101 research outputs found

    SUPPLEMENTARY TECHNICAL BASIS FOR ASME SECTION XI CODE CASE N-597-2

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    ABSTRACT Section XI of the American Society of Mechanical Engineers (ASME) Boiler and Pressure Vessel Code provides rules and requirements for maintaining pressure boundary integrity of components, piping, and equipment during the life of a nuclear power plant. Code Case N-597-2 of Section XI, Requirements for Analytical Evaluation of Pipe Wall Thinning, provides evaluation procedures and acceptance criteria to justify continued operation of Class 1, 2 and 3 piping items subjected to wall thinning by a mechanism such as flow-accelerated corrosion. The acceptance criteria ensure that margins equivalent to those of the ASME B&PV Code are maintained. The technical basis for Code Case N-597-2 was previously presented at the 1999 ASME Pressure Vessels and Piping Conference. Since then, the ASME Section XI Working Group on Pipe Flaw Evaluation has identified the need for further explanation of the technical basis for the Code Case, such as the procedures for evaluation of wall thickness less than the Construction Code Design Pressure-based minimum allowable wall thickness, t min . This paper provides an additional description of the Code Case technical basis and validation against experimental and historic wall thinning events. NOMENCLATURE a = depth of an axial flaw A = reinforcement area required for a Class 1 pipe under internal pressure in accordance with rules in Section III of the ASME B&PV Code A i = predicted inside area of the cross-section of the pipe A o = total cross-sectional area of the pipe based on nominal outside diameter A p = predicted metal cross-sectional area of the pipe A rein = reinforcement area required for a Class 2 or 3 pipe under internal pressure in accordance with rules in Section III of the ASME B&PV Code B = parameter used to calculate maximum allowable length of an axial flaw in ANSI/ASME B31G d = distance from the center of a local thinned area defining the limits of reinforcement for Class 2 and 3 piping in accordance with the Construction Code D o = nominal outside diameter of the piping item f = stress range reduction factor for cyclic conditions for Class 2 and 3 piping i = stress intensification factor for Class 2 and 3 piping i 0 = stress intensification factor based on the design-basis geometry of the piping item k = constant used to describe the assumed linear increase in stress intensification factor i L = maximum extent of a local thinned area with t p < t nom L A = distance used to define limits of reinforcement for Class 1 piping in accordance with rules in Section III of the ASME B&PV Code L ax = maximum allowable length of an axial flaw from ANSI/ASME B31G L m = maximum extent of a local thinned area with t p < t min L m(a) = axial extent of a local thinned area with t p < t min L m(t) = transverse (circumferential) extent of a local thinned area with t p < t min M b = bending moment n = number of load cycles N = number of allowable load cycles N' = number of allowable load cycles corresponding to an assumed linear increase in stress intensification factor i N 0 = number of allowable load cycles based on the as-installed geometry of the piping item P = Design Pressure R = mean radius of the piping item based on nominal outside radius and nominal wall thickness R min = mean radius of the piping item based on nominal outside radius and t min s = stress range due to cyclic loading s 0 = stress range due to cyclic loading based on the design basis geometry of the piping item 1 Copyright © 2006 by ASME = predicted distribution of wall thickness at the end of the evaluation period t p,min = minimum predicted wall thickness at the end of the evaluation period y = factor required by the applicable piping Construction Code in the calculation of t min , and is equal to 0.4 Z min = predicted minimum section modulus of the thinned section of pipe δ = nominal distance between the center of the pipe and the neutral axis of the thinned pipe section σ

    A review of silhouette extraction algorithms for use within visual hull pipelines

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    © 2020, © 2020 Informa UK Limited, trading as Taylor & Francis Group. Markerless motion capture would permit the study of human biomechanics in environments where marker-based systems are impractical, e.g. outdoors or underwater. The visual hull tool may enable such data to be recorded, but it requires the accurate detection of the silhouette of the object in multiple camera views. This paper reviews the top-performing algorithms available to date for silhouette extraction, with the visual hull in mind as the downstream application; the rationale is that higher-quality silhouettes would lead to higher-quality visual hulls, and consequently better measurement of movement. This paper is the first attempt in the literature to compare silhouette extraction algorithms that belong to different fields of Computer Vision, namely background subtraction, semantic segmentation, and multi-view segmentation. It was found that several algorithms exist that would be substantial improvements over the silhouette extraction algorithms traditionally used in visual hull pipelines. In particular, FgSegNet v2 (a background subtraction algorithm), DeepLabv3+ JFT (a semantic segmentation algorithm), and Djelouah 2013 (a multi-view segmentation algorithm) are the most accurate and promising methods for the extraction of silhouettes from 2D images to date, and could seamlessly be integrated within a visual hull pipeline for studies of human movement or biomechanics

