Influence of nanotube length and density on the plasmonic terahertz response of single-walled carbon nanotubes

We measure the conductivity spectra of thin films comprising bundled single-walled carbon nanotubes (CNTs) of different average lengths in the frequency range 0.3-1000 THz and temperature interval 10-530 K. The observed temperature-induced changes in the terahertz conductivity spectra are shown to depend strongly on the average CNT length, with a conductivity around 1 THz that increases/decreases as the temperature increases for short/long tubes. This behaviour originates from the temperature dependence of the electron scattering rate, which we obtain from Drude fits of the measured conductivity in the range 0.3-2 THz for 10 $\mu$m length CNTs. This increasing scattering rate with temperature results in a subsequent broadening of the observed THz conductivity peak at higher temperatures and a shift to lower frequencies for increasing CNT length. Finally, we show that the change in conductivity with temperature depends not only on tube length, but also varies with tube density. We record the effective conductivities of composite films comprising mixtures of WS$_2$ nanotubes and CNTs vs CNT density for frequencies in the range 0.3-1 THz, finding that the conductivity increases/decreases for low/high density films as the temperature increases. This effect arises due to the density dependence of the effective length of conducting pathways in the composite films, which again leads to a shift and temperature dependent broadening of the THz conductivity peak.Comment: Submitted to Journal of Physics D. Main manuscript: 9 pages, 8 figures. Supplementary material: 5 pages, 6 figure

Performance of a novel wafer scale CMOS active pixel sensor for bio-medical imaging

Recently CMOS Active Pixels Sensors (APSs) have become a valuable alternative to amorphous Silicon and Selenium Flat Panel Imagers (FPIs) in bio-medical imaging applications. CMOS APSs can now be scaled up to the standard 20 cm diameter wafer size by means of a reticle stitching block process. However despite wafer scale CMOS APS being monolithic, sources of non-uniformity of response and regional variations can persist representing a significant challenge for wafer scale sensor response. Non-uniformity of stitched sensors can arise from a number of factors related to the manufacturing process, including variation of amplification, variation between readout components, wafer defects and process variations across the wafer due to manufacturing processes. This paper reports on an investigation into the spatial non-uniformity and regional variations of a wafer scale stitched CMOS APS. For the first time a per-pixel analysis of the electro-optical performance of a wafer CMOS APS is presented, to address inhomogeneity issues arising from the stitching techniques used to manufacture wafer scale sensors. A complete model of the signal generation in the pixel array has been provided and proved capable of accounting for noise and gain variations across the pixel array. This novel analysis leads to readout noise and conversion gain being evaluated at pixel level, stitching block level and in regions of interest, resulting in a coefficient of variation ≤ 1.9%. The uniformity of the image quality performance has been further investigated in a typical X-ray application, i.e. mammography, showing a uniformity in terms of CNR among the highest when compared with mammography detectors commonly used in clinical practise. Finally, in order to compare the detection capability of this novel APS with the currently used technology (i.e. FPIs), theoretical evaluation of the Detection Quantum Efficiency (DQE) at zero-frequency has been performed, resulting in a higher DQE for this detector compared to FPIs. Optical characterization, X-ray contrast measurements and theoretical DQE evaluation suggest that a trade off can be found between the need of a large imaging area and the requirement of a uniform imaging performance, making the DynAMITe large area CMOS APS suitable for a range of bio-medical applications

Business modeling and requirements in RUP: a dependency analysis of activities, tasks and work products

Most artifacts developed during the requirements engineering process relate themselves in different ways. In order to understand in detail how they affect each other during the software development process, it is relevant to iden-tify their interdependencies. This paper presents a systematization of the existing interdependencies between the different elements of the Rational Unified Process (RUP) in the Business Modeling and Requirements disciplines. This work, which highlights knowledge about the different interdependencies and traceability of RUP elements, is useful to avoid unconscious decisions during software the de-velopment process and also, to detect potential problems due to the violation of the existing interdependencies.This work has been supported by COMPETE: POCI-01-0145-FEDER-007043 and FCT – Fundação para a Ciência e a Tecnologia within the Project Scope: UID/CEC/00319/2013.info:eu-repo/semantics/publishedVersio

Partitioning heritability by functional annotation using genome-wide association summary statistics

Recent work has demonstrated that some functional categories of the genome contribute disproportionately to the heritability of complex diseases. Here we analyze a broad set of functional elements, including cell type-specific elements, to estimate their polygenic contributions to heritability in genome-wide association studies (GWAS) of 17 complex diseases and traits with an average sample size of 73,599. To enable this analysis, we introduce a new method, stratified LD score regression, for partitioning heritability from GWAS summary statistics while accounting for linked markers. This new method is computationally tractable at very large sample sizes and leverages genome-wide information. Our findings include a large enrichment of heritability in conserved regions across many traits, a very large immunological disease-specific enrichment of heritability in FANTOM5 enhancers and many cell type-specific enrichments, including significant enrichment of central nervous system cell types in the heritability of body mass index, age at menarche, educational attainment and smoking behavior

