Quantum Reed-Solomon Codes

After a brief introduction to both quantum computation and quantum error correction, we show how to construct quantum error-correcting codes based on classical BCH codes. With these codes, decoding can exploit additional information about the position of errors. This error model - the quantum erasure channel - is discussed. Finally, parameters of quantum BCH codes are provided.Comment: Summary only (2 pages), for the full version see: Proceedings Applied Algebra, Algebraic Algorithms and Error-Correcting Codes (AAECC-13), Lecture Notes in Computer Science 1719, Springer, 199

MuRF1 mono-ubiquitinates TRα to inhibit T3-induced cardiac hypertrophy in vivo

Thyroid hormone (TH) is recognized for its role in cellular metabolism and growth and participates in homeostasis of the heart. T3 activates pro-survival pathways including Akt and mTOR. Treatment with T3 after myocardial infarction is cardioprotective and promotes elements of physiological hypertrophic response after cardiac injury. Although T3 is known to benefit the heart, very little about its regulation at the molecular level has been described to date. The ubiquitin proteasome system (UPS) regulates nuclear hormone receptors such as estrogen, progesterone, androgen, and glucocorticoid receptors by both degradatory and non-degradatory mechanisms. However, how the UPS regulates T3-mediated activity is not well understood. In this study, we aim to determine the role of the muscle-specific ubiquitin ligase muscle ring finger-1 (MuRF1) in regulating T3-induced cardiomyocyte growth. An increase in MuRF1 expression inhibits T3-induced physiological cardiac hypertrophy, whereas a decrease in MuRF1 expression enhances T3’s activity both in vitro and in cardiomyocytes in vivo. MuRF1 interacts directly with TRα to inhibit its activity by posttranslational ubiquitination in a non-canonical manner. We then demonstrated that a nuclear localization apparatus that regulates/inhibits nuclear receptors by sequestering them within a subcompartment of the nucleus was necessary for MuRF1 to inhibit T3 activity. This work implicates a novel mechanism that enhances the beneficial T3 activity specifically within the heart, thereby offering a potential target to enhance cardiac T3 activity in an organ-specific manner

Prolonged refractory status epilepticus following acute traumatic brain injury: a case report of excellent neurological recovery

INTRODUCTION: Refractory status epilepticus (RSE) secondary to traumatic brain injury (TBI) may be under-recognized and is associated with significant morbidity and mortality. METHODS: This case report describes a 20 year old previously healthy woman who suffered a severe TBI as a result of a motor vehicle collision and subsequently developed RSE. Pharmacological coma, physiological support and continuous electroencephalography (cEEG) were undertaken. RESULTS: Following 25 days of pharmacological coma, electrographic and clinical seizures subsided and the patient has made an excellent cognitive recovery. CONCLUSION: With early identification, aggressive physiological support, appropriate monitoring, including cEEG, and an adequate length of treatment, young trauma patients with no previous seizure history and limited structural damage to the brain can have excellent neurological recovery from prolonged RSE

Inhibition of the translesion synthesis polymerase REV1 exploits replication gaps as a cancer vulnerability

The replication stress response, which serves as an anticancer barrier, is activated not only by DNA damage and replication obstacles but also oncogenes, thus obscuring how cancer evolves. Here, we identify that oncogene expression, similar to other replication stress-inducing agents, induces single-stranded DNA (ssDNA) gaps that reduce cell fitness. DNA fiber analysis and electron microscopy reveal that activation of translesion synthesis (TLS) polymerases restricts replication fork slowing, reversal, and fork degradation without inducing replication gaps despite the continuation of replication during stress. Consistent with gap suppression (GS) being fundamental to cancer, we demonstrate that a small-molecule inhibitor targeting the TLS factor REV1 not only disrupts DNA replication and cancer cell fitness but also synergizes with gap-inducing therapies such as inhibitors of ATR or Wee1. Our work illuminates that GS during replication is critical for cancer cell fitness and therefore a targetable vulnerability

Mesoscopic superpositions of vibronic collective states of N trapped ions

We propose a scalable procedure to generate entangled superpositions of motional coherent states and electronic states in N trapped ions. Beyond their fundamental importance, these states may be of interest for quantum information processing and may be used in experimental studies of decoherence.Comment: Final version, as published in Physical Review Letters. See also further developments and applications in quant-ph/020207

Experimental realization of the one qubit Deutsch-Jozsa algorithm in a quantum dot

We perform quantum interference experiments on a single self-assembled semiconductor quantum dot. The presence or absence of a single exciton in the dot provides a qubit that we control with femtosecond time resolution. We combine a set of quantum operations to realize the single-qubit Deutsch-Jozsa algorithm. The results show the feasibility of single qubit quantum logic in a semiconductor quantum dot using ultrafast optical control.Comment: REVTex4, 4 pages, 3 figures. Now includes more details about the dephasing in the quantum dots. The introduction has been reworded for clarity. Minor readability fixe

Trial-unique, delayed nonmatching-to-location (TUNL) touchscreen testing for mice: sensitivity to dorsal hippocampal dysfunction.

