守恒律的分析和数值学

本书是一本专题论文集，汇集了1997年设立的德国研究基金项目（DFG）“守恒律的分析和数值学”在近6年来的成果报告，共计22篇。该项目的参加者除数学家外，还有来自多种不同的科学分支的研究人员。他们通过交叉学科的协作攻关，应用数学方法解决来自物理、化学、生物、天文及工程等不同领域的各种问题。这些问题主要集中表现为发散形式的双曲型一阶偏微分方程组（2维和多维空间双曲型守恒律）的解的分析和数值近似，这是当代数学的一个具有挑战性的课题。     

新仙女木时期东亚夏季风降水不稳定的证据

通过位于沙漠 /黄土边界带的杨桃峁剖面AMS14 C年代和磁化率、粒度、有机质总量等气候代用指标的测定分析 ,认为新仙女木 (Youngerdryas)气候事件在该区存在夏季风降水波动和不稳定性 ,反映了东亚季风区和极地高纬地区Youngerdryas时期的气候差异 ,其原因可能是南北半球大气相互作用以及赤道太平洋地区气压异常 (ENSO)所致 .     

Reciprocal regulation of CD4/CD8 expression by SWI/SNF-like BAF complexes

Thymic development produces two sub-lineages of T cells expressing either CD4 or CD8 co-receptors that assist antibody production and mediate cell killing, respectively. The mechanisms for mutually exclusive co-receptor expression remain poorly defined. We find that mutations in the high mobility group (HMG) domain of BAF57--a DNA-binding subunit of the mammalian SWI/SNF-like chromatin-remodelling BAF complexes--or in the BAF complex ATPase subunit Brg, impair both CD4 silencing and CD8 activation. Brg is haploinsufficient for CD8 activation, but not for CD4 silencing, whereas BAF57 mutations preferentially impair CD4 silencing, pointing to target- and subunit-specific mechanisms of chromatin remodelling. BAF complexes directly bind the CD4 silencer, but the BAF57 HMG domain is dispensable for tethering BAF complexes to the CD4 silencer or other chromatin loci in vivo, or for remodelling reconstituted templates in vitro, suggesting that chromatin remodelling in vivo requires HMG-dependent DNA bending. These results indicate that BAF complexes contribute to lineage bifurcation by reciprocally regulating lineage-specific genes, reminiscent of the role of the yeast SWI/SNF complex in mediating mating-type switching.     

Sporadic immunogenic tumours avoid destruction by inducing T-cell tolerance

The recognition and elimination of tumours by T cells, a process termed cancer immunosurveillance, is effective against certain virus-associated cancers. Spontaneous tumours often induce a specific immune response and are therefore also immunogenic. However, it is not clear whether they can be controlled by T cells. The immunosurveillance hypothesis postulates that tumours, if they eventually grow, escaped T-cell recognition by losing immunogenicity. Here we show, by generating a mouse model of sporadic cancer based on rare spontaneous activation of a dormant oncogene, that immunogenic tumours do not escape their recognition but induce tolerance. In this model, tumours derive from single cells and express a tumour-specific transplantation rejection antigen. Whereas vaccinated mice remain tumour-free throughout their lifetime, naive mice always develop a progressively growing tumour. We also show that despite specific recognition by T cells, the tumours do not lose their intrinsic immunogenicity and are rejected after transplantation in T-cell-competent recipients. Furthermore, in the primary host tumour-induced tolerance is associated with the expansion of non-functional T cells. Together, our data argue against immunosurveillance of spontaneous cancer.