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)

Thirty patients of both sexes (15 males and 15 females) with chronic renal failure who had under gone hemodialysis for 2-184 months (mean 45.1 months) were examined with conventional radiographs of the cervical spine and thin-layer CT of C4-C5-C6 to evaluate the radiographic patterns of destructive spondyloarthropathy. The radiographic patterns obtained with conventional and CT exams were compared with one another and with clinical (carpal tunnel syndrome) and biochemical data (alkaline phosphatase, parathormon, Ca, P, Ca/P, Al, beta 2-microglobulin). DSA (erosion and narrowing of the intervertebral space, collapse of the vertebral body and erosion of the vertebral plates) was recognized in 7 patients with conventional radiographs and in 11 patients with CT thanks to greater CT capabilities to recognize minimal osteolytic lesions of the vertebral body. All the patients with destructive spondyloarthropathy had personal and hemodialysis age higher than those without destructive spondyloarthropathy: 59.3 vs 57.7 years; 49 vs 39 months. Parathormon and alkaline phosphatase were increased while beta 2-microglobulin was normal. Only 2 patients with DSA had carpal tunnel syndrome. In conclusion, CT is a valuable technique for the diagnosis of destructive spondyloarthropathy but it must be performed only after conventional radiographs of the cervical spine or in the presence of clinical signs of destructive spondyloarthropathy (parathormon and beta 2-microglobulin increased, long-term hemodialysis).
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PMID:[Computerized tomography and conventional radiography in the diagnosis of destructive spondyloarthropathy. Our experience with 30 patients undergoing periodic hemodialysis]. 149 70

In order to identify sensitive and specific biochemical indicators of pulmonary damages caused by industrial contaminants, male Long-Evans rats were exposed to a cadmium chloride (CdCl2) aerosol (5 mg Cd/m3; MMAD = 1.4 microns; SDg = 1.8) for 1 hr. The rats were sacrificed at 1, 4, 8, and 16 days after treatment. The response of the pulmonary surfactant (SF) system, which prevents alveolar collapse during expiration by lowering the surface tension at the air-liquid interface, was of particular interest. The effect of CdCl2 inhalation on the SF system was monitored by assaying the alkaline phosphatase (AKP) activity and phospholipid (PL) content in an enriched surface active SF fraction purified from bronchoalveolar lavages. The AKP activity of the SF fraction was markedly decreased (99%) on Day 1, indicating an inhibition of AKP by Cd. The PL content remained at control level while the total protein content was significantly increased (199%). On day 4, the high recovery of PL (207%) and AKP activities (639%) may reflect an increased secretion caused by Type II cell hyperplasia. By Day 8 these parameters returned to baseline levels. On Day 16 both the AKP activity and the PL content of the SF fraction were decreased significantly. Concurrently, the activities of the acid phosphatase and the B-N-acetylglucosaminidase followed, but to a lesser extent, the response of the AKP activity on Days 1 and 4. They differed from AKP, however, in that their activities remained significantly elevated on Day 8 and in that they returned to baseline levels on Day 16.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The response of the pulmonary surfactant-associated alkaline phosphatase following acute cadmium chloride inhalation. 275 63

The cytochemical localization of enzymatic activity by means of backscattered electron imaging (BEI) is reviewed and the application of BEI to changes in acid phosphatase and ATPase distribution during physiological (programmed) cell death in Heliothis midgut is explored. Programmed cell death entails the release of nascent free acid phosphatase as extracisternal hydrolase. This shift can readily be detected by means of the atomic number contrast imparted by BEI of the lead phosphatase reaction product, thus enabling the distribution of dying cells to be mapped. BEI is particularly useful in this context as it allows the examination of bulk specimens at low magnification. Death of cells is also accompanied by a collapse in ATPase activity which shows up as cytochemically negative areas in the X-ray microscope and by means of BEI. Acid phosphatase in normal cells is localized in the apical microvilli and lysosomes. Senescent or dying cells, however, clearly show a basally situated free hydrolase which migrates throughout the cell. Parallel TEM results confirm that this enzyme is ribosomal and extracisternal rather than lysosomal in origin. ATPase activity is largely limited to the apical microvilli, although there is some activity associated with the basal plasma membranes. The apical ATPase, however is partially resistant to ouabain. Young and mature cells are positive although in the latter case some microvilli may be lost as the cells acquire a negative cap or dome. Inhibition by bromotetramizole indicates that apical activity is not to any significant extent contributed to by alkaline phosphatase. Degenerate or dead cells are negative and can be seen as a mozaic of "black patches" among normal cells when imaged by means of BEI or X-ray microscopy.
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PMID:The use of backscattered electron imaging, X-ray microanalysis and X-ray microscopy in demonstrating physiological cell death. 297 76

