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)

beta,beta'-Iminodipropionitrile (IDPN) administration produces giant neurofilament-filled axonal swellings in the first proximal internodes of large myelinated sensory and motor fibers without any accompanying axonal degeneration. In the present study, we asked whether proximal giant axonal swellings are sufficient to elicit aberrant neurofilament (NF) phosphorylation in neuronal perikarya. Rats were given a single intraperitoneal (i.p.) injection of IDPN (2 g/kg) followed by IDPN (0.1%) in the drinking water (continuous IDPN exposure) or tap water (single IDPN exposure) for two days to 7 weeks. Immunoreactivity to phosphorylated NF (pNF) epitopes (using monoclonal antibodies 6-17 and 7-05) was observed in L4 and L5 dorsal root ganglia (DRG) neurons beginning between one and 5 days, corresponding to the development of proximal giant axonal swellings. Quantitation of DRG neurons demonstrated maximal numbers of immunoreactive cell bodies to pNF epitopes (46-51%) by one week. The number of immunostained DRG cells was maintained in animals given continuous IDPN exposure, but declined significantly (P less than 0.001) in rats given a single injection of IDPN to 26 +/- 0.80% and 6 +/- 0.04% at 3 and 5 weeks, respectively. Ventral and dorsal root fibers, which undergo axonal atrophy distal to axonal swellings, showed intense immunoreactivity to pNF epitopes and a marked reduction or a complete lack of immunostaining to antibody 2-135 (directed against non-phosphorylated NF epitopes); pretreatment with alkaline phosphatase reversed this staining pattern. In a separate study, a similar alkaline phosphatase-sensitive lack of staining to antibody 2-135 was also observed in atrophic motor fibers in the DRG 4 weeks following nerve crush. It is suggested that aberrant NF phosphorylation in DRG neuronal cell bodies from IDPN-treated rats arises secondarily to an alteration in a retrogradely transported 'trophic' signal(s) to the neuron due to the presence of giant axonal swellings. Furthermore, pNFs in atrophic axons may correspond to stationary or slowly moving NFs in the axoplasm.
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PMID:Regulation of aberrant neurofilament phosphorylation in neuronal perikarya. III. Alterations following single and continuous beta, beta'-iminodipropionitrile administrations. 172 19

A case of primary myelofibrosis complicated with pericardial effusion and proteinuria is described. A 66-year-old female was admitted to our hospital because of abdominal fullness and shortness of breath. On admission, hepatosplenomegaly and pericardial effusion were observed. Blood examination revealed leukoerythroblastic anemia and thrombocytosis with tear drop cells and giant platelets. Bone marrow aspiration was dry tap and its biopsy showed remarkable myelofibrosis. Urinalysis indicated severe proteinuria. Although neutrophilic alkaline phosphatase score was low, no signs of acute blastic crisis of chronic myelogenous leukemia was found. The diagnosis of an atypical type of primary myelofibrosis was obtained. Administration of MCNU was started in August 1987. Hepatosplenomegaly, pericardial effusion and proteinuria were gradually improved after the administration. The etiology of the pericardial effusion and proteinuria were not obvious, however, these facts suggest that these abnormal findings might be related to PMF itself and MCNU was effective to PNF.
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PMID:[The use of MCNU to a patient of primary myelofibrosis complicated with pericardial effusion and proteinuria]. 276 70

A total of 1,026 patients undergoing haemodialysis as the only chronic treatment were studied in all the dialysis units of the Veneto region, Italy. Aluminium was determined in water, dialysis fluids, and patients' serum. Aluminium mean concentration was 9.1 micrograms/l in tap water and 13.3 and 15.7 micrograms/l in bicarbonate and acetate haemodialysis fluids, respectively. Patients' serum aluminium mean level was 52.0 micrograms/l with the following frequency distribution: 59.2% below 60 micrograms/l, 25.5% between 60 and 100 micrograms, and 15.3% above 100 micrograms/l. The mean serum aluminium level was higher in patients undergoing haemodialysis with aluminium concentration in fluids over 10 micrograms/l. This was true also in patients not receiving aluminium hydroxide. Furthermore, we found higher average serum aluminium in those treated with aluminium hydroxide more than 3 g/day. No relationship was found between serum aluminium and sex, age, dialytic age, parathyroid hormone, and vitamin D treatment. Moreover, the patients with serum aluminium above 100 micrograms/l had higher serum alkaline phosphatase and lower mean cell volume values. Thus, in our haemodialysis population aluminium overloading occurred in spite of low concentration in water and fluid, and it was a result more of fluid pollution (over 10 micrograms/l) than aluminium hydroxide ingestion (over 3 g/day).
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PMID:Serum aluminium level in the veneto chronic haemodialysis population: cross-sectional study on 1,026 patients. 278

