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Selected AbstractsIn vitro evaluation of Er:YAG laser scaling of subgingival calculus in comparison with ultrasonic scalingJOURNAL OF PERIODONTAL RESEARCH, Issue 5 2000A. Aoki The purpose of the present study was to evaluate the effectiveness of Er:YAG laser scaling and the morphological and histological changes of the laser-scaled root surface in comparison with the effectiveness and root surface changes produced by conventional ultrasonic scaling. Fifty-three periodontally involved human extracted teeth with a band of subgingival calculus were used. The teeth were divided randomly into 2 groups for laser scaling and ultrasonic scaling. Laser irradiation was performed at an energy output of 40 mJ/pulse and 10 pulses/s under water spray, with the probe tip contacted obliquely to the root surface. Ultrasonic scaling was performed at a clinically standard power setting. The time required for scaling, the scaled area and the temperature changes were determined using both methods of treatment. The features of the scaled surfaces were examined by histological and scanning electron microscope (s.e.m.) observations. The Er:YAG laser provided subgingival calculus removal on a level equivalent to that provided by the ultrasonic scaler, without major thermal elevation. Macroscopically, the laser-treated root surface was somewhat rougher than or similar to the ultrasonically scaled root. However, the efficiency of the laser scaling was lower than that of the ultrasonic scaling. In addition, histological examination revealed a thin deeply stained zone on the lased root surface, and s.e.m. analysis revealed a characteristic microroughness on the lased surface. The laser scaling provided a level of calculus removal that was similar to that provided by the ultrasonic scaling. However, the Er:YAG laser produced superficial, structural and thermal microchanges on the root cementum. [source] Increasing the Effectiveness of Reed canary grass (Phalaris arundinacea L.) Control in Wet Meadow RestorationsRESTORATION ECOLOGY, Issue 3 2006Carrie Reinhardt Adams Abstract Restoration practices are often based on trial and error or anecdotal information because data from controlled experiments are not available. In wet meadow restorations of the upper Midwest United States, Reed canary grass (Phalaris arundinacea L.) is controlled with spring burning and spring glyphosate herbicide applications, but the relative effectiveness of either treatment with respect to P. arundinacea growth and life history has not been assessed. We designed a multiyear field experiment to evaluate effects of burning and herbicide application timings on P. arundinacea populations. Burning did not reduce P. arundinacea biomass but reduced the P. arundinacea seed bank, potentially limiting recolonization of P. arundinacea. Glyphosate applications in late August and late September were more effective than in mid-May (due to enhanced glyphosate translocation to rhizomes), such that two mid-May applications reduced P. arundinacea biomass to a level equivalent to that achieved by one late-season application. Phalaris. arundinacea recolonized rapidly from the seed bank and, in plots that received suboptimally timed (mid-May) herbicide, from rhizomes. Establishment of native species was very low, likely due to competition with recolonizing P. arundinacea. Unplanted species (from the seed bank and refugial populations) accounted for the majority of non- P. arundinacea biomass. Recolonization of other species was strongly limited by a threshold level of P. arundinacea biomass. Adequate site preparation (over multiple growing seasons) and aftercare (selective removal of P. arundinacea) will be the key to facilitating subsequent wet meadow vegetation establishment. This research provides an example of the importance of experimental evidence as the basis to improve the efficiency of restoration practices. [source] Accelerated plasminogen activator inhibitor may prevent late restenosis after coronary stenting in acute myocardial infarctionCLINICAL CARDIOLOGY, Issue 3 2003Teruo Inoue M.D. Abstract Background: Although acceleration of plasma plasminogen activator inhibitor-1 (PAI-1) level after emergent coronary angioplasty in acute myocardial infarction (AMI) has been documented, its pathophysiologic role is still unknown. Hypothesis: This study was designed to elucidate the role of PAI-1 in the development of restenosis after primary coronary stenting in AMI. Methods: We selected for this study 66 patients with AMI, who underwent primary coronary stenting for infarct-related coronary artery lesions in an emergent situation. In all patients, plasma PAI-1 level was measured