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)

Twelve severely emaciated patients with emphysema and 4 control patients with mild emaciation were studied. Arterial blood gas analysis, pulmonary function tests, and muscle biopsy were performed. According to the percentage of ideal body weight (%IBW), patients were divided into two groups of 6 patients each; one with %IBW values greater than 70.0 (group 1) and the other with %IBW values less than 70.0 (group 2), and 4 control patients with emphysema whose %IBW values were greater than 85.5. %FEV1.0, PaO2 and Hugh-Jones scores in group 2 patients were consistent with significantly greater deterioration as compared with those in group 1 patients and controls. In the muscle fibers of 11 patients and 4 controls, nicotinamide and adenosine dinucleotide tetrazolium reductase activity was studded with spots. Nemalin rods were detected in 3 specimens in group 2 and in 1 specimen each in both group 1 and controls. These changes probably result from chronic hypoxemia. Fiber type grouping accompanied by type II dominant fiber atrophy was demonstrated in 5 patients of group 2, whereas type II fiber atrophy was shown in 2 specimens from patients of group 1. Diameters of both types I and II fibers in group 2 were smaller than those in group 1 and controls. Significant correlations were observed between fiber diameters and %IBW, %FEV1.0 and %IBW, and PaO2 and %IBW. Neurogenic and disuse muscular atrophy due to both hypoxic axonal disorder and disuse is likely to be the cause of the emaciation, and a 'vicious circle' between muscular atrophy, respiratory function and hypoxemia probably exists in group 2. Since mild or moderate emaciation was observed in controls and group 1 in spite of the lack of fiber atrophy, involvement of fat and connective tissue should also be taken into consideration to determine the cause of emaciation.
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PMID:Morphologic and histochemical evaluation of muscle in patients with chronic pulmonary emphysema manifesting generalized emaciation. 905 68

A 1-yr-old male leopard (Panthera pardus) presented for intermittent anorexia, emaciation, and generalized muscle wasting. Plain radiographs, ultrasonography, and esophageal endoscopy led to a diagnosis of diaphragmatic eventration with probable concurrent hiatal hernia. An exploratory laparotomy confirmed both diagnoses, and surgical repair and stabilization were performed. After surgery, the leopard was maintained on small liquid meals for 4 days, with a gradual return to normal diet over 2 wk. By 4 wk after surgery, the leopard was eating well and gaining weight, and it showed no recurrence of clinical signs for 2 yr subsequently, becoming mildly obese.
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PMID:Hiatal hernia and diaphragmatic eventration in a leopard (Panthera pardus). 1123 47

The occurrence of hereditary premature senescence in a family of pure bred Belgian hares belonging to a rabbit-breeding colony organized for the investigation of constitutional problems, has been described. Representatives of 20 generations of the complex have been studied. The condition was a degeneration of variable degrees of severity and two principal forms were recognized, the acute and the chronic, the chronic being the more frequent. The chronic form has now been described in terms of the principal local or external manifestations; that is, degeneration of the coat and skin, lesions of the eyes and feet, and reproductive abnormalities, and of the general deterioration which in severe cases pursued a progressive course characterized by muscle wasting, fat reduction, emaciation, weakness, and death. The acute form will be described in the next paper (2).
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PMID:Hereditary premature sensescence of the rabbit. I. Chronic form; general features. 1373 54

Spontaneous and experimental poisoning with the swainsonine-containing and calystegine-containing plant Ipomoea carnea subsp fistulosa is described. Three of 8 goats presenting with emaciation, weakness, symmetrical ataxia, posterior paresis, proprioceptive deficits, abnormal posture, abnormal postural reaction, and muscle hypertonia were necropsied. I fistulosa was suspected to be the cause of the neurologic disease in all cases. An experiment was conducted to confirm the diagnosis using 12 goats and diets containing 3 different concentrations of the plant. All goats fed I fistulosa developed neurological signs that were similar to those observed in the spontaneous intoxication. Muscle atrophy and pallor were the only macroscopic changes observed in spontaneous and in experimental intoxication. Histological lesions of spontaneous and experimental animals were similar. The most prominent lesion was cytoplasmic vacuolation in neurons of the central and the autonomous nervous system, pancreatic acinar cells, hepatocytes, Kupffer cells, follicular epithelial cells of the thyroid gland, and macrophages of the lymphatic tissues. Neuronal necrosis, axonal spheroids formation, and astrogliosis were additionally observed in the brain. Ultrastructurally, the cytoplasmic vacuoles consisted of distended lysosomes surrounded by a single-layered membrane. Nonreduced end-rests or sequence of alpha-Man, alpha-Glc, beta(1-4)-GlcNAc, and NeuNAc on lysosomal membrane were revealed by lectin histochemistry. Samples of plants used in the experimental trial contained swainsonine and calystegine and their intermediary derivate. We conclude that I fistulosa induces a glycoprotein storage disease primarily based on the inhibition of the lysosomal alpha-mannosidase by the alkaloid swainsonine.
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PMID:Spontaneous and experimental glycoprotein storage disease of goats induced by Ipomoea carnea subsp fistulosa (Convolvulaceae). 1731 94