SON-POWERED DYNAMIC OPTIMIZATION OF RELAY LAYER TO ENHANCE COVERAGE AND CAPACITY OF A CELLULAR NETWORK COMBINED WITH CENTRALIZED SON ON MACRO LAYER

The usage patterns of cellular networks can change dramatically over short periods of time, such as when a large number of people crowd a very small space within a cell\u27s coverage area for only a short period of time. In order to save on costly and inefficient current solutions, the techniques presented herein suggest a Self-Organizing Network (SON)-optimized system of relays as a layer on top of an existing system. Such relays can be deployed ad hoc, such as in the cars of people arriving at a troubled location, to alleviate temporary coverage and load issues. SON will control the activation and deactivation of these ad hoc relays and the joint optimization of both the macro and relay layers

Precursors prior to Type IIn supernova explosions are common: precursor rates, properties, and correlations

There is a growing number of supernovae (SNe), mainly of Type IIn, which present an outburst prior to their presumably final explosion. These precursors may affect the SN display, and are likely related to some poorly charted phenomena in the final stages of stellar evolution. Here we present a sample of 16 SNe IIn for which we have Palomar Transient Factory (PTF) observations obtained prior to the SN explosion. By coadding these images taken prior to the explosion in time bins, we search for precursor events. We find five Type IIn SNe that likely have at least one possible precursor event, three of which are reported here for the first time. For each SN we calculate the control time. Based on this analysis we find that precursor events among SNe IIn are common: at the one-sided 99% confidence level, more than 50% of SNe IIn have at least one pre-explosion outburst that is brighter than absolute magnitude -14, taking place up to 1/3 yr prior to the SN explosion. The average rate of such precursor events during the year prior to the SN explosion is likely larger than one per year, and fainter precursors are possibly even more common. We also find possible correlations between the integrated luminosity of the precursor, and the SN total radiated energy, peak luminosity, and rise time. These correlations are expected if the precursors are mass-ejection events, and the early-time light curve of these SNe is powered by interaction of the SN shock and ejecta with optically thick circumstellar material.Comment: 15 pages, 20 figures, submitted to Ap

Interaction-powered supernovae: Rise-time vs. peak-luminosity correlation and the shock-breakout velocity

Interaction of supernova (SN) ejecta with the optically thick circumstellar medium (CSM) of a progenitor star can result in a bright, long-lived shock breakout event. Candidates for such SNe include Type IIn and superluminous SNe. If some of these SNe are powered by interaction, then there should be a relation between their peak luminosity, bolometric light-curve rise time, and shock-breakout velocity. Given that the shock velocity during shock breakout is not measured, we expect a correlation, with a significant spread, between the rise time and the peak luminosity of these SNe. Here, we present a sample of 15 SNe IIn for which we have good constraints on their rise time and peak luminosity from observations obtained using the Palomar Transient Factory. We report on a possible correlation between the R-band rise time and peak luminosity of these SNe, with a false-alarm probability of 3%. Assuming that these SNe are powered by interaction, combining these observables and theory allows us to deduce lower limits on the shock-breakout velocity. The lower limits on the shock velocity we find are consistent with what is expected for SNe (i.e., ~10^4 km/s). This supports the suggestion that the early-time light curves of SNe IIn are caused by shock breakout in a dense CSM. We note that such a correlation can arise from other physical mechanisms. Performing such a test on other classes of SNe (e.g., superluminous SNe) can be used to rule out the interaction model for a class of events.Comment: Accepted to ApJ, 6 page

Age-related biological differences in children's and adolescents' very rare tumors

Very rare tumors (VRTs) in pediatric age represent many different diseases. They present an annual incidence < 2/1000,000 and correspond to about 11% of all cancers in patients aged 0–14 years. They can be roughly divided into two groups: one including tumors that are also rare in adults, and the other group includes adult-type tumors rarely encountered in children and adolescents. Although there is an obvious gap in knowledge regarding oncogenesis in pediatric cancers, there is some evidence of the involvement of various signalling pathways in the development of tumors in children and adolescents and sometimes in young adults. In addition, despite the rarity of these neoplasms, several attempts have been made to disclose the underlying mechanisms. More effort and resources have urgently to be devoted to deepening current knowledge and integrating new findings into the therapeutic approach, which nowadays relies on the treatment modalities used in adult oncology. The aim of this paper is to provide a review of the main solid VRTs occurring in both the pediatric and the adult age groups, highlighting the variability between groups in their biological and clinical course

