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:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability of epsilon-amino caproic acid (EACA)-treated normal serum and of cystic fibrosis (CF)-affected and carrier sera to promote the release of lysosomal enzymes from sensitized human polymorphonuclear leukocytes (PMN) was assessed through the measurement of beta-glucuronidase and myeloperoxidase activity after exposure of these cells to the various test sera. This study was initiated to extend the analogies between preciliary dyskinesia factor (pre-CDF), separated from the cell-free media of cultures derived from CF homozygous and heterozygous individuals, and C3a anaphylatoxin. The extent of lysosomal degranulation of human PMN exposed to fresh untreated sera of each of five controls, seven CF homozygotes, and eight heterozygotes, as expressed by the amount of beta-glucuronidase releases, was 7.84% (+/- 0.934) for countrol sera, 14.01% (+/- 1.79) for CF-affected sera, and 10.61% (+/- 1.43) for heterozygous sera. The difference between CF homozygotes and control subjects is significatn (P less than 0.0001), as is the difference between CF-affected and carrier individuals (0.001 less than P less than 0.005) and between control subjects and carriers (0.001 less than P less than 0.005), when beta-glucuronidase. However, the differences between control subjects and CF heterozygous individuals are not significant. Treatment of these sera with 1 M EACA gave values for beta-glucuronidase and myeloperoxidase release which are slightly reduced when compared with those obtained with fresh, untreated samples. EACA apparently reduces the activity of beta-glucuronidase released from PMN. Amicon filtration studies of these serum samples demonstrated that degranulating ability and the presence of cilicary dyskinesia, as assessed by rabbit tracheal bioassay, are not always associated. Therefore, the relationship between pre-CDF and the degranulator activity in native CF-affected and carrier sera is unclear, in part because of the limitations inherent in the test systems employed.
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PMID:Demonstration of human leukocyte degranulation induced by sera from homozygotes and heterozygotes for cystic fibrosis. 17 51

The acid concentration and quantity, the pH and the peptic activity of the gastric juice were measured after stimulation with pentagastrin in 10 children with cystic fibrosis between the ages 2 and 12 years and in 20 healthy children of the same age group. Furthermore, the basal, maximal and peak volume outputs (BVO, MVO and PVO), the basal, maximal and peak acid outputs (BAO, MAO and PAO) and the basal, maximal and peak pepsin output (BPO, MPO and PPO) were determined. The statistical calculations were carried out with the help of partial hierarchical analysis of variance, comparison of regression curves, simple analysis of covariance and the t test. After stimulation with pentagastrin, the volume of the gastric juice, the acid quantity and the peptic activity were found to be dependent on age in healthy children as well as in children with cystic fibrosis. The maximal volume of secretion in children with cystic fibrosis is less than that of healthy children; however, the acid quantity and peptic activity show no significant difference in both groups. The volume of the gastric juice, acid quantity and peptic activity in basal and stimulated secretions, expressed in kilograms per body weight or surface area in square meters, are independent of age and show no significant difference between the two groups. In the two groups the curves for the three parameters differ significantly from one to another. There is a significant shift in the time course of the curves that depict the acid secretion and peptic activity. Contrary to the accepted views, the acid and enzyme secretions are not closely interrelated. Based on the acidity and peptic activity, the digestive capacity of the stomach is the same for healthy children and children with cystic fibrosis. In contrast to the pancreas, there is no impairment in the exocrine function of the stomach. The gastric secretions of children with cystic fibrosis are not completely the same as in healthy children.
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PMID:[The acidity and peptic activity of gastric juice in healthy children and in children suffering from cystic fibrosis (author's transl)]. 24 Nov 64

Concanavalin A (Con A) binding sites were visualized ultrastructurally in the cultured fibroblasts from cystic fibrosis patients, obligatory heterozygotes, and normal individuals by peroxidase labeling technique. Con A binding sites were localized as a continuous layer on the external side of the plasma membrane in fixed fibroblasts of the three genotypes. In living cells, Con A induces both lateral and vertical movements of binding sites as expressed by cap formation and internalization of the plasma membrane. Fibroblasts of the three genotypes responded similarly to Con A treatment and failed to show significant detectable differences.
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PMID:An electron microscopic cytochemical study on concanavalin A binding sites and their mobility in normal and cystic fibrosis fibroblasts in vitro. 86 21

