On the Possibility of Quasi Small-World Nanomaterials

The possibility of materials that are governed by a fixed point related to small world networks is discussed. In particular, large-scale Monte Carlo simulations are performed on Ising ferromagnetic models on two different small-world networks generated from a one-dimensional spin chain. One has the small-world bond strengths independent of the length, and exhibits a finite-temperature phase transition. The other has small-world bonds built from atoms, and although there is no finite-temperature phase transition the system shows a slow power-law change of the effective critical temperature of a finite system as a function of the system size. An outline of a possible synthesis route for quasi small-world nanomaterials is presented.Comment: 13 pages, 9 figures, submitted to Brazilian Journal of Physics, conference proceedings for III Brazilian Meeting on Simulational Physics (2003

Information preserving structures: A general framework for quantum zero-error information

Quantum systems carry information. Quantum theory supports at least two distinct kinds of information (classical and quantum), and a variety of different ways to encode and preserve information in physical systems. A system's ability to carry information is constrained and defined by the noise in its dynamics. This paper introduces an operational framework, using information-preserving structures to classify all the kinds of information that can be perfectly (i.e., with zero error) preserved by quantum dynamics. We prove that every perfectly preserved code has the same structure as a matrix algebra, and that preserved information can always be corrected. We also classify distinct operational criteria for preservation (e.g., "noiseless", "unitarily correctible", etc.) and introduce two new and natural criteria for measurement-stabilized and unconditionally preserved codes. Finally, for several of these operational critera, we present efficient (polynomial in the state-space dimension) algorithms to find all of a channel's information-preserving structures.Comment: 29 pages, 19 examples. Contains complete proofs for all the theorems in arXiv:0705.428

On Interferometric Duality in Multibeam Experiments

We critically analyze the problem of formulating duality between fringe visibility and which-way information, in multibeam interference experiments. We show that the traditional notion of visibility is incompatible with any intuitive idea of complementarity, but for the two-beam case. We derive a number of new inequalities, not present in the two-beam case, one of them coinciding with a recently proposed multibeam generalization of the inequality found by Greenberger and YaSin. We show, by an explicit procedure of optimization in a three-beam case, that suggested generalizations of Englert's inequality, do not convey, differently from the two-beam case, the idea of complementarity, according to which an increase of visibility is at the cost of a loss in path information, and viceversa.Comment: 26 pages, 1 figure, substantial changes in the text, new material has been added in Section 3. Version to appear in J.Phys.

Lactate signalling regulates fungal β-glucan masking and immune evasion

AJPB: This work was supported by the European Research Council (STRIFE, ERC- 2009-AdG-249793), The UK Medical Research Council (MR/M026663/1), the UK Biotechnology and Biological Research Council (BB/K017365/1), the Wellcome Trust (080088; 097377). ERB: This work was supported by the UK Biotechnology and Biological Research Council (BB/M014525/1). GMA: Supported by the CNPq-Brazil (Science without Borders fellowship 202976/2014-9). GDB: Wellcome Trust (102705). CAM: This work was supported by the UK Medical Research Council (G0400284). DMM: This work was supported by UK National Centre for the Replacement, Refinement and Reduction of Animals in Research (NC/K000306/1). NARG/JW: Wellcome Trust (086827, 075470,101873) and Wellcome Trust Strategic Award in Medical Mycology and Fungal Immunology (097377). ALL: This work was supported by the MRC Centre for Medical Mycology and the University of Aberdeen (MR/N006364/1).Peer reviewedPostprin

Relational Quantum Mechanics

I suggest that the common unease with taking quantum mechanics as a fundamental description of nature (the "measurement problem") could derive from the use of an incorrect notion, as the unease with the Lorentz transformations before Einstein derived from the notion of observer-independent time. I suggest that this incorrect notion is the notion of observer-independent state of a system (or observer-independent values of physical quantities). I reformulate the problem of the "interpretation of quantum mechanics" as the problem of deriving the formalism from a few simple physical postulates. I consider a reformulation of quantum mechanics in terms of information theory. All systems are assumed to be equivalent, there is no observer-observed distinction, and the theory describes only the information that systems have about each other; nevertheless, the theory is complete.Comment: Substantially revised version. LaTeX fil

Anti-de Sitter black holes, perfect fluids, and holography

We consider asymptotically anti-de Sitter black holes in $d$-spacetime dimensions in the thermodynamically stable regime. We show that the Bekenstein-Hawking entropy and its leading order corrections due to thermal fluctuations can be reproduced by a weakly interacting fluid of bosons and fermions (`dual gas') in $\Delta=\alpha(d-2)+1$ spacetime dimensions, where the energy-momentum dispersion relation for the constituents of the fluid is assumed to be $\epsilon = \kappa p^\alpha$. We examine implications of this result for entropy bounds and the holographic hypothesis.Comment: Minor changes to match published version. 9 Pages, Revte

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Application of Stem Cell Derived Neuronal Cells to Evaluate Neurotoxic Chemotherapy

The generation of induced pluripotent stem cells (iPSCs) and differentiation to cells composing major organs has opened up the possibility for a new model system to study adverse toxicities associated with chemotherapy. Therefore, we used human iPSC-derived neurons to study peripheral neuropathy, one of the most common adverse effects of chemotherapy and cause for dose reduction. To determine the utility of these neurons in investigating the effects of neurotoxic chemotherapy, we measured morphological differences in neurite outgrowth, cell viability as determined by ATP levels and apoptosis through measures of caspase 3/7 activation following treatment with clinically relevant concentrations of platinating agents (cisplatin, oxaliplatin and carboplatin), taxanes (paclitaxel, docetaxel and nab-paclitaxel), a targeted proteasome inhibitor (bortezomib), an antiangiogenic compound (thalidomide), and 5-fluorouracil, a chemotherapeutic that does not cause neuropathy. We demonstrate differential sensitivity of neurons to mechanistically distinct classes of chemotherapeutics. We also show a dose-dependent reduction of electrical activity as measured by mean firing rate of the neurons following treatment with paclitaxel. We compared neurite outgrowth and cell viability of iPSC-derived cortical (iCell® Neurons) and peripheral (Peri.4U) neurons to cisplatin, paclitaxel and vincristine. Goshajinkigan, a Japanese herbal neuroprotectant medicine, was protective against paclitaxel-induced neurotoxicity but not oxaliplatin as measured by morphological phenotypes. Thus, we have demonstrated the utility of human iPSC-derived neurons as a useful model to distinguish drug class differences and for studies of a potential neuroprotectant for the prevention of chemotherapy-induced peripheral neuropathy

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN