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)

Developmental profiles describing the expression of lactase, alpha-glucosidase, and alkaline phosphatase activities have been determined quantitatively in mouse jejunal enterocytes during migration over villi and Peyer's patch lymphoid tissue. The predicted maximal lactase and alpha-glucosidase activities expressed by enterocytes migrating over Peyer's patch follicles were about one-quarter and one-half of values found in control villi. Alkaline phosphatase activity was, on the other hand, one third greater in Peyer's patch compared with villus enterocytes. Expression of lactase and alpha-glucosidase activities was initially less in enterocytes migrating along interfollicular compared with control villi. Subsequent increase in hydrolase activities occurred during the later stages of enterocyte migration over interfollicular villi. Lactase activity in athymic mice Peyer's patch enterocytes was identical to that recorded for control mice. The corresponding value for villus lactase was, however, only half that found in control tissue. Factors produced locally in lymphoid follicles are probably responsible for selective effects on enterocyte differentiation.
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PMID:Selective expression of brush border hydrolases by mouse Peyer's patch and jejunal villus enterocytes. 393 May 23

In vitro studies of certain lymphoid tumor cells show potentiation of 1-beta-D-arabinofuranosylcytosine (ara-C) effects by uridine because it elevates intracellular uridine triphosphate, resulting in increased ara-C triphosphate levels. Seven-day continuous i.v. infusions of uridine at 123 mg/kg/h (2.5 g/sq m/h) were studied in 5 male beagles. Steady state levels of uridine were reached within 4 to 6 h and ranged from 2 to 5 X 10(-4) M over the course of the infusion. Steady state uracil levels ranged from 4 to 10 X 10(-4) M. After the end of infusion, uridine and uracil levels fell with a half-life of approximately 15 and 18 min, respectively. Toxicity in 2 dogs treated at this dose was limited to minimal diarrhea and a transient rise of alkaline phosphatase to 2 to 3 times normal. No drug toxicity was evident at sacrifice on Days 7 or 72. Three dogs received a 7-day infusion of ara-C plus uridine followed approximately 4 weeks later by an infusion of ara-C alone (or the same drugs in the reverse sequence). Coinfusion of 2.5 or 5.0 mg/kg/day (50 or 100 mg/sq m/day) of ara-C had no significant effects on uridine plasma levels or postinfusion half-lives. Similarly, no consistent effect was seen of uridine on ara-C plasma levels. Uridine coinfusion with ara-C resulted in a definite potentiation of myelosuppression; at 5.0 mg/kg/day X 7 of ara-C white blood cell and platelet nadirs (X 10(3)/microliters) were 0.8 and 15 as compared to 3.6 and 66, respectively, with ara-C alone. One-third of the dogs developed reversibly elevated transaminases with the combination treatment. The results show that a minimally toxic dose of uridine enhances bone marrow and probably hepatic toxicity of coadministered ara-C.
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PMID:Pharmacology and toxicology of a seven-day infusion of 1-beta-D-arabinofuranosylcytosine plus uridine in dogs. 398 95

Histochemical investigations were carried out to demonstrate the activity of succinic dehydrogenase, diphosphopyridine-nucleotid-diaphorase, alkaline phosphatase, and acid phosphatase in the liver, kidneys, lymph nodes, and heart muscle of a total of 20 cows with positive serologic response for leukosis as well as in organs of 2 normal controls. It was found that the lymphoid cells of the leukotic proliferations and the activated endothelial and adventitial cells of the blood vessels had high alkaline phosphatase activity and negligibly expressed acid phosphatase activity. Dehydrogenase activity was low in the lymphoid-cell proliferations and in the activated cell of the vessels. The cell metabolism of the leukotic proliferations was like-wise disturbed. Histochemical methods of investigations could be used test-like in the diagnosis of bovine leukosis.
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PMID:[Histochemical changes in leukemia in cattle]. 399 26

The lungs of mice having survived three inoculations with influenza virus A/PR8/34 (H1N1) repeated at 7-day intervals (an experimentally induced "chronic" influenza infection) were subjected to histological, electron optic, histochemical and histoenzymatic investigations. Hyperemia, edema and infiltration of the alveolar walls with lymphoid and monocytic elements could be observed. Electron microscopy revealed changes at the level of different ultrastructures of both lung and infiltration cells. A decrease in the levels of alkaline phosphatase, lactate, malate, succinate dehydrogenases and monoaminoxidase, an elevated amount of lipids and of mucopolysaccharides were made evident in the lung cells of mice chronically infected with influenza virus type A.
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PMID:Morphological, histochemical and histoenzymatic investigations on the lungs of mice chronically infected with influenza virus type A. 400 17

