Geometric quantum computation using nuclear magnetic resonance

A significant development in computing has been the discovery that the computational power of quantum computers exceeds that of Turing machines. Central to the experimental realization of quantum information processing is the construction of fault-tolerant quantum logic gates. Their operation requires conditional quantum dynamics, in which one sub-system undergoes a coherent evolution that depends on the quantum state of another sub-system; in particular, the evolving sub-system may acquire a conditional phase shift. Although conventionally dynamic in origin, phase shifts can also be geometric. Conditional geometric (or 'Berry') phases depend only on the geometry of the path executed, and are therefore resilient to certain types of errors; this suggests the possibility of an intrinsically fault-tolerant way of performing quantum gate operations. Nuclear magnetic resonance techniques have already been used to demonstrate both simple quantum information processing and geometric phase shifts. Here we combine these ideas by performing a nuclear magnetic resonance experiment in which a conditional Berry phase is implemented, demonstrating a controlled phase shift gate.     

Crossing paths: interactions between the cell death machinery and growth factor survival signals

Cytokines and growth factors play a crucial role in the maintenance of haematopoietic homeostasis. They transduce signals that regulate the competing commitments of haematopoietic stem cells, quiescence or proliferation, retention of stem cell pluripotency or differentiation, and survival or demise. When the balance between these commitments and the requirements of the organisms is disturbed, particularly when it favours survival and proliferation, cancer may result. Cell death provoked by loss of growth factor signalling is regulated by the Bcl-2 family of apoptosis regulators, and thus survival messages transduced by growth factors must regulate the activity of these proteins. Many aspects of direct interactions between cytokine signalling and regulation of apoptosis remain elusive. In this review, we explore the mechanisms by which cytokines, in particular Interleukin-3 and granulocyte–macrophage colony-stimulating factor, promote cell survival and suppress apoptosis as models of how cytokine signalling and apoptotic pathways intersect.     

热轧带钢层流冷却设定模型的开发与实现

分析了热轧带钢层流冷却的传热过程,基于传热过程给出了冷却控制的空冷和水冷温降计算模型,该模型为线性回归模型,不同于理论的指数温降模型,回归数据取自于现场,更具有实用性,具有模型结构简单、精度高的特点·对层流冷却的设定计算(预设定和修正设定计算)的程序实现方法进行了详细描述,讨论了层流冷却系统中的组别划分,并给出了冷却控制系统的数据流程·本系统的冷却能力强,具有较宽的冷却速率调整范围,运行情况以及使用控制效果良好,能满足现场生产以及新品种开发的要求·     

Apoptosis initiated by Bcl-2-regulated caspase activation independently of the cytochrome c/Apaf-1/caspase-9 apoptosome

Apoptosis is an evolutionarily conserved cell suicide process executed by cysteine proteases (caspases) and regulated by the opposing factions of the Bcl-2 protein family. Mammalian caspase-9 and its activator Apaf-1 were thought to be essential, because mice lacking either of them display neuronal hyperplasia and their lymphocytes and fibroblasts seem resistant to certain apoptotic stimuli. Because Apaf-1 requires cytochrome c to activate caspase-9, and Bcl-2 prevents mitochondrial cytochrome c release, Bcl-2 is widely believed to inhibit apoptosis by safeguarding mitochondrial membrane integrity. Our results suggest a different, broader role, because Bcl-2 overexpression increased lymphocyte numbers in mice and inhibited many apoptotic stimuli, but the absence of Apaf-1 or caspase-9 did not. Caspase activity was still discernible in cells lacking Apaf-1 or caspase-9, and a potent caspase antagonist both inhibited apoptosis and retarded cytochrome c release. We conclude that Bcl-2 regulates a caspase activation programme independently of the cytochrome c/Apaf-1/caspase-9 'apoptosome', which seems to amplify rather than initiate the caspase cascade.