A Streamwise Constant Model of Turbulence in Plane Couette Flow

Streamwise and quasi-streamwise elongated structures have been shown to play a significant role in turbulent shear flows. We model the mean behavior of fully turbulent plane Couette flow using a streamwise constant projection of the Navier Stokes equations. This results in a two-dimensional, three velocity component ($2D/3C$) model. We first use a steady state version of the model to demonstrate that its nonlinear coupling provides the mathematical mechanism that shapes the turbulent velocity profile. Simulations of the $2D/3C$ model under small amplitude Gaussian forcing of the cross-stream components are compared to DNS data. The results indicate that a streamwise constant projection of the Navier Stokes equations captures salient features of fully turbulent plane Couette flow at low Reynolds numbers. A system theoretic approach is used to demonstrate the presence of large input-output amplification through the forced $2D/3C$ model. It is this amplification coupled with the appropriate nonlinearity that enables the $2D/3C$ model to generate turbulent behaviour under the small amplitude forcing employed in this study.Comment: Journal of Fluid Mechanics 2010, in pres

Avaliação dos efeitos do sulfato de atropina em filhotes de cães

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Relevance of laboratory testing for the diagnosis of primary immunodeficiencies: a review of case-based examples of selected immunodeficiencies

The field of primary immunodeficiencies (PIDs) is one of several in the area of clinical immunology that has not been static, but rather has shown exponential growth due to enhanced physician, scientist and patient education and awareness, leading to identification of new diseases, new molecular diagnoses of existing clinical phenotypes, broadening of the spectrum of clinical and phenotypic presentations associated with a single or related gene defects, increased bioinformatics resources, and utilization of advanced diagnostic technology and methodology for disease diagnosis and management resulting in improved outcomes and survival. There are currently over 200 PIDs with at least 170 associated genetic defects identified, with several of these being reported in recent years. The enormous clinical and immunological heterogeneity in the PIDs makes diagnosis challenging, but there is no doubt that early and accurate diagnosis facilitates prompt intervention leading to decreased morbidity and mortality. Diagnosis of PIDs often requires correlation of data obtained from clinical and radiological findings with laboratory immunological analyses and genetic testing. The field of laboratory diagnostic immunology is also rapidly burgeoning, both in terms of novel technologies and applications, and knowledge of human immunology. Over the years, the classification of PIDs has been primarily based on the immunological defect(s) ("immunophenotype") with the relatively recent addition of genotype, though there are clinical classifications as well. There can be substantial overlap in terms of the broad immunophenotype and clinical features between PIDs, and therefore, it is relevant to refine, at a cellular and molecular level, unique immunological defects that allow for a specific and accurate diagnosis. The diagnostic testing armamentarium for PID includes flow cytometry - phenotyping and functional, cellular and molecular assays, protein analysis, and mutation identification by gene sequencing. The complexity and diversity of the laboratory diagnosis of PIDs necessitates many of the above-mentioned tests being performed in highly specialized reference laboratories. Despite these restrictions, there remains an urgent need for improved standardization and optimization of phenotypic and functional flow cytometry and protein-specific assays. A key component in the interpretation of immunological assays is the comparison of patient data to that obtained in a statistically-robust manner from age and gender-matched healthy donors. This review highlights a few of the laboratory assays available for the diagnostic work-up of broad categories of PIDs, based on immunophenotyping, followed by examples of disease-specific testing

Large-eddy-simulations of the unsteady behaviour of a mach 5 hypersonic intake

Numerical simulations of a hypersonic ramjet intake at Mach 5 are performed combining a high-order and time-accurate Large-Eddy-Simulation model with a sharp-interface Immersed Boundary Method. The study aims at proving that advanced fluid dynamics techniques, such as LES, in combination with an ad-hoc method for embedded geometries, represent a robust and accurate framework to deal with the unsteady and off-design behavior of highly-turbulent flows in the field of hypersonic applications. The authors show that the present methodology well reproduces the unsteady behavior observed in the experiment of Berto et al. [1] in corresponding conditions, and allows a complete characterization of the 3D time-resolved flow fields

Loss of TET2 Affects Proliferation and Drug Sensitivity through Altered Dynamics of Cell-State Transitions

A persistent puzzle in cancer biology is how mutations, which neither alter growth signaling pathways nor directly interfere with drug mechanism, can still recur and persist in tumors. One example is the mutation of the DNA demethylase tet methylcytosine dioxygenase 2 (TET2) in acute myeloid leukemias (AMLs) that frequently persists from diagnosis through remission and relapse, but whose fitness advantage in chemotherapy is unclear. Here, we use isogenic human AML cell lines to show that TET2 loss of function alters the dynamics of transitions between differentiated and stem-like states. A conceptual mathematical model and experimental validation suggest that these altered cell-state dynamics can benefit the cell population by slowing population decay during drug treatment and lowering the number of survivor cells needed to re-establish the initial population. These studies shed light on the functional and phenotypic effects of a TET2 mutation in AML and illustrate how a single gene mutation can alter a cells' phenotypic plasticity. A record of this paper's transparent peer review process is included in the Supplemental Information