UMLS:C0432222 - FACTA Search

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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

Intact single twitch fibers from frog muscle were stretched to long sarcomere length, micro-injected with the pH indicator dye phenol red, and activated by action potential stimulation. Indicator-related absorbance changes (denoted by delta A0 and delta A90) were measured with 0 degree and 90 degrees polarized light (oriented, respectively, parallel and perpendicular to the fiber axis). Two components of delta A were detected that had generally similar time courses. The "isotropic" component, calculated as the weighted average (delta A0 + 2 delta A90)/3, had the wavelength dependence expected for a change in myoplasmic pH. If calibrated in pH units, this signal's peak amplitude, which occurred 15-20 ms after stimulation, corresponded to a myoplasmic alkalization of average value 0.0025 +/- 0.0002 (+/- SEM; n = 9). The time course of this change, as judged from a comparison with that of the fibers' intrinsic birefringence signal, was delayed slightly with respect to that of the myoplasmic free [Ca2+] transient. On average, the times to half-peak and peak of the phenol red isotropic signal lagged those of the birefringence signal by 2.4 +/- 0.2 ms (+/- SEM; n = 8) and 8.4 +/- 0.5 ms (+/- SEM; n = 4), respectively. The other component of the phenol red signal was "dichroic," i.e., detected as a difference (delta A0-delta A90 greater than 0) between the two polarized absorbance changes. The wavelength dependence of this signal was similar to that of the phenol red resting dichroic signal (Baylor and Hollingworth. 1990. J. Gen. Physiol. 96:449-471). Because of the presence of the active dichroic signal, and because approximately 80% of the phenol red molecules appear to be bound in the resting state to either soluble or structural sites, the possibility exists that myoplasmic events other than a change in pH underlie the phenol red isotropic signal.
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PMID:Changes in phenol red absorbance in response to electrical stimulation of frog skeletal muscle fibers. 223 Jul 9

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

Propofol, a phenol compound with a short elimination half-life, was compared with thiopental and isoflurane for induction and maintenance of general anesthesia in 60 consenting ASA I, II, and III patients. The study was randomized and open label in design. Hemodynamically, the propofol patients showed a mean +/- SEM decrease in systolic blood pressure in comparison with the thiopental/isoflurane group at 2 (115.1 +/- 4.9 vs. 136.6 +/- 6.0 mmHg), 3 (125.7 +/- 5.1 vs. 149.4 +/- 5.6 mmHg), and 5 min (126.6 +/- 3.8 vs. 144.4 +/- 6.1 mmHg) postinduction and at intubation (135.2 +/- 4.7 vs. 157.8 +/- 6.0 mmHg) (p less than 0.05). The heart rate was lower in the propofol group throughout the induction period (p less than 0.05). Patients who received propofol were ready for discharge from the recovery room sooner (67.9 +/- 4.0 vs. 80.0 +/- 3.6 min) than the thiopental/isoflurane-treated patients (p less than 0.05). Propofol is as safe and effective for induction and maintenance of general anesthesia as thiopental and isoflurane.
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PMID:Comparison of propofol with thiopental and isoflurane for induction and maintenance of general anesthesia. 269 40

Granulocyte-macrophage colony-stimulating factor (GM-CSF) was shown to modulate different granulocyte functions. In the present study we investigated the effect of purified and recombinant human GM-CSF, particularly on the oxidative metabolism of isolated human granulocytes. In addition, ultrastructural changes upon stimulation were evaluated. For detection of granulocyte activation the following 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, and 6) scanning and transmission electron microscopy (SEM and TEM, respectively). A significant CL response was seen upon stimulation with recombinant human GM-CSF at concentrations ranging from 1 to 10(3) U/ml. The CL response started within 5-10 min with a maximum at 60-90 min and lasted more than 3 h. Thereafter granulocytes were completely deactivated to restimulation with the same mediator and with Tumor Necrosis Factor, but responded to other triggers of the oxidative burst, whereas the response to f-met-leu-phe was significantly increased. The CL signal was completely blocked by an antiserum to GM-CSF. Moreover, the response was significantly inhibited by SOD and D-Mannitol, suggesting the involvement of distinct reactive oxygen species (ROS) in generating the CL response. Significant amounts of superoxide were detected within 180 min after stimulation with GM-CSF, whereas release of hydrogen peroxide and peroxidase were only minimal as shown by functional and ultrastructural assays. Activation of granulocytes could be visualized by SEM and TEM. GM-CSF stimulated cells showed an increased adherence to the substratum developing polarized filopodia and an increased number of intracellular vesicles within 30 min after addition of the stimulus. The results clearly demonstrate that GM-CSF directly stimulates granulocytes and, particularly, their oxidative metabolism. Therefore, GM-CSF which is probably released by epidermal cells appears to be a candidate for neutrophil activation in the skin, and thereby may play a crucial role in inflammatory skin diseases.
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PMID:Human granulocyte-macrophage colony stimulating factor: an effective direct activator of human polymorphonuclear neutrophilic granulocytes. 283 54

