用于VLSI的新型介质膜界面陷阱的特征

采用雪崩热电子注入技术和高频Ｃ－Ｖ准静态Ｃ－Ｖ特性测试,研究了新型快速热氮化的ＳｉＯｘＮｙ介质膜界面陷阱的特征,侧重于研究界面陷阱的特性与分布。结果表明：这种ＳｉＯｘＮｙ薄膜禁带中央界面陷阱密度随氮化时间的分布变化呈现”回转效应“,且存在着不同类型、密度悬殊很大的电子陷阱、指出雪崩热电子注入过程中在Ｓｉ／ＳｉＯｘＮｙ界面上产生两种性质不同的快界面态陷阱;给出了这两种界面态陷阱密度在禁带中能量的分布     

碘放射性核素在土壤－蔬菜系统中的转移系数

人工引入核电站排放的关键核素￣（１３１）Ｉ，采用γ能谱和总β计数两种方法确定核素在土壤－蔬菜系统中的转移系数。测得核素不同迁移时间、不同生长期的蔬菜、以及土壤中不同核素浓度等各种情况下的转移系数。给出转移系数的频数分布及变异性。γ能谱法测得的￣（１３１）Ｉ在广东土壤－蔬菜系统中转移系数的观察值范围为１．２８×１０￣（－２）～２．１０×１０￣（－１），几何平均值为５．０５×１０￣（－２），几何标准偏差为１．９６．实验中观察到蔬菜棵株大小、不同气候条件等因素对转移系数的影响。     

A complementary transposon tool kit for Drosophila melanogaster using P and piggyBac

With the availability of complete genome sequence for Drosophila melanogaster, one of the next strategic goals for fly researchers is a complete gene knockout collection. The P-element transposon, the workhorse of D. melanogaster molecular genetics, has a pronounced nonrandom insertion spectrum. It has been estimated that 87% saturation of the approximately 13,500-gene complement of D. melanogaster might require generating and analyzing up to 150,000 insertions. We describe specific improvements to the lepidopteran transposon piggyBac and the P element that enabled us to tag and disrupt genes in D. melanogaster more efficiently. We generated over 29,000 inserts resulting in 53% gene saturation and a more diverse collection of phenotypically stronger insertional alleles. We found that piggyBac has distinct global and local gene-tagging behavior from that of P elements. Notably, piggyBac excisions from the germ line are nearly always precise, piggyBac does not share chromosomal hotspots associated with P and piggyBac is more effective at gene disruption because it lacks the P bias for insertion in 5' regulatory sequences.     

Upper intestinal lipids regulate energy and glucose homeostasis

Upon the entry of nutrients into the small intestine, nutrient sensing mechanisms are activated to allow the body to adapt appropriately to the incoming nutrients. To date, mounting evidence points to the existence of an upper intestinal lipid-induced gut–brain neuronal axis to regulate energy homeostasis. Moreover, a recent discovery has also revealed an upper intestinal lipid-induced gut–brain–liver neuronal axis involved in the regulation of glucose homeostasis. In this mini-review, we will focus on the mechanisms underlying the activation of these respective neuronal axes by upper intestinal lipids.     

Differential effects of oncogenic K-Ras and N-Ras on proliferation, differentiation and tumor progression in the colon

Kras is commonly mutated in colon cancers, but mutations in Nras are rare. We have used genetically engineered mice to determine whether and how these related oncogenes regulate homeostasis and tumorigenesis in the colon. Expression of K-Ras(G12D) in the colonic epithelium stimulated hyperproliferation in a Mek-dependent manner. N-Ras(G12D) did not alter the growth properties of the epithelium, but was able to confer resistance to apoptosis. In the context of an Apc-mutant colonic tumor, activation of K-Ras led to defects in terminal differentiation and expansion of putative stem cells within the tumor epithelium. This K-Ras tumor phenotype was associated with attenuated signaling through the MAPK pathway, and human colon cancer cells expressing mutant K-Ras were hypersensitive to inhibition of Raf, but not Mek. These studies demonstrate clear phenotypic differences between mutant Kras and Nras, and suggest that the oncogenic phenotype of mutant K-Ras might be mediated by noncanonical signaling through Ras effector pathways.     

Mitogens trigger a calcium-independent signal for proliferation in phorbol-ester-treated lymphocytes

The activation of T lymphocytes by mitogens requires at least two signals; the first, delivered to T cells by a mitogen in conjunction with accessory cells (monocytes/macrophages), leads to the generation of the second signal, interleukin-2 (IL-2). The first signal also induces the expression of IL-2 receptors on the surface of a subpopulation of T cells; binding of IL-2 to its receptor then initiates a cascade of events culminating in DNA synthesis by these cells. Certain compounds act synergistically with mitogens in promoting T-cell proliferation by substituting for the activities of interacting cells or their products. For example, the phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (TPA) has been shown to restore the ability of macrophage-depleted T-cell populations to respond to mitogenic lectins. Transmembrane fluxes of calcium, leading to increased free cytosolic calcium concentrations ([Ca2+]), have been demonstrated following mitogen binding to lymphocytes and have been implicated in the initiation of cell proliferation. We show here that the effect of TPA on lymphocyte proliferation occurs in the absence of extracellular Ca2+ or detectable changes in [Ca2+]i, but only in the presence of mitogens. This suggests that in cells which have been incubated with the phorbol ester, mitogens can induce proliferation by a calcium-independent signal.     

The effects of cocaine in the production of cardiovascular anomalies inβ-Adrenoreceptor stimulated chick embryos

Summary Cocaine potentiates the effects of epinephrine and norepinephrine in terms of aortic arch malformation in embryonic chicks. Cocaine itself induces aortic arch malformations when administered in large doses.This study was supported by grant No. HL 18050, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland.