α－FeOOH超微粒的制备及热处理

利用化学沉淀法制备了α－ＦｅＯＯＨ超微粒，将其在不同温度下于空气氛中进行热处理，并使用ｘ－ｒａｙ衍射和透射电镜及热重分析仪对样品进行了测试与分析．     

Local changes in snow depth dominate the evolving pattern of elevation-dependent warming on the Tibetan Plateau

Elevation-dependent warming (EDW),whereby warming rates are stratified by elevation,may increase the threat to the life-supporting solid water reservoir on the ...     

燃速低温感的高能硝胺发射药研究

利用差示扫描量热法和密闭爆发器测试方法对含有NX燃速改良剂的高能硝胺发射药的热分解和燃烧性能及燃速温度系数进行研究。研究结果表明，NX燃速改良剂对改善硝胺发射药的燃烧性能和降低燃速温度系数有很好的效果。     

塑性变形和热处理工艺对白口铸铁组织及性能的改善

大于2.11％C的白口铸铁中含有大块且又分布不均匀的渗碳体,其塑性和韧性很差。本文采用塑性变形及热处理等4种方法,最终得到了细小碳化物均匀分布在铁素体基体上的理想组织。具有这种球化组织的铸铁,强韧性有了提高,且在650～850℃温度范围变形表现出良好的超塑特性。     

用粘度法研究石油中沥青质沉积的起始点

介绍了测定混合物粘度以确定沥青质沉积起始点的方法，考察了将正庚烷或甲苯加入油样过程中体系粘度的变化规律．结果发现，随着正庚烷的加入，体系的粘度呈下降趋势，但在某一浓度时出现明显的偏离，该点即被定义为沥青质沉积的起始点．而用甲苯作溶剂时，体系粘度则始终呈平缓下降趋势，无偏离现象研究还发现，各种原油的沥青质沉积的起始点明显早于其相应的减压渣油，这表明渣油胶体体系比原油的更为稳定，上述结果借助显微照相观察得以证实     

The parameter determination in the design of 3-D spherically symmetric FIR filters via the McClellan transformation

In the design of 3-D spherically symmetric FIR filters via the McClellan transformation, two methods are proposed to determine the transformation parameters. The first is to improve the original 3-D algorithm by exploiting the 2-D effective methods in 3-D. This method can change the constrained optimization algorithm into the unconstrained one and makes the design easier to realize. The second method is to solve the coupled equations under constrained conditions and a set of ideal parameters can be gotten. The design example shows that the two methods are all efficient and easier than the original algorithm. Supported by the National Natural Science Foundation of China Jin Xiaoying: born in 1975, Graduate student     

拟南芥逆境胁迫诱导转录因子DREB1A基因的克隆和序列分析

以拟南芥基因组DNA为模板,通过PCR扩增得到逆境胁迫诱导转录因子DREB1A基因,将其克隆到pUC19质粒中.序列分析表明获得的基因序列与已报道的该基因的序列完全相同.     

模糊信息系统知识约简的分辨函数法

知识约简是粗糙集理论的重要研究内容.针对不同的粗糙集模型和约简定义,给出相应的知识约简方法一直是知识约简的主要任务.以分辩函数法为代表的各种符号值信息系统知识约简方法已得到深入研究.将分辨函数引入模糊信息系统,得到相应的知识约简分辨函数法,并通过实例分析说明了该方法的具体计算步骤.这为从模糊信息系统中获取知识提供了一种有效的粗糙集方法.     

Zebrafish miR-214 modulates Hedgehog signaling to specify muscle cell fate

Numerous microRNAs (miRNAs) have been discovered in the genomes of higher eukaryotes, and functional studies indicate that they are important during development. However, little is known concerning the function of individual miRNAs. We approached this problem in zebrafish by combining identification of miRNA expression, functional analyses and experimental validation of potential targets. We show that miR-214 is expressed during early segmentation stages in somites and that varying its expression alters the expression of genes regulated by Hedgehog signaling. Inhibition of miR-214 results in a reduction or loss of slow-muscle cell types. We show that su(fu) mRNA, encoding a negative regulator of Hedgehog signaling, is targeted by miR-214. Through regulation of su(fu), miR-214 enables precise specification of muscle cell types by sharpening cellular responses to Hedgehog.     

Germline gain-of-function mutations in SOS1 cause Noonan syndrome

Noonan syndrome, the most common single-gene cause of congenital heart disease, is characterized by short stature, characteristic facies, learning problems and leukemia predisposition. Gain-of-function mutations in PTPN11, encoding the tyrosine phosphatase SHP2, cause approximately 50% of Noonan syndrome cases. SHP2 is required for RAS-ERK MAP kinase (MAPK) cascade activation, and Noonan syndrome mutants enhance ERK activation ex vivo and in mice. KRAS mutations account for <5% of cases of Noonan syndrome, but the gene(s) responsible for the remainder are unknown. We identified missense mutations in SOS1, which encodes an essential RAS guanine nucleotide-exchange factor (RAS-GEF), in approximately 20% of cases of Noonan syndrome without PTPN11 mutation. The prevalence of specific cardiac defects differs in SOS1 mutation-associated Noonan syndrome. Noonan syndrome-associated SOS1 mutations are hypermorphs encoding products that enhance RAS and ERK activation. Our results identify SOS1 mutants as a major cause of Noonan syndrome, representing the first example of activating GEF mutations associated with human disease and providing new insights into RAS-GEF regulation.