Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the precise etiologic incitant of the minimal lesion idiopathic nephrotic syndrome of childhood is not known, it is likely that a host mechanism mediates the permeability alterations of the glomerular capillary wall resulting in massive proteinuria. As a first step in examining the possibility that local kinin release may account for the proteinuria in this disorder, two parameters of the plasma kinin-generating system, plasma prekallikrein and kallikrein inhibitor, were assayed during 27 nephrotic episodes in 21 corticosteroid-responsive children. Plasma kallikrein was assayed by means of its esterase activity on a synthetic arginine ester substrate, N-alpha-tosyl-L-arginine methyl ester (TAMe), after activation of Hageman factor by kaolin. This activity, after subtraction of spontaneous arginine esterase activity (i.e., TAMe esterase activity measured in plasma not exposed to kaolin) is derived from prekallikrein. Plasma prekallikrein activity in 11 normal children was 99.6 +/- 2.9 mumol TAMe hydrolyzed/ml plasma/hr (mean +/- SEM). Kallikrein inhibitor was quantified in arbitrary units. Kallifrein inhibitor activity in 11 normal children was 0.94 +/- 0.04 units. During the overt nephrotic syndrome, before initiation of intensive daily corticosteroid treatment, mean values were: prekallikrein, 58.5 +/- 7.24 mumol/ml/hr; and kallikrein inhibitor, 0.35 +/- 0.06 units. After corticosteroid-induced remission occurred, mean values were: plasma prekallikrein, 118.6 +/- 3.2 mumol/ml/hr; and kallikrein inhitor, 0.78 +/- 0.03 mumol/ml/hr. Both parameters were again assayed in 14 of the 21 children after complete cessation of corticosteroid treatment. Plasma prekallikrein was normal, 99.6 +/- 4.8 mumol/ml/hr; but kallikrein inhibitor was still somewhat depressed, 0.84 +/- 0.03 units. A subset of 9 patients had marked depression of plasma prekallikrein to levels less than 20 mumol/ml/hr and essentially undetectable inhibitor activity. Serum alpha-2 macroglobulin was elevated in nephrotic patients: mean value during relapse, 862 +/- 29 mg/100 ml; during corticosteroid-maintaining remission, 615 +/- 29 mg/100 ml. After cessation of corticosteroids, mean serum level was 481 +/- 20 mg/100 ml. The proportional reduction of plasma prekallikrein and kallikrein inhibitor suggested that an enzyme-inhibitor complex formed in vivo, perhaps at a local site of activation in proximity to the glomerular basement membrane. These data suggest that the plasma kinin-generating system may be the host effector mechanism subserving the increased glomerular capillary permeability in the minimal lesion nephrotic syndrome of childhood.
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PMID:A study of the plasma kinin-generating system in children with the minimal lesion, idiopathic nephrotic syndrome. 5 8

Non-specific acid alpha-naphthyl acetate esterase (ANAE) activity was demonstrated in a majority of bovine peripheral blood lymphocytes, confirming and extending the observations on murine and human lymphocytes made by previous workers. Simultaneous study of both ANAE activity and spontaneous erythrocyte (E) or erythrocyte-antibody-complement (EAC) rosetting capability of the same bovine lymphocytes showed directly that, while 64.2 +/- 4.6 (SEM) % of bovine lymphocytes capable of forming E rosettes were ANAE positive, 38.3 +/- 0.8% of those forming EAC rosettes were also ANAE positive. Similar studies of human peripheral blood lymphocytes showed also that, while 80.6 +/- 2.2% of the lymphocytes capable of forming E rosettes were ANAE positive, 44.1 +/- 2.6% of EAC forming lymphocytes were ANAE positive. Thus the presence of ANAE activity in a majority of T lymphocytes and a significant proportion of B lymphocytes of both human and bovine peripheral blood is indicated. Human and bovine lymphocytes from phytohaemagglutinin (PHA)-stimulated cultures demonstrated greatly enhanced intensity of ANAE activity.
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PMID:Acid alpha-naphthyl acetate esterase: presence of activity in bovine and human T and B lymphocytes. 31 18

A system is described for determination of LC50 or IC50 by an iterative process based on data obtained from a plate reader using a marine unicellular alga as a target species. The esterase activity of Tetraselmis suesica on fluorescein diacetate as a substrate was measured using a fluorescence titerplate. Simultaneous analysis of results was performed using an iterative process adopting the sigmoid function Y = y/1 (dose of toxicant/IC50)slope for dose-response relationships. IC50 (+/- SEM) was estimated (P less than 0.05). An application with phosalone as a toxicant is presented.
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PMID:Simultaneous and iterative weighted regression analysis of toxicity tests using a microplate reader. 137 29

