Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0205700 (ash)
 15,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two groups of weanling pigs, injected with 45Ca, were fed diets containing optimal calcium and phosphorus, and vitamin D3 at 1320 IU/kg feed in the control group, and 825,000 IU/kg feed in the test group. The groups were further subdivided with 2 pigs in each subgroup, with survival times of 1, 2, 3, 4, 7, and 14 days. Pigs fed the high level of vitamin D3 lost weight and anorexia, weakness, rough hair coat and labored breathing were observed. Hypercalcemia began at 12 hours and progressed rapidly after 2 days. Radioisotope sutdies interpreted in the light of histopathologic findings indicated that bone was the primary source of increased plasma calcium. Calcium was released at a rapid rate into blood from prelabeled bone which was undergoing necrosis; it was also removed from blood and deposited into bone at a slower rate due to decreased apposition. Histopathologic examination of bones from test pigs showed regressive changes in the osteocytes, chondrocytes and osteoblasts which bean within 1 day of treatment and resulted in evidence osteopenia within 7 days. Arrested osteocytic osteolysis led to the appearance of cementing lines and to chondroid core retention. Further regressive changes in the osteocytes resulted in osteocytic death and osteonecrosis with subsequent osteoclasia and osteopenia. Retardation and arrest of cartilage maturation as well as osteoblastic deficiency contributed to the osteopenia. The osteopenia was further evidenced by decreased specific gravity and ash content per unit volume of humerus. The initial negative effect on the osteocytes, chondrocytes and osteoblasts is attributed to a direct toxic effect of excessive dietary vitamin D3 since hypoparathyroidism and hypercalcitoninism, which occur secondarily to hypercalcemia, could not account for the rapid appearance of this effect, nor are they known to induce osteocytic death. The release of bone calcium and the resulting hypercalcemia in vitamin D3 toxicosis is therefore due to a direct toxic effect of the vitamin, or its metabolites, on the osteocyte resulting in osteonecrosis. It is not due to increased resorption as has been reported previously from both in vivo and in vitro investigations. Degeneration, with subsequent inflammation, but without calcification, was observed in the kidneys and in the lungs. Epithelial cells, basement membranes, and smooth muscle were affected. This conclusively demonstrates that degeneration is the primary soft tissue lesion in vitamin D3 toxicosis, and that the subsequent calcification is therefore dystrophic. Degenerative changes occurred in the parathyroid glands within 1 day of treatment resulting in necrosis, inflammation and atrophy within 4 days. Relative fibrosis was seen as the parenchyma receded. The parathyroid gland changes were considered a direct effect of vitamin D3 toxicity since they occurred with only mild hypercalcemia and since necrosis of parathyroid cells has not been demonstrated with hypercalcemia either in vivo or in vitro.
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PMID:Vitamin D toxicity. Initial site and mode of action. 66 94

Acute accidental vitamin D2 (ergocalciferol) toxicosis was diagnosed in a 6-month-old foal with extensive lesions of soft tissue mineralization. In an experimental study, three 18-month-old horses were given ergocalciferol per os at a rate of 9,300, 22,200, or 47,200 IU/kg of body weight/day for 21 days. Clinical signs or lesions were not seen in horses given the low and intermediate doses, whereas the horse receiving the highest dose developed clinical signs and lesions similar to those noted in the foal. Signs included depression, loss of appetite, weakness, limb stiffness with impaired mobility, and cessation of growth or weight loss. Gross and histologic lesions of mineralization of various soft tissues, especially of the endocardium and wall of large blood vessels, were seen in the foal and the horse given the high dose. Marked, persistent, hyperphosphatemia (7.0 to 13.0 mg of P/dl of serum) developed in each horse. The horse given the intermediate dose remained normocalcemic. Horses given the low and high doses became hypercalcemic (13.6 to 14.5 mg of Ca/dl of serum), but serum calcium concentrations varied from day to day and both horses were normocalcemic at necropsy (12.4 to 12.7 mg of Ca/dl of serum). Distal metacarpal bone ash concentrations of calcium, phosphorus, and magnesium of the foal were mg/g of bone ash) 400.5, 180.5, and 5.30, respectively. In the horses, treatment with ergocalciferol also had no significant effect on serum magnesium (1.88 to 2.18 mg/dl of serum) or distal metacarpal bone ash concentrations of calcium (352.5 to 362.5 mg/g of bone ash), phosphorus (182.5 to 184.0 mg/g of bone ash), or magnesium (5.48 to 6.02 mg/g of bone ash).
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PMID:Acute vitamin D2 (ergocalciferol) toxicosis in horses: case report and experimental studies. 697 34