Colonization in the respiratory tracts of cystic fibrosis (CF) patients by mucoid Pseudomonas aeruginosa correlates with the progression of bronchial airway pathology. There is a direct correlation between the incidence of Pseudomonas colonization and age, clinical score, extent of pulmonary disease, severity of radiographic changes, and level of serum immunoglobulins. The central propensity to Pseudomonas colonization in patients with CF is not freely understood, but we discuss the acquisition and persistence of P aeruginosa in the CF airway. Elucidation of pathogenetic mechanisms of CF inflammatory airways disease is the first essential step to initiating novel therapies. It has been difficult to prove that the ability of P aeruginosa to adhere to the respiratory epithelium and provide selective advantage for this gram-negative bacillus over other potential pathogens for infection in the CF airway. However, flexible filaments (pili) extending from the Pseudomonas cell wall are thought to medicate epithelial cell adherence for nonmucoid P aeruginosa, and similarly, the gelatinous exopolysaccharide alginate produced by mucoid variants of P aeruginosa seems to be the adhesive to tracheal cells. Following the signal event of adherence, this bacterial pathogen competes successfully for iron cofactor and multiplies, releasing proteases with broad substrate specificities that dramatically alter the airway antiprotease screen, and the pathogen creates defects in local antibacterial defenses. Lung inflammation in CF is characterized by massive neutrophil infiltration. Although critical to host defense, neutrophils also cause progressive airway damage by release of bioactive lipids, oxygen metabolites, and granule enzymes such as hydrolases, myeloperoxidase (MPO), lysozyme, and neutral serine proteases. The necessarily circumscribed discussion that follows will focus narrowly on the host cell-derived factors (macrophages and neutrophils) proposed as important components in this pathogenetic scheme.
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PMID:Emergence and persistence of Pseudomonas aeruginosa in the cystic fibrosis airway. 147 41

An enzyme-linked immunosorbent assay system was developed and used to study adhesion of Pseudomonas aeruginosa to human epithelial cells and the abilities of specific antibodies to inhibit this process. Human buccal epithelial cells coated onto microtiter plates were incubated with P. aeruginosa suspensions, and adherent bacteria were detected by using anti-P. aeruginosa serum and a horseradish peroxidase-conjugated secondary antiserum. Adhesion, quantitated as an increase in A405, varied linearly with increasing numbers of bacterial CFU added per well in the range of 10(5) to 10(8) CFU per well. Adhesion of P. aeruginosa increased following trypsinization of buccal epithelial cells. Preincubation of bacteria with monoclonal antibodies directed against P. aeruginosa outer membrane protein H2 inhibited adhesion with all eight of the isolates tested. Preincubation of P. aeruginosa with sera from infected cystic fibrosis patients also resulted in inhibition of adhesion in the enzyme-linked immunosorbent assay system. This inhibitory activity was shown to be due to two factors: P. aeruginosa-specific immunoglobulin G and a non-immunoglobulin G serum component. These data support the hypothesis that bacterial components other than pili are involved in adhesion and suggest that anti-P. aeruginosa antibodies may be of use in preventing adhesion and subsequent colonization with P. aeruginosa.
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PMID:Characterization of antibody-mediated inhibition of Pseudomonas aeruginosa adhesion to epithelial cells. 163 1

From preclimacteric women (n = 10, 45-50 years of age) with gross cystic breast disease, levels of beta-endorphin, estradiol, progesterone, luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, cortisol and prolactin were assayed radiochemically in the breast cyst fluid and in plasma. The beta-endorphin concentration (fmol/ml) was increased more than fourfold in the breast cyst fluid (17.6 +/- 4.6 SEM) than in plasma (4.2 +/- 0.5 SEM). In the breast cyst fluid, estradiol was increased 41-fold (1738.2 +/- 350.5 SEM pg/ml), and progesterone 47-fold (65.47 +/- 8.25 SEM ng/ml) more than in plasma. The significantly increased values of beta-endorphin, estradiol and progesterone in the breast cyst fluid and the identification of beta-endorphin in cyst-lining epithelia demonstrate the local synthesis. Growth factor-like properties of beta-endorphin and estradiol are accountable for the propagation of cystic changes. The autonomic formation and function of beta-endorphin, estradiol and progesterone in cyst compartments can not be related with the levels of luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone and cortisol, which were significantly higher in plasma than in the breast cyst fluid. In the breast cyst fluid, prolactin could not detected to be significantly higher than in plasma. In addition the plasma-concentration of testosterone, androstenedione, thyroxin, triiodothyronine, thyroid-binding globulin, sexual-hormone-binding-globulin could be detected within the normal range. In this study we could demonstrate the synergism of beta-endorphin, steroid hormones and peptide hormones which advance the growth of gross cystic disease of preclimacteric women. Beta-endorphin was also examined by immunocytochemical assays (fluorescence, alkaline phosphatase and horseradish peroxidase method), in 11 women with pure fibrocystic disease, in 7 women with fibrocystic disease combined with a carcinoma in situ and in 15 women with fibrocystic disease combined with invasive carcinoma of the breast. Sections of frozen and paraffin embedded tissue of the same patient were reacted with anti-beta-endorphin antiserum. The immunoreactivity of beta-endorphin was intense in normal, proliferative altered and cyst-lining epithelia of fibrocystic disease and decreased in atypical epithelia and carcinoma cells of the breast. The degree of beta-endorphin staining is related to the degree of cell differentiation. In addition, nuclear receptors for estrogen and progesterone were assayed by peroxidase antiperoxidase technique.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Interaction between beta-endorphin, steroids and peptide hormones in fibrocystic lesions of the female breast]. 164 46