It has been speculated whether the recently developed non-sedating antihistamines may possess other properties than merely being antagonists at the H1-receptors. To investigate this suggestion 12 patients with strictly seasonal allergic rhinitis participated in a double-blind placebo controlled randomized cross-over study outside the pollen season. At steady state levels of 10 mg loratadine, a new non-sedating antihistamine, the patients were challenged with methacholine. This was followed by a nasal challenge with increasing doses of allergen. 24 h later the patients were rechallenged nasally with the same methacholine dose as the day before. The volume of the methacholine-induced nasal secretion was measured and the response to allergen was determined by scoring technique. In returned nasal lavage fluid the levels of histamine and TAME-esterase activity were measured. It was found that loratadine significantly reduced the immediate allergic nasal symptoms compared with placebo (P less than 0.01). Loratadine also reduced the allergen-induced release of histamine into the nasal cavity after the strongest allergen dose, from 9.6 +/- 1.5 (mean +/- SEM) to 6.4 +/- 1.4 ng/ml (P less than 0.05). A similar decrease in the TAME-esterase activity after treatment with loratadine was observed. The TAME-esterase activity decreased from 11.6 *10(3) +/- 2.47 *10(3) to 5.60 *10(3) +/- 1.45 *10(3) CMP (P less than 0.05). There were no significant changes between the active and placebo treatments regarding the methacholine-induced secretory response. This was true for the initial methacholine challenge as well as the secretory response 24 h later.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Suppressive effect of loratadine on allergen-induced histamine release in the nose. 172 92

Based on the identification of intracellular esterase activity as one early target of sulfamethoxazole hydroxylamine (SMX-HA), we wished to determine if the metabolite affected immune functions which involve esterases. The natural killer (NK) activity of human peripheral blood mononuclear cells (PBMC) was assessed with a cell concentration fluorescence technique following exposure to SMX-HA. When K562 target cells were incubated (4 hr/37 degrees) with various ratios of untreated PBMC effector to K562 target cells (E:T), NK activity increased from 17.8 +/- 3.1% (mean +/- SEM; N = 12) at an E:T ratio of 5:1 to 46.2 +/- 2.0% at an E:T ratio of 40:1. Pretreatment of fresh PBMC with 0.1 to 1.0 mM SMX-HA produced a concentration-dependent inhibition of NK activity (E:T ratio 40:1) reaching approximately 80% at 1 mM SMX-HA. Maximum suppression of NK activity was completed within a 60-min pretreatment period with measurable inhibition detected within 30 min. The viability of effector cells was not affected by the metabolite during the pretreatment period. Therefore, the SMX-HA effects could not be directly attributed to decreased viability of the effector cells; they were irreversible and could be prevented by the inclusion of exogenous reduced glutathione (GSH) in a concentration-dependent manner. Given the important roles of NK cells in immune responsiveness and host resistance, our findings of rapid functional inactivation of the cytolytic effector function provide a possible link between idiosyncratic drug toxicity and drug effects directly on components of the immune system.
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PMID:Cellular toxicity of sulfamethoxazole reactive metabolites--II. Inhibition of natural killer activity in human peripheral blood mononuclear cells. 199 6

Monocytes have been demonstrated to play an important role in acute serum sickness (AcSS) nephritis. Because accumulation of monocytes within the glomeruli could be the result of local lymphokine production, we studied migration inhibition factor (MIF) activity in supernatants from glomerular cultures, analyzed its temporal relationship with monocyte and lymphocyte accumulation, and tested the effect of anti-T lymphocyte monoclonal antibody on local MIF production. AcSS was induced in 12 rabbits, and one additional rabbit had antigen elimination without proteinuria. Single nephrectomy was performed at the time of antigen elimination in all animals; the remaining kidney was removed four days (4 rabbits) or 14 days afterwards (5 rabbits). In glomerular cross sections (gcs), lymphocytes were identified using monoclonal antibody M108, and monocytes by nonspecific esterase stain (ES). MIF activity was determined in supernatants of cultures of isolated glomeruli by the agarose microdroplet method. Peak of MIF activity (84.3 +/- 2.6%, SEM) was observed the first day of proteinuria in association with peak of lymphocyte infiltration (1.15 +/- 0.1 lymphocytes/gcs) and monocyte infiltration (2.4 +/- 0.3 mean ES score/gcs). MIF activity diminished by day 4 (66.0 +/- 6.3%) and reached control levels by day 14 (12.8 +/- 3.2%). There was a significant correlation between lymphocyte infiltration and MIF activity (r = 0.776, P less than 0.0001) as well as between MIF activity and monocyte accumulation (r = 0.858, P less than 0.0001). In five additional rabbits with AcSS, glomeruli were isolated, treated successively with M108 and normal rabbit serum, and supernatants harvested from 24-hour cultures were tested for MIF activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Migration inhibition factor in acute serum sickness nephritis. 207 55

