Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normal reference values for total serum protein, albumin, cholesterol, alanine aminotransferase (ALT), aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH), gamma glutamyl transferase (GGT), alkaline phosphatase (AP), and total bilirubin were established in 48 clinically healthy woodchucks. To validate the use of these biochemical tests in the woodchuck for assessment of liver injury, carbon tetrachloride was administered to produce hepatocellular necrosis and the common bile duct was surgically occluded to produce cholestasis. Biochemical tests were performed prior to experimental treatment and thereafter in surviving woodchucks for a period of 6 weeks. There were marked increases in the serum activities of AST, ALT, and SDH following carbon tetrachloride administration and all 3 enzymes appeared to be useful markers of acute hepatocellular injury. The predominate biochemical abnormalities in woodchucks with bile duct obstruction were hyperbilirubinemia, hypercholesterolemia and increased serum AP and GGT activities. The increase of GGT occurred earlier following bile duct obstruction and the magnitude of increase was greater than that of AP, suggesting that GGT would be the preferred serum enzyme test in the woodchuck for assessment of cholestatic liver injury.
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PMID:Laboratory assessment of hepatic injury in the woodchuck (Marmota monax). 286 72

The case records of 21 dogs with congenital portosystemic encephalopathy are reviewed. The disorder was most common in Australian cattledogs (blue heelers; 8 cases), Old English sheepdogs (3 cases) and Maltese terriers (3 cases). Extra-hepatic shunts occurred in small breeds, with the exception of 1 cattledog, while intra-hepatic shunts occurred in the medium to large breeds. The most common clinical pathology abnormalities were abnormal ammonia tolerance, mild to moderate increases in plasma alanine aminotransferase or alkaline phosphatase concentrations, decreased total serum protein concentrations, increased fasting ammonia concentrations and ammonium biurate crystalluria. Radiological examination revealed that all the dogs had a small liver. The kidneys were enlarged in 5 of 10 dogs in which kidney size could be estimated. Surgical ligation of an extra-hepatic shunt was successful in 2 of 4 dogs in which it was attempted. Medical management resulted in alleviation of clinical signs in 5 of 8 dogs. The period of successful treatment ranged from a few months to over a year.
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PMID:Canine congenital portosystemic encephalopathy. 319 May 91

The individual and combined effects of aflatoxin and T-2 toxin were studied in male broiler chicks (Hubbard X Hubbard). The experimental design was a 2 X 2 factorial design with dietary treatments of 0 and 2.5 micrograms/g aflatoxin and 0 and 4.0 micrograms/g T-2 toxin. The broilers were obtained at 1 day of age and housed in electrically heated batteries with feed and water available ad libitum until they reached 3 wk of age. Aflatoxicosis in this study was characterized by a significant (P less than .05) reduction in body weight, changes in red blood cell counts and serum levels of protein, albumin, glucose, cholesterol, and calcium, and magnesium, activity of the serum enzymes lactic dehydrogenase and alkaline phosphatase, and a significant (P less than .05) increase in relative weights of the liver, kidney, spleen, pancreas, proventriculus, and heart. Dietary T-2 toxin alone caused oral lesions, a significant (P less than .05) decrease in serum protein, albumin, potassium, and magnesium levels, and a significant (P less than .05) decrease in the activity of the serum enzymes lactic dehydrogenase and alkaline phosphatase. In the combination treatment of aflatoxin and T-2 toxin, significant (P less than .05) interactive effects were seen through a decrease in body weights, increase in the relative weights of the kidney, gizzard, and heart, and decrease in mean corpuscular volume and serum levels of potassium. These data indicate that aflatoxin and T-2 toxin can interact to produce synergistic toxicity. This synergism is a threat to poultry production due to the prevalence of these mycotoxins and severity of the interactive toxicity of these mycotoxins.
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PMID:Toxic synergism between aflatoxin and T-2 toxin in broiler chickens. 319 34

