钢筋与钢纤维混凝土的黏结滑移性能及其关系模型

基于内贴应变片的钢筋与钢纤维混凝土局部黏结试件的拉拔试验,研究钢筋与不同强度钢纤维混凝土的黏结性能。通过对实测钢筋应变的分析,建立了以三次多项式表达的黏结应力分布函数,得到了各级荷载作用下钢筋与钢纤维混凝土黏结应力和相对滑移沿黏结区段的分布,进一步分析了钢纤维和混凝土强度对黏结性能的影响。结果表明,随钢纤维的体积率和混凝土强度的增大,黏结试件加载端附近的黏结应力提高,黏结应力极值总体向加载端靠拢;同时,加载端与自由端的滑移减小。最后,提出了能够较好反映钢筋与钢纤维混凝土受力过程的黏结-滑移关系模型。     

Fragility assessment of high‐rise reinforced concrete buildings considering the effects of shear wall contributions

The effect of shear wall configurations on seismic responses of high‐rise RC buildings is investigated in this paper using fragility analysis method. Four lower high‐rise RC buildings that have the same plan dimensions and height but are different in configurations in lateral force resisting systems, were firstly designed following the standard code procedure. To consider uncertainties in earthquake motions, 16 real ground motion pairs were selected and scaled, then applied orthogonally to the four RC building models during the Incremental Dynamic Analysis (IDA). Fragility relationships were therefore derived based on the IDA results for the three limit states including slight damage, moderate damage and collapse to show the probabilistic comparison of seismic responses among the four buildings in both x and y‐directions. It was observed that generally adding shear walls will improve buildings' seismic performance at all limit states. However, shear wall configuration also plays a significant role in seismic behavior of the lower high‐rise regular RC buildings' and internal shear walls are generally more effective than external shear walls in improving building's seismic resistance. Copyright © 2016 John Wiley & Sons, Ltd.     

Domains of interaction between alpha interferon and its receptor components

We describe how constraints on the binding of human interferons (IFNs), alpha1 and alpha2 and alpha8 on mouse cells are partially relieved by the expression of the bovine (Bo) or human (Hu) IFN alpha/beta receptor (IFNAR) component in these cells. We show that, while the binding of all three is substantially increased by the transfection of Bo IFNAR, it is accompanied by an increase in activity only in the case of alpha2 and alpha8 (IFNs that otherwise have little activity on mouse cells). IFN alpha1, which shows some partial activity on mouse cells, responds to the presence of Bo IFNAR by acting, at low concentrations, as a competitive antagonist to IFNs alpha2 and alpha8. A review of published results on IFN hybrid scanning and on the effects of expressing Bo IFNAR in human cells led us to propose that an N-terminal segment of the IFN molecule interacts directly with IFNAR. Applying site-directed mutagenesis to an IFN hybrid; alpha8[60]alpha1[92]alpha8, we show that the point mutations K84 to E84 and Y90 to D90 act synergistically to cause the hybrid to behave as the parental IFN alpha8, switching the preference from Mu to Hu IFNAR in transfected mouse cells. The published structural models for IFN reveal that positions 84 and 90 span the exposed residues of the alpha-helix C of the IFN molecule. We derive a model of IFN-receptor interaction in which the A helix and the C helix of IFN interact with IFNAR and in which a binding phase can be distinguished from a binding/activity phase. We propose that the so-called "hot" domains of the IFN molecule (the AB loop and the D helix) are presented by IFNAR to interact with an additional component of the functional receptor.