The track finding algorithm of the Belle II vertex detectors

The Belle II experiment is a high energy multi purpose particle detector operated at the asymmetric e+e-- collier SuperKEKB in Tsukuba (Japan). In this work we describe the algorithm performing the pattern recognition for inner tracking detector which consists of two layers of pixel detectors and four layers of double sided silicon strip detectors arranged around the interaction region. The track finding algorithm will be used both during the High Level Trigger on-line track reconstruction and during the off-line full reconstruction. It must provide good efficiency down to momenta as low as 50 MeV/c where material effects are sizeable even in an extremely thin detector as the VXD. In addition it has to be able to cope with the high occupancy of the Belle II detectors due to the background. The underlying concept of the track finding algorithm, as well as details of the implementation are outlined. The algorithm is proven to run with good performance on simulated Y (4S) â\u86\u92 BB events with an efficiency for reconstructing tracks of above 90% over a wide range of momentum

A Chromosomal Inversion Unique to the Northern White-Cheeked Gibbon

The gibbon family belongs to the superfamily Hominoidea and includes 15 species divided into four genera. Each genus possesses a distinct karyotype with chromosome numbers varying from 38 to 52. This diversity is the result of numerous chromosomal changes that have accumulated during the evolution of the gibbon lineage, a quite unique feature in comparison with other hominoids and most of the other primates. Some gibbon species and subspecies rank among the most endangered primates in the world. Breeding programs can be extremely challenging and hybridization plays an important role within the factors responsible for the decline of captive gibbons. With less than 500 individuals left in the wild, the northern white-cheeked gibbon (Nomascus leucogenys leucogenys, NLE) is the most endangered primate in a successful captive breeding program. We present here the analysis of an inversion that we show being specific for the northern white-cheeked gibbon and can be used as one of the criteria to distinguish this subspecies from other gibbon taxa. The availability of the sequence spanning for one of the breakpoints of the inversion allows detecting it by a simple PCR test also on low quality DNA. Our results demonstrate the important role of genomics in providing tools for conservation efforts

MYCN mediates cysteine addiction and sensitizes neuroblastoma to ferroptosis

Aberrant expression of MYC transcription factor family members predicts poor clinical outcome in many human cancers. Oncogenic MYC profoundly alters metabolism and mediates an antioxidant response to maintain redox balance. Here we show that MYCN induces massive lipid peroxidation on depletion of cysteine, the rate-limiting amino acid for glutathione (GSH) biosynthesis, and sensitizes cells to ferroptosis, an oxidative, non-apoptotic and iron-dependent type of cell death. The high cysteine demand of MYCN-amplified childhood neuroblastoma is met by uptake and transsulfuration. When uptake is limited, cysteine usage for protein synthesis is maintained at the expense of GSH triggering ferroptosis and potentially contributing to spontaneous tumor regression in low-risk neuroblastomas. Pharmacological inhibition of both cystine uptake and transsulfuration combined with GPX4 inactivation resulted in tumor remission in an orthotopic MYCN-amplified neuroblastoma model. These findings provide a proof of concept of combining multiple ferroptosis targets as a promising therapeutic strategy for aggressive MYCN-amplified tumors

Trajectories from extinction: Where are missing mammals rediscovered?

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The track finding algorithm of the Belle II vertex detectors

The Belle II experiment is a high energy multi purpose particle detector operated at the asymmetric e+e− - collider SuperKEKB in Tsukuba (Japan). In this work we describe the algorithm performing the pattern recognition for inner tracking detector which consists of two layers of pixel detectors and four layers of double sided silicon strip detectors arranged around the interaction region. The track finding algorithm will be used both during the High Level Trigger on-line track reconstruction and during the off-line full reconstruction. It must provide good efficiency down to momenta as low as 50 MeV/c where material effects are sizeable even in an extremely thin detector as the VXD. In addition it has to be able to cope with the high occupancy of the Belle II detectors due to the background. The underlying concept of the track finding algorithm, as well as details of the implementation are outlined. The algorithm is proven to run with good performance on simulated ϒ(4S) → BB̄ events with an efficiency for reconstructing tracks of above 90% over a wide range of momentum

Alternative lengthening of telomeres in childhood neuroblastoma from genome to proteome

Telomere maintenance by telomerase activation or alternative lengthening of telomeres (ALT) is a major determinant of poor outcome in neuroblastoma. Here, we screen for ALT in primary and relapsed neuroblastomas (n=760) and characterize its features using multi-omics profiling. ALT-positive tumors are molecularly distinct from other neuroblastoma subtypes and enriched in a population-based clinical sequencing study cohort for relapsed cases. They display reduced ATRX/DAXX complex abundance, due to either ATRX mutations (55%) or low protein expression. The heterochromatic histone mark H3K9me3 recognized by ATRX is enriched at the telomeres of ALT-positive tumors. Notably, we find a high frequency of telomeric repeat loci with a neuroblastoma ALT-specific hotspot on chr1q42.2 and loss of the adjacent chromosomal segment forming a neo-telomere. ALT-positive neuroblastomas proliferate slowly, which is reflected by a protracted clinical course of disease. Nevertheless, children with an ALT-positive neuroblastoma have dismal outcome. Alternative lengthening of telomeres (ALT) is associated with a poor outcome in neuroblastoma. Here, the authors find that ALT is associated with mutated ATRX and/or reduced protein abundance, frequent telomeric repeat loci and heterochromatic telomeric chromatin