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)

Excessive W-6 PUFA metabolism due to high levels of dietary fat intake can encourage infection via prolonged inflammation, enhanced Gram negative survival, reticuloendothelial blockage, immunosuppression, and monokine depression. Lipids can influence host immunity by altering eicosanoid metabolism and membrane structure and function. Further investigations are essential to answer questions regarding the levels and properties of various essential fatty acids in TPN lipid emulsions. Combining the features of LCT in the form of W-3 PUFA (fish oil) and MCT in the form of medium-chain triglyceride in a "structured lipid" may decrease infection and may improve survival rates by producing fewer inflammatory eicosanoids of the two- and four-series, and serving as a more "efficient fuel." The introduction of W-3 polyunsaturated fatty acids into the TPN emulsions as well as into normal diets may provide an important therapeutic advance in the pathogenesis of disease. Such unique antiinflammatory properties of W-3 PUFA require intensive research.
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PMID:Invited comment: lipids and the development of immune dysfunction and infection. 306 38

The LOMIR-MCT-IL study was designed to investigate the effects of different antihypertensive drugs on the quality of life (QoL) of men with mild-to-moderate hypertension. This report focuses on the subgroup of patients treated with the combination of the angiotensin converting enzyme (ACE) inhibitor captopril and the calcium antagonist isradipine. The LOMIR-MCT-IL was a double-blind multicenter, placebo-controlled, one-year follow-up study in which 368 hypertensive men, aged 40-65 years, were randomly allocated to receive either isradipine, methyldopa or placebo at three titration levels. If diastolic blood pressure (DBP) remained > 90 mmHg, captopril was added openly. The QoL evaluation introduced a qualitative self-structured subjective measure in addition to prestructured quantitative measures. The quality of life was assessed at baseline, after 6 months and at the end of the study. Methyldopa normalized DBP in 50% of patients when given as monotherapy and an additional 34% with the addition of captopril (84% total). With placebo, 36% normalized DBP and another 39% on addition of captopril (75% total) and, with isradipine, 64% normalized DBP and an additional 26% with added captopril (90% total). Assessment of QoL showed that both the placebo and the isradipine+captopril groups showed significant improvement in semantic memory after antihypertensive treatment. The isradipine+captopril group showed a clear tendency towards lower depression scores, better quality of sleep, better subjective evaluation of QoL and a more positive evaluation of personal life events in comparison to the other groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does the combination of ACE inhibitor and calcium antagonist control hypertension and improve quality of life? The LOMIR-MCT-IL study experience. 820 97

gamma-Hydroxybutyrate (sodium oxybate, GHB) is an approved therapeutic agent for cataplexy with narcolepsy. GHB is widely abused as an anabolic agent, euphoriant, and date rape drug. Recreational abuse or overdose of GHB (or its precursors gamma-butyrolactone or 1,4-butanediol) results in dose-dependent central nervous system (CNS) effects (respiratory depression, unconsciousness, coma, and death) as well as tolerance and withdrawal. An understanding of the CNS transport mechanisms of GHB may provide insight into overdose treatment approaches. The hypothesis that GHB undergoes carrier-mediated transport across the BBB was tested using a rat in situ brain perfusion technique. Various pharmacological agents were used to probe the pharmacological characteristics of the transporter. GHB exhibited carrier-mediated transport across the BBB consistent with a high-capacity, low-affinity transporter; averaged brain region parameters were V(max) = 709 +/- 214 nmol/min/g, K(m) = 11.0 +/- 3.56 mM, and CL(ns) = 0.019 +/- 0.003 cm(3)/min/g. Short-chain monocarboxylic acids (pyruvic, lactic, and beta-hydroxybutyric), medium-chain fatty acids (hexanoic and valproic), and organic anions (probenecid, benzoic, salicylic, and alpha-cyano-4-hydroxycinnamic acid) significantly inhibited GHB influx by 35 to 90%. Dicarboxylic acids (succinic and glutaric) and gamma-aminobutyric acid did not inhibit GHB BBB transport. Mutual inhibition was observed between GHB and benzoic acid, a well known substrate of the monocarboxylate transporter MCT1. These results are suggestive of GHB crossing the BBB via an MCT isoform. These novel findings of GHB BBB transport suggest potential therapeutic approaches in the treatment of GHB overdoses. We are currently conducting "proof-of-concept" studies involving the use of GHB brain transport inhibitors during GHB toxicity.
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PMID:GHB (gamma-hydroxybutyrate) carrier-mediated transport across the blood-brain barrier. 1517 14

