Full-spectrum noise prediction of the high-speed train head under multi-physics coupling excitations based on statistical energy analysis

The force between wheels and rails of the high-speed train was firstly extracted and applied into the computational model of radiation noises of wheels and rail respectively. As a result, the radiation noise of wheels and rails was obtained. As can be seen from the result, radiation noises of wheels had an obvious directivity on the body surface, while radiation noises of rails had an obvious periodicity on the body surface. With the increase of the analyzed frequency, both directivity and periodicity were shown more obviously. Then the aerodynamic model of the high-speed train was established, and the pressure and velocity distributions on the train surface were computed. The maximum pressure was at the tip of the nose of the high-speed train, the maximum velocity was at the transition of the cabin, and more serious eddy was in the rear of the high speed train. Based on the computed pressure distribution, the aerodynamic noise was distributed evenly on the entire body surface, which was gradually increased with the increasing analyzed frequency. Finally, the wheel radiation noise, rail radiation noise and aerodynamic noise were extracted as excitations and applied into the SEA (Statistical Energy Analysis) model of the high-speed train, in order to compute its full-spectrum noise under multi-physics coupling excitations. The computational result was compared with the experimental result. It was presented that the difference of average sound pressure level (SPL) was 2.8 dB between the experimental and numerical simulations within the entire analytical frequency band. The SEA model with considering the multi-physics coupling was effective

Paxillin facilitates timely neurite initiation on soft-substrate environments by interacting with the endocytic machinery.

Neurite initiation is the first step in neuronal development and occurs spontaneously in soft tissue environments. Although the mechanisms regulating the morphology of migratory cells on rigid substrates in cell culture are widely known, how soft environments modulate neurite initiation remains elusive. Using hydrogel cultures, pharmacologic inhibition, and genetic approaches, we reveal that paxillin-linked endocytosis and adhesion are components of a bistable switch controlling neurite initiation in a substrate modulus-dependent manner. On soft substrates, most paxillin binds to endocytic factors and facilitates vesicle invagination, elevating neuritogenic Rac1 activity and expression of genes encoding the endocytic machinery. By contrast, on rigid substrates, cells develop extensive adhesions, increase RhoA activity and sequester paxillin from the endocytic machinery, thereby delaying neurite initiation. Our results highlight paxillin as a core molecule in substrate modulus-controlled morphogenesis and define a mechanism whereby neuronal cells respond to environments exhibiting varying mechanical properties

Arrangement for K2∗K_2^* meson family

Two observed structures with $M=1868 \pm 8^{+ 40}_{- 57}$ MeV and $M=2073 \pm 94^{+ 245}_{- 240}$ MeV are the same states ($K_2^*(1980)$) in PDG.The analysis of the mass spectrum and the calculation of the strong decay of $K_2^*$ mesons support the low mass state of $K_2^*(1980)$ as $2^3P_2$ and the high mass state of $K_2^*(1980)$ as $1^3F_2$ in this letter. This analysis brings us very important criterion for the assignment of the observed $K_2^* (1980)$ and experimental findings for this assignment is suggested. Additionally, prediction of some partial decay widths are made on the high excitations of $K_2^*$ family. This study is crucial to establishing and searching for their higher excitations in the future.Comment: 9 pages, 6 figures. arXiv admin note: text overlap with arXiv:1810.0269

Stanniocalcin-1 promotes tumor angiogenesis through up-regulation of VEGF in gastric cancer cells