at admission, and at 3 h, 24 h, 48 h, and 1 month after coronary stenting. Results: At admission, the PAI-1 level was equivalent in 24 patients who experienced restenosis and in 42 patients without restenosis (28 ± 4 vs. 29 ± 4 ng/ml). In patients with restenosis, the levels did not change during the course after coronary stenting. In patients without restenosis, however, the level significantly increased at 3 h (48 ± 9 ng/ml, p < 0.001), 24 h (42 ± 9, p < 0.01), and 48 h (38 ± 7, p < 0.05) after coronary stenting, and was restored to the level equivalent to that at admission (27 ± 2 ng/ml) 1 month after coronary stenting. The PAI-1 level at 3 h after coronary stenting in patients without restenosis was significantly higher (p < 0.05) than the level (33 ± 6 ng/ml) in patients with restenosis. Multiple logistic regression analysis indicated that the PAI-1 level 3 h after coronary stenting was an independent predictor of restenosis (Wald x2 = 3.826, p = 0.019, odds ratio 0.921, 95% confidence interval 0.866-0.961). Conclusion: Accelerated PAI-1 after coronary stenting in patients with AMI may protect against the development of late restenosis. [source] Pharmacology and safety of glycerol phenylbutyrate in healthy adults and adults with cirrhosis,,HEPATOLOGY, Issue 6 2010Brendan M. McGuire Phenylbutyric acid (PBA), which is approved for treatment of urea cycle disorders (UCDs) as sodium phenylbutyrate (NaPBA), mediates waste nitrogen excretion via combination of PBA-derived phenylacetic acid with glutamine to form phenylactylglutamine (PAGN) that is excreted in urine. Glycerol phenylbutyrate (GPB), a liquid triglyceride pro-drug of PBA, containing no sodium and having favorable palatability, is being studied for treatment of hepatic encephalopathy (HE). In vitro and clinical studies have been performed to assess GPB digestion, safety, and pharmacology in healthy adults and individuals with cirrhosis. GPB hydrolysis was measured in vitro by way of pH titration. Twenty-four healthy adults underwent single-dose administration of GPB and NaPBA and eight healthy adults and 24 cirrhotic subjects underwent single-day and multiple-day dosing of GPB, with metabolites measured in blood and urine. Simulations were performed to assess GPB dosing at higher levels. GPB was hydrolyzed by human pancreatic triglyceride lipase, pancreatic lipase-related protein 2, and carboxyl-ester lipase. Clinical safety was satisfactory. Compared with NaPBA, peak metabolite blood levels with GPB occurred later and were lower; urinary PAGN excretion was similar but took longer. Steady state was achieved within 4 days for both NaPBA and GPB; intact GPB was not detected in blood or urine. Cirrhotic subjects converted GPB to PAGN similarly to healthy adults. Simulations suggest that GPB can be administered safely to cirrhotic subjects at levels equivalent to the highest approved NaPBA dose for UCDs. Conclusion: GPB exhibits delayed release characteristics, presumably reflecting gradual PBA release by pancreatic lipases, and is well tolerated in adults with cirrhosis, suggesting that further clinical testing for HE is warranted. (HEPATOLOGY 2010;) [source] Cumulative effects of in utero administration of mixtures of reproductive toxicants that disrupt common target tissues via diverse mechanisms of toxicityINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 2 2010C. V. Rider Summary Although risk assessments are typically conducted on a chemical-by-chemical basis, the 1996 Food Quality Protection Act required the US Environmental Protection Agency to consider cumulative risk of chemicals that act via a common mechanism of toxicity. To this end, we are conducting studies with mixtures of chemicals to elucidate mechanisms of joint action at the systemic level with the goal of providing a framework for assessing the cumulative effects of reproductive toxicants. Previous mixture studies conducted with antiandrogenic chemicals are reviewed briefly and two new studies are described. In all binary mixture studies, rats were dosed during pregnancy with chemicals, singly or in pairs, at dosage levels equivalent to approximately one-half of the ED50 for hypospadias or epididymal agenesis. The binary mixtures included androgen receptor (AR) antagonists (vinclozolin plus procymidone), phthalate esters [di(n-butyl) phthalate (DBP) plus benzyl n-butyl phthalate (BBP) and diethyl hexyl phthalate (DEHP) plus DBP], a phthalate ester plus an AR antagonist (DBP plus procymidone), a mixed mechanism androgen signalling disruptor (linuron) plus BBP, and two chemicals which disrupt epididymal differentiation through entirely different toxicity pathways: DBP (AR pathway) plus 2,3,7,8 TCDD (AhR pathway). We also