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:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Conditioned medium (CM) prepared from bone marrow (BM) or spleen (SPL) cells from mice injected with PGE2 in doses ranging from 0.0001 to 10 micrograms was found to contain an activity inhibitory to the proliferation of granulocyte-monocyte progenitor cells (CFU-GM). This activity was found in medium conditioned for 24 to 48 h, but was not present in medium conditioned for longer time intervals. BM cells from PGE2-treated mice incubated over a concentration range of 0.1 to 1.0 x 10(6) cells/ml and SPL cells over a range of 1.0 to 10 x 10(6) cells/ml produced CM with equivalent degrees of inhibition for CFU-GM proliferation. Titration of this activity revealed a significant inhibitory effect still present at a 1/256 dilution. Inhibitory activity was similar whether or not CM was prepared in the presence or absence of FCS. Inhibition of CFU-GM development was approximately equal in the presence of either PWM SPL CM or L cell CM as sources of CSF activity. Morphologic analysis of CFU-GM revealed an equivalent inhibition of monocyte, monocyte-neutrophil, and neutrophil CFU-GM by the PGE2-stimulated inhibitory activity. Equivalent picogram amounts of PGE were measured in CM derived from BM or SPL cells from either control or PGE2-treated mice, indicating a low probability that injected PGE2 was carried over in the CM and contributed to CFU-GM inhibition. Protease digestion of BM or SPL cell CM from PGE2-treated mice revealed a loss of inhibitory activity after trypsin, chymotrypsin, pronase, and neuraminidase treatment. Inhibitory activity was also ablated by heat treatment at 56 degrees C for 30 min and 100 degrees C for 5 min. Acrylamide-agarose gel filtration of BM CM revealed an active inhibitory fraction in the Mr range of 5.5 to 8.0 kDa. The results of the present study suggest that one of the mechanisms by which PGE2 exerts its in vivo myelopoietic inhibitory action may be by stimulating the production of an inhibitory factor or factors from BM and SPL cells.
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PMID:In vivo modulation of myelopoiesis by prostaglandin E2. IV. Prostaglandin E2 induction of myelopoietic inhibitory activity. 317 Nov 82

Mouse splenocytes are induced by pokeweed mitogen to secrete a factor that stimulates mouse hemopoetic (spelling per Nomina Histologica in the Nomina Anatomica, 5th edition, 1983, Williams and Wilkins, Baltimore) progenitor cells to undergo proliferation and differentiation into granulocytes and macrophages in a semi-solid culture system. The granulocyte and macrophage colony-stimulating factor (GM-CSF) was purified with a four-step procedure that includes ultrafiltration, chromatography on DEAE-agarose, Sephacryl S-200, and chromatofocusing gel. The isoelectric point (pI) of 4.2 of the GM-CSF was determined by analytical isoelectrofocusing gel electrophoresis. The sensitivity of the biological activity of GM-CSF to digestion by trypsin and neuraminidase suggests that GM-CSF is a glycoprotein with its sugar moieties at the active site. The GM-CSF is also sensitive to heat denaturation at 60 degrees C or higher suggesting that a three-dimensional conformation is required for its biological activity. The molecular weight of GM-CSF is approximately 57,000 Daltons as determined by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate.
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PMID:Properties and purification of a colony-stimulating factor of granulocytes and macrophages produced by mouse spleen cells. 349 11

