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)

In a double-blind clinical trial comprising 29 depressed patients citalopram, a highly selective 5-HT re-uptake inhibitor and maprotiline, a specific NA re-uptake inhibitor, were compared. Allowing for the small sample and taking into consideration that both groups consisted of severely ill, hospitalized patients, it is notable that half of them appeared to respond to treatment. Comparison of the clinical efficacy of the two drugs showed no significant difference, but the profiles of the side-effects appeared to be different. The patients treated with citalopram showed increased sweating, drowsiness, restlessness and headache. These side-effects were almost entirely reported by the non-responders. The maprotiline patients had anticholinergic symptoms, such as dryness of mouth and constipation, side-effects which were also reported by the responders. No correlation was found between plasma steady-state levels of either drug and clinical outcome. The Dexamethasone Suppression Test (DST) appeared to show some predictive value as regards treatment response. There was a tendency towards better overall treatment results in the non-suppressor group. Determination of post-probenecid 5-HIAA, HVA and MHPG concentrations in lumbar-CSF was made in 22 patients. There was a significant negative correlation between HVA and the severity of depression, as well as a significant negative correlation of MHPG with the Newcastle score. The 5-HIAA concentration was found to be correlated with HVA, but not with MHPG. Rather surprisingly significant negative correlation between 5-HIAA and treatment results with maprotiline was found, but no correlation with MHPG. The lumbar-CSF MHPG and HVA values did not appear to have any predictive value as regards treatment response to citalopram or maprotiline. As expected the serotonin (5-HT) concentration in blood and thrombocytes in patients treated with citalopram showed a highly significant reduction after 2 and 4 weeks of treatment.
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PMID:A double-blind comparative clinical trial of citalopram vs maprotiline in hospitalized depressed patients. 244 51

Metabolites of selected neurotransmitters (5-HIAA, HVA and DOPAC) and beta-endorphin were measured in the CSF of 39 chronic pain patients and compared to controls. Twelve of the pain patients also fulfilled criteria for major depression. The concentration of 5-HIAA was increased in female but not male pain patients; there was no significant difference in the CSF concentrations of HVA and DOPAC. The presence of depression did not influence the concentrations of neurotransmitters. No correlation was found between the concentrations of monoamine metabolites and beta-endorphin. However, there was a positive correlation between 5-HIAA and HVA in controls and chronic pain patients without depression but not in depressed patients. It is concluded: chronic pain states are associated with elevation of CSF 5-HIAA in female patients; depression abolishes a positive correlation between 5-HIAA and HVA.
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PMID:CSF monoamine metabolites in chronic pain. 244 27

We have investigated the effects of granulocyte-macrophage (GM) CSF on two biochemical responses thought to play internal signaling roles in the neutrophils, namely the increase in the concentration of free calcium and the changes in the internal pH. The changes in the right-angle light scatter of the cell suspensions were also examined. GM-CSF was found not to affect the resting levels of calcium or the internal pH of the cells. However, pre-incubation of the neutrophils with the growth factor resulted in an increase in the magnitude of the calcium transients that follow the stimulation of the cells with chemotactic factors as well as a profound depression of the cell alkalinization that is induced by fMet-Leu-Phe, leukotriene B4, and platelet-activating factor, as well as by phorbol esters. The rapid cytoplasmic acidification elicited by these agents was apparently magnified. GM-CSF did not directly affect the Na+/H+ antiport as GM-CSF-treated cells were as capable as untreated cells of recovering from an acid load. The right-angle light scatter responses of the cells to the chemotactic factors were found not to be affected by GM-CSF. These results provide an initial description of the effects of GM-CSF on the cellular physiology of the neutrophils and insights into the mechanism of action of this factor as well as into the excitation-response coupling sequence activated by chemotactic factors.
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PMID:Granulocyte-macrophage colony-stimulating factor modulates the excitation-response coupling sequence in human neutrophils. 245 91

