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)

The authors studied depression after focal subcortical lesions (SCLs) in 45 highly selected subjects. Secondary major depression (secondary MD) occurred in 20.0%, depressive disorder NOS (secondary DDNOS) in 4.4%, and secondary dysthymia in 0.0%. secondary MD after SCLs was associated with pallidal lesions (88.9%) and dystonia without geste antagonistique; subjects with secondary DDNOS had nigrotegmental lesions and parkinsonism. Depressive severity after SCLs correlated positively with severity of parkinsonism and dystonia. Pallidal lesions disrupting neurotransmitter systems and pallidothalamic and parietal input to the frontal lobe may lead to secondary MD, whereas nigrotegmental lesions may predispose to secondary MD forme fruste (secondary DDNOS) through disruption of mesocortical frontal or nigrostriatal dopamine tracts. Patients should be closely followed over several years for depression after such lesions, especially when accompanied by parkinsonism or dystonia without geste antagonistique.
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PMID:Clinical, motor, and biological correlates of depressive disorders after focal subcortical lesions. 914 6

We studied 149 subjects admitted to hospital with operable, untreated breast cancer (108) or benign (41) breast disease (control group). Depression was evaluated before diagnosis and surgery, using MMPI and Rorschach tests, HDRS scale, and DSM-III-R diagnostic criteria during a semistructured interview. 62% of patients and 34% of controls (p<0.005) presented some depressive symptoms, whereas only 55% of patients and 18% of controls (p<0.001) met criteria for depressive mood disorders: 2% of patients and 0% of controls for major depression, 13% and 5% for dysthymia (p<0.05), 40% and 13% for depressive disorders NOS (p<0.001). No correlation was observed with respect to stage of disease, histopathologic grade, age and menopause except for ER status (p=0.03). During interview, 89% of patients and 65% of controls reported severe stressful life events 5+/-4 years before the clinical onset of the breast node. No differences were observed in the depression rating scales mean value whereas patients resulted more inhibited in their affection and emotionally controlled (Rorschach data) compared to controls (p<0.05). In conclusion, although the depression diagnostic criteria used may not be strictly correlated higher prevalence of depressive mood disorders and stressful life events were observed in patients in the pre-clinical phase of operable breast cancer. This may suggest an involvement of depression in the natural history of breast cancer.
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PMID:Depressive mood disorders in patients with operable breast cancer. 914 71

Examines the relation between depression, self-esteem, sex, and age to determine if the previously reported associations between these variables in nonreferred samples remain consistent in a sample of clinically referred patients. Two hundred thirty-six participants between the ages of 6 and 17 years were included. All were consecutive referrals to an outpatient child and adolescent mood disorders program. Eighty-four percent met the criteria for at least 1 depressive disorder from the third and revised edition of the Diagnostic and Statistical Manual of Mental Disorders (major depressive disorder, dysthymia, both, depression NOS, or adjustment disorder with depressive mood). In keeping with previous reports, the data indicate an inverse relation between age and self-esteem and an even stronger inverse relation between depression and self-esteem. However, there was no evidence for a sex difference for self-esteem, alone or interactively with age. The implications of these findings in relation to the importance of self-esteem in depressed youth are discussed.
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PMID:Depression, self-esteem, sex, and age in a child and adolescent clinical sample. 929 86

The study consisted of evaluating 80 out-patients for DSM-IV diagnoses and giving 75 mg trazodone for four months to children aged 9-13 who fulfilled DSM-IV criteria for Major Depressive Disorder (n = 22); Major Depressive Disorder and Generalized Anxiety Disorder (n = 24), Major Depressive Disorder and Learning Disorder NOS (n = 24); Major Depressive Disorder and Oppositional Defiant Disorder (n = 10). They were followed up weekly by a psychiatrist blind to the original evaluations and to the precise purpose of the study. Trazodone emerges as safe and effective for over 50% of the sample. Those with depression alone and with LD NOS did particularly well, and those with ODD did particularly badly. The presence of psychopathology in the parents was associated with poorer response to trazodone, and life events were also associated with a poor response.
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PMID:Depressive disorder in pre-adolescence: comorbidity or different clinical subtypes? (A pharmacological contribution). 933 23