Nine- to ten-week-old, male castrated, specific pathogen-free derived pigs, weighing 34 to 42 kg, were exposed to a T-2 toxin aerosol (390 micrograms/liter, 1.5 microM mass median aerodynamic diameter) for a time period which allowed an amount equivalent to 8 mg/kg to be nebulized (six pigs). Control animals (five pigs) were exposed to an equivalent amount of the nebulized vehicle. Pigs were immunized subcutaneously with sheep red blood cells on Days 0 and 21. Whole blood and serum samples were taken periodically for clinical pathologic and immunologic studies. Pigs were closely observed, and daily rectal temperatures and weekly weights were measured. The T-2-treated pigs vomited and exhibited cyanosis, anorexia, lethargy, lateral recumbency, slightly elevated rectal temperature, and depressed body weight gain. The lymphocyte count decreased while the neutrophil count increased. The concentrations of total serum protein and hemoglobin declined. There was a marked increase in serum alkaline phosphatase activity on Day 1, followed by a marked and persistent decrease. Mitogen-induced (Con A, PHA, and PWM) blastogenic responses of peripheral blood mononuclear cells and hemagglutination titers to SRBC were also transiently decreased. Thus, inhalation exposure of pigs to a sublethal dose of T-2 toxin caused clinical signs of toxicity and adverse effects on clinical pathologic parameters and immune responses; however, most of these effects were short-lived. The changes described in our study resemble those reported in pigs given T-2 toxin by intravascular injection.
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PMID:Experimental T-2 toxicosis in swine following inhalation exposure: clinical signs and effects on hematology, serum biochemistry, and immune response. 320 8

Eighteen xenogeneic chimeric rats (survival: greater than 100 days) were established by transplanting bone marrow cells from femurs of 10 gnotobiotic CFW mice into each germfree Sprague-Dawley or Wistar rat. The erythrocytes circulating in the rats were of mouse origin as determined by hemagglutination. Hemoglobin electrophoresis, radial immunodiffusion for IgG, and assay of granulocytic neutrophils for leukocyte alkaline phosphatase verified that true chimerism was achieved. The extent of hematological and immunological reconstitution varied. In general, hematocrit levels were low to normal, white blood cell counts and differentials were within normal limits, and serum protein levels were normal. Levels of circulating IgG of each species were comparable to those of germfree rat and mouse controls. Natural killer (NK) activity was depressed, a phenomenon that may be attributable to the radiation treatment of recipients, or to failure to transfer NK cells or precursors. Mitogenic stimulation reactions were varied, but most chimeric rats demonstrated moderately depressed responses. Reactions as a whole suggested that gnotobiotic rats with xenogeneic bone marrow are incompletely reconstituted, both hematologically and immunologically. No acute graft-versus-host reaction was seen.
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PMID:Characterization of xenogeneic mouse-to-rat bone marrow chimeras. I. Examination of hematologic and immunologic function. 329 26

This study was carried out on 18 albino rats. The control group, consisting of six rats, was fed a normal diet and tap water. The other rats were given a zinc-deficient diet and deionized water. Two weeks later the latter group was again divided into two into smaller groups. The first of these groups was given an given an additional 100 ppm of zinc acetate. From the fifteenth day onwards, the human growth hormone (Nanormon) was injected intra-peritoneally to each group at a dose of 80 micrograms/day for two weeks. At the end of the experiment, it was found that body weights were markedly increased in the control and zinc-added groups compared with the zinc-deficient rats. In the zinc-deficient group, serum zinc, hair zinc levels, alkaline phosphatase activity and serum protein levels were lower than those of the control and zinc-added groups. The zinc-deficient group had narrower tibial epiphyseal growth plates than those of the control group. The count of hypertrophied cells was also less in the zinc-deficient group. Based on these data, our conclusion was that the growth hormone becomes ineffective under conditions of zinc deficiency. This means that zinc deficiency has multidimensional effects on growth hormone activity.
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PMID:Effect of growth hormone on epiphyseal growth plates in zinc deficiency. 350 57

