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Query: UMLS:C0003123 (anorexia)
 13,794 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The plasma alpha-lipoprotein bands seen on starch-gel electrophoresis are progressively split and retarded as avian erythroblastosis progresses. Similar changes may be produced in normal birds by starvation, and by pair-feeding methods. Anorexia appears to be a major cause, if not the total cause, of the plasma alpha-lipoprotein changes seen in erythroblastosis.
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PMID:Anorexia as the probable cause of plasma alpha-lipoprotein changes seen in avian erythroblastosis. 18 Sep 63

Gross and microscopic lesions of Bolivian hemorrhagic fever (BHF) are described in 10 rhesus monkeys that survived from 30 to 78 days after subcutaneous inoculation with a dose of 10(3) plaque-forming units (PFU) of Machupo virus, a dose which produces a severe and generally fatal disease. Six of the monkeys had been given low doses of homologous immune globulin when initial signs of infection appeared. Monkeys exhibited clinical signs in two phases. The initial signs of acute infection which began to appear about 1 week following inoculation included: diarrhea, depression, anorexia, dehydration, and skin rash. The survivors of this early phase of the illness usually showed improvement before relapsing into the second (or chronic) phase, which was characterized clinically by central nervous system disturbances including incoordination, tremors, convulsions, paresis, and muscle atrophy. Microscopic lesions were similar in both immune globulin-treated and untreated animals. These included widespread lymphoreticular infiltrates in the walls and adventitia of blood vessels of the brain, spinal cord, pancreas, intestine, liver kidney, adrenal, parathyroid, heart, and skeletal muscle. Diffuse lymphocytic infiltrates not confined to the vascular or perivascular tissues were present to a variable degree in many of these and other organs. Several monkeys exhibited lymphocytic inflammation of the choroid, meninges, peripheral nerves, and ganglia.
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PMID:Pathology of chronic Bolivian hemorrhagic fever in the rhesus monkey. 18 94

Toxicosis was induced in pregnant Holstein-Friesian heifers by giving polybrominated biphenyls a in gelatin capsules at the rate of 25 g/day. Initially, this dosage was approximately 67 mg/kg of body weight. Clinical signs were anorexia, excessive lacrimation and salivation, diarrhea, emaciation, dehydration, depression, and abortion. Fever was not evident during the experiment. Values for serum glutamic-oxalacetic transaminase, lactic dehydrogenase, blood urea nitrogen, and bilirubin were increased. Changes in packed cell volume, hemoglobin content, total erythrocyte and leukocyte counts, and differential leukocyte counts were minimal and reflected dehydration and secondary infection. The principal urine changes were decreased specific gravity and moderate proteinuria. Gross necropsy findings included dehydration; subcutaneous emphysema and hemorrhage; atrophy of the thymus; fetal death with concomitant necrosis of cotyledons; kidneys that were enlarged, pale tan to gray; thickened wall of the gallbladder; inspissated bile; edema of abomasal folds; mucoid enteritis; linear hemorrhage and edema of the rectal mucosa; and secondary pneumonia. Microscopic changes were most marked in the kidneys, gallbladder, and eyelid. In the kidney, the principal changes were extreme dilatation of collecting ducts and convoluted tubules, with epithelial degenerative changes of cloudy swelling, hydropic degeneration, and separation from the basement membrane. Common changes in the gallbladder were moderate to marked hyperplasia and cystic dilatation of the mucous glands in the lamina propria. The changes in the eyelids were characterized by hyperkeratosis, with accumulations of keratin in hair follicles of the epidermis and squamous metaplasia with keratin cysts in the tarsal glands. Clinical signs and lesions of toxicosis did not develop in heifers given the polybrominated biphenyls at the rate of 0.25 mg and 250 mg/day for 60 days. Initially these rates were approximately 0.00065 mg/kg and 0.65 mg/kg of body weight, respectively.
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PMID:Pathology of experimentally induced polybrominated biphenyl toxicosis in pregnant heifers. 18 92

