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)

The concentration of phospholipids is well suited as indicator for the prognosis of a possibly postnatal respiratory distress syndrome. The method used most frequently up to now has been the determination of the lecithin/sphingomyelin ratio (L/S ratio) by thin layer chromatography. We have developed a specific assay for the quantitative determination of lecithin in amniotic fluid, which yields absolute concentration values and does not require the determination of a concentration ratio. Lecithin is hydrolized by phospholipase C and alkaline phosphatase. Choline is determined afterwards by a highly specific choline kinase from yeast. The total time required is less than 2 h. The usual lecithin concentration present in the 35th to 38th wk of gestation can be determined with a coefficient of variation of 2-3% (n=30). Fetal lung maturity can be expected at a lecithin concentration above 4.7-5.1 mg/100 ml. The method compares well with the L/S ratio. Detailed data about clinical significance will be presented. Good precision accuracy and simple handling make enzymatic lecithin determinations suitable for routine use.
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PMID:A new method of evaluating fetal lung maturity: the enzymatic lecithin determination in amniotic fluid. 711 59

An outbreak of bacillary haemoglobinuria was recorded in 60 out of 110 sheep in Ludhiana, Punjab, India. The condition was clinically characterised by fever, haemoglobinuria, constipation, weakness of hind quarters followed by recumbency, respiratory distress and death in 16 sheep. Haematological studies revealed moderate to severe degrees of anaemia associated with leucocytosis. Plasma gamma-glutamyl transferase, alkaline phosphatase and creatinine phosphokinase activities were significantly higher in haemoglobinuric sheep. Babesiosis and copper poisoning were ruled out on stained blood film examination and from blood mineral profiles, respectively. Post-mortem examination of affected sheep revealed no gross changes. Pure cultures of Clostridium haemolyticum isolated from heart blood, liver, kidney and spleen of freshly killed sheep confirmed the disease. Parenteral administration of procaine penicillin was effective in the treatment of affected sheep.
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PMID:An outbreak of bacillary haemoglobinuria in sheep in India. 777 Sep 49

Fumonisin B1 (FB1), a mycotoxin produced by Fusarium moniliforme and F. proliferatum, induces liver damage and pulmonary edema in swine. We examined the temporal and dose-response features of FB1 toxicosis in male weanling crossbred pigs fed nutritionally balanced diets, containing corn screenings naturally contaminated with fumonisins, for 14 days. Total fumonisins (FB1 and FB2) in diets 1 through 6 were assayed at 175, 101, 39, 23, 5, and < 1 ppm (below detectable concentrations), respectively. Clinical signs, serum biochemical alterations, and morphologic changes were evaluated. Pigs were weighed, and bled for hematologic and clinical chemistry evaluation on days 5 and 14. They were euthanized on day 14, or earlier if respiratory distress was observed. Respiratory distress developed in 3/5 pigs fed diet 1 between days 4 and 6 due to severe pulmonary edema and pleural effusion. Histologic evidence of hepatic injury was present in all pigs fed diets 1 and 2, 3/5 on diet 3, and 1/5 on diet 4. Serum bilirubin and cholesterol concentrations, gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and arginase (ARG) activities were elevated in pigs fed diets 1 and 2. Based on liver histopathology, the no observed adverse effect level (NOAEL) for fumonisin toxicity in swine was < 23 ppm total fumosins for the 14-day period. Based on regression analyses of the clinical chemistry profiles at 14 days, the NOAEL was < 12 ppm, with ALP being the most sensitive parameter. In conclusion, pulmonary edema occurred only at the highest fumonisin concentration (175 ppm), while liver damage occurred at much lower concentrations with a NOAEL of < 12 ppm.
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PMID:Temporal and dose-response features in swine fed corn screenings contaminated with fumonisin mycotoxins. 805 90

The cases of fetal intrauterine hypotrophy syndrome were subjected to rest, dietetic and pharmacological treatment which included intravenous infusions of low molecular Dekstrane, intramuscular injections of Synacthen-Depot, Sadamine and Partusisten. The clear improvement of selected parameters of placenta efficiency during the management was observed. It included: mean increase of blood serum oxytocinase activity about 2.1 U, mean increase of quantity of estrogens excreted in 24-hour urine about 4.1 mg/24 hours, mean decrease of term-stabile alkaline phosphatase activity in blood serum about 16 U. The comparison of the state of hypotrophic newborns found in the group with hypotrophy treated during the course of pregnancy with the group of untreated hypotrophy permits to conclude: statistically significant more rarefied occurrence of newborns of low values according to Apgar scale, hypoglycemia, acidosis, anemia as well as respiratory distress syndrome and five-fold diminished perinatal mortality. It was demonstrated a clear correlation between many parameters of structure and activity of oxygenizing enzymes of placentae existed between the group with treated and untreated hypotrophy.
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PMID:[Microstructure of placenta and activity of some respiratory enzymes --in pregnancy with treated and untreated fetal intrauterine hypotrophy syndrome]. 835 45

