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)

Lactose-intolerant children manifest diminished or nonexistent intestinal lactase activity, resulting in flatulence, abdominal pain, and diarrhea. To assess the hydrolytic capability of lactase-containing tablets taken immediately before oral lactose challenge, we studied 18 children previously identified as being lactose intolerant and having no underlying organic gastrointestinal disease. Subjects had a mean (+/- SEM) age of 11.4 +/- 3.4 years; 72% were male. At time of the study, lactase-containing tablets or placebo tablets were ingested (double-blind) immediately before drinking a solution of lactose. Breath samples were obtained for hydrogen analysis at 30-minute intervals during a 2-hour period, and clinical symptoms were monitored. In lactose-intolerant patients, hydrogen production was significantly greater following placebo (maximum hydrogen excretion, approximately 60 ppm) compared with lactase-containing tablets (maximum hydrogen excretion, 7 ppm). Increased hydrogen production was associated with clinical symptoms including abdominal pain (89% of subjects following placebo ingestion), bloating (83%), diarrhea (61%), and flatulence (44%). These results indicate, therefore, that coingestion of lactose and lactase-containing tablets significantly reduces both breath hydrogen excretion and clinical symptoms associated with lactose intolerance.
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PMID:Beta-galactosidase tablets in the treatment of lactose intolerance in pediatrics. 212 19

To predict the presence and thickness of the acid-proof dentin layer by the method of combining the halogenated methacrylate and electron-probe microanalyzer (EPMA), 2-methacryloyloxyethyl hydrogen chloromaleate (CIMEM) used as a base monomer for a bonding agent and 2-bromoethyl methacrylate (2 BEM), 2-(4-bromophenyl)ethyl methacrylate (BPy1EM), 2-(4-bromo-1-naphthyl)ethyl methacrylate (BNEM) and 2,4,6-tribromophenoxy methacrylate (TriBr-PM) used as tracers were synthesized. The bond strength to dentin treated with 37% phosphoric acid solution for 30 sec. was not statistically different for the bonding agents with and without tracers. The SEM micrographs revealed that the layers, which may be acid-proof dentin layers, were 3-4 microns thick at the resin-dentin interface for all bonding agents. According to EPMA analysis, cps of C1Ka and BrLa increase at the same points and the acid-proof dentin layer thickness was about 4 microns.
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PMID:[Electron-probe microanalysis examination of acid-proof dentin layer]. 213 37

In a previous study, we reported that fragment Bb of bovine complement factor B activated bovine monocytes, as demonstrated by the uptake of 3H-deoxyglucose. In the present study, the effects of Bb on the production of superoxide anion and hydrogen peroxide by bovine monocytes was investigated. The production of superoxide was measured by the superoxide dismutase inhibitable reduction of cytochrome c. The change in absorbance was determined by a spectrophotometer at a wavelength of 550 nm. Hydrogen peroxide production was measured by the horse-radish peroxidase-dependent oxidation of phenol red. The resulting color change was measured by a spectrophotometer at a wavelength of 620 nm. Fragment Bb (20 micrograms/mL) induced the generation of 0.96 +/- 0.2 (mean +/- SEM) nanomoles of superoxide/2.5 x 10(5) monocytes at 5 min. The production of superoxide peaked at 15 min (1.24 +/- 0.3 nanomoles). The production of hydrogen peroxide was also rapid: 0.195 +/- 0.05 nanomoles/2.5 x 10(5) monocytes at 5 min with a peak at 15 min (0.250 +/- 0.04 nanomoles). These observations show that fragment Bb, which has serine protease activity, induces bovine monocytes to generate reactive oxygen intermediates such as superoxide and hydrogen peroxide.
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PMID:Bb fragment of bovine complement factor B: stimulation of the oxidative burst in bovine monocytes. 217 93

An enzyme immunoassay (EIA) was developed using unlabelled and peroxidase-labelled rabbit antibodies to assess urinary rat beta 2-microglobulin (beta 2-m) excretion. It consisted in the adsorption of rabbit anti-rat beta 2-m immunoglobulin to a polystyrene surface, the addition of beta 2-m samples or standard and the addition of peroxidase-labelled rabbit anti-rat beta 2-m immunoglobulin. After addition of hydrogen peroxide and o-phenylenediamine, the enzyme activity of the solid phase was measured photometrically at 490 nm. Analytical recovery of pure beta 2-m in urine was 102%. From determinations made on normal female and male rats, the ranges of 24-h urine beta 2-m individually excreted were found to be 0.84-4.77 and 3.7-17.3 micrograms, respectively. The means +/- SEM were 2.49 +/- 0.17 and 10.2 +/- 0.55 micrograms. EIA was of value in evidencing the tubule-damaging properties of sodium chromate and hexachloro-1,3-butadiene in rats.
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PMID:Assessment of urinary rat beta 2-microglobulin by enzyme immunoassay. 220 81

