Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biochemical parameters (dry matter, DNA, protein, cAMP, and calmodulin) were measured in tibial dyschondroplastic (TD) cartilage. This abnormal cartilage, which is a mass of unmineralized, unvascularized cartilage found in the proximal metaphysis of the tibiotarsus and tarsometatarsus, was compared with normal epiphyseal growth plate and hypertrophic cartilage obtained from day-old embryonic cone. The latter tissue is an example of cartilage which rapidly undergoes vascularization and mineralization. When compared with normal growth plate, tibial dyschondroplastic cartilage was found to contain lower amounts of dry matter, DNA, protein, cAMP, and calmodulin. This cartilage did not respond to factors in serum which stimulate 35S uptake. Although the above two types of cartilage contained similar amounts of ash, TD cartilage had less phosphorus and potassium and more sodium than the growth plate. The two types of cartilage had similar lysozyme activity and proteoglycan (hexosamine) content. In many of the parameters measured, day-old hypertrophic cartilage was similar to the normal growth plate. However, these tissues did differ in DNA, protein, ash, and lysozyme content. Substantially greater amounts of ash and lysozyme were found in the hypertrophic cartilage, which appeared to be related to events of mineralization and vascularization of this cartilage. These events did not occur in the abnormal cartilage cells found in the tibial dyschondroplastic lesion.
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PMID:Avian tibial dyschondroplasia. II. Biochemical changes. 399 38

Monocyte and neutrophil function assessed as antibody-dependent cell-mediated cytotoxicity (ADCC) using IgG-sensitizing human erythrocytes as target cells was enhanced in patients with severe psoriasis when compared to healthy controls. We found significant correlation between increased monocyte ADCC and increased neutrophil ADCC, No differences in basal cAMP levels and cAMP responses during initiation of the ADCC reaction was observed between psoriatics and normals. Also degranulation determined as lysozyme release during ADCC was normal. In contrast, the increase in ADCC was significantly correlated to an enhanced hexose monophosphate shunt activation in the effector cells during the cytotoxic reaction. Activity of enzymes responsible for the respiratory burst was not altered in psoriasis since superoxide production after stimulation with phorbol myristate acetate was normal. Likewise, oxygen consumption and degranulation following phagocytosis of opsonized zymosan particles in neutrophils was found normal in psoriasis. Since monocytes showed increased binding of IgG-sensitized erythrocytes these data indicate that the enhanced monocyte and neutrophil ADCC is caused by an enhancement of the respiratory burst possibly induced by increased Fc receptor activity.
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PMID:On the mechanism of enhanced monocyte and neutrophil cytotoxicity in severe psoriasis. 628 40

A total of 28 psoriatics and the same number of healthy individuals as controls were subjected to chemical analyses of their lacrimal fluid and parotid saliva to assess whether any functional disturbances attributable to psoriasis were detectable, i.e. if they have sicca syndrome (SS) or not. The stimulated parotid flow rate and Schirmer test I proved to be normal in both series. A significant elevation of salivary IgA, alpha-amylase, and Na+ was found in psoriatics when compared with the controls. On the other hand, salivary lysozyme values in psoriatics were markedly lowered. There was a distinct interrelationship between salivary IgA, beta 2-microglobulin, and lysozyme detectable in both series. The findings are discussed in terms of the increased immunological activity in psoriasis, and the possible role of cAMP and neural regulation in the causation of elevated amylase and Na+ levels in psoriatics is hypothesized. These alterations in salivary constituents might provide a protective system for oral mucous membranes against this skin disease.
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PMID:Chemical analysis of parotid saliva and lacrimal fluid in psoriatics. 635 61

Choline, acetylcholine and betaine used as a sole carbon source, effectuate in Ps. aeruginosa an acid phosphatase activity in addition to a cholinesterase activity. Induction of both enzyme activities was repressed by succinate or glucose. Cyclic AMP failed to relieve the repression produced by these compounds. Substrates not related to choline and used as a sole source of carbon, were inefficient to produce induction of both enzymes. The in-vitro action of choline, acetylcholine and betaine on Ps. aeruginosa acid phosphatase and cholinesterase has also been studied. To perform these studies periplasmic extracts obtained by EDTA-lysozyme treatment of the cells grown on choline or betaine as sole source of carbon, were used. Acid phosphatase activity was competitively inhibited by betaine, whereas the inhibition produced by choline and acetylcholine showed competitive and noncompetitive components. Cholinesterase activity was noncompetitively inhibited by betaine. At low acetylthiocholine concentration choline was an inhibitor of cholinesterase, whereas at high substrate concentration choline raised the hydrolysis rate of acetylthiocholine. These findings allow the conclusion that acid phosphatase and cholinesterase are specifically induced by choline and its metabolites derivatives. Kinetic results led us to postulate that acid phosphatase and cholinesterase contain a similar allosteric site. This site would either be of an anionic nature or show affinity to a methyl group or display both characteristics.
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PMID:Induction of acid phosphatase and cholinesterase activities in Ps. aeruginosa and their in-vitro control by choline, acetylcholine and betaine. 640 29