Although the antioxidant properties of N-acetylcysteine (NAC) in vitro are widely accepted, the efficacy of NAC in the prevention of O2 toxicity in vivo is poorly documented. The aim of our study was to investigate the presumed protective effect of NAC on hyperoxic lung injury, focusing on gamma-glutamyltransferase (gamma-GT) activity and glutathione (GSH) levels in lung tissue, epithelial lining fluid (ELF), and isolated rat type II cells immediately after their isolation and 48 h later when kept in culture in normoxia. Thirty-four male Wistar rats were divided in three groups (n = 10-14) and were exposed to air or to 60 or 85% O2 for 7 days. One-half of the rats in each group received 200 mg/kg NAC intraperitoneally one time per day from 3 days before exposure until the end of the experiment, and the other one-half received the vehicle. In the 85% O2-exposed animals, NAC led to more respiratory distress and weight loss. NAC did not prevent the rise in bronchoalveolar lavage lactate dehydrogenase and alkaline phosphatase, but it did prevent the rise in calculated ELF volume. NAC decreased GSH levels (1.4-fold) and gamma-GT activity (1.8-fold) in the air-exposed type II cells. In the 60% O2-exposed group, no effects of NAC were seen (except for a decrease in gamma-GT mRNA expression), but, in the 85% O2-exposed group, NAC gave rise to higher GSH (2.6-fold) and higher gamma-GT activity (2.9-fold) in the ELF and lower GSH (6.9-fold) and higher gamma-GT activity (3.6-fold) in the type II cells. Even in culture, GSH levels remained 1.5-fold lower than in the cells from the air-exposed animals and 2-fold lower than in the cells from the 85% O2-exposed animals. There was increased DNA damage (as assessed by thymidine incorporation) and apoptosis after hyperoxia, especially after 60% O2, and this effect was amplified after NAC treatment. Although protective at the endothelial side, NAC treatment led to adverse effects at the epithelial side, despite, or probably because of, restoration of the ELF GSH levels in the presence of high O2 levels. Because NAC is rapidly metabolized to cysteine, it is plausible that the effects of NAC are manifested through the toxic effects of cysteine.
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PMID:N-acetylcysteine does not protect against type II cell injury after prolonged exposure to hyperoxia in rats. 931 88

Pyridoxine dependency and congenital hypophosphatasia are unusual metabolic disorders. We report a female infant born from healthy consanguineous parents with shortening of limbs, detected during pregnancy by ultrasonography. Immediately after delivery, the baby was admitted to the neonatal intensive care unit because of respiratory distress. A bone radiograph showed hypomineralization of all bones, and serum alkaline phosphatase was very low (10 U/L). Within the first day of life, seizures (focal clonic and tonic) started. The seizures were refractory to phenobarbital and other antiepileptic drugs. The first electroencephalogram (EEG) showed a burst-suppression pattern. Pyridoxine was administered (50 mg/kg) and completely controlled the seizures. Antiepileptic drugs were discontinued, and a maintenance dose of pyridoxine (10 mg/day) was established. A postpyridoxine EEG revealed the disappearance of the burst-suppression pattern. The patient died at age 26 days. Pyridoxine-dependent seizures, when recognized early and treated, have a more favorable prognosis. However, hypophosphatasia detected at birth almost always has a lethal outcome.
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PMID:Pyridoxine-dependent seizures associated with hypophosphatasia in a newborn. 1202 40

