Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The microcirculatory state (by the method of conjunctival biomicroscopy) and ADP-induced platelet aggregation were examined in 42 patients with atherosclerotic and 34 patients with involutional depression both before and after the treatment which included vasoactive preparations and calcium antagonists. It was determined vascular and intravascular alterations predominance and increase of platelet aggregation in patients with atherosclerotic depression independently of leading syndrome, in patients with involutional depression with anxiety prevalence as well as in patients in stuporous state. The tendency was revealed of such disturbances increasing as for as psychosis was extended. Trental and Cavinton antiplatelet and spasmolytic properties were potentiated by inclusion of Corinfar in complex therapy and that promoted earlier microcirculatory alterations removal as well as aggregatograms and patient mental state normalization.
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PMID:[Changes in the microcirculatory rheological properties of the blood and their correction in patients with atherosclerotic and involutional depressions]. 858 81

Tumor necrosis factor (TNF, cachectin), a cytokine secreted by macrophages and T-cells, mediates inflammatory and immune responses, and is associated with wasting in persons with malignancies or AIDS. In inflammation, TNF attracts and activates neutrophils, stimulating phagocytic function of neutrophils and macrophages. TNF also increases hepatic cell resistance to damaging parasitic effects; enhances endothelial permeability, causing edema; aids in wound healing by stimulating tissue and vascular growth; enhances lymphocytic activity through cytokine activation; acts with interleukin (IL) to produce fever, anorexia, lethargy and sleep; and possesses antitumor activity, particularly against the presumed origin of Kaposi's sarcoma, capillary endothelial cells. The host has an acute phase response (APR) following TNF- and IL-induced immunologic activation. TNF and IL decrease production and activity of lipoprotein lipase (LPL), resulting in reduced uptake and improper storage of fat; and they stimulate anabolism of fatty acids, causing hypertriglyceridemia. This "futile cycling" causes shuttling of fatty acids between adipose tissue and the liver, and use of muscle protein as the main fuel source. This, along with further muscular breakdown due to the increased caloric demands of fever, may affect cachexia. TNF benefits the HIV-infected through selective killing of HIV-infected cells, although effects may be dose and time dependent. The negative effects of TNF may be impeded by anti-cytokine therapy. Possible therapies include dietary N-3 fatty acid (fish oil), an inhibitor of TNF and IL production in vitro; pentoxifylline (Trental), another TNF production inhibitor; anti-TNF monoclonal antibodies; and soluble TNF receptors.
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PMID:Tumor necrosis factor: its role in HIV/AIDS. 1136 96