Gentile statistics and restricted partitions

In a recent paper (Tran et al, Ann. Phys.311, 204 (2004)), some asymptotic number theoretical results on the partitioning of an integer were derived exploiting its connection to the quantum density of states of a many-particle system. We generalise these results to obtain an asymptotic formula for the restricted or coloured partitions pks (n), which is the number of partitions of an integer n into the summand of sth powers of integers such that each power of a given integer may occur utmost k times. While the method is not rigorous, it reproduces the well-known asymptotic results for s = 1 apart from yielding more general results for arbitrary values of s

Counterfactual Explanation Policies in RL

As Reinforcement Learning (RL) agents are increasingly employed in diverse decision-making problems using reward preferences, it becomes important to ensure that policies learned by these frameworks in mapping observations to a probability distribution of the possible actions are explainable. However, there is little to no work in the systematic understanding of these complex policies in a contrastive manner, i.e., what minimal changes to the policy would improve/worsen its performance to a desired level. In this work, we present COUNTERPOL, the first framework to analyze RL policies using counterfactual explanations in the form of minimal changes to the policy that lead to the desired outcome. We do so by incorporating counterfactuals in supervised learning in RL with the target outcome regulated using desired return. We establish a theoretical connection between Counterpol and widely used trust region-based policy optimization methods in RL. Extensive empirical analysis shows the efficacy of COUNTERPOL in generating explanations for (un)learning skills while keeping close to the original policy. Our results on five different RL environments with diverse state and action spaces demonstrate the utility of counterfactual explanations, paving the way for new frontiers in designing and developing counterfactual policies.Comment: ICML Workshop on Counterfactuals in Minds and Machines, 202

A genetic network that suppresses genome rearrangements in Saccharomyces cerevisiae and contains defects in cancers.

Gross chromosomal rearrangements (GCRs) play an important role in human diseases, including cancer. The identity of all Genome Instability Suppressing (GIS) genes is not currently known. Here multiple Saccharomyces cerevisiae GCR assays and query mutations were crossed into arrays of mutants to identify progeny with increased GCR rates. One hundred eighty two GIS genes were identified that suppressed GCR formation. Another 438 cooperatively acting GIS genes were identified that were not GIS genes, but suppressed the increased genome instability caused by individual query mutations. Analysis of TCGA data using the human genes predicted to act in GIS pathways revealed that a minimum of 93% of ovarian and 66% of colorectal cancer cases had defects affecting one or more predicted GIS gene. These defects included loss-of-function mutations, copy-number changes associated with reduced expression, and silencing. In contrast, acute myeloid leukaemia cases did not appear to have defects affecting the predicted GIS genes

Searching for Dark Matter with a Superconducting Qubit

Detection mechanisms for low mass bosonic dark matter candidates, such the axion or hidden photon, leverage potential interactions with electromagnetic fields, whereby the dark matter (of unknown mass) on rare occasion converts into a single photon. Current dark matter searches operating at microwave frequencies use a resonant cavity to coherently accumulate the field sourced by the dark matter and a near standard quantum limited (SQL) linear amplifier to read out the cavity signal. To further increase sensitivity to the dark matter signal, sub-SQL detection techniques are required. Here we report the development of a novel microwave photon counting technique and a new exclusion limit on hidden photon dark matter. We operate a superconducting qubit to make repeated quantum non-demolition measurements of cavity photons and apply a hidden Markov model analysis to reduce the noise to 15.7 dB below the quantum limit, with overall detector performance limited by a residual background of real photons. With the present device, we perform a hidden photon search and constrain the kinetic mixing angle to $\epsilon \leq 1.68 \times 10^{-15}$ in a band around 6.011 GHz (24.86 $\mu$eV) with an integration time of 8.33 s. This demonstrated noise reduction technique enables future dark matter searches to be sped up by a factor of 1300. By coupling a qubit to an arbitrary quantum sensor, more general sub-SQL metrology is possible with the techniques presented in this work.Comment: 15 pages, 14 figures, 2 table. Dark matter exclusion analysis modified to include experimental systematics. Discussion of background calibration and detector compatibility with tunable cavity added to conclusion. Future optimizations and integration into axion search sections moved to Supplemental Material. References update

One in Four Individuals of African-American Ancestry Harbors a 5.5kb Deletion at chromosome 11q13.1

Cloning and sequencing of 5.5kb deletion at chromosome 11q13.1 from the HeLa cells, tumorigenic hybrids and two fibroblast cell lines has revealed homologous recombination between AluSx and AluY resulting in the deletion of intervening sequences. Long-range PCR of the 5.5kb sequence in 494 normal lymphocyte samples showed heterozygous deletion in 28.3% of African- American ancestry samples but only in 4.8% of Caucasian samples (p<0.0001). This observation is strengthened by the copy number variation (CNV) data of the HapMap samples which showed that this deletion occurs in 27% of YRI (Yoruba – West African) population but none in non- African populations. The HapMap analysis further identified strong linkage disequilibrium between 5 single nucleotide polymorphisms and the 5.5kb deletion in the people of African ancestry. Computational analysis of 175kb sequence surrounding the deletion site revealed enhanced flexibility, low thermodynamic stability, high repetitiveness, and stable stem-loop/ hairpin secondary structures that are hallmarks of common fragile sites

