Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013911 (emaciation)
 1,059 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Naturally occurring bovine sarcocystosis caused death and illness in eight dairy heifers. Clinical disease was characterized by cachexia, peripheral lymph node enlargement, and anemia. Increased amounts of serum enzymes and anti-Sarcocystis antibody titers were present in affected animal. Macroscopic findings in two heifers at necropsy included emaciation and serous atrophy. Necropsied heifers (No. 1 and 2) contained different developmental stages of Sarcocystis cruzi; each stage was characterized by specific histopathologic findings. Heifer 1 had vascular endothelial schizonts in various soft tissues, with mild mononuclear cell infiltration, alveolar capillary fibrinous thrombi, and multifocal splenic necrosis. Heifer 2 had developing young S cruzi cysts, in myofibrils of cardiac and skeletal muscles, with a concurrent multifocal degenerative myositis. Marked lymphoid hyperplasia occurred in both heifers.
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PMID:Bovine saccocystosis: patholgic features of naturally occurring infection with Sarcocystis cruzi. 11 89

Three female patients with cachexia are reported in whom a psychogenic emaciation (anorexia nervosa) had been assumed. The postpubertal onset of the disease, deliberate limitation of diet, vomiting and subsequent emaciation and--in 2 patients--amenorrhea, as well as demonstrable experience of conflict supported this. The disease ran a lethal course. Autopsy revealed serious somatic diseases (stenosis of the ileum in two cases and brain tumor in one); their symptoms had been largely overlapped by those of anorexia nervosa.
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PMID:[The differential diagnosis of anorexia nervosa. Coincidence of somatic disease and psychogenic emaciation (author's transl)]. 81 92

A child, aged 6 years 3 months, with a triglyceride storage disorder in peripheral adipose tissue, microcephaly, and gross emaciation has been studied at autopsy. The mean triglyceride content of adipocytes in hand and foot was 0.17 +/- 0.02 mug/cell and 0.18 +/- 0.02 mug/cell. Adipocytes from abdominal tissue were small, irregular, and difficult to measure accurately, reflecting the degree of cachexia. Basal tissue contents of cyclic AMP and release of glycerol and fatty acid from peripheral tissue of the child were in the same range as adult tissues. None of these measurements, however, were increased by incubation with isoprenaline (10(-5 M), compared to a three- to seven-fold increment in adult subcutaneous tissues and to a four- to ten-fold increment of glycerol and cyclic AMP in peripheral adipose tissue of a control child aged 10 years. We postulate that the proband may have had a defect of adenyl cyclase or catecholamine receptor, which has a role in the abnormal storage of triglyceride in peripheral adipose tissue.
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PMID:Triglyceride storage disease: a defect in activation of lipolysis in adipose tissue. 84 May 64

Thirty-five 6-week-old guinea fowl keets, seronegative for maternal antibodies to Newcastle disease virus, were infected with Herts strain (33/56) and Kumarov strain of Newcastle disease virus intramucularly (IM) or intranasally (IN). Clinical signs were first noticed four days post infection (PI) in the group infected IM but five days PI in the group infected IN with Herts strain of Newcastle disease virus. These clinical signs were similar in both groups and included anorexia, droopiness, huddling together, greenish diarrhoea and marked cachexia. Prominent nervous signs, including spasms of the head and neck, were observed in groups infected with Herts strain. The major gross lesions observed were emaciation with prominent keel bone, empty intestinal tract and distended gall bladder in most keets. The histological lesions were characterised by meningoencephalitis, necrosis and loss of lymphocytes from splenic and lymphoid aggregates. There was muscular degeneration and necrosis in the gizzard and mild pulmonary congestion and oedema in some keets. Neither gross or microscopic lesions were observed in keets that had received the Kumarov strain.
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PMID:Pathogenicity of two strains of Newcastle disease virus in the grey-breasted helmet guinea fowl. 150 75

The case of an infant admitted for evaluation of severe emaciation with intermittent ocular anomalies including strabismus and nystagmus is reported. This case demonstrates the value of magnetic resonance imaging and transfontanellar ultrasonography for the diagnosis of diencephalic syndrome of infancy. The prognosis of this condition is usually grim, in particular because of the severe emaciation which is disproportionate with the tumour spread. Pathophysiologic hypotheses put forward to explain this cachexia are reviewed. Although cytokines such as TNF alpha are currently incriminated in the pathophysiology of cachexia induced by a number of conditions, they have not yet been studied in diencephalic syndrome of infancy. TNF alpha is a potent lipolytic agent. Excessive production of TNF alpha may be involved in the genesis of the emaciation characteristic of diencephalic syndrome. Inappropriate production of TNF alpha may respond to the administration of specific anti-TNF monoclonal antibodies. This approach may be considered as a means for treating emaciation in patients with diencephalic syndrome of infancy.
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PMID:[A case report of Russel's diencephalic cachexia]. 157 Sep 47

Hypopituitarism depends on the history of the obstetric cause, on the subsequent amenorrhoea and the usual absence of lactation, on the biochemical abnormalities found later, and on the effect of therapy. Nevertheless, an initial clinical inspection of the untreated patient gives important clues to the diagnosis. Cachexia does not occur in true hypopituitarism, unless there is some intercurrent factor which causes emaciation, such as carcinoma, tuberculosis, ulceration in the alimentary tract etc.
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PMID:[The clinical picture of postpartum hypopituitarism]. 317 80