By photon absorptiometry, extrauterine bone mineralization was evaluated in preterm infants (less than 1,600 g birth weight) fed either a commercial premature formula containing 117 mg calcium, 58.5 mg phosphorus/100 kcal, the same formula containing higher phosphorus (82 mg/100 kcal), the same formula with higher calcium (140 mg Ca) and phosphorus (82 mg/100 kcal), or their own mother's milk. All infants had serum protein, albumin, calcium, phosphorus, bicarbonate, 25-hydroxyvitamin D, and alkaline phosphatase levels done at the start of the study and every 2 weeks until they weighed 1,900 g. At the start of the study, birth weight and gestational ages were similar in all four groups. There were no biochemical differences among the four groups except for a lower serum P in the human milk group. The human milk group had lower bone mineralization rate compared with the three formula groups. Bone mineral content was similar in the three formula-fed groups. However, only formulas containing 117 mg Ca and 58.5 mg P or 140 mg Ca and 82 P mg/100 kcal approximated intrauterine bone mineralization. Human milk fed infants did not approximate and were significantly different from the intrauterine rate.
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PMID:Effects of increased calcium and phosphorous formulas and human milk on bone mineralization in preterm infants. 372 65

The nutritional status of 145 black preschool children aged 3-5 years living in Letaba near Tzaneen was evaluated biochemically; 20.7% weighed less than 80% of the 50th percentile. Mean levels of red cell thiamine, serum protein and albumin, 25-hydroxyvitamin D, alkaline phosphatase, calcium and phosphorus were similar in underweight children and children not classified as underweight. The precise bearing of slower growth and associated biochemical parameters on present and future health needs elucidation.
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PMID:Biochemical evaluation of black preschool children in the northern Transvaal. 373 40

We compared the growth, biochemical status, and mineral status of 30 very-low-birth-weight infants randomly assigned to receive preterm human milk (Group I, 10 infants) from their own mothers, fortified preterm human milk (Group II, 8 infants), or a high-caloric-density premature formula (Group III, 12 infants). Added to the infant's own mother's milk, a human milk fortifier at full strength provided additional protein (60:40 whey/casein, 0.7 g/dl), calories (4 kcal/oz), and minerals. Volume of intake, feeding tolerance, and complications were similar in the three groups. Infants receiving fortified preterm human milk showed growth, biochemical status, and mineral status similar to those receiving high-caloric-density formula, but infants receiving fortified preterm human milk grew faster (12.0 +/- 3.2 vs. 8.9 +/- 1.1 days/300 g, p less than 0.05), had higher serum protein (4.6 +/- 0.5 vs. 4.2 +/- 0.2 g/dl, p less than 0.05), and tended to have better mineral status (higher serum calcium, lower alkaline phosphatase, and higher serum phosphorus, none individually significant) than infants receiving preterm human milk alone. This study supports previous observations that fortified preterm human milk provides nutritional advantages for very-low-birth-weight infants.
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PMID:Growth, biochemical status, and mineral metabolism in very-low-birth-weight infants receiving fortified preterm human milk. 376 Nov 7

VP 16-213 (etoposide, abbr. to VP), an oncostatic drug, was administered orally to Crj : CD (Sprague-Dawley) rats of both sexes at dose levels of 3, 10, 30 and 100 mg/kg/day for one month with the object of examining its subacute toxicity and the reversibility of toxic effects. The summarized results obtained are as follows: VP 30 mg/kg suppressed body weight increase and feed intake, and brought soft stool. VP 100 mg/kg decreased body weight and feed intake, and induced diarrhea, depilation and so forth. Furthermore, half of the animals at this dose level died showing systemic debility and emaciation. VP 30 and 100 mg/kg predominantly decreased red blood cell count as well as white blood cell count accompanied with lowered lymphocyte fraction. VP 10 mg/kg and higher lowered total serum protein content and serum alkaline phosphatase activity, and elevated A/G ratio. VP 10 mg/kg and higher caused thymic atrophy and a decrease in testicular weight; 30 and 100 mg/kg brought suppression of spermatogenesis; and 100 mg/kg predominantly induced appearance of giant cells in epididymis, hypoplasia of bone marrow, ileocecitis, and atrophy of prostate, seminal vesicle and splenic germinal centers. Above-described changes excluding exacerbation of the findings on testis and epididymis were shown to be generally reversible. Based on these results, the no-effect dose level of VP under the present experimental condition was estimated to be 3 mg/kg/day against rats of both sexes.
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PMID:[Toxicity studies of VP 16-213 (II)--Oral one-month subacute toxicity in rats]. 376 92


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