1000 resultados para I-a(g7)


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利用1 2 4 Sn( 7Li,4n) 1 2 7I反应研究了1 2 7I核的在束γ谱 ,建立了包括 2 5个新能级和 52条新γ射线构成的新能级纲图 .将基于πh1 1 2 粒子态 ( 1 1 2 - )的负宇称能级推高到 ( 3 5 2 - ) ,在较重的1 2 7I核中得到了退耦合能级结构 .由于在两个正宇称带ΔI=2能级系列中观测到了强的带间跃迁 ,建议此带的主要成分为g7 2质子的组态 .另外还观测到了两个正宇称ΔI=2和ΔI=1能级系列 ,它们可能基于πd5 2 的单准粒子带和一个 3准粒子带 .

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Finding motifs that can elucidate rules that govern peptide binding to medically important receptors is important for screening targets for drugs and vaccines. This paper focuses on elucidation of peptide binding to I-A(g7) molecule of the non-obese diabetic (NOD) mouse - an animal model for insulin-dependent diabetes mellitus (IDDM). A number of proposed motifs that describe peptide binding to I-A(g7) have been proposed. These motifs results from independent experimental studies carried out on small data sets. Testing with multiple data sets showed that each of the motifs at best describes only a subset of the solution space, and these motifs therefore lack generalization ability. This study focuses on seeking a motif with higher generalization ability so that it can predict binders in all A(g7) data sets with high accuracy. A binding score matrix representing peptide binding motif to A(g7) was derived using genetic algorithm (GA). The evolved score matrix significantly outperformed previously reported

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Prueba de campo de las vendimiadoras autopropulsadas G7 y G8 y de las arrastradas G1 y G2

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To better understand the role of class II major histocompatibility complex molecules in both normal and autoimmune responses, we have produced a series of I-Ab transgenic mice. One of these transgenic constructs, designated NOD.PD, has the sequence of the NOD beta chain (Abeta(g7)) except at positions 56 and 57, where Pro-Asp replaces His-Ser. Several NOD.PD transgenic lines have been produced. One line of these mice carried a very high number of copies (>50) of the NOD.PD transgene. As has been described in other mice carrying high copy numbers of I-Ab transgenes, B-cell development was abnormal. The steady state numbers of mature B cells (IgM+/IgD(hi)) in the periphery were greatly reduced in transgenic mice compared to nontransgenic littermates. Surprisingly, rather than being accompanied by a generalized hypogammaglobulinemia, this B-cell deficiency was accompanied by elevated concentrations of IgG1 and IgE in the serum. Conversely, the levels of IgG2a were reduced in transgenic mice compared to nontransgenic littermates. Because this isotype pattern was characteristic of interleukin (IL)-4-induced class-switching, we then investigated the role of IL-4 in causing the observed phenotype. We crossed the high copy number transgenic mice with an IL-4-deficient strain of mice. As expected, the elevated levels of IgE in high copy number transgenic mice were eliminated when the IL-4 gene was inactivated. However, the reduction in the number of B cells was not ameliorated. These data indicate that the primary defect caused by the transgene was to reduce the number of B cells in these mice. This reduction was accompanied by a secondary increase in IL-4 production, which drove the remaining B cells toward the production of IgGl and IgE.

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Mode of access: Internet.

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Contiene una segunda obra con portada propia: "Pomponi Melae de situ orbis libris tres, cum annotationibus Petri Ioannis Olivarij Valentini ..."