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)

In basal conditions, NB4 and HL-60, two acute promyelocytic leukemia cell lines, express high levels of tumor necrosis factor (TNF-alpha) mRNA, whereas they do not synthesize appreciable amounts of the transcripts coding for interleukin-1 beta (IL-1 beta) or interleukin-8 (IL-8). Upon granulocytic differentiation with all-trans retinoic acid (ATRA) or the combination of ATRA and granulocyte-colony-stimulating factor (G-CSF), significant amounts of IL-1 beta and IL-8 mRNAs accumulated in both cell types. These changes in mRNA levels were parallelled by the increased secretion of the two cytokines. Dexamethasone (DEX) had no effect on the induction of IL-1 beta mRNA, while it enhanced the G-CSF-, ATRA- and (ATRA+G-CSF) dependent secretion of the cytokine. In combination with ATRA and G-CSF, the corticosteroid increased the expression of leukocyte alkaline phosphatase, a late marker of granulocytic differentiation.
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PMID:Effects of dexamethasone on pro-inflammatory cytokine expression, cell growth and maturation during granulocytic differentiation of acute promyelocytic leukemia cells. 858 72

Locally produced pro-inflammatory cytokines are considered to play an important role in the initiation and/or maintenance of inflammatory diseases. In cholesteatomatous lesions there are increased levels of some cytokines and inflammatory mediators like interleukin 1, tumor necrosis factor and colony-stimulating factor, etc. Interleukin 6 (IL-6) can be produced by different cells present in cholesteatoma (e.g. keratinocytes, lymphocytes, fibroblasts and macrophages). Until now, no data have been available on the role of IL-6 in cholesteatoma. In this study we used immunohistochemistry to investigate the presence and distribution of IL-6 in tissue samples from cholesteatoma patients. Levels of the cytokine were quantified in tissue extracts using an enzyme-linked immunosorbent assay. Finally, the presence of biologically active IL-6 was analyzed in the murine cell line 7TD1. Human skin samples obtained from the external ear canal were used as controls. Using the anti-IL-6 antibody in an alkaline phosphatase anti alkaline phosphatase technique, a moderate diffuse staining of the whole epidermis was observed in sections of normal skin. In cryostat sections of cholesteatoma samples, a stronger staining of the whole epithelium was observed. Many of the cells infiltrating the cholesteatoma stroma also showed positive immunostainings. The concentration of IL-6 in relation to the total protein concentration in cholesteatoma (119.33 +/- 30) were higher than in human skin (9.16 +/- 13). While IL-6 activity was not detected in skin samples, two of the ten cholesteatoma samples studied showed a stimulatory effect when incubated with the cell line 7TD1. The overexpression of IL-6 in middle ear cholesteatoma suggests a participation of this cytokine in some of the clinical features seen: epithelial hyperproliferation and bone resorption. The absence of biological activity in the majority of the cholesteatoma samples points to the presence of natural inhibitors for IL-6.
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PMID:Role of interleukin 6 in epithelial hyperproliferation and bone resorption in middle ear cholesteatomas. 865 57

Tissue injury is a common occurrence in multiple organ failure, a possible clinical complication of Gram-negative bacterial sepsis. Gram-negative bacteria, in part through lipopolysaccharide (LPS), tumor necrosis factor, and other cytokines, activate neutrophils to increase oxygen consumption and produce reactive oxygen species (ROS). ROS have been suggested to play a critical role in the pathogenesis of multiple organ failure. Accordingly, we hypothesized that the susceptibility of tissues to ROS can be reduced by augmenting the antioxidant status of the affected tissues. Rats were challenged intravenously with LPS (Escherichia coli: 0111:B4) at a dose of 1 mg/kg body weight, and 0, 2, 4, or 6 h later were treated intravenously with plain liposomes or alpha-tocopherol liposomes (20 mg alpha-tocopherol/kg body weight); treated rats were then killed 24 h after LPS challenge. Animals challenged with LPS were extensively damaged in the liver, as evidenced by an increase in plasma alanine aminotransferase and aspartate aminotransferase activities, and also in the lung, as indicated by a decrease in pulmonary angiotensin-converting enzyme and alkaline phosphatase activities. The injection of LPS also resulted in increased myeloperoxidase activities in the two organs, suggestive of activation of the inflammatory response. Within the pulmonary and hepatic organs of LPS-challenged animals, the involvement of oxidative stress mechanisms was evident, because a significant decrease in reduced glutathione and an increase in lipid peroxidation were observed. In contrast, the administration of alpha-tocopherol liposomes in the post-LPS-challenge period resulted in a significant alleviation of both lung and liver injuries, evidenced by a general reversal of the altered biochemical indices toward normal among treated animals. The therapeutic effect was found to be greater when liposomal alpha-tocopherol treatment was given earlier during the development of injury. Plain liposomes administered immediately after LPS injection also protected hepatic and pulmonary tissues from injuries. However, unlike alpha-tocopherol liposomes, plain liposomes did not confer any beneficial effect when administered at later timepoints post-LPS injection. These data suggest that alpha-tocopherol, administered in a liposomal form, may serve as a potentially effective pharmacological agent in the treatment of LPS-induced tissue injuries.
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PMID:Treatment of LPS-induced tissue injury: role of liposomal antioxidants. 882 99

