Static and unsteady pressure measurements on a 50 degree clipped delta wing at M = 0.9

Pressures were measured with Freon as the test medium. Data taken at M = 0.9 is presented for static and oscillatory deflections of the trailing edge control surface and for the wing in pitch. Comparisons of the static measured data are made with results computed using the Bailey-Ballhaus small disturbance code

Steady and unsteady transonic pressure measurements on a clipped delta wing for pitching and control-surface oscillations

Steady and unsteady pressures were measured on a clipped delta wing with a 6-percent circular-arc airfoil section and a leading-edge sweep angle of 50.40 deg. The model was oscillated in pitch and had an oscillating trailing-edge control surface. Measurements were concentrated over a Mach number range from 0.88 to 0.94; less extensive measurements were made at Mach numbers of 0.40, 0.96, and 1.12. The Reynolds number based on mean chord was approximately 10 x 10 to the 6th power. The interaction of wing or control-surface deflection with the formation of shock waves and with a leading-edge vortex generated complex pressure distributions that were sensitive to frequency and to small changes in Mach number at transonic speeds

Transonic steady- and unsteady-pressure measurements on a high-aspect-ratio supercritical-wing model with oscillating control surfaces

A supercritical wing with an aspect ratio of 10.76 and with two trailing-edge oscillating control surfaces is described. The semispan wing is instrumented with 252 static orifices and 164 in situ dynamic-pressure gages for studying the effects of control-surface position and motion on steady- and unsteady-pressures at transonic speeds. Results from initial tests conducted in the Langley Transonic Dynamics Tunnel at two Reynolds numbers are presented in tabular form

Transonic unsteady airloads on an energy efficient transport wing with oscillating control surfaces

An aspect ratio 10.8 supercritical wing with oscillating control surfaces is described. The wing is instrumental with 252 static orifices and 164 in situ dynamic pressure transducers for studying the effects of control surface deflection on steady and unsteady pressures at transonic speeds. Results from initial wind tunnel tests conducted in the Langley Transonic Dynamics Tunnel are discussed. Unsteady pressure results are presented for two trailing edge control surfaces oscillating separately at the design Mach number of 0.78. Some experimental results are compared with analytical results obtained by using linear lifting surface theory

Analysis of colorectal cancers in British Bangladeshi identifies early onset, frequent mucinous histotype and a high prevalence of RBFOX1 deletion

PMCID: PMC3544714This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

Topological Analysis of Metabolic Networks Integrating Co-Segregating Transcriptomes and Metabolomes in Type 2 Diabetic Rat Congenic Series

Background: The genetic regulation of metabolic phenotypes (i.e., metabotypes) in type 2 diabetes mellitus is caused by complex organ-specific cellular mechanisms contributing to impaired insulin secretion and insulin resistance. Methods: We used systematic metabotyping by 1H NMR spectroscopy and genome-wide gene expression in white adipose tissue to map molecular phenotypes to genomic blocks associated with obesity and insulin secretion in a series of rat congenic strains derived from spontaneously diabetic Goto-Kakizaki (GK) and normoglycemic Brown-Norway (BN) rats. We implemented a network biology strategy approach to visualise shortest paths between metabolites and genes significantly associated with each genomic block. Results: Despite strong genomic similarities (95-99%) among congenics, each strain exhibited specific patterns of gene expression and metabotypes, reflecting metabolic consequences of series of linked genetic polymorphisms in the congenic intervals. We subsequently used the congenic panel to map quantitative trait loci underlying specific metabotypes (mQTL) and genome-wide expression traits (eQTL). Variation in key metabolites like glucose, succinate, lactate or 3-hydroxybutyrate, and second messenger precursors like inositol was associated with several independent genomic intervals, indicating functional redundancy in these regions. To navigate through the complexity of these association networks we mapped candidate genes and metabolites onto metabolic pathways and implemented a shortest path strategy to highlight potential mechanistic links between metabolites and transcripts at colocalized mQTLs and eQTLs. Minimizing shortest path length drove prioritization of biological validations by gene silencing. Conclusions: These results underline the importance of network-based integration of multilevel systems genetics datasets to improve understanding of the genetic architecture of metabotype and transcriptomic regulations and to characterize novel functional roles for genes determining tissue-specific metabolism

Parametric flutter studies of an arrow-wing configuration: Some early results

Some early experimental results from a combined experimental and analytical study being conducted at NASA-Langley of the transonic flutter characterisitics of a generic arrow wing configuration are presented. The planned study includes the parametric variation of a variety of structural and geometric characteristics. Presented here are flutter results of the basic arrow wing, for the basic wing with the addition of two simulated lower-surface-mounted engine nacelles, and for the basic wing with the addition of both the fin and the engine nacelles

Whole-genome sequencing of bladder cancers reveals somatic CDKN1A mutations and clinicopathological associations with mutation burden

Bladder cancers are a leading cause of death from malignancy. Molecular markers might predict disease progression and behaviour more accurately than the available prognostic factors. Here we use whole-genome sequencing to identify somatic mutations and chromosomal changes in 14 bladder cancers of different grades and stages. As well as detecting the known bladder cancer driver mutations, we report the identification of recurrent protein-inactivating mutations in CDKN1A and FAT1. The former are not mutually exclusive with TP53 mutations or MDM2 amplification, showing that CDKN1A dysfunction is not simply an alternative mechanism for p53 pathway inactivation. We find strong positive associations between higher tumour stage/grade and greater clonal diversity, the number of somatic mutations and the burden of copy number changes. In principle, the identification of sub-clones with greater diversity and/or mutation burden within early-stage or low-grade tumours could identify lesions with a high risk of invasive progression

Combined exome and transcriptome sequencing of non-muscle-invasive bladder cancer: associations between genomic changes, expression subtypes, and clinical outcomes.

BACKGROUND: Three-quarters of bladder cancer patients present with early-stage disease (non-muscle-invasive bladder cancer, NMIBC, UICC TNM stages Ta, T1 and Tis); however, most next-generation sequencing studies to date have concentrated on later-stage disease (muscle-invasive BC, stages T2+). We used exome and transcriptome sequencing to comprehensively characterise NMIBCs of all grades and stages to identify prognostic genes and pathways that could facilitate treatment decisions. Tumour grading is based upon microscopy and cellular appearances (grade 1 BCs are less aggressive, and grade 3 BCs are most aggressive), and we chose to also focus on the most clinically complex NMIBC subgroup, those patients with grade 3 pathological stage T1 (G3 pT1) disease. METHODS: Whole-exome and RNA sequencing were performed in total on 96 primary NMIBCs including 22 G1 pTa, 14 G3 pTa and 53 G3 pT1s, with both exome and RNA sequencing data generated from 75 of these individual samples. Associations between genomic alterations, expression profiles and progression-free survival (PFS) were investigated. RESULTS: NMIBCs clustered into 3 expression subtypes with different somatic alteration characteristics. Amplifications of ARNT and ERBB2 were significant indicators of worse PFS across all NMIBCs. High APOBEC mutagenesis and high tumour mutation burden were both potential indicators of better PFS in G3pT1 NMIBCs. The expression of individual genes was not prognostic in BCG-treated G3pT1 NMIBCs; however, downregulated interferon-alpha and gamma response pathways were significantly associated with worse PFS (adjusted p-value < 0.005). CONCLUSIONS: Multi-omic data may facilitate better prognostication and selection of therapeutic interventions in patients with G3pT1 NMIBC. These findings demonstrate the potential for improving the management of high-risk NMIBC patients and warrant further prospective validation