    Association of Methylentetraydrofolate Reductase (MTHFR) 677 C > T gene polymorphism and homocysteine levels in psoriasis vulgaris patients from Malaysia: a case-control study

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    <p>Abstract</p> <p>Background</p> <p>The methylenetetrahydrofolate reductase (MTHFR) enzyme catalyzes the reduction of 5, 10-methylenetetrahydrofolate to 5-methyltetrahydrofolate and methyl donors. The methyl donors are required for the conversion of homocysteine to methionine. Mutation of MTHFR 677 C > T disrupts its thermostability therefore leads to defective enzyme activities and dysregulation of homocysteine levels.</p> <p>Methods</p> <p>This case-control study (n = 367) was conducted to investigate the correlation of the MTHFR gene polymorphism [NM_005957] and psoriasis vulgaris amongst the Malaysian population. Overnight fasting blood samples were collected from a subgroup of consented psoriasis vulgaris patients and matched controls (n = 84) for the quantification of homocysteine, vitamin B<sub>12 </sub>and folic acid levels.</p> <p>Results</p> <p>There was no significant increase of the MTHFR 677 C > T mutation in patients with psoriasis vulgaris compared with controls (<it>χ</it><sup>2 </sup>= 0.733, p = 0.392). No significant association between homocysteine levels and MTHFR gene polymorphism in cases and controls were observed (F = 0.91, df = 3, 80, p = 0.44). However, homocysteine levels in cases were negatively correlated with vitamin B<sub>12 </sub>(r = -0.173) and folic acid (r = -0.345) levels. Vitamin B<sub>12 </sub>and folic acid levels in cases were also negatively correlated (r = -0.164).</p> <p>Conclusions</p> <p>Our results indicate that there was no significant association between the MTHFR gene polymorphism and psoriasis vulgaris in the Malaysian population. There was no significant increase of the plasma homocysteine level in the psoriasis patients compared to the controls.</p

    Neoplastic transformation of rat liver epithelial cells is enhanced by non-transferrin-bound iron

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    <p>Abstract</p> <p>Background</p> <p>Iron overload is associated with liver toxicity, cirrhosis, and hepatocellular carcinoma in humans. While most iron circulates in blood as transferrin-bound iron, non-transferrin-bound iron (NTBI) also becomes elevated and contributes to toxicity in the setting of iron overload. The mechanism for iron-related carcinogenesis is not well understood, in part due to a shortage of suitable experimental models. The primary aim of this study was to investigate NTBI-related hepatic carcinogenesis using T51B rat liver epithelial cells, a non-neoplastic cell line previously developed for carcinogenicity and tumor promotion studies.</p> <p>Methods</p> <p>T51B cells were loaded with iron by repeated addition of ferric ammonium citrate (FAC) to the culture medium. Iron internalization was documented by chemical assay, ferritin induction, and loss of calcein fluorescence. Proliferative effects were determined by cell count, toxicity was determined by MTT assay, and neoplastic transformation was assessed by measuring colony formation in soft agar. Cyclin levels were measured by western blot.</p> <p>Results</p> <p>T51B cells readily internalized NTBI given as FAC. Within 1 week of treatment at 200 μM, there were significant but well-tolerated toxic effects including a decrease in cell proliferation (30% decrease, p < 0.01). FAC alone induced little or no colony formation in soft agar. In contrast, FAC addition to cells previously initiated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) resulted in a concentration dependent increase in colony formation. This was first detected at 12 weeks of FAC treatment and increased at longer times. At 16 weeks, colony formation increased more than 10 fold in cells treated with 200 μM FAC (p < 0.001). The iron chelator desferoxamine reduced both iron uptake and colony formation. Cells cultured with 200 μM FAC showed decreased cyclin D1, decreased cyclin A, and increased cyclin B1.</p> <p>Conclusion</p> <p>These results establish NTBI as a tumor promoter in T51B rat liver epithelial cells. Changes in cyclin proteins suggest cell cycle disregulation contributes to tumor promotion by NTBI in this liver cell model.</p