The pathophysiology, clinical presentation, prevention, and treatment of aluminum-related osteomalacia in renal-failure patients are reviewed. Aluminum-related osteomalacia can develop in patients exposed to high concentrations of aluminum either in dialysis solutions or through gastrointestinal aluminum absorption from aluminum-containing antacids used to treat hyperphosphatemia. Although the exact etiology of aluminum-related osteomalacia is unknown, aluminum is believed to inhibit bone mineralization by forming an inhibitory complex with citric acid at physiologic concentrations. The complex is deposited along bone mineralization fronts and in bone marrow. The major symptoms of aluminum-related osteomalacia include skeletal pain, fractures, and vertebral collapse. The disease is difficult to diagnose because patients may have normal or slightly elevated serum concentrations of calcium, phosphate, alkaline phosphatase, and parathyroid hormone. Direct measurement of bone aluminum content (using biopsy) is often needed to confirm diagnosis. The aluminum-chelating agent deferoxamine mesylate can be used to measure bone aluminum content indirectly. Aluminum intoxication can be managed either by preventing exposure to aluminum or by removing deposited aluminum from bone. New standards restrict aluminum content in dialysis solutions, and prevention now focuses on the use of aluminum-free phosphate binders for treatment of hyperphosphatemia. Calcium carbonate may be as effective as aluminum-containing antacids in controlling serum phosphate concentrations, but it should be used cautiously in patients who are hypercalcemic or at risk of developing metastatic calcification. Chelation therapy with deferoxamine has improved the symptoms and bone histology in a small number of patients. Clinical improvements have been seen in patients receiving intravenous deferoxamine 2-6 g per week for 20 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aluminum-related osteomalacia in renal-failure patients. 389 71

Juvenile osteoporosis is a disease of childhood and adolescence exhibiting marked clinical variability in bone change. The disease usually begins in the prepubertal period or even younger. A case of a Chinese boy suffering from back pain and generalized osteoporosis since 9 yr of age who spontaneously recovered at 14 yr of age when entering puberty is reported. The affected patient was clinically normal (as shown by X rays), until he fractured his left humerus. Metabolic studies indicated a negative calcium balance, but serum calcium, phosphorus, alkaline phosphatase, parathyroid hormone, calcifediol, calcitriol, cortisol and sex hormones were normal. X ray showed typical generalized osteoporosis with vertebral collapse. The disease markedly improved within 5 yr. No family history of inherited skeletal disorders or presenile osteoporosis was noted. The diagnosis of idiopathic juvenile osteoporosis was made.
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PMID:Idiopathic juvenile osteoporosis: five-year case follow-up. 761 64

A crude, whole-body extract of female or male heartworms was injected IV into 28 dogs with and 22 dogs without heartworm (HW) infection. The female HW extract caused shock in 22 of 24 dogs with and 12 of 20 dogs without HW infection. The male HW extract induced shock in 4 of 4 dogs with and 1 of 2 dogs without HW infection. Prevalence of shock caused by female HW extract was significantly (P < 0.05) higher in dogs with than without HW infection; shock developed 5 to 30 minutes after HW injection. These signs were observed: marked decrease in blood pressure; collapse (initial collapse); paleness of mucous membranes; weak heart sounds; dyspnea; skin coldness; intestinal hyperperistalsis, and defecation; increases in RBC count, serum total protein concentration, serum osmolality, serum Na and blood glucose concentrations; and decreases in neutrophil, eosinophil, and platelet counts. Alanine transaminase, alkaline phosphatase, and lactate dehydrogenase activities increased substantially from the time of initial collapse to 24 hours after HW injection. Of 39 dogs with shock, 29 recovered from initial collapse, but 5 of the 29 subsequently collapsed again (secondary collapse), with bloody diarrhea followed by death. Of these 39 dogs, 6 died during initial collapse without bloody diarrhea, and 4 were euthanatized during initial collapse. It was confirmed that HW extract had, in fact, induced shock. These clinical, hematologic, and biochemical findings were fundamentally similar to those associated with shock resulting from administration of drugs, such as diethylcarbamazine and milbemycin D, in microfilaremic dogs with HW infection.
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PMID:Clinical, hematologic, and biochemical findings in dogs after induction of shock by injection of heartworm extract. 787 76