Responses to i.v. injected E. coli endotoxin (E), followed by saline infusion, as compared with saline infusion alone, were studied for 24 h in 1-week-old calves. After administration of E, respiratory rate (RR), heart rate (HR), rectal temperature (RT), serum iron, insulin, (I), cortisol and tumor necrosis factor-alpha, transiently, and urea, continuously, increased. Isoleucine and leucine became elevated at 24 h, whereas white-blood-cell number, free fatty acids (FFA) and triglycerides (TG) increased after an initial fall. After administration of E, packed-cell volume, erythrocyte number, haemoglobin, glucose (G), cholesterol, phospholipids (PL), lysine, arginine, proline, citrulline, calcium (Ca), inorganic phosphorus, insulin-like growth factor I (IGF-I) and 3,5,3'-triiodothyronine (T3) concentrations and alkaline phosphatase (AP) and gamma-glutamyl transferase (gamma GT) activities increased significantly while growth hormone decreased non-significantly. When saline was infused alone, G, TG, PL, Ca, AP, gamma GT, I, IGF-I and T3 decreased, while FFA, urea and sodium increased, but, changes of G, urea, AP, IGF-I and T3 were less marked than after injection of E. Potassium, total protein and albumin concentrations, and glutamyl dehydrogenase and glutamate oxalacetate transaminase activities were not significantly affected by either treatment. In conclusion, metabolic and endocrine changes during saline infusion alone were typical for food withdrawal. Changes of variables after administration of E were transient, biphasic or sustained, thus expressing complex interactions between metabolic parameters, endocrine factors and cytokines.
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PMID:Metabolic, endocrine and haematological responses to intravenous E. coli endotoxin administration in 1-week-old calves. 883 Dec 69

The synthetic polynucleotide polyadenylic-polyuridylic acid (polyA:polyU) has shown antitumor activity in murine studies and human breast cancer. PolyA:polyU was evaluated in 25 cancer patients receiving weekly intravenous doses between 3 and 600 mg/m2. PolyA:polyU was well tolerated up to 600 mg/m2, with no doselimiting toxicity (all < grade 3). Side effects included mild elevation in temperature, fatigue, and mild hyperglycemia. No changes outside of the normal range in hematocrit, WBC count, platelet count, total bilirubin, or alkaline phosphatase were observed. Of 25 patients, 18 completed at least one cycle of 6 weeks, and 5 completed two cycles (median 6 weeks). Four patients had stable disease over 11-13 weeks of treatment, and no clinical responses were observed. At 24 h after the first treatment, there were no significant increases in biologic response (beta 2-microglobulin and neopterin in serum, or 2',5'-oligoadenylate synthetase in peripheral blood mononuclear cells). A small increase in beta 2-microglobulin was observed 24 h after the week 3 treatment (1.1-fold, p < 0.01). By the third week of treatment, 2-5A synthetase levels decreased slightly (to 80% of baseline, p < 0.01). No changes in cytokines IL-6, IL-12, tumor necrosis factor (TNF), or IL-2 receptor in serum were detected after 24 h of treatment. Thus, at these doses, polyA:polyU had no marked modulation on biologic responses in vivo, although this preparation significantly induced 2-5A synthetase in peripheral blood mononuclear cells in vitro. PolyA:polyU was well tolerated. An MTD was not reached but was greater than 600 mg/m2 on this weekly schedule.
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PMID:Phase I/IB study of polyadenylic-polyuridylic acid in patients with advanced malignancies: clinical and biologic effects. 887 34