PIQA: pipeline for Illumina G1 genome analyzer data quality assessment

Summary: PIQA is a quality analysis pipeline designed to examine genomic reads produced by Next Generation Sequencing technology (Illumina G1 Genome Analyzer). A short statistical summary, as well as tile-by-tile and cycle-by-cycle graphical representation of clusters density, quality scores and nucleotide frequencies allow easy identification of various technical problems including defective tiles, mistakes in sample/library preparations and abnormalities in the frequencies of appearance of sequenced genomic reads. PIQA is written in the R statistical programming language and is compatible with bustard, fastq and scarf Illumina G1 Genome Analyzer data formats

Multimode photon blockade

Interactions are essential for the creation of correlated quantum many-body states. While two-body interactions underlie most natural phenomena, three- and four-body interactions are important for the physics of nuclei [1], exotic few-body states in ultracold quantum gases [2], the fractional quantum Hall effect [3], quantum error correction [4], and holography [5, 6]. Recently, a number of artificial quantum systems have emerged as simulators for many-body physics, featuring the ability to engineer strong interactions. However, the interactions in these systems have largely been limited to the two-body paradigm, and require building up multi-body interactions by combining two-body forces. Here, we demonstrate a pure N-body interaction between microwave photons stored in an arbitrary number of electromagnetic modes of a multimode cavity. The system is dressed such that there is collectively no interaction until a target total photon number is reached across multiple distinct modes, at which point they interact strongly. The microwave cavity features 9 modes with photon lifetimes of $\sim 2$ ms coupled to a superconducting transmon circuit, forming a multimode circuit QED system with single photon cooperativities of $\sim10^9$. We generate multimode interactions by using cavity photon number resolved drives on the transmon circuit to blockade any multiphoton state with a chosen total photon number distributed across the target modes. We harness the interaction for state preparation, preparing Fock states of increasing photon number via quantum optimal control pulses acting only on the cavity modes. We demonstrate multimode interactions by generating entanglement purely with uniform cavity drives and multimode photon blockade, and characterize the resulting two- and three-mode W states using a new protocol for multimode Wigner tomography.Comment: 5 pages of main text with 5 figures. 11 pages of supplementary information with 10 figure

Loss of epigenetic regulator TET2 and oncogenic KIT regulate myeloid cell transformation via PI3K pathway

Mutations in KIT and TET2 are associated with myeloid malignancies. We show that loss of TET2-induced PI3K activation and -increased proliferation is rescued by targeting the p110α/δ subunits of PI3K. RNA-Seq revealed a hyperactive c-Myc signature in Tet2-/- cells, which is normalized by inhibiting PI3K signaling. Loss of TET2 impairs the maturation of myeloid lineage-derived mast cells by dysregulating the expression of Mitf and Cebpa, which is restored by low-dose ascorbic acid and 5-azacytidine. Utilizing a mouse model in which the loss of TET2 precedes the expression of oncogenic Kit, similar to the human disease, results in the development of a non-mast cell lineage neoplasm (AHNMD), which is responsive to PI3K inhibition. Thus, therapeutic approaches involving hypomethylating agents, ascorbic acid, and isoform-specific PI3K inhibitors are likely to be useful for treating patients with TET2 and KIT mutations

Propofol induces MAPK/ERK cascade dependant expression of cFos and Egr-1 in rat hippocampal slices

Background: Propofol is a commonly used intravenous anesthetic agent, which produce rapid induction of and recovery from general anesthesia. Numerous clinical studies reported that propofol can potentially cause amnesia and memory loss in human subjects. The underlying mechanism for this memory loss is unclear but may potentially be related to the induction of memory-associated genes such as c-Fos and Egr-1 by propofol. This study explored the effects of propofol on c-Fos and Egr-1 expression in rat hippocampal slices. Findings: Hippocampal brain slices were exposed to varying concentrations of propofol at multiple time intervals. The transcription of the immediate early genes, c-Fos and Egr-1, was quantified using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). MAPK/ERK inhibitors were used to investigate the mechanism of action. We demonstrate that propofol induced the expression of c-Fos and Egr-1 within 30 and 60 min of exposure time. At 16.8 μM concentration, propofol induced a 110% increase in c-Fos transcription and 90% decrease in the transcription of Egr-1. However, at concentrations above 100 μM, propofol failed to induce expression of c-Fos but did completely inhibit the transcription of Egr-1. Propofol-induced c-Fos and Egr-1 transcription was abolished by inhibitors of RAS, RAF, MEK, ERK and p38-MAPK in the MAPK/ERK cascade. Conclusions: Our study shows that clinically relevant concentrations of propofol induce c-Fos and down regulated Egr-1 expression via an MAPK/ERK mediated pathway. We demonstrated that propofol induces a time and dose dependant transcription of IEGs c-Fos and Egr-1 in rat hippocampal slices. We further demonstrate for the first time that propofol induced IEG expression was mediated via a MAPK/ERK dependant pathway. These novel findings provide a new avenue to investigate transcription-dependant mechanisms and suggest a parallel pathway of action with an unclear role in the activity of general anesthetics

Polymerase-directed synthesis of C5-ethynyl locked nucleic acids

Modified nucleic acids have considerable potential in nanobiotechnology for the development of nanomedicines and new materials. Locked nucleic acid (LNA) is one of the most prominent nucleic acid analogues reported so far and we herein for the first time report the enzymatic incorporation of LNA-U and C5-ethynyl LNA-U nucleotides into oligonucleotides. Phusion High Fidelity and KOD DNA polymerases efficiently incorporated LNA-U and C5-ethynyl LNA-U nucleotides into a DNA strand and T7 RNA polymerase successfully accepted the LNA-U nucleoside 5′-triphosphate as substrate for RNA transcripts