690 research outputs found

    A Study of the Stress Corrosion Crack Initiation Stage in Alpha-Brass.

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    The objective of the present work was to provide an insight to the nucleation and evolution of deformation patterns occurring during transgranular stress corrosion cracking (TGSCC) and produce new alternatives for addressing the nature of the embrittlement process. Flat, tensile α\alpha-brass (72Cu-28Zn) specimens were tested in 5 M NH\sb4OH, 0.1 M CuSO\sb4 and 1 M NaNO\sb2 solutions at a strain rate of 1\times 10\sp{-5} s\sp{-1}. Slip band spacing (SBS) and slip band heights (SBH) were measured as a function of strain by conducting interrupted experiments in the SCC environments and were compared with those developed during laboratory air experiments. The presence of the TGSCC-causing environment during straining was found to promote localized plastic deformation at the near-surface region, induce strain hardening and more importantly to produce an entirely different deformation pattern compared to that developed in laboratory air. The deformation evolved in the presence of the TGSCC electrolytes was highly localized, exhibiting a dense SBS but coarse SBH. Also, a periodicity was exhibited by the crack initiation process. The amount of localized strain developed at the specimen near-surface region prior to nucleation of stress corrosion cracks was found to be equivalent to the strain required for ductile fracture of the material in air, suggesting the existence of a fundamental fracture criterion. In view of the present observations, an environment-induced deformation localization mechanism is introduced to explain TGSCC initiation and propagation. The main elements of the proposed mechanism are: (i) strain localization due to corrosion instability and periodicity; (ii) vacancy-induced dislocation emission at the surface region and (iii) vacancy-dislocation interaction localizing deformation and modifying dislocation arrangement

    Design and Evaluation of Digital Baseband Converter Sub-channel Delay Compensation Method on Bandwidth Synthesis

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    The effect of sub-channel delay on bandwidth synthesis is investigated to eliminate the “phase step” phenomenon in bandwidth synthesis during the test of CDBE (Chinese Digital Backend). Through formula derivation, we realize that sub-channel delay may cause phase discontinuity between different sub-channels. Theoretical analysis shows that sub-channel delay can induce bandwidth synthesis error in group delay measurement of the linear system. Furthermore, in the differential delay measurement between two stations, bandwidth synthesis error may occur when the LO (Local Oscillator) frequency differences of corresponding sub-channels are not identical. Error-free conditions are discussed under different applications. The phase errors among different sub-channels can be removed manually. However, the most effective way is the compensation of sub-channel delay. A sub-channel delay calculation method based on Modelsim is proposed. The compensation method is detailed. Simulation and field experiments are presented to verify our approach

    A Gas-Kinetic Scheme for Reactive Flows

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    In this paper, the gas-kinetic BGK scheme for the compressible flow equations is extended to chemical reactive flow. The mass fraction of the unburnt gas is implemented into the gas kinetic equation by assigning a new internal degree of freedom to the particle distribution function. The new variable can be also used to describe fluid trajectory for the nonreactive flows. Due to the gas-kinetic BGK model, the current scheme basically solves the Navier-Stokes chemical reactive flow equations. Numerical tests validate the accuracy and robustness of the current kinetic method

    Top Yukawa Coupling Determination at High Energy Muon Collider

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    The Top Yukawa coupling profoundly influences several core mysteries linked to the electroweak scale and the Higgs boson. We study the feasibility of measuring the Top Yukawa coupling at high-energy muon colliders by examining the high-energy dynamics of the weak boson fusion to top quark pair processes. A deviation of the Top Yukawa coupling from the Standard Model would lead modified VVttˉV V \rightarrow t\bar{t} process, violating unitarity at high energy. Our analysis reveals that utilizing a muon collider with a center-of-mass energy of 10 TeV and an integrated luminosity of 10 ab1^{-1} allows us to investigate the Top Yukawa coupling with a precision surpassing 1.5\%, more than one order of magnitude better than the precision from ttˉht\bar t h channel at muon colliders. This precision represents a notable enhancement compared to the anticipated sensitivities of the High-Luminosity LHC (3.4\%) and those at muon colliders derived from the ttˉHt\bar{t} H process.Comment: 33 pages, 13 figure

