An efficient mixed algorithm of L-MEI and DDM for the wavescattering by a concave cylinder

In this paper, a localized MEI method (L-MEI) is developed and combined with the domain decomposition method (DDM) for the simulation of scattering by a concave cylinder. In the L-MEI, the whole domain is decomposed into many subdomains. Different from the conventional MEI method, the MEI coefficients of the L-MEI method in each subdomain are only dependent on the localized metrons that are defined in the subdomain. The localization of metrons has the following advantages: (1) speeding up the calculation of MEI coefficients and saving memory, (2) making the MEI method available for concave structures, and (3) obtaining a band sparse matrix directly without any modification     

一种实验炼钢渣的穆斯堡尔谱研究

一种实验炼钢渣不同炉次样品的室温透射穆斯堡尔谱由两组裂距较大的四极分裂双峰和一组裂距较小的双峰组成，它们分别相应于具有不同微观环境的Ｆｅ＾２＋和Ｆｅ＾３＋。参照文献中已知ＦｅｘＯ的穆斯堡尔谱数据，可确定该渣中的主要含铁相为ＦｅｘＯ。Ｘ射线衍射相分析给出相同的结果。按亚谱的面积比计算出Ｆｅ＾２＋和Ｆｅ＾３＋的相对含量分别为８５％和１５％左右。进一步选取与样品晶体结构相联系的原子簇模型。用ＭＳ－Ｘａ方     

Integrated magnetic full wave converter with flexible output inductor

A new integrated magnetic full wave DC/DC power converter that provides flexible transformer design by incorporating an independent output inductor winding is introduced. The transformer is implemented on a traditional three-leg magnetic core. The inductor winding can be separately designed to control the output current ripple. The cross-sectional area of the inductor core leg can be reduced dramatically. The operation and performance of the proposed circuit are verified on a 100 W prototype converter.     

聚吡咯导电材料合成方法的进展

本文对聚吡咯及聚吡咯导电复合物的合成方法进行了综述。     

TEM study of PLZT ceramics

The microscopic structures of PLZT(7.9/70/30 and x/65/35, x = 7 or 8) ceramics were studied by means of transmission electron microscopy. The presence of micro-regions in PLZTs was first verfied.     

Nucleotide sequence and genome structure of mink enteritis virus

Diabetes mellitus is a common disease. It affects multiple organ systems. Adverse effects of hyperglycemia on infection, fracture healing, and bone remodeling have been recently reported. This study was conducted to evaluate the clinical and radiographic results of 93 total hip arthroplasties in 78 consecutive patients with diabetes. All femoral components were cemented using contemporary cementing techniques. Prophylactic antibiotics were given in each case. The mean follow-up period was 4.1 years (range, 2-6.5 years). Ninety-six percent of the hips were rated excellent or good. Radiolucencies were observed in only 3.7% of the stems, while 22.2% of the cups showed radiolucencies. There was a 4% revision incidence. There was no postoperative infection in this series--a distinct improvement from previously reported series. However, complications remained high at 24.3%. The most frequent complication was urinary tract infection (14.2%). The most serious complication was myocardial infarction. The authors believe total hip arthroplasty can be safely performed in patients with diabetes, provided that adequate medical and follow-up evaluations are performed. The medium-term clinical and radiographic follow-up evaluations are not inferior to reported series in patients without diabetes.     

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.