6G networks : is this an evolution or a revolution?

The lessons learned from the third industrial revolution taught us that the transformation from mechanical and analog technology to digital electronics have changed the world once and forever. While computers and communication networks have become the new oil that defines the wealth of countries, research and industrial communities have been the driving forces that have made this transition possible. In the future, the same communities and stakeholders are required to enable the transition to net-zero communication networks. With reference to mobile communications, 5G is an evolution from all previous networks with the adoption of new radio access technologies, multisliced architecture, cloud-native and automation, and so on. By definition, 5G is a network that adapts to user needs and dynamic changes in traffic, designed to serve a new class of users: “machines.” Therefore, latency has become a critical metric in 5G. Looking forward, 6G shall employ cell-less access networks, integrated nonterrestrial networks, joint sensing and communications, new spectrums such as terahertz (THz) communications, switching from traditional channel-based design paradigms to designing channels through novel technologies such as intelligent reconfigurable surfaces, open interfaces that interconnect all network functions, end-to-end orchestrators, and, most noticeably, artificial intelligence (AI) machines that govern all functional modules and operational services. The various network functions generate traces of various operations that are ingested into databases; then AI will leverage this data for optimized decisions that are reflected into network status transitions, resource utilization, service enhancement, and ultimately lead to self-synthesizing networks. Built upon commercial clouds, 6G will have the flexibility to scale and restructure for more resilient response to traffic fluctuations and user requirements. To this end, cybersecurity features will become an embedded part of network functions to shield the network services not only from external threats but also from hosting domains. From an air interface perspective, 6G will integrate nonterrestrial (space, air, drone, and ocean) communications technologies to connect and route new users such as drones and coastal trading vessels. Furthermore, future wireless networks need to make use of a spectrum that extends into the optical spectrum and includes the THz range. The channel becomes a critical component due to the impact of blockages and random orientations at these frequencies. Active and passive intelligent reflecting surfaces (IRSs) will become a new wireless system element that will help overcome new challenges related to coverage and the propagation channel

Delayed puberty and abnormal anthropometry and its associations with quality of life in young Fontan survivors: A multicenter crossâ sectional study

IntroductionWe sought to evaluate the prevalence of delayed puberty and abnormal anthropometry and its association with quality of life (QoL) in young Fontan survivors.MethodsThis was a crossâ sectional study at 11 Pediatric Heart Network centers. Demographic and clinical data, anthropomety, and Tanner stage were collected. Anthropometric measurements and pubertal stage were compared to US norms. QoL was assessed using Pediatric Quality of Life inventory (PedsQL). Mixed effects regression modeling adjusting for clustering by center was used to evaluate factors associated with abnormal anthropometry and delayed puberty and associations with QoL.ResultsOf the 299 subjects, 42% were female. The median enrollment age was 13.9 years, and the median age at Fontan was 3 years. Fontan survivors had a higher prevalence of short stature relative to normative data (20% vs 5%, P 2 surgeries before Fontan was associated with delayed puberty. Lower family income (<$25 000) and hypoplastic left heart syndrome were associated with lower QoL.ConclusionCompared to the normal population, Fontan survivors have high prevalence of short stature, abnormal BMI and delayed puberty. Abnormal anthropometry, but not delayed puberty, was associated with lower overall QoL and perceived physical appearance scores. Routine screening for abnormal anthropometry, especially in HLHS and in lower socioeconomic status families, should be considered to allow interventions, which might ameliorate the negative psychosocial impact.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/144293/1/chd12597.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/144293/2/chd12597_am.pd

Mutational patterns in chemotherapy resistant muscle-invasive bladder cancer

Despite continued widespread use, the genomic effects of cisplatin-based chemotherapy and implications for subsequent treatment are incompletely characterized. Here, we analyze whole exome sequencing of matched pre- and post-neoadjuvant cisplatin-based chemotherapy primary bladder tumor samples from 30 muscle-invasive bladder cancer patients. We observe no overall increase in tumor mutational burden post-chemotherapy, though a significant proportion of subclonal mutations are unique to the matched pre- or post-treatment tumor, suggesting chemotherapy-induced and/or spatial heterogeneity. We subsequently identify and validate a novel mutational signature in post-treatment tumors consistent with known characteristics of cisplatin damage and repair. We find that post-treatment tumor heterogeneity predicts worse overall survival, and further observe alterations in cell-cycle and immune checkpoint regulation genes in post-treatment tumors. These results provide insight into the clinical and genomic dynamics of tumor evolution with cisplatin-based chemotherapy, suggest mechanisms of clinical resistance, and inform development of clinically relevant biomarkers and trials of combination therapies

Polymorphisms near TBX5 and GDF7 are associated with increased risk for Barrett's esophagus.

