有机-无机压电材料TMCM-MnCl3的研究

有机-无机压电材料是一种分子铁电体，具有柔性、结构灵活、易成膜、全液相合成及环保节能等优点，可满足新一代薄膜器件及可穿戴设备的需求。该文以三甲基卤代甲基铵(TMXM, X=F, Cl, Br)为有机部分，MnCl₂为无机部分，通过溶液蒸发法制备了具有钙钛矿分子结构的有机-无机压电材料三甲基氯三氯化锰(TMCM-MnCl₃)，并对其分子结构组成、压电、热学、声学及铁电性进行表征。结果表明，TMCM-MnCl₃的压电常数为106 pC/N，居里温度为130 ℃，声阻抗值约为16.5 MRayl，低于压电陶瓷PZT-4(大于33 MRayl)，具有广阔的应用前景。     

Scaling planar silicon devices

The generation-over-generation scaling of critical CMOS technology parameters is ultimately bound by nonscalable limitations, such as the thermal voltage and the elementary electronic charge. Sustained improvement in performance and density has required the introduction of new device structures and materials. Partially depleted SOI, a most recent MOSFET innovation, has extended VLSI performance while introducing unique idiosyncrasies. Fully depleted SOI is one logical extension of this device design direction. Gate dielectric tunneling, device self-heating, and single-event upsets present developers of these next-generation devices with new challenges. Strained silicon and high-permittivity gate dielectric are examples of new materials that will enable CMOS developers to continue to deliver device performance enhancements in the sub-100 nm regime.     

The Role of the γ/ γeutectic and porosity on the tensile behavior of a single-crystal nickel-base superalloy

The microstructure of a single-crystal nickel-base superalloy, PWA 1480, has been varied by heat treatment and hot isostatic pressing in order to study the role of the γ/yγ′ eutectic and porosity on subsequent tensile behavior. The level of porosity was found not to affect any of the tensile properties, while the γ/γ′ eutectic strongly influenced ductility. Eliminating the γ/γ′ eutectic increased ductility which was attributed to the cleavage fracture of this constituent. It is proposed that such cleavage of the γ/γ′ eutectic is initiated by the stress created from impinging slip bands, promoting shear localization, and final fracture along {111} slip planes. The precise nature of this fracture process is discussed with emphasis on the role of the γ/′ micro-structure. The deformation structure of PWA 1480 was also studied, and while different in some respects from many other single-crystal superalloys, its fracture process appears to be similar. Formerly Graduate Student, Department of Metallurgical Engineering and Materials Science, Carnegie Mellon University.     

基于小波神经网络的信号识别

信号的分选和识别技术在当今信号处理的系统中占有相当重要的地位.小波分析和神经网络是近年来兴起的一种分析信号方法.文中对二者的结合问题进行了研究.小波空间可以作为信号分类的特征空间,进而可以通过神经网络对信号进行特征识别.小波神经网络是基于小波分析而构造的神经网络模型.在信号调制类型识别中,利用小波伸缩平移把信号分解到不同频道上进行特征提取;把提取的特征信息输入神经网络进行分类.仿真结果表明,利用此方法可以较好的对信号进行分选和识别.     

Dependence on the motif YIPP for the physical association of Jak2 kinase with the intracellular carboxyl tail of the angiotensin II AT1 receptor

Angiotensin II is the effector molecule of the renin-angiotensin system. Virtually all of its biochemical actions are mediated through a single class of cell-surface receptors called AT1. These receptors contain the structural features of the seven-transmembrane, G-protein-coupled receptor superfamily. Angiotensin II, acting through the AT1 receptor, also stimulates the Jak/STAT pathway by inducing ligand-dependent Jak2 tyrosine phosphorylation and activation. Here, we show that a glutathione S-transferase fusion protein containing the carboxyl-terminal 54 amino acids of the rat AT1A receptor physically binds to Jak2 in an angiotensin II-dependent manner. Deletional analysis, using both in vitro protocols and cell transfection analysis, showed that this association is dependent on the AT1A receptor motif YIPP (amino acids 319-322). The wild-type AT1A receptor can induce Jak2 tyrosine phosphorylation. In contrast, an AT1A receptor lacking the YIPP motif is unable to induce ligand-dependent phosphorylation of Jak2. Competition experiments with synthetic peptides suggest that each of the YIPP amino acids, including tyrosine 319, is important in Jak2 binding to the AT1A receptor. The binding of the AT1A receptor to the intracellular tyrosine kinase Jak2 supports the concept that the seven-transmembrane superfamily of receptors can physically associate with enzymatically active intracellular proteins, creating a signaling complex mechanistically similar to that observed with growth factor and cytokine receptors.     

