陕西球迷从众行为分析与对策研究

运用文献资料、问卷调查、逻辑分析和数理统计等方法对陕西球迷的从众行为进行了调查,从群体因素、情景因素、个人因素等方面进行了分析,并提出建议与对策.     

部分线性模型的渐近性

考虑Ｙｉ＝Ｘ＾ｔｉβ＋ｇ（ｔｉ）＋εｉ，１≤ｉ≤，忱里Ｘｉ是一固定设计点列，ｔｉ是独立同分布随机变量并且服从［０，１］上均匀分布。     

淬火工艺对铬结构钢显微组织和机械性能的影响

本文研究了淬火工艺对低和中碳铬钢的显微组织,冲击韧性和断裂机制的影响,得出了无论是低碳,还是中、高碳钢,当奥氏体长大倾向稍大时,采取提高加热温度进行淬火的工艺均为不可取的结论。     

一种改进的实信号IFFT算法

由于重量轻、体积小、功耗低、功能强的小卫星工作在无人干预的低温 ,高辐射的空间环境中 ,因此星上计算机系统必须满足集成度高、寿命长、可靠性高、抗辐射能力强的要求。针对立体测绘小卫星的特点 ,我们设计了满足上述要求的集集中控制与分布控制优点于一身的星上计算机系统 ,对其可靠性进行了分析 ,并对提高其可靠性应采取的关键技术进行了简要的论述。     

金汤桥开启系统的复原与改进

介绍了天津金汤桥活动跨开启系统的原貌、原状以及原缺陷，阐述了复原手动和电动开启系统的原则，并介绍了平转式开启桥的原理及构成．通过反复探索与研究，成功地复原了金汤桥活动跨手动和电动开启系统．提出了平转式活动跨机械传动系统的回转中心、活动跨的回转中心，以及桥墩中心的设计基准与安装基准必须服从三者同一性原理，并解决了这一平转式开启桥的难题．实践证明，复原后的活动跨开启系统安全、可靠、平稳、灵活．     

Mutation of the matrix metalloproteinase 2 gene (MMP2) causes a multicentric osteolysis and arthritis syndrome.

The inherited osteolyses or 'vanishing bone' syndromes are a group of rare disorders of unknown etiology characterized by destruction and resorption of affected bones. The multicentric osteolyses are notable for interphalangeal joint erosions that mimic severe juvenile rheumatoid arthritis (OMIMs 166300, 259600, 259610 and 277950). We recently described an autosomal recessive form of multicentric osteolysis with carpal and tarsal resorption, crippling arthritic changes, marked osteoporosis, palmar and plantar subcutaneous nodules and distinctive facies in a number of consanguineous Saudi Arabian families. We localized the disease gene to 16q12-21 by using members of these families for a genome-wide search for homozygous-by-descent microsatellite markers. Haplotype analysis narrowed the critical region to a 1.2-cM region that spans the gene encoding MMP-2 (gelatinase A, collagenase type IV; (ref. 3). We detected no MMP2 enzymatic activity in the serum or fibroblasts of affected family members. We identified two family-specific homoallelic MMP2 mutations: R101H and Y244X. The nonsense mutation effects a deletion of the substrate-binding and catalytic sites and the fibronectin type II-like and hemopexin/TIMP2 binding domains. Based on molecular modeling, the missense mutation disrupts hydrogen bond formation within the highly conserved prodomain adjacent to the catalytic zinc ion.