RATIONALE: The hippocampus is implicated in many of the cognitive impairments observed in conditions such as Alzheimer's disease (AD) and schizophrenia (SCZ). Often, mice are the species of choice for models of these diseases and the study of the relationship between brain and behaviour more generally. Thus, automated and efficient hippocampal-sensitive cognitive tests for the mouse are important for developing therapeutic targets for these diseases, and understanding brain-behaviour relationships. One promising option is to adapt the touchscreen-based trial-unique nonmatching-to-location (TUNL) task that has been shown to be sensitive to hippocampal dysfunction in the rat. OBJECTIVES: This study aims to adapt the TUNL task for use in mice and to test for hippocampus-dependency of the task. METHODS: TUNL training protocols were altered such that C57BL/6 mice were able to acquire the task. Following acquisition, dysfunction of the dorsal hippocampus (dHp) was induced using a fibre-sparing excitotoxin, and the effects of manipulation of several task parameters were examined. RESULTS: Mice could acquire the TUNL task using training optimised for the mouse (experiments 1). TUNL was found to be sensitive to dHp dysfunction in the mouse (experiments 2, 3 and 4). In addition, we observed that performance of dHp dysfunction group was somewhat consistently lower when sample locations were presented in the centre of the screen. CONCLUSIONS: This study opens up the possibility of testing both mouse and rat models on this flexible and hippocampus-sensitive touchscreen task.CHK received funding from the Korean Health Technology R&D Project, Ministry of Health & Welfare, Republic of Korea (HI11C1183). CJH, LMS and TJB were funded by Medical Research Council/Wellcome Trust grant 089703/Z/09/Z. CR, LMS and TJB were funded by Alzheimer’s Research UK [ART/ESG2010/1]. ACM, MHE, CAO, LMS and TJB also received funding from the Innovative Medicine Initiative Joint Undertaking under grant agreement no 115008 of which resources are composed of EFPIA in-kind contribution and financial contribution from the European Union’s Seventh Framework Programme (FP7/2007-2013).This is the final version of the article. It first appeared from Springer via http://dx.doi.org/10.1007/s00213-015-4017-

Two-Bit Gates are Universal for Quantum Computation

A proof is given, which relies on the commutator algebra of the unitary Lie groups, that quantum gates operating on just two bits at a time are sufficient to construct a general quantum circuit. The best previous result had shown the universality of three-bit gates, by analogy to the universality of the Toffoli three-bit gate of classical reversible computing. Two-bit quantum gates may be implemented by magnetic resonance operations applied to a pair of electronic or nuclear spins. A ``gearbox quantum computer'' proposed here, based on the principles of atomic force microscopy, would permit the operation of such two-bit gates in a physical system with very long phase breaking (i.e., quantum phase coherence) times. Simpler versions of the gearbox computer could be used to do experiments on Einstein-Podolsky-Rosen states and related entangled quantum states.Comment: 21 pages, REVTeX 3.0, two .ps figures available from author upon reques

The Road to Quantum Computational Supremacy

We present an idiosyncratic view of the race for quantum computational supremacy. Google's approach and IBM challenge are examined. An unexpected side-effect of the race is the significant progress in designing fast classical algorithms. Quantum supremacy, if achieved, won't make classical computing obsolete.Comment: 15 pages, 1 figur

Entropy and Quantum Kolmogorov Complexity: A Quantum Brudno's Theorem

In classical information theory, entropy rate and Kolmogorov complexity per symbol are related by a theorem of Brudno. In this paper, we prove a quantum version of this theorem, connecting the von Neumann entropy rate and two notions of quantum Kolmogorov complexity, both based on the shortest qubit descriptions of qubit strings that, run by a universal quantum Turing machine, reproduce them as outputs.Comment: 26 pages, no figures. Reference to publication added: published in the Communications in Mathematical Physics (http://www.springerlink.com/content/1432-0916/