The content of membrane-bound ribosomes in normal rat liver cells is 3 times as high as compared to that of free ribosomes. (K=membrane-bound ribosome RNAs divided by free ribosome RNAs=3, the opposite effect being observed in case of ascites hepatoma cells. A considerable increase in the free ribosome fraction in the liver of hepatoma-bearing rats occurs by the sixth day due to a decrease in the content of hepatoma-bearing rats occurs by the sixth day due to a decrease in the content of membrane-bound ribosomes (K=0.6). Similar, but less-pronounced changes were observed in liver cells of control animals after 48-hour starvation (K=0.9), simulating the condition occurring during the last days of tumour animals' life. Thus, changes in the rativ of membrane-bound to free ribosomes in liver during the ascites tumour growth are probably specifics and are not only due to anorexia in Zajdela hepatoma animals.
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PMID:[Correlation of membrane-bound and free ribosomes in normal rat liver, Zajdela hepatoma rat liver and ascite cells proper]. 19 Nov

Six serologically negative sows were infected by intranasal instillation of porcine cytomegalovirus (PCMV) between 31 and 85 days of pregnacy. Four sows showed an afebrile anorexia and lethargy 14-25 days after infection and all 6 developed significant increases in indirect immunofluorescent (IIF) antibody titres within 35 days. Virus was recovered from nasal and/or cervical swabs from 2 sows during life and from lung macrophage cultures after death. At term the sows were killed and their fetuses harvested by caesarean section. The number of mummified and stillborn fetuses increased from 4/63 in 6 previous litters to 18/60 in the 6 present litters. Nine of 43 fetuses born alive were reared in isolators for up to 6 weeks but the majority were killed for examination on the day of birth. Virus was isolated from 16 piglets from 4 of the 6 litters examined; it was isolated most frequently from lungs and liver but also from spleen, kidney, brain and nasal mucosa. Unsuckled day-old pigs had insignificant IIF titres, irrespective of whether they were excreting virus or not. The 5 congenital excretors which were reared all died within 7 days but no death occurred among their 4 litter-mates. Post-natal infection of 2 of these piglets reared in contact with congenitally infected pigs was suggested by the recovery of virus from nasal swabs 17 and 27 days after birth and the subsequent rise in IIF titre to 1/256 by day 42.
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PMID:Experimental transplacental transmission of porcine cytomegalovirus. 19 22

The small number of cases of Aujeszky's disease in goats referred to in the literature is stressed, and an outbreak in goats causing many deaths is reported. The flock of goats concerned was occasionally housed in a barn during the night in which there also were fattening pigs. The first deaths occurred without previous symptoms, the animals being found dead in the morning. In subsequent cases, symptoms were observed which continued for a few or several hours and consisted in agitation, lying down and rising, screaming plaintively, profuse sweating and, in the terminal stage, spasms and paralysis. Pruritus was not observed in any of the animals. Of the fifteen goats which had been housed in the pig-sty, thirteen died during ten days. In the same period, only one out of forty pigs died, and the others showed anorexia and somnolence for a couple of days but soon recovered. In two goats studied, the virus of Aujeszky's disease was isolated from the central nervous system. It is suggested that, in cases of disease or death in ruminants occurring in the proximity of pigs, there should primarily be a strong suspicion of Aujeszky's disease, regardless of the symptoms observed.
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PMID:[Aujeszky's disease in goats (authors transl)]. 19 54

Fifty-five hepatocarcinomas were found in a review of approximately 7,500 surgical biopsies done on Nigerian Igbos during a period of 6 years. The male: female ratio was 2.9:1 and the age peak was between 20 and 49 years. The main symptoms were abdominal swelling, pain, emaciation, jaundice, fever, anorexia and diarrhea. Physical examination revealed a palpable liver in nearly all patients. Two patients presented acutely with hemoperitoneum due to rupture of necrotic tumor nodule. Cirrhosis was found in 60% of the adequately sized specimens. In comparison with published data, this series from an ethnic group in Nigeria, West Africa, reveals both similarities and dissimilarities which are noteworthy.
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PMID:Biopsy study of hepatocarcinomas in Nigerian Igbos. 19 27

