Linear dynamics of a stably-neutrally stratified ocean

Linear dynamics of stably-neutrally stratified fluid consisting of the stably stratified upper layer and the homogeneous lower layer is studied with and without rotation. The density and other fields are continuous at the interface between the layers. A special feature of this configuration is existence of the wave mode related to the homogeneous layer. In non-rotating fluid this is the homogeneous layer vortex mode characterized by a stationary three-dimensional velocity field confined to the lower layer. In the presence of rotation, the mode turns into the gyroscopic waves. Besides the mode, the wave spectrum contains internal waves and the zero frequency horizontal vortex mode with zero vertical velocity. In non-rotating fluid, the vertical velocity consists of the dispersive internal waves and of a steady component in the homogeneous layer. With increasing time the internal waves decay at a fixed point because of dispersion, and the vertical velocity decays in the upper layer and becomes stationary in the lower layer. A non-stationary boundary layer develops near the interface in the stratified layer at large times. In rotating fluid we examined the wave spectrum not using the traditional and hydrostatic approximations, and found the spectrum consists of the super-inertial internal waves, the sub-inertial gyroscopic waves and the sub- and super-inertial internal inertio-gravity waves. In the case of strong stratification f/N \u3c\u3c 1(f is the inertial frequency and N is the stratified layer buoyancy frequency) and for the long wave scales f2/N2 \u3c\u3c H/L \u3c\u3c 1(H and L are the fluid depth and the horizontal scale), the internal and the super-inertial inertio-gravity waves freely penetrate into the lower layer, and the gyroscopic waves are localized in the lower layer and are close to the inertial oscillations. Any long-wave field of the vertical velocity is split into the internal waves, and the inertial oscillations (long gyroscopic waves) confined to the lower layer. With time, the internal waves decay because of dispersion, and the vertical velocity goes to zero in the upper layer and in the lower layer only the inertial oscillations remain

Footprints of quantum pigeons

We show that in the mathematical framework of the quantum theory the classical pigeonhole principle can be violated more directly than previously suggested, i.e., in a setting closer to the traditional statement of the principle. We describe how the counterfactual reasoning of the paradox may be operationally grounded in the analysis of the tiny footprints left in the environment by the pigeons. After identifying the drawbacks of recent experiments of the quantum pigeonhole effect, we argue that a definitive experimental violation of the pigeonhole principle is still needed and propose such an implementation using modern quantum computing hardware: a superconducting circuit with transmon qubits

Failed attempt to escape from the quantum pigeon conundrum

A recent criticism by Kunstatter et al. [Phys. Lett. A 384, 126686 (2020)] of a quantum setup violating the pigeon counting principle [Aharonov et al. PNAS 113, 532 (2016)] is refuted. The quantum nature of the violation of the pigeonhole principle with pre- and postselection is clarified.Comment: to be published in Physics Letters

Photons are lying about where they have been, again

Bhati and Arvind [Phys. Lett. A, 127955 (2022)] recently argued that in a specially designed experiment the timing of photon detection events demonstrate photon presence in a location in which they are not present according to the weak values approach. The alleged contradiction is resolved by a subtle interference effect resulting in anomalous sensitivity for the interaction in this location, similarly to the case of a nested Mach-Zehnder interferometer with a Dove prism [Quant. Stud.: Mat. Found. 2, 255 (2015)]. The theoretical results are tested by a computer simulation of the proposed experiment

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

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

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Spatial Organization and Molecular Correlation of Tumor-Infiltrating Lymphocytes Using Deep Learning on Pathology Images

Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images of TCGA samples remain underutilized. To highlight this resource, we present mappings of tumorinfiltrating lymphocytes (TILs) based on H&E images from 13 TCGA tumor types. These TIL maps are derived through computational staining using a convolutional neural network trained to classify patches of images. Affinity propagation revealed local spatial structure in TIL patterns and correlation with overall survival. TIL map structural patterns were grouped using standard histopathological parameters. These patterns are enriched in particular T cell subpopulations derived from molecular measures. TIL densities and spatial structure were differentially enriched among tumor types, immune subtypes, and tumor molecular subtypes, implying that spatial infiltrate state could reflect particular tumor cell aberration states. Obtaining spatial lymphocytic patterns linked to the rich genomic characterization of TCGA samples demonstrates one use for the TCGA image archives with insights into the tumor-immune microenvironment

Integrated Genomic Analysis of the Ubiquitin Pathway across Cancer Types

Protein ubiquitination is a dynamic and reversibleprocess of adding single ubiquitin molecules orvarious ubiquitin chains to target proteins. Here,using multidimensional omic data of 9,125 tumorsamples across 33 cancer types from The CancerGenome Atlas, we perform comprehensive molecu-lar characterization of 929 ubiquitin-related genesand 95 deubiquitinase genes. Among them, we sys-tematically identify top somatic driver candidates,including mutatedFBXW7with cancer-type-specificpatterns and amplifiedMDM2showing a mutuallyexclusive pattern withBRAFmutations. Ubiquitinpathway genes tend to be upregulated in cancermediated by diverse mechanisms. By integratingpan-cancer multiomic data, we identify a group oftumor samples that exhibit worse prognosis. Thesesamples are consistently associated with the upre-gulation of cell-cycle and DNA repair pathways, char-acterized by mutatedTP53,MYC/TERTamplifica-tion, andAPC/PTENdeletion. Our analysishighlights the importance of the ubiquitin pathwayin cancer development and lays a foundation fordeveloping relevant therapeutic strategies