<p>Abstract</p> <p>Background</p> <p>Stanniocalcin-1(STC-1) is up-regulated in several cancers including gastric cancer. Evidences suggest that STC-1 is associated with carcinogenesis and angiogenic process. However, it is unclear on the exact role for STC-1 in inducing angiogenesis and tumorigeneisis.</p> <p>Method</p> <p>BGC/STC cells (high-expression of STC-1) and BGC/shSTC cells (low- expression of STC-1) were constructed to investigate the effect of STC-1 on the xenograft tumor growth and angiogenesis <it>in vitro </it>and <it>in vivo</it>. ELISA assay was used to detect the expression of vascular endothelial growth factor (VEGF) in the supernatants. Neutralizing antibody was used to inhibit VEGF expression in supernatants. The expression of phosphorylated -PKCβII, phosphorylated -ERK1/2 and phosphorylated -P38 in the BGC treated with STC-1protein was detected by western blot.</p> <p>Results</p> <p>STC-1 could promote angiogenesis <it>in vitro </it>and <it>in vivo</it>, and the angiogenesis was consistent with VEGF expression <it>in vitro</it>. Inhibition of VEGF expression in supernatants with neutralizing antibody markedly abolished angiogenesis induced by STC-1 <it>in vitro</it>. The process of STC-1-regulated VEGF expression was mediated via PKCβII and ERK1/2.</p> <p>Conclusions</p> <p>STC-1 promotes the expression of VEGF depended on the activation of PKCβII and ERK1/2 pathways. VEGF subsequently enhances tumor angiogenesis which in turn promotes the gastric tumor growth.</p

Myeloid autophagy genes protect mice against fatal TNF- and LPS-induced cytokine storm syndromes

ATG5: autophagy related 5; ATG7: autophagy related 7; ATG14: autophagy related 14; ATG16L1: autophagy related 16-like 1 (S. cerevisiae); BECN1: beclin 1, autophagy related; CASP1: caspase 1; CASP4/CASP11: caspase 4, apoptosis-related cysteine peptidase; CIM: conditionally immortalized macrophage; CLP: cecal ligation and puncture; CSS: cytokine storm syndrome; DC: dendritic cell; IFNG/IFNγ: interferon gamma; IFNGR1: interferon gamma receptor 1; ip: intraperitoneal; iv: intravenous; IL12/p70: interleukin 12, p70 heterodimer; IL18: Interleukin 18; ITGAX/CD11c: integrin alpha X; LAP: LC3-associated phagocytosis; LPS: lipopolysaccharide; LYZ2/LYSM: lysozyme 2; MAP1LC3A/LC3: microtubule-associated protein 1 light chain 3 alpha; RB1CC1/FIP200: RB1-inducible coiled-coil 1; S100A8/MRP8: S100 calcium binding protein A8 (calgranulin A); TICAM1/TRIF: TIR domain containing adaptor molecule 1; TLR4: toll-like receptor 4; TNF: tumor necrosis factor

Modulation of nucleosome-binding activity of FACT by poly(ADP-ribosyl)ation

Chromatin-modifying factors play key roles in transcription, DNA replication and DNA repair. Post-translational modification of these proteins is largely responsible for regulating their activity. The FACT (facilitates chromatin transcription) complex, a heterodimer of hSpt16 and SSRP1, is a chromatin structure modulator whose involvement in transcription and DNA replication has been reported. Here we show that nucleosome binding activity of FACT complex is regulated by poly(ADP-ribosyl)ation. hSpt16, the large subunit of FACT, is poly(ADP-ribosyl)ated by poly(ADP-ribose) polymerase-1 (PARP-1) resulting from physical interaction between these two proteins. The level of hSpt16 poly(ADP-ribosyl)ation is elevated after genotoxic treatment and coincides with the activation of PARP-1. The enhanced hSpt16 poly(ADP-ribosyl)ation level correlates with the dissociation of FACT from chromatin in response to DNA damage. Our findings suggest that poly(ADP-ribosyl)ation of hSpt16 by PARP-1 play regulatory roles for FACT-mediated chromatin remodeling

Predicting one-year mortality among elderly survivors of hospitalization for an acute myocardial infarction: results from the Cooperative Cardiovascular Project

