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Direct cardiac effects of vasopressin and their reversal by a vascular antagonist. 376 50

Osmolalities of selected defined-formula products for use in treatment of inherited disorders of amino acid metabolism were measured at 12 energy concentrations. Osmotic behaviors of six carbohydrate modules as components of L-amino acid formulas were also studied. Osmolality measurements were made using a Wescor vapor pressure depression osmometer (model 5100 C). Phenyl-Free at concentrations greater than 10 kcal/oz yielded high osmolalities that exceeded the recommended level for infants. Lofenalac, Low Phe/Tyr Diet Powder, and MSUD Diet Powder at concentrations up to but no greater than 20 kcal/oz exerted osmolalities acceptable for use with infants. Low Methionine Diet Powder produced the lowest osmolality of the products tested. Differences among products can be explained by the formulations of the products, with sources of nitrogen and carbohydrate and percents of protein, carbohydrate, and fat considered. Carbohydrate type significantly affected formula osmolality; differences among carbohydrate sources can be attributed to their molecular sizes. Formulas that contained glucose exerted the highest osmolalities, while those with corn syrup or sucrose yielded the next highest. Protein Free Diet Powder, Polycose, and Moducal exerted reasonably low osmolalities.
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PMID:Osmolalities of selected enteral products and carbohydrate modules used to treat inherited metabolic disorders. 379 33

After an initial period of depression which lasted up to 90 min following injection, bromocriptine (BRC, 5-20 mg/kg, IP) produced dose-dependent and long lasting (7 h) locomotor stimulation in mice. The locomotor stimulation was antagonised by reserpine, alpha-methyl-p-tyrosine (AMPT) or haloperidol. The blockade by AMPT of BRC's locomotor stimulant effect was reversed by prior treatment of the mice with a low, behaviourally inactive dose of L-Dopa plus benserazide. In mice pretreated with reserpine, BRC enhanced the stimulant action of d-amphetamine. Moreover, in mice pretreated with reserpine plus AMPT, BRC significantly enhanced the locomotor stimulant effect of apomorphine. This ability of BRC to enhance the effect of apomorphine commenced as soon as 20 min after BRC administration and lasted for at least 8 h. The dopamine (DA) uptake inhibitor and DA receptor agonist nomifensine potentiated and prolonged the stimulant effect of BRC while inhibitors of the neuronal uptake of noradrenaline (desipramine) and 5-hydroxytryptamine (fluoxetine) were without marked effect. The results clearly show that BRC, in behavioural terms, has no efficacy per se at the postsynaptic DA receptor and that it requires either DA or the administration of an exogenous agonist such as apomorphine for the expression of its effects.
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PMID:Bromocriptine potentiates the behavioural effects of directly and indirectly acting dopamine receptor agonists in mice. 387 78

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