Nitric oxide (NO) is an effector molecule with multiple effects on various organ systems. The most prominent physiological actions of NO as a biological mediator include cGMP-dependent vasodilation and cytotoxicity against pathogens in the unspecific immune defense. Sepsis syndrome is a complex disease entity mostly caused by overwhelming bacterial infections. It has a high mortality rate of 40 to 60%. Catecholamine-resistant hypotension and myocardial depression are regarded as major factors contributing to death in septic patients. In septic shock, a pathophysiologically increased NO production occurs due to an excessive induction of the inducible NO synthase (iNOS). Inducible nitric oxide synthase up-regulation is probably caused by bacterial endo- and exotoxins as well as by an increase of circulating pro-inflammatory cytokines. It may be a key factor leading to pronounced vasodilation and myocardial toxicity. Experimental studies have confirmed that NO overproduction causes severe hypotension in septic animals. Treatment with competitive NOS-inhibitors abolishes this hypotension in animals as well as in septic patients. However, their use is complicated by concomitant decreases in cardiac index and oxygen delivery. Conclusive data on mortality in animals and patients with sepsis-syndrome treated by NOS antagonists are not available. This article discusses current concepts concerning the L-arginine/NO system in the pathophysiology of and as a potential therapeutic target in septic shock.
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PMID:Nitric oxide in sepsis-syndrome: potential treatment of septic shock by nitric oxide synthase antagonists. 947 85

Nitric oxide (NO) is one of many vasoactive substances released, from a variety of cells, under conditions of endotoxaemia and sepsis. Under physiological conditions it is produced by two constitutive calcium-dependent enzymes (nitric oxide synthase; NOS) in neurones (nNOS) and endothelial cells (eNOS) and has functions ranging from neurotransmission and vasodilatation to inhibition of platelet adhesion and aggregation. Following bacterial infection, especially with Gram-negative organisms, its formation from L-arginine is enhanced due to the cytokine-mediated induction of a NOS enzyme (iNOS) in cells (e.g. cardiac myocytes, vascular smooth muscle) that do not normally have the ability to synthesize NO. The result of this excessive NO production is enhanced bacterial lysis by activated macrophages, vasoplegia and myocardial depression. These cardiovascular effects can be alleviated by inhibitors of the L-arginine NO pathway, which results in elevated perfusion pressure, restored responsiveness to sympathetic nerve stimulation and to exogenous catecholamines, and to enhanced (endothelin-dependent) myocardial contractility. In patients in shock this approach also leads to detrimental effects (increased systemic vascular resistance, elevated pulmonary artery pressure, reduced cardiac output and oxygen delivery, increased platelet accumulation) and survival is not improved. Because some of these detrimental effects are due to inhibition of eNOS, attempts have been made to examine the effects of substances with a higher selectivity for the induced form of the enzyme. In experimental animals, one of these (L-canavanine) protects endothelial cells from damage, increases survival time and restores vascular responsiveness without increasing blood pressure or peripheral vascular resistance. However, whether even this approach will be of benefit to patients with sepsis remains in doubt since studies in iNOS knock-out mice do not support the concept that eliminating this particular source of NO improves ultimate survival.
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PMID:Nitric oxide in sepsis and endotoxaemia. 951 Oct 84

Inflammatory cytokines have been implicated in the reversible depression of cardiac contractile function accompanying local or systemic immune stimulation. Incubation of cardiac myocytes with soluble components in the supernatant from cultured rat lung macrophages activated with endotoxin decreases their contractile response to beta-adrenergic stimulation through the induction of iNOS and the subsequent production of nitric oxide by these cells. In the present study, we characterize the mechanisms underlying NO's attenuation of adrenergic responsiveness in cardiac myocytes. iNOS was induced in cultured ventricular myocytes from adult rats by incubation for 20 h with conditioned medium from lipopolysaccharide (LPS)-activated macrophages. iNOS induction did not induce any alteration in beta-adrenergic receptor density or affinity, Galphai protein abundance, or adenylyl cyclase activity in cultured myocytes. Myocyte exposure to activated macrophage-conditioned medium markedly attenuated the elevation of cAMP in response to isoproterenol (Iso, 2 nM). Induction of iNOS with the macrophage-conditioned medium also potentiated the Iso-induced increase in myocyte cGMP. This cGMP increase was totally abolished by NOS inhibitors. NOS inhibition also returned the attenuated cAMP response to 2 nM Iso to levels observed in control cells. Pre-incubation of the cells in isobutylmethylxanthine (IBMX), a phosphodiesterase inhibitor, also partly reversed the attenuation of cAMP increase with 2 nM Iso in cells expressing iNOS. Brief (15 min) exposure of myocytes to the NO donor, S-nitrosoacetylcysteine (SNAC, 100 micro M) which produced a three-fold increase in intracellular cGMP, also decreased by half the contractile response of cardiac myocytes to Iso (2 nM). We conclude that NO endogenously produced by iNOS decreases the intracellular levels of cAMP in response to beta-adrenergic stimulation in isolated cardiac myocytes, in part through a cGMP-mediated mechanism. This effect may participate in the NO-dependent depression of cardiac function following cytokine exposure.
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PMID:Regulation of cardiac myocyte contractile function by inducible nitric oxide synthase (iNOS): mechanisms of contractile depression by nitric oxide. 951 7

