化学镀非晶态Ni—B合金的研究

本文通过化学镀方法在铜和钢上沉积非晶态Ni-B合金。着重讨论了还原剂浓度、络合剂浓度对化学镀沉积速率的影响;分析了它的耐蚀原因和其显微硬度随退火温度的变化情况并就其应用和发展略作说明。     

清华屏蔽实验反应堆中子注量率能谱的调节和测量

叙述了采用多种屏蔽过滤方法,通过实验获得多种条件下的中子注量率能谱的调节和测量。     

雷达仿真系统中电磁干扰环境的仿真设计和实施

雷达仿真系统是为检测雷达设备的抗干扰能力以及在各种电磁环境下的工作性能而设计的，包括有源干扰和无源干扰的模拟仿真。本文阐述了无源干扰即杂波的散射模型和仿真过程；从同步脉冲干扰的基本原理出发，阐明在雷达工作环境仿真系统中距离拖引、速度拖引、虚假目标等同步脉冲有源干扰的设计和实施过程；并针对工作在搜索和跟踪交替模式下的相控阵雷达提出自适应综合干扰方式；最后分析并总结了系统仿真时为真实、有效地模拟电磁干扰环境应注意的关键问题。     

Gate and drain currents in off-state buried-type p-channel LDDMOSFETs

The buried-type p-channel LDD MOSFETs biased at high positive gate voltage exhibit novel characteristics: (1) the ratio of the drain to gate currents is about 1×10^-3 to 5×10^-3; and (2) the gate and drain currents both are functions of only the gate voltage minus the n-well bias. Such characteristics are addressed based on the formation of the surface n ⁺ inversion layer due to the punchthrough of the buried channel to the underlying shallow p-n junction. The measured gate current is due to the Fowler-Nordheim tunneling of electrons from this inversion layer surface and the holes generated within the high-field oxide constitute the drain current. The n⁺ inversion layer surface potential is found to be equal to the n-well bias plus 0.55 V. As a result, both the oxide field and the gate and drain currents are independent of drain voltage     

光纤的淬冷增强原理

本文从拉丝工艺技术的角度出发，讨论了高速、高温拉丝工艺方法对光纤的淬冷增强原理。     

Penicilloyl peptides are recognized as T cell antigenic determinants in penicillin allergy

Although hapten immune responses have been intensively studied in the mouse, very little is known about hapten determinants involved in human allergic reactions. Penicillins, as chemically reactive compounds of low molecular weight, constitute typical examples of hapten allergens for humans. Penicillins become immunogenic only after covalent binding to carrier proteins and in this form frequently induced IgE-mediated allergic reactions in patients subjected to antibiotic treatment. However, our previous data strongly indicated that penicillins also form part of the epitopes contacting the antigen receptors of beta lactam-specific T cells in allergic individuals. We have therefore investigated the molecular constraints involved in the T cell immune response to penicillin G (Pen G). Designer peptides containing a DRB1*0401-binding motif and covalently modified with Pen G via a lysine epsilon-amino group were found to induce proliferation of Pen G-specific T cell clones. A precise positioning of the hapten molecule on the peptide backbone was required for optimal T cell recognition. Furthermore, we extended these observations from our designer peptides to show that a peptide sequence derived from a natural DRB1*1101-binding peptide modified in vitro with Pen G, also acquired antigenic properties. Our data for the first time provide insight into the manner in which allergenic haptens are recognized by human T cells involved in allergic reactions to drugs and suggest possible mechanisms leading to the onset of these adverse immune responses.     

The effect of pack-aluminisation on the microstructure of MCrAlY and the performance of thermal barrier coatings

Plasma spraying and pack-aluminising processes were combined and applied to the nickel-base superalloy Mar-M247 to improve its cyclic oxidation resistance. The performance tests of duplex ZrO₂-8 wt.%Y₂O₃/MCrAlY thermal barrier coatings (TBCs) were conducted at 1050 °C, 1075 °C, 1100 °C, 1150 °C and 1200 °C. The results of the experiments in this study showed that TBC specimens with the aluminised MCrAlY bond coat exhibited higher cyclic lives (except for the Ni-22Cr-10Al-1Y bond coat), at all the temperatures tested, than specimens on which the bond coat was not aluminised. The microstructures of the Co-29Cr-6Al-1Y, Co-32Ni-21Cr-8Al-0.5Y and Ni-22Cr-10Al-1Y bond coats with or without aluminising treatment were examined in detail using a scanning electron microscope equipped with an electron probe microanalyzer.     

An efficient approach for calculating the dispersions of photonic-crystal fibers: design of the nearly zero ultra-flattened dispersion

A novel and efficient approach is proposed to calculate the dispersions of the guided modes of the photonic-crystal fibers (PCFs). Based on the vector boundary-element method (VBEM), the surface integral equations for the first and second derivatives of the propagation constants with respect to the wavelength are explicitly derived. Compared with the three-point finite-difference approach, which needs to solve and search three effective indexes near the interested wavelength, this approach can determine the dispersions of the PCFs by only solving one effective index at this wavelength based on the derived formulations. This novel approach saves over 60% computing time without losing the accuracy. Based on this approach, a novel four-ring PCF is designed by optimizing only three geometrical parameters to achieve the nearly zero ultra-flattened dispersion property. Compared with previously presented dispersion-flattened PCFs, the design procedure for the four-ring structure could be more efficient and easier because relatively lesser parameters need to be optimized.     

BID: a novel BH3 domain-only death agonist

The BCL-2 family of proteins consists of both antagonists (e.g., BCL-2) and agonists (e.g., BAX) that regulate apoptosis and compete through dimerization. The BH1 and BH2 domains of BCL-2 are required to heterodimerize with BAX and to repress cell death; conversely, the BH3 domain of BAX is required to heterodimerize with BCL-2 and to promote cell death. To extend this pathway, we used interactive cloning to identify Bid, which encodes a novel death agonist that heterodimerizes with either agonists (BAX) or antagonists (BCL-2). BID possesses only the BH3 domain, lacks a carboxy-terminal signal-anchor segment, and is found in both cytosolic and membrane locations. BID counters the protective effect of BCL-2. Moreover, expression of BID, without another death stimulus, induces ICE-like proteases and apoptosis. Mutagenesis revealed that an intact BH3 domain of BID was required to bind the BH1 domain of either BCL-2 or BAX. A BH3 mutant of BID that still heterodimerized with BCL-2 failed to promote apoptosis, dissociating these activities. In contrast, the only BID BH3 mutant that retained death promoting activity interacted with BAX, but not BCL-2. This BH3-only molecule supports BH3 as a death domain and favors a model in which BID represents a death ligand for the membrane-bound receptor BAX.