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 investigated the effect of urinastatin on energy metabolism disorder during shock. Intravenous administration of urinastatin at the dose of 50,000 U/kg ameliorated the decrease in total adenine nucleotide (TA) levels and in energy charge (EC) of liver and pancreas during traumatic-shock induced by the Noble-Collip drum method in rats. Urinastatin, at a concentration of 3,000 U/ml, suppressed the decrease in EC of rat liver slices exposed to the medium including 10% serum obtained from traumatic-shock rats. Aprotinin showed a similar effect. Depression in respiratory activity of liver mitochondria exposed to the shock rat serum was also ameliorated by 1,000 U/ml of urinastatin, but aprotinin failed to reverse this depression. In the isolated rat livers perfused with normal rat serum, urinastatin at the concentration of 3,000 U/ml did not affect ATP and TA levels and EC. These results suggest that, unlike aprotinin, urinastatin ameliorates the depression of energy metabolism in liver during shock without affecting normal energy metabolism, probably by antagonizing the actions of depressant factors released into blood during the shock state and by protecting against the decrease in the adenine nucleotide pool.
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PMID:[Effects of urinastatin on an energy metabolism disorder during shock]. 243 82

The monoamine hypothesis of depression originally proposed that depression is caused by a central deficiency of biogenic amines, and antidepressants were considered to work by correcting this deficiency. In the course of time, many studies have analysed monoamine metabolites in the urine, plasma and cerebrospinal fluid of patients and healthy controls under different conditions to test the hypothesis. These studies have failed to identify a robust metabolic disorder in depressive patients as a group. Certain subgroups of depressed patients have shown deviations in biogenic amine metabolism, the most consistent being reduced levels of the major serotonin and dopamine metabolites in the cerebrospinal fluid. Noradrenaline metabolism is influenced by the activity of the sympathetic nervous system, and thus increases in anxious patients regardless of their clinical diagnosis. On the other hand, development of new antidepressants and advances in receptor techniques, together with modern electrophysiologic and behavioural studies have given increasing support to a receptor supersensitivity hypothesis of depression, based on the evidence that antidepressants lead to subsensitivity or down regulation of beta-adrenoceptors, and adaptive changes may occur also in other receptor systems after two three weeks of antidepressant treatment. There is also growing evidence on the manifold interplay of noradrenergic and serotonergic systems in the mechanism of actions of effective antidepressant treatments, including the new and more selective therapeutic compounds. The rapidly increasing knowledge of the neurotransmitter receptors as well as of the relations between the different regulatory systems may lead to more specific intervention strategies in efforts to correct the biological malfunction in the heterogeneous collection of diseases classified as affective disorders.
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PMID:Monoaminergic mechanisms in affective disorders. 288 34

Myalgic Encephalomyelitis or post-viral fatigue syndrome is a common disorder, which has been known previously under a variety of different names, i.e., Iceland disease or Royal Free disease. It may occur in epidemics or sporadically. The cause is unknown, with patients complaining of exhaustion, fatigue, muscle aches and pains, and invariable psychiatric symptoms such as emotional lability, poor memory/concentration, and depression. Present-day research points to the cause as a metabolic disorder secondary to persistent viral infection.
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PMID:Postviral fatigue syndrome. 306 94

An adequate history from the patient and a family member, an examination for signs and symptoms suggestive of contributing organic disease, plus an individualized diagnostic battery of laboratory tests are sufficient workup for most patients presenting with the dementia syndrome. Electroencephalography, computerized axial tomographic scanning, or psychometric testing are not usually required. The results of eight studies investigating demented individuals are reviewed. Across these studies, 56 percent of cases were attributable to primary dementia, 15 percent were secondary to reversible causes, 13 percent were secondary to irreversible conditions, and 15 percent of individuals had been wrongly labeled demented. Of reversible dementias including depression, 56 percent of patients improved with therapy. Metabolic disorders were associated with about 25 percent of reversible dementias and accounted for less than 5 percent of all patients investigated for the dementia syndrome.
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PMID:Evaluation of the demented patient. 310 30

