单一颗粒流分形模型及有效热导率计算

首次提出了颗粒流中粒子的分形模型，得到粒子在不同分维下的分形分布，并和麦克斯韦分布进行比较，分析了两种分布产生差异的物理机制．在此基础上研究了单一颗粒流的有效热导率，得到其解析表达式，并分析了有效热导率随粒子温度、粒子分维的变化规律．     

Inactivation of the apoptosis effector Apaf-1 in malignant melanoma

Metastatic melanoma is a deadly cancer that fails to respond to conventional chemotherapy and is poorly understood at the molecular level. p53 mutations often occur in aggressive and chemoresistant cancers but are rarely observed in melanoma. Here we show that metastatic melanomas often lose Apaf-1, a cell-death effector that acts with cytochrome c and caspase-9 to mediate p53-dependent apoptosis. Loss of Apaf-1 expression is accompanied by allelic loss in metastatic melanomas, but can be recovered in melanoma cell lines by treatment with the methylation inhibitor 5-aza-2'-deoxycytidine (5aza2dC). Apaf-1-negative melanomas are invariably chemoresistant and are unable to execute a typical apoptotic programme in response to p53 activation. Restoring physiological levels of Apaf-1 through gene transfer or 5aza2dC treatment markedly enhances chemosensitivity and rescues the apoptotic defects associated with Apaf-1 loss. We conclude that Apaf-1 is inactivated in metastatic melanomas, which leads to defects in the execution of apoptotic cell death. Apaf-1 loss may contribute to the low frequency of p53 mutations observed in this highly chemoresistant tumour type.     

带哨嘴喷嘴射流流场的离散涡模拟

采用离散涡方法模拟了两种不同形状哨嘴的喷嘴出口流场旋涡结构和压力分布。模拟结果表明 ,射流在喷嘴出口和哨嘴出口形成的旋涡结构在流场及其他涡元的作用下 ,向下游运动 ,在流场中某个地方形成低压区 ,这有助于诱发空化现象。对两种不同喷嘴的出口流场进行比较发现 ,哨嘴形状对形成的射流流场的旋涡结构有很大影响。因此 ,研究和应用空化射流必须考虑喷嘴出口哨嘴形状的影响     

高容量温盘驱动器伺服码同步时钟录写技术

提出了可变频时钟写入方法和锁相环倍频时钟写入方法，给出了这两种写入法的读／写电路，并分析了其性能。结果证明，可变频时钟写入方法电路简单，刻写时钟周期短；锁相环倍频时钟写入过程较前者长，但其频率范围容易调整。两者均适合高密度小型温盘的时钟录写。     

T形线散射电流的麦克斯韦电路

运用最新提出的麦克斯韦电路理论,分析T形线的散射电流,将该结构等效为LC电路,求解与之对应的微分方程,得到该结构的散射电流,数值实验分别计算了T形线的等效电路参数L,C,α,β,以及相应的散射电流,分析结果表明,所得电路参数和散射电流符合物理现象,并且与矩量法的结果以及相关文献中的结果均吻合,从而证明了该方法的正确性和...     

Prion-like behaviour and tau-dependent cytotoxicity of pyroglutamylated amyloid-β