Methotrexate appears to be an effective alternative to corticosteroid therapy for some patients with sarcoidosis. The mechanism of action of methotrexate as an immunosuppressive is unknown. Patients with symptomatic pulmonary sarcoidosis underwent pulmonary function tests and bronchoscopy with bronchoalveolar lavage. Patients were treated with 10 mg methotrexate or prednisone weekly for at least 6 months and repeat studies were performed. A comparison was made between those patients receiving methotrexate (12 patients) and those receiving prednisone (12 patients). For both groups, there was a significant improvement in the vital capacity with therapy (Prednisone: Pre = 2.5 +/- 0.14 L (Mean +/- SEM); Post = 3.1 +/- 0.18 L, p less than 0.01; Methotrexate: Pre = 2.4 +/- 0.14 L; Post = 2.8 +/- 0.18 L, p less than 0.01). In addition, the percentage of lymphocytes in the lavage fell significantly for both the prednisone (Pre: 30 +/- 3.5%; Post: 16 +/- 2.7%, p less than 0.001) and methotrexate (Pre: 37 +/- 3.4%; Post: 13 +/- 2.9%, p less than 0.001) groups. Alveolar macrophages from the symptomatic sarcoid patients were found to be spontaneously releasing hydrogen peroxide and tumor necrosis factor. After treatment with either prednisone or methotrexate, alveolar macrophages retrieved by lavage spontaneously released less of either macrophage product. We found that effective doses of methotrexate for sarcoidosis led to significant changes in lymphocyte and macrophages retrieved by lavage.
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PMID:The effect of corticosteroid or methotrexate therapy on lung lymphocytes and macrophages in sarcoidosis. 225 43

Disturbances of gastrointestinal motility are a common feature of diabetes mellitus and are usually ascribed to autonomic neuropathy. In order to assess the role of other factors on changes in motility in diabetes we have studied the stomach to caecum transit time (SCTT) during the progression of streptozotocin induced diabetes in the rat. Rats were used one, two, four, and eight weeks after a single injection of streptozotocin and age matched animals were used as controls. In further experiments non-diabetic rats received a bolus injection of pancreatic glucagon (50 or 75 micrograms intraperitoneally) or its diluent. SCTT was estimated using the non-invasive hydrogen excretion method. SCTT was unaffected by the age of the animal (mean (SEM) value: 101 (5) min), but was significantly delayed at one week (139 (11) min, p less than 0.01), two weeks (163 (16) min, p less than 0.01), four weeks (148 (9) min, p less than 0.01), and eight weeks (171 (13) min, p less than 0.01) after streptozotocin. SCTT was also slower during hyperglucagonaemia (control 96 (6) min; glucagon treated 50 micrograms: 120 (7) min, p less than 0.05 and 75 micrograms: 127 (8), p less than 0.05). Since autonomic neuropathy is not a recognised feature of the initial stages of diabetes hyperglucagonaemia may be responsible, at least in part, for diabetes induced changes in gastrointestinal motility.
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PMID:Delayed stomach to caecum transit time in the diabetic rat. Possible role of hyperglucagonaemia. 237 69

Alveolar macrophages (AM) were retrieved by bronchoalveolar lavage from 20 patients. Following AM purification by glass adherence, the effect of bleomycin on hydrogen peroxide and lactic dehydrogenase release was assessed by colorimetric methods. All AM from nine nonsmokers had no detectable spontaneous release of hydrogen peroxide. The AM did not release hydrogen peroxide when stimulated with bleomycin (25 mU/mL). AM from all eleven smokers spontaneously released hydrogen peroxide (36 +/- 5.3 nm/10(6) AM, mean +/- SEM). AM from eight of the eleven smokers released more hydrogen peroxide when incubated with bleomycin (smokers 55 +/- 6.8 nm/10(6) AM, p less than 0.05). There was no difference in the amount of lactic dehydrogenase released by AM spontaneously or when incubated with bleomycin at 25 mU/mL, suggesting that this dose of bleomycin was not directly toxic to the AM. Results from this study further support the premise that bleomycin pulmonary toxicity may result from the generation of reactive oxygen metabolites and that cigarette smoking may predispose to bleomycin pulmonary toxicity.
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PMID:Bleomycin causes alveolar macrophages from cigarette smokers to release hydrogen peroxide. 245 24