conducted multi-component mixture studies combining several ,antiandrogens'. In the first study, seven chemicals (four pesticides and three phthalates) that elicit antiandrogenic effects at two different sites in the androgen signalling pathway (i.e. AR antagonist or inhibition of androgen synthesis) were combined. In the second study, three additional phthalates were added to make a 10 chemical mixture. In both the binary mixture studies and the multi-component mixture studies, chemicals that targeted male reproductive tract development displayed cumulative effects that exceeded predictions based on a response-addition model and most often were in accordance with predictions based on dose-addition models. In summary, our results indicate that compounds that act by disparate mechanisms of toxicity to disrupt the dynamic interactions among the interconnected signalling pathways in differentiating tissues produce cumulative dose-additive effects, regardless of the mechanism or mode of action of the individual mixture component. [source] Resistance to acidic and alkaline environments in the endodontic pathogen Enterococcus faecalisMOLECULAR ORAL MICROBIOLOGY, Issue 5 2006K. Nakajo Background/aims:, This study aimed to investigate the biochemical mechanisms employed by the endodontic pathogen Enterococcus faecalis to confer acid- and alkali-resistance and to compare these with the mechanisms of representative oral streptococci. Methods:,E. faecalis JCM8728, Streptococcus mutans NCTC10449 and Streptococcus sanguinis ATCC10556 were used to assess both acid- and alkali-resistance by examining: (i) growth in complex media; (ii) stability of intracellular pH (pHin); (iii) cell durability to leakage of preloaded BCECF (2,,7,-bis-(2-carboxyethyl)-5,6-carboxy-fluorescein); and (iv) cell permeability to SYTOX-Green. Results:, Growth was initiated by E. faecalis at pH 4.0,11.0, by S. mutans at pH 4.0,9.0 and by S. sanguinis at pH 5.0,9.0. The pHin was similar to the extracellular pH in S. mutans and S. sanguinis at pH 5,10, while the pHin of E. faecalis was maintained at approximately 7.5,8.5 when extracellular pH was 7.5,10 and was maintained at levels equivalent to the extracellular pH when pH < 7.5. Cell membranes of E. faecalis were resistant to BCECF leakage when extracellular pH was 2.5,12 and to SYTOX-Green permeability at pH 4,10. The cell membrane durability to extracellular pH in E. faecalis was higher than that observed in the Streptococcus strains. Conclusion:, Compared to S. mutans, E. faecalis was found to be equally resistant to acid and more resistant to alkalis. The results suggest that pH-resistance in E. faecalis is attributed to membrane durability against acid and alkali, in addition to cell membrane-bound proton-transport systems. These characteristics may account for why E. faecalis is frequently isolated from acidic caries lesions and from persistently infected root canals where calcium hydroxide medication is ineffective. [source] The role of seeds and airborne inoculum in the initiation of leaf blotch (Rhynchosporium secalis) epidemics in winter barleyPLANT PATHOLOGY, Issue 2 2010J. M. Fountaine Both airborne spores of Rhynchosporium secalis and seed infection have been implied as major sources of primary inoculum for barley leaf blotch (scald) epidemics in fields without previous history of barley cropping. However, little is known about their relative importance in the onset of disease. Results from both quantitative real-time PCR and visual assessments indicated that seed infection was the main source of inoculum in the field trial conducted in this study. Glasshouse studies established that the pathogen can be transmitted from infected seeds into roots, shoots and leaves without causing symptoms. Plants in the field trial remained symptomless for approximately four months before symptoms were observed in the crop. Covering the crop during part of the growing season was shown to prevent pathogen growth, despite the use of infected seed, indicating that changes in the physiological condition of the plant and/or environmental conditions may trigger disease development. However, once the disease appeared in the field it quickly became uniform throughout the cropping area. Only small amounts of R. secalis DNA were measured in 24 h spore-trap tape samples using PCR. Inoculum levels equivalent to spore concentrations between 30 and 60 spores per m3 of air were only detected on three occasions during the growing season. The temporal pattern and level of detection of R. secalis DNA in spore tape samples indicated that airborne inoculum was limited and most likely represented rain-splashed conidia rather than putative ascospores. [source] | |||||||||||||