Citations

The goal of this study was to excite and measure, in a noncontact manner, the vibrational modes of the reed from a reed organ pipe. To perform ultrasound stimulated excitation, the audio-range difference frequency between a pair of ultrasound beams produced a radiation force that induced vibrations. The resulting vibrational deflection shapes were measured with a scanning laser vibrometer. The resonances of any relatively small object can be studied in air using this technique. For a 36mm×6mm brass reed, displacements and velocities in excess of 5μm and 4mm∕s could be imparted at the fundamental frequency of 145Hz. Using the same ultrasound transducer, excitation across the entire range of audio frequencies was obtained. Since the beam was focused on the reed, ultrasound stimulated excitation eliminated background effects observed during mechanical shaker excitation, such as vibrations of clamps and supports. The results obtained using single, dual and confocal ultrasound transducers in AM and two-beam modes, along with results obtained using a mechanical shaker and audio excitation using a speaker are discussed.

ABSTRACT The activity of garenoxacin was compared to that of levofloxacin or penicillin in a rabbit model of Streptococcus mitis group (penicillin MIC, 0.125 μg/ml) and Streptococcus sanguinis group (penicillin MIC, 0.25 μg/ml) endocarditis. Garenoxacin and levofloxacin had MICs of 0.125 and 0.5 μg/ml, respectively, for both study isolates. Rabbits with catheter-induced aortic valve endocarditis were given no treatment, penicillin at 1.2 × 10 6 IU/8 h intramuscularly, garenoxacin at 20 mg/kg of body weight/12 h intravenously, or levofloxacin at 40 mg/kg/12 h intravenously. For both isolates tested, garenoxacin area under the curve (AUC)/MIC and maximum concentration of drug in serum ( C max )/MIC ratios were 368 and 91, respectively. Rabbits were sacrificed after 3 days of treatment; cardiac valve vegetations were aseptically removed and quantitatively cultured. For S. mitis group experimental endocarditis, all studied antimicrobial agents were more active than no treatment ( P < 0.001), whereas for S. sanguinis group endocarditis, no studied antimicrobial agents were more active than no treatment. We conclude that AUC/MIC and C max /MIC ratios may not predict activity of some quinolones in experimental viridans group endocarditis and that garenoxacin and levofloxacin may not be ideal choices for serious infections caused by some quinolone-susceptible viridans group streptococci.

The microtubule-binding protein tau has been implicated in the pathogenesis of Alzheimer's disease and related disorders. However, the mechanisms underlying tau-mediated neurotoxicity remain unclear. We created a genetic model of tau-related neurodegenerative disease by expressing wild-type and mutant forms of human tau in the fruit fly Drosophila melanogaster . Transgenic flies showed key features of the human disorders: adult onset, progressive neurodegeneration, early death, enhanced toxicity of mutant tau, accumulation of abnormal tau, and relative anatomic selectivity. However, neurodegeneration occurred without the neurofibrillary tangle formation that is seen in human disease and some rodent tauopathy models. This fly model may allow a genetic analysis of the cellular mechanisms underlying tau neurotoxicity.

Abstract Background: The American Heart Association (AHA) case definition for acute myocardial infarction (AMI) requires an “adequate set” of biomarkers: 2 measurements of the same marker at least 6 h apart. A sensitive troponin assay might detect significant changes in concentration earlier. We determined AMI prevalence, using protocols with shorter intervals between measurements, with and without incorporating the time from onset of symptoms. Methods: The AHA case definition was used to retrospectively assign a diagnosis in 258 patients presenting to the emergency department with symptoms of cardiac ischemia. AMI was diagnosed if either specimen in an adequate set had a cardiac troponin I (cTnI) above the 99th percentile (AccuTnI® &gt;0.04 μg/L; Beckman Coulter) with a ≥20% change in concentration between specimens. We assessed positivity for AMI after progressively decreasing the time interval between specimens in specimen sets. In addition, for each patient, 2 additional specimen pairs were selected: pairs collected at least 1 h apart with 1 specimen being either ≥3 h after onset or ≥6 h after onset. Results: When we used the AHA definition, the AMI prevalence was 35.7%. Prevalence was not significantly diminished when the interval between specimens was ≥5, ≥4, or ≥3 h (36.4%, 34.5%, and 33.7%, respectively) compared with the AHA ≥6 h interval. When the time from onset of symptoms was included in the specimen selection algorithm, a 1-h interval was sufficient provided that at least one specimen was collected ≥6 h after onset (prevalence, 34.1%; P = 0.48 vs AHA definition). Conclusion: A sensitive cTnI assay in specimen sets with time intervals ≥3 h, or having one specimen ≥6 h after onset, gave an AMI prevalence equivalent to the AHA definition.