Analysis of Aspergillus fumigatus water soluble fractions by electrophoresis on non-denaturing polyacrylamide gels (PAGE) showed the presence of at least three catalase bands. They were designated F, S1 and S2 in order of descending electrophoretic mobility with respect to the anode. The multiple enzyme forms appear to be distinct in their physicochemical properties. Enzyme bands S1 and S2 were simple catalases; the F band had an additional peroxidase function. All of the components were antigenic and differed in their binding to specific antibodies raised in rabbits with separate fractions of A. fumigatus mycelium. When serum from patients with aspergilloma, allergic bronchopulmonary aspergillosis, cystic fibrosis and chronic asthma were pre-incubated with A. fumigatus antigens and analysed by PAGE, 17 of 26 samples either abolished or reduced catalase activity. Enzyme F was a non-Concanavalin A (ConA)-binding antigen; the S1 and S2 enzymes were ConA-binding glycoprotein antigens. The major catalase band present in A. niger preparations represented only a minor component in A. fumigatus.
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PMID:Analysis of Aspergillus fumigatus catalases possessing antigenic activity. 173 Oct 61

Abnormal fucosylation of cystic fibrosis mucin was previously shown using peroxidase conjugated lectins on ileal tissue sections. These abnormally fucosylated glycoproteins were investigated further using monoclonal antibodies to fucosyl oligosaccharides based on type 1 and type 2 blood group precursor chains. The results of this study, using monoclonal antibodies to blood group glycoproteins in cystic fibrosis, were negative, yet abnormal fucosylation had been found using lectin histochemistry. Using monoclonal antibodies, lectins, and appropriate enzymes, such as glycosyl hydrolases, it should be possible to delineate further the abnormality found in glycoproteins in cystic fibrosis on appropriately fixed ileal sections, obtained from infants at term presenting with meconium ileus.
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PMID:Abnormal fucosylation of-ileal mucus in cystic fibrosis: II. A histochemical study using monoclonal antibodies to fucosyl oligosaccharides. 226 74

In serum and sputum samples from 15 patients with cystic fibrosis (CF) suffering from chronic Pseudomonas aeruginosa lung infections, concentrations and/or activities of elastase derived from polymorphonuclear leukocytes (PMN), cathepsin G, myeloperoxidase (MPO), and superoxide dismutase (SOD), as well as concentrations of the proteinase inhibitors alpha 1-proteinase inhibitor (alpha 1-PI) and alpha 2-macroglobulin (alpha 2-M), were determined. High enzyme concentrations compared with those in normal control subjects were found for PMN elastase (mean, 96.1 +/- 91.7 micrograms/ml), cathepsin G (mean, 5.9 +/- 6.0 micrograms/ml), and MPO (mean, 138.0 +/- 177 micrograms/ml) in patients' sputum samples. Superoxide dismutase was not detectable in any of the sputum specimens (below 1 ng/ml). Proteinase inhibitor concentrations were elevated in serum samples (alpha 1-PI: mean, 3,457 +/- 1,084 micrograms/ml; alpha 2-M: mean, 4,835 +/- 1,334 micrograms/ml). Means of 61 +/- 38 micrograms/ml alpha 1-PI and 29 +/- 31 micrograms/ml alpha 2-M were present in the sputum specimens. Both proteinase inhibitors were functional in the serum samples. However, sputum alpha 1-PI was proteolytically degraded, as shown by western blot technique, and was not able to bind 125I-labeled PMN elastase, as shown by autoradiography. Only 10.9 +/- 8.5% of the total alpha 1-PI in the sputum samples was complexed to PMN elastase and 3.6 +/- 3.2% to cathepsin G. On the other hand, 96.2 +/- 96.8% of the total PMN elastase and 78.0 +/- 100% of cathepsin G were unbound in the sputum samples. The study suggests that the imbalance between PMN proteinases and their inhibitors is due to inactivation of alpha 1-PI in the sputum caused by proteolytic or oxidative attack from PMN enzymes.
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PMID:Lysosomal enzymes from polymorphonuclear leukocytes and proteinase inhibitors in patients with cystic fibrosis. 242 73

The peroxidase-antiperoxidase histochemical method of staining for tissue carcinoembryonic antigen (CEA) was performed on 20 samples of malignant breast tissue, 20 samples of fibroadenomatous breast tissue, and 15 samples of breast tissue that variably contained minimal fibrosis (N = 7), ductal ectasia (N = 5), and sclerosing adenosis (N = 3; the fibrocystic changes of the breast). The intensity of staining was described to be either negative, weak, intermediate, or strong and was assigned a point value of 1, 2, 3, or 4, respectively. The following weighted average values of tissue CEA were obtained: carcinoma, 3.35 +/- 0.88; fibroadenomas, 2.85 +/- 0.67; fibrocystic changes, 2.13 +/- 0.52. Carcinomatous tissue is likely (55%) to display intense tissue staining, whereas fibrocystic disease (0%) or fibroadenoma (15%) are unlikely to exhibit such a reaction. The tissue CEA content between carcinoma and fibrocystic changes (P less than 0.01), carcinoma and fibroadenoma (P less than 0.01), and fibroadenoma and fibrocystic changes (P less than 0.05) are statistically significant.
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PMID:Tissue carcinoembryonic antigen levels in benign and malignant diseases of the breast. 246 56


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