In this study, Sprague-Dawley rats were exposed in a TEM chamber to 20-MHz (HF-band) continuous-wave radiofrequency radiation (RFR) for 6 hr/day, 5 days/week up to 6 weeks. The average E-field intensity was 2686 +/- 164 V/m (mean +/- SD) and the calculated specific absorption rate was 0.3 W/kg. Randomly sampled rats killed on Days 8, 22, 39, and 42 after initiation of exposure showed no statistically significant differences from controls for body mass, spleen cell density, erythrocyte and leukocyte counts, hematocrit, hemoglobin, methemoglobin, erythrocyte fragility, bilirubin, creatinine, SGPT, alkaline phosphatase, calcium, sodium, potassium, and spleen cell chemiluminescence. Splenic mass differences were statistically significant (p less than 0.05) only on Day 22. Spleen to body mass ratios differed significantly between exposed and control groups on Days 22 and 39 (P less than 0.05 and P less than 0.025, respectively). Histologic examination of the rats revealed the successive accumulation of phagocytic cells, lymphoid proliferation, development of lesions, and tissue necrosis characteristic of respiratory mycoplasmosis. In a followup experiment, a separate set of rats was exposed for 6 weeks to identical levels of RFR. No significant differences were found in splenic parameters and spleen cell peroxidative activity. Histologic examination of these animals revealed no evidence of mycoplasma infection. The observed differences between exposed and control animals of the first experiment appear to have resulted from subclinical respiratory mycoplasmosis rather than exposure to RFR.
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PMID:Effects of 20-MHz radiofrequency radiation on rat hematology, splenic function, and serum chemistry. 402 74

Normal and malignant lymphocytes can migrate from the bloodstream into lymph nodes and Peyer's patches. This process helps distribute normal lymphocytes throughout the lymphoid system and may provide a portal of entry for circulating malignant cells. An adhesive interaction between lymphocytes and the endothelium of postcapillary venules is the first step in the migratory process. We have recently shown that the simple sugars L-fucose and D-mannose, and an L-fucose-rich polysaccharide (fucoidin), can inhibit this adhesive interaction in vitro. We now report that mannose-6-phosphate, the structurally related sugar fructose-1-phosphate, and a phosphomannan, core polysaccharide from the yeast Hansenula holstii (PPME) are also potent inhibitors. Inhibitory activity was assessed by incubating freshly prepared suspensions of lymphocytes, containing the various additives, over air-dried, frozen sections of syngeneic lymph nodes at 7-10 degrees C. Sections were then evaluated in the light microscope for the binding of lymphocytes to postcapillary venules. Mannose-6-phosphate and fructose-1-phosphate were potent inhibitors of lymphocyte attachment (one-half maximal inhibition at 2-3 mM). Mannose-1-phosphate and fructose-6-phosphate had slight inhibitory activity, while glucose-1-phosphate, glucose-6-phosphate, galactose-1-phosphate, and galactose-6-phosphate had no significant activity (at 10 mM). In addition, the phosphomannan core polysaccharide was a potent inhibitor (one-half maximal inhibition at 10-20 micrograms/ml); dephosphorylation with alkaline phosphatase resulted in loss of its inhibitory activity. Preincubation of the lymphocytes, but not the lymph node frozen sections, with PPME resulted in persistent inhibition of binding. Neither the monosaccharides nor the polysaccharide suppressed protein synthesis nor decreased the viability of the lymphocytes. Furthermore, inhibitory activity did not correlate with an increase in negative charge on the lymphocyte surface (as measured by cellular electrophoresis). These data suggest that a carbohydrate-binding molecule on the lymphocyte surface, with specificity for mannose-phosphates and structurally related carbohydrates, may be involved in the adhesive interaction mediating lymphocyte recirculation.
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PMID:Phosphomannosyl receptors may participate in the adhesive interaction between lymphocytes and high endothelial venules. 609 Apr 73

Alkaline phosphatase (EC 3.1.3.1) was assayed in a large number of cultured mouse tumor cell line using p-nitrophenylphosphate as the substrate. Of 19 lines of the B lymphoid lineage, including Abelson pre-B, B lymphoma, and plasma cell tumor lines, all but 1 had substantial activity averaging 407 nmol/min/mg protein (with a range from 5 to 900). Nine T lymphoid and 9 nonlymphoid hematopoietic lines examined had low activity of 0.7 to 4.2 nmol/min/mg protein. The enzyme was markedly enriched in plasma membrane preparations from the B lymphoid cells, but not in those from most T lymphoma cells. The activity of another plasma-membrane-bound enzyme, gamma-glutamyl transferase, did not vary systematically with the type of cell line but was exceptionally high in 1 T lymphoma line. Investigation of pH dependence and susceptibility to inhibition by L-phenylalanine and L-homoarginine indicated similarity of the alkaline phosphatase from B cell lines to the enzyme recoverable from normal mouse kidney, placenta, bone marrow, and lymphoid organs. The enzyme seems to provide a useful marker for tumor lines of the B lymphoid lineage and for their plasma membranes.
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PMID:Alkaline phosphatase in hematopoietic tumor cell lines of the mouse: high activity in cells of the B lymphoid lineage. 616 25

