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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objectives of this study were to investigate the torsional bond strength of ceramic brackets bonded to composite resin veneer laminates and to human enamel. Microfilled resin veneers were bonded directly to prepared, etched bovine teeth embedded in epoxy resin. Brackets [Allure IV (NSB), Fascination, Starfire TMB, and Transcend 2000] were bonded to abraded, acid-etched resin veneers with a light-cured or a chemically-cured adhesive. Brackets were also bonded to human teeth with light-cured and chemically-cured adhesives for comparison purposes. After 24 hours storage in water, specimens were subjected to torsional stress and the maximum shear stress tau max, was calculated. The debonded brackets, the veneer, and enamel surfaces were examined under a stereomicroscope and a SEM to study the failure modes. Three-way ANOVA with a Tukey multiple comparisons test revealed significant differences in bond strengths among bracket types and bonding substrate at P = 0.05 level. Highest bond strength was observed in brackets with a combination of micromechanical retention and chemical adhesion. Significant interactions among bracket, substrate (enamel or resin) and mode of cure of adhesive were observed. Analysis of the failure pattern of brackets revealed adhesive and/or cohesive resin failures in all brackets studied, while cohesive bracket failures occurred in the single-crystal Starfire TMB bracket and the polycrystalline Transcend 2000 bracket. Debonding ceramic brackets under a steady torsional load caused no substrate surface alterations regardless of adhesive used.
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PMID:Torsional bond strength and failure pattern of ceramic brackets bonded to composite resin laminate veneers. 868 71

Several new light-cured glass-ionomer materials have been developed for restorative use. It is not yet clear, however, whether the ability of the conventional glass ionomers to bond chemically to dentin has been preserved in the new light-cured glass ionomers whose chemical compositions have been modified. The fracture toughness test was recently introduced as an appropriate method of measuring the fracture resistance of an interface. We have applied this test to the glass ionomer/dentin interface for the first time. Ten mini short-rod fracture-toughness specimens were fabricated for each group. Each specimen contained a chevron-shaped glass ionomer/dentin interface along its midplane. After 24 hours in 37 degrees C water, the specimens were tested by loading at 0.5 mm/min. The interfacial Kic results (MPa X m (1/2)) (SD), analyzed by ANOVA and Fisher's LSD test (P<0.05), were: Chem-fil II, 0.17 (0.04); Vitremer, 0.18 (0.15); Fuji II LC, 0.33 (0.16). There were no significant differences in interfacial Kic between the conventional and light-cured glass ionomers. Interfacial Kic's for a light-cured glass ionomer were, however, significantly higher when an intermediary dentin bonding agent was used. SEM examinations of the fractured surfaces indicated that crack propagation generally occurred along the bond interface, and indicated the formation of a resin-infiltrated layer when the dentin bonding agents were used. It was concluded that the fracture-toughness test could be a useful measure of the integrity of the glass ionomer/dentin interface. The clinical effect of an intermediary layer between the glass ionomer and the tooth structure is, however, unknown and requires further investigation.
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PMID:Fracture toughness ov conventional or photopolymerized glass ionomer/dentin interfaces. 870 Jul 82

A prescale gel product, designed to facilitate the removal of calculus, has recently been introduced and marketed to the dental profession. The purpose of this study was to evaluate the effectiveness of this gel on the removal of subgingival calculus. 10 patients, each with 5 periodontally diseased teeth scheduled for extraction, participated in this in vivo/in vitro study. 4 teeth per patient were randomly assigned using a 2-by-2 block design and treated in vivo with either active or placebo gel, with or without scaling, prior to extraction. To assess possible overexposure to the product, 10 selected teeth from the sample were treated with active gel for an extended exposure time. Standardized scaling was performed on a 4x4 mm treated root area in vitro on groups as assigned. Quantification of residual calculus was determined by one examiner blind to treatment group assignment using SEM photomicrograph montages and the Java image analysis computer system. Repeated measures ANOVA showed no statistically significant treatment effect for gel (p > 0.05) in the scaled and no-scaled groups. The 5th group exposed to the prescale gel for an extended time was evaluated descriptively for root surface morphological changes with no noticeable effect. Based on the results of this investigation, treatment of subgingival calculus with prescale gel offers no advantage for calculus removal over scaling alone. The findings suggest no significant clinical impact of product use.
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PMID:Effectiveness of a prescale gel on subgingival calculus. 870 71

