451 research outputs found

    DIGITAL SUBTRACTION ANGIOGRAPHY: PROBLEM SOLVING TOOL IN DECISION MAKING IN EQUIVOCAL CASES OF POLYTRAUMA

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    We are reporting a case of polytrauma having head injury and fracture in both bone lower limb, highlighting the importance of Digital Subtraction Angiography (DSA) in patient care and management and how important it is to be aware of normal anatomical variations. It can lead to an erroneous diagnosis and therefore change the entire management protocol of the patient. Polytrauma is an emergency , immediate and judicious intervention is the mainstay in patient's management

    Efficiency enhancement in dye sensitized solar cells through step wise cosensitization of TiO2 electrode with N719 and metal free dye

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    656-664We have used a step-wise cosensitization process to improve the power conversion efficiency (PCE) of dye sensitized solar cells employing N719 and metal free dye TA-St-CA. The DSSC sensitized with N719/TA-St-CA shows a PCE of 8.27% which is higher than for the DSSCs sensitized with either N719 (5.78 %) or TA-St-CA (4.45%). The improved PCE is attributed to the enhanced overall dye loading as well the reduced dye aggregation that has resulted from the usage of dyes with different anchoring units. The enhancement in the PCE has also been attributed to increase in both short circuit photocurrent and open circuit voltage. This was due to the reduced dark current and suppression of back recombination of injected electrons in the conduction band of TiO2 photoanode with the Iions in the electrolyte

    Rectus sheath haematoma or leaking aortic aneurysm - a diagnostic challenge: a case report

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    © 2009 Shaw et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

    Progress report no. 5

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    Includes bibliographical referencesProgress report; June 30, 1974U.S. Atomic Energy Commission contract AT(11-1)225

    A polymorphism in the base excision repair gene PARP2 is associated with differential prognosis by chemotherapy among postmenopausal breast cancer patients

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    Background: Personalized therapy considering clinical and genetic patient characteristics will further improve breast cancer survival. Two widely used treatments, chemotherapy and radiotherapy, can induce oxidative DNA damage and, if not repaired, cell death. Since base excision repair (BER) activity is specific for oxidative DNA damage, we hypothesized that germline genetic variation in this pathway will affect breast cancer-specific survival depending on treatment. Methods: We assessed in 1,408 postmenopausal breast cancer patients from the German MARIE study whether cancer specific survival after adjuvant chemotherapy, anthracycline chemotherapy, and radiotherapy is modulated by 127 Single Nucleotide Polymorphisms (SNPs) in 21 BE

    Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.

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    Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition

    Fine-mapping of the HNF1B multicancer locus identifies candidate variants that mediate endometrial cancer risk.

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    Common variants in the hepatocyte nuclear factor 1 homeobox B (HNF1B) gene are associated with the risk of Type II diabetes and multiple cancers. Evidence to date indicates that cancer risk may be mediated via genetic or epigenetic effects on HNF1B gene expression. We previously found single-nucleotide polymorphisms (SNPs) at the HNF1B locus to be associated with endometrial cancer, and now report extensive fine-mapping and in silico and laboratory analyses of this locus. Analysis of 1184 genotyped and imputed SNPs in 6608 Caucasian cases and 37 925 controls, and 895 Asian cases and 1968 controls, revealed the best signal of association for SNP rs11263763 (P = 8.4 × 10(-14), odds ratio = 0.86, 95% confidence interval = 0.82-0.89), located within HNF1B intron 1. Haplotype analysis and conditional analyses provide no evidence of further independent endometrial cancer risk variants at this locus. SNP rs11263763 genotype was associated with HNF1B mRNA expression but not with HNF1B methylation in endometrial tumor samples from The Cancer Genome Atlas. Genetic analyses prioritized rs11263763 and four other SNPs in high-to-moderate linkage disequilibrium as the most likely causal SNPs. Three of these SNPs map to the extended HNF1B promoter based on chromatin marks extending from the minimal promoter region. Reporter assays demonstrated that this extended region reduces activity in combination with the minimal HNF1B promoter, and that the minor alleles of rs11263763 or rs8064454 are associated with decreased HNF1B promoter activity. Our findings provide evidence for a single signal associated with endometrial cancer risk at the HNF1B locus, and that risk is likely mediated via altered HNF1B gene expression
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