The compromised host has recently increased because of the improvement of medical diagnosis and technology. Infection in the compromised host is somewhat different from that in common patients, since this infection is caused by impairment of the host defense mechanism. And the compromised host easily suffers from opportunistic infections. This situation prompted us to study the effect of biological response modifiers (BRMs), which activate the host defense mechanism against infections in the compromised host. We used streptozotocin (STZ)-induced diabetic mice, as experimental models of the compromised host. First, we investigated the bactericidal capacity of the perineal exudating neutrophils in diabetic mice, as one of the host defense mechanism. Second, we also studied the effect of Granulocyte-Colony Stimulating Factor (G-CSF) on diabetic mice with ascending pyelonephritis by P. aeruginosa. At 1 and 2 weeks after inducing the diabetic state, no difference was found in the bactericidal capacity of the perineal exudating neutrophils between normal mice and diabetic mice. At 3 weeks, however, this bactericidal capacity was markedly suppressed in these mice. This result suggested that a depression of host defense mechanisms in diabetics was caused by, in part, a suppression of bactericidal capacity of neutrophils. When G-CSF (2 micrograms/mouse) was injected subcutaneously once a day into diabetic mice, the suppression of the bactericidal capacity of neutrophils significantly recovered. We thus studied the effect of G-CSF on diabetic mice against infection. Diabetic mice increased their susceptibility to bacterial infection more than normal mice. In diabetic mice, administration of G-CSF (2 micrograms/mouse) yielded a lower incidence of infection and infection-induced mortality than those of controls. These data show that G-CSF may be of great value for prevention and treatment of opportunistic infections in the compromised host, especially in patients whose bactericidal capacity of neutrophils is depressed, as in diabetics.
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PMID:[Study of the prophylactic effect of human granulocyte-colony stimulating factor (G-CSF) on experimental pyelonephritis induced by Pseudomonas aeruginosa in diabetic mice]. 248 17

A 5-year-old mixed breed dog was presented with a history of depression and anorexia. Physical examination revealed a pharyngeal tumour and a neurological examination indicated the presence of a possible space-occupying lesion in the brain. Investigative procedures included a bloodsmear, impression smears and cytology of the pharyngeal tumour, haematology, chemical pathology, faecal analysis, urinalysis, electrocardiography, cerebrospinal fluid analysis, hormone assays and a computerised axial tomography scan. Results of these investigations revealed a round cell tumour in the pharynx, hypergammaglobulinaemia (34 g l-1), azotaemia (urea 8.6 mmol l-1 and creatinine 170 mumol l-1), hypoalbuminaemia (20 g l-1), proteinuria, sinus bradycardia (heart rate 60 beats per min), increased concentration of protein in the CSF (1.1 g l-1), hypoadrenocorticism (base line cortisol less than 55 nmol l-1) and hypothyroidism (T4 less than 13 nmol l-1). The computerised axial tomography scan revealed a brain tumour in the region of the hypophysis. The dog was euthanased and a post mortem examination confirmed the presence of a pharyngeal tumour with apparent direct extension of the tumour into the brain. Both tumours were confirmed histologically as mastocytomas.
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PMID:An expansile secondary hypophyseal mastocytoma in a dog. 251 66

Feline parvovirus (FPV) causes leukopenia in naturally infected cats. We investigated the mechanism of hematopoietic depression by this virus in feline bone marrow cultured in vitro. In suspension cultures we demonstrated FPV propagation and replication using DNA molecular hybridization. Viral RNA and DNA were observed by in situ hybridization in about 10% of marrow cells at day 3. Granulocytes and their precursors were virtually absent from infected cultures after six days. Infected cells showed viral capsid protein predominantly in nuclei by immunofluorescence. In clonal assays, FPV most efficiently inhibited hematopoietic colony formation by myeloid progenitor cells (CFU-GM), but erythroid colony formation (BFU-E and CFU-E-derived) was also depressed in the presence of virus. Inhibition of colony formation could be abrogated by physical inactivation of the virus or preincubation with specific neutralizing antibodies. Recombinant human colony stimulating factors GM-CSF and G-CSF supported feline myelopoiesis in progenitor assays, and FPV completely inhibited factor dependent colony formation.
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PMID:Feline parvovirus propagates in cat bone marrow cultures and inhibits hematopoietic colony formation in vitro. 254 25