Prospective data on 1,360 consecutive inpatients referred to the consultation-liaison psychiatry service of 2 metropolitan general teaching hospitals and diagnoses as having a Depressive Illness Spectrum Disorder were collected by using the MICRO-CARES clinical database system. The distribution of DSM-III-R diagnoses was major depression (MD) 49%; dysthymia (DYS) 15%; organic or substance-induced mood disorder or depressive disorder not otherwise specified (ORG/NOS) 14%; and adjustment disorder with depressed mood (AD) 29%s. Antidepressants were prescribed in 59% of the MD cases, 40% of the DYS cases, 36% of the ORG/NOS cases, and 17% of the AD cases. In confirmed MD, antidepressants were prescribed in 69%, and significantly more often in those who were older, female, had a prior history of physical illness, had a neoplasm or a disorder of the nervous or musculoskeletal systems, had higher Axis IV scores, or were referred because of pain or terminal illness. The patients with confirmed MD prescribed antidepressants had a longer length of stay and were referred later than those not prescribed antidepressants. The results illustrate the importance of all the forms of depression in consultation-liaison psychiatry and the vigor with which all forms are treated.
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PMID:Consultation-liaison psychiatrists management of depression. 966 71

In adult mammalian cardiomyocytes, stimulation of muscarinic receptors counterbalances the beta-adrenoceptor-mediated increase in myocardial contractility and heart rate by decreasing the L-type Ca2+ current (ICa) (1, 2). This effect is mediated via inhibition of adenylyl cyclase and subsequent reduction of cAMP-dependent phosphorylation of voltage-dependent L-type Ca2+ channels (3). Little is known, however, about the nature and origin of this pivotal inhibitory pathway. Using embryonic stem cells as an in vitro model of cardiomyogenesis, we found that muscarinic agonists depress ICa by 58 +/-3% (n=34) in early stage cardiomyocytes lacking functional beta-adrenoceptors. The cholinergic inhibition is mediated by the nitric oxide (NO)/cGMP system since it was abolished by application of NOS inhibitors (L-NMA, L-NAME), an inhibitor of the soluble guanylyl cyclase (ODQ), and a selective phosphodiesterase type II antagonist (EHNA). The NO/cGMP-mediated ICa depression was dependent on a reduction of cAMP/protein kinase A (PKA) levels since application of the catalytic subunit of PKA or of the PKA inhibitor PK) prevented the carbachol effect. In late development stage cells, as reported for ventricular cardiomyocytes (2, 4), muscarinic agonists had no effect on basal ICa but antagonized beta-adrenoceptor-stimulated ICa by 43 +/-4% (n=16). This switch in signaling pathways during development is associated with distinct changes in expression of the two NO-producing isoenzymes, eNOS and iNOS, respectively. These findings indicate a fundamental role for NO as a signaling molecule during early embryonic development and demonstrate a switch in the signaling cascades governing ICa regulation.
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PMID:Regulation of the L-type Ca2+ channel during cardiomyogenesis: switch from NO to adenylyl cyclase-mediated inhibition. 997 19

Nitric oxide is formed in the brain primarily by neurons containing neuronal nitric oxide synthase (nNOS), though some neurons may express endothelial NOS (eNOS), and inducible NOS (iNOS) only occurs in neurons following toxic stimuli. Mice with targeted disruption of nNOS (nNOS-) display distended stomachs with hypertrophied pyloric sphincters reflecting loss of nNOS in myenteric plexus neurons. nNOS- animals resist brain damage following middle cerebral artery occlusions consistent with evidence that excess release of nitric oxide mediates neurotoxicity in ischemic stroke. Neuronal NOS- mice have no grossly evident defects in locomotor activity, breeding long-term depression in the cerebellum, long-term potentiation in the hippocampus, and overall sensorimotor function. However, nNOS- animals display excessive, inappropriate sexual behavior and dramatic increases in aggression. Because the cerebellum possesses the greatest levels of nNOS neurons in the brain, it was surprising that presumed cerebellar functions such as balance and coordination were grossly normal in nNOS- mice. These previous studies were all conducted during the day (between 1400 and 1600, lights on at 0700). We now report striking, discrete abnormalities in balance and motor coordination in nNOS-mice reflected selectively at night.
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PMID:Nocturnal motor coordination deficits in neuronal nitric oxide synthase knock-out mice. 1007 13


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