Osteocytes are differentiated forms of osteoblasts that arise upon entrapment within the bone matrix. In this report, we describe the establishment and hormonal regulation of the first conditionally transformed human preosteocytic cell line. Primary adult bone cells were obtained from protease cell line. Primary adult bone cells were obtained from protease digestion of cancellous chips. The cells were infected with adenovirus-ori- SV40 tsA 209, which encodes for a temperature-sensitive large T-antigen. After immortalization, we isolated a clone designated HOB-01-C1. This cell line expressed the mutant T-antigen and proliferated at the permissive temperature (34 C) but stopped dividing at the nonpermissive temperature (39-40 C). Electron microscopy of cells incubated at 39 C demonstrated the presence of preosteocytic cellular processes, some of which appeared to form gap junctions or were rich in microfilaments. The clone expressed alpha 1 type (I) procollagen messenger RNA (mRNA) and secreted type I procollagen C peptide at both temperatures, and this expression was elevated 1.6-fold to 1.8-fold at 40 degrees C. The cells expressed very low basal levels of alkaline phosphatase activity (approximately 0.02 nmol/min.mg), which was increased 2- to 5-fold in a dose-dependent manner by 0.1-100 nM 1 alpha,25-dihydroxyvitamin D3 (vitamin D3) at both temperatures. Vitamin D3 also increased osteocalcin secretion in a dose-dependent manner when the clone was maintained at 34 C (approximately 6-fold), and this stimulation was enhanced > 5 fold at 40 C. In contrast to the low expression of alkaline phosphatase, the cells secreted high amounts of osteocalcin in response to vitamin D3 (approximately 15 ng/mg cell protein); this biochemical profile also resembled that of preosteocytes. Alizarin red-S histochemical staining demonstrated that these cells rapidly produced mineralized nodules at both temperatures. PTH (10 and 100 nM) had no effect on the intracellular accumulation of cAMP at 34 C but stimulated a 14- to 18-fold increase in the production of this second messenger at 40 C. In contrast, 100 nM prostaglandin E2 and 1 microM forskolin stimulated cAMP synthesis better at 34 C. Western blot analysis indicated that the cells expressed CD44, a putative osteocytic marker, at both temperatures. Finally, interleukin-1 beta and tumor necrosis factor-alpha (1-1000 pM) stimulated dose-dependent increases in the secretion of interleukin-6 and monocyte chemoattractant protein-1 at 34 C and 40C. We conclude that the HOB-01-C1 cell line has a preosteocytic phenotype. Moreover, these cells respond to calcitropic hormones and bone resorbing cytokines.
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PMID:Establishment and hormonal regulation of a conditionally transformed preosteocytic cell line from adult human bone. 889 22

The macrophage cell line J774, primary rat osteoblasts, and the osteoblast cell line MC3T3-E1 were used to examine the biocompatibility of a newly developed polyesterurethane foam and the possible use of this structure as bone-repair materials. The newly developed, biodegradable, and highly porous (pore size 100-150 microns) DegraPol/btc polyesterurethane foam was found to exhibit good cell compatibility; the cell-to-substrate interactions induced neither cytotoxic effects nor activation of macrophages. Osteoblasts and macrophages exhibited normal cell morphology. No signs of cell damage were detected using scanning electron microscopy (SEM). No significant increase in the production of tumor necrosis factor-alpha (TNF-alpha) or nitric oxide (NO) was detected in macrophages. Compared with cells cultured on tissue culture polystyrene (TCPS), macrophages exhibited relatively high cell attachment (150% of TCPS) but significantly high doubling time (about 8 days) compared with TCPS (4.6 days). Primary rat osteoblasts and the osteoblast cell line exhibited relatively high attachment (140% and 180% of TCPS, respectively) and a doubling time of about 5 days, compared with TCPS (6 days and 8.8 days, respectively). Eight days after cell seeding, osteoblasts exhibited a confluent cell multilayer and migrated into the pores of the polymer. In addition they produced high concentrations of collagen type I, the main protein of the bone, and expressed increasing alkaline phosphatase activity and osteocalcin production throughout the 12 days of the experiment. During degradation of these polymers, small crystalline particles of short-chain poly[(R)-3-hydroxybutyric acid] (M(n) approximately 2300) (PHB-P) are released. Therefore PHB-P (diameter, 2-20 microns), as possible degradation products of the polymer, are investigated here for their effects on macrophages and osteoblasts. Results obtained in the present study clearly indicate that macrophages and, to a lesser degree, osteoblasts have the ability to take up (phagocytose) PHB-P. At low concentrations particles of PHB failed to induce cytotoxic effects or to activate macrophages. Osteoblasts showed only limited PHB-P phagocytosis and no signs of cellular damage. At high concentrations of PHB-P, this process was accompanied by cytotoxic effects in macrophages (> 200 pg PHB-P/cell) and to a lesser extent in osteoblasts (> 400 pg PHB-P/cell).
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PMID:Interactions of osteoblasts and macrophages with biodegradable and highly porous polyesterurethane foam and its degradation products. 889 40