    脑舒胶囊对衰老小鼠免疫功能的调节作用

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    Objective: To observe the effects of NaoShu capsule on immune function of aging mice. Methods: Aging mice was induced by subcutaneous injections model was induced by subcutaneous injections with 5% D-galactose at the neck for 6 weeks, IL-2 and IL-6 content in serum were detected by means of radio-immunity, and calculating the index of organ by a ratio of the weight of thymus and spleen and the weight of mice. Results: Compared with the control group, the thymus and spleen index of mice was decreased obvious; the IL-2 content was obvious decreased, and the IL-6 content was obvious increased in aging model group. Compared with the model group, the the IL-2 content was enhanced and the IL-6 content was obvious decreased in the therapeutic group with 1.33g/kg and 2.66g/kg Naoshu capsule (P<0.05, 0.01). Conclusion: There has a certain correlation between aging and immune, and there are obvious accommodation of Naoshu capsule on immune function of aging mice.目的  观察脑舒胶囊对衰老小鼠免疫功能的调节作用。方法  5%D-半乳糖颈背部皮下注射连续6周制备衰老小鼠模型;放射免疫法测小鼠血清IL-2和IL-6含量;胸腺、脾脏重量比小鼠体重,计算脏器指数。结果  与对照组比较,衰老模型组小鼠胸腺、脾脏指数明显下降,血清IL-2含量明显降低,IL-6的含量明显提高。与模型组比较,1.33g/kg和2.66g/kg脑舒胶囊可明显提高衰老小鼠的胸腺和脾指数(P<0.05,0.01),升高衰老小鼠血清IL-2含量(P<0.05,0.01),降低血清IL-6含量(P<0.05,0.01)。结论  衰老与免疫存在相关性,脑舒胶囊对衰老小鼠的免疫功能具有明显的调节作用

    C1q/TNF-related protein 3 (CTRP3) and 9 (CTRP9) concentrations are decreased in patients with heart failure and are associated with increased morbidity and mortality.

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    BACKGROUND: Biochemical marker has revolutionized the approach to the diagnosis of heart failure. However, it remains difficult to assess stability of the patient. As such, novel means of stratifying disease severity are needed. C1q/TNF-Related Protein 3 (CTRP3) and C1q/TNF-Related Protein 9 (CTRP9) are novel adipokines that contribute to energy homeostasis with additional anti-inflammatory and anti-ischemic properties. The aim of our study is to evaluate concentrations of CTRP3 and CTRP9 in patients with HFrEF (heart failure with reduced ejection fraction) and whether associated with mortality. METHODS: Clinical data and plasma were obtained from 176 healthy controls and 168 patients with HFrEF. CTRP3 and CTRP9 levels were evaluated by enzyme-linked immunosorbent assay. RESULTS: Both CTRP3 and CTRP9 concentrations were significantly decreased in the HFrEF group compared to the control group (p \u3c 0.001). Moreover, patients with higher New York Heart Association class had significantly lower CTRP3 or CTRP9 concentrations. Correlation analysis revealed that CTRP3 and CTRP9 levels were positively related with LVEF% (CTRP3, r = 0.556, p \u3c 0.001; CTRP9, r = 0.526, p \u3c 0.001) and negatively related with NT-proBNP levels (CTRP3, r = - 0.454, p \u3c 0.001; CTRP9, r = - 0.483, p \u3c 0.001). After a follow up for 36 months, after adjusted for age, LVEF and NT-proBNP, we observed that CTRP3 or CTRP9 levels below the 25th percentile was a predictor of total mortality (CTRP3,HR:1.93,95%CI1.03~3.62,P = 0.042;CTRP9,HR:1.98,95%CI:1.02~3.85,P = 0.044) and hospitalizations (CTRP3,HR:2.34,95% CI:1.43~3.82,P = 0.001;CTRP9,HR:2.67,95%CI:1.58~4.50,P \u3c 0.001). CONCLUSIONS: CTRP3 and CTRP9 are decreased in patients with HFrEF, proportionate to disease severity, and each is associated with increased morbidity and mortality. TRIAL REGISTRATION: NCT01372800 . Registered May 2011
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