Abstract:
In this study, we demonstrate that the ability of LMP1 to induce the phosphorylation and inactivation of Foxo3a is linked to the upregulation of Id1. Furthermore, we show that the induction of Id1 is essential for the transforming function of LMP1 as over-expression of Id1 increases cell proliferation, attenuates TGFβ-SMAD-mediated transcription and renders cells refractory to TGFβ-mediated cytostasis. Id1 silencing in LMP1-expressing epithelial cells abolishes the inhibitory effect of LMP1 on TGFβ-mediated cell growth arrest and reduces the ability of LMP1 to attenuate SMAD transcriptional activity. In response to TGFβ stimulation, LMP1 does not abolish SMAD phosphorylation but inhibits p21 protein expression. In addition, we found the induction of Id1 in LMP1-expressing cells upon stimulation by TGFβ. We provide evidence that LMP1 suppresses the transcriptional repressor ATF3, possibly leading to the TGFβ-induced Id1 upregulation.The current data provide novel information regarding the mechanisms by which LMP1 suppresses TGFβ-induced cytostasis, highlighting the importance of Id1 in LMP1 mediated cell transformationThe Epstein-Barr virus (EBV)-encoded latent membrane protein (LMP1) is commonly expressed in nasopharyngeal carcinoma (NPC) and is believed to play important role in NPC pathogenesis [1]. LMP1 is an oncogenic protein, inducing lymphomagenesis in transgenic mice and transforming rodent fibroblasts in vitro, rendering them tumourigenic in vivo. In vitro studies show that LMP1 is essential for EBV immortalisation of primary B cells, and can induce a state of cell activation in B lymphoma-derived cell lines. In epithelial cells, LMP1 increases cell proliferation, promotes anchorage independent growth, protects cells from apoptosis, induces an epithelial-mesenchymal transformation, promotes cell invasion and perturbs epithelial cell differentiation [2,3]. LMP1 is an integral membrane protein comprising a 24 amino acid N-terminal cytoplasmic domain, six trans

Abstract:
Which gates are universal for quantum computation? Although it is well known that certain gates on two-level quantum systems (qubits), such as the controlled-not (CNOT), are universal when assisted by arbitrary one-qubit gates, it has only recently become clear precisely what class of two-qubit gates is universal in this sense. Here we present an elementary proof that any entangling two-qubit gate is universal for quantum computation, when assisted by one-qubit gates. A proof of this important result for systems of arbitrary finite dimension has been provided by J. L. and R. Brylinski [arXiv:quant-ph/0108062, 2001]; however, their proof relies upon a long argument using advanced mathematics. In contrast, our proof provides a simple constructive procedure which is close to optimal and experimentally practical [C. M. Dawson and A. Gilchrist, online implementation of the procedure described herein (2002), http://www.physics.uq.edu.au/gqc/].

Abstract:
How useful is a quantum dynamical operation for quantum information processing? Motivated by this question we investigate several strength measures quantifying the resources intrinsic to a quantum operation. We develop a general theory of such strength measures, based on axiomatic considerations independent of state-based resources. The power of this theory is demonstrated with applications to quantum communication complexity, quantum computational complexity, and entanglement generation by unitary operations.

Abstract:
A globalized food trade, extensive production and complex supply chains are contributing toward an increased number of microbiological food safety outbreaks. Moreover, the volume of international food trade has increased to become very large. All of these factors are putting pressure on the food companies to meet global demand in order to be competitive. This scenario could force manufacturers to be lenient toward food safety control intentionally, or unintentionally, and result in a major foodborne outbreak that causes health problems and economic loss. The estimated cost of food safety incidents for the economy of the United States is around $7 billion per year which comes from notifying consumers, removing food from shelves, and paying damages as a result of lawsuits. Most other countries similarly have economic losses. Much of these losses represent lost markets, loss of consumer demand, litigation and company closures. Concrete steps are needed to improve safety of foods produced for local or overseas markets to avoid unexpected food scandals and economic losses.

Abstract:
The one-way quantum computing model introduced by Raussendorf and Briegel [Phys. Rev. Lett. 86 (22), 5188-5191 (2001)] shows that it is possible to quantum compute using only a fixed entangled resource known as a cluster state, and adaptive single-qubit measurements. This model is the basis for several practical proposals for quantum computation, including a promising proposal for optical quantum computation based on cluster states [M. A. Nielsen, arXiv:quant-ph/0402005, accepted to appear in Phys. Rev. Lett.]. A significant open question is whether such proposals are scalable in the presence of physically realistic noise. In this paper we prove two threshold theorems which show that scalable fault-tolerant quantum computation may be achieved in implementations based on cluster states, provided the noise in the implementations is below some constant threshold value. Our first threshold theorem applies to a class of implementations in which entangling gates are applied deterministically, but with a small amount of noise. We expect this threshold to be applicable in a wide variety of physical systems. Our second threshold theorem is specifically adapted to proposals such as the optical cluster-state proposal, in which non-deterministic entangling gates are used. A critical technical component of our proofs is two powerful theorems which relate the properties of noisy unitary operations restricted to act on a subspace of state space to extensions of those operations acting on the entire state space.

Abstract:
This pedagogical review presents the proof of the Solovay-Kitaev theorem in the form of an efficient classical algorithm for compiling an arbitrary single-qubit gate into a sequence of gates from a fixed and finite set. The algorithm can be used, for example, to compile Shor's algorithm, which uses rotations of $\pi / 2^k$, into an efficient fault-tolerant form using only Hadamard, controlled-{\sc not}, and $\pi / 8$ gates. The algorithm runs in $O(\log^{2.71}(1/\epsilon))$ time, and produces as output a sequence of $O(\log^{3.97}(1/\epsilon))$ quantum gates which is guaranteed to approximate the desired quantum gate to an accuracy within $\epsilon > 0$. We also explain how the algorithm can be generalized to apply to multi-qubit gates and to gates from $SU(d)$.

