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)

Male rats weighing 180-220 g were given CdSO4, 0,4 mg/kg body weight subcutaneously once a week for 6-12 months. The animals were killed after 6, 9, 12 months and following blood serum levels were determined: total protein, albumin, globulin, GPT, GOT, Al.P. and urea. The tissue tissue samples from liver and kidneys were examined histologically (acid and alkaline phosphatase). After 9 months, the difference between values of biochemical indices in the exposed and control groups was statistically significant. It has been found that the observed biochemical indices show correlation with the extent of morphological changes in liver and kidneys. These degenerative changes became more intense in the liver than in the kidneys.
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PMID:[Effect of chronic action of cadmium sulfate on various biochemical indices of blood serum and on the histological picture of rat liver and kidneys]. 19 73

Simultaneous measurements of serum immunoreactive thyrocalcitonin (iTCT), immunoreactive parathyroid hormone (iPTH), calcium, inorganic phosphate, magnesium, and alkaline phosphatase were made in 37 normal children whose ages ranged from 6-12 years. Between the ages of 6 and 12 there is a statistically significant rise in serum iTCT levels (r = 0.4638; P less than 0.01), and a fall in serum iPTH levels (r = 0.4976; P less than 0.01). There is a highly significant inverse correlation between serum iTCT and iPTH levels (r = 0.5248; P less than 0.005). Serum iTCT levels were inversely correlated with phosphate levels (r = 0.4989; P less than 0.01), the latter being age dependent and falling significantly between the ages of 6 and 12 (r = 0.4802; P less than 0.001). There was no significant relationship between serum calcium levels and iTCT, iPTH, or age. Serum magnesium levels were not correlated with calcium, iTCT, or iPTH levels.
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PMID:Serum calcitonin and blood mineral interrelationships in normal children aged six to twelve years. 84 May

A comparative study of enzyme alkaline phosphatase (AP) of plasma and chorion placental extracts was made in various terms of pregnancy by PAAG electrophoresis. It is shown that the first three month chorion extract contained 1 thermolabile (TL) and 1 or 3 thermostable (TS) fractions of AP. In the second trimester of intrauterine development the activity of TL fraction disappeared, the number of TS forms increased. The early plasma period (6-12 weeks) was characterized by 2 TL non-placental forms, from the second half they added to 1 or 3 TS placental fractions, and before delivery TS enzyme appeared in the liver AP which had no analogue in the placenta. It is concluded that only the fastest placental TS AP forms (1 or 3) appear in maternal blood from the second trimester of gestation.
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PMID:[Comparative electrophoretic characteristics of alkaline phosphatase isoforms in maternal blood and shaggy chorion extracts at various periods of pregnancy]. 147 40

Intestinal Ca2+ malabsorption has been described in spontaneously hypertensive rats (SHRs), but the molecular basis for this defect is unknown. In this study, we measured intestinal alkaline phosphatase and vitamin D-dependent Ca(2+)-binding protein (calbindin-D9k), two proteins implicated in the active pathway of intestinal Ca2+ absorption. Both proteins were measured in the small intestines of SHRs and their normotensive controls, Wistar-Kyoto rats, before, during, and after development of hypertension (4, 9, 14, 18, and 28 wk of age). At all ages, alkaline phosphatase activity in duodenum (0-6 cm) was decreased by 30-57% (P less than 0.001) and by 47-75% in the 2nd intestinal segment (6-12 cm) (P less than 0.001-0.05). Calbindin-D9k was decreased similarly. The decreases of calbindin were statistically significant (P less than 0.001-0.05) in the duodena at 4, 14, 18, and 28 wk (9-30% decreases) and in the 2nd segment at 4, 14, and 18 wk (38-69% decreases; P less than 0.001-0.005). Decreased calbindin in SHRs was documented in animals from two suppliers. The deficiencies of calbindin-D9k and alkaline phosphatase could not be attributed to malnutrition or to a generalized brush-border defect as indicated by body weights and the intestinal marker enzyme sucrase. Although calbindin-D9k was decreased in young SHRs, the serum 1,25-dihydroxycholecalciferol [1,25(OH)2D3] was increased by 59 and 129% in 4- and 9-wk-old SHRs (P less than 0.001), respectively; by contrast, serum 1,25(OH)2D3 was unchanged or decreased in older SHRs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intestinal vitamin D-dependent calbindin-D9k and alkaline phosphatase in spontaneously hypertensive rats. 203 38

Clinical investigations have shown that 1 alpha-hydroxycholecalciferol (oxydevit, alphacalcidiol) and 1 alpha, 25-dihydroxycholecalciferol (rocaltrol) are act vitamin D3 agents producing a positive clinical effect in different types of osteoporosis and osteomalacia. Clinical improvement of the patients' status (alleviation of the pain syndrome, an increase in motor activity) was noted in 1-2 mos., an x-ray picture of regeneration of the bone structure of both axial and peripheral skeleton--in 6-12 mos. after the initiation of therapy. Therapy was attended by an increase in the serum content of total and ionized calcium, the return of alkaline phosphatase activity to normal, and a decrease in the level of parathormone. During prolonged therapy these agents administered at daily doses of 0.25-2 micrograms caused no pathological side-effects and hypercalcemia. In osteoporotic conditions all these drugs were equal in their clinical effectiveness. Rocaltrol has some advantages in the presence of associated liver pathology.
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PMID:[Comparative evaluation of the effectiveness of vitamin D3 preparations (1-alpha-hydroxy- and 1-alpha,25-dihydroxycholecalciferol in various forms of osteoporosis and osteomalacia]. 276 60

