179 research outputs found
Deep learning cardiac motion analysis for human survival prediction
Motion analysis is used in computer vision to understand the behaviour of
moving objects in sequences of images. Optimising the interpretation of dynamic
biological systems requires accurate and precise motion tracking as well as
efficient representations of high-dimensional motion trajectories so that these
can be used for prediction tasks. Here we use image sequences of the heart,
acquired using cardiac magnetic resonance imaging, to create time-resolved
three-dimensional segmentations using a fully convolutional network trained on
anatomical shape priors. This dense motion model formed the input to a
supervised denoising autoencoder (4Dsurvival), which is a hybrid network
consisting of an autoencoder that learns a task-specific latent code
representation trained on observed outcome data, yielding a latent
representation optimised for survival prediction. To handle right-censored
survival outcomes, our network used a Cox partial likelihood loss function. In
a study of 302 patients the predictive accuracy (quantified by Harrell's
C-index) was significantly higher (p < .0001) for our model C=0.73 (95 CI:
0.68 - 0.78) than the human benchmark of C=0.59 (95 CI: 0.53 - 0.65). This
work demonstrates how a complex computer vision task using high-dimensional
medical image data can efficiently predict human survival
Reparameterization Invariance Revisited
Reparameterization invariance, a symmetry of heavy quark effective theory,
appears in different forms in the literature. The most commonly cited forms of
the reparameterization transformation are shown to induce the same constraints
on operators that do not vanish under the equation of motion to order ,
and to be related by a redefinition of the heavy quark field. We give a new,
very straightforward proof that that the reparameterization invariance
constraints apply to all orders in under matching to full QCD and
renormalization-group running, at least up to and including .Comment: 20 pages, no figures, Latex. Revised version: Discussion of
reparameterization invariance constraints on class-II operators adde
Characteristics and risk factors for post-COVID-19 breathlessness after hospitalisation for COVID-19
Methods for specifying the target difference in a randomised controlled trial : the Difference ELicitation in TriAls (DELTA) systematic review
Peer reviewedPublisher PD
Glucosinolates, myrosinase hydrolysis products, and flavonols found in rocket (Eruca sativa and Diplotaxis tenuifolia)
Rocket species have been shown to have very high concentrations of glucosinolates and flavonols, which have numerous positive health benefits with regular consumption. In this review we highlight how breeders and processors of rocket species can utilize genomic and phytochemical research to improve varieties and enhance the nutritive benefits to consumers. Plant breeders are increasingly looking to new technologies such as HPLC, UPLC, LC-MS and GC-MS to screen populations for their phytochemical content to inform plant selections. Here we collate the research that has been conducted to-date in rocket, and summarise all glucosinolate and flavonol compounds identified in the species. We emphasize the importance of the broad screening of populations for phytochemicals and myrosinase degradation products, as well as unique traits that may be found in underutilized gene bank resources. We also stress that collaboration with industrial partners is becoming essential for long-term plant breeding goals through research
Immune-related genetic enrichment in frontotemporal dementia:An analysis of genome-wide association studies
Background: Converging evidence suggests that immune-mediated dysfunction plays an important role in the pathogenesis of frontotemporal dementia (FTD). Although genetic studies have shown that immune-associated loci are associated with increased FTD risk, a systematic investigation of genetic overlap between immune-mediated diseases and the spectrum of FTD-related disorders has not been performed. Methods and findings: Using large genome-wide association studies (GWASs) (total n = 192,886 cases and controls) and recently developed tools to quantify genetic overlap/pleiotropy, we systematically identified single nucleotide polymorphisms (SNPs) jointly associated with FTD-related disorders—namely, FTD, corticobasal degeneration (CBD), progressive supranuclear palsy (PSP), and amyotrophic lateral sclerosis (ALS)—and 1 or more immune-mediated diseases including Crohn disease, ulcerative colitis (UC), rheumatoid arthritis (RA), type 1 diabetes (T1D), celiac disease (CeD), and psoriasis. We found up to 270-fold genetic enrichment between FTD and RA, up to 160-fold genetic enrichment between FTD and UC, up to 180-fold genetic enrichment between FTD and T1D, and up to 175-fold genetic enrichment between FTD and CeD. In contrast, for CBD and PSP, only 1 of the 6 immune-mediated diseases produced genetic enrichment comparable to that seen for FTD, with up to 150-fold genetic enrichment between CBD and CeD and up to 180-fold enrichment between PSP and RA. Further, we found minimal enrichment between ALS and the immune-mediated diseases tested, with the highest levels of enrichment between ALS and RA (up to 20-fold). For FTD, at a conjunction false discovery rate < 0.05 and after excluding SNPs in linkage disequilibrium, we found that 8 of the 15 identified loci mapped to the human leukocyte antigen (HLA) region on Chromosome (Chr) 6. We also found novel candidate FTD susceptibility loci within LRRK2 (leucine rich repeat kinase 2), TBKBP1 (TBK1 binding protein 1), and PGBD5 (piggyBac transposable element derived 5). Functionally, we found that the expression of FTD–immune pleiotropic genes (particularly within the HLA region) is altered in postmortem brain tissue from patients with FTD and is enriched in microglia/macrophages compared to other central nervous system cell types. The main study limitation is that the results represent only clinically diagnosed individuals. Also, given the complex interconnectedness of the HLA region, we were not able to define the specific gene or genes on Chr 6 responsible for our pleiotropic signal. Conclusions: We show immune-mediated genetic enrichment specifically in FTD, particularly within the HLA region. Our genetic results suggest that for a subset of patients, immune dysfunction may contribute to FTD risk. These findings have potential implications for clinical trials targeting immune dysfunction in patients with FTD
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