GAN Augmentation: Augmenting Training Data using Generative Adversarial Networks

One of the biggest issues facing the use of machine learning in medical imaging is the lack of availability of large, labelled datasets. The annotation of medical images is not only expensive and time consuming but also highly dependent on the availability of expert observers. The limited amount of training data can inhibit the performance of supervised machine learning algorithms which often need very large quantities of data on which to train to avoid overfitting. So far, much effort has been directed at extracting as much information as possible from what data is available. Generative Adversarial Networks (GANs) offer a novel way to unlock additional information from a dataset by generating synthetic samples with the appearance of real images. This paper demonstrates the feasibility of introducing GAN derived synthetic data to the training datasets in two brain segmentation tasks, leading to improvements in Dice Similarity Coefficient (DSC) of between 1 and 5 percentage points under different conditions, with the strongest effects seen fewer than ten training image stacks are available

Perceived Product Hazard Norms in Younger and Older Adults

Designers and researchers have often assumed that individuals rely to some degree on individual perceptions of a product's hazard when interacting with warning systems that accompany the product. However, few investigations have been made to determine what precisely these perceptions are, and how they may differ across diverse populations (such as age). Younger and older adults were tested for perceived product hazards over a diverse group of products using a Battig and Montague (1969) style procedure. Participants were presented with a total of 78 products, and asked to list the first hazards that came to their mind (up to 7 per product) for each. Comparisons revealed age-related differences between the most commonly perceived hazards for 28 of the products, with many of the age-related differences not predicted prior to data collection. The resulting data additionally form a tool for designing warning systems and research stimuli based on the products or classes of products represented in this sample.M.S.Committee Chair: Arthur Fisk; Committee Member: Ute Fischer; Committee Member: Wendy Roger

INGLATERRA (Reino Unido). Mapas generales (1754-1763?). 1:460000

Comprende además las costas de la zona más meridional de Escocia, oriental de Irlanda e Irlanda del Norte y noroccidental de FranciaDedicatoria : "To the Right Honourable and Right Reverend Father in God Peter Lord Bishop of Winchester Prelate of the most Noble Order of the Gart. &c. This Map of England Is humbly dedicated and presented"Fecha de publicación deducida teniendo en cuenta el período en el que pudieron colaborar los editoresEscalas gráficas de 50 millas grandes [= 23 cm], 50 millas medianas [= 20'8 cm] y 50 millas pequeñas [= 19,1 cm]. Coordenadas referidas a un meridiano que no se especifica (E 15°17'--E 26°56'/N 55°52'--N 49°58'). Orientado con lis en dos rosas de treinta y dos vientos, presentando una de ellas la mención nominal de los puntos cardinalesOrografía de perfilLíneas divisorias entre los condados diferenciados por colorTabla de signos convencionales para indicar distintos tipos de población y carreteras, haciendo mención de las distancias que aparecen indicadas en el mapa entre ciudadesRelación de las principales ciudades indicando el condado al que pertenecen y sus coordenadas geográficasLeyendas relativas a los reinados de Enrique II y III de Inglaterra y a características geográficas, económicas y de poblaciónAdornado con barcos y monstruos marinosCartelas barrocas, enmarcando todos los datos que figuran en el documento, entre las que destacan la que recoje el título y la de la dedicatoria, al estar coronadas por los escudos de la Casa Real inglesa y del obispo de Winchester, respectivamenteForma parte de la colección Mendoz

An Overview of the Role of Systems Analysis in NASA's Hypersonics Project

NASA's Aeronautics Research Mission Directorate recently restructured its Vehicle Systems Program, refocusing it towards understanding the fundamental physics that govern flight in all speed regimes. Now called the Fundamental Aeronautics Program, it is comprised of four new projects, Subsonic Fixed Wing, Subsonic Rotary Wing, Supersonics, and Hypersonics. The Aeronautics Research Mission Directorate has charged the Hypersonics Project with having a basic understanding of all systems that travel at hypersonic speeds within the Earth's and other planets atmospheres. This includes both powered and unpowered systems, such as re-entry vehicles and vehicles powered by rocket or airbreathing propulsion that cruise in and accelerate through the atmosphere. The primary objective of the Hypersonics Project is to develop physics-based predictive tools that enable the design, analysis and optimization of such systems. The Hypersonics Project charges the systems analysis discipline team with providing it the decision-making information it needs to properly guide research and technology development. Credible, rapid, and robust multi-disciplinary system analysis processes and design tools are required in order to generate this information. To this end, the principal challenges for the systems analysis team are the introduction of high fidelity physics into the analysis process and integration into a design environment, quantification of design uncertainty through the use of probabilistic methods, reduction in design cycle time, and the development and implementation of robust processes and tools enabling a wide design space and associated technology assessment capability. This paper will discuss the roles and responsibilities of the systems analysis discipline team within the Hypersonics Project as well as the tools, methods, processes, and approach that the team will undertake in order to perform its project designated functions

Myeloma-derived macrophage inhibitory factor regulates bone marrow stromal cell-derived IL-6 via c-MYC

Multiple myeloma (MM) remains an incurable malignancy despite the recent advancements in its treatment. The protective effects of the niche in which it develops has been well documented; however, little has been done to investigate the MM cell’s ability to ‘re-program’ cells within its environment to benefit disease progression. Here, we show that MM-derived macrophage migratory inhibitory factor (MIF) stimulates bone marrow stromal cells to produce the disease critical cytokines IL-6 and IL-8, prior to any cell-cell contact. Furthermore, we provide evidence that this IL-6/8 production is mediated by the transcription factor cMYC. Pharmacological inhibition of cMYC in vivo using JQ1 led to significantly decreased levels of serum IL-6—a highly positive prognostic marker in MM patients

NADPH oxidase-2 derived superoxide drives mitochondrial transfer from bone marrow stromal cells to leukemic blasts

Improvements in the understanding of the metabolic cross-talk between cancer and its micro-environment are expected to lead to novel therapeutic approaches. Acute myeloid leukemia (AML) cells have increased mitochondria compared to non-malignant CD34+ hematopoietic progenitor cells. Furthermore, contrary to the Warburg hypothesis, (AML) relies on oxidative phosphorylation to generate ATP. Here we report that in human AML, NOX2 generates superoxide which stimulates bone marrow stromal cells (BMSC) to AML blast transfer of mitochondria through AML derived tunnelling nanotubes. Moreover, inhibition of NOX2 was able to prevent mitochondrial transfer, increase AML apoptosis and improve NSG AML mouse survival. Although mitochondrial transfer from BMSC to non-malignant CD34+ cells occurs in response to oxidative stress, NOX2 inhibition had no detectable effect on non-malignant CD34+ cell survival. Taken together we identify tumor-specific dependence on NOX2 driven mitochondrial transfer as a novel therapeutic strategy in AML

What factors influence the rediscovery of lost tetrapod species?

We created a database of lost and rediscovered tetrapod species, identified patterns in their distribution and factors influencing rediscovery. Tetrapod species are being lost at a faster rate than they are being rediscovered, due to slowing rates of rediscovery for amphibians, birds and mammals, and rapid rates of loss for reptiles. Finding lost species and preventing future losses should therefore be a conservation priority. By comparing the taxonomic and spatial distribution of lost and rediscovered tetrapod species, we have identified regions and taxa with many lost species in comparison to those that have been rediscovered—our results may help to prioritise search effort to find them. By identifying factors that influence rediscovery, we have improved our ability to broadly distinguish the types of species that are likely to be found from those that are not (because they are likely to be extinct). Some lost species, particularly those that are small and perceived to be uncharismatic, may have been neglected in terms of conservation effort, and other lost species may be hard to find due to their intrinsic characteristics and the characteristics of the environments they occupy (e.g. nocturnal species, fossorial species and species occupying habitats that are more difficult to survey such as wetlands). These lost species may genuinely await rediscovery. However, other lost species that possess characteristics associated with rediscovery (e.g. large species) and that are also associated with factors that negatively influence rediscovery (e.g. those occupying small islands) are more likely to be extinct. Our results may foster pragmatic search protocols that prioritise lost species likely to still exist

CD38-driven mitochondrial trafficking promotes bioenergetic plasticity in multiple myeloma

Metabolic adjustments are necessary for the initiation, proliferation, and spread of cancer cells. Although mitochondria have been shown to move to cancer cells from their microenvironment, the metabolic consequences of this phenomenon have yet to be fully elucidated. Here we report that multiple myeloma (MM) cells use mitochondrial-based metabolism as well as glycolysis when located within the bone marrow microenvironment (BMM). The reliance of MM cells on oxidative phosphorylation was caused by intercellular mitochondrial transfer to MM cells from neighboring non-malignant bone marrow stromal cells (BMSC). This mitochondrial transfer occurred through tumor-derived tunneling nanotubes (TNT). Moreover, shRNA mediated knockdown of CD38 inhibits mitochondrial transfer and TNT formation in-vitro and blocks mitochondrial transfer and improves animal survival in vivo. This study describes a potential treatment strategy to inhibit mitochondrial transfer for clinical benefit and scientifically expands the understanding of the functional effects of mitochondrial transfer on tumor metabolism

PGC-1 alpha induced mitochondrial biogenesis in stromal cells underpins mitochondrial transfer to melanoma

INTRODUCTION: Progress in the knowledge of metabolic interactions between cancer and its microenvironment is ongoing and may lead to novel therapeutic approaches. Until recently, melanoma was considered a glycolytic tumour due to mutations in mitochondrial-DNA, however, these malignant cells can regain OXPHOS capacity via the transfer of mitochondrial-DNA, a process that supports their proliferation in-vitro and in-vivo. Here we study how melanoma cells acquire mitochondria and how this process is facilitated from the tumour microenvironment. METHODS: Primary melanoma cells, and MSCs derived from patients were obtained. Genes’ expression and DNA quantification was analysed using Real-time PCR. MSC migration, melanoma proliferation and tumour volume, in a xenograft subcutaneous mouse model, were monitored through bioluminescent live animal imaging. RESULTS: Human melanoma cells attract bone marrow-derived stromal cells (MSCs) to the primary tumour site where they stimulate mitochondrial biogenesis in the MSCs through upregulation of PGC1a. Mitochondria are transferred to the melanoma cells via direct contact with the MSCs. Moreover, inhibition of MSC-derived PGC1a was able to prevent mitochondrial transfer and improve NSG melanoma mouse tumour burden. CONCLUSION: MSC mitochondrial biogenesis stimulated by melanoma cells is prerequisite for mitochondrial transfer and subsequent tumour growth, where targeting this pathway may provide an effective novel therapeutic approach in melanoma