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)

A healthy twenty-month-old boy ingested a maximal dose of valproate from which about 750 mg/kg were absorbed. Cerebral coma, which lasted for twenty hrs, was followed by an undisturbed period of approximately sixteen hrs. Death from cardiorespiratory failure due to severe bronchopneumonia occurred 46.5 hrs after the ingestion of the drug. The serum valproic acid concentration reached a peak of 1061 micrograms/ml within three hours, and fifteen minutes before death it had fallen to 187 micrograms/ml. The half-life of 16.6 hrs was within the range usually found. Metabolic acidosis, hypernatraemia and hyperosmolarity could be corrected, unlike the hypocalcaemia, which developed later. Bilirubin, GOT, GPT, gamma-GT, alkaline phosphatase, blood glucose, diastase, urea, creatinine, haemoglobin as well as PT and PTT and the platelet count were all normal. Leucopenia with 1,600 per microliter developed only during the bronchopneumonial stage. The histo-pathological findings were acute hypoxic damage of the myocardium, kidneys and certain neurones of vulnerable areas of the brain (neuronal microvesiculation and tigrolysis) in addition to a severe cerebral oedema in the final stage. A morphological substrate of an acute valproate encephalopathy was not demonstrable. The liver showed no necrosis or cholostasis. The vertebral marrow was inconspicuous. All the results indicate that liver function was not impaired in spite of the initial maximal concentration of valproic acid. In all probability the patient might have survived the acute valproate intoxication had it not been for the bronchopneumonia.
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PMID:Acute valproate intoxication with fatal outcome in an infant. 393 45

The sodium excess (Naes) which represents the nonexchangeable sodium compartment of bone was calculated from the total body sodium and total body chlorine of 95 women with vertebral crush fracture syndrome. No evidence was found for a subpopulation with increased or decreased Naes or Naes:TBCa ratio (TBCa is total body calcium which reflects total skeletal mass). Correlations in the osteoporotic women were found between the Naes and serum alkaline phosphatase (r = 0.31), PTH (r = 0.53), urinary hydroxyproline excretion (r = 0.42) and serum 250H vitamin D (r = -0.32). These data suggest that the state of vitamin D nutrition as well as parathyroid hormone levels may influence the quantity of sodium in bone in osteoporotic women. It is of great interest that these relationships were not observed in two control populations consisting of elderly women and women who recently underwent spontaneous menopause.
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PMID:Sodium excess in postmenopausal osteoporosis. 641 12

Investigations in animals have shown that nicotinic acid, an intestinal cyclic-AMP inhibitor, partially corrects the metabolic changes associated with urinary diversion through intestinal segments. Blood and serum chemistry were studied in patients before and 3 to 5 months after undergoing urinary diversion through ileal segments, both with and without nicotinic acid treatment. It was found that diverted patients had metabolic acidosis, an increased anion gap and increased levels of serum alkaline phosphatase; there were no significant changes in serum PTH and vitamin D levels, calcaemia and phosphoraemia. There was a tendency towards dehydration, hypernatraemia, hyperchloraemia and secondary hyperaldosteronism produced by ileal secretion of a hypotonic fluid. Nicotinic acid 3 g/day significantly reduced the chloraemia but did not correct the metabolic acidosis, although it reduced its severity, since blood pH decreased when treatment was suspended. Nicotinic acid cannot be recommended for routine use in the management of metabolic acidosis after urinary diversion, and patients with a marginal renal reserve should not be considered for trans-intestinal urinary diversion.
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PMID:Changes in acid-base balance and calcium metabolism after urinary diversion through ileal segments. II. Treatment with nicotinic acid. 830 47

It is recognized that biocomputing can provide intelligent solutions to complex biosensing projects. However, it remains challenging to transform biomolecular logic gates into convenient, portable, resettable and quantitative sensing systems for point-of-care (POC) diagnostics in a low-resource setting. To overcome these limitations, the first design of biocomputing on personal glucose meters (PGMs) is reported, which utilizes glucose and the reduced form of nicotinamide adenine dinucleotide as signal outputs, DNAzymes and protein enzymes as building blocks, and demonstrates a general platform for installing logic-gate responses (YES, NOT, INHIBIT, NOR, NAND, and OR) to a variety of biological species, such as cations (Na+ ), anions (citrate), organic metabolites (adenosine diphosphate and adenosine triphosphate) and enzymes (pyruvate kinase, alkaline phosphatase, and alcohol dehydrogenases). A concatenated logical gate platform that is resettable is also demonstrated. The system is highly modular and can be generally applied to POC diagnostics of many diseases, such as hyponatremia, hypernatremia, and hemolytic anemia. In addition to broadening the clinical applications of the PGM, the method reported opens a new avenue in biomolecular logic gates for the development of intelligent POC devices for on-site applications.
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PMID:Biocomputing for Portable, Resettable, and Quantitative Point-of-Care Diagnostics: Making the Glucose Meter a Logic-Gate Responsive Device for Measuring Many Clinically Relevant Targets. 2989 2