    The Thyroid Hormone Receptors Modulate the Skin Response to Retinoids

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    [Background]: Retinoids play an important role in skin homeostasis and when administered topically cause skin hyperplasia, abnormal epidermal differentiation and inflammation. Thyroidal status in humans also influences skin morphology and function and we have recently shown that the thyroid hormone receptors (TRs) are required for a normal proliferative response to 12-O-tetradecanolyphorbol-13-acetate (TPA) in mice. [Methodology/Principal Findings]: We have compared the epidermal response of mice lacking the thyroid hormone receptor binding isoforms TRα1 and TRβ to retinoids and TPA. Reduced hyperplasia and a decreased number of proliferating cells in the basal layer in response to 9-cis-RA and TPA were found in the epidermis of TR-deficient mice. Nuclear levels of proteins important for cell proliferation were altered, and expression of keratins 5 and 6 was also reduced, concomitantly with the decreased number of epidermal cell layers. In control mice the retinoid (but not TPA) induced parakeratosis and diminished expression of keratin 10 and loricrin, markers of early and terminal epidermal differentiation, respectively. This reduction was more accentuated in the TR deficient animals, whereas they did not present parakeratosis. Therefore, TRs modulate both the proliferative response to retinoids and their inhibitory effects on skin differentiation. Reduced proliferation, which was reversed upon thyroxine treatment, was also found in hypothyroid mice, demonstrating that thyroid hormone binding to TRs is required for the normal response to retinoids. In addition, the mRNA levels of the pro-inflammatory cytokines TNFα and IL-6 and the chemotactic proteins S1008A and S1008B were significantly elevated in the skin of TR knock-out mice after TPA or 9-cis-RA treatment and immune cell infiltration was also enhanced. [Conclusions/significance]: Since retinoids are commonly used for the treatment of skin disorders, these results demonstrating that TRs regulate skin proliferation, differentiation and inflammation in response to these compounds could have not only physiological but also therapeutic implications.This work was supported by grants BFU2007-62402 and SAF2008-00121 from Ministerio de Ciencia e Innovación, RD06/0020/0036 and RD06/0020/0029 from the Fondo de Investigaciones Sanitarias and by the European Grant CRESCENDO (FP-018652).Peer reviewe

    Tai Chi on psychological well-being: systematic review and meta-analysis

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    <p>Abstract</p> <p>Background</p> <p>Physical activity and exercise appear to improve psychological health. However, the quantitative effects of Tai Chi on psychological well-being have rarely been examined. We systematically reviewed the effects of Tai Chi on stress, anxiety, depression and mood disturbance in eastern and western populations.</p> <p>Methods</p> <p>Eight English and 3 Chinese databases were searched through March 2009. Randomized controlled trials, non-randomized controlled studies and observational studies reporting at least 1 psychological health outcome were examined. Data were extracted and verified by 2 reviewers. The randomized trials in each subcategory of health outcomes were meta-analyzed using a random-effects model. The quality of each study was assessed.</p> <p>Results</p> <p>Forty studies totaling 3817 subjects were identified. Approximately 29 psychological measurements were assessed. Twenty-one of 33 randomized and nonrandomized trials reported that 1 hour to 1 year of regular Tai Chi significantly increased psychological well-being including reduction of stress (effect size [ES], 0.66; 95% confidence interval [CI], 0.23 to 1.09), anxiety (ES, 0.66; 95% CI, 0.29 to 1.03), and depression (ES, 0.56; 95% CI, 0.31 to 0.80), and enhanced mood (ES, 0.45; 95% CI, 0.20 to 0.69) in community-dwelling healthy participants and in patients with chronic conditions. Seven observational studies with relatively large sample sizes reinforced the beneficial association between Tai Chi practice and psychological health.</p> <p>Conclusions</p> <p>Tai Chi appears to be associated with improvements in psychological well-being including reduced stress, anxiety, depression and mood disturbance, and increased self-esteem. Definitive conclusions were limited due to variation in designs, comparisons, heterogeneous outcomes and inadequate controls. High-quality, well-controlled, longer randomized trials are needed to better inform clinical decisions.</p

