Effects of grazing flow on the steady-state flow resistance and acoustic impedance of thin porous-faced liners

The effects of grazing flow on the steady state flow resistance and acoustic impedance of seven Feltmetal and three Rigimesh thin porous faced liners were studied. The steady-state flow resistance of the ten specimens was measured using standard fluid mechanical experimental techniques. The acoustic impedance was measured using the two microphone method. The principal findings of the study are that the effects of grazing flow were measured and found to be small; small differences were measured between steady-state and acoustic resistance, and a semi-empirical model was derived that correlated the steady-state resistance data of the seven Feltmetal liners and the face sheet reactance of both the Feltmetal and Rigimesh liners

Fluid mechanical model of the Helmholtz resonator

A semi-empirical fluid mechanical model of the acoustic behavior of Helmholtz resonators is presented which predicts impedance as a function of the amplitude and frequency of the incident sound pressure field and resonator geometry. The model assumes that the particle velocity approaches the orifice in a spherical manner. The incident and cavity sound fields are connected by solving the governing oscillating mass and momentum conservation equations. The model is in agreement with the Rayleigh slug-mass model at low values of incident sound pressure level. At high values, resistance is predicted to be independent of frequency, proportional to the square root of the amplitude of the incident sound pressure field, and virtually independent of resonator geometry. Reactance is predicted to depend in a very complicated way upon resonator geometry, incident sound pressure level, and frequency. Nondimensional parameters are defined that divide resonator impedance into three categories corresponding to low, moderately low, and intense incident sound pressure amplitudes. The two-microphone method was used to measure the impedance of a variety of resonators. The data were used to refine and verify the model

Insulin Degrading Enzyme Assays for Treatment of Alzheimer\u27s Disease

Estrogen has been shown to increase the expression and activity of amyloid peptide inactivating enzymes in the brain. Peptides have been shown to increase the activity of an amyloid peptide inactivating enzyme. Methods of identifying compounds for, and methods of treating patients with, Alzheimer\u27s Disease is disclosed

The utility of general purpose versus specialty clinical databases for research: Warfarin dose estimation from extracted clinical variables

AbstractThere is debate about the utility of clinical data warehouses for research. Using a clinical warfarin dosing algorithm derived from research-quality data, we evaluated the data quality of both a general-purpose database and a coagulation-specific database. We evaluated the functional utility of these repositories by using data extracted from them to predict warfarin dose. We reasoned that high-quality clinical data would predict doses nearly as accurately as research data, while poor-quality clinical data would predict doses less accurately. We evaluated the Mean Absolute Error (MAE) in predicted weekly dose as a metric of data quality. The MAE was comparable between the clinical gold standard (10.1mg/wk) and the specialty database (10.4mg/wk), but the MAE for the clinical warehouse was 40% greater (14.1mg/wk). Our results indicate that the research utility of clinical data collected in focused clinical settings is greater than that of data collected during general-purpose clinical care

Amyloid Peptide Inactivating Enzyme to Treat Alzheimer\u27s Disease Peripherally

Methods for treatment and/or prevention of Alzheimer\u27s disease comprising inactivating peripheral AP in serum to a reduce A(3 in the brain. Methods comprise expression of amyloid peptide inactivating enzyme on bone marrow cells; and coupling of amyloid peptide inactivating enzyme to hematopoietic cells

Generalized Ginsparg-Wilson relations

We give a general derivation of Ginsparg-Wilson relations for both Dirac and Majorana fermions in any dimension. These relations encode continuous and discrete chiral, parity and time reversal anomalies and will apply to the various classes of free fermion topological insulators and superconductors (in the framework of a relativistic quantum field theory in Euclidean spacetime). We show how to formulate the exact symmetries of the lattice action and the relevant index theorems for the anomalies.Comment: 14 pages. Submitted Version. Section III.D revised, and other minor improvement

Aminopeptidases do not directly degrade tau protein

BACKGROUND: Tau hyperphosphorylation and aggregation to form intracellular neurofibrillar tangles is prevalent in a number of tauopathies. Thus there is current interest in the mechanisms involved in Tau clearance. It was recently reported that Tau can be degraded by an aminopeptidase known as the puromycin sensitive aminopeptidase (PSA). Until now PSA has been reported to only cleave peptides, with the largest reported substrates having 30-50 amino acids. We have studied this unique PSA cleavage reaction using a number of different PSA preparations. RESULTS: An N-terminally His tagged-PSA was expressed and purified from Sf9 insect cells. Although this PSA preparation cleaved Tau, product analysis with N and C terminal Tau antibodies coupled with mass spectrometry showed an endoproteolytic cleavage atypical for an aminopeptidase. Furthermore, the reaction was not blocked by the general aminopeptidase inhibitor bestatin or the specific PSA inhibitor puromycin. In order to test whether Tau hydrolysis might be caused by a protease contaminant the enzyme was expressed in E. coli as glutathione S-transferase and maltose binding protein fusion proteins or in Sf9 cells as a C-terminally His-tagged protein. After purification to near homogeneity none of these other recombinant forms of PSA cleaved Tau. Further, Tau-cleaving activity and aminopeptidase activities derived from the Sf9 cell expression system were separable by molecular sieve chromatography. When tested in a cellular context we again failed to see a PSA dependent cleavage of Tau. A commercial preparation of a related aminopeptidase, aminopeptidase N, also exhibited Tau cleaving activity, but this activity could also be separated from aminopeptidase activity. CONCLUSION: It is concluded that PSA does not directly cleave Tau

Aminopeptidases do not directly degrade tau protein

BACKGROUND: Tau hyperphosphorylation and aggregation to form intracellular neurofibrillar tangles is prevalent in a number of tauopathies. Thus there is current interest in the mechanisms involved in Tau clearance. It was recently reported that Tau can be degraded by an aminopeptidase known as the puromycin sensitive aminopeptidase (PSA). Until now PSA has been reported to only cleave peptides, with the largest reported substrates having 30-50 amino acids. We have studied this unique PSA cleavage reaction using a number of different PSA preparations. RESULTS: An N-terminally His tagged-PSA was expressed and purified from Sf9 insect cells. Although this PSA preparation cleaved Tau, product analysis with N and C terminal Tau antibodies coupled with mass spectrometry showed an endoproteolytic cleavage atypical for an aminopeptidase. Furthermore, the reaction was not blocked by the general aminopeptidase inhibitor bestatin or the specific PSA inhibitor puromycin. In order to test whether Tau hydrolysis might be caused by a protease contaminant the enzyme was expressed in E. coli as glutathione S-transferase and maltose binding protein fusion proteins or in Sf9 cells as a C-terminally His-tagged protein. After purification to near homogeneity none of these other recombinant forms of PSA cleaved Tau. Further, Tau-cleaving activity and aminopeptidase activities derived from the Sf9 cell expression system were separable by molecular sieve chromatography. When tested in a cellular context we again failed to see a PSA dependent cleavage of Tau. A commercial preparation of a related aminopeptidase, aminopeptidase N, also exhibited Tau cleaving activity, but this activity could also be separated from aminopeptidase activity. CONCLUSION: It is concluded that PSA does not directly cleave Tau