Quantum Computer Emulator

We describe a quantum computer emulator for a generic, general purpose quantum computer. This emulator consists of a simulator of the physical realization of the quantum computer and a graphical user interface to program and control the simulator. We illustrate the use of the quantum computer emulator through various implementations of the Deutsch-Jozsa and Grover's database search algorithm.Comment: 28 pages, 4, figures, see also http://rugth30.phys.rug.nl/compphys/qce.htm ; figures updated, instructions change

Feedback Effect on Landau-Zener-Stueckelberg Transitions in Magnetic Systems

We examine the effect of the dynamics of the internal magnetic field on the staircase magnetization curves observed in large-spin molecular magnets. We show that the size of the magnetization steps depends sensitively on the intermolecular interactions, even if these are very small compared to the intra-molecular couplings.Comment: 4 pages, 3 Postscript figures; paper reorganized, conclusions modifie

Fast Algorithm for Finding the Eigenvalue Distribution of Very Large Matrices

A theoretical analysis is given of the equation of motion method, due to Alben et al., to compute the eigenvalue distribution (density of states) of very large matrices. The salient feature of this method is that for matrices of the kind encountered in quantum physics the memory and CPU requirements of this method scale linearly with the dimension of the matrix. We derive a rigorous estimate of the statistical error, supporting earlier observations that the computational efficiency of this approach increases with matrix size. We use this method and an imaginary-time version of it to compute the energy and the specific heat of three different, exactly solvable, spin-1/2 models and compare with the exact results to study the dependence of the statistical errors on sample and matrix size.Comment: 24 pages, 24 figure

Regulation of the host immune system by helminth parasites

Helminth parasite infections are associated with a battery of immunomodulatory mechanisms, which impact all facets of the host immune response to ensure their persistence within the host. This broad-spectrum modulation of host immunity has intended and unintended consequences, both advantageous and disadvantageous. Thus the host may benefit from suppression of collateral damage during parasite infection, and from reduced allergic, autoimmune and inflammatory reactions. However, helminth infection can also be detrimental in reducing vaccine responses, increasing susceptibility to co-infection, and potentially reducing tumor immunosurveillance. In this review we will summarize the panoply of immunomodulatory mechanisms used by helminths, their potential utility in human disease, and prospective areas of future research

Concerted IL-25R and IL-4Rα signaling drive innate type 2 effector immunity for optimal helminth expulsion

Interleukin 25 (IL-25) is a major 'alarmin' cytokine, capable of initiating and amplifying the type 2 immune response to helminth parasites. However its role in the later effector phase of clearing chronic infection remains unclear. The helminth Heligmosomoides polygyrus establishes long-term infections in susceptible C57BL/6 mice, but is slowly expelled in BALB/c mice from day 14 onwards. We noted that IL-25R (Il17rb)-deficient BALB/c mice were unable to expel parasites despite type 2 immune activation comparable to the wild-type. We then established that in C57BL/6 mice, IL-25 adminstered late in infection (days 14-17) drove immunity. Moreover when IL-25 and IL-4 were delivered to Rag1-deficient mice, the combination resulted in near complete expulsion of the parasite, even following administration of an anti-CD90 antibody to deplete innate lymphoid cells (ILCs). Hence, effective anti-helminth immunity during chronic infection requires an innate effector cell population that is synergistically activated by the combination of IL-4Rα and IL-25R signaling

Host protective roles of type 2 immunity:Parasite killing and tissue repair, flip sides of the same coin

AbstractMetazoan parasites typically induce a type 2 immune response, characterized by T helper 2 (Th2) cells that produce the cytokines IL-4, IL-5 and IL-13 among others. The type 2 response is host protective, reducing the number of parasites either through direct killing in the tissues, or expulsion from the intestine. Type 2 immunity also protects the host against damage mediated by these large extracellular parasites as they migrate through the body. At the center of both the innate and adaptive type 2 immune response, is the IL-4Rα that mediates many of the key effector functions. Here we highlight the striking overlap between the molecules, cells and pathways that mediate both parasite control and tissue repair. We have proposed that adaptive Th2 immunity evolved out of our innate repair pathways to mediate both accelerated repair and parasite control in the face of continual assault from multicellular pathogens. Type 2 cytokines are involved in many aspects of mammalian physiology independent of helminth infection. Therefore understanding the evolutionary relationship between helminth killing and tissue repair should provide new insight into immune mechanisms of tissue protection in the face of physical injury