The role of cancer predisposition syndrome in children and adolescents with very rare tumours

Germline predisposing pathogenic variants (GPVs) are present in approximately 8 to 10% of children with all cancer types. Very rare tumours (VRTs) represent many different diseases, defined with an annual incidence < 2 / 1,000,000, and correspond to 11% of all cancers in patients aged 0-14 years. Some of these VRTs, including cancer typical for adults, develop in children with a cancer predisposition syndrome (CPS). Classically, three situations lead to consider this association: Some patients develop a VRT for which histology itself strongly suggests a GPV related to a CPS; others are referred for germline genetic testing because of a family or personal history and finally, a systematic molecular genomic tumour analysis, reveals a PV typical to a CPS. Depending on the samples tested and type of analysis performed, information can be directly available about the germline status of such a PV. Depicting the association between CPS and VRT is clinically important as some of these tumour types require adapted therapy, sometimes in the frontline setting, and the proposal of a specific surveillance programme to detect other malignancies. The diagnosis of CPS necessitates a careful familial evaluation and genetic counselling regarding the risks faced by the child or other family members. The aim of this paper is to propose a literature review of solid VRTs occurring in paediatric and young adult patients associated with CPSs

A Wolf-Rayet-Like Progenitor of SN 2013cu from Spectral Observations of a Stellar Wind

The explosive fate of massive Wolf-Rayet stars (WRSs) is a key open question in stellar physics. An appealing option is that hydrogen- deficient WRSs are the progenitors of some hydrogen-poor supernova explosions of types IIb, Ib and Ic. A blue object, having luminosity and colours consistent with those of some WRSs, has recently been identified in pre-explosion images at the location of a supernova of type Ib, but has not yet been conclusively determined to have been the progenitor. Similar work has so far only resulted in non-detections. Comparison of early photometric observations of type Ic supernovae with theoretical models suggests that the progenitor stars had radii of less than 10(exp 12) centimetres, as expected for some WRSs. The signature of WRSs, their emission line spectra, cannot be probed by such studies. Here we report the detection of strong emission lines in a spectrum of type IIb supernova 2013cu (iPTF13ast) obtained approximately 15.5 hours after explosion (by 'flash spectroscopy', which captures the effects of the supernova explosion shock breakout flash on material surrounding the progenitor star).We identify Wolf-Rayet-like wind signatures, suggesting a progenitor of the WN(h) subclass (those WRSs with winds dominated by helium and nitrogen, with traces of hydrogen). The extent of this dense wind may indicate increased mass loss from the progenitor shortly before its explosion, consistent with recent theoretical predictions

Interaction-powered Supernovae: Rise-time versus Peak-luminosity Correlation and the Shock-breakout Velocity

Interaction of supernova (SN) ejecta with the optically thick circumstellar medium (CSM) of a progenitor star can result in a bright, long-lived shock-breakout event. Candidates for such SNe include Type IIn and superluminous SNe. If some of these SNe are powered by interaction, then there should be a specific relation between their peak luminosity, bolometric light-curve rise time, and shock-breakout velocity. Given that the shock velocity during shock breakout is not measured, we expect a correlation, with a significant spread, between the rise time and the peak luminosity of these SNe. Here, we present a sample of 15 SNe IIn for which we have good constraints on their rise time and peak luminosity from observations obtained using the Palomar Transient Factory. We report on a possible correlation between the R-band rise time and peak luminosity of these SNe, with a false-alarm probability of 3%. Assuming that these SNe are powered by interaction, combining these observables and theory allows us to deduce lower limits on the shock-breakout velocity. The lower limits on the shock velocity we find are consistent with what is expected for SNe (i.e., ~10^(4) km s^(–1)). This supports the suggestion that the early-time light curves of SNe IIn are caused by shock breakout in a dense CSM. We note that such a correlation can arise from other physical mechanisms. Performing such a test on other classes of SNe (e.g., superluminous SNe) can be used to rule out the interaction model for a class of events