The aim of the study was the evaluation of survival of 140 cirrhotic patients who had a liver biopsy between 1970 and 1987. It is interesting to point out that all the patients with cirrhosis were included in the study and that they were all coming from a limited geographic area. This justifies the limited drop-out (7/147 patients). The high survival rate could be due to the fact that only patients suitable to receive a liver biopsy were elected for the study. We found that factors critical for prognosis in the short term (6-12 months) are biochemical values such as prothrombin index, serum albumin, serum bilirubin, alkaline phosphatase, while the factors affecting long-term prognosis are age, sex, etiology of cirrhosis, high alcohol intake after biopsy, ascites and untreated portal hypertension.
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PMID:[Liver cirrhosis. Survival of a homogeneous population]. 276 65

We have studied some effects of small doses of 1,25-dihydroxycalciferol (calcitriol) and calcium, either combined or separately, in 45 patients with osteoporosis and malabsorption of calcium. In 24 patients on 0.25 micrograms/d of calcitriol the hourly fractional rate of radiocalcium absorption rose from 0.37 +/- 0.02 to 0.55 +/- 0.04 (p less than 0.001) and in 21 patients on 0.50 micrograms/d it rose from 0.36 +/- 0.02 to 0.69 +/- 0.05 (p less than 0.001). These responses were seen within 5 days and were not increased further at 6 weeks to 3 months. The combined therapy significantly reduced the fasting urinary hydroxyproline/creatine ratio (OHPr/Cr) and plasma alkaline phosphatase activity (ALP) in 6-12 weeks, the smaller dose of calcitriol (0.25 micrograms/d) being as effective as the larger one (0.50 micrograms/d) in this respect. Calcium alone (1 g/d) had no effect and calcitriol alone (0.25 mcg/d) had a lesser effect on both OHPr/Cr and ALP than the combined therapy. The falls in OHPr/Cr and ALP tended to be greatest in the cases with the highest initial levels but constituted only partial suppression of these variables towards the theoretical non-bone components. These results suggest that treatment with calcitriol and calcium suppresses bone resorption in osteoporosis associated with malabsorption of calcium and is more effective than calcium or calcitriol given alone.
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PMID:1,25-Dihydroxycalciferol and calcium therapy in osteoporosis with calcium malabsorption. Dose response relationship of calcium absorption and indices of bone turnover. 383 58

In 42 uraemic patients radiological skeletal survey, biochemistry and bone histology were compared before and at 6-12 months (42 patients), 12-24 months (26 patients) or 24-48 months (12 patients) after parathyroidectomy. The presence of small vessel or non-visceral soft tissue calcification was not related to the age, sex, duration of end-stage renal failure treatment, total serum calcium, magnesium, phosphate, Ca x P product, alkaline phosphatase, ionised calcium, serum aluminium, iPTH, severity of radiological and histological osteitis fibrosa or parathyroid gland weight. Twenty-three patients (55%) had small vessel and 20 (48%) soft tissue calcification before parathyroidectomy. Despite a marked improvement in subperiosteal erosions (37 healed, 5 improved) and healing of osteitis fibrosa histologically, seven patients developed new and six developed increased peripheral arterial calcification while in 10 patients non-visceral soft tissue calcification disappeared and in two decreased. Successful parathyroidectomy improves non-visceral calcification but not arterial calcification despite reduction in Ca x P product and iPTH.
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PMID:Ectopic calcification. The role of parathyroid hormone. 399 87

The effect of vincristine treatment on the morphofunctional status of the small intestine was studied morphologically in 80 Wistar rats. The drug was found to possess a general toxic effect. Diarrhea was matched by the arrest of crypt cell-proliferation at metaphase, lysis, a decreased disaccharidase activity and increased levels of cytoplasmic alkaline phosphatase and dipeptidyl(amino)peptidase-IV in enterocytes of the villi. Exudation and degenerated cell organellae prevailed in intramural nervous ganglion cells, smooth muscle cells of intestinal tunica muscularis and vessels and in endothelium. The said changes were transitory in epithelium, but never regressed in nervous structures. At later stages (6-12 months after vincristine, but never regressed in endothelium. The later stages (6-12 months after vincristine treatment), secondary dystrophic changes developed in the small intestine wall, being predominantly confined to neuromuscular and vascular elements.
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PMID:[The effect of vincristine on the morpho-functional state of the rat small intestine]. 648 90

Clinical observations suggest that the onset and severity of glucocorticoid (GC) induced osteoporosis is dependent on the duration of the GC treatment and the applied GC compound. To test whether these in vivo observations are reflected by different in vitro effects of various synthetic GCs on human bone cell metabolism we isolated human osteoblast-like cells (HOC) from bone biopsies of healthy (no clinical symptoms of arthritis or arthrosis) adults who underwent selective orthopedic surgery. HOC were identified as bone cells by 1,25-vitamin D3-stimulated increase of specific alkaline phosphatase (ALP) activity, secretion of osteocalcin and type-I procollagen peptide, and the ability to form mineral in vitro. We investigated the effects of dexamethasone (dexa), methylprednisolone (mpred), prednisolone (pred), and deflazacort (defla) on DNA-synthesis, ALP, and osteocalcin (OC)- and type-I procollagen peptide secretion of HOC in vitro. In summary, (1) GC exposure stimulates DNA synthesis after 6-12 hour treatment periods; (2) dex and mpred strongly inhibit DNA (48-hour treatment) and collagen synthesis but stimulate ALP, whereas pred and defla exhibit smaller effects on DNA synthesis, ALP, and collagen production; and (3) all tested glucocorticoids inhibit OC secretion by HOC in vitro. Thus, the effect of GC on DNA synthesis of HOC varies with the duration of GC exposure, and dex and mpred more potently affect HOC metabolism in vitro than pred and defla.
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PMID:Differential effects of glucocorticoids on human osteoblastic cell metabolism in vitro. 758 72


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