As shown previously monocytes upon stimulation with bacterial lipopolysaccharides (LPS) release granulocyte-activating mediator(s) (M-GRAM) which induced a long-lasting chemiluminescence (CL) response in human granulocytes. M-GRAM could be separated from interleukin-1 alpha and beta, interleukin-2, interferon alpha and gamma, granulocyte colony stimulating factor (G-CSF) and macrophage colony stimulating factor (M-CSF), since these cytokines are shown to be unable to induce a significant CL response. In contrast, granulocyte macrophage colony stimulating factor (GM-CSF) and particularly tumor necrosis factor (TNF) are important triggers of the oxidative burst and they are capable of inducing a CL response. TNF activity but not lymphotoxin (LT) activity could be demonstrated in M-GRAM samples. A polyclonal rabbit IgG as well as a monoclonal antibody to recombinant human TNF which neutralized the TNF activity in M-GRAM preparations did not substantially block the CL signal. Furthermore, M-GRAM-induced CL response was not significantly inhibited by a polyclonal calf antiserum to human recombinant GM-CSF. For further functional characterization of M-GRAM-induced granulocyte activation different assays were performed in order to compare GM-CSF and TNF: (a) SOD-inhibitable cytochrome C-reduction (.O2-); (b) horseradish peroxidase-mediated oxidation of phenol red (H2O2); (c) the release of peroxidase; (d) ultrastructural detection of hydrogen peroxide production; and (e) scanning and transmission electron microscopy (SEM and TEM). Significant release of .O2- was induced by M-GRAM, TNF, and GM-CSF, whereas H2O2 production was significantly stimulated only by M-GRAM and TNF, as shown by functional and ultrastructural assays.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Granulocyte-activating mediators (GRAM): III. Further functional characterization of monocyte-derived GRAM. 284 61

The mechanism of the genotoxicity and metabolism of benzene (BZ) was investigated by using a free-radical scavenger, dimethyl sulfoxide (DMSO), to investigate the free radical mechanism in BZ metabolism. The presence of chromosomal breakage expressed as micronuclei (MN) in bone marrow polychromatic erythrocytes (PCE) and the presence of several BZ metabolites in the urine were monitored. Adult male ICR mice were exposed orally to DMSO after oral exposure to BZ (440 mg/kg b.w.). DMSO was administered either in different concentrations (1.25, 3.75 or 12.5% given at a volume of 0.01 ml/gm b.w.) or at different intervals after BZ exposure (1, 3 or 5 h). Each group consisted of five mice. It was found that the BZ-induced MN frequency was reduced by DMSO from 48.8 +/- 5.6 (SEM) to 2.6 +/- 0.7 per 1000 PCE when DMSO (12.5%) was administered at 1 h after BZ exposure (P less than 0.01), to 3.4 +/- 0.8 at 3 h (P less than 0.01) and to 36.2 +/- 12.1 at 5 h (P less than 0.01). The reduction of the clastogenic effect of BZ by DMSO was also dependent upon the DMSO doses. The MN frequency was significantly reduced from 48.8 +/- 5.6 to 29.4 +/- 10.9 with 1.25% DMSO (P less than 0.01) to 20 +/- 7.6 with 3.75% (P less than 0.01) and to 2.6 +/- 0.7 with 12.5% DMSO (P less than 0.01). The presence of different metabolites of BZ such as hydroquinone, catechol, trans-trans muconic acid (MA, the oxidized form of trans-trans muconaldehyde, ttM), and total and conjugated phenol was evaluated in the urine of the exposed mice using HPLC. Among these metabolites, the quantity of MA was found to have the closest positive correlation with the MN frequency (P less than 0.007). Phenol but not the other monitored metabolites was also positively correlated with MN frequency (P less than 0.03). Thus, our data show that the formation of genotoxic metabolites from BZ probably involves hydroxyl radicals and ttM as well as phenol are likely to be responsible for the clastogenic effect of benzene in vivo.
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PMID:Effect of dimethyl sulfoxide on the genotoxicity and metabolism of benzene in vivo. 292 92