To test the role of sows in spreading transmissible gastroenteritis (TGE), 11 sows were intravenously, intranasally, or intramammarily inoculated with virulent virus within 5 days of farrowing. Six of the sows were separated from their offspring, and 5 were allowed to nurse their litters. All sows became clinically ill with sign of anorexia, depression, and fever that persisted until postinoculation day 4 or 5. They shed virus through milk, nasal secretions, and feces, with individual variations occurring in degree and duration of shedding in the 1st week after inoculation. Of 40 pigs separately fed milk samples from the 6 inoculated sows, 19 pigs (47.5%) became sick in 24 to 40 hours, and virus was isolated from them at necropsy. Of 43 pigs in the 5 litters that nursed exposed dams, all became sick with typical signs of TGE, and 29 (67.4%) died in 2 to 9 days. Sows given the single intramammary inoculation of virus developed statistically significant higher levels of TGE virus-neutralizing antibodies than did sows inoculated intravenously or intranasally.
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PMID:Quantitative transmissible gastroenteritis virus shedding patterns in lactating sows. 19 8

The toxicity of a commercial blend of polybrominated biphenyls was determined in 24 pregnant Holstein heifers that were allotted randomly to one of four experimental groups given 0, .25, 250, or 25,000 mg/day of fire-Master BP-6. The polybrominated biphenyls were mixed with finely ground corn and given by bolus for 60 days or until the animal became moribund. Average body weight of heifers at onset of experiment was 381 kg. No clinical signs of toxicosis were evident in heifers fed 0, .25 or 250 mg/day. Toxicosis was induced in heifers fed 25,000 mg/day resulting in reduced dry matter intake, body weight, heart rate, and respiration rate. Clinical signs were anorexia, emaciation, dehydration, excessive lacrimation and salivation, diarrhea, depression, and abortion or fetal death. All heifers fed 25,000 mg/day became moribund within 33 to 66 days.
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PMID:Effects of polybrominated biphenyls on health and performance of pregnant Holstein heifers. 19 46

The chief causes of liver disease in Ethiopia are reviewed, considering hospital data on admissions for hepatitis, cirrhosis, ascites and hepatoma. Liver diseases account for 11.4% of all medical admissions in 3 medical wards in Addis Ababa. The causes are viral hepatitis, post- hepatic and post necrotic and mixed cirrhosis and hepatocellular carcinoma. Alcoholic cirrhosis is rare. Viral hepatitis with shivering, rigor and fever and elevated direct bilirubin levels are common in Ethiopians, especially in child-bearing women. The hepatitis B surface antigen (HBsAg) is often associated with hepatitis. The disease may be transmitted by several species of mosquitoes, placental transmission, or feces, urine, saliva or semen. Blood products are not screened for hepatitis B. Cirrhosis is common, and causes significant mortality, usually from esophageal varices and hepatic coma. Chronic active hepatitis patients may live for a time, especially if they are near a hospital and are treated with steroids. In Ethiopia presenting symptoms for hepatoma are anorexia, weight loss, persistent, burning, right upper quadrant pain, and a hard, nodular, tender RUQ mass. Over 5% of malignancies seen are primary hepatocellular carcinomas. 50% have HBsAG, compared to 3.8% of controls. 65% have alpha-fetoglobulins. It is suggested that some viral hepatitis cases progress to cirrhosis, of which some go on to hepatocellular carcinoma. Herbal medicines, aflatoxins and other toxins may also contribute to liver disease.
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PMID:Current views on liver diseases in Ethiopia. 20 62


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