Performance Modelling and Analysis of Mobile Wireless Networks

Non

Looking the void in the eyes - the kSZ effect in LTB models

As an alternative explanation of the dimming of distant supernovae it has recently been advocated that we live in a special place in the Universe near the centre of a large void described by a Lemaitre-Tolman-Bondi (LTB) metric. The Universe is no longer homogeneous and isotropic and the apparent late time acceleration is actually a consequence of spatial gradients in the metric. If we did not live close to the centre of the void, we would have observed a Cosmic Microwave Background (CMB) dipole much larger than that allowed by observations. Hence, until now it has been argued, for the model to be consistent with observations, that by coincidence we happen to live very close to the centre of the void or we are moving towards it. However, even if we are at the centre of the void, we can observe distant galaxy clusters, which are off-centre. In their frame of reference there should be a large CMB dipole, which manifests itself observationally for us as a kinematic Sunyaev-Zeldovich (kSZ) effect. kSZ observations give far stronger constraints on the LTB model compared to other observational probes such as Type Ia Supernovae, the CMB, and baryon acoustic oscillations. We show that current observations of only 9 clusters with large error bars already rule out LTB models with void sizes greater than approximately 1.5 Gpc and a significant underdensity, and that near future kSZ surveys like the Atacama Cosmology Telescope, South Pole Telescope, APEX telescope, or the Planck satellite will be able to strongly rule out or confirm LTB models with giga parsec sized voids. On the other hand, if the LTB model is confirmed by observations, a kSZ survey gives a unique possibility of directly reconstructing the expansion rate and underdensity profile of the void.Comment: 20 pages, 9 figures, submitted to JCA

Mutations in SPG11, encoding spatacsin, are a major cause of spastic paraplegia with thin corpus callosum.

Autosomal recessive hereditary spastic paraplegia (ARHSP) with thin corpus callosum (TCC) is a common and clinically distinct form of familial spastic paraplegia that is linked to the SPG11 locus on chromosome 15 in most affected families. We analyzed 12 ARHSP-TCC families, refined the SPG11 candidate interval and identified ten mutations in a previously unidentified gene expressed ubiquitously in the nervous system but most prominently in the cerebellum, cerebral cortex, hippocampus and pineal gland. The mutations were either nonsense or insertions and deletions leading to a frameshift, suggesting a loss-of-function mechanism. The identification of the function of the gene will provide insight into the mechanisms leading to the degeneration of the corticospinal tract and other brain structures in this frequent form of ARHSP

Brain-predicted age difference mediates the association between PROMIS sleep impairment, and self-reported pain measure in persons with knee pain

Knee pain, the most common cause of musculoskeletal pain (MSK), constitutes a severe public health burden. Its neurobiological causes, however, remain poorly understood. Among many possible causes, it has been proposed that sleep problems could lead to an increase in chronic pain symptomatology, which may be driven by central nervous system changes. In fact, we previously found that brain cortical thickness mediated the relationship between sleep qualities and pain severity in older adults with MSK. We also demonstrated a significant difference in a machine-learning-derived brain-aging biomarker between participants with low-and high-impact knee pain. Considering this, we examined whether brain aging was associated with self-reported sleep and pain measures, and whether brain aging mediated the relationship between sleep problems and knee pain. Exploratory Spearman and Pearson partial correlations, controlling for age, sex, race and study site, showed a significant association of brain aging with sleep related impairment and self-reported pain measures. Moreover, mediation analysis showed that brain aging significantly mediated the effect of sleep related impairment on clinical pain and physical symptoms. Our findings extend our prior work demonstrating advanced brain aging among individuals with chronic pain and the mediating role of brain-aging on the association between sleep and pain severity. Future longitudinal studies are needed to further understand whether the brain can be a therapeutic target to reverse the possible effect of sleep problems on chronic pain

Amplification of IGH/MYC fusion in clinically aggressive IGH/BCL2-positive germinal center B-cell lymphomas

Activation of an oncogene via its juxtaposition to the IGH locus by a chromosomal translocation or, less frequently, by genomic amplification is considered a major mechanism of B-cell lymphomagenesis. However, amplification of an IGH/oncogene fusion, coined a complicon, is a rare event in human cancers and has been associated with poor outcome and resistance to treatment. In this article are descriptions of two cases of germinal-center-derived B-cell lymphomas with IGH/BCL2 fusion that additionally displayed amplification of an IGH/MYC fusion. As shown by fluorescence in situ hybridization, the first case contained a IGH/MYC complicon in double minutes, whereas the second case showed a BCL2/IGH/MYC complicon on a der(8)t(8;14)t(14;18). Additional molecular cytogenetic and mutation analyses revealed that the first case also contained a chromosomal translocation affecting the BCL6 oncogene and a biallelic inactivation of TP53. The second case harbored a duplication of REL and acquired a translocation affecting IGL and a biallelic inactivation of TP53 during progression. Complicons affecting Igh/Myc have been reported previously in lymphomas of mouse models simultaneously deficient in Tp53 and in genes of the nonhomologous end-joining DNA repair pathway. To the best of our knowledge, this is the first time that IGH/MYC complicons have been reported in human lymphomas. Our findings imply that the two mechanisms resulting in MYC deregulation, that is, translocation and amplification, can occur simultaneously

Matrix representation and simulation algorithm of spiking neural P systems with structural plasticity

Abstract(#br)In this paper, we create a matrix representation for spiking neural P systems with structural plasticity (SNPSP, for short), taking inspiration from existing algorithms and representations for related variants. Using our matrix representation, we provide a simulation algorithm for SNPSP systems. We prove that the algorithm correctly simulates an SNPSP system: our representation and algorithm are able to capture the syntax and semantics of SNPSP systems, e.g. plasticity rules, dynamism in the synapse set. Analyses of the time and space complexity of our algorithm show that its implementation can benefit using parallel computers. Our representation and simulation algorithm can be useful when implementing SNPSP systems and related variants with a dynamic topology, in software or..