Episodic elevation of air pollutants may exacerbate respiratory distress associated with chronic obstructive pulmonary disease (COPD), yet few experiments have been performed to determine how continuously polluted atmospheres may contribute to the etiology of COPD, in general and pulmonary emphysema in particular. This study describes the effects of concurrent exposure to ozone (O(3)) in the pathogenesis of cigarette smoke (CS)-induced emphysema in the mouse. Female B6C3F1 mice were whole-body exposed either to filtered air (FA) or to mainstream CS at a concentration of 250 mg total particulate material/m(3) for 6 h/day, 5 days/wk for 15 or 32 wk. Concurrently, mice were exposed either to FA or to O(3) at 0.3 ppm for 8 h/night, 5 nights/wk for the same time periods. At necropsy, mouse lungs were lavaged, and bronchoalveolar lavage fluid (BALF) was analyzed for inflammatory cell numbers, total protein, lactate dehydrogenase (LDH) and alkaline phosphatase (AP) activities, superoxide production by isolated alveolar macrophages, glutathione content, inflammatory cytokines, and proteolytic activity. Other lungs were inflated at constant pressure for 6 h with formalin for fixation, routine histopathology, and stereology. After 32 wk of exposure, CS with or without concurrent O(3) exposure produced stereologic evidence of emphysema as previously described. Concurrent O(3) exposure did not worsen any of these parameters, nor did O(3) by itself cause stereologic changes that were consistent with emphysema. The O(3) exposure caused only slight elevations of BALF macrophages, while CS exposure caused marked increases in the numbers of both BALF macrophages and neutrophils. Neutrophils in the BALF in response to CS exposure were also more numerous at 32 wk than at 15 wk. Exposure to CS caused an increase in BALF total protein, LDH, AP, and interleukin (IL)-1beta. After 32 wk, CS exposure was associated with decreased superoxide production from isolated alveolar macrophages. The CS exposure elevated BALF total glutathione primarily at 15 wk. Overall, O(3) had little effect on endpoints that were significantly affected by CS exposure. We conclude that concurrent O(3) exposure has no effect on the induction of emphysema by CS in this animal model.
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PMID:Effects of concurrent ozone exposure on the pathogenesis of cigarette smoke-induced emphysema in B6C3F1 mice. 1245 86

A two-hour-old female infant presented with respiratory distress and short limbs. Neonatal radiographs showed micromelic dwarfism and generalised demineralisation, especially at the ribs, long bones of both forearms and both fibulae. The spine showed a flattened shape. All long bones showed metaphyseal irregularities and flaring. Normal serum calcium and elevated serum phosphorus were found, while serum alkaline phosphatase was markedly reduced. A diagnosis of perinatal lethal hypophosphatasia was made. The aetiology, clinical manifestations, radiographical findings, laboratory assays, prenatal diagnosis and treatment of hypophosphatasia are discussed.
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PMID:Clinics in diagnostic imaging (112). Perinatal lethal hypophosphatasia (PLH). 1707 71

Hypophosphatasia is a rare inborn disease of metabolism. This paper reviewed its pathogenesis, forms, clinical manifestations, differential diagnosis,treatment and prognosis. Here a case of neonatal hypophosphatasia is reported. This baby was female (30 minutes old). Prenatal ultrasound showed disproportionate biparietal diameter and long bones of limbs in the baby. After birth, she presented with obvious craniomalacia, respiratory distress and cyanosis. Serum alkaline phosphatase level was significantly reduced. Both X-ray and autopsy showed extremely insufficient skeletal mineralization. Four days later she died of respiratory failure.
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PMID:[Neonatal hypophosphatasia]. 1855 53

The mode of cellular toxicity of aqueous extract of Fadogia agrestis stem in male rats was investigated. Rats were grouped into four: A, B, C and D where A (the control) received orally 1 mL of distilled water; B, C and D (test groups) received orally 18, 50 and 100 mg/kg body weight of the extract, respectively, for 28 days. Infrared spectroscopy indicated the presence of hydroxyl (OH) and primary amine (CONH). Clinical toxicity symptoms such as respiratory distress, epistasis, salivation, hypo- and hyperactivity were not observed at any period of the experiment. No mortality was also recorded. Extract administration significantly reduced (p < .05) the activities of alkaline phosphatase, lactate dehydrogenase and gamma glutamyl transferase in the liver and kidney with corresponding increases in the serum. Serum malondialdehyde also increased significantly in all the extract-treated groups. The liver and kidney body weight ratios of the extract-treated animals compared well (P > .05) with their controls throughout the experimental period. The extract did not cause any swelling, atrophy or hypertrophy of the organs. The other evidence in this study suggests disruption of the ordered lipid bilayer of the plasma membranes of the hepatocytes and nephrons. This might have resulted from peroxidation of the polyunsaturated fatty acids on the membranes of the hepatocytes and nephrons made possible by the functional groups or the product of metabolism of the extract. This may be responsible for the compromise of the integrity of the plasma membranes of the hepatocytes and nephrons.
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PMID:Mode of cellular toxicity of aqueous extract of Fadogia agrestis (Schweinf. Ex Hiern) stem in male rat liver and kidney. 1975 38


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