Static fracture and modal analysis simulation of a gas turbine compressor blade and bladed disk system

This paper presents a methodology for conducting a 3-D static fracture analysis with applications to a gas turbine compressor blade. An open crack model is considered in the study and crack-tip driving parameters are estimated by using 3-D singular crack-tip elements in ANSYS. The static fracture analysis is verified with a special purpose fracture code (FRANC3D). Once the crack front is perfectly defined and validated, a free vibration study is conducted by analyzing the natural frequencies and modeshapes for both a single blade and bladed disk system. Taking advantage of high performance computing resources, a high fidelity finite element model is considered in the parametric investigation. In the fracture simulation, the influence of the size of a single edged crack as well as the rotational velocity on fracture parameters (stress intensity factors and J-Integral) are evaluated. Results demonstrate that for the applied loading condition, a mixed mode crack propagation is expected. In the modal analysis study, increasing the depth of the crack leads to a decrease in the natural frequencies of both the single blade and bladed disk system, while increasing the rotational velocity increases the natural frequencies. The presence of a crack also leads to mode localization for all mode families, a phenomenon that cannot be captured by a single blade analysis.The authors gratefully acknowledge the support of the Qatar National Research Fund through Grant number NPRP 7-1153-2-432. The authors also thank Texas A&M at Qatar?s Advanced Scientific Computing (TASC) for access to the RAAD Supercomputer.Scopu

A study on the mutagenic effect of dichloromethane extract of pickled vegetables from high risk area for nasopharyngeal carcinoma (NPC)-in Sihui County

The mutagenic effect of dichloromethane extract of pickles collected from Sinhui County was examined. Sample I markedly increased the frequency of sister chromatid exchange (SCE) and the rate of micronucleus (MN) in mice. Sample II also induced an increase in SCE frequency significantly, but the increase in MN rate was slight. Chemical analyses showed that two samples of pickles contained 37.83ppb and 33.38ppb of volatile nitrosamines, respectively, which alone could not explain the observed mutagenic effect. These results sug ested that the pickled vegetables taken from NPC high-risk area, Sihui County, may contain some mutagen(s) besides volatile nitrosamines. 本文報告四會縣醃菜二氯甲烷提取液的誘變性試驗。醃菜樣本提取液Ⅰ號引起姐妹染色單體交換(SCE)率及微核(MN)率顯著升高,醃菜樣本提取液Ⅱ號亦引起SCE率明顯升高,但MN率僅略有升高。化學分析表明,該兩份醃菜的揮發性亞硝胺含量分別為37.83、33.38 ppb。醃菜提取液的誘變性似不能單用亞硝胺來解釋。實驗結果提示,鼻咽癌高發區四會縣醃菜中可能含有除揮發性亞硝胺以外的其他誘變性物質

Transition of tumor-associated macrophages from MHC class IIhi to MHC class IIlow mediates tumor progression in mice

<p>Abstract</p> <p>Background</p> <p>Tumor-associated macrophages (TAMs) are the most abundant immune cells within the tumor stroma and play a crucial role in tumor development. Although clinical investigations indicate that high levels of macrophage (MΦ) infiltration into tumors are associated with a poor prognosis, the exact role played by TAMs during tumor development remains unclear. The present study aimed to investigate dynamic changes in TAM major histocompatibility complex (MHC) class II expression levels and to assess the effects of these changes on tumor progression.</p> <p>Results</p> <p>Significant inhibition of tumor growth in the murine hepatocellular carcinoma Hepa1-6 model was closely associated with partial TAM depletion. Strikingly, two distinct TAM subsets were found to coexist within the tumor microenvironment during Hepa1-6 tumor development. An MHC class II^hiTAM population appeared during the early phase of tumor development and was associated with tumor suppression; however, an MHC class II^lowTAM population became increasingly predominant as the tumor progressed.</p> <p>Conclusions</p> <p>Tumor progression was positively correlated with increasing infiltration of the tumor tissues by MHC class II^lowTAMs. Thus, targeting the transition of MΦ may be a novel strategy for drug development and immunotherapy.</p

Solution structure of a repeated unit of the ABA-1 nematode polyprotein allergen of ascaris reveals a novel fold and two discrete lipid-binding sites

Parasitic nematode worms cause serious health problems in humans and other animals. They can induce allergic-type immune responses, which can be harmful but may at the same time protect against the infections. Allergens are proteins that trigger allergic reactions and these parasites produce a type that is confined to nematodes, the nematode polyprotein allergens (NPAs). These are synthesized as large precursor proteins comprising repeating units of similar amino acid sequence that are subsequently cleaved into multiple copies of the allergen protein. NPAs bind small lipids such as fatty acids and retinol (Vitamin A) and probably transport these sensitive and insoluble compounds between the tissues of the worms. Nematodes cannot synthesize these lipids, so NPAs may also be crucial for extracting nutrients from their hosts. They may also be involved in altering immune responses by controlling the lipids by which the immune and inflammatory cells communicate. We describe the molecular structure of one unit of an NPA, the well-known ABA-1 allergen of Ascaris and find its structure to be of a type not previously found for lipid-binding proteins, and we describe the unusual sites where lipids bind within this structur

TRIM32 Regulates Skeletal Muscle Stem Cell Differentiation and Is Necessary for Normal Adult Muscle Regeneration

Limb girdle muscular dystrophy type 2H (LGMD2H) is an inherited autosomal recessive disease of skeletal muscle caused by a mutation in the TRIM32 gene. Currently its pathogenesis is entirely unclear. Typically the regeneration process of adult skeletal muscle during growth or following injury is controlled by a tissue specific stem cell population termed satellite cells. Given that TRIM32 regulates the fate of mammalian neural progenitor cells through controlling their differentiation, we asked whether TRIM32 could also be essential for the regulation of myogenic stem cells. Here we demonstrate for the first time that TRIM32 is expressed in the skeletal muscle stem cell lineage of adult mice, and that in the absence of TRIM32, myogenic differentiation is disrupted. Moreover, we show that the ubiquitin ligase TRIM32 controls this process through the regulation of c-Myc, a similar mechanism to that previously observed in neural progenitors. Importantly we show that loss of TRIM32 function induces a LGMD2H-like phenotype and strongly affects muscle regeneration in vivo. Our studies implicate that the loss of TRIM32 results in dysfunctional muscle stem cells which could contribute to the development of LGMD2H