Clinical and biochemical effects of two selective 5-HT uptake inhibitors, zimeldine and alaproclate, were studied in 24 hospitalized patients with endogenous depression. According to a randomized parallel group design 14 patients were treated with zimeldine and 10 with alaproclate. The dosage of both zimeldine and alaproclate was 200 mg daily. For the evaluation of the clinical effect, Montgomery & Asberg Depression Rating Scale (MADRS) was used. Seven of 14 patients treated with zimeldine and seven of 10 treated with alaproclate improved. 5-HT uptake inhibition in patients' platelets and concentration of amine metabolites (5-HIAA, HVA, HMPG) in CSF were studied before and during treatment. After 3 weeks of treatment with zimeldine 5-HIAA and HMPG in CSF decreased significantly while HVA in CSF increased significantly. Zimeldine produced a significant 5-HT uptake inhibition in platelets. During treatment with alaproclate no significant change in amine metabolites concentration in CSF was found and there were no mean changes on 5-HT uptake inhibition in platelets.
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PMID:Alaproclate a novel antidepressant? A biochemical and clinical comparison with zimeldine. 258 Apr 22

Experimental animal models have been introduced to study aspects of psychiatric symptoms of depression and anxiety; however, there is no comprehensive animal model for these conditions. The models introduced may simulate certain symptoms (despair), be used to evaluate behavioral theories (cognitive theory of learned helplessness), allow study of underlying neurochemical mechanisms (CSF metabolites, genetic, neurotransmitter model), be used to evaluate developmental issues, and lead to finding new treatments through preclinical pharmacologic trials. A variety of models are needed, as each one attempts to deal with a particular aspect of a syndrome. Pharmacologic models, the model of uncontrollability, separation models, and genetic approaches have been summarized. Depression is viewed as a complex, multifactorial illness. Anxiety models have focused on pharmacologic treatment of motivational conflict and the elicitation of fear and panic through environmental and drug manipulations. The most recent investigations in this area address separation calls and alarm calls in primates as potential models for separation distress and panic symptomatology, arguing that the behavioral context as well as the specific behavior be considered. Animal models have emphasized adult psychopathology in the past. However, with increased recognition of psychiatric disorders in children and adolescents, animal modeling of disorders that begin in the development period assumes importance. Studies in the animal modeling of depression and anxiety involving genetic models, psychosocial models, and stress-induction models are the focus of continuing investigations and may be pertinent to child and adolescent psychopathology. They offer hope for learning more about the neurobiologic mechanisms involved in these conditions and for testing new treatment approaches.
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PMID:Experimental animal modeling of depression and anxiety. 269 27

The different methods of measuring the intracranial CSF spaces on CT images are described. The values obtained are demonstrated to separate the normal aging brain from the brain in senile dementia of Alzheimer's type. The CT criteria for the diagnosis of multi-infarct dementia are shown. The significance of CT studies in senile depression is discussed. The problem of vascular encephalopathy (leuko-araiosis) in normal aging of the brain and in dementia is considered in particular, and even the occurrence of intracranial space-occupying lesions and normal pressure hydrocephalus, as treatable causes of dementia and depression, are mentioned. The data and results of my own CT research on normal brain aging, dementia and depression are presented with reference to the literature.
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PMID:[Problems in CT diagnosis of the aging brain]. 269 69

In order to investigate the mechanisms leading to respiratory depression after lumbar administration of opioids, plasma and ventricular CSF pharmacokinetics of intrathecal meperidine (1 mg.kg-1) were studied in five head-injured patients undergoing surgery for lower limb fracture. Meperidine was detected both in the plasma (arterial catheter) and in the ventricular CSF (intracranial catheter) soon after intrathecal administration: 45 +/- 17 min and 100 +/- 14 min, respectively. The maximal plasma concentration was 341 +/- 133 ng.ml-1, whereas, in ventricular CSF, it was 64.5 +/- 14.9 ng.ml-1. The ventricular CSF-plasma ratio increased with time (r = 0.82) from 0.18 +/- 0.04 at the first hour to 0.38 +/- 0.1 at 16th hour. It is concluded that the putative risk of respiratory depression appears to be mainly related to the absorption into the systemic circulation and to redistribution back into CSF.
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PMID:Arterial and ventricular CSF pharmacokinetics after intrathecal meperidine in humans. 272 38


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