A subchronic oral toxicity study with potassium nitrite (KNO2) was carried out in rats. Groups of ten male and ten female 6-wk-old rats received KNO2 in the drinking-water (tap-water) at levels of 0, 100, 300, 1000 and 3000 mg/litre for a period of 13 wk. The potassium concentration in the nitrite solutions was equalized by adding potassium chloride (KCl) up to the potassium level of the 3000-mg KNO2/litre solution. An additional group of ten males and ten females received drinking-water supplemented with KCl only, at an amount resulting in a potassium concentration equivalent to that of the 3000-mg KNO2/litre solution. Body weight, food intake and food efficiency were decreased at 3000-mg/litre level in males, while liquid intake was decreased in males given 1000 and 3000 mg/litre and in females given 3000 mg/litre. There was significant increase in the methaemoglobin concentration in animals given 3000 mg/litre, while slight decreases in red blood cell variables occurred at the 1000- and 3000-mg/litre dose. No impaired renal function was observed in any of the test groups, although the relative weight of the kidneys and the plasma urea nitrogen level was increased at 3000 mg/litre. There was a slight decrease in plasma alkaline phosphatase activity at 3000 mg/litre. A small amount of nitrite was present in the saliva of the rats receiving 3000 mg/litre but there was no evidence of increased mutagenic activity in the urine of these rats. Interestingly, hypertrophy of the adrenal zone glomerulosa was observed in all test groups, the incidence and degree being dose related. It was concluded that in the study reported here the no-effect level is lower than 100 mg KNO2/litre in the drinking-water, which is equivalent to a level lower than 10 mg KNO2/kg body weight/day.
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PMID:Evaluation of the oral toxicity of potassium nitrite in a 13-week drinking-water study in rats. 322 Mar 28

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

Male Porton-Wistar rats, 32 weeks old, were given i.p. one of the following doses of HgCl2; 0.5, 1.0 or 1.5 mg Hg/kg. In the preceding 4-week period and throughout the experiment the animals had free access to either tap water or 1.0% saline. The urinary excretion of alkaline phosphatase measured in urine samples, collected during the first 24 h after treatment with mercury, indicated that chronic saline loading significantly attenuated tubular damage caused by 0.5 mg or 1.0 mg Hg/kg, but not by 1.5 mg Hg/kg. Tubular necrosis 12 and 24 h after mercury was also less severe and extensive in saline than in tap water-drinking rats. This difference was still noticeable 4 days after mercury treatment in rats dosed with 0.5 mg Hg/kg, but death in the two higher dose groups prevented further pair-to-pair histological comparison. At the selected dose levels chronic saline loading did not decrease renal mercury content at 12 or 24 h and therefore protection was not associated with decrease in renal mercury uptake. The experiment indicates that chronic saline drinking, which at higher doses attenuates HgCl2-induced acute renal failure but not tubular necrosis, is able to moderate the severity of tubular necrosis when the dose of HgCl2 is as low as 0.5 mg Hg/kg. This protective effect diminishes as the dose is increased.
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PMID:Effect of prolonged saline loading on HgCl2-induced renal tubular damage. 648 35

Fresh-brewed regular coffee at concentrations of 25, 50, and 100% was consumed ad libitum as the sole fluid intake of F1 Sprague-Dawley rats (55 male and 55 female/group), derived from P0-treated females which were provided 50% coffee for about 5 weeks prior to copulation and throughout gestation and lactation. P0 males, P0 control females, and two groups of F1 control rats received tap water. Ten rats/sex/level were killed and examined after 1 year; survivors were killed after 2 years. Smaller mean body weights (50 and 100% coffee concentrations) occurred with increased feed and liquid consumption. Mean serum alkaline phosphatase, bilirubin, BUN, and calcium values occasionally were elevated. Serum cholesterol levels at 2 years were elevated in males (25 and 100%) and at 1 and 2 years in females (100%). Bone calcium was slightly reduced in females consuming 25 or 100% coffee for 1 year, but not after 2 years. Treatment-related increases in relative weights of lungs, kidneys, liver, and epididymides were recorded. Significantly increased mortality was observed in females receiving 50 or 100% coffee. There also was some evidence of a relationship between coffee consumption and the number of primary tumor-bearing animals; however, this finding appeared ambiguous, dependent on the assumption that tumors were the probable cause of death.
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PMID:Two-year toxicity/carcinogenicity study of fresh-brewed coffee in rats initially exposed in utero. 674 Jun 85

