Towards Accurate One-Stage Object Detection with AP-Loss

One-stage object detectors are trained by optimizing classification-loss and localization-loss simultaneously, with the former suffering much from extreme foreground-background class imbalance issue due to the large number of anchors. This paper alleviates this issue by proposing a novel framework to replace the classification task in one-stage detectors with a ranking task, and adopting the Average-Precision loss (AP-loss) for the ranking problem. Due to its non-differentiability and non-convexity, the AP-loss cannot be optimized directly. For this purpose, we develop a novel optimization algorithm, which seamlessly combines the error-driven update scheme in perceptron learning and backpropagation algorithm in deep networks. We verify good convergence property of the proposed algorithm theoretically and empirically. Experimental results demonstrate notable performance improvement in state-of-the-art one-stage detectors based on AP-loss over different kinds of classification-losses on various benchmarks, without changing the network architectures. Code is available at https://github.com/cccorn/AP-loss.Comment: 13 pages, 7 figures, 4 tables, main paper + supplementary material, accepted to CVPR 201

Mammalian DNA2 helicase/nuclease cleaves G-quadruplex DