Segmentation of pneumonia lesions from CT scans of COVID-19 patients is important for accurate diagnosis and follow-up. Deep learning has a potential to automate this task but requires a large set of high-quality annotations that are difficult to collect. Learning from noisy training labels that are easier to obtain has a potential to alleviate this problem. To this end, we propose a novel noise-robust framework to learn from noisy labels for the segmentation task. We first introduce a noise-robust Dice loss that is a generalization of Dice loss for segmentation and Mean Absolute Error (MAE) loss for robustness against noise, then propose a novel COVID-19 Pneumonia Lesion segmentation network (COPLE-Net) to better deal with the lesions with various scales and appearances. The noiserobust Dice loss and COPLE-Net are combined with an adaptive self-ensembling framework for training, where an Exponential Moving Average (EMA) of a student model is used as a teacher model that is adaptively updated by suppressing the contribution of the student to EMA when the student has a large training loss. The student

Human DNA helicase II (HDH II) is a novel ATP‐dependent DNA unwinding enzyme, purified to apparent homogeneity from HeLa cells, which (i) unwinds exclusively DNA duplexes, (ii) prefers partially unwound substrates and (iii) proceeds in the 3′ to 5′ direction on the bound strand. HDH II is a heterodimer of 72 and 87 kDa polypeptides. It shows single‐stranded DNA‐dependent ATPase activity, as well as double‐stranded DNA binding capacity. All these activities comigrate in gel filtration and glycerol gradients, giving a sedimentation coefficient of 7.4S and a Stokes radius of approximately 46 A, corresponding to a native molecular weight of 158 kDa. The antibodies raised in rabbit against either polypeptide can remove from the solution all the activities of HDH II. Photoaffinity labelling with [alpha‐32P]ATP labelled both polypeptides. Microsequencing of the separate polypeptides of HDH II and cross‐reaction with specific antibodies showed that this enzyme is identical to Ku, an autoantigen recognized by the sera of scleroderma and lupus erythematosus patients, which binds specifically to duplex DNA ends and is regulator of a DNA‐dependent protein kinase. Recombinant HDH II/Ku protein expressed in and purified from Escherichia coli cells showed DNA binding and helicase activities indistinguishable from those of the isolated protein. The exclusively nuclear location of HDH II/Ku antigen, its highly specific affinity for double‐stranded DNA, its abundance and its newly demonstrated ability to unwind exclusively DNA duplexes, point to an additional, if still unclear, role for this molecule in DNA metabolism.

Background and aims: Reduced ileal Paneth cell adefensin expression has been reported to be associated with Crohn's disease, especially in patients carrying NOD2 mutations. The aim of this study was to independently assess whether NOD2, a-defensins and Crohn's disease are linked. Methods: Using quantitative real-time polymerase chain reaction (RT-PCR), we measured the mRNA expression levels of key Paneth cell antimicrobial peptides (DEFA5, DEFA6, LYZ, PLA2G2A), inflammatory cytokines [interkelukin 6 (IL6) and IL8], and a marker of epithelial cell content, villin (VIL1) in 106 samples from both affected ileum (inflamed Crohn's disease cases, n = 44) and unaffected ileum (non-inflamed; Crohn's disease cases, n = 51 and controls, n = 11). Anti-human defensin 5 (HD-5) and haematoxylin/eosin immunohistochemical staining was performed on parallel sections from NOD2 wild-type and NOD2 mutant ileal Crohn's disease tissue. Results: In Crohn's disease patients, DEFA5 and DEFA6 mRNA expression levels were 1.9-and 2.2-fold lower, respectively, in histologically confirmed inflamed ileal mucosa after adjustment for confounders (DEFA5, p,0.001; DEFA6, p = 0.001). In contrast to previous studies, we found no significant association between adefensin expression and NOD2 genotype. HD-5 protein data supports these RNA findings. The reduction in HD-5 protein expression appears due to surface epithelial cell loss and reduced Paneth cell numbers as a consequence of tissue damage. Conclusions: Reduction in a-defensin expression is independent of NOD2 status and is due to loss of surface epithelium as a consequence of inflammatory changes rather than being the inciting event prior to inflammation in ileal Crohn's disease.Crohn's disease is one of two major forms of inflammatory bowel disease (IBD), and is a chronic, debilitating disorder with increasing incidence and prevalence globally.

This is a repository copy of A global benchmark of algorithms for segmenting the left atrium from late gadolinium-enhanced cardiac magnetic resonance imaging.