与分圆方程有关的差集的不可能性

设f=Ord_p(q), ε_p为本原p次单位方根,γ∈Z[ε_p]。若f是奇数且γγ^-=n（其中n∈Z, q|n）,加上别的一些条件,Arasu和Pott证明了γ具有形式：γ＝∑^e_i=1a∑^f-1_j=0ε^iqj_p其中p-1=ef, 并且指出如果条件“f是奇数”能去掉的话,将是一个很好的结果,本文作者研究了f为偶数的情形并得到相应的结论。     

4p4阶群的差集

设G是具有二面体群同态象D_4p²的4p⁴阶群,通过考察其相交数得到如下结论：当p是素数且p≥5时,G上的差集不存在。     

W(2)到Kac模的一阶上同调

确定了特征p>2的域上Witt型模李超代数W(2)到两类Kac模K(λ)的一阶上同调。得出以下结论: W(2)到K(2ξ2)的一阶上同调空间是一维的; W(2)到K(ξ1+ξ2)的一阶上同调空间是零维的。     

关于Sylow交的共轭类

设G为有限群,p是G阶数的一个素因子,即p||G|。在有限群的研究中,Sylow p-子群无疑起到了非常重要的作用;同样,Sylow p-子群交在有限群不可分解模和块论研究当中的作用也是不容忽视的。文中研究了有限群G的 Sylow p-子群交的共轭类个数n_p(G)对于有限群结构的影响,并且着重讨论了n_p(G)=2的有限群的性质,特别地,给出了有限群G满足n_p(G)=2时2个不同Sylow p-子群的交与O_p(G)相等的几个充分必要条件。     

Adams谱序列E2项的一些注记

利用May谱序列的相关理论对Adams谱序列的E2项,即模p Steenrod代数A的上同调进行讨论。具体给出了(~overγ)_s+3b1h_n(n≥4, 0≤s4)在Adams谱序列中的非平凡性,并且说明其不是任何元素微分的像。这些结论对球面稳定同伦群新元素的发掘具有重要意义。     

单李群齐性空间中的相交理论

考虑齐性空间U_n/T_n的整系数上同调环H^*(U_n/T_n , Z)。它是n元多项式环的一个商环。特别地,商环的d=dimU_n/T_n次齐次部分对应于顶维上同调群Z,即每个d次齐次多项式 f都对应于一个整数 χ(f)。本文具体计算出了此对应。在几何上,这一对应给出了到U_n/T_n的连续映射的相交数的计算方法。同样的方法也适用于Sp_n/T_n上的相交理论的研究。     

膜反应器中生物质甘油制氢反应的热力学研究

采用吉布斯自由能最小化方法对膜反应器中生物质甘油水汽重整制氢反应进行热力学研究,考察了温度、压力、水与甘油进料比(S/G)等条件对反应性能的影响,并分析副产物CO和CH₄的生成、积炭的生成、移去CO₂、O₂的添加等对氢气产量和反应体系平衡组成的影响.结果表明:T=900 K,p=100 kPa,S/G=12时,在膜反应器中及时移除CO₂可提高氢气产量和选择性,氢气产量高达6.86 mol H₂/摩尔甘油,选择性98.00%; 在反应体系中添加少量的O₂(摩尔分数<1%)有利于抑制CO和CH₄的生成,而氢气产量几乎不受影响.     

X65碳钢的H2S/CO2腐蚀控制因素研究

目前,H₂S/CO₂腐蚀过程的控制因素判定依据主要参考Dunlop等的研究结果,但该判定结果经常与油田实际腐蚀情况不相符。为找到造成偏差的主要原因,更好地指导生产实践,采用动态高温高压釜,使用扫描电子显微镜（SEM）、能谱仪（EDS）和X射线衍射（XRD）等手段对X65碳钢在H₂S/CO₂共存体系中的腐蚀控制因素进行了研究。结果表明,不同温度下平均腐蚀速率随H₂S/CO₂分压比（p_H2S/p_CO2）的变化呈现两种不同的规律,这与腐蚀产物的膜形态和组成密切相关;腐蚀控制因素与p_H2S/p_CO2有关,而p_H2S/p_CO2临界值大小与温度密切相关。对于H₂S腐蚀控制,当温度低于40℃时,Dunlop等的研究结果仍然适用;当温度从40℃升高至60℃时,本研究的p_H2S/p_CO2临界值由0.05升高到0.10。对于CO₂腐蚀控制,本研究的p_H2S/p_CO2临界值在85℃以上时由原来的0.002逐渐升高到0.003。根据以上研究结果,修正了X65碳钢的H₂S/CO₂腐蚀过程的控制因素与p_H2S/p_CO2及体系温度的关系图。     