During ischemic heart diseases and when heart failure progresses depletion of myocardial energy stores occurs. D-Ribose (R) has been shown to improve cardiac function and energy status after ischemia. Folic acid (FA) is an essential cofactor in the formation of adenine nucleotides. Therefore, we assessed whether chronic R-FA administration during the development of hypertrophy resulted in an improved cardiac function and energy status. In Wistar rats (n = 40) compensatory right ventricular (RV) hypertrophy was induced by monocrotaline (30 mg/kg; MCT), whereas saline served as control. Both groups received a daily oral dose of either 150 mg.kg(-1).day(-1) dextrose (placebo) or R-FA (150 and 40 mg.kg(-1).day(-1), respectively). In Langendorff-perfused hearts, RV and left ventricular (LV) pressure development and collagen content as well as total RV adenine nucleotides (TAN), creatine content, and RV and LV collagen content were determined. In the control group R-FA had no effect. In the MCT-placebo group, TAN and creatine content were reduced, RV and LV diastolic pressure-volume relations were steeper, RV systolic pressures were elevated, RV and LV collagen content was increased, and RV-LV diastolic interaction was altered compared with controls. In the MCT-R-FA group, TAN, RV and LV diastolic stiffness, RV and LV collagen content, and RV-LV diastolic interaction were normalized to the values in the control group while creatine content remained depressed and RV systolic function remained elevated. In conclusion, the depression of energy status in compensated hypertrophic myocardium observed was partly prevented by chronic R-FA administration and accompanied by a preservation of diastolic function and collagen deposition.
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PMID:Preservation of diastolic function in monocrotaline-induced right ventricular hypertrophy in rats. 1760 25

Search for new therapeutic methods applied in psychiatric disorders, especially in depression--concern not only pharmacotherapy, but also physical techniques. Electroconvulsive treatment is a recognised and effective method for receiving of antidepressant effects by means of electric head stimulation with eliciting of seizures. During two past decades, a few new techniques using the electrical or magnetic stimulation were tested with respect to their therapeutic antidepressant activity. The trancranial magnetic stimulation TMS, vagus nerve stimulation VNS, magnetic seizure therapy/magnetoconvulsive therapy MST/MCT, deep brain stimulation DBS, and trancranial direct current stimulation tDCS are involved among these techniques. The paper discusses those above mentioned techniques and it makes a critical comparison--in relation to several criteria--with the electroconvulsive treatment and pharmacotherapy.
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PMID:[New techniques of electrical and magnetic stimulation in treatment of depression--comparison with electroconvulsive treatment and pharmacotherapy]. 2144 68

This study analyzed the interrelationships between key constructs of cognitive therapy (CT; depressogenic schemas), metacognitive therapy (MCT; dysfunctional metacognitive beliefs), and acceptance and commitment therapy (ACT; psychological inflexibility) in the prediction of depressive symptoms. With a lapse of nine months, 106 nonclinical participants responded twice to an anonymous online survey containing the following questionnaires: the Depression subscale of the Depression Anxiety and Stress Scales (DASS), the Dysfunctional Attitude Scale Revised (DAS-R), the Positive beliefs, Negative beliefs and Need to control subscales of the Metacognitions Questionnaire-30 (MCQ-30), and the Acceptance and Action Questionnaire - II (AAQ-II). Results showed that when controlling for baseline levels of depressive symptoms and demographic variables, psychological inflexibility longitudinally mediated the effect of depressogenic schemas (path ab = .023, SE = .010; 95% BC CI [.008, .048]) and dysfunctional metacognitive beliefs on depressive symptoms (positive metacognitive beliefs: path ab = .052, SE = .031; 95% BC CI [.005, .134]; negative metacognitive beliefs: path ab = .087, SE = .049; 95% BC CI [.016, .214]; need to control: path ab = .087, SE = .051; 95% BC CI [.013, .220]). Results are discussed emphasizing the role of psychological inflexibility in the CT and MCT models of depression.
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PMID:Comparing Cognitive, Metacognitive, and Acceptance and Commitment Therapy Models of Depression: a Longitudinal Study Survey. 2607 77