The aim of the present study was to investigate the pathways of platelet-activating factor (PAF) production and release from human monocytes. For this purpose, both phagocytic stimuli and stimuli induced by soluble agents were used. The phagocytic stimuli exerted their effect in a receptor-specific mechanism related to surface Fc, C3b and C3d receptors. Stimuli induced by soluble agents, such as A23187 and pH 10.6, which do not require interaction with specific receptors, were also effective in inducing PAF release. In contrast, C5a, a soluble agent which induces a receptor-mediated release of PAF from neutrophils, failed to induce PAF release from monocytes. PAF release from monocytes could be dissociated from phagocytosis and from release of lysozyme. The PAF release required the presence of extracellular cations, the activation of membrane esterase and phospholipase A2 and the integrity of the microfilament system. Moreover, PAF release was modulated by lipoxygenase and intracellular cAMP levels. The relevance of an acetylation process in the biosynthesis of PAF was suggested by the increase of PAF yields in the presence of sodium acetate and by the incorporation of 14C-sodium acetate into molecules of active PAF.
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PMID:Biosynthesis and release of platelet-activating factor from human monocytes. 682 35

The arginase produced by peritoneal macrophages is not synthesized de novo in short-term (3 h) cultures after harvesting the cells. In long-term cultures the arginase synthesis is restored. In contrast to arginase lysozyme is continuously synthesized in short-term cultures. These statements were proved by the following experimental results: 1. Protein synthesis inhibitor and lysosomotropic agents did not alter the arginase level. 2. Arginine and its analogue, canavanine and ornithine were not able to change the arginase activity. 3. The product of an alternative metabolic pathway of arginine, sodium nitrite, did not affect arginase activity. 4. Effectors influencing the synthesis of cyclic nucleotides (cAMP, cGMP), indomethacin, sodium nitroprusside and an analogue of cAMP had no effect on the arginase activity. 5. Arginase activity could not be significantly modified either by an in vitro Micrococcus luteus treatment or by changing the adherence period of peritoneal exudate cells. 6. When arginase was produced in murine peritoneal macrophages at various periods with medium change, the total arginase released into the media from murine and rat macrophages did not exceed the original intracellular arginase content of the adhered cells during the first 6 hours.
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PMID:Evidence for the pre-synthesized state of secreted macrophage arginase: arginase activity cannot be modified in short-term cultures. 817 55

The FACS-analysis of diseases as different as cancer, autoimmune disorders and chronic (retro)viral infections, including HIV-infection, shows -at least temporarily- a common feature of lymphocyte hyperactivation, characterized by cellular activation markers (HLA-DR, CD26, CD38, CD69, CD2R and/or CD30), as well as by solubilized membrane structures, such as beta-2m, sICAM-I, sIL-2R/sCD25, sCD8, and by some oversecreted immunocyte products (e.g. neopterin, lysozyme and/or cathepsin D). We tested two potential approaches to down-regulate the pathologically elevated CD8+ and HLA-DR+ T cells: (a) In animal model, we tested the sensibility of these, disease inducing and maintaining T cell subsets to in vitro pretreated (cell death preprogrammed) semi-syngeneic and allogeneic donor T cells in tumor-bearing mice. (b) In the first clinical study, we used a novel combination of FDA-approved drugs which inhibits Ca(2+)-influx and concomitantly down-regulates cytosolic cAMP in patient's overstimulated immunocompetent cells. We could achieve a 94.6-100% long-term survival in tumor-bearing mice. In patients, large primary tumors and large metastases shrinked by 80-85% and small metastases disappeared completely. Since in HIV-infected persons, the increased number of HLA-DR+ CD38+T (T8) cells is associated with a fall in CD4-level and with development of AIDS, we are looking for the elimination of these HLA-DR+ targets by our novel technique in two AIDS-simulating (FIV/FeLV and SIV) animal models.
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PMID:Treatment of solid tumors should obligatorily be combined with the in vivo codepletion of tumor-protecting, CD8+/HLA-DR(+)-suppressor T cells by alloreactive donor T cells whose preprogrammed cell death allows a high GvL-effect before GvHD can be established. Results of animal experiments, including more than 6000 mice. 873 48