B2-型量子群的不可约模的Gröbner-Shirshov对

首先用B2-型量子群U_q(B2)的已知Gröbner-Shirshov基和双自由模方法,给出B2-型量子群上不可约模V_q(λ)的Gröbner-Shirshov对,然后通过在U_q(B2)的适当形式中取q=1给出B2型单Lie代数的泛包络代数U(B2)的Gröbner-Shirshov基和不可约U(B2)-模V(λ)的Gröbner-Shirshov对。     

[C(NH2)3]2{[MoO(H2O)C2O4]2(μ-O)2}·2H2O的合成与结构

合成并用元素分析和单晶X射线衍射表征了一个新的化合物[C(NH₂)₃]₂{[MoO(H₂O)C₂O₄]₂(μ-O)₂}·2H₂O,测定结果表明该化合物中存在金属Mo-Mo键,通过计算知道钼原子是+5价的,两个钼氧八面体是共边连接的,每个钼上有一个螯合的草酸根,而胍作为阳离子存在于晶体中,参与构筑有特色的氢键网络。该化合物属单斜晶系,空间群P2₁/c, a=0.7956(2)nm, b=1.8996(4)nm, c=1.2832(3)nm, β=106.78(3)^o, V=1.8568(7)nm³, R₁=0.0243, ωR₂=0.0672.     

Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis.

The cyclin-dependent kinase inhibitor p16INK4a can induce senescence of human cells, and its loss by deletion, mutation or epigenetic silencing is among the most frequently observed molecular lesions in human cancer. Overlapping reading frames in the INK4A/ARF gene encode p16INK4a and a distinct tumour-suppressor protein, p19ARF (ref. 3). Here we describe the generation and characterization of a p16Ink4a-specific knockout mouse that retains normal p19Arf function. Mice lacking p16Ink4a were born with the expected mendelian distribution and exhibited normal development except for thymic hyperplasia. T cells deficient in p16Ink4a exhibited enhanced mitogenic responsiveness, consistent with the established role of p16Ink4a in constraining cellular proliferation. In contrast to mouse embryo fibroblasts (MEFs) deficient in p19Arf (ref. 4), p16Ink4a-null MEFs possessed normal growth characteristics and remained susceptible to Ras-induced senescence. Compared with wild-type MEFs, p16Ink4a-null MEFs exhibited an increased rate of immortalization, although this rate was less than that observed previously for cells null for Ink4a/Arf, p19Arf or p53 (refs 4, 5). Furthermore, p16Ink4a deficiency was associated with an increased incidence of spontaneous and carcinogen-induced cancers. These data establish that p16Ink4a, along with p19Arf, functions as a tumour suppressor in mice.     

p15Ink4b is a critical tumour suppressor in the absence of p16Ink4a

The CDKN2b-CDKN2a locus on chromosome 9p21 in human (chromosome 4 in mouse) is frequently lost in cancer. The locus encodes three cell cycle inhibitory proteins: p15INK4b encoded by CDKN2b, p16INK4a encoded by CDKN2a and p14ARF (p19Arf in mice) encoded by an alternative reading frame of CDKN2a (ref. 1). Whereas the tumour suppressor functions for p16INK4a and p14ARF have been firmly established, the role of p15INK4b remains ambiguous. However, many 9p21 deletions also remove CDKN2b, so we hypothesized a synergistic effect of the combined deficiency for p15INK4b, p14ARF and p16INK4a. Here we report that mice deficient for all three open reading frames (Cdkn2ab-/-) are more tumour-prone and develop a wider spectrum of tumours than Cdkn2a mutant mice, with a preponderance of skin tumours and soft tissue sarcomas (for example, mesothelioma) frequently composed of mixed cell types and often showing biphasic differentiation. Cdkn2ab-/- mouse embryonic fibroblasts (MEFs) are substantially more sensitive to oncogenic transformation than Cdkn2a mutant MEFs. Under conditions of stress, p15Ink4b protein levels are significantly elevated in MEFs deficient for p16Ink4a. Our data indicate that p15Ink4b can fulfil a critical backup function for p16Ink4a and provide an explanation for the frequent loss of the complete CDKN2b-CDKN2a locus in human tumours.     