Twenty-two dogs with superficial necrolytic dermatitis were evaluated prospectively, twenty-one of which had characteristic crusting lesions of the paw pads. Histologically, epidermal lesions included parakeratosis and laminar intracellular edema. The plasma amino acid concentrations of eight dogs were markedly depressed. Nine dogs had terminal diabetes mellitus. These clinical and morphologic findings were strikingly similar to those of necrolytic migratory erythema in human beings, the most common cause of which is hyperglucagonemia due to islet cell tumor of the pancreas. No pancreatic tumors were found in these dogs; plasma glucagon concentrations in the five dogs tested were normal. The serum alkaline phosphatase concentrations were elevated in all dogs. Severe vacuolar hepatopathy, suggesting metabolically or hormonally induced hepatic dysfunction, was found in 21 dogs at necropsy or by biopsy; one dog had ultrasonographic abnormalities of the liver. Histopathologically, severe vacuolar alteration resulted in parenchymal collapse and nodular regeneration, which grossly mimicked cirrhosis. Although the definitive metabolic stimulus was not discovered for the cutaneous and hepatic lesions, the similarity of the cutaneous and biochemical features of canine superficial necrolytic dermatitis to human necrolytic migratory erythema warrants further investigation into possible underlying pancreatic hormonal dysfunction.
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PMID:Superficial necrolytic dermatitis (necrolytic migratory erythema) in dogs. 844 31

Collapsin-1 is a member of the semaphorin family of signaling molecules that acts as a repellent for growing spinal sensory axons. We have constructed a chimeric collapsin-1/alkaline phosphatase probe to visualize putative collapsin-1 receptors in vitro and in situ. As predicted by the activity profile of collapsin-1, the probe binds spinal sensory tracts, ventral spinal roots, and the sympathetic chain but does not bind retinal axons. In addition, we find that the probe binds sensory axons arising from the olfactory epithelium and some, but not all, cranial sensory nerves. As predicted by these binding studies, in vitro assays demonstrate that primary olfactory sensory, trigeminal, and jugular ganglion growth cones collapse in the presence of soluble collapsin-1. Comparing the expression pattern of collapsin-1 with the trajectories of collapsin-1 responsive axons suggests that in both the spinal cord and the olfactory bulb, collapsin-1 prevents premature entry of sensory axons into their target and helps determine the final location of sensory terminations.
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PMID:A role for collapsin-1 in olfactory and cranial sensory axon guidance. 933 8

This pilot study sought associations between liver function tests (LFTs) and membership in homogeneous exposure groups (HEGs) at a target plant as pre-clinical indications of possible future occupational health problems. A large company database yielded linear models for each of six LFTs (total bilirubin, alkaline phosphatase, gammaglutamyl transferase, lactate dehydrogenase, aspartate transaminase, and alanine transaminase) in terms of sex, body mass index, age, race (white/non-white), alcohol and cigarette consumption, and production/non-production (P/NP) job, permitting control for these in analyses of LFTs vs HEGs at the plant. These analyses, with HEG substituted for P/NP in the large group model, resulted in loosely "suspect" associations significant at P < 0.10. Collapsed HEG variable (containing "suspects" separately and all other non-significant HEG levels pooled) yielded "confirmed suspects" at P < 0.05 in the analysis of an independent LFT set taken at the plant approximately one year later.
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PMID:Health surveillance using an occupational medical database. 972 51

Collapsin-1/Sema III, a member of the semaphorin family, has been implicated in axonal pathfinding as a repulsive guidance cue. Cellular and molecular mechanisms by which collapsin-1 exerts its action are not fully understood. Collapsin-1 induces growth cone collapse via a pathway which may include neuropilin-1, a cellsurface collapsin-1 binding protein, as well as intracellular CRMP-62 and heterotrimeric G proteins. We previously identified a second action of collapsin-1, the facilitation of antero- and retrograde axoplasmic transport. This response occurs via a mechanism distinct from that causing growth cone collapse. To investigate the possible involvement of neuropilin-1 in the action of collapsin-1 on axoplasmic transport, we produced a soluble neuropilin-1 (sNP-1) lacking the transmembrane and intracellular region. sNP-1 progressively displaced the dose-response curve for collapsin-1 to induce growth cone collapse to higher concentrations. sNP-1 also inhibited collapsin-1-induced augmentation of both antero- and retrograde axoplasmic transport. Furthermore, an anti-neuropilin-1 antibody blocked the collapsin-induced axoplasmic transport. These results together indicate that neuropilin-1 mediates collapsin-1 action on axoplasmic transport. To visualize collapsin-1 binding to endogenous neuropilin-1, we used a truncated collapsin-1-alkaline phosphatase fusion protein (CAP-4). CAP-4 stains the growth cone, neurite, and cell body. However, local application of collapsin-1 to growth cone but to neither neurite nor cell body promotes axoplasmic transport. Thus, growth cone NP-1 mediates the facilitatory action of collapsin-1 on antero- and retrograde axoplasmic transport.
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PMID:Growth cone neuropilin-1 mediates collapsin-1/Sema III facilitation of antero- and retrograde axoplasmic transport. 1038 79


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