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)

Two breeds of commercial broiler chicks were used to investigate possible breed differences and to determine the effect of methionine and lysine on arginine requirements. Graded levels of arginine were added to a glucose-casein diet with or without added methionine and to a corn-soybean meal diet with and without added lysine and/or methionine. The arginine requirement of chicks receiving the glucose-casein diet with and without supplemental methionine was found to be 1.46 per cent and 1.55 per cent of the diet, respectively. No breed differences were found. When arginine was added to a corn-soy diet containing 1.53 per cent arginine, with or without supplemental methionine, no response was obtained indicating that this level of arginine was adequate. When this diet was supplemented with lysine to bring it up to the lysine level of the casein diet, a growth depression occurred which was overcome by the addition of 0.20 and 0.25 per cent arginine, respectively, in the absence and presence of supplemental methione. These levels of arginine exceeded the requirements determined for chicks fed the glucose-casein diet. In chicks fed the glucose-casein diet, muscle creatine increased with each level of added arginine with or without supplemental methionine. Creatinine excretion also increased with each level of added arginine in the absence of supplementary methionine but when methionine was added creatine excretion reached a plateau at the level of arginine which satisfied the chick's growth requirement.
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PMID:The effect of methionine and lysine levels on the arginine requirement of the chick. 116 68

Effects of histidine or methionine imbalance and dietary levels (3-50%) of casein on food intake and preference of young, adult, and diabetic (2.5 month old) rats were examined. Depressions in food intake and growth caused by ingestion of the imbalanced diet were greatest in young rats and least or absent in diabetic rats. Alloxan diabetes induced hyperphagia and elevated concentrations of plasma branched-chain amino acids and decreased concentrations of tryptophan and tyrosine. The diabetic rats fed the imbalanced diet for 9 days had a higher concentration of the limiting amino acid in the plasma than the adult normal rats fed the same diet. The diabetic rats preferred the imbalanced diet over a protein-free diet when they were fed these diets concurrently. Ingestion of the imbalanced diet by normal rats caused greater changes in plasma and brain amino acid patterns than did the protein-free diet. Unlike the diabetic rats, the normal rats, especially the young rats, strongly preferred the protein-free diet over the imbalanced diet. The normal rats also preferred a 10% casein diet supplemented with L-methionine over a low or high casein diet. It seemed that young rats were able to select a protein diet that supported maximal growth when proportions of dietary amino acids were balanced. It also seemed that the susceptibility of the rats to amino acid imbalance varied directly with the status of overall protein synthesis of the animals.
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PMID:Effects of amino acid imbalance and protein content of diets on food intake and preference of young, adult, and diabetic rats. 119 6

Methionine incorporation into proteins of the fibrillating dog heart perfused by donor circulation was investigated. In the heart in which fibrillation was induced by electric current under conditions of adequate oxygen supply a 50-55% increase of methionine S35 incorporation into the contractile protein fraction of both ventricles was observed. In the heart in which fibrillation appeared after anoxia, methionine S35 incorporation into the sum total proteins of the atria showed 40-60% depression, into the sarcoplasmic - 36 -53%, and into the contractile proteins of both ventricles - 18 -30% decrease.
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PMID:[Protein biosynthesis in the fibrillating perfused heart during normal oxygenation and following anoxia]. 127 12

A double-blind clinical trial was carried out to evaluate the efficacy of S-adenosyl-L-methionine (SAMe) in speeding the onset of action of imipramine (IMI). SAMe is a naturally occurring substance that has been shown to possess antidepressant activity with a rapid mode of onset and minimal side effects. Sixty-three outpatients with moderate to severe depression were included in the study. After an initial 1-week placebo period, only 40 patients entered the active treatment phase. During the first 2 weeks of the trial, half of these patients received 200 mg/day of SAMe intramuscularly, while the other half received placebo. Simultaneously, oral IMI was administered to all patients at a fixed dose of 150 mg/day. The onset of clinical response was determined by evaluating patients every second day. By the end of week 2, the parenteral treatment was suppressed and IMI was adjusted according to individual needs. Depressive symptoms decreased earlier in the patients who were receiving the SAMe-IMI combination than in those who were receiving the placebo-IMI combination.
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PMID:Efficacy of S-adenosyl-L-methionine in speeding the onset of action of imipramine. 128 23