In earlier experiments we had noted that transformed and leukemic leukocytes produced an RNA-rich angiogenic lymphokine. The formation of capillaries is a stepwise process in which reticulum cells first become detached and attracted to a site (mobilization and migration along a reticulin network). This is followed by local proliferation and finally by elongation and alignment against a basal membrane in tubular geometry. Coincidental with the last step is a biochemical and immunochemical differentiation of the endothelial cells manifested by the appearance of alkaline phosphatase, angiotensin-converting enzyme, factor VIII and the generation of receptors for thrombin as well as the capacities to produce prostacyclin and fibronectin on demand. It is postulated that there may be not one but several angiogenic lymphokines (angiokines) for each step of capillary development. Angiokine 1 (AK1) for the mobilization-chemotactic-migration, AK2 for the local proliferative, and AK3 for differentiating-morphogenic events. The above postulate aids in the classification and understanding of a number of angiolymphoproliferative syndromes since these reflect different disorders of the stepwise vessel formation. The association and the simultaneous proliferation of vascular and lymphoid elements is a feature that a number of lymphoproliferative disorders, of otherwise differing nature, have in common. To this effect they have been grouped in this study as angiolymphoproliferative syndromes (ALPS). These are a group of prelymphomatous or prelymphomogenic clinicopathologic entities in which proliferation of a lymphoid element (cell) is coupled with the accelerated development of blood capillaries and postcapillary venules.
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PMID:Angiokines, angiogenesis and angiolymphoproliferative syndromes (ALPS). 618 89

Human placental cell suspensions prepared by trypsin digestion were analyzed with several monoclonal antibodies on a multiparameter fluorescence-activated cell sorter (FACS). Five distinct cell populations were isolated on the basis of size and quantitative differences in the coordinate expression of cell surface antigens detected by monoclonal antibodies against an HLA-A,B,C monomorphic determinant (MB40.5) and against human trophoblasts (anti-Trop-2). By FACS analysis and after sorting we clearly identified the major cell population as cytotrophoblasts based on several independent criteria, including presence of trophoblast-specific surface antigens, Trop-1, and Trop-2; absence of all HLA class I, class II, and beta 2-microglobulin (beta 2m) antigens; absence of the pan-leucocyte and monocyte antigens, HLe1 and LeuM1, respectively; presence of Y-chromatin in a male placenta; presence of placental and not liver alkaline phosphatase; and a large, mononuclear morphology. These procedures provide a reproducible method for obtaining highly purified human cytotrophoblast populations for further studies. We measured by molecular hybridization (RNA or Northern blots) the HLA-A,B,C and beta 2m mRNA in total RNA extracted from sorted cytotrophoblasts. We find that normal human cytotrophoblasts have extremely small amounts of HLA-A,B,C mRNA: approximately 300 times less than that in the lymphoid cell line LCL-721 or normal lymphocytes. In contrast, they have approximately 11% the level of beta 2m mRNA present in LCL-721 cells. Thus, HLA-A,B,C antigen expression on human cytotrophoblasts is limited by the level of HLA heavy chain mRNA.
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PMID:Transcriptional control of HLA-A,B,C antigen in human placental cytotrophoblast isolated using trophoblast- and HLA-specific monoclonal antibodies and the fluorescence-activated cell sorter. 620 84

Cytochemical methods at the light and electron microscopic level were used to define the pattern of alkaline phosphatase (APase) activity in normal thymus and to study its modifications after inoculation with the thymotropic leukemogenic radiation leukemia virus in correlation with the emergence of preleukemic cells and their thymus dependency. APase was found in numerous lymphoblasts of the fetal thymus. The enzyme was also detected in a few lymphoid blast cells of the normal young adult thymus, which were closely associated with thymic nurse cells. The observed distribution of APase in normal thymus suggests that its expression could be limited to an early stage of the T-cell differentiation pathway. After inoculation with radiation leukemia virus, APase activity remained normal for almost the entire latency period, during which virus replication spread to the cortex and thymus-dependent preleukemic cells appeared. An important increase in the number of APase-positive cells occurred later, i.e., at the end of the latency period, in nontumoral thymus, which displayed lymphocytic depletion and contained autonomous thymus-independent preleukemic cells. These latter features obviously reflected the malignant transformation of thymus lymphoblasts, which eventually led to the development of the thymic lymphomas. The results raise the question of the possible filiation between the thymic nurse cell-associated APase-positive lymphoid cells of the normal thymus and the target cells susceptible to productive infection and to neoplastic transformation after radiation leukemia virus infection.
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PMID:Correlation of alkaline phosphatase activity to normal T-cell differentiation and to radiation leukemia virus-induced preleukemic cells in the C57BL mouse thymus. 631 7


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