Paratuberculosis in sheep usually is manifested as emaciation and decreased wool production. Diarrhea occurred in only 18% of affected animals. Significant hematologic changes included decreased RBC count, hemoglobin level and hematocrit. Necropsy revealed pallor, cachexia and serous fluid in body cavities. Staining of intestinal mucosal scrapings and mesenteric lymph node impression smears for acid-fast organisms revealed bright-red clumps of Mycobacterium paratuberculosis bacilli. Fecal examination identified 70% of affected animals, intradermal injection of johnin 60%, and avian tuberculin 39%.
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PMID:Diagnosis of paratuberculosis in sheep. 672 47

The Leydig cell tumor has been reported to produce tumor necrosis factor (TNF) and induce cachexia in rats. TNF is thought to reduce lipoprotein lipase (LPL) activity, decrease fat deposits, induce emaciation, and worsen cachexia. Therefore, we thought emaciation might be prevented and thus cachexia improved by increasing LPL activity. We administered NO-1886, a lipoprotein lipase activator, to rats bearing Leydig cell tumor and observed its effect on improving the cachexia induced by the tumor. In Leydig cell tumor-bearing rats, the emaciation progressed after tumor inoculation and the general condition worsened daily. Plasma levels of total protein, albumin, and glucose, which are biological parameters of malnutrition, were found to decrease soon after tumor inoculation in tumor-bearing rats. In contrast, rats given NO-1886 showed less malnutrition than tumor-bearing rats. LPL activity of rat adipose tissue was decreased, the weight of adipose tissue was decreased, carcass weight was reduced, and food consumption was decreased after Leydig cell tumor inoculation. NO-1886 increased adipose tissue LPL activity and suppressed the decrease in the weight of adipose tissue, carcass weight, and food consumption due to cachexia without influencing tumor growth. The present results suggest that the novel compound NO-1886 may suppress carcass weight loss in rats bearing Leydig cell tumor by suppressing the decrease in food consumption and LPL activity.
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PMID:Suppression of carcass weight loss in cachexia in rats bearing Leydig cell tumor by the novel compound NO-1886, a lipoprotein lipase activator. 944 Apr 86

Cachexia in cancer is characterized by progressive emaciation involving depletion of host adipose tissue stores, the molecular mechanism of which remains largely unknown. In this study, we have attempted to clarify the biologic characteristics of lipid-depleting factor in a mouse cachexia model. Utilizing differentiated 3T3-L1 adipocytes, we established an assay method quantifying the lipid-depleting activity in plasma derived from colon-26-inoculated mice and then analyzed the associated molecular mechanism. Injection (s.c.) of a mouse colon adenocarcinoma cell line, colon-26 clone 20, induced cachexia, as evidenced by progressive weight loss. Addition of clone 20-derived cachexigenic, but not clone 5-derived noncachexigenic, plasma to the culture medium of differentiated 3T3-L1 adipocytes reduced the TG content in cultured cells. The ability of the introduced plasma to induce TG loss in 3T3-L1 cells paralleled the body weight changes of tumor-inoculated host mice. Clone 20 plasma, but not clone 5 plasma or recombinant IL-6, elicited lipolytic activity, which induced glycerol release from 3T3-L1 cells. Addition of clone 20 plasma to cultured 3T3-L1 adipocytes reduced TG synthesis from [(14)C]-glucose compared to clone 5 plasma, indicating that the lipid-depleting activity resulting from addition of clone 20 plasma depended not only on induction of lipolysis but also on inhibition of lipogenesis. Addition of clone 20 plasma to cultured 3T3-L1 adipocytes reduced the quantity of mature SREBP-1 in the nucleus of 3T3-L1 cells without affecting PPAR-gamma and C/EBP-alpha. Although TNF-alpha induced apoptosis in 3T3-L1 cells, clone 20 plasma did not. These results suggest that the lipid-depleting factor in clone 20 plasma is different from either IL-6 or TNF-alpha, and that this factor interfered with not only lipolysis but also lipogenesis through SREBP-1 of 3T3-L1 adipocytes.
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PMID:Molecular analysis of lipid-depleting factor in a colon-26-inoculated cancer cachexia model. 1220 86

Using a swine abdominal organ cluster transplantation model, we investigated the postoperative function and immunological reactions of a cluster graft and evaluated the immunosuppressive activity of FK506. The animals were divided into two groups. Group I (n = 6) served as controls, while in group II (n = 6) a daily dose of 0.1 mg/kg FK506 was given intramuscularly. Postoperative pancreatitis was the most important factor influencing the early outcome in both groups. In group I, the cause of late death was cachexia due to diabetes mellitus induced by pancreatic rejection. In group II, emaciation despite a well-functioning graft was the principal cause of late death. Histologically, in group I the grade of rejection in the pancreas was more severe than in the liver, and no sign of rejection was observed in group II. In conclusion, the pancreas suffered more severe rejection than the liver, and FK506 could significantly prevent cluster allograft rejection in this model.
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PMID:Abdominal organ cluster transplantation in pigs and FK506. 1462 61


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