Various mechanisms may exist for activation of polymorphonuclear (PMN) leukocytes during hemorrhagic shock and reinfusion. During activation of PMN leukocytes, hypochlorous acid (HOCl) is produced in addition to oxygen free radicals. We studied the effects of hemorrhagic shock and reinfusion on cardiac function and contractility, oxygen free radical producing activity of PMN leukocytes (PMN chemiluminescence), and serum and cardiac tissue malondialdehyde (MDA), a lipid peroxidation product, with and without methionine (quencher of hypochlorous acid) in anesthetized dogs, in order to assess the role of hypochlorous acid in depression of cardiac function and contractility in hemorrhagic shock. The dogs were divided into two groups: group I, hemorrhagic shock (2 hr) followed by reinfusion (2 hr); and group II, hemorrhagic shock and reinfusion similar to group I but methionine (30 mg/kg i.v.) was administered before bleeding, before reinfusion, and after 1 hr of reinfusion in this group. Mean arterial pressure (mAo), mean pulmonary arterial pressure (mPAP), index of myocardial contractility (dp/dtmax), and cardiac function (stroke volume index [SVI], left-ventricular work index [LVWI]) decreased significantly during shock and the decreases were similar in both groups. The indices of myocardial contractility which are independent of pre- and/or afterload ([dp/dt]/IIP and [dp/dt]/IIP/CPIP) were affected to a lesser degree than the other indices of myocardial contractility (dp/dtmax) during shock and reinfusion. However, the systemic and pulmonary vascular resistance increased significantly in both groups. Postinfusion recovery of cardiac function and contractility in group II was greater than in group I. Cardiac function and contractility after reinfusion returned to preshock levels initially followed by a decrease below the preshock values in group I. However, these parameters remained at or above preshock levels after reinfusion in group II. Cardiac tissue MDA levels were higher in group I, as compared to those in control dogs. The tissue levels of MDA in group II were lower than in group I but similar to those of control. The serum MDA did not change significantly during shock and reinfusion in either group. Although there were increases in the serum MDA after reinfusion in group I, they were not significant. While the chemiluminescent activity of PMN leukocyte increased significantly in group I, this activity decreased significantly in group II during shock and reinfusion. Methionine in in vitro studies did not affect the oxygen free radical producing activity of PMN leukocyte. These results suggest that hypochlorous acid is produced during shock and reinfusion. The decrease in the cardiac function and contractility after reinfusion may be due to hypochlorous acid.
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PMID:Methionine in protection of hemorrhagic shock: role of oxygen free radicals and hypochlorous acid. 132 Apr 67

The biochemistry of migraine is complex. Many contradictory or never replicated findings in often small patient groups have been published. The following observations in the platelet-free plasma and urine appear to have some solid basis and will be discussed: 1) systemic derangement of 5-HT metabolism, relevant to the peripheral vascular component of migraine pathophysiology, 2) changes in neuroexcitatory amino acids and magnesium, which may reflect a predisposition of the migraine patient, notably those having attacks with aura, to develop spreading depression, 3) alterations in methionine-enkephalin levels, which may be a useful marker to discriminate between tension headache and migraine, 4) hormonal fluctuations which seem important to set the threshold for an attack, 5) changes of vasoactive peptides in the cranio-vascular circulation, providing the first human evidence that the trigemino-vascular system indeed is relevant in migraine, and 6) catecholaminergic changes suggesting sympathetic overactivity. Finally distinct biochemical differences between patients with migraine without aura and patients with tension headache on one hand, and between patients with migraine with aura and patients with migraine without aura on the other hand will be emphasized. Findings in platelets will be discussed only if they are complementary and supportive to the plasma and urine data.
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PMID:Biochemistry of migraine. 137 6

The initiator of coliphage lambda DNA replication, lambda O protein, may be detected among other 35S-labeled phage and bacterial proteins by a method based on immunoprecipitation. This method makes it possible to study lambda O proteolytic degradation in lambda plasmid-harboring or lambda phage-infected cells; it avoids ultraviolet (u.v.)-irradiation of bacteria, used for depression of host protein synthesis, prior to lambda phage infection. We confirm the rapid decay of lambda O protein (half-time of 80 s), but we demonstrate the existence of a stable lambda O fraction. In the standard five minute pulse-chase experiments, 20% of synthesized lambda O is stable. The extension of the [35S]methionine pulse, possible in lambda plasmid-harboring cells, leads to a linear increase of this fraction, as if a part of the synthesized lambda O was constantly made resistant to proteolysis. Less than 5% of lambda O protein synthesized during one minute is transformed into a stable form. We presume that the stable lambda O is identical with lambda O present in the normal replication complex and thus protected from proteases. We cannot find any stable lambda O in Escherichia coli recA+ cells that were irradiated with u.v. light prior to lambda phage infection, but their recA- counterparts behave normally, suggesting that recA function interferes in the assembly of a normal replication complex in u.v.-irradiated bacteria. The stable lambda O found in lambda plasmid-harboring, amino acid-starved relA cells is responsible for the lambda O-dependent lambda plasmid replication that occurs in this system in the absence of lambda O synthesis. The existence of stable lambda O raises doubt concerning its role as the limiting initiator protein in the control of replication. Another significance of lambda O rapid degradation is proposed.
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PMID:Stability of coliphage lambda DNA replication initiator, the lambda O protein. 138 70