The hydrogen-poor superluminous supernova iPTF 13ajg and its host galaxy in absorption and emission

We present imaging and spectroscopy of a hydrogen-poor superluminous supernova (SLSN) discovered by the intermediate Palomar Transient Factory, iPTF 13ajg. At a redshift of z = 0.7403, derived from narrow absorption lines, iPTF 13ajg peaked at an absolute magnitude of M u, AB = -22.5, one of the most luminous supernovae to date. The observed bolometric peak luminosity of iPTF 13ajg is 3.2 × 1044 erg s-1, while the estimated total radiated energy is 1.3 × 1051 erg. We detect narrow absorption lines of Mg I, Mg II, and Fe II, associated with the cold interstellar medium in the host galaxy, at two different epochs with X-shooter at the Very Large Telescope. From Voigt profile fitting, we derive the column densities log N(Mg I) =11.94 ± 0.06, log N(Mg II) =14.7 ± 0.3, and log N(Fe II) =14.25 ± 0.10. These column densities, as well as the Mg I and Mg II equivalent widths of a sample of hydrogen-poor SLSNe taken from the literature, are at the low end of those derived for gamma-ray bursts (GRBs) whose progenitors are also thought to be massive stars. This suggests that the environments of hydrogen-poor SLSNe and GRBs are different. From the nondetection of Fe II fine-structure absorption lines, we derive a lower limit on the distance between the supernova and the narrow-line absorbing gas of 50 pc. The neutral gas responsible for the absorption in iPTF 13ajg exhibits a single narrow component with a low velocity width, ΔV = 76 km s-1, indicating a low-mass host galaxy. No host galaxy emission lines are detected, leading to an upper limit on the unobscured star formation rate (SFR) of SFR. Late-time imaging shows the iPTF 13ajg host galaxy to be faint, with g AB 27.0 and R AB ≥ 26.0 mag, corresponding to M B, Vega ≳ -17.7 mag. © 2014. The American Astronomical Society. All rights reserved.

Structural and non-coding variants increase the diagnostic yield of clinical whole genome sequencing for rare diseases

BACKGROUND: Whole genome sequencing is increasingly being used for the diagnosis of patients with rare diseases. However, the diagnostic yields of many studies, particularly those conducted in a healthcare setting, are often disappointingly low, at 25-30%. This is in part because although entire genomes are sequenced, analysis is often confined to in silico gene panels or coding regions of the genome.METHODS: We undertook WGS on a cohort of 122 unrelated rare disease patients and their relatives (300 genomes) who had been pre-screened by gene panels or arrays. Patients were recruited from a broad spectrum of clinical specialties. We applied a bioinformatics pipeline that would allow comprehensive analysis of all variant types. We combined established bioinformatics tools for phenotypic and genomic analysis with our novel algorithms (SVRare, ALTSPLICE and GREEN-DB) to detect and annotate structural, splice site and non-coding variants.RESULTS: Our diagnostic yield was 43/122 cases (35%), although 47/122 cases (39%) were considered solved when considering novel candidate genes with supporting functional data into account. Structural, splice site and deep intronic variants contributed to 20/47 (43%) of our solved cases. Five genes that are novel, or were novel at the time of discovery, were identified, whilst a further three genes are putative novel disease genes with evidence of causality. We identified variants of uncertain significance in a further fourteen candidate genes. The phenotypic spectrum associated with RMND1 was expanded to include polymicrogyria. Two patients with secondary findings in FBN1 and KCNQ1 were confirmed to have previously unidentified Marfan and long QT syndromes, respectively, and were referred for further clinical interventions. Clinical diagnoses were changed in six patients and treatment adjustments made for eight individuals, which for five patients was considered life-saving.CONCLUSIONS: Genome sequencing is increasingly being considered as a first-line genetic test in routine clinical settings and can make a substantial contribution to rapidly identifying a causal aetiology for many patients, shortening their diagnostic odyssey. We have demonstrated that structural, splice site and intronic variants make a significant contribution to diagnostic yield and that comprehensive analysis of the entire genome is essential to maximise the value of clinical genome sequencing.</p