Body composition changes with increasing age in men, in that lean body mass decreases whereas fat mass increases. Whether this altered body composition is related to decreasing physical activity or to the known age-associated decrease in growth hormone secretion is uncertain. To address this question, three groups of healthy men (n = 14 in each group), matched for weight, height and body mass index, were investigated using dual-energy X-ray absorptiometry, indirect calorimetry and estimate of daily growth hormone secretion [i.e. plasma insulin-like growth factor I (IGF-I-) levels]. Group 1 comprised young untrained subjects aged 31.0 +/- 2.1 years (mean +/- SEM) taking no regular physical exercise; group 2 consisted of old untrained men aged 68.6 +/- 1.2 years; and group 3 consisted of healthy old men aged 67.4 +/- 1.2 years undergoing regular physical training for more than 10 years with a training distance of at least 30 km per week. Subjects in group 3 had for the past three years taken part in the 'Grand Prix of Berne', a 16.5-km race run at a speed of 4.7 +/- 0.6 min km-1 (most recent race). Fat mass was more than 4 kg higher in old untrained men (P < 0.01, ANOVA) than in the other groups (young untrained men, 12.0 +/- 0.9 kg; old untrained men, 16.1 +/- 1.0 kg; old trained men, 11.0 +/- 0.8 kg), whereas body fat distribution (i.e. the ratio of upper to lower body fat mass) was similar between the three groups. The lean mass of old untrained men was more than 3.5 kg lower (P < 0.02, ANOVA) than in the other two groups (young untrained men, 56.4 +/- 1.0 kg; old untrained men, 52.4 +/- 1.0 kg; old trained men, 56.0 +/- 1.0 kg), mostly because of a loss of skeletal muscle mass in the arms and legs (young untrained men, 24.0 +/- 0.5 kg; old untrained men 20.8 +/- 0.5 kg; old trained men, 23.6 +/- 0.7 kg; P < 0.01, ANOVA). Resting metabolic rate per kilogram lean mass decreased with increasing age independently of physical activity (r = -0.42, P < 0.005). Fuel metabolism was determined by indirect calorimetry at rest. Protein oxidation was similar in the three groups. Old untrained men had higher (P < 0.001) carbohydrate oxidation (young untrained men, 13.2 +/- 1.0 kcal kg-1 lean mass; old untrained men, 15.2 +/- 1.3 kcal Kg-1; old trained men, 7.8 +/- 0.8 kcal kg-1), but lower (P < 0.05, ANOVA) fat oxidation (young untrained men, 10.1 +/- 1.2 kcal kg-1 lean mass; old untrained men, 6.5 +/- 1.0 kcal kg-1; old trained men, 13.7 +/- 1.0 kcal kg-1) than the other two groups. Mean plasma IGF-I level in old trained men was higher than in old untrained men (P < 0.05), but was still lower than that observed in young untrained men (P < 0.005) (young untrained men, 236 +/- 24 ng mL-1; old untrained men, 119 +/- 13 ng mL-1; old trained men, 166 +/- 14 ng mL-1). In summary, regular physical training in older men seems to prevent the changes in body composition and fuel metabolism normally associated with ageing. Whether regular physical training in formerly untrained old subjects would result in similar changes awaits further study.
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PMID:Effect of regular physical training on age-associated alteration of body composition in men. 873 84

The ciliary beat frequency (CBF) of the tracheal epithelial cells controls in part the respiratory tract mucociliary transport efficiency. We investigated the effects on CBF of PAF-acether (PAF) and its metabolite/precursor lyso-PAF. Guinea-pig tracheal rings were incubated for 3 to 6h with 1 microM PAF (C16, C18, C16/C18: 80/20%), lyso-PAF C16 or lyso-phosphatidylcholine (LPC). CBF changes were assessed by microphotooscillography (mean number of measures per ring = 14). We also examined the effect on PAF-induced CBF changes of the PAF receptor-antagonist WEB 2086, the anti-asthmatic/anti-anaphylactic drug ketotifen and the anti-histamine H1 pyribenzamine. CBF of control rings exposed to vehicle only from 0 to 6h showed no significant statistical variations (hertz, mean +/- SEM): 10.8 +/- 0.1 (n of measures = 890). By contrast, 1 microM C16, C18, and C16/C18 PAF significantly inhibited CBF after 3 to 6h incubation. C16 and C16/C18 PAF were more potent than C18 PAF (8.8 +/- 0.2, n = 112, 8.7 +/- 0.2, n = 64, and 9.6 +/- 0.1, n = 537 respectively; ANOVA analysis, p < 0.001 from control). At the same concentration, lyso-PAF also inhibited CBF, 9.5 +/- 0.1 (n = 197, p < 0.001) but not LPC, 10.5 +/- 0.2 (n = 127). WEB 2086 inhibited lyso-PAF and C16/18 PAF-induced CBF decrease. Preincubation (20 min) with ketotifen but not with pyribenzamine (1 microM) also suppressed the CBF inhibitory effect of PAF and lyso-PAF. Incubation of [3H]PAF with tracheal rings from 10 min to 6h resulted in its partial metabolism (25%) into [3H]lyso-PAF and a compound with a short retention time (10 min). [3H]lyso-PAF incubated for 3h with tracheal rings was partially metabolized (10%) into [3H]PAF and a compound with a short retention time. The PAF-induced decrease of CBF is congruent with its influence on pulmonary clearance, possibly via a specific receptor, since WEB 2086 abolished the effect of PAF. The inhibition of the PAF-induced CBF decrease by ketotifen may contribute to the therapeutic properties of this antiallergic drug.
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PMID:Decrease of ciliary beat frequency by platelet activating factor: protective effect of ketotifen. 873 46

The purpose of this study was to determine whether treatment with intravenous basic fibroblast growth factor (bFGF) would protect histopathologically in a rat model of traumatic brain injury (TBI). Twenty-four hours prior to TBI, the fluid-percussion interface was positioned parasagittally over the right cerebral cortex. On the second day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37-37.5 degrees C), rats were injured with a fluid-percussion pulse ranging from 1.6 to 1.9 atm. Rats were randomized into two groups where either bFGF (45 micrograms/kg/h) in vehicle (n = 7) or vehicle alone (n = 7) was infused intravenously for 3 h, beginning 30 min after TBI. Three days later, brains were perfusion-fixed for histopathological assessment and quantitative analysis of contusion volume and numbers of necrotic cortical neurons. In vehicle-treated animals, necrotic neurons were observed throughout the lateral cerebral cortex remote from the impact site. In addition, an intracerebral contusion was present in all rats at the gray-white interface underlying the injured cortical areas. Posttraumatic administration of bFGF significantly reduced the numbers of damaged cortical neuron profiles at several coronal levels and reduced the total number of damaged neurons (696 +/- 148 vs. 1,248 +/- 198, means +/- SEM), p < 0.05, ANOVA). In addition, contusion ares at several coronal levels as well as total contusion volume was significantly reduced (1.13 +/- 0.39 mm(3) vs. 3.18 +/- 0.81 mm(3), p < 0.05). These data demonstrate neuroprotection with intravenous bFGF infusion in the posttraumatic setting.
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PMID:Posttreatment with intravenous basic fibroblast growth factor reduces histopathological damage following fluid-percussion brain injury in rats. 883 98

Cardiovascular adenosine-5'-triphosphate-sensitive potassium (KATP) channels have been reported to play an important role in endogenous cardioprotective mechanisms. Sulphonylurea derivatives can inhibit these cardioprotective mechanisms in animal models. We investigated whether therapeutic concentrations of sulphonylurea derivatives can block vascular KATP channels in humans. The forearm vasodilator responses to administration of the specific KATP channel opener diazoxide into the brachial artery of healthy male volunteers were recorded by venous occlusion plethysmography. This procedure was repeated with concomitant intraarterial infusion of:1) the sulphonylurea derivative glibenclamide (0.33 or 3.3 micrograms. min-1. dl-1, both n = 12), 2) the new sulphonylurea derivative glimepiride (2.5 micrograms.min-1. dl-1, n = 12) or 3) placebo (n = 12). The effects of glibenclamide on the vasodilator responses to sodium nitroprusside were also studied (n = 12). Glibenclamide significantly inhibited the diazoxide-induced increase in forearm blood flow ratio (ANOVA with repeated measures: p < 0.01). During the highest diazoxide dose this ratio (mean +/- SEM) was lowered from 892 +/- 165 to 449 +/- 105%, and from 1044 +/- 248 to 663 +/- 114% by low- and high-dose glibenclamide, respectively. In contrast, neither glimepiride nor placebo attenuate diazoxide-induced vasodilation. Furthermore, glibenclamide did not affect nitroprusside-induced vasodilation. We conclude that therapeutic concentrations of the classical sulphonylurea derivative glibenclamide result in significant blockade of vascular KATP channels in humans. The newly developed glimepiride seems to be devoid of these properties.
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PMID:Interaction of sulphonylurea derivatives with vascular ATP-sensitive potassium channels in humans. 887 93

