Grid-Adapted FUN3D Computations for the Second High Lift Prediction Workshop

Contributions of the unstructured Reynolds-averaged Navier-Stokes code FUN3D to the 2nd AIAA CFD High Lift Prediction Workshop are described, and detailed comparisons are made with experimental data. Using workshop-supplied grids, results for the clean wing configuration are compared with results from the structured code CFL3D Using the same turbulence model, both codes compare reasonably well in terms of total forces and moments, and the maximum lift is similarly over-predicted for both codes compared to experiment. By including more representative geometry features such as slat and flap brackets and slat pressure tube bundles, FUN3D captures the general effects of the Reynolds number variation, but under-predicts maximum lift on workshop-supplied grids in comparison with the experimental data, due to excessive separation. However, when output-based, off-body grid adaptation in FUN3D is employed, results improve considerably. In particular, when the geometry includes both brackets and the pressure tube bundles, grid adaptation results in a more accurate prediction of lift near stall in comparison with the wind-tunnel data. Furthermore, a rotation-corrected turbulence model shows improved pressure predictions on the outboard span when using adapted grids

Extraskeletal Chondrosarcoma of Labium Majus

Extraskeletal myxoid chondrosarcoma (ESMC) is a rare tumor seen more often in men. It is seen to arise from soft tissue of lower extremity or buttocks. We report a case of soft tissue swelling of left labium majus in a 66-year-old female. Patient underwent wide excision with uneventful postoperative course. Histopathology of specimen confirmed it to be ESMC. Patient refused adjuvant therapy. Followup of 1 year has shown her to be disease- and symptom- free. Only two cases arising from vulva have been reported in literature . This is the third case and first from Indian subcontinent. A brief review of clinical features, diagnosis, treatment, and outcome of patients with extraskeletal chondrosarcoma is presented

Can creatine supplementation improve body composition and objective physical function in rheumatoid arthritis patients? A randomised controlled trial.

OBJECTIVE: Rheumatoid cachexia (muscle wasting) in rheumatoid arthritis (RA) patients contributes to substantial reductions in strength and impaired physical function. The objective of this randomised control trial was to investigate the effectiveness of oral creatine (Cr) supplementation in increasing lean mass and improving strength and physical function in RA patients. METHOD: In a double-blind design, 40 RA patients, were randomised to either 12 weeks supplementation of Cr or placebo. Body composition (dual energy x-ray absorptiometry, DXA, and bioelectrical impedance spectroscopy, BIS), strength and objectively-assessed physical function were measured at: baseline, day 6, week 12 and week 24. Data analysis was performed by ANCOVA. RESULTS: Creatine supplementation increased appendicular lean mass (ALM; a surrogate measure of muscle mass) by 0.52 (± 0.13) kg (P = 0.004 versus placebo), and total LM by 0.60 (± 0.37) kg (P = 0.158). The change in LM concurred with the gain in intracellular water (0.64 ± 0.22 L, P = 0.035) measured by BIS. Despite increasing ALM, Cr supplementation, relative to placebo, failed to improve isometric knee extensor (P = 0.408), handgrip strength (P = 0.833), or objectively-assessed physical function (P's = 0.335 - 0.764). CONCLUSION: In patients with RA, creatine supplementation increased muscle mass, but not strength or objective physical function. No treatment-related adverse effects were reported suggesting that Cr supplementation may offer a safe and acceptable adjunct treatment for attenuating muscle loss; this treatment may be beneficial for patients suffering from severe rheumatoid cachexia. This article is protected by copyright. All rights reserved

Pseudosarcomatous myofibroblastic proliferations of the genitourinary tract are genetically different from nodular fasciitis and lack USP6, ROS1 and ETV6 gene rearrangements

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/145266/1/his13526_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/145266/2/his13526.pd

The landscape of somatic copy-number alteration across human cancers

available in PMC 2010 August 18.A powerful way to discover key genes with causal roles in oncogenesis is to identify genomic regions that undergo frequent alteration in human cancers. Here we present high-resolution analyses of somatic copy-number alterations (SCNAs) from 3,131 cancer specimens, belonging largely to 26 histological types. We identify 158 regions of focal SCNA that are altered at significant frequency across several cancer types, of which 122 cannot be explained by the presence of a known cancer target gene located within these regions. Several gene families are enriched among these regions of focal SCNA, including the BCL2 family of apoptosis regulators and the NF-κΒ pathway. We show that cancer cells containing amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend on the expression of these genes for survival. Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in several cancer types.National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, P50CA90578)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, R01CA109038))National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, R01CA109467)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, P01CA085859)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, P01CA 098101)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, K08CA122833

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

Solitary skin metastasis from sarcomatoid carcinoma of the bladder: a case report

<p>Abstract</p> <p>Introduction</p> <p>Cutaneous metastases from carcinomas of the bladder are very rare. They are related to advanced stages of the disease and have poor prognosis with low survival rates. The common treatment modality of cutaneous metastases from a primary bladder cancer is wide local excision followed by chemotherapy.</p> <p>Case presentation</p> <p>We report a case of solitary skin metastasis from a rare type of urinary bladder carcinoma in a 68 year-old Caucasian man. Urinary bladder carcinoma metastasizing to the skin is an uncommon finding despite the high incidence of this tumor. Skin metastasis generally presents in the late stages of this disease and indicates a poor outcome.</p> <p>Conclusions</p> <p>Because of the extremely aggressive malignant potential of sarcomatoid carcinomas, the indications for a transurethral resection of the bladder should be carefully assessed and suitable therapeutic strategies should be examined further.</p

BORIS, a paralogue of the transcription factor, CTCF, is aberrantly expressed in breast tumours

BORIS (for brother of the regulator of imprinted sites), a paralogue of the transcription factor, CTCF, is a novel member of the cancer-testis antigen family. The aims of the present study were as follows: (1) to investigate BORIS expression in breast cells and tumours using immunohistochemical staining, western and real-time RT–PCR analyses and (2) assess potential correlation between BORIS levels in tumours with clinical/pathological parameters. BORIS was detected in all 18 inspected breast cell lines, but not in a primary normal breast cell culture. In 70.7% (41 of 58 cases) BORIS was observed in breast tumours. High levels of BORIS correlated with high levels of progesterone receptor (PR) and oestrogen receptor (ER). The link between BORIS and PR/ER was further confirmed by the ability of BORIS to activate the promoters of the PR and ER genes in the reporter assays. Detection of BORIS in a high proportion of breast cancer patients implies potential practical applications of BORIS as a molecular biomarker of breast cancer. This may be important for diagnosis of the condition and for the therapeutic use of BORIS. The ability of BORIS to activate promoters of the RP and ER genes points towards possible involvement of BORIS in the establishment, progression and maintenance of breast tumours