一个非奇异H矩阵实用充分条件的改进

对干泰彬(计算数学,2004,(1):109-116)给出的非奇异H矩阵的实用充分条件进行了改进,使得判定范围明显扩大,并且这个充分条件只与给定矩阵的本身元素有关,避免了胡家赣(线性方程组的迭代解法,1991.63-65)中判别H矩阵要计算Jacobi迭代矩阵的特征值的过程,大大简化了计算的复杂性,并给出了一个例子说明这种方法在实际中是十分方便和有用的.     

Acute mutation of retinoblastoma gene function is sufficient for cell cycle re-entry

Cancer cells arise from normal cells through the acquisition of a series of mutations in oncogenes and tumour suppressor genes. Mouse models of human cancer often rely on germline alterations that activate or inactivate genes of interest. One limitation of this approach is that germline mutations might have effects other than somatic mutations, owing to developmental compensation. To model sporadic cancers associated with inactivation of the retinoblastoma (RB) tumour suppressor gene in humans, we have produced a conditional allele of the mouse Rb gene. We show here that acute loss of Rb in primary quiescent cells is sufficient for cell cycle entry and has phenotypic consequences different from germline loss of Rb function. This difference is explained in part by functional compensation by the Rb-related gene p107. We also show that acute loss of Rb in senescent cells leads to reversal of the cellular senescence programme. Thus, the use of conditional knockout strategies might refine our understanding of gene function and help to model human cancer more accurately.     

PSD迭代法收敛的一个充分必要条件

在线性方程组Ax=b的系数矩阵A为相容次序矩阵及A的Jacobi迭代矩阵的特征值μj均为纯虚数且｜μj｜〈1的条件下得到了PSD收敛的一个充分必要条件,并给出数值例子．     

第一类平面图的一个充分条件

对于最大度为5的平面图,既有第一类,也有第二类.运用Discharge方法以及临界图的一些重要性质证明了:每个最大度为5且不含相交三角形的简单平面图的边色数等于5,即这样的平面图是第一类的.因此,给出了最大度为5的平面图分类的一个特征刻画.     

The human CST complex is a terminator of telomerase activity

The lengths of human telomeres, which protect chromosome ends from degradation and end fusions, are crucial determinants of cell lifespan. During embryogenesis and in cancer, the telomerase enzyme counteracts telomeric DNA shortening. As shown in cancer cells, human telomerase binds the shelterin component TPP1 at telomeres during the S phase of the cell cycle, and adds ~60 nucleotides in a single round of extension, after which telomerase is turned off by unknown mechanisms. Here we show that the human CST (CTC1, STN1 and TEN1) complex, previously implicated in telomere protection and DNA metabolism, inhibits telomerase activity through primer sequestration and physical interaction with the protection of telomeres 1 (POT1)–TPP1 telomerase processivity factor. CST competes with POT1–TPP1 for telomeric DNA, and CST–telomeric-DNA binding increases during late S/G2 phase only on telomerase action, coinciding with telomerase shut-off. Depletion of CST allows excessive telomerase activity, promoting telomere elongation. We propose that through binding of the telomerase-extended telomere, CST limits telomerase action at individual telomeres to approximately one binding and extension event per cell cycle. Our findings define the sequence of events that occur to first enable and then terminate telomerase-mediated telomere elongation.     

DNA sequence for a low-level promoter of the lac repressor gene and an 'up' promoter mutation.

The promoter for a weakly expressed constitutive gene, the lactose repressor gene (lacI), has been sequenced, along with an 'up' promoter mutation Iq. The 10-fold enhancement in I expression found in Iq is the result of a single base change at position -35. To facilitate the sequencing, the lacI gene was cloned in a small plasmid.     

BAI1 is an engulfment receptor for apoptotic cells upstream of the ELMO/Dock180/Rac module

Engulfment and subsequent degradation of apoptotic cells is an essential step that occurs throughout life in all multicellular organisms. ELMO/Dock180/Rac proteins are a conserved signalling module for promoting the internalization of apoptotic cell corpses; ELMO and Dock180 function together as a guanine nucleotide exchange factor (GEF) for the small GTPase Rac, and thereby regulate the phagocyte actin cytoskeleton during engulfment. However, the receptor(s) upstream of the ELMO/Dock180/Rac module are still unknown. Here we identify brain-specific angiogenesis inhibitor 1 (BAI1) as a receptor upstream of ELMO and as a receptor that can bind phosphatidylserine on apoptotic cells. BAI1 is a seven-transmembrane protein belonging to the adhesion-type G-protein-coupled receptor family, with an extended extracellular region and no known ligands. We show that BAI1 functions as an engulfment receptor in both the recognition and subsequent internalization of apoptotic cells. Through multiple lines of investigation, we identify phosphatidylserine, a key 'eat-me' signal exposed on apoptotic cells, as a ligand for BAI1. The thrombospondin type 1 repeats within the extracellular region of BAI1 mediate direct binding to phosphatidylserine. As with intracellular signalling, BAI1 forms a trimeric complex with ELMO and Dock180, and functional studies suggest that BAI1 cooperates with ELMO/Dock180/Rac to promote maximal engulfment of apoptotic cells. Last, decreased BAI1 expression or interference with BAI1 function inhibits the engulfment of apoptotic targets ex vivo and in vivo. Thus, BAI1 is a phosphatidylserine recognition receptor that can directly recruit a Rac-GEF complex to mediate the uptake of apoptotic cells.     

分解矩阵具有广义Moore-Penrose逆的充要条件

给出了矩阵乘积PAQ关于对合*和相对于M,N的一个广义Moore-Penrose逆的充分必要条件,其中*为环R的一个对合,A,P,Q为环R上的矩阵,M,N为环R上的可逆矩阵,并推广了Patricio的结果.     

一类n维自映射无异状点的充要条件

若f是可降的n维自映射,则可以利用可降映射的特征,给出了这类自映射无异状点的一个充要条件,当f限制在周期点集上时,是等度连续的。     

一类广义恰当罚函数存在的一个充要条件

就一个广义的数学规划问题(PH),研究了其恰当罚函数存在的条件.在已有结果的基础上给出了一类涵义较为广泛的罚函数,撇开象空间的正则性条件,得到了问题(PH)恰当罚函数存在的一个充要条件,并且把得到的结果推广到广义分式规划中去.     

一类n-阶非线性边值问题正解的存在性与唯一性的几个充分条件

利用不动点定理和积分方程研究了一类非线性n-阶边值问题,获得了其非平凡正解存在性的新结果.在此基础上给出了此边值问题非平凡正解的存在性与唯一性的几个充分条件,推广和改进了以前文献的相关结果.