A note on the Landauer principle in quantum statistical mechanics

The Landauer principle asserts that the energy cost of erasure of one bit of information by the action of a thermal reservoir in equilibrium at temperature T is never less than $kTlog 2$. We discuss Landauer's principle for quantum statistical models describing a finite level quantum system S coupled to an infinitely extended thermal reservoir R. Using Araki's perturbation theory of KMS states and the Avron-Elgart adiabatic theorem we prove, under a natural ergodicity assumption on the joint system S+R, that Landauer's bound saturates for adiabatically switched interactions. The recent work of Reeb and Wolf on the subject is discussed and compared

Opening up the Quantum Three-Box Problem with Undetectable Measurements

One of the most striking features of quantum mechanics is the profound effect exerted by measurements alone. Sophisticated quantum control is now available in several experimental systems, exposing discrepancies between quantum and classical mechanics whenever measurement induces disturbance of the interrogated system. In practice, such discrepancies may frequently be explained as the back-action required by quantum mechanics adding quantum noise to a classical signal. Here we implement the 'three-box' quantum game of Aharonov and Vaidman in which quantum measurements add no detectable noise to a classical signal, by utilising state-of-the-art control and measurement of the nitrogen vacancy centre in diamond. Quantum and classical mechanics then make contradictory predictions for the same experimental procedure, however classical observers cannot invoke measurement-induced disturbance to explain this discrepancy. We quantify the residual disturbance of our measurements and obtain data that rule out any classical model by > 7.8 standard deviations, allowing us for the first time to exclude the property of macroscopic state-definiteness from our system. Our experiment is then equivalent to a Kochen-Spekker test of quantum non-contextuality that successfully addresses the measurement detectability loophole

A novel class of microRNA-recognition elements that function only within open reading frames.

MicroRNAs (miRNAs) are well known to target 3' untranslated regions (3' UTRs) in mRNAs, thereby silencing gene expression at the post-transcriptional level. Multiple reports have also indicated the ability of miRNAs to target protein-coding sequences (CDS); however, miRNAs have been generally believed to function through similar mechanisms regardless of the locations of their sites of action. Here, we report a class of miRNA-recognition elements (MREs) that function exclusively in CDS regions. Through functional and mechanistic characterization of these 'unusual' MREs, we demonstrate that CDS-targeted miRNAs require extensive base-pairing at the 3' side rather than the 5' seed; cause gene silencing in an Argonaute-dependent but GW182-independent manner; and repress translation by inducing transient ribosome stalling instead of mRNA destabilization. These findings reveal distinct mechanisms and functional consequences of miRNAs that target CDS versus the 3' UTR and suggest that CDS-targeted miRNAs may use a translational quality-control-related mechanism to regulate translation in mammalian cells

Consequences of temperature fluctuations in observables measured in high energy collisions

We review the consequences of intrinsic, nonstatistical temperature fluctuations as seen in observables measured in high energy collisions. We do this from the point of view of nonextensive statistics and Tsallis distributions. Particular attention is paid to multiplicity fluctuations as a first consequence of temperature fluctuations, to the equivalence of temperature and volume fluctuations, to the generalized thermodynamic fluctuations relations allowing us to compare fluctuations observed in different parts of phase space, and to the problem of the relation between Tsallis entropy and Tsallis distributions. We also discuss the possible influence of conservation laws on these distributions and provide some examples of how one can get them without considering temperature fluctuations.Comment: Revised version of the invited contribution to The European Physical Journal A (Hadrons and Nuclei) topical issue about 'Relativistic Hydro- and Thermodynamics in Nuclear Physics' guest eds. Tamas S. Biro, Gergely G. Barnafoldi and Peter Va

eIF4A2 drives repression of translation at initiation by Ccr4-Not through purine-rich motifs in the 5'UTR

Background: Regulation of the mRNA life cycle is central to gene expression control and determination of cell fate. miRNAs represent a critical mRNA regulatory mechanism, but despite decades of research, their mode of action is still not fully understood. Results: Here, we show that eIF4A2 is a major effector of the repressive miRNA pathway functioning via the Ccr4-Not complex. We demonstrate that while DDX6 interacts with Ccr4-Not, its effects in the mechanism are not as pronounced. Through its interaction with the Ccr4-Not complex, eIF4A2 represses mRNAs at translation initiation. We show evidence that native eIF4A2 has similar RNA selectivity to chemically inhibited eIF4A1. eIF4A2 exerts its repressive effect by binding purine-rich motifs which are enriched in the 5′UTR of target mRNAs directly upstream of the AUG start codon. Conclusions: Our data support a model whereby purine motifs towards the 3′ end of the 5′UTR are associated with increased ribosome occupancy and possible uORF activation upon eIF4A2 binding

A Candidate Approach Implicates the Secreted Salmonella Effector Protein SpvB in P-Body Disassembly

P-bodies are dynamic aggregates of RNA and proteins involved in several post-transcriptional regulation processes. P-bodies have been shown to play important roles in regulating viral infection, whereas their interplay with bacterial pathogens, specifically intracellular bacteria that extensively manipulate host cell pathways, remains unknown. Here, we report that Salmonella infection induces P-body disassembly in a cell type-specific manner, and independently of previously characterized pathways such as inhibition of host cell RNA synthesis or microRNA-mediated gene silencing. We show that the Salmonella-induced P-body disassembly depends on the activation of the SPI-2 encoded type 3 secretion system, and that the secreted effector protein SpvB plays a major role in this process. P-body disruption is also induced by the related pathogen, Shigella flexneri, arguing that this might be a new mechanism by which intracellular bacterial pathogens subvert host cell function