We have previously shown that human megakaryocyte colony-stimulating activity (Meg-CSA) is present in sera from patients with bone marrow megakaryocyte aplasia. In this report, we demonstrate that Meg-CSA is also present in sera from dogs rendered aplastic by 1000 rad total body irradiation. Canine serum Meg-CSA has activity comparable to human when assayed in plasma clot cultures containing human bone marrow mononuclear cells. Because of the uniform high potency and ready availability of aplastic canine sera, it was utilized initially for Meg-CSA purification. Sequential ammonium sulfate precipitation to approximately 80% saturation resulted in recovery of 59%-69% of the serum protein and of 75%-103% of the original serum Meg-CSA. The fraction precipitable between ammonium sulfate saturations of 0% and 44%-50% (fraction I) contained 53%-76% of the initial serum Meg-CSA and 25%-32% of the initial serum protein. This represents an enrichment of Meg-CSA specific activity by over 100%. The Meg-CSA eluted from Sephacryl S-300 in a single peak corresponding to a molecular weight of 175,000. This Meg-CSA peak also contained IgG, but the Meg-CSA did not bind to protein A-agarose. Meg-CSA was 90% inactivated by trypsin digestion for 4 h at 37 degrees C and by exposure to 5mM dithiothreitol for 2 h at room temperature. Exposure to either 6 M guanidine for 1 h at room temperature or 8 M urea for 1 h at 4 degrees C resulted in a 70% loss of Meg-CSA. At culture concentrations capable of stimulating maximal megakaryocyte colony formation, fraction I supported no colony growth by myeloid (CFU-GM) or late erythroid (CFU-E) human hematopoietic progenitor cells. Erythroid burst-promoting activity (BPA) was not detected in fraction I from two of three different aplastic canine sera tested. Therefore, Meg-CSA is functionally distinct from granulocyte-monocyte colony-stimulating factor (GM-CSF), erythropoietin, and BPA. The data indicate that serum Meg-CSA is a 175,000-dalton protein (megakaryocyte colony-stimulating factor, Meg-CSF) in which higher order structure and disulfide bonding are necessary for biologic activity. Partially purified Meg-CSF manifests functional specificity for the CFU-Meg hematopoietic progenitor cell.
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PMID:Human megakaryocyte colony-stimulating factor in sera from aplastic dogs: partial purification, characterization, and determination of hematopoietic cell lineage specificity. 387 46

Immunoenzymatic, clinical and follow up study of 3500 patients suffering from nervous forms of epidemic parotitis was performed. It is concluded that the adaptive humoral enzymes, ribonuclease and trypsin, the persistence of antigen to epidemic parotitis virus in CSF lymphocytes as well as the immunologic status of the patient at the disease onset play the leading role in the pathogenesis of its acute phase. It advisable to examine the factors enumerated in order to predict the clinical course of the disease. The treatment with adaptive enzymes was of great efficacy in 660 patients.
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PMID:[Various mechanisms of the pathogenesis and etiotropic therapy of neurologic forms of epidemic parotitis]. 398 4

In chronic experiments on dogs with fistulae of pancreas, administration of pancreozymin into the cerebral ventricles activated the lipase activity of pancreatic juice whereas secretin inhibited the trypsin activity. The pancreozymin administration into the anterior hypothalamus activated the pancreatic lipase whereas administration of this hormone into the RF exerts no effect on the basal secretion of juice and enzymes. The secretin administration into the hypothalamus or RF leaves the pancreatic secretion intact. Administration of CSF from dogs-donors with pancreozymin in their cisterna magna activated the lipase activity of the juice. Central action of cholecystokinin-pancreozymin on the pancreatic secretion of enzymes seems to be actualized through the hypothalamic structures.
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PMID:[Central action of cholecystokinin-pancreozymin and secretin on pancreatic enzyme secretion]. 617 May 32

A model of human Hemophilus influenzae type b meningitis was developed in infant rabbits infected intranasally. The pathogenesis and course resembled that in human beings; bacteremia was followed by meningitis with a high mortality. Pretreatment of the nasopharyngeal mucosa with 0.5% trypsin or normal saline significantly increased the rate of bacteremia. Death was age related. Intranasal challenge with type f and nontypeable H influenzae was associated with transient bacteremia. Our results suggest that factors on the respiratory tract epithelial cell surface influence colonization and infection with H influenzae type b and confirm the importance of other host and parasite factors. Intravenous aztreonam resulted in a peak CSF concentration that was 6% to 7% of the serum concentration in infected meninges but only 2% to 3% in normal meninges. Aztreonam reduced mortality in established H influenzae type b meningitis from 88% in untreated animals to 9%.
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PMID:Hemophilus influenzae type b meningitis in infant rabbits. Pathogenesis and therapy. 653 45

