162 research outputs found

    Universal quantum computation with unlabeled qubits

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    We show that an n-th root of the Walsh-Hadamard transform (obtained from the Hadamard gate and a cyclic permutation of the qubits), together with two diagonal matrices, namely a local qubit-flip (for a fixed but arbitrary qubit) and a non-local phase-flip (for a fixed but arbitrary coefficient), can do universal quantum computation on n qubits. A quantum computation, making use of n qubits and based on these operations, is then a word of variable length, but whose letters are always taken from an alphabet of cardinality three. Therefore, in contrast with other universal sets, no choice of qubit lines is needed for the application of the operations described here. A quantum algorithm based on this set can be interpreted as a discrete diffusion of a quantum particle on a de Bruijn graph, corrected on-the-fly by auxiliary modifications of the phases associated to the arcs.Comment: 6 page

    Embedding complete binary trees into star networks

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    Abstract. Star networks have been proposed as a possible interconnection network for massively parallel computers. In this paper we investigate embeddings of complete binary trees into star networks. Let G and H be two networks represented by simple undirected graphs. An embedding of G into H is an injective mapping f from the vertices of G into the vertices of H. The dilation of the embedding is the maximum distance between f(u), f(v) taken over all edges (u, v) of G. Low dilation embeddings of binary trees into star graphs correspond to efficient simulations of parallel algorithms that use the binary tree topology, on parallel computers interconnected with star networks. First, we give a construction of embeddings of dilation 1 of complete binary trees into n-dimensional star graphs. These trees are subgraphs of star graphs. Their height is fl(n log n), which is asymptotically optimal. Constructions of embeddings of complete binary trees of dilation 28 and 26 + 1, for 8 > 1, into star graphs are then given. The use of larger dilation allows embeddings of trees of greater height into star graphs. For example, the difference of the heights of the trees embedded with dilation 2 and 1 is greater than n/2. All these constructions can be modified to yield embeddings of dilation 1, and 26, for ~ > 1, of complete binary trees into pancake graphs. Our results show that massively parallel computers interconnected with star networks are well suited for efficient simulations of parallel algorithms with complete binary tree topology

    "Of Mice and Measures": A Project to Improve How We Advance Duchenne Muscular Dystrophy Therapies to the Clinic

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    A new line of dystrophic mdx mice on the DBA/2J (D2) background has emerged as a candidate to study the efficacy of therapeutic approaches for Duchenne muscular dystrophy (DMD). These mice harbor genetic polymorphisms that appear to increase the severity of the dystropathology, with disease modifiers that also occur in DMD patients, making them attractive for efficacy studies and drug development. This workshop aimed at collecting and consolidating available data on the pathological features and the natural history of these new D2/mdx mice, for comparison with classic mdx mice and controls, and to identify gaps in information and their potential value. The overall aim is to establish guidance on how to best use the D2/mdx mouse model in preclinical studies

    The battle over Syria's reconstruction

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    Reconstruction is becoming the new battleground in the Syrian conflictβ€”its continuation by other means. It is instrumentalized by the regime as a way to reconsolidate its control over the country and by rival regional and international powers to shape the internal balance of power and establish spheres of influence in the country. The paper examines the Asad regime’s practices, including co-optation of militia leaders via reconstruction concessions and use of reconstruction to clear strategic areas of opposition-dominated urban settlements. The paper then surveys how the geopolitical struggle in Syria has produced an asymmetry as regards reconstruction: those powers that lost the geo-political contest on the ground seek to use geo-economic superiority to reverse the geo-political outcome. Then the impact of proxy wars and spheres of influence in the country on the security context for reconstruction is examined. Finally, the reconstruction initiatives of the various external parties are assessed, including Russia, Iran and Turkey as well as the spoiler role by which the US seeks to obstruct reconstruction that would spell victory in Syria for its Russian and Iranian rivals.PostprintPeer reviewe

    The theory and method of comparative area studies

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    Though many now downplay the tension between area studies and disciplinary political science, there has been little substantive guidance on how to accomplish complementarity between their respective approaches. This article seeks to develop the idea of comparative area studies (CAS) as a rubric that maintains the importance of regional knowledge while contributing to general theory building using inductive intra-regional, cross-regional, inter-regional comparison. Treating regions as theoretically-grounded analytical categories, rather than inert or innate geographical entities, can help inform both quantitative and qualitative attempts to build general theory.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