Circulating phenolsulfotransferase M and P and monoamine oxidase activities were determined in 18 untreated essential hypertensive patients and in 35 normotensive healthy controls. Phenolsulfotransferase M is involved in the sulfoconjugation of catecholamines and their metabolites while PST P preferentially sulfates phenolic substrates. After lysis of whole blood, enzymatic activities were determined by radioenzymatic techniques using as substrates 3-methoxy-4-phenoxyphenylglycol for PST M, phenol for PST P and [14C] beta-phenylethylamine for MAO. Blood MAO activity measured by this method is fully accounted for by platelet MAO-B activity. Concerning blood PST activities, no significant difference was found in hypertensive patients compared to normotensive controls (PST M: 1.69 +/- 0.17 versus 1.66 +/- 0.08 nmoles of MHPG-sulfate/ml of blood/hour; PST P: 0.36 +/- 0.05 versus 0.27 +/- 0.04 nmoles of phenol-sulfate/ml of blood/hour). MAO activity was higher in women than in men. Significantly lower MAO B activities were observed in hypertensive patients both in men (19.25 +/- 2.20, n = 8 versus 24.35 +/- 2.22, n = 14, desaminated beta-phenyl-ethylamine/10(9) platelets/hour, x +/- SEM, p less than 0.05) and in women (23.92 +/- 2.74, n = 10 versus 35.76 +/- 2.35, n = 21, p less than 0.01) when compared to normotensive controls of the same sex. Recent in vitro studies have suggested that a reduction in platelet MAO B activity may be induced by an alteration in the phospholipidic and/or calcium environment of the enzyme. Low MAO activity in other tissues such as liver or vascular endothelium could contribute to the high sympathetic tone observed in these patients.
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PMID:[Blood phenolsulfotransferase and monoamine oxidase-B activity in essential arterial hypertension]. 311 77

A survey was carried out in a steel foundry in Brisbane to evaluate the nature and frequency of respiratory symptoms and to assess ventilatory function. The foundry used many moulding processes including the Furane, Isocure, Shell, carbon dioxide, and oil sand systems. Nasal symptoms and wheeze were often reported, particularly by workers in the general foundry and core shop, and on a semiautomated line. By contrast, workers in the aftercast section not exposed to fumes or vapours from the various moulding processes reported these symptoms less often. Of 46 workers exposed to moulding fumes and vapours, 11 had developed a wheeze while working at the foundry. Wheeze and other respiratory tract symptoms were often attributed by the workers to exposure to substances at work, particularly from the Shell process which uses phenol formaldehyde resin and hexamethylenetetramine. Symptoms were reported also, but less often, on exposure to materials used in the Furane process (urea formaldehyde and furfuryl alcohol) and the Isocure process (methylene diphenyl diisocyanate, phenol formaldehyde, and dimethylethylamine). Ventilatory function studied over Monday and Friday showed a small and inconsistent changes. The six subjects working on the semiautomated line showed a small decrease in FEV1 (+/- SEM) (208 +/- 70 ml) only on Monday; this differed significantly from that in 17 aftercast workers (9 +/- 50 ml, p less than 0.05). Ventilatory function recorded before work on Monday morning showed no evidence of chronic airway obstruction in any group. Most environmental measurements were below the threshold limit values (TLV) except in the general foundry, where furfuryl alcohol was detected at concentrations of up to 50 ppm and formaldehyde at 4 ppm. The onset of symptoms in relation to exposure to various fumes and vapours suggests that both irritant and hypersensitivity mechanisms are present. As environmental modifications had occurred recently the apparent hypersensitivity may relate to past exposure levels above the TLV.
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PMID:Respiratory disease in foundry workers. 397 Aug 67

The effects of severe hypoxemia on gastrointestinal (GI) blood flow and gastric emptying were studied in nine 2- to 4-day-old piglets which were mechanically ventilated while receiving nitrous oxide anesthesia. Each animal was studied during a control period of oxygenation (PaO2 91 +/- 8 torr), 35 min of hypoxemia (PaO2 29 +/- 1 torr), and a recovery period (PaO2 90 +/- 5 torr) (mean +/- SEM). During each study period, the animal received a 10% dextrose test meal with phenol red marker (22 ml/kg), gastric residual volumes were determined at 10-min intervals over 30-min study periods using a dye dilution double sampling technique, and GI blood flow (radionuclide-labeled microspheres), O2 delivery, O2 extraction, and O2 consumption were measured at the end of the 30-min period. Hypoxemia resulted in decreased blood flow to the following GI organs: stomach, jejunal and ileal mucosa-submucosa, and colon decreased 62, 31, and 35%, respectively (p less than 0.05). Jejunal and ileal muscularis blood flow remained unchanged. Oxygen delivery and consumption by GI tract decreased 79 and 58%, respectively; whereas oxygen extraction of GI tract increased 115%. Values returned toward baseline levels during the recovery period. The hypoxemic gastric emptying pattern showed significantly greater gastric residuals at 20 min compared to the 10-min value (p less than 0.05). This pattern was different than that observed during control and recovery periods. We conclude that severe hypoxemia results in decreased GI blood flow, tissue oxygenation, and an altered gastric emptying pattern. These observations may have clinical significance for feeding infants following an hypoxemic episode.
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PMID:Effects of hypoxemia on gastrointestinal blood flow and gastric emptying in the newborn piglet. 400 Jul 73

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