Numerical study of large-eddy breakup and its effect on the drag characteristics of boundary layers

The break-up of a field of eddies by a flat-plate obstacle embedded in a boundary layer is studied using numerical solutions to the two-dimensional Navier-Stokes equations. The flow is taken to be incompressible and unsteady. The flow field is initiated from rest. A train of eddies of predetermined size and strength are swept into the computational domain upstream of the plate. The undisturbed velocity profile is given by the Blasius solution. The disturbance vorticity generated at the plate and wall, plus that introduced with the eddies, mix with the background vorticity and is transported throughout the entire flow. All quantities are scaled by the plate length, the unidsturbed free-stream velocity, and the fluid kinematic viscosity. The Reynolds number is 1000, the Blasius boundary layer thickness is 2.0, and the plate is positioned a distance of 1.0 above the wall. The computational domain is four units high and sixteen units long

Neuroantigen-specific, tolerogenic vaccines: GM-CSF is a fusion partner that facilitates tolerance rather than immunity to dominant self-epitopes of myelin in murine models of experimental autoimmune encephalomyelitis (EAE)

<p>Abstract</p> <p>Background</p> <p>Vaccination strategies that elicit antigen-specific tolerance are needed as therapies for autoimmune disease. This study focused on whether cytokine-neuroantigen (NAg) fusion proteins could inhibit disease in chronic murine models of experimental autoimmune encephalomyelitis (EAE) and thus serve as potential therapeutic modalities for multiple sclerosis.</p> <p>Results</p> <p>A fusion protein comprised of murine GM-CSF as the N-terminal domain and the encephalitogenic MOG35-55 peptide as the C-terminal domain was tested as a tolerogenic, therapeutic vaccine (TTV) in the C57BL/6 model of EAE. Administration of GMCSF-MOG before active induction of EAE, or alternatively, at the onset of EAE blocked the development and progression of EAE. Covalent linkage of the GM-CSF and MOG35-55 domains was required for tolerogenic activity. Likewise, a TTV comprised of GM-CSF and PLP139-151 was a tolerogen in the SJL model of EAE.</p> <p>Conclusion</p> <p>These data indicated that fusion proteins containing GM-CSF coupled to myelin auto-antigens elicit tolerance rather than immunity.</p

Shigella spp. surveillance in Indonesia: the emergence or reemergence of S. dysenteriae.

From June 1998 through November 1999, Shigella spp. were isolated in 5% of samples from 3,848 children and adults with severe diarrheal illness in hospitals throughout Indonesia. S. dysenteriae has reemerged in Bali, Kalimantan, and Batam and was detected in Jakarta after a hiatus of 15 years

Ethnicity Modifies the Relationships of Insulin Resistance, Inflammation, and Adiponectin With Obesity in a Multiethnic Asian Population

10.2337/dc10-2097Diabetes Care3451120-1126DICA

ChIPseqR: analysis of ChIP-seq experiments

<p>Abstract</p> <p>Background</p> <p>The use of high-throughput sequencing in combination with chromatin immunoprecipitation (ChIP-seq) has enabled the study of genome-wide protein binding at high resolution. While the amount of data generated from such experiments is steadily increasing, the methods available for their analysis remain limited. Although several algorithms for the analysis of ChIP-seq data have been published they focus almost exclusively on transcription factor studies and are usually not well suited for the analysis of other types of experiments.</p> <p>Results</p> <p>Here we present ChIPseqR, an algorithm for the analysis of nucleosome positioning and histone modification ChIP-seq experiments. The performance of this novel method is studied on short read sequencing data of <it>Arabidopsis thaliana </it>mononucleosomes as well as on simulated data.</p> <p>Conclusions</p> <p>ChIPseqR is shown to improve sensitivity and spatial resolution over existing methods while maintaining high specificity. Further analysis of predicted nucleosomes reveals characteristic patterns in nucleosome sequences and placement.</p