Molecular imaging of cell death in vivo by a novel small molecule probe

Apoptosis has a role in many medical disorders, therefore assessment of apoptosis in vivo can be highly useful for diagnosis, follow-up and evaluation of treatment efficacy. ApoSense is a novel technology, comprising low molecular-weight probes, specifically designed for imaging of cell death in vivo. In the current study we present targeting and imaging of cell death both in vitro and in vivo, utilizing NST-732, a member of the ApoSense family, comprising a fluorophore and a fluorine atom, for both fluorescent and future positron emission tomography (PET) studies using an 18F label, respectively. In vitro, NST-732 manifested selective and rapid accumulation within various cell types undergoing apoptosis. Its uptake was blocked by caspase inhibition, and occurred from the early stages of the apoptotic process, in parallel to binding of Annexin-V, caspase activation and alterations in mitochondrial membrane potential. In vivo, NST-732 manifested selective uptake into cells undergoing cell-death in several clinically-relevant models in rodents: (i) Cell-death induced in lymphoma by irradiation; (ii) Renal ischemia/reperfusion; (iii) Cerebral stroke. Uptake of NST-732 was well-correlated with histopathological assessment of cell-death. NST-732 therefore represents a novel class of small-molecule detectors of apoptosis, with potential useful applications in imaging of the cell death process both in vitro and in vivo

Human leukocyte antigen supertype matching after myeloablative hematopoietic cell transplantation with 7/8 matched unrelated donor allografts: a report from the Center for International Blood and Marrow Transplant Research

The diversity of the human leukocyte antigen (HLA) class I and II alleles can be simplified by consolidating them into fewer supertypes based on functional or predicted structural similarities in epitope-binding grooves of HLA molecules. We studied the impact of matched and mismatched HLA-A (265 versus 429), -B (230 versus 92), -C (365 versus 349), and -DRB1 (153 versus 51) supertypes on clinical outcomes of 1934 patients with acute leukemias or myelodysplasia/myeloproliferative disorders. All patients were reported to the Center for International Blood and Marrow Transplant Research following single-allele mismatched unrelated donor myeloablative conditioning hematopoietic cell transplantation. Single mismatched alleles were categorized into six HLA-A (A01, A01A03, A01A24, A02, A03, A24), six HLA-B (B07, B08, B27, B44, B58, B62), two HLA-C (C1, C2), and five HLA-DRB1 (DR1, DR3, DR4, DR5, DR9) supertypes. Supertype B mismatch was associated with increased risk of grade II-IV acute graft-versus-host disease (hazard ratio =1.78, P=0.0025) compared to supertype B match. Supertype B07-B44 mismatch was associated with a higher incidence of both grade II-IV (hazard ratio=3.11, P=0.002) and III-IV (hazard ratio=3.15, P=0.01) acute graft-versus-host disease. No significant associations were detected between supertype-matched versus -mismatched groups at other HLA loci. These data suggest that avoiding HLA-B supertype mismatches can mitigate the risk of grade II-IV acute graft-versus-host disease in 7/8-mismatched unrelated donor hematopoietic cell transplantation when multiple HLA-B supertype-matched donors are available. Future studies are needed to define the mechanisms by which supertype mismatching affects outcomes after alternative donor hematopoietic cell transplantation

Earth observations into action: the systemic integration of earth observation applications into national risk reduction decision structures

Purpose - As stated in the United Nations Global Assessment Report 2022 Concept Note, decision-makers everywhere need data and statistics that are accurate, timely, sufficiently disaggregated, relevant, accessible and easy to use. The purpose of this paper is to demonstrate scalable and replicable methods to advance and integrate the use of earth observation (EO), specifically ongoing efforts within the Group on Earth Observations (GEO) Work Programme and the Committee on Earth Observation Satellites (CEOS) Work Plan, to support risk-informed decision-making, based on documented national and subnational needs and requirements. Design/methodology/approach - Promotion of open data sharing and geospatial technology solutions at national and subnational scales encourages the accelerated implementation of successful EO applications. These solutions may also be linked to specific Sendai Framework for Disaster Risk Reduction (DRR) 2015–2030 Global Targets that provide trusted answers to risk-oriented decision frameworks, as well as critical synergies between the Sendai Framework and the 2030 Agenda for Sustainable Development. This paper provides examples of these efforts in the form of platforms and knowledge hubs that leverage latest developments in analysis ready data and support evidence-based DRR measures. Findings - The climate crisis is forcing countries to face unprecedented frequency and severity of disasters. At the same time, there are growing demands to respond to policy at the national and international level. EOs offer insights and intelligence for evidence-based policy development and decision-making to support key aspects of the Sendai Framework. The GEO DRR Working Group and CEOS Working Group Disasters are ideally placed to help national government agencies, particularly national Sendai focal points to learn more about EOs and understand their role in supporting DRR. Originality/value - The unique perspective of EOs provide unrealized value to decision-makers addressing DRR. This paper highlights tangible methods and practices that leverage free and open source EO insights that can benefit all DRR practitioners

