Self-organising comprehensive handover strategy for multi-tier LTE-advanced heterogeneous networks

Long term evolution (LTE)-advanced was introduced as real fourth generation (4G) with its new features and additional functions, satisfying the growing demands of quality and network coverage for the network operators' subscribers. The term muti-tier has also been recently used with respect to the heterogeneity of the network by applying the various subnetwork cooperative systems and functionalities with self-organising capabilities. Using indoor short-range low-power cellular base stations, for example, femtocells, in cooperation with existing long-range macrocells are considered as the key technical challenge of this multi-tier configuration. Furthermore, shortage of network spectrum is a major concern for network operators which forces them to spend additional attentions to overcome the degradation in performance and quality of services in 4G HetNets. This study investigates handover between the different layers of a heterogeneous LTE-advanced system, as a critical attribute to plan the best way of interactive coordination within the network for the proposed HetNet. The proposed comprehensive handover algorithm takes multiple factors in both handover sensing and decision stages, based on signal power reception, resource availability and handover optimisation, as well as prioritisation among macro and femto stations, to obtain maximum signal quality while avoiding unnecessary handovers

Lineage-Independent Tumors in Bilateral Neuroblastoma

Childhood tumors that occur synchronously in different anatomical sites usually represent metastatic disease. However, such tumors can be independent neoplasms. We investigated whether cases of bilateral neuroblastoma represented independent tumors in two children with pathogenic germline mutations by genotyping somatic mutations shared between tumors and blood. Our results suggested that in both children, the lineages that had given rise to the tumors had segregated within the first cell divisions of the zygote, without being preceded by a common premalignant clone. In one patient, the tumors had parallel evolution, including distinct second hits in SMARCA4, a putative predisposition gene for neuroblastoma. These findings portray cases of bilateral neuroblastoma as having independent lesions mediated by a germline predispositio

Dysfunction of phospholipase Cγ in immune disorders and cancer

The surge in genetic and genomic investigations over the past 5 years has resulted in many discoveries of causative variants relevant to disease pathophysiology. Although phospholipase C (PLC) enzymes have long been recognized as important components in intracellular signal transmission, it is only recently that this approach highlighted their role in disease development through gain-of-function mutations. In this review we describe the new findings that link the PLCγ family to immune disorders and cancer, and illustrate further efforts to elucidate the molecular mechanisms that underpin their dysfunction

Chromosome segregation errors generate a diverse spectrum of simple and complex genomic rearrangements

Cancer genomes are frequently characterized by numerical and structural chromosomal abnormalities. Here we integrated a centromere-specific inactivation approach with selection for a conditionally essential gene, a strategy termed CEN-SELECT, to systematically interrogate the structural landscape of mis-segregated chromosomes. We show that single-chromosome mis-segregation into a micronucleus can directly trigger a broad spectrum of genomic rearrangement types. Cytogenetic profiling revealed that mis-segregated chromosomes exhibit 120-fold-higher susceptibility to developing seven major categories of structural aberrations, including translocations, insertions, deletions, and complex reassembly through chromothripsis coupled to classical non-homologous end joining. Whole-genome sequencing of clonally propagated rearrangements identified random patterns of clustered breakpoints with copy-number alterations resulting in interspersed gene deletions and extrachromosomal DNA amplification events. We conclude that individual chromosome segregation errors during mitotic cell division are sufficient to drive extensive structural variations that recapitulate genomic features commonly associated with human disease

Recurrent histone mutations in T-cell acute lymphoblastic leukaemia.

Mutations affecting key modifiable histone type 3 (H3; Supplementary Table 1) residues are frequent oncogenic events in certain solid tumours (Feinberg, et al 2016), and have also recently been implicated in a subset of acute myeloid leukaemia (AML)(Lehnertz, et al 2017). Here, we systematically reviewed the somatic mutations in >20,000 cancer specimens to identify tumours harbouring H3 mutations. In a subset of T-cell acute lymphoblastic leukaemia (T-ALL) we identified non-methionine mutations of the key modifiable H3 residues, lysine (K) 27 and 36

EEG-based functional connectivity analysis of brain abnormalities: A systematic review study

Several imaging modalities and many signal recording techniques have been used to study the brain activities. Significant advancements in medical device technologies like electroencephalographs have provided conditions for recording neural information with high temporal resolution. These recordings can be used to calculate the connections between different brain areas. It has been proved that brain abnormalities affect the brain activity in different brain regions and the connectivity patterns between them are changed as a result. This paper studies the electroencephalogram (EEG) functional connectivity methods and investigates the impacts of brain abnormalities on brain functional connectivities. The effects of different brain abnormalities including stroke, depression, emotional disorders, epilepsy, attention deficit hyperactivity disorder (ADHD), autism, and Alzheimer's disease on functional connectivity of the EEG recordings have been explored in this study. The EEG-based metrics and network properties of different brain abnormalities have been discussed to present a comparison of the connectivities affected by each abnormality. Also, the effects of therapy and medical intake on the EEG functional connectivity network of each abnormality have been reviewed.This research received no external funding

Wilms tumour

Wilms tumour (WT) is a childhood embryonal tumour that is paradigmatic of the intersection between disrupted organogenesis and tumorigenesis. Many WT genes play a critical (non-redundant) role in early nephrogenesis. Improving patient outcomes requires advances in understanding and targeting of the multiple genes and cellular control pathways now identified as active in WT development. Decades of clinical and basic research have helped to gradually optimize clinical care. Curative therapy is achievable in 90% of affected children, even those with disseminated disease, yet survival disparities within and between countries exist and deserve commitment to change. Updated epidemiological studies have also provided novel insights into global incidence variations. Introduction of biology-driven approaches to risk stratification and new drug development has been slower in WT than in other childhood tumours. Current prognostic classification for children with WT is grounded in clinical and pathological findings and in dedicated protocols on molecular alterations. Treatment includes conventional cytotoxic chemotherapy and surgery, and radiation therapy in some cases. Advanced imaging to capture tumour composition, optimizing irradiation techniques to reduce target volumes, and evaluation of newer surgical procedures are key areas for future research

A rare case of paediatric astroblastoma with concomitant MN1-GTSE1 and EWSR1-PATZ1 gene fusions altering management

In a case of astroblastoma, methylation analysis was uninformative, with no clustering with known CNS-HGNET-MN1 cases. Whole genome sequencing however identified a novel MN1-GTSE1 gene fusion (image), confirming the diagnosis of astroblastoma, as well as an EWSR1-PATZ1 gene fusion. Whole genome sequencing, alongside methylation profiling and conventional neuropathology, will continue to lead to improved diagnostics and prognostication for children with brain tumours