    Marginal Level Dystrophin Expression Improves Clinical Outcome in a Strain of Dystrophin/Utrophin Double Knockout Mice

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    Inactivation of all utrophin isoforms in dystrophin-deficient mdx mice results in a strain of utrophin knockout mdx (uko/mdx) mice. Uko/mdx mice display severe clinical symptoms and die prematurely as in Duchenne muscular dystrophy (DMD) patients. Here we tested the hypothesis that marginal level dystrophin expression may improve the clinical outcome of uko/mdx mice. It is well established that mdx3cv (3cv) mice express a near-full length dystrophin protein at ∼5% of the normal level. We crossed utrophin-null mutation to the 3cv background. The resulting uko/3cv mice expressed the same level of dystrophin as 3cv mice but utrophin expression was completely eliminated. Surprisingly, uko/3cv mice showed a much milder phenotype. Compared to uko/mdx mice, uko/3cv mice had significantly higher body weight and stronger specific muscle force. Most importantly, uko/3cv outlived uko/mdx mice by several folds. Our results suggest that a threshold level dystrophin expression may provide vital clinical support in a severely affected DMD mouse model. This finding may hold clinical implications in developing novel DMD therapies

    Worsening of Cardiomyopathy Using Deflazacort in an Animal Model Rescued by Gene Therapy

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    We have previously demonstrated that gene therapy can rescue the phenotype and extend lifespan in the delta-sarcoglycan deficient cardiomyopathic hamster. In patients with similar genetic defects, steroids have been largely used to slow down disease progression. Aim of our study was to evaluate the combined effects of steroid treatment and gene therapy on cardiac function. We injected the human delta-sarcoglycan cDNA by adeno-associated virus (AAV) 2/8 by a single intraperitoneal injection into BIO14.6 Syrian hamsters at ten days of age to rescue the phenotype. We then treated the hamsters with deflazacort. Treatment was administered to half of the hamsters that had received the AAV and the other hamsters without AAV, as well as to normal hamsters. Both horizontal and vertical activities were greatly enhanced by deflazacort in all groups. As in previous experiments, the AAV treatment alone was able to preserve the ejection fraction (70Β±7% EF). However, the EF value declined (52Β±14%) with a combination of AAV and deflazacort. This was similar with all the other groups of affected animals. We confirm that gene therapy improves cardiac function in the BIO14.6 hamsters. Our results suggest that deflazacort is ineffective and may also have a negative impact on the cardiomyopathy rescue, possibly by boosting motor activity. This is unexpected and may have significance in terms of the lifestyle recommendations for patients

    Genetic Background of Prop1df Mutants Provides Remarkable Protection Against Hypothyroidism-Induced Hearing Impairment

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    Hypothyroidism is a cause of genetic and environmentally induced deafness. The sensitivity of cochlear development and function to thyroid hormone (TH) mandates understanding TH action in this sensory organ. Prop1df and Pou1f1dw mutant mice carry mutations in different pituitary transcription factors, each resulting in pituitary thyrotropin deficiency. Despite the same lack of detectable serum TH, these mutants have very different hearing abilities: Prop1df mutants are mildly affected, while Pou1f1dw mutants are completely deaf. Genetic studies show that this difference is attributable to the genetic backgrounds. Using embryo transfer, we discovered that factors intrinsic to the fetus are the major contributor to this difference, not maternal effects. We analyzed Prop1df mutants to identify processes in cochlear development that are disrupted in other hypothyroid animal models but protected in Prop1df mutants by the genetic background. The development of outer hair cell (OHC) function is delayed, but Prestin and KCNQ4 immunostaining appear normal in mature Prop1df mutants. The endocochlear potential and KCNJ10 immunostaining in the stria vascularis are indistinguishable from wild type, and no differences in neurofilament or synaptophysin staining are evident in Prop1df mutants. The synaptic vesicle protein otoferlin normally shifts expression from OHC to IHC as temporary afferent fibers beneath the OHC regress postnatally. Prop1df mutants exhibit persistent, abnormal expression of otoferlin in apical OHC, suggesting delayed maturation of synaptic function. Thus, the genetic background of Prop1df mutants is remarkably protective for most functions affected in other hypothyroid mice. The Prop1df mutant is an attractive model for identifying the genes that protect against deafness
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