Rabbits parasitized by Obeliscoides cuniculi were used as models for stomach worm parasitism in ruminants. A 3 X 4 randomized complete block design containing three levels of of infection (NI, no infection; LI and HI, infections produced by 1,800 and 30,000 larvae, respectively) and four levels of diet (PC, high protein and carbohydrate; pc, low protein and carbohydrate; Pc, high protein, and low carbohydrate; pC, low protein and high carbohydrate) was replicated four times. Mean weight gains for rabbits on diets pc or PC were not influenced by infection level, whereas LI rabbits on diets Pc and pC gained as well as the NI animals and more than the HI ones. Only HI rabbits exhibited anorexia. NI and LI rabbits has positive feed conversion efficiencies, whereas those of HI rabbits were negative. The apparent digestibilities of organic matter, protein, and ash in rabbits with different infection levels varied with diet. Daily nitrogen balances were positive. The changes in concentrations of amino acids in the plasma typically associated with systemic, fever-producing infections or with starvation or protein-calorie malnutrition did not occur in infected rabbits. Only the high level infections produced adverse effects on productivity. These effects occurred on diets pc, Pc and pC and were mediated by anorexia.
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PMID:Metabolic effects of infection by the stomach worm Obeliscoides cuniculi in rabbits fed diets varying in nutritive quality. 713 Oct 89

The apparent digestibilities (AD) of dry matter (DM), organic matter (OM), crude ash (CA), crude fiber (CFi), crude fat (CFa) crude protein (CP) and nitrogen-free extracts (NFE) and the nitrogen balance were investigated during experimental Eimeria bovis coccidiosis in calves. noninfected pair-fed controls and controls fed on a normal plan of nutrition were included in the study to allow differentiation between the effects of infection and of changes in feed intake. Primary infection with 5 x 10(4) oocysts (n = 4, group A) caused mild diarrhea and calves infected primarily with 1 X 10(5) oocysts (n = 5, group B) suffered from mild (three calves) to severe hemorrhagic (two calves) diarrhea. No clinical disease was seen after reinfection of the group A calves with 1 X 10(5) oocysts. The primary infection with 5 X 10(4) oocysts or reinfection with twice the primary inoculum did not affect AD of nutrients or the overall nitrogen balance (RT). AD of DM, NFE or OM were higher in group B during patency and in the pair-fed group C calves (n = 5) than in the reinfected but healthy group A calves. AD of CFi of the group B calves even exceeded the values of the pair-fed controls. The two calves of group B that suffered from hemorrhagic diarrhea and anorexia had low values of AD of CP during the acute phase of the disease and the plasma nitrogen levels were reduced in this group. Severe clinical coccidiosis transiently reduced the nitrogen balance. It is concluded that the transient increase of AD of nutrients, especially of CFi, during clinical coccidiosis reflect hypomotility and that anorexia and intestinal leakage impair the nitrogen balance and cause weight depression.
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PMID:Apparent digestibility of nutrients and nitrogen balance during experimental infection of calves with Eimeria bovis. 974 79

