Symmetry algebra of a generalized anisotropic harmonic oscillator

It is shown that the symmetry Lie algebra of a quantum system with accidental degeneracy can be obtained by means of the Noether's theorem. The procedure is illustrated by considering a generalized anisotropic two dimensional harmonic oscillator, which can have an infinite set of states with the same energy characterized by an u(1,1) Lie algebra

A square root of the harmonic oscillator

Allowing for the inclusion of the parity operator, it is possible to construct an oscillator model whose Hamiltonian admits an EXACT square root, which is different from the conventional approach based on creation and annihilation operators. We outline such a model, the method of solution and some generalizations.Comment: RevTex, 10 pages in preprint form, no figure

Bell's inequalities in the tomographic representation

The tomographic approach to quantum mechanics is revisited as a direct tool to investigate violation of Bell-like inequalities. Since quantum tomograms are well defined probability distributions, the tomographic approach is emphasized to be the most natural one to compare the predictions of classical and quantum theory. Examples of inequalities for two qubits an two qutrits are considered in the tomographic probability representation of spin states.Comment: 11 pages, comments and references adde

The pseudo-spin symmetry in Zr and Sn isotopes from the proton drip line to the neutron drip line

Based on the Relativistic continuum Hartree-Bogoliubov (RCHB) theory, the pseudo-spin approximation in exotic nuclei is investigated in Zr and Sn isotopes from the proton drip line to the neutron drip line. The quality of the pseudo-spin approximation is shown to be connected with the competition between the centrifugal barrier (CB) and the pseudo-spin orbital potential (PSOP). The PSOP depends on the derivative of the difference between the scalar and vector potentials $dV/dr$. If $dV/dr = 0$, the pseudo-spin symmetry is exact. The pseudo-spin symmetry is found to be a good approximation for normal nuclei and to become much better for exotic nuclei with highly diffuse potential, which have $dV/dr \sim 0$. The energy splitting of the pseudo-spin partners is smaller for orbitals near the Fermi surface (even in the continuum) than the deeply bound orbitals. The lower components of the Dirac wave functions for the pseudo-spin partners are very similar and almost equal in magnitude.Comment: 22 pages, 9figure

T. brucei Infection Reduces B Lymphopoiesis in Bone Marrow and Truncates Compensatory Splenic Lymphopoiesis through Transitional B-Cell Apoptosis

African trypanosomes of the Trypanosoma brucei species are extracellular protozoan parasites that cause the deadly disease African trypanosomiasis in humans and contribute to the animal counterpart, Nagana. Trypanosome clearance from the bloodstream is mediated by antibodies specific for their Variant Surface Glycoprotein (VSG) coat antigens. However, T. brucei infection induces polyclonal B cell activation, B cell clonal exhaustion, sustained depletion of mature splenic Marginal Zone B (MZB) and Follicular B (FoB) cells, and destruction of the B-cell memory compartment. To determine how trypanosome infection compromises the humoral immune defense system we used a C57BL/6 T. brucei AnTat 1.1 mouse model and multicolor flow cytometry to document B cell development and maturation during infection. Our results show a more than 95% reduction in B cell precursor numbers from the CLP, pre-pro-B, pro-B, pre-B and immature B cell stages in the bone marrow. In the spleen, T. brucei induces extramedullary B lymphopoiesis as evidenced by significant increases in HSC-LMPP, CLP, pre-pro-B, pro-B and pre-B cell populations. However, final B cell maturation is abrogated by infection-induced apoptosis of transitional B cells of both the T1 and T2 populations which is not uniquely dependent on TNF-, Fas-, or prostaglandin-dependent death pathways. Results obtained from ex vivo co-cultures of living bloodstream form trypanosomes and splenocytes demonstrate that trypanosome surface coat-dependent contact with T1/2 B cells triggers their deletion. We conclude that infection-induced and possibly parasite-contact dependent deletion of transitional B cells prevents replenishment of mature B cell compartments during infection thus contributing to a loss of the host's capacity to sustain antibody responses against recurring parasitemic waves

Comprehensive genomic profiles of small cell lung cancer

We have sequenced the genomes of 110 small cell lung cancers (SCLC), one of the deadliest human cancers. In nearly all the tumours analysed we found bi-allelic inactivation of TP53 and RB1, sometimes by complex genomic rearrangements. Two tumours with wild-type RB1 had evidence of chromothripsis leading to overexpression of cyclin D1 (encoded by the CCND1 gene), revealing an alternative mechanism of Rb1 deregulation. Thus, loss of the tumour suppressors TP53 and RB1 is obligatory in SCLC. We discovered somatic genomic rearrangements of TP73 that create an oncogenic version of this gene, TP73Dex2/3. In rare cases, SCLC tumours exhibited kinase gene mutations, providing a possible therapeutic opportunity for individual patients. Finally, we observed inactivating mutations in NOTCH family genes in 25% of human SCLC. Accordingly, activation of Notch signalling in a pre-clinical SCLC mouse model strikingly reduced the number of tumours and extended the survival of the mutant mice. Furthermore, neuroendocrine gene expression was abrogated by Notch activity in SCLC cells. This first comprehensive study of somatic genome alterations in SCLC uncovers several key biological processes and identifies candidate therapeutic targets in this highly lethal form of cancer