Large amounts of homogeneous cells are not always available for in vitro studies of inflammatory skin disorders. Here we demonstrate that a novel cell line, termed YAA, has been established from peripheral blood mononuclear cells, which were separated by the Ficoll method, of a patient with atopic dermatitis. YAA cells were grown in suspension culture. The cytochemical staining showed a positive reaction for alpha-naphthyl butyrate esterase, which was completely inhibited by sodium fluoride, but a negative result for periodic acid-Schiff, peroxidase and alkaline phosphatase. A large population of YAA cells exhibited phenotype of CD33 and CD56 but neither of CD2 nor CD3. The phorbol ester-stimulated YAA cells produced a considerable amount of tumor necrosis factor-alpha. These findings suggest that YAA might be a monocytoid line with an additional phenotype specific for natural killer cells.
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PMID:Establishment and characterization of a novel human cell line exhibiting both immunophenotypic markers of monocyte/macrophage and natural killer cell lineages from peripheral blood of a patient with atopic dermatitis. 906 7

We have developed enhanced immunohistochemical protocols for detecting autonomic nerve fibers and splenocyte-associated proteins in rat spleen. This includes norepinephrine-synthesizing enzymes (dopamine-beta hydroxylase (DBH) and tyrosine hydroxylase (TH)), neuropeptide Y (NPY), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), c-fos protein, inducible nitric oxide synthase (iNOS), and the macrophage cell marker ED1. Animals were divided into sham-operated and splenic nerve-sectioned groups for detection of DBH, TH, and NPY. For immunodetection of TNF-alpha, iNOS, IFN-gamma and c-fos, animals were injected IV with saline or 100 microg of lipopolysaccharide (LPS) and were sacrificed at various time intervals post injection. Rats were perfused with 4% paraformaldehyde, spleens removed and cryoprotected, and 50-microm floating sections were cut on a freezing microtome. Immunodetection was performed with various detection systems and substrate/chromogen solutions, and in some cases using pretreatment with proteinase K (PK) for antigen unmasking. PK pretreatment increased immunostaining for DBH, TH, NPY, IFN-gamma, iNOS, and ED1, and the improvement was concentration-dependent. Using NPY immunostaining to index the signal-to-noise ratio for various substrates and detection systems, we found that an alkaline phosphatase detection system with NBT/BCIP as a substrate was the best procedure for light microscopy, whereas the CY3-labeled secondary antibody technique proved optimal for fluorescent microscopy. Surgical transection of the splenic nerve eliminated all nerve fiber staining for DBH, TH, and NPY. TNF-alpha, IFN-gamma, c-fos, and iNOS proteins were observed in the spleen in a time-dependent manner after LPS stimulation. Fluorescent double labeling, visualized with fluorescent confocal scanning laser microscopy, revealed many NPY fibers distributed among the ED1-labeled macrophages. These results demonstrate that immunohistochemistry can be used to index the activational effects of an immune challenge on splenocytes in situ and verifies that splenic immune cells are innervated by the sympathetic nervous system.
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PMID:Enhanced immunohistochemical detection of autonomic nerve fibers, cytokines and inducible nitric oxide synthase by light and fluorescent microscopy in rat spleen. 911 Dec 38

The modulatory effects of interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha on bone morphogenetic protein (BMP)-2- and -4-induced alkaline phosphatase (ALP) activity were examined in cultures of mouse MC3T3-E1 osteoblastic cells. Both BMP-2 and -4 significantly induced ALP in these cells. IL-1 beta alone had no effect on ALP activity, but it significantly enhanced BMP-2- and -4-induced ALP activity. TNF-alpha suppressed the induction of ALP by BMP-2 or -4. The results suggest that the action of BMP on osteogenic differentiation may be regulated by such immuno/inflammatory cytokines as IL-1 beta and TNF-alpha.
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PMID:Interleukin-1 beta enhances and tumor necrosis factor-alpha inhibits bone morphogenetic protein-2-induced alkaline phosphatase activity in MC3T3-E1 osteoblastic cells. 921 3


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