Extracellular plaques of amyloid-β and intraneuronal neurofibrillary tangles made from tau are the histopathological signatures of Alzheimer's disease. Plaques comprise amyloid-β fibrils that assemble from monomeric and oligomeric intermediates, and are prognostic indicators of Alzheimer's disease. Despite the importance of plaques to Alzheimer's disease, oligomers are considered to be the principal toxic forms of amyloid-β. Interestingly, many adverse responses to amyloid-β, such as cytotoxicity, microtubule loss, impaired memory and learning, and neuritic degeneration, are greatly amplified by tau expression. Amino-terminally truncated, pyroglutamylated (pE) forms of amyloid-β are strongly associated with Alzheimer's disease, are more toxic than amyloid-β, residues 1-42 (Aβ(1-42)) and Aβ(1-40), and have been proposed as initiators of Alzheimer's disease pathogenesis. Here we report a mechanism by which pE-Aβ may trigger Alzheimer's disease. Aβ(3(pE)-42) co-oligomerizes with excess Aβ(1-42) to form metastable low-n oligomers (LNOs) that are structurally distinct and far more cytotoxic to cultured neurons than comparable LNOs made from Aβ(1-42) alone. Tau is required for cytotoxicity, and LNOs comprising 5% Aβ(3(pE)-42) plus 95% Aβ(1-42) (5% pE-Aβ) seed new cytotoxic LNOs through multiple serial dilutions into Aβ(1-42) monomers in the absence of additional Aβ(3(pE)-42). LNOs isolated from human Alzheimer's disease brain contained Aβ(3(pE)-42), and enhanced Aβ(3(pE)-42) formation in mice triggered neuron loss and gliosis at 3 months, but not in a tau-null background. We conclude that Aβ(3(pE)-42) confers tau-dependent neuronal death and causes template-induced misfolding of Aβ(1-42) into structurally distinct LNOs that propagate by a prion-like mechanism. Our results raise the possibility that Aβ(3(pE)-42) acts similarly at a primary step in Alzheimer's disease pathogenesis.     

Bone marrow cells regenerate infarcted myocardium

Myocardial infarction leads to loss of tissue and impairment of cardiac performance. The remaining myocytes are unable to reconstitute the necrotic tissue, and the post-infarcted heart deteriorates with time. Injury to a target organ is sensed by distant stem cells, which migrate to the site of damage and undergo alternate stem cell differentiation; these events promote structural and functional repair. This high degree of stem cell plasticity prompted us to test whether dead myocardium could be restored by transplanting bone marrow cells in infarcted mice. We sorted lineage-negative (Lin-) bone marrow cells from transgenic mice expressing enhanced green fluorescent protein by fluorescence-activated cell sorting on the basis of c-kit expression. Shortly after coronary ligation, Lin- c-kitPOS cells were injected in the contracting wall bordering the infarct. Here we report that newly formed myocardium occupied 68% of the infarcted portion of the ventricle 9 days after transplanting the bone marrow cells. The developing tissue comprised proliferating myocytes and vascular structures. Our studies indicate that locally delivered bone marrow cells can generate de novo myocardium, ameliorating the outcome of coronary artery disease.     

Human gamma-chain genes are rearranged in leukaemic T cells and map to the short arm of chromosome 7

Three gene families that rearrange during the somatic development of T cells have been identified in the murine genome. Two of these gene families (alpha and beta) encode subunits of the antigen-specific T-cell receptor and are also present in the human genome. The third gene family, designated here as the gamma-chain gene family, is rearranged in murine cytolytic T cells but not in most helper T cells. Here we present evidence that the human genome also contains gamma-chain genes that undergo somatic rearrangement in leukaemia-derived T cells. Murine gamma-chain genes appear to be encoded in gene segments that are analogous to the immunoglobulin gene variable, constant and joining segments. There are two closely related constant-region gene segments in the human genome. One of the constant-region genes is deleted in all three T-cell leukaemias that we have studied. The two constant-region gamma-chain genes reside on the short arm of chromosome 7 (7p15); this region is involved in chromosomal rearrangements identified in T cells from individuals with the immunodeficiency syndrome ataxia telangiectasia and observed only rarely in routine cytogenetic analyses of normal individuals. This region is also a secondary site of beta-chain gene hybridization.     

Early Cambrian phosphatized blastula- and gastrula-stage animal fossils from southern Shaanxi

Marine invertebrate animal embryos and their early developmental products are of great significance to the study of taxonomy and phylogeny of early animals. A great number of phosphatized globular fossils were collected fromthe early Cambrian Kuanchuanpu Member (upper Dengying Formation), southern Shaanxi, and a nearly complete develo-pmental sequence—from a fertilized egg, via blastodisc formation, blastula development, blastodisc enlargement toward gastrulae, to tissue differentiation—can be discerned in this collection. This discovery provides unmatchable material for studies on the origin, taxonomy, radiation, and ontogeny of early metazoans.