The purpose of this study was to investigate the in vitro viability and secretory behaviour of human main and accessory lacrimal glands using an organ culture technique. We evaluated the influence of the second messengers cAMP and cGMP on secretion. Fragments less than 1 mm3 of main and accessory lacrimal glands as well as conjunctiva were cultured for 2-72 hr at 37 degrees C in an atmosphere consisting of 50% O2, 45% N2 and 5% CO2, using a specially devised culture medium (+/- cAMP or cGMP). The conjunctival tissue served as negative control. Supernatants were assayed for secretory-component-bound IgA, lactoferrin and lysozyme using ELISA. Cultured tissue pieces were embedded in paraffin, serially sectioned, stained and their volumes calculated using an image-analysis system. This enabled us to differentiate between secretory, connective and fatty tissue. Secreted exudate was correlated to the volume of secretory tissue. Viability of cultured organ pieces was determined by electron microscopic examination. Suitable organ culture conditions for human lacrimal glands were successfully established. Electron microscopic examinations proved that the structural characteristics of the organ and the polarity of the individual cells were well preserved up to 22 days of culture. Culture supernatants were assayed for secretory-component-bound IgA, lactoferrin, and lysozyme and showed that the amount of protein secreted increased with time. Upon addition of cAMP (1 x 10(-3) M) and cGMP (4 x 10(-3) M), secretion was elevated in both main and accessory lacrimal glands. An organ culture system for lacrimal glands was developed that maintains their structural and cellular characteristics as well as their secretory function for up to 22 days. We believe that this system mimics the in vitro state of the organ better than monolayer cultures and thus proves to be a valuable tool when examining lacrimal function in vitro. The fact that both cAMP and cGMP enhance secretion may help to shed some light on the cellular pathways human main and accessory lacrimal glands use for signal transduction.
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PMID:Organ culture of human main and accessory lacrimal glands and their secretory behaviour. 875 22

An aqueous fraction (10-300 micrograms/mL) of the ethanol extract of the leaves of Cissampelos sympodialis Eichl inhibited N-formyl-Met-Leu-Phe (fMLP)-induced release of lysozyme and myeloperoxidase from human neutrophils. Inhibition by the fraction, as well as by dibutyryl-cAMP and prostaglandin E2, was substantially greater when the cells were pretreated with the phosphodiesterase (PDE) inhibitor isobutyl methyl xanthine (IBMX) indicating that the effect may be mediated by cAMP. Measurement of intracellular cAMP levels showed that the fraction (30-100 micrograms/mL) increased the nucleotide levels in IBMX-pretreated neutrophils which was unaffected by propranolol. Cyclic AMP dependent protein kinase A activity was also increased by the fraction (1.5-100 micrograms/mL). Superoxide anion generation induced by fMLP in cytochalasin B-treated cells primed with PAF was not inhibited by the aqueous fraction. The results indicate that the aqueous fraction of Cissampelos sympodialis inhibits neutrophil degranulation by a cAMP-dependent mechanism which may be relevant to the use of the plant as an anti-asthmatic agent in folk medicine.
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PMID:Effects of the aqueous fraction of the ethanol extract of the leaves of Cissampelos sympodialis Eichl. in human neutrophils. 1018 43

The MLL gene is fused with the cAMP-responsive element binding protein-binding protein (CBP) gene in t(11;16)(q23;p13), which has been reported to be associated with therapy-related acute leukemia. We established a novel myeloid cell line, SN-1, from a patient with T-cell acute lymphoblastic leukemia with t(11;16)(q23;p13) having in-frame MLL-CBP fusion transcripts. The majority of the SN-1 cells were positive for myeloperoxidase when examined using an electron microscope and expressed CD13, CD33, CD56, and HLA-DR antigens, but not CD7, CD10, CD19, CD34, or CD41 antigens, suggesting that these cells are of myeloid origin. SN-1 cells underwent functional and morphological differentiation when treated with actinomycin D or sodium butyrate, but not with all-trans-retinoic acid (ATRA) or 1alpha,25-dihydroxyvitamin D3 (VD3). Exposure of SN-1 cells to ATRA hardly affected cell growth and differentiation, whereas the growth of HL-60 and NB4 cells treated with ATRA was effectively inhibited, and differentiation into mature granulocytes was induced. SN-1 cells were relatively insensitive to VD3 with respect to inhibiting the cell growth and inducing the ability to reduce nitroblue tetrazolium, lysozyme activity, and morphological differentiation, although the expression of CD11b was slightly induced by VD3. These results suggest that the cell line was impaired in the signal transduction systems of ATRA and VD3. This cell line should be useful for the study of the role of CBP as a transcriptional regulator in leukemia differentiation and for the functional analysis of the MLL-CBP fusion gene, which will provide new insights into leukemogenesis caused by 11q23 translocations.
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PMID:SN-1, a novel leukemic cell line with t(11;16)(q23;p13): myeloid characteristics and resistance to retinoids and vitamin D3. 1070 36


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