Maturation of blood monocytes into macrophages is accompanied by a number of functional changes including decreased IL-1 beta release in response to LPS. This limitation has previously been ascribed to transcriptional regulation. However, in seeming conflict with the observed depression in IL-1 beta mRNA levels, recent work demonstrates increased intracellular IL-1 beta in macrophages. Therefore, the present study sought to explain these differences by comparing IL-1 beta production from autologous alveolar macrophage and blood monocyte pairs at multiple regulatory sites, including endotoxin responsiveness, mRNA expression, protein translation, and post-translational processing. Macrophages did not differ from monocytes in endotoxin sensitivity, but when analyzed by both ELISA and Western blot, were confirmed to have limitations in IL-1 beta release. Gene expression studies demonstrated that at 4 h, macrophage IL-1 beta steady state mRNA levels were 3-fold lower than the monocyte's. However, total IL-1 beta protein production, as measured by [35S]methionine labeling with immunoprecipitation, demonstrated three- to sixfold higher amounts in macrophages at comparable time points. The enhanced protein production in the face of relatively low mRNA levels suggests that macrophages translate IL-1 beta mRNA more efficiently. Furthermore, characterization of IL-1 beta release into supernatants revealed that whereas monocyte release occurred early, represented 5 to 20% of the intracellular amounts, and contained largely processed IL-1 beta, macrophage release was delayed, represented 1 to 5% of the intracellular amounts, and contained primarily unprocessed IL-1 beta. Taken together, these data demonstrate that the limitations in alveolar macrophage IL-1 beta release occur due to slower export and conversion of 35- to 17-kDa protein and are not due to differences in sensitivity to endotoxin or to transcriptional control mechanisms.
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PMID:Macrophage and monocyte IL-1 beta regulation differs at multiple sites. Messenger RNA expression, translation, and post-translational processing. 140 31

We evaluated the predictive value of the thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) in 32 depressed outpatients completing a double-blind placebo-controlled trial of s-adenosyl-l-methionine (SAMe), which failed to show any significant difference between SAMe and placebo. Treatment response was defined as the change in Hamilton Rating Scale for Depression (HRSD-24) score between baseline and the end of the six-week trial. Subjects with TSH response outside the normal range (7-25 uU/ml) had a significantly greater response than patients with a normal response. There was also a significant correlation between absolute deviations from the mean TSH response (16 uU/ml) and changes in HRSD-24 scores.
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PMID:The thyrotropin response to thyrotropin-releasing hormone as a predictor of response to treatment in depressed outpatients. 141 98

Hepatic cysteine sulfinic acid decarboxylase (EC 4.1.1.29) activity has been reported to decrease in response to both L-methionine (Met) feeding and adrenalectomy in rats. A series of experiments was conducted to (a) determine if CSAD depression was evident in female rats fed a methionine-supplemented diet; and (b) determine if adrenal hormones mediated the response of CSAD to dietary methionine. Cysteine sulfinic acid decarboxylase (CSAD) activity was measured in livers of male and female rats fed a methionine-supplemented diet. In female rat liver, CSAD activity was only 25% of the activity measured in livers of male rats. Hepatic enzyme activity in male rats fed a casein-based basal diet containing 0.6% L-methionine was 2.5-fold higher than activity in male rats fed a methionine-supplemented diet containing 1.35% L-methionine (+Met). Similarly, enzyme activity in livers of female rats fed the basal diet was 1.7-fold higher than in female rats fed a methionine-supplemented diet. CSAD activity in adrenalectomized (ADX) male rats fed the basal diet was depressed (990 +/- 120 nmol/min.g liver) compared to activity in intact controls (2347 +/- 89) and sham controls (2040 +/- 143) fed the basal diet. CSAD activity was further depressed in ADX, intact controls, and sham controls fed +Met. Immunochemical detection and quantification of CSAD protein in rat liver demonstrated that changes in CSAD protein were consistent with the observed decreased enzyme activity in female rats, ADX rats, and rats fed +Met. S-Adenosylmethionine and S-adenosylhomocysteine concentrations tended to increase in livers of rats fed +Met. ADX rats fed +Met had the greatest increase in S-adenosylmethionine and S-adenosylhomocysteine concentrations. The depression in hepatic CSAD observed after feeding +Met to rats does not appear to involve adrenal function.
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PMID:Quantification of cysteine sulfinic acid decarboxylase in male and female rats: effect of adrenalectomy and methionine. 156 10


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