Esophageal cancer is among the 10 most frequent cancers in the world. Iran is one of the known areas with a high incidence of esophageal cancer. Most of the patients in Iran have been reported from the north and northeast regions of the country. In one survey by the Iran Cancer Institute, 9% of all cancers and 27% of gastrointestinal cancers were esophageal carcinoma. The male to female ratio was 1.7/1. The distal portion of the esophagus is involved more often than other parts. Consumption of wheat flour, exposure to residues from opium pipes, drinking hot tea, and chewing nass (a mixture of tobacco, lime, ash, and other ingredients) are the suspect etiologic agents for esophageal cancer in Iran. Dysphagia, weight loss, anorexia, abdominal pain, and odynophagia are the common symptoms and signs of Iranian patients with esophageal cancer. For clinical staging, chest computed tomographic scanning is performed. Adenocarcinoma of the esophagus is not as common in Iran as in western countries. Public education, nutritional support, and eradication of opium addiction may decrease the morbidity and mortality that result from esophageal cancer. Surgery has traditionally been the mainstay of esophageal cancer treatment in Iran. Radiotherapy is mainly used postoperatively. The usual combination chemotherapy regimen is cisplatin plus flurouracil (5-Fu). Semin Oncol 28:153-157.
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PMID:Esophageal cancer in Iran. 1130 77

In a dairy herd of 21 cows which were on pasture during the day at the end of May 2002, four eight years old cows were suddenly inappetent and showed severe diarrhoea consisting of black discolorate feces. A few days after the onset of the disease, three affected cows exhibited neurological disorders. These cows were admitted to the IInd Medical Clinic of the University for Veterinary Medicine in Vienna. Following clinical signs were observed: circulatory weakness, anorexia, atony of the rumen, diarrhoea and in accordance with acute lead poisoning typical signs of the central nervous system. One cow died and the other two animals were euthanized. Results of blood testing were anaemia, basophil spotting of erythrocytes, increase of liver enzymes and CK, hypocalcaemia, decrease of potassium and phosphate. The cerebrospinal fluid of two cows showed increased CK-, LDH- and AST-values. The lead contents of whole blood samples were between 0.486 and 0.928 mg/kg, of liver samples 13.3 to 114.4 mg/kg, of kidney samples 172.2 to 448 mg/kg and of rumen content 59 mg/kg fresh matter. At necropsy, enteritis, liver fluke disease and severe interstitial and alveolar pulmonary emphysema were found. Pathohistologically typical ischaemic necrosis of neurons predominantly at the tips of the gyri, disseminated petechial hemorrhages and moderate diffuse neovascularisation, but no acid-fast intranucleolar inclusion bodies in the renal tubules were observed. As causative agent of the acute lead poisoning a residue on combustion, taken up by the cows on the pasture, was confirmed. The ash residue was formed by combustion of three tires which contained 450 g heavy weights of 96.5% lead for wheel balance. The lead content of the ash residue was between 2.9 and 28 g/kg dry matter.
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PMID:[Acute lead poisoning in cows due to feeding of lead contaminated ash residue]. 1496 24

Lead poisoning was diagnosed in three cattle along with increased mercury levels in the liver and kidney tissues of two of these animals. The clinical signs were different in each case and included salivation, anorexia, delayed menace response, delayed withdrawal reflex, head pressing, localized muscle fasciculation, reduced tongue tone, ataxia, rumen atony and seizures. Blood lead concentration was increased in all three cases to 0.76, 0.37 and 0.454ppm. Post mortem changes characteristic of lead poisoning were only recognized in one case and included cerebro-cortical oedema, cortical neuronal necrosis and endothelial proliferation, especially at the tips of the cerebral gyri. The animals were poisoned by ingestion of lead-contaminated ash residues from a bonfire. The abnormal levels of mercury in the liver and kidney tissues of two animals may also be at least partly attributable to the intake of the metal in the ash residues. The levels of mercury in the three samples from the ash residue were relatively low (1.31, 0.7 and 2.1ppm).
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PMID:Toxic effects seen in a herd of beef cattle following exposure to ash residues contaminated by lead and mercury. 1675 17