A 57-year-old man was admitted to hospital because of leukocytosis. He showed mild splenomegaly and, laboratory studies revealed elevated mature neutrophil count without morphological abnormality, mild anemia and elevated neutrophil alkaline phosphatase score. The serum granulocyte colony stimulating factor concentration was below 30 pg/ml. Bone marrow was a dry tap, and biopsy specimen revealed severe fibrosis. The peripheral blood karyotype was 46, XY with no rearrangement of bcr-abl. The patient was diagnosed as having chronic neutrophilic leukemia (CNL) with bone marrow fibrosis. He was successfully treated with hydroxyurea (HU) 1000 mg/day. The peripheral blood leukocyte was decreased to the normal level and, the bone marrow biopsy specimen changed mild fibrosis. During the follow up period of 11 months, the neutrophil count was well controlled without any side effect. This is a rare case of CNL accompanied with bone marrow fibrosis which was effectively treated by the administration of HU.
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PMID:[A case of chronic neutrophilic leukemia accompanied with severe bone marrow fibrosis which was effectively treated by hydroxyurea]. 782

Forty-two hematological and biochemical variables routinely measured in dogs as part of a preoperative protocol have been analyzed for circannual changes by analysis of variance (ANOVA) and single cosinor procedures. Data were available from up to 489 adult mongrel dogs of both sexes studied on weekdays over a 5-year span (January 5, 1987 to December 18, 1991). Dogs were housed in individual cages at 24 +/- 1 degrees C with dog chow and tap water available ad libitum and lights on between 06:00 and 18:00 h. A single blood sample/dog was collected by jugular venipuncture between 08:00 and 09:00 h and sent to a commercial laboratory for hematological and biochemical determinations. Data were assigned to date and time of sampling and analyzed for the effect of time of year by ANOVA (across 12 months and 4 seasons), and by the least-squares fit of a precise 1-year cosine. ANOVA and single cosinor described a significant circannual time effect and rhythm for the following: total leukocytes, lymphocytes, hemoglobin, mean corpuscular hemoglobin (MCH), MCH concentration, red cell distribution width, mean platelet volume, creatinine, blood urea nitrogen (BUN), BUN/creatinine ratio, amylase, glucose, chloride, uric acid, direct bilirubin, total protein, albumin, globulin, albumin/globulin ratio, lactate dehydrogenase, alkaline phosphatase, gamma-glutamyltransferase, alanine aminotransferase (ALT), and aspartate aminotransferase (AST)/ALT ratio. A significant effect of season by ANOVA only was found for: Ca, Na, phosphorus, total bilirubin, hematocrit, mean corpuscular volume, and neutrophils. No significant time effect could be found at p < or = 0.05 by either statistical method for: K, Mg, Fe, cholesterol, triglycerides, ASP, red blood cells, monocytes, eosinophils, basophils, or platelets. Acrophases occurred for the most part in either the winter or summer.
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PMID:Circannual variations in baseline blood values of dogs. 826 36

We studied the effect of chronic exposure (6 weeks and 6 months) of mice to drinking (tap) water containing 1.76% (0.06 M) aluminum lactate on some cytochemical properties of the blood-brain barrier (BBB). The plasmalemma-bound enzymatic activities of alkaline phosphatase (AP) and Ca(2+)-activated adenosine triphosphatase (Ca(2+)-ATPase) were studied at the ultrastructural level. Anionic sites were localized with cationized ferritin in a pre-embedding procedure and with cationic colloidal gold in a post-embedding procedure applied to brain samples embedded in Lowicryl K4M. Intravenously injected Evans blue and horseradish peroxidase (HRP) were used for evaluation of the functional state of the BBB. The results indicate that chronic exposure to aluminum does not noticeably affect barrier function of the endothelium of cerebral cortex blood microvessels. Focal leakage of larger than capillary microvessels (presumably arterioles and venules) was observed only in a few areas, such as the basal ganglia and amygdaloid nuclei. The localization of both enzymatic activities (AP and Ca(2+)-ATPase) in microvessels remained essentially unchanged. The localization of anionic sites was also unchanged except on the luminal surface of the endothelium of a few blood microvessels located in areas of the brain where leakage of the injected HRP was noted. In these vessels the injected HRP was often attached to the luminal surface of the endothelial cells, suggesting its increased stickiness. These data, compared with our previous observations on brain microvascular endothelial cells growing in vitro, indicate that cytotoxicity of aluminum is evidently less pronounced in the living organism, presumably due to action of detoxicating and regulatory mechanisms.
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PMID:Ultracytochemical studies of the effects of aluminum on the blood-brain barrier of mice. 828 66


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