Intravenous anesthesia is a method rarely used during infancy. Only neuroleptanalgesia has a number of indications, especially in major surgery and for seriously ill children. There are several advantages of inhalation anesthesia in infancy: good control of anesthesia because of low fat-muscle mass, low functional residual capacity, relatively increased alveolar ventilation, and increased cardiac output. Potential disadvantages of inhalation anesthesia in infancy are numerous: The necessity of high concentrations of inhalational agents may cause myocardial depression and blood pressure drops, the analgetic potency is very low, damage to surfactant is possible, there is a prolonged awakening period in many cases, and cerebral blood flow and intracranial pressure can be increased by inhalation anesthetics. Positive results with the short-acting opiate alfentanil in adult lead us to the idea of replacing routine inhalation anesthesia by a combination of low-dose halothane and intermittent injections of alfentanil. Fifty infants undergoing corrective orthopedic surgery of the hip and lower limb were anesthetized with the combination of alfentanil and halothane described in Fig. 1. Patient data are shown in Table 2. All children were premedicated orally with flunitrazepam 0.1 mg/kg body weight and Bellafolin 1 drop/kg and were primarily anesthetized via inhalation of oxygen/N2O/halothane. After relaxation with vecuronium, intubation and administration of alfentanil, halothane concentrations were reduced to low maintenance doses. Intraoperative und postoperative circulatory parameters showed remarkable stability. Postoperative blood gas analyses--in 8 cases done using capillary blood--gave no hint of any respiratory or metabolic disorder caused by the anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intravenous combination anesthesia using alfentanil in infants]. 314 88

Morphofunctional studies of muscles, heart, liver and kidneys after different periods of compression and decompression, as well as literature data indicate that crush syndrome is one of the most severe forms of traumatic shock. A wide range of pathologic effects of catecholamines and other shock-causing agents in response to the emotional stress and pain occurs already at the compression period and results in hemodynamic disturbances in microcirculation of organs and tissues with the development of dystrophic and necrobiotic processes, depression of the monocytic phagocyte system and immune system. The consequences of shock are mostly manifest after decompression: hypercatecholaminemia, hypovolemia, intoxication with myolysis and pathogenic microflora products result in aggravation of monocytic phagocyte failure, as well as immune system, intravascular coagulation, membrane penetration insufficiency, cell necrosis. Monocytic macrophage depletion favours the progression of hepatic necrobiosis, formation of renal failure and detritus organization in the muscles of the extremities. Hypercatecholaminemia and hypoxia (leading to electrolyte-imbalance contractures of myofibrillar apparatus, metabolism disorder and intracellular conductivity disturbance) from the basis for cardiac insufficiency. Inadequate cardiac function, in its turn, maintains hemodynamic and hypoxic disturbances in tissues. Changes in renal blood flow, hemofiltration and tubular system are shown to reflect different aspects of pathogenesis of the acute renal failure in crush syndrome.
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PMID:[Morphology and pathogenetic problems of the crush syndrome]. 355 89

Thiamine-deficient encephalopathy is characterized by morphologic lesions in the brainstem and less extensively in the cerebellum, but the early neurologic signs reverse rapidly and fully with thiamine, indicating a metabolic disorder. The suggested causal mechanisms of the encephalopathy involve two thiamine-dependent enzymes: (a) impairment of pyruvate decarboxylase activity with decreased cerebral energy (ATP) synthesis, and (b) reduction of transketolase activity with possible impairment of the hexose monophosphate shunt and subsequent decrease in NADPH formation. The latter may be important in maintaining glutathione in a reduced form (GSH), which apparently functions by keeping enzymes in a reduced (active) conformation. To examine some of these postulated mechanisms, in this study we measured pyruvate decarboxylase and transketolase activity, lactate, ATP and GSH levels in the cerebral cortex, cerebellum, and brainstem, and thiamine concentration in whole brain of rats with diet-induced low thiamine encephalopathy. Pair-fed and normally fed asymptomatic control animals were similarly investigated. To assess the functional importance of some of our results, we repeated the studies in rats, immediately (16-36 hr) after reversal of the neurological signs with thiamine administration. THE DATA OBTAINED LED TO THE FOLLOWING CONCLUSIONS: (a) Brain contains a substantial reserve of thiamine in that thiamine level has to fall to below 20% of normal before the onset of overt encephalopathy and an increase in brain thiamine to only 26% of normal results in rapid reversal of neurologic signs. (b) Both cerebral transketolase and pyruvate decarboxylase activities are impaired in low thiamine encephalopathy and the abnormality in the pyruvate decarboxylase is reflected in a rise in brain lactate. These biochemical abnormalities occur primarily in the brainstem and cerebellum, the sites of the morphologic changes. (c) Although the fall in cerebral transketolase is about twofold greater than that of pyruvate decarboxylase activity during encephalopathy, both enzymes rise on reversal of neurologic signs and the degree of the transketolase rise is slight. Accordingly, this study cannot ascertain the relative functional importance of these two pathways in the induction of the encephalopathy. The data suggest, however, that the depression of transketolase is not functionally important per se, but may only be an index of some other critical aspect of the hexose monophosphate shunt. (d) The normal cerebral ATP concentration and small GSH fall during encephalopathy, with little GSH rise on reversal of neurologic signs, suggest that a depletion of neither substance is instrumental in inducing thiamine-deficient encephalopathy.
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PMID:Encephalopathy of thiamine deficieny: studies of intracerebral mechanisms. 567 22