This study investigated the human erythropoietin (EPO) response to short-term hypocapnic hypoxia, its relationship to a normoxic or hypoxic increase of the haemoglobin oxygen affinity, and its suppression by the addition of CO2 to the hypoxic gas. On separate days, eight healthy male subjects were exposed to 2 h each of hypocapnic hypoxia, normocapnic hypoxia, hypocapnic normoxia, and normal breathing of room air (control experiment). During the control experiment, serum-EPO showed significant variations (ANOVA P = 0.047) with a 15% increase in mean values. The serum-EPO measured in the other experiments were corrected for these spontaneous variations in each individual. At 2 h after ending hypocapnic hypoxia (10% O2 in nitrogen), mean serum-EPO increased by 28% [baseline 8.00 (SEM 0.84) U.l-1, post-hypoxia 10.24 (SEM 0.95) U.l-1, P = 0.005]. Normocapnic hypoxia was produced by the addition of CO2 (10% Co2 with 10% O2) to the hypoxic gas mixture. This elicited an increased ventilation, unaltered arterial pH and haemoglobin oxygen affinity, a lower degree of hypoxia than during hypocapnic hypoxia, and no significant changes in serum-EPO (ANOVA P > 0.05). Hypocapnic normoxia, produced by hyperventilation of room air, elicited a normoxic increase in the haemoglobin oxygen affinity without changing serum-EPO. Among the measured blood gas and acid-base parameters, only the partial pressures of oxygen in arterial blood during hypocapnic hypoxia were related to the peak values of serum-EPO (r = -0.81, P = 0.01). The present human EPO responses to hypoxia were lower than those which have previously been reported in rodents and humans. In contrast with the earlier rodent studies, it was found that human EPO production could not be triggered by short-term increases in pH and haemoglobin oxygen affinity per se, and the human EPO response to hypoxia could be suppressed by concomitant normocapnia without acidosis.
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PMID:Human erythropoietin response to hypocapnic hypoxia, normocapnic hypoxia, and hypocapnic normoxia. 895 96

Aprotinin (AP) is a plasmin inhibitor commonly used to limit bleeding during reoperative coronary bypass surgery. The effect on smooth muscle cell (SMC) behavior and the development of intimal hyperplasia has not been evaluated. This study examines the effect of AP on SMC proliferation, migration, and extracellular matrix synthesis. Bovine aortic SMCs (three to five passages) plated at 5 x 10(4) cells/ml were treated with 1.0, 10, 100, and 1000 microg/ml AP. Proliferation was measured as micrograms of DNA per well, after 3 days in culture. SMC migration was measured after treatment with mitomycin C (20 microg/ml, to study migration in the absence of proliferation) by means of a fence assay. Extracellular matrix was quantitated utilizing a tritiated proline assay and corrected for cell density (cpm/microg DNA). Data are presented as means +/- SEM; ANOVA and post hoc Tuckey test were used to test for significant differences. AP stimulated SMC proliferation at dosages of 100 microg/ml (353 +/- 6 microg DNA, SMC control vs 440 +/- 11, 100 microg/ml; P < 0.05) and 1000 microg/ml (353 +/- 6, SMC control vs 503 +/- 14, 1000 microg/ml; P < 0.01). AP concentrations less than 100 microg/ml had no effect on SMC proliferation. A dose-response relationship existed between AP and SMC migration. AP doses as low as 10 microg/ml increased SMC migration from 66 +/- 4 mm2 (control SMC) to 90 +/- 4 mm2 (P < 0.02) while the maximal dose of AP (1000 microg/ml) produced an almost twofold increase in migration (66 +/- 4, SMC control vs 113 +/- 3, 1000 microg/ml group; P < 0.0001). AP had no effect on extracellular matrix synthesis. AP stimulated vascular SMC migration and proliferation but not matrix synthesis in vitro. These data suggest that AP could augment the development of intimal hyperplasia following bypass surgery.
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PMID:Effect of aprotinin on smooth muscle cell proliferation, migration, and extracellular matrix synthesis. 902 21

Endurance performance is a common criterion used to evaluate training or dietary interventions. However, to accurately appraise the effects of an intervention, the endurance performance measure must be reliable. The purpose of the investigation was to establish the reliability of a 1-h endurance performance test. Twenty trained female subjects (peak VO2 = 47.4 +/- 7.2 ml.kg-1.min-1) completed two trials in which they had to generate the highest power output possible throughout 60 min of cycling. Heart rates (HR) and ratings of perceived exertion (RPE) were also recorded during these two trials. All tests were conducted on a wind-braked cycle ergometer set up to closely resemble the subject's own cycle. The trials were separated by 1 wk, conducted on the same day of the week, and completed at a similar time of the day. The average power outputs (+/-SD) for the two trials were 180.0 (+/-18.1) W and 180.0 (+/-20.6) W. The results revealed that average absolute power output, HR, and RPE were not significantly different between trials. The intraclass correlation coefficient (one way ANOVA) for average absolute power output was 0.97, the coefficient of variation was 2.7%, and the SEM was 3.4 W. These results suggest that under controlled conditions average absolute power output during a 1-h endurance test is a reliable measure for trained female cyclists.
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PMID:Reliability of a 1-h endurance performance test in trained female cyclists. 910 40


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