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)

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

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

A brief characterization of 27 neurologic syndromes occurring in 44 AIDS patients during two years is presented. In 4 out of 7, intrathecal Ig synthesis was demonstrated without the CSF cell count and blood brain barrier values being within a normal range. Ig intrathecal formation was also observed in 2 LAS patients without neurological symptoms. Similar changes in CSF findings occur in other subacute encephalitis, particularly in multiple sclerosis. Activation of CSF B-cells or their depression due to impairment of CD8 T-lymphocytes was indicated as the cause of this phenomenon. In the Authors' opinion this explanation is somewhat general. The possibility of an immune response in CNS was clearly demonstrated, but in the CSF neither B-cells nor Ig producing plasma cells are evident. In addition, it should be noted that the reliability of blood brain barrier and Ig intrathecal assessment procedures is doubtful in ADC disease, because of the severe alterations in serum albumin and Ig concentrations seen in these patients.
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PMID:Cerebral spinal fluid IgG production in HIV-positive patients. 274 Jun 4

The ventilatory pharmacodynamics of morphine sulfate (MS) in the awake dog (n = 14) were investigated. Two routes of MS administration were employed: 1) 4 h continuous intravenous (iv) infusion (1 mg.kg-1 loading dose, 10 micrograms.kg-1.min-1 thereafter); and 2) fourth ventricle to cisterna magna perfusion (VCP) at increasing infusate morphine concentrations (0.1-100 micrograms.ml-1). The former was associated with a constant plasma and cisternal CSF (and presumably tissue) free morphine concentration. The latter produced, over 1 h at a constant infusate morphine delivery, a cisternal CSF free morphine concentration that leveled off by 30 min, little or no distribution of drug beyond superficial dorsal and superficial ventral brainstem tissue, and no detectable levels of morphine in plasma. When comparing the two routes of administration, ventilatory depression for a given cisternal free morphine level in the iv infusion studies was of a much greater magnitude than that seen in VCP experiments. Differences in the ventilatory patterns were also noted. Thus, iv delivery produced a decrease in tidal volume (VT) and no change or reduced respiratory frequency (f) with prolonged exposure. VCP delivery was also associated with reduction in VT but produced significant increases in f. An apparent maximal ventilatory depression with 1 h VCP administration was observed at morphine infusate levels of greater than 10 micrograms.ml-1, with higher infusate concentrations and extension of the perfusion period to 3 h producing no significant additional changes. Finally, VCP delivery of the mu-antagonist nalbuphine could only partially reverse the ventilatory depression accompanying iv morphine administration. These findings suggest that the ventilatory depression associated with iv morphine is a result of interactions with brain u-opiate receptors in superficial brainstem tissue and in deep brainstem and/or suprapontine tissue as well.
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PMID:Comparative ventilatory effects of intravenous versus fourth cerebroventricular infusions of morphine sulfate in the unanesthetized dog. 275 45

Recently sufficient evidence has accumulated to propose that a central GABAergic dysfunction may be primarily related to the pathology of affective disorders and that antidepressant mechanisms (pharmacological or electroconvulsive therapy, ECT) have an intrinsic GABAergic component. In depressed patients GABA levels are reported to be low in the CSF and plasma, and GABA synthesis is decreased in some brain areas, including the frontal cortex. GABAmimetics such as progabide and fengabine exert a therapeutic effect in depression. In behavioural laboratory models GABAmimetics exhibit antidepressant-like actions in the olfactory bulbectomized rat and in rats submitted to an inescapable shock (learned helplessness). Furthermore, antidepressant GABAmimetics decrease paradoxical sleep. In the olfactory bulbectomized rat, GABAB receptors are downregulated in the frontal cortex and in the learned helplessness model, GABA release is diminished in the hippocampus. These decreases are reversed by antidepressants in parallel with their behavioural activities. An intrinsic activity of widely varied antidepressants and ECT is the upregulation of GABAB receptors in the frontal cortex. This, together with the downregulation of beta-adrenergic receptors induced by these compounds, and the GABAB modulation of the beta-adrenergic second messenger system, strongly suggest that both GABAergic and beta-adrenergic responses are inherent to an antidepressant effect.
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PMID:GABA and affective disorders. 282 30


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