Free-particle and harmonic-oscillator propagators in two and three dimensions

This contribution illustrates how to construct free-particle and harmonic-oscillator quantum-mechanical propagators in two and three dimensions in cartesian, and in circular and spherical coordinates, respectively, starting from the corresponding one-dimensional propagators in cartesian coordinates

Connection Between Type A and E Factorizations and Construction of Satellite Algebras

Recently, we introduced a new class of symmetry algebras, called satellite algebras, which connect with one another wavefunctions belonging to different potentials of a given family, and corresponding to different energy eigenvalues. Here the role of the factorization method in the construction of such algebras is investigated. A general procedure for determining an so(2,2) or so(2,1) satellite algebra for all the Hamiltonians that admit a type E factorization is proposed. Such a procedure is based on the known relationship between type A and E factorizations, combined with an algebraization similar to that used in the construction of potential algebras. It is illustrated with the examples of the generalized Morse potential, the Rosen-Morse potential, the Kepler problem in a space of constant negative curvature, and, in each case, the conserved quantity is identified. It should be stressed that the method proposed is fairly general since the other factorization types may be considered as limiting cases of type A or E factorizations.Comment: 20 pages, LaTeX, no figure, to be published in J. Phys.

Generalized Morse Potential: Symmetry and Satellite Potentials

We study in detail the bound state spectrum of the generalized Morse potential~(GMP), which was proposed by Deng and Fan as a potential function for diatomic molecules. By connecting the corresponding Schr\"odinger equation with the Laplace equation on the hyperboloid and the Schr\"odinger equation for the P\"oschl-Teller potential, we explain the exact solvability of the problem by an $so(2,2)$ symmetry algebra, and obtain an explicit realization of the latter as $su(1,1) \oplus su(1,1)$. We prove that some of the $so(2,2)$ generators connect among themselves wave functions belonging to different GMP's (called satellite potentials). The conserved quantity is some combination of the potential parameters instead of the level energy, as for potential algebras. Hence, $so(2,2)$ belongs to a new class of symmetry algebras. We also stress the usefulness of our algebraic results for simplifying the calculation of Frank-Condon factors for electromagnetic transitions between rovibrational levels based on different electronic states.Comment: 23 pages, LaTeX, 2 figures (on request). one LaTeX problem settle

The extraordinary evolutionary history of the reticuloendotheliosis viruses

The reticuloendotheliosis viruses (REVs) comprise several closely related amphotropic retroviruses isolated from birds. These viruses exhibit several highly unusual characteristics that have not so far been adequately explained, including their extremely close relationship to mammalian retroviruses, and their presence as endogenous sequences within the genomes of certain large DNA viruses. We present evidence for an iatrogenic origin of REVs that accounts for these phenomena. Firstly, we identify endogenous retroviral fossils in mammalian genomes that share a unique recombinant structure with REVs—unequivocally demonstrating that REVs derive directly from mammalian retroviruses. Secondly, through sequencing of archived REV isolates, we confirm that contaminated Plasmodium lophurae stocks have been the source of multiple REV outbreaks in experimentally infected birds. Finally, we show that both phylogenetic and historical evidence support a scenario wherein REVs originated as mammalian retroviruses that were accidentally introduced into avian hosts in the late 1930s, during experimental studies of P. lophurae, and subsequently integrated into the fowlpox virus (FWPV) and gallid herpesvirus type 2 (GHV-2) genomes, generating recombinant DNA viruses that now circulate in wild birds and poultry. Our findings provide a novel perspective on the origin and evolution of REV, and indicate that horizontal gene transfer between virus families can expand the impact of iatrogenic transmission events

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

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