The following paper deals with the current research in hyperthyroidism, with special accent to Graves' disease. Besides severe psychological trauma a breakdown of neurotic defense mechanism on the ground of a special personality structure was thought to be the trigger of the disease. The metabolic changes became the main point of interest. The influence of thyrostatic, surgical and radioactive therapies on psychological symptoms, was investigated. Thereby, the previously anticipated emotional factors became less significant in the aetiology of the disease. A recent study (Paschke 1990) suggests that patient with hyperthyroidism have, even in an euthyrotic state, an increased vulnerability to anxiety provoking situations. At this point it is not clear, due to the retrospective nature of the study, whether the vulnerability exists prior to the unset of the disease or is a result of the metabolic disorder. Both thyroxin and TRH are being successfully used in the treatment of major depression. TRH acts as a neurotransmitter in the autonomic nervous system and can be demonstrated in the peripheral lymphocytes. However, the exact mechanisms of action of thyroxin and TRH are still unknown. Graves' disease is an autoimmune disease, that can be caused by specific HLA antigens. Thereby, a changed subpopulation of lymphocytes can be demonstrated, as well as there disturbed functions. A correlation between high scores for anxiety and depression on one hand and the occurrence of an abnormal T4/T8 ratio on the other hand, have been reported in a small number of cases (Paschke 1990). The psychological symptoms in hyperthyroidism are similar to the symptomatology of neurotic anxiety and the anxious depressive syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Psychosomatic aspects of hyperthyroidism with special reference to Basedow's disease. An overview]. 837 18

The purpose of this prospective study was to identify the incidence of a distinct central anticholinergic syndrome following routine anaesthesia. For 2 months, all inpatients aged more than 15 years scheduled for elective procedures and cared for in the recovery room were investigated for symptoms of the syndrome. Patients with neuropsychiatric disease or other disorders that could alter consciousness were excluded. Prolonged action of anaesthetics or relaxants, respiratory depression and metabolic disorder were ruled out before making the diagnosis. Out of 962 patients (366 men, 596 women), 18 (4 men, 14 women) developed the syndrome. The difference between men and women was not statistically significant. Six out of 60 women developed the syndrome after a hysterectomy with or without adnectomy/oophorectomy, and this high incidence was significantly different from that observed after all other procedures in women (P = 0.003) or all other gynaecological procedures (P = 0.013). The reason for this is unknown. In six of the 18 cases, untreated prolonged somnolence lasted for more than 2 h. All patients woke up after an injection of physostigmine, but six of them relapsed into somnolence and needed a second, and in one case a third, injection. The findings of the study emphasize that, when there is delayed recovery from anaesthesia, the diagnosis of central anticholinergic syndrome should be considered if other accessible causes for that condition have been excluded.
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PMID:Distinct central anticholinergic syndrome following general anaesthesia. 904 53

Growing understanding of the pathogenetic process of insulin-dependent diabetes mellitus diabetes has favoured attempts to predict the clinical manifestation of the metabolic disorder in people at risk by some easily measurable marker or markers and, subsequently, to prevent its onset. This complicated process includes the screening procedure based on the assumption of an eventually positive finding, the detection of islet cell antibody positivity, metabolic tests for the evaluation of the actual state of energy metabolism, the categorization of the respective individual's risk to develop diabetes, the commencement of some placebo-controlled interventive measure, and finally the chance to fail to prevent the disease. Every step in this process may constitute both a threat and a severe burden to the affected individual and his/her family, eventually arousing conflicts and depression, and hopefully also attempts to deal and cope with them. The coping procedure, however, may be greatly influenced by various pre-existing primary and acquired secondary factors. Because at present prevention trials are justified only in families already exposed to this disease, the latter may depend upon the impact of diabetes in one (or more) member(s) of the family, and upon their acquired competence to cope with the various challenges it brings. On the other hand, personal characteristics, such as individual maturity, emotional stability and the integrity of one's self-image in spite of this threat, and the competence of the family to support the threatened member may be important codeterminants of the individual's response to disease prediction and preventive activities. In order to understand the impact of disease prediction and prevention on the individual better, but also to increase his coping potential by competent advice, future prevention trials should be accompanied by psychological research and competent offers of support for the affected individuals and their families.
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PMID:Psychological aspects in diabetes prevention trials. 945 95


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