Abstract:
Entanglement in the ground state of a many-body quantum system may arise when the local terms in the system Hamiltonian fail to commute with the interaction terms in the Hamiltonian. We quantify this phenomenon, demonstrating an analogy between ground-state entanglement and the phenomenon of frustration in spin systems. In particular, we prove that the amount of ground-state entanglement is bounded above by a measure of the extent to which interactions frustrate the local terms in the Hamiltonian. As a corollary, we show that the amount of ground-state entanglement is bounded above by a ratio between parameters characterizing the strength of interactions in the system, and the local energy scale. Finally, we prove a qualitatively similar result for other energy eigenstates of the system.

Abstract:
In this report we demonstrate that EBNA1 inhibits the canonical NF-κB pathway in carcinoma lines by inhibiting the phosphorylation of IKKα/β. In agreement with this observation we find a reduction in the phosphorylation of IκBα and reduced phosphorylation and nuclear translocation of p65, resulting in a reduction in the amount of p65 in nuclear NF-κB complexes. Similar effects were also found in carcinoma lines infected with recombinant EBV and in the EBV-positive NPC-derived cell line C666-1. Inhibition of NF-κB was dependent upon regions of EBNA1 essential for gene transactivation whilst the interaction with the deubiquitinating enzyme, USP7, was entirely dispensable. Furthermore, in agreement with EBNA1 inhibiting p65 NF-κB we demonstrate that p65 was exclusively cytoplasmic in 11 out of 11 NPC tumours studied.Inhibition of p65 NF-κB in murine and human epidermis results in tissue hyperplasia and the development of squamous cell carcinoma. In line with this, p65 knockout fibroblasts have a transformed phenotype. Inhibition of p65 NF-κB by EBNA1 may therefore contribute to the development of NPC by inducing tissue hyperplasia. Furthermore, inhibition of NF-κB is employed by viruses as an immune evasion strategy which is also closely linked to oncogenesis during persistent viral infection. Our findings therefore further implicate EBNA1 in playing an important role in the pathogenesis of NPC.Epstein-Barr virus (EBV) is a ubiquitous human γ-herpesvirus that is associated with both lymphoid and epithelial tumours [1], including undifferentiated NPC where there is a near 100% association with EBV infection. Whilst the pattern of EBV latent protein expression varies in different tumour types the EBV nuclear antigen, Epstein-Barr nuclear antigen-1 (EBNA1), is expressed in all EBV-associated malignancies due to its indispensable role in the maintenance and replication of the EBV genome via sequence-specific binding to the viral origin of replication, oriP [2]. Furthermore

Abstract:
Our data confirm that in epithelial cells EBNA1 can enhance cellular pol III transcription. Transient expression of EBNA1 in Ad/AH cells stably expressing the EBERs led to induction of both EBER1 and EBER2 and conversely, expression of a dominant negative EBNA1 led to reduced EBER expression in EBV-infected Ad/AH cells. EBNA1 can induce transcription factors used by EBER genes, including TFIIIC, ATF-2 and c-Myc. A variant chromatin precipitation procedure showed that EBNA1 is associated with the promoters of these genes but not with the promoters of pol III-transcribed genes, including the EBERs themselves. Using shRNA knock-down, we confirm the significance of both ATF-2 and c-Myc in EBER expression. Further, functional induction of a c-Myc fusion protein led to increased EBER expression, providing c-Myc binding sites upstream of EBER1 were intact. In vivo studies confirm elevated levels of the 102 kD subunit of TFIIIC in the tumour cells of EBV-positive nasopharyngeal carcinoma biopsies.Our findings reveal that EBNA1 is able to enhance EBER expression through induction of cellular transcription factors and add to the repertoire of EBNA1's transcription-regulatory properties.In the 46 years since its discovery, the ubiquitous Epstein-Barr Virus (EBV) has been found to be closely associated with a wide range of epithelial and lymphoid malignancies [1]. During all typical forms of latent EBV infection and B-cell immortalisation, two highly expressed gene products are the non-polyadenylated RNAs, Epstein-Barr Virus encoded RNAs 1 and 2 (EBER1 and EBER2). Although no definitive role for the EBERs in cell transformation or malignant growth has been elucidated, several studies highlight the EBERs as making a significant contribution to EBV-associated malignancies [2-5] probably through direct interactions with cellular proteins with which they are known to form complexes. These include PKR [6,7], RIG-I [8], La [9] and ribosomal protein L22 [10-12]. In addition, the EBERs

Abstract:
We introduce a new method for constraining the redshift distribution of a set of galaxies, using weak gravitational lensing shear. Instead of using observed shears and redshifts to constrain cosmological parameters, we ask how well the shears around clusters can constrain the redshifts, assuming fixed cosmological parameters. This provides a check on photometric redshifts, independent of source spectral energy distribution properties and therefore free of confounding factors such as misidentification of spectral breaks. We find that ~40 massive ($\sigma_v=1200$ km/s) cluster lenses are sufficient to determine the fraction of sources in each of six coarse redshift bins to ~11%, given weak (20%) priors on the masses of the highest-redshift lenses, tight (5%) priors on the masses of the lowest-redshift lenses, and only modest (20-50%) priors on calibration and evolution effects. Additional massive lenses drive down uncertainties as $N_{lens}^0.5$, but the improvement slows as one is forced to use lenses further down the mass function. Future large surveys contain enough clusters to reach 1% precision in the bin fractions if the tight lens mass priors can be maintained for large samples of lenses. In practice this will be difficult to achieve, but the method may be valuable as a complement to other more precise methods because it is based on different physics and therefore has different systematic errors.