A suitable model of Haemophilus influenzae meningitis will facilitate better understanding of the pathophysiology, therapy, and prevention of the disease and its sequelae. Bacteremia and meningitis were induced in infant New Zealand white rabbits by intranasal inoculation of H. influenzae type b. Intranasal trypsin prior to challenge significantly increased (p = 0.002) the rate of bacteremia from 64% (7/11) to 100% (45/45). In the trypsin-treated group, H. influenzae b was isolated from the CSF of 89% (25/28) of 17- to 21-day-old rabbits and from 76% (13/17) of 23- to 30-day-old animals, p = 0.3; fatality rates were 88% and 31%, respectively, p = 0.001. Bacteremia developed within 24 hr of inoculation and meningitis within 96 hr. Death occurred 1 to 7 days after the development of meningitis. Histologic evidence of nasopharyngitis and meningitis was found at autopsy. The intranasal route of infection, the age-dependent outcome, the size of the animal, and its low cost and availability make the infant rabbit an appropriate model of H. influenzae b meningitis.
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PMID:Haemophilus influenzae b bacteremia and meningitis in infant rabbits after intranasal inoculation. 660 8

A granulocyte colony-stimulating factor (G-CSF) was highly purified from the serum-free culture medium of RSP -2 X P3 cells. The G-CSF had an apparent molecular weight of 33,000 as determined by high speed gel permeation chromatography, but its molecular weight was decreased to 15,000 by 0.1% sodium dodecyl sulfate. A small amount of monocyte/macrophage CSF (M-CSF) also was separated from the same medium. The production of this M-CSF was increased markedly by bacterial lipopolysaccharides. The M-CSF had an apparent molecular weight of 77,000 in the absence of 0.1% SDS and 49,000 in its presence. The G-CSF was stable against 5 mM dithiothreitol, whereas the M-CSF was slowly inactivated. The two CSFs also differed in their heat-stability and resistance to trypsin. Neuraminidase changed the isoelectric point of both CSFs. Anti-L cell CSF serum severely inhibited the activity of M-CSF but not that of G-CSF. A 1 : 1 mixture of M-CSF and G-CSF developed colonies of the respective types, both in excess of the number predicted. The RSP -2 X P3 G-CSF reported here should prove very useful in the study of differentiation in myeloid stem cells.
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PMID:A granulocyte colony-stimulating factor from serum-free cultures of RSP-2 X P 3 cells: its separation from a macrophage colony-stimulating factor and its biological and molecular characterization. 660 80

Recently developed enzyme tests that are used in (a) identifying high risk populations, (b) diagnosing cancer, (c) following treatment response of cancer patients, and (d) the selection of cancer therapy are summarized. The diagnostic role of methionine adenosyltransferase and CSF monoamine oxidase activity measurements in the diagnosis of schizophrenia are discussed. The role of N-acetyltransferase in the conversion of serotonin to melatonin in the pineal gland and the importance of these changes for the synchronization of the functioning of cells throughout the organism are described. New developments in the determination of immunoreactive trypsin in the early diagnosis of pancreatic diseases are summarized.
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PMID:Present and future trends in selected areas of clinical enzymology. 677 51

Long-term in vitro growth of murine mast cells was dependent on the presence of a mast cell growth factor (MCGF) present in media conditioned by mitogen-activated splenic leukocytes or by various murine leukemic cell lines. MCGF shared a number of properties with granulocyte colony-stimulating factor (G-CSF). Both factors were present in media conditioned by the myelomonocytic leukemic WEHI-3 and the T cell lymphoma, LBRM-33 cell lines. They were relatively sensitive to trypsin treatment, and were resistant to boiling temperature. NZB mice that failed to respond to WEHI-3-derived G-CSF also failed to respond to MCGF. MCGF differed from G-CSF, however, in sensitivity to neuraminidase and lactoferrin, an inhibitor of macrophage CSF production, suppressed G-CSF production by WEHI-3 cells without affecting MCGF production. Furthermore, peritoneal cells produced G-CSF but not MCGF when stimulated with lipopolysaccharide. In vitro production of MCGF by normal spleen cells required the presence of T lymphocytes and is relatively macrophage-independent. The role of T cells in the maturation and growth of mast cells and the physiologic function of MCGF are discussed.
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PMID:Long-term in vitro culture of murine mast cells. III. Discrimination of mast cells growth factor and granulocyte-CSF. 680 16


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