Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Within a period of 5 consecutive days after the initial observation of illness was made, 7 of 12 Siberian Husky dogs developed clinical signs of Rickettsia rickettsii infection. One dog died and was necropsied. Clinical signs of infection consisted of lethargy, anorexia, ocular and nasal discharges, and neurologic disorder (incoordination and rolling). Scleral blood vessel injection, fever, lymphadenomegaly, splenomegaly, and increased bronchovesicular lung sounds were prominent findings. Clinical laboratory test results identified decreased platelet numbers, variable neutrophil counts, increased serum alkaline phosphatase activity, hyponatremia, hypokalemia, and bilirubinuria. Diagnosis of Rocky Mountain spotted fever was confirmed by serologic evaluation of acute and convalescent sera, using the micro-immunofluorescence technique, and R rickettsii antigen was determined by demonstration of intracellular rickettsial organisms in vascular endothelial cells of brain and lung (stained with carbol-basic fuchsin and aqueous malachite green) and by demonstration of spotted fever-group rickettsiae in tissues by direct fluorescent antibody technique. Near-simultaneous naturally occurring tick-borne infection of 7 dogs with R rickettsii documents an unreported occurrence.
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PMID:Canine Rocky Mountain spotted fever: a kennel epizootic. 406 17

Three Shetland ponies were given a single oral dose of ground Cassia occidentalis seeds in aqueous suspension. The clinical signs observed resembled those seen in naturally occurring and experimental cases in cattle. The syndrome was characterized by an afebrile course, incoordination, recumbency and death. Elevations of blood alkaline phosphatase, CPK, LDH, and SGOT were observed. Although muscle lesions were not seen grossly, microscopic lesions included segmental necrosis of skeletal muscle fibers. The findings were regarded as sufficiently characteristic of C. occidentalis poisoning to be useful in differential diagnosis. When Cassia poisoning is suspected, access of the affected horses to the plant should be demonstrated.
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PMID:Toxicity of Cassia occidentalis in the horse. 733 63

The acute toxicity of 2,4-dichlorophenoxyacetic acid (2,4-D), a herbicide, was studied in chicks dosed with 100, 300, 500, or 600 mg 2,4-D/kg BW, by the oral route. Clinical, laboratory, and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased motor activity and induced muscular weakness and motor incoordination; decreased weight gain; increased serum creatine kinase (CK) and alkaline phosphatase (AP) activities and serum uric acid (UA), creatinine (CR), and total proteins (TP) levels; and did not change serum aspartate aminotransferase (AST) or alanine aminotransferase (ALT) activities. These changes were time- and dose-dependent and reversible. The LD50 (lethal dose 50%) calculated for oral 2,4-D in chicks was 420 mg/kg BW (385 to 483). Chromatographic analysis of the serum of the intoxicated chicks showed the presence of the herbicide; the amount found was dose- and time-dependent, increasing from 2 to 8 h after exposure and decreasing afterwards. Histopathological post-mortem studies conducted on intoxicated chicks showed hepatic (vacuolar degeneration of the hepatocytes), renal (tubular nephrosis), and intestinal (hemorrhagic) lesions. Taken together, the observed alterations mainly reflected kidney and muscle tissue damage, although hepatic toxicity may also have occurred after acute 2,4-D intoxication.
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PMID:Acute 2,4-dichlorophenoxyacetic acid intoxication in broiler chicks. 956 31

Changes in hematological and serum biochemistry parameters in female zinc (Zn)-dosed farm-raised mallards (Anas platyrhynchos) fed four different diets were examined. Sixty ducks received an average dose of 0.97 g of Zn in the form of eight, 3.30-mm diameter shot pellets containing 98% Zn and 2% tin, and another 60 ducks were sham-dosed as controls. Fifteen ducks from each of the two dosing groups were assigned to one of four dietary treatments: corn only, corn with soil, commercial duck ration only, or commercial duck ration with soil. Shot-pellet dissolution rates ranged from 7 mg/Zn/day to 27 mg/Zn/day. Regardless of diet, the Zn dose resulted in mortality; incoordination; paralysis and anorexia; decreased body, liver, pancreas, gonad, and gizzard weight; increased kidney weight; and macroscopic lesions. Zn-dosed ducks had a lower mean erythrocyte packed cell volume (PCV), higher mean reticulocyte count, and a greater number of individuals with immature and/or abnormal erythrocytes, than did control mallards. Mean total leucocyte counts were higher in Zn-dosed ducks than in controls. Zn-dosed ducks that had soil available had higher leucocyte counts than those without soil. Zn-dosed ducks were characterized by a marked heterophilia and relative lymphopenia. In Zn-dosed ducks, the mean lymphocyte count was highest in those provided a commercial duck ration, and lowest in those fed corn. In control ducks, the mean lymphocyte count was highest in ducks fed corn, and lowest in those provided soil along with a commercial duck ration. Zn-dosed mallards had higher serum aspartate aminotransferase and amylase levels, and lower alkaline phosphatase activities than control ducks. Serum phosphorus and uric acid concentrations were higher, and calcium, glucose, and total protein levels lower, in Zn-dosed ducks than in control ducks. Diet did affect serum calcium, phosphorus, total protein, and uric acid concentrations. Differences in erythrocyte and leucocyte parameters, serum enzyme activities, and metabolite concentrations were associated with dose and diet effects. Diets high in protein and other organic matter and calcium and phosphorus did not prevent or substantially alleviate Zn toxicosis in farm-raised mallard ducks.
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PMID:Influence of diet on the hematology and serum biochemistry of zinc-intoxicated mallards. 1068 52

A five-year-old female dog was presented with a four-week history of inappetence, weight loss, and skin and gait abnormalities. Physical examination revealed weakness, depression, incoordination of the posterior limbs, emaciation, skin and hair coat alterations, peripheral lymphadenopathy, pale mucous membranes and fever. Laboratory analysis of samples revealed abnormalities which included anaemia, neutrophilic leucocytosis, thrombocytopenia, low serum glucose and albumin concentrations, and increased serum alkaline phosphatase activity. The diagnosis was confirmed microscopically, by demonstrating the presence of Hepatozoon canis gametocytes within neutrophils in Giemsa-stained peripheral blood smears. Treatment consisting of toltrazuril and a trimethoprim-sulfamethoxazole combination was effective in relieving the clinical signs and clearing the blood of H. canis gametocytes. To the authors' knowledge, this is the first detailed clinical description of H. canis infection in a dog in Turkey.
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PMID:Clinical Hepatozoon canis infection in a dog in Turkey. 1560 Feb 73