AbstractOBJECTIVESWe sought to develop a model based on information available from the medical record that would accurately stratify elderly patients who survive hospitalization with an acute myocardial infarction (AMI) according to their risk of one-year mortality.BACKGROUNDPrediction of the risk of mortality among older survivors of an AMI has many uses, yet few studies have determined the prognostic importance of demographic, clinical and functional data that are available on discharge in a population-based sample.METHODSIn a cohort of patients aged ≥65 years who survived hospitalization for a confirmed AMI from 1994 to 1995 at acute care, nongovernmental hospitals in the U.S., we developed a parsimonious model to stratify patients by their risk of one-year mortality.RESULTSThe study sample of 103,164 patients, with a mean age of 76.8 years, had a one-year mortality of 22%. The factors with the strongest association with mortality were older age, urinary incontinence, assisted mobility, presence of heart failure or cardiomegaly any time before discharge, presence of peripheral vascular disease, body mass index <20 kg/m2, renal dysfunction (defined as creatinine >2.5 mg/dl or blood urea nitrogen >40 mg/dl) and left ventricular dysfunction (left ventricular ejection fraction <40%). On the basis of the coefficients in the model, patients were stratified into risk groups ranging from 7% to 49%.CONCLUSIONSWe demonstrate that a simple risk model can stratify older patients well by their risk of death one year after discharge for AMI

Numerical computation of aerodynamic noises of the high speed train with considering pantographs

With the improvement of the speed, aerodynamic noises of trains also become more obvious. Reducing the aerodynamic noise has become a key factor to control noises of the high speed train. This paper uses large eddy simulation and boundary element method to compute the flow field and aerodynamic noises of pantographs and trains. The result presents that there are obvious eddies at the head, push rod, and base. Two obvious separation eddies can be found around the guide rod of the head and the push rod of pantographs. The front part of the base has a layer of shear flow, which leads to a separation eddy in the back of the base while the flow moves backward. Noises of pantographs mainly concentrate around the head, base and pushrod. With the increase of the analyzed frequency, the strength of pantograph noise source is weaker and weaker. When the analyzed frequency is 500 Hz, the noise source of pantographs is mainly around joints of several structures. By comparing the computational and the experimental result of aerodynamic noises of pantographs, this result presents that they are consistent with each other in the change tendency and value within the whole analyzed frequency. This indicates that the computational model of aerodynamic noises of pantographs is effective. Pantographs have an obvious influence on the distribution of the flow field around high speed trains, especially at the end of high speed trains. High speed trains with pantographs only have an eddy at the end, but high speed trains without pantographs have two eddies at the end. When this paper conducts on numerical computation for high speed trains, pantographs should not be ignored. In the low frequency, radiation noises of high speed trains can be found mainly around pantographs and at the end of trains. At the longitudinal symmetric plane of high speed trains, the sound pressure level at the end of trains is the highest. The radiation noise around pantographs mainly concentrates around the pushrod, then base, and the last is the head

The role of EGFR mutation as a prognostic factor in survival after diagnosis of brain metastasis in non-small cell lung cancer: A systematic review and meta-analysis

Abstract Background The brain is a common site for metastasis in non-small-cell lung cancer (NSCLC). This study was designed to evaluate the relationship between the mutational of the epidermal growth factor receptor (EGFR) and overall survival (OS) in NSCLC patients with brain metastases. Methods Searches were performed in PubMed, EmBase, and the Cochrane Library to identify studies evaluating the association of EGFR mutation with OS in NSCLC patients through September 2017. Results 4373 NSCLC patients with brain metastases in 18 studies were involved. Mutated EGFR associated with significantly improved OS compared with wild type. Subgroup analyses suggested that this relationship persisted in studies conducted in Eastern, with retrospective design, with sample size ≥500, mean age of patients ≥65.0 years, percentage male < 50.0%, percentage of patients receiving tyrosine kinase inhibitor ≥30.0%. Finally, although significant publication bias was observed using the Egger test, the results were not changed after adjustment using the trim and fill method. Conclusions This meta-analysis suggests that EGFR mutation is an important predictive factor linked to improved OS for NSCLC patients with brain metastases. It can serve as a useful index in the prognostic assessment of NSCLC patients with brain metastases