Metacognitive Training for Depression (D-MCT), a low-threshold group intervention, has been shown to improve depressive symptoms. It aims at the reduction of depression by changing dysfunctional cognitive as well as metacognitive beliefs. The purpose of the present study was to investigate whether the mechanisms of change in D-MCT are cognitive (and thus primarily concern the content of cognition) or metacognitive in nature. Eighty-four outpatients with depression were included in a randomized controlled trial comparing D-MCT to an active control intervention. Level of depression, dysfunctional cognitive beliefs (DAS), and metacognitive beliefs (MCQ subscales: Positive Beliefs, Negative Beliefs, Need for Control) were assessed before (t0) and after treatment (t1). Severity of depression was also assessed 6 months later (t2). Linear regression analyses were used to determine whether change in depression from t0 to t2 was mediated by change in cognitive vs. metacognitive beliefs from t0 to t1. D-MCT's effect on change in depression was mediated by a decrease in dysfunctional metacognitive beliefs, particularly 'need for control'. Our findings underline that one of the key mechanisms of improvement in D-MCT is the change in metacognitive beliefs. The current study provides further support for the importance of metacognition in the treatment of depression.
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PMID:Cognitive and Metacognitive Mechanisms of Change in Metacognitive Training for Depression. 2861 51

'Metacognitive training for borderline personality disorder' (B-MCT) represents a complementary group intervention. It aims at raising awareness for cognitive biases that may play an important role in the development and maintenance of borderline symptomatology. For the present study, we evaluated the effectiveness of this new approach against a control condition. Seventy-four inpatients with borderline personality disorder (BPD) were randomly assigned to metacognitive training for BPD or progressive muscle relaxation training as an add-on intervention to treatment as usual. Severity of symptomatology was assessed at baseline, four weeks after beginning and six months after completion of the intervention. The per-protocol and intention-to-treat analyses revealed that patients in the metacognitive training group showed significantly greater reductions on the primary outcome (Borderline Symptom List-23) after six months. Progressive muscle relaxation was superior in alleviating depressive symptoms (secondary outcome: Beck Depression Inventory) at the long-term follow-up. Findings provide preliminary evidence that metacognitive training for BPD yields surplus effects to standard treatment.
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PMID:Efficacy of metacognitive training for patients with borderline personality disorder: Preliminary results. 2892 66

Metacognitive Training for Depression (D-MCT) is a highly standardized group program targeted at depression-related ("Beckian") emotional as well as cognitive biases, including mood-congruent and false memory. While prior results are promising with respect to psychopathological outcomes (depression), it is unclear whether D-MCT also meets its goal of improving cognitive biases, such as false memories. In the framework of a randomized controlled trial (registered trial, DRKS00007907), we investigated whether D-MCT is superior to an active control condition (health training, HT) in reducing the susceptibility of depressed patients for false memories. False memories were examined using parallel versions of a visual variant of the Deese-Roediger McDermott paradigm. Both groups committed less false memories at post assessment after 4 weeks compared to baseline. Relative to HT, D-MCT led to a significant decrease in high-confident false memories over time. The study presents first evidence that D-MCT decreases the susceptibility of depressed patients for false memories, particularly for errors made with high confidence that are presumably the most "toxic" in terms of mood-congruent memory distortions.
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PMID:Metacognitive Training for Depression (D-MCT) reduces false memories in depression. A randomized controlled trial. 2989 Mar 66

The aim of this study was to indentify the involvement of leptin receptors (LepR) in astrocytes in hippocampal synaptic transmission and plasticity and metabolism. To this end we used a genetic mouse model (GFAP-LepR-/-) of specific LepR ablation in GFAP positive cells and recorded excitatory postsynaptic potentials (fEPSPs) within the CA1 area. Glutamate (Glu) uptake and the expression of Glu transporters (EEAT3, GLT-1 and GLAST) and enzymes involved in Glu metabolism (glutamine synthase, GABA decarboxylase 65 and 67) were quantified. Modifications in the expression of GFAP, the glucose transporter (GLUT)-1, and the monocarboxylate transporters MCT-2 and MCT-4, were also analyzed. The results show that depletion of LepR in GFAP positive cells reduced basal synaptic transmission within the CA1 area and impaired N-methyl-d-aspartate (NMDA)-evoked long-term depression (NMDA-LTD). Hippocampal slices from GFAP-LepR-/- mice displayed lower Glu uptake efficacy together with up-regulation of GLT-1, glutamine synthase, GFAP and GLUT-1. In conclusion, astrocyte LepRs are involved in the maintenance of Glu homeostasis and Glu neurotransmission within the hippocampus. Our findings support a role of hippocampal LepRs in synaptic plasticity, which could have an impact on memory and learning processes.
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PMID:Specific Deletion of the Astrocyte Leptin Receptor Induces Changes in Hippocampus Glutamate Metabolism, Synaptic Transmission and Plasticity. 3170 91


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