Q&A: ChIP-seq technologies and the study of gene regulation

10.1186/1741-7007-8-56BMC Biology85

CO2 dissolution and design aspects of a multiorifice oscillatory baffled column

Dissolution of CO2 in water was studied for a batch vertical multiorifice baffled column (MOBC) with varying orifice diameters (d0) of 6.4-30 mm and baffle open area (α) of 15-42%. Bubble size distributions (BSDs) and the overall volumetric CO2 mass transfer coefficient (KLa) were experimentally evaluated for very low superficial gas velocities, UG of 0.12-0.81 mm s-1, using 5% v/v CO2 in the inlet gas stream at a range of fluid oscillations (f = 0-10 Hz and x0 = 0-10 mm). Remarkably, baffles presenting large do = 30 mm and α = 36%, therefore in the range typically found for single-orifice oscillatory baffled columns, were outperformed with respect to BSD control and CO2 dissolution by the other baffle designs or the same aerated column operating without baffles or fluid oscillations. Flow visualization and bubble tracking experiments also presented in this study established that a small do of 10.5 mm combined with a small value of α = 15% generates sufficient, strong eddy mixing capable of generating and trapping an extremely large fraction of microbubbles in the MOBC. This resulted in increased interfacial area yielding KLa values up to 65 ± 12 h-1 in the range of the UG tested, representing up to 3-fold increase in the rate of CO2 dissolution when compared to the unbaffled, steady column. In addition, a modi fied oscillatory Reynolds number, Re′o and Strouhal number, St' were presented to assist on the design and scale-up of gas-liquid systems based on multiorifice oscillatory ba ffled columns. This work is relevant to gas-liquid or multiphase chemical and biological systems relying on efficient dissolution of gaseous compounds into a liquid medium.BBSRC -European Commissio

An Integrated Model of Multiple-Condition ChIP-Seq Data Reveals Predeterminants of Cdx2 Binding

Regulatory proteins can bind to different sets of genomic targets in various cell types or conditions. To reliably characterize such condition-specific regulatory binding we introduce MultiGPS, an integrated machine learning approach for the analysis of multiple related ChIP-seq experiments. MultiGPS is based on a generalized Expectation Maximization framework that shares information across multiple experiments for binding event discovery. We demonstrate that our framework enables the simultaneous modeling of sparse condition-specific binding changes, sequence dependence, and replicate-specific noise sources. MultiGPS encourages consistency in reported binding event locations across multiple-condition ChIP-seq datasets and provides accurate estimation of ChIP enrichment levels at each event. MultiGPS's multi-experiment modeling approach thus provides a reliable platform for detecting differential binding enrichment across experimental conditions. We demonstrate the advantages of MultiGPS with an analysis of Cdx2 binding in three distinct developmental contexts. By accurately characterizing condition-specific Cdx2 binding, MultiGPS enables novel insight into the mechanistic basis of Cdx2 site selectivity. Specifically, the condition-specific Cdx2 sites characterized by MultiGPS are highly associated with pre-existing genomic context, suggesting that such sites are pre-determined by cell-specific regulatory architecture. However, MultiGPS-defined condition-independent sites are not predicted by pre-existing regulatory signals, suggesting that Cdx2 can bind to a subset of locations regardless of genomic environment. A summary of this paper appears in the proceedings of the RECOMB 2014 conference, April 2–5.National Science Foundation (U.S.) (Graduate Research Fellowship under Grant 0645960)National Institutes of Health (U.S.) (grant P01 NS055923)Pennsylvania State University. Center for Eukaryotic Gene Regulatio

The Extracellular Domain of Myelin Oligodendrocyte Glycoprotein Elicits Atypical Experimental Autoimmune Encephalomyelitis in Rat and Species

Atypical models of experimental autoimmune encephalomyelitis (EAE) are advantageous in that the heterogeneity of clinical signs appears more reflective of those in multiple sclerosis (MS). Conversely, models of classical EAE feature stereotypic progression of an ascending flaccid paralysis that is not a characteristic of MS. The study of atypical EAE however has been limited due to the relative lack of suitable models that feature reliable disease incidence and severity, excepting mice deficient in gamma-interferon signaling pathways. In this study, atypical EAE was induced in Lewis rats, and a related approach was effective for induction of an unusual neurologic syndrome in a cynomolgus macaque. Lewis rats were immunized with the rat immunoglobulin variable (IgV)-related extracellular domain of myelin oligodendrocyte glycoprotein (IgV-MOG) in complete Freund’s adjuvant (CFA) followed by one or more injections of rat IgV-MOG in incomplete Freund’s adjuvant (IFA). The resulting disease was marked by torticollis, unilateral rigid paralysis, forelimb weakness, and high titers of anti-MOG antibody against conformational epitopes of MOG, as well as other signs of atypical EAE. A similar strategy elicited a distinct atypical form of EAE in a cynomolgus macaque. By day 36 in the monkey, titers of IgG against conformational epitopes of extracellular MOG were evident, and on day 201, the macaque had an abrupt onset of an unusual form of EAE that included a pronounced arousal-dependent, transient myotonia. The disease persisted for 6–7 weeks and was marked by a gradual, consistent improvement and an eventual full recovery without recurrence. These data indicate that one or more boosters of IgV-MOG in IFA represent a key variable for induction of atypical or unusual forms of EAE in rat and Macaca species. These studies also reveal a close correlation between humoral immunity against conformational epitopes of MOG, extended confluent demyelinating plaques in spinal cord and brainstem, and atypical disease induction