Pseudo-Riemannian geodesic foliations by circles

We investigate under which assumptions an orientable pseudo-Riemannian geodesic foliations by circles is generated by an $S^1$-action. We construct examples showing that, contrary to the Riemannian case, it is not always true. However, we prove that such an action always exists when the foliation does not contain lightlike leaves, i.e. a pseudo-Riemannian Wadsley's Theorem. As an application, we show that every Lorentzian surface all of whose spacelike/timelike geodesics are closed, is finitely covered by $S^1\times \R$. It follows that every Lorentzian surface contains a non-closed geodesic.Comment: 14 page

Stability of the lattice formed in first-order phase transitions to matter containing strangeness in protoneutron stars

Well into the deleptonization phase of a core collapse supernova, a first-order phase transition to matter with macroscopic strangeness content is assumed to occur and lead to a structured lattice defined by negatively charged strange droplets. The lattice is shown to crystallize for expected droplet charges and separations at temperatures typically obtained during the protoneutronstar evolution. The melting curve of the lattice for small spherical droplets is presented. The one-component plasma model proves to be an adequate description for the lattice in its solid phase with deformation modes freezing out around the melting temperature. The mechanical stability against shear stresses is such that velocities predicted for convective phenomena and differential rotation during the Kelvin-Helmholtz cooling phase might prevent the crystallization of the phase transition lattice. A solid lattice might be fractured by transient convection, which could result in anisotropic neutrino transport. The melting curve of the lattice is relevant for the mechanical evolution of the protoneutronstar and therefore should be included in future hydrodynamics simulations.Comment: accepted for publication in Physical Review

Epstein-Barr virus: clinical and epidemiological revisits and genetic basis of oncogenesis

Epstein-Barr virus (EBV) is classified as a member in the order herpesvirales, family herpesviridae, subfamily gammaherpesvirinae and the genus lymphocytovirus. The virus is an exclusively human pathogen and thus also termed as human herpesvirus 4 (HHV4). It was the first oncogenic virus recognized and has been incriminated in the causation of tumors of both lymphatic and epithelial nature. It was reported in some previous studies that 95% of the population worldwide are serologically positive to the virus. Clinically, EBV primary infection is almost silent, persisting as a life-long asymptomatic latent infection in B cells although it may be responsible for a transient clinical syndrome called infectious mononucleosis. Following reactivation of the virus from latency due to immunocompromised status, EBV was found to be associated with several tumors. EBV linked to oncogenesis as detected in lymphoid tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), post-transplant lymphoproliferative disorders (PTLD) and T-cell lymphomas (e.g. Peripheral T-cell lymphomas; PTCL and Anaplastic large cell lymphomas; ALCL). It is also linked to epithelial tumors such as nasopharyngeal carcinoma (NPC), gastric carcinomas and oral hairy leukoplakia (OHL). In vitro, EBV many studies have demonstrated its ability to transform B cells into lymphoblastoid cell lines (LCLs). Despite these malignancies showing different clinical and epidemiological patterns when studied, genetic studies have suggested that these EBV- associated transformations were characterized generally by low level of virus gene expression with only the latent virus proteins (LVPs) upregulated in both tumors and LCLs. In this review, we summarize some clinical and epidemiological features of EBV- associated tumors. We also discuss how EBV latent genes may lead to oncogenesis in the different clinical malignancie

Detectable clonal mosaicism and its relationship to aging and cancer

In an analysis of 31,717 cancer cases and 26,136 cancer-free controls from 13 genome-wide association studies, we observed large chromosomal abnormalities in a subset of clones in DNA obtained from blood or buccal samples. We observed mosaic abnormalities, either aneuploidy or copy-neutral loss of heterozygosity, of >2 Mb in size in autosomes of 517 individuals (0.89%), with abnormal cell proportions of between 7% and 95%. In cancer-free individuals, frequency increased with age, from 0.23% under 50 years to 1.91% between 75 and 79 years (P = 4.8 × 10(-8)). Mosaic abnormalities were more frequent in individuals with solid tumors (0.97% versus 0.74% in cancer-free individuals; odds ratio (OR) = 1.25; P = 0.016), with stronger association with cases who had DNA collected before diagnosis or treatment (OR = 1.45; P = 0.0005). Detectable mosaicism was also more common in individuals for whom DNA was collected at least 1 year before diagnosis with leukemia compared to cancer-free individuals (OR = 35.4; P = 3.8 × 10(-11)). These findings underscore the time-dependent nature of somatic events in the etiology of cancer and potentially other late-onset diseases