BACKGROUND & AIMS: Barrett's esophagus (BE) increases the risk of esophageal adenocarcinoma (EAC). We found the risk to be BE has been associated with single nucleotide polymorphisms (SNPs) on chromosome 6p21 (within the HLA region) and on 16q23, where the closest protein-coding gene is FOXF1. Subsequently, the Barrett's and Esophageal Adenocarcinoma Consortium (BEACON) identified risk loci for BE and esophageal adenocarcinoma near CRTC1 and BARX1, and within 100 kb of FOXP1. We aimed to identify further SNPs that increased BE risk and to validate previously reported associations. METHODS: We performed a genome-wide association study (GWAS) to identify variants associated with BE and further analyzed promising variants identified by BEACON by genotyping 10,158 patients with BE and 21,062 controls. RESULTS: We identified 2 SNPs not previously associated with BE: rs3072 (2p24.1; odds ratio [OR] = 1.14; 95% CI: 1.09-1.18; P = 1.8 × 10(-11)) and rs2701108 (12q24.21; OR = 0.90; 95% CI: 0.86-0.93; P = 7.5 × 10(-9)). The closest protein-coding genes were respectively GDF7 (rs3072), which encodes a ligand in the bone morphogenetic protein pathway, and TBX5 (rs2701108), which encodes a transcription factor that regulates esophageal and cardiac development. Our data also supported in BE cases 3 risk SNPs identified by BEACON (rs2687201, rs11789015, and rs10423674). Meta-analysis of all data identified another SNP associated with BE and esophageal adenocarcinoma: rs3784262, within ALDH1A2 (OR = 0.90; 95% CI: 0.87-0.93; P = 3.72 × 10(-9)). CONCLUSIONS: We identified 2 loci associated with risk of BE and provided data to support a further locus. The genes we found to be associated with risk for BE encode transcription factors involved in thoracic, diaphragmatic, and esophageal development or proteins involved in the inflammatory response

The epigenetic landscape of renal cancer

This is an accepted manuscript of an article published by Nature in Nature Reviews: Nephrology on 28/11/2016, available online: https://doi.org/10.1038/nrneph.2016.168 The accepted version of the publication may differ from the final published version.The majority of kidney cancers are associated with mutations in the von Hippel-Lindau gene and a small proportion are associated with infrequent mutations in other well characterized tumour-suppressor genes. In the past 15 years, efforts to uncover other key genes involved in renal cancer have identified many genes that are dysregulated or silenced via epigenetic mechanisms, mainly through methylation of promoter CpG islands or dysregulation of specific microRNAs. In addition, the advent of next-generation sequencing has led to the identification of several novel genes that are mutated in renal cancer, such as PBRM1, BAP1 and SETD2, which are all involved in histone modification and nucleosome and chromatin remodelling. In this Review, we discuss how altered DNA methylation, microRNA dysregulation and mutations in histone-modifying enzymes disrupt cellular pathways in renal cancers

Sequential bottom-up and top-down processing for the synthesis of transition metal dichalcogenide nanosheets: the case of rhenium disulfide (ReS2)

Bottom-up (aerosol-assisted chemical vapor deposition, AACVD) and top-down (liquid phase exfoliation, LPE) processing methodologies are used in tandem to produce colloids of few-layer thick rhenium disulfide (ReS2) in N-methyl pyrrolidone.</p

The influence of precursor on rhenium incorporation into Re-doped MoS₂ (Mo_1-:XRe_xS₂) thin films by aerosol-assisted chemical vapour deposition (AACVD)

The molecular precursors [Mo(S2CNEt2)4] (1), [Re(S2CC6H5)(S3CC6H5)2] (2), and [Re2(μ-S)2(S2CNEt2)4] (3) were used to deposit thin films of Re-doped MoS2.</p