The Genomic and Immune Landscapes of Lethal Metastatic Breast Cancer.

The detailed molecular characterization of lethal cancers is a prerequisite to understanding resistance to therapy and escape from cancer immunoediting. We performed extensive multi-platform profiling of multi-regional metastases in autopsies from 10 patients with therapy-resistant breast cancer. The integrated genomic and immune landscapes show that metastases propagate and evolve as communities of clones, reveal their predicted neo-antigen landscapes, and show that they can accumulate HLA loss of heterozygosity (LOH). The data further identify variable tumor microenvironments and reveal, through analyses of T cell receptor repertoires, that adaptive immune responses appear to co-evolve with the metastatic genomes. These findings reveal in fine detail the landscapes of lethal metastatic breast cancer.CRUK

Coral-Bacterial Communities before and after a Coral Mass Spawning Event on Ningaloo Reef

Bacteria associated with three coral species, Acropora tenuis, Pocillopora damicornis and Tubastrea faulkneri, were assessed before and after coral mass spawning on Ningaloo Reef in Western Australia. Two colonies of each species were sampled before and after the mass spawning event and two additional samples were collected for P. damicornis after planulation. A variable 470 bp region of the 16 S rRNA gene was selected for pyrosequencing to provide an understanding of potential variations in coral-associated bacterial diversity and community structure. Bacterial diversity increased for all coral species after spawning as assessed by Chao1 diversity indicators. Minimal changes in community structure were observed at the class level and data at the taxonomical level of genus incorporated into a PCA analysis indicated that despite bacterial diversity increasing after spawning, coral-associated community structure did not shift greatly with samples grouped according to species. However, interesting changes could be detected from the dataset; for example, α-Proteobacteria increased in relative abundance after coral spawning and particularly the Roseobacter clade was found to be prominent in all coral species, indicating that this group may be important in coral reproduction

Post-Transcriptional Regulation of BCL2 mRNA by the RNA-Binding Protein ZFP36L1 in Malignant B Cells

The human ZFP36 zinc finger protein family consists of ZFP36, ZFP36L1, and ZFP36L2. These proteins regulate various cellular processes, including cell apoptosis, by binding to adenine uridine rich elements in the 3′ untranslated regions of sets of target mRNAs to promote their degradation. The pro-apoptotic and other functions of ZFP36 family members have been implicated in the pathogenesis of lymphoid malignancies. To identify candidate mRNAs that are targeted in the pro-apoptotic response by ZFP36L1, we reverse-engineered a gene regulatory network for all three ZFP36 family members using the ‘maximum information coefficient’ (MIC) for target gene inference on a large microarray gene expression dataset representing cells of diverse histological origin. Of the three inferred ZFP36L1 mRNA targets that were identified, we focussed on experimental validation of mRNA for the pro-survival protein, BCL2, as a target for ZFP36L1. RNA electrophoretic mobility shift assay experiments revealed that ZFP36L1 interacted with the BCL2 adenine uridine rich element. In murine BCL1 leukemia cells stably transduced with a ZFP36L1 ShRNA lentiviral construct, BCL2 mRNA degradation was significantly delayed compared to control lentiviral expressing cells and ZFP36L1 knockdown in different cell types (BCL1, ACHN, Ramos), resulted in increased levels of BCL2 mRNA levels compared to control cells. 3′ untranslated region luciferase reporter assays in HEK293T cells showed that wild type but not zinc finger mutant ZFP36L1 protein was able to downregulate a BCL2 construct containing the BCL2 adenine uridine rich element and removal of the adenine uridine rich core from the BCL2 3′ untranslated region in the reporter construct significantly reduced the ability of ZFP36L1 to mediate this effect. Taken together, our data are consistent with ZFP36L1 interacting with and mediating degradation of BCL2 mRNA as an important target through which ZFP36L1 mediates its pro-apoptotic effects in malignant B-cells