Cloning, tissue expression, and chromosomal localization of the mouse IRS-3 gene

Insulin receptor substrate (IRS) proteins are key regulators of basic functions such as cellular growth and metabolism. They provide an interface between multiple receptors and a complex network of intracellular signaling molecules. Two members of this family (IRS-1 and IRS-2) have been identified previously. In this investigation, we analyzed a mouse expressed sequence tag clone that proved to be a new member of the IRS family. Sequence analysis of this clone and comparison with the sequences deposited in GenBank demonstrates this protein may be the murine homolog of rat IRS-3, recently purified and cloned from rat adipocytes. Accordingly, we have named our protein mouse IRS-3. The expressed sequence tag clone contains the complete coding sequence of 1485 bp, encoding a protein of 495 amino acids. Sequence alignment with the other members of the IRS family shows that this protein contains pleckstrin homology and phosphotyrosine-binding domains that are highly conserved. In addition, there is conservation of many tyrosine phosphorylation motifs responsible for interactions with downstream signaling molecules containing SH2 domains. The murine IRS-3 messenger RNA (2.4 kilobases in length) is expressed in many tissues, with highest levels in liver and lung. Mouse IRS-3 is highly expressed in the first part of the embryonic life, when IRS-1 messenger RNA is barely detectable. Unlike the genes encoding IRS-1 and IRS-2, the IRS-3 gene contains an intron (344 bp in length) in the region between the pleckstrin homology and the phosphotyrosine-binding domains. Fluorescent in situ hybridization localized the mouse IRS-3 gene on the telomeric region of chromosome 5G2. Cloning of the murine IRS-3 gene will make it possible to apply genetic approaches to elucidate the physiological role of this new member of the IRS family of proteins.     

Molecular cloning of CYP1A from the estuarine fish Fundulus heteroclitus and phylogenetic analysis of CYP1 genes: update with new sequences

Since we published a phylogenetic analysis of the CYP1A subfamily in 1995, several additional full-length sequences have been reported, including three members of an entirely new subfamily, CYP1B. Two avian sequences were recently published, so that CYP1A sequence data are now available from three of the five major vertebrate lineages. The two new branches that have been added to the CYP1 family tree significantly add to our understanding of P450 evolution. The inclusion of the CYP1Bs to the phylogenetic analysis allows us to root inferred trees. Addition of the avian CYP1As indicates that the CYP1A1/CYP1A2 duplication present in the mammalian lineage may have occurred after the divergence of birds and mammals. The number of fish species from which full-length coding regions of CYP1A genes have been sequenced has increased from four (trout, plaice, toadfish, and scup) to nine. These include CYP1A sequences from tomcod, butterflyfish, sea bream, sea bass, and the full-length sequence of CYP1A from the killifish Fundulus heteroclitus that is reported here. Phylogenetic analyses incorporating the new fish CYP1A sequences support our original conclusion that the fish CYP1As are monophyletic and indicate that the genes are evolving at very different rates in different species.     

Temporal order and functional analysis of mutations within the Fli-1 and p53 genes during the erythroleukemias induced by F-MuLV

The erythroleukemias induced by Friend murine leukemia virus (F-MuLV) result from the accumulation of a number of genetic changes, including activation of the Fli-1 proto-oncogene and inactivation of the p53 tumor suppressor gene. We have determined the temporal order of mutation of the genes involved in this multistage malignancy, by serial in vivo transplantation of F-MuLV induced primary erythroleukemias into syngenic Balb/c mice. These primary tumors are capable of growing when transplanted into syngenic mice, but die after several days of in vitro culture. From the transplanted tumors grown in syngenic mice, erythropoietin-dependent cell lines were established in culture that are clonally related to cells in the primary tumors. We show that retroviral insertional activation of the Fli-1 ets family member is the first detectable genetic event in F-MuLV induced primary erythroleukemias. Mutations in the p53 gene were observed in the Epo-dependent cell lines but not in the transplanted erythroleukemias used to establish these cell lines in culture. These data suggest that activation of Fli-1 plays an important role in the early stages of F-MuLV-induced leukemia, perhaps by altering the self-renewal probabilities of erythroid progenitor cells and that p53 mutations immortalize these cells, enabling them to grow in vitro in the presence of Epo.