    Defining the Role of the MHC in Autoimmunity: A Review and Pooled Analysis

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    The major histocompatibility complex (MHC) is one of the most extensively studied regions in the human genome because of the association of variants at this locus with autoimmune, infectious, and inflammatory diseases. However, identification of causal variants within the MHC for the majority of these diseases has remained difficult due to the great variability and extensive linkage disequilibrium (LD) that exists among alleles throughout this locus, coupled with inadequate study design whereby only a limited subset of about 20 from a total of approximately 250 genes have been studied in small cohorts of predominantly European origin. We have performed a review and pooled analysis of the past 30 years of research on the role of the MHC in six genetically complex disease traits – multiple sclerosis (MS), type 1 diabetes (T1D), systemic lupus erythematosus (SLE), ulcerative colitis (UC), Crohn's disease (CD), and rheumatoid arthritis (RA) – in order to consolidate and evaluate the current literature regarding MHC genetics in these common autoimmune and inflammatory diseases. We corroborate established MHC disease associations and identify predisposing variants that previously have not been appreciated. Furthermore, we find a number of interesting commonalities and differences across diseases that implicate both general and disease-specific pathogenetic mechanisms in autoimmunity

    Joining S100 proteins and migration:for better or for worse, in sickness and in health

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    The vast diversity of S100 proteins has demonstrated a multitude of biological correlations with cell growth, cell differentiation and cell survival in numerous physiological and pathological conditions in all cells of the body. This review summarises some of the reported regulatory functions of S100 proteins (namely S100A1, S100A2, S100A4, S100A6, S100A7, S100A8/S100A9, S100A10, S100A11, S100A12, S100B and S100P) on cellular migration and invasion, established in both culture and animal model systems and the possible mechanisms that have been proposed to be responsible. These mechanisms involve intracellular events and components of the cytoskeletal organisation (actin/myosin filaments, intermediate filaments and microtubules) as well as extracellular signalling at different cell surface receptors (RAGE and integrins). Finally, we shall attempt to demonstrate how aberrant expression of the S100 proteins may lead to pathological events and human disorders and furthermore provide a rationale to possibly explain why the expression of some of the S100 proteins (mainly S100A4 and S100P) has led to conflicting results on motility, depending on the cells used. © 2013 Springer Basel

    Comparative performances of machine learning methods for classifying Crohn Disease patients using genome-wide genotyping data

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    Abstract: Crohn Disease (CD) is a complex genetic disorder for which more than 140 genes have been identified using genome wide association studies (GWAS). However, the genetic architecture of the trait remains largely unknown. The recent development of machine learning (ML) approaches incited us to apply them to classify healthy and diseased people according to their genomic information. The Immunochip dataset containing 18,227 CD patients and 34,050 healthy controls enrolled and genotyped by the international Inflammatory Bowel Disease genetic consortium (IIBDGC) has been re-analyzed using a set of ML methods: penalized logistic regression (LR), gradient boosted trees (GBT) and artificial neural networks (NN). The main score used to compare the methods was the Area Under the ROC Curve (AUC) statistics. The impact of quality control (QC), imputing and coding methods on LR results showed that QC methods and imputation of missing genotypes may artificially increase the scores. At the opposite, neither the patient/control ratio nor marker preselection or coding strategies significantly affected the results. LR methods, including Lasso, Ridge and ElasticNet provided similar results with a maximum AUC of 0.80. GBT methods like XGBoost, LightGBM and CatBoost, together with dense NN with one or more hidden layers, provided similar AUC values, suggesting limited epistatic effects in the genetic architecture of the trait. ML methods detected near all the genetic variants previously identified by GWAS among the best predictors plus additional predictors with lower effects. The robustness and complementarity of the different methods are also studied. Compared to LR, non-linear models such as GBT or NN may provide robust complementary approaches to identify and classify genetic markers
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