We investigated: (1) the capacity to digest and tolerate the lactose administered by continuous infusion of intact milk to undernourished tube-fed patients, and (2) the effectiveness of lactose-prehydrolyzed milk, and of the addition of exogenous lactase to milk at infusion time, to reduce lactose maldigestion and increase clinical tolerance. Carbohydrate digestion was evaluated in 10 subjects with the hydrogen breath analysis test during 8 hr of observation. Lactose intolerance was determined by evaluation of subject's symptoms. With the infusion of intact milk (IM), none of the subjects were able to efficiently digest the lactose infused (5.6 +/- 0.35 g/hr, mean +/- SEM) and 86% of them experienced major symptoms of intolerance. With the infusion of lactose-prehydrolyzed milk (HM) and enzyme-added milk (EM) there was a highly significant reduction in lactose maldigestion. More importantly, major symptoms were present in only 10% of subjects with EM, and were completely eliminated with HM. Lactose maldigestion and intolerance represent a major limitation for the application of milk-based polymeric formula for liquid diets in undernourished subjects. The use of exogenous beta-galactosidases represents an alternative to avoid such reactions.
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PMID:Lactose digestion and clinical tolerance to milk, lactose-prehydrolyzed milk and enzyme-added milk: a study in undernourished continuously enteral-fed patients. 249 46

Besides their cytotoxic effects, Tumor necrosis factor (TNF) and Lymphotoxin (LT) were shown to modulate distinct PMN functions. Therefore, in the present study we evaluated the effect of recombinant human TNF and LT on the oxidative metabolism of isolated human PMN. In addition ultrastructural changes upon stimulation were evaluated. For detection of granulocyte activation different assay systems were used: 1) lucigenin-dependent chemiluminescence (CL), 2) superoxide-dismutase (SOD) inhibitable cytochrome C-reduction (superoxide), 3) horseradish peroxidase-mediated oxidation of phenol red (hydrogen peroxide), 4) release of myeloperoxidase, 5) ultrastructural detection of hydrogen peroxide-production, 6) scanning and transmission electron microscopy (SEM and TEM). TNF at concentrations as low as 10(-3) U/ml induced a distinct CL response, whereas LT appeared to be less active. PMN preincubated with TNF or LT for 150 min were completely deactivated to renewed stimulation with TNF, LT, and with GM-CSF, but responded to other triggers of the oxidative burst. Moreover, stimulation with f-met-leu-phe resulted in an enhanced response after preincubation with TNF or LT. The CL response was significantly inhibited by SOD, but not by catalase, D-mannitol, and DMTU, suggesting that mainly .O2- is responsible for the CL signal. The effect on PMN could be completely blocked by antibodies to TNF. Significant release of reactive oxygen species upon stimulation with TNF was also demonstrated by cytochrome C reduction and by detection of H2O2 using functional and ultrastructural assays. Only minimal amounts of peroxidase were released. Activation of PMN could be visualized by SEM and TEM. After addition of TNF at concentrations as low as 10(-1) U/ml PMN adhered to the substratum and were typically polarized within 15 min. Stimulation with LT resulted in comparable results, but based on its biologic activity in the cytotoxicity assay LT, in comparison to TNF, was significantly less active. Based on the data presented LT and, particularly, TNF appear to be potent activators of PMN oxidative metabolism.
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PMID:Human tumor necrosis factor is a potent activator of the oxidative metabolism in human polymorphonuclear neutrophilic granulocytes: comparison with human lymphotoxin. 253 65

Oxygen free radicals and Ca2+ overload have been implicated in the genesis of reperfusion induced arrhythmia and injury. Effects of hydrogen peroxide (H2O2) on action potentials and intracellular Ca2+ concentration ([Ca2+]i) were studied using guinea pig papillary muscles and ventricular myocytes. High concentration of H2O2 (10 mmol.litre-1) caused delayed afterdepolarisations in all six papillary muscles, and induced triggered activity in 3/6 preparations. Pretreatment with ryanodine (1 mumol.litre-1) abolished delayed afterdepolarisations and triggered activity induced by H2O2. [Ca2+]i and morphological changes in isolated ventricular myocytes of guinea pig were measured using fura-2. Quiescent and rod shaped myocytes became shortened and rounded (contracture) after the application of 0.1 and 1 mmol.litre-1 H2O2. [Ca2+]i increased from the control values of 53 (SEM 4) and 62(8) nmol.litre-1 to 110(29) and 105(24) nmol.litre-1 (p less than 0.05 v control) when cells were shortened during perfusion with 0.1 and 1 mmol.litre-1 H2O2, respectively. The values were 130(26) nmol.litre-1 (p less than 0.05 v control) and 100(18) nmol.litre-1 (p less than 0.05 v control) when the cells became rounded during perfusion with 0.1 and 1 mmol.litre-1 H2O2. We suggest that the arrhythmia caused by Ca2+ overload was induced by H2O2, possibly by lipid peroxidation of cell membrane. H2O2 was also shown to shorten cells and cause cell contracture (rounding). The mechanism of cell injury is not likely to be due to the Ca2+ overload, since the increase in [Ca2+]i during perfusion with H2O2 was not large.
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PMID:Effects of hydrogen peroxide on action potentials and intracellular Ca2+ concentration of guinea pig heart. 261 15


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