To determine if atopic subjects without asthma naturally exposed to antigens to which they are sensitized demonstrate evidence of lower airway inflammation, we studied 10 subjects with recurrent seasonal allergic rhinitis to pollens. Each subject had a monthly methacholine challenge and two bronchoalveolar lavages (BAL), one during symptoms of allergic rhinitis and one out of season. The percentage of macrophages, lymphocytes, neutrophils, eosinophils, and mast cells in the lavage fluid were determined on Diff-Quik, nonspecific esterase, or toluidine blue-stained cytocentrifuge preparations. The total number of cells recovered on BAL was 23.2 +/- 3.5 X 10(6) (mean +/- SEM) (13.3 +/- 2.3 X 10(4) cells per milliliter) in season, during symptoms of allergic rhinitis, and 33.8 +/- 7.4 X 10(6) (15.2 +/- 3.1 X 10(4) cells per milliliter) out of season (p greater than 0.05). BAL cell-differential counts (percent) in/out season were similar for macrophages (89.0/84.6), lymphocytes (9.1/12.8), neutrophils (1.3/2.1), eosinophils (0.5/0.5), epithelial cells (0.37/0.46), and mast cells (0.0008/0.0013). Blood eosinophil counts, taken, respectively, in and out of season, were 135.5 +/- 26.8 X 10(6)/L and 102.8 +/- 20.6 X 10(6)/L (p greater than 0.05). Although overall airway responsiveness increased slightly during the pollen season, it did not reach statistical significance (geometric mean of provocative concentration causing a 20% fall in FEV1 [milligrams per milliliter], 98.8 during antigenic exposure compared to 121.4 out of season) (p greater than 0.05. These observations suggest that in subjects without asthma, no changes in cell differential are detected on BAL at the time of maximal symptoms of allergic rhinitis.
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PMID:Influence of natural antigenic exposure on bronchoalveolar lavage in subjects with pollen-induced rhinitis. 237 Mar 87

Cell suspension prepared from the lymph node biopsy of patients with non-Hodgkin's lymphoma (NHL), metastatic carcinoma (MC) and non-neoplastic lymphadenopathies (NL) were analyzed by the Hemalog D, automated differential counter. The preparation of lymph node cells is described first in this study. The results show that the percentage of large cells (diameter greater than 13.5 micron) stained negatively with peroxidase (LUC, large unstained cells) was remarkably increased in patients with NHL (mean +/- SEM = 18.6 +/- 3.1%) and was particularly increased in the subgroup, diffuse histiocytic type (31.1 +/- 5.3%). Patients with MC had a raised percentage of nonspecific esterase-positive cells (9.2 +/- 1.4%) compared to patients in the NHL and NL groups. Patients in the NL group had low percentages of both LUC (5.3 +/- 0.7%) and nonspecific esterase-positive cells (1.8 +/- 0.2%). Quantitation of cells in the lymph node by using the Hemalog D may assist in the diagnosis of lymph node diseases.
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PMID:Automated cytochemistry in non-Hodgkin's lymphoma: a new method for determination of cells from lymph node biopsy. 243 Apr 21

It has been suggested that the IgE-dependent late-phase reaction to allergen exposure, with the features of an inflammatory cellular infiltration and airway hyperreactivity, is a link between anaphylaxis and continuous allergic airway disease. Our main knowledge of the cellular response to allergen in sensitized individuals has been derived from allergen-challenge models. To explore the dynamics of the cellular response during the actual disease, patients with a strictly seasonal allergic rhinitis were studied during natural allergen exposure. Ten patients suffering from an isolated birch-pollen allergy were followed from a symptom-free state before, during, and to the height of the birch-pollen season. Repeated parallel cell samplings from the nasal mucosa were performed with cytologic imprints on plastic strips, nasal lavages with the recovery of the cells in the lavage fluid with cytocentrifugation on object slides for cytologic study, and scrapings from the nasal surface with a curette for histologic and ultrastructural evaluation. The histamine content was determined in lavage fluid and cell pellets. The tosyl-alpha-tosyl-L-arginine methyl esterase activity of the nasal lavage fluid was also determined as a biochemical marker of the allergic inflammatory reaction. The birch-pollen season was moderate in terms of pollen counts, and this resulted in mild to moderate nasal symptoms that ran parallel to the birch-pollen counts. The total number of cells recovered in the lavage fluid was 1.2 +/- 0.4 (SEM) x 10(6) before and 3.2 +/- 2.0 per 10(6) cells (not significant) during pollen exposure. Most cells were neutrophils and mononuclear cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The cellular response of the human allergic mucosa to natural allergen exposure. 246 80

We developed a method for avoiding contamination by fibroblasts when cultures of peritoneal cells are initiated. Macrophages were identified by immunogold detection [light microscope, transmission (TEM) and scanning (SEM) electron microscopes] of membrane antigens (Mac-1+, Thy-1,2-), non-specific esterase activity and ultrastructural features (TEM). As compared with controls, the yield of peritoneal macrophages was 2- and 12-fold higher, respectively, in acutely and chronically infected mice. In all, 30 "chronic", 18 "acute" and 18 control cultures were followed up. At a given cell-density seeding, the decline of control, "acute" and "chronic" cultures starts at about day 10, 15, and 27, respectively. In "chronic" cultures only, fibroblast-like cells appear from day 6 onwards; their number increases with time. Cells showing characters intermediary between macrophages and fibroblasts were observed. We suggest that fibroblast-like cells result from the in vitro transdifferentiation of a limited number of in vivo committed macrophages.
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PMID:Schistosomiasis and in vitro transdifferentiation of murine peritoneal macrophages into fibroblastic cells. 251 39


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