▽n(G)={1}的有限群

设Ｇ满足标题的条件。１、若ｎ＝４,则下述结论之一成立;;（１）Ｇ可解;;（２）Ｇ≌Ａ~５;;（３）Ｇ≌ＰＳＬ（２,１３）;;（４）Ｇ≌ＰＳＬ（２,ｐ）,满足ｐ＝４ｐ１＋１＝６ｐ２－１,这里ｐ１≥４３,ｐ２≥２９;;（５）Ｇ≌ＰＳＬ（２,ｐ）,满足ｐ＝６ｐ１＋１＝４ｐ２—１,这里ｐ１≥７,ｐ２≥１１;;２、若ｎ＝５且Ｇ与ＰＳＬ（２,ｐ）无关,则下述结论之一成立：（１）Ｇ可解;;（２）Ｇ≌ＰＳＬ（２,２~３）;;（３）Ｇ≌ＰＳＬ（２,３~３）;;３、设３　π（Ｇ）,８≤ｎ≤２ｐ＋１．若对任ｑ＜ｐ,Ｇ与Ｓｚ（２~ｑ）无关,则Ｇ可解。     

人p16~(INK4) cDNA探针在非小细胞肺癌研究中的应用

制备总RNA ,RT PCR克隆p16 INK4 cDNA ,测序验证 ,制备探针 .进行PCR产物Southern杂交检测非小细胞肺癌组织标本中p16 INK4 基因第二外显子阴性杂交率为 12 .9% (4 / 31) .原位杂交显示p16 INK4 基因转录阴性率为2 2 .6 % (7/ 31) .结果说明克隆的p16 INK4 cDNA是正确的 ,可用于临床基因诊断 ,p16 INK4 基因变异及表达在非小细胞肺癌的发生、发展中起作用     

关于余氏猜测的一个命题

设ａ，ｂ１，ｂ２是整数，ａ＞１，（ａ，ｂ１）－（ａ，ｂ２）＝１．则偶数ｍｂ１＋ｂ２（ｍｏｄａ）都可以表示为ｐ＋ｐ４，这里ｐ是素数，ｐ４是至多４个素数的积，且Ｐｂ１（ｍｏｄａ），ｐ４ｂ２（ｍｏｄａ）．     

Frame自正交拉丁方中的截态

本文证明当ｐ为质数幂时．在型为２ｐ的Ｆｒａｍｅ自正拉丁方中存在２（Ｐ－１）个互不相交的截态，且（ｉ）当ｐ大于３且时ｐ≡１（ｍｏｄ４）时这２（ｐ－１）个截态表现为ｐ－１个自对称的截态和（ｐ－１）／２对相互对称的截态；（ｉｉ）当ｐ大于５且ｐ≡３（ｍｏｄ４）时这２（ｐ－１）个截态在现为ｐ－１对相互对称的截态．     

Enhancement of T-cell responsiveness by the lymphocyte-specific tyrosine protein kinase p56lck.

Lymphocyte-specific tyrosine protein kinase p56lck is physically associated with CD4 and CD8 T-cell surface molecules, suggesting that it may transduce CD4/CD8-triggered tyrosine phosphorylation signals during antigen stimulation. Indeed, antibody-mediated aggregation of CD4 (to mimic interaction with its ligand, major histocompatibility complex (MHC) class II molecules), rapidly elevates the kinase activity of p56lck and is associated with marked changes in tyrosine protein phosphorylation. Genetic analyses suggest that the interaction of CD4/CD8 with p56lck results in a positive signal during antigen-induced T-cell activation. To evaluate directly the role of p56lck in T-cell activation, we introduced a constitutively activated form of Lck protein (tyrosine 505 to phenylalanine 505 mutant); in a CD4-negative, MHC-class II restricted mouse T-cell hybridoma. We report here that, as for transfection of CD4, expression of the Lck mutant enhanced T-lymphocyte responsiveness. This finding provides direct evidence that p56lck can positively regulate T-cell functions and that it mediates at least some of the effects of CD4 and CD8 on T-cell activation.     

Z4上长度为p的三次剩余码

利用Hensel提升,文章定义了Z4上长度为p的三次剩余码,其中素数p满足p≡1(mod 3)以及2是模p的三次剩余,给出了这些三次剩余码的幂等生成元,证明了这些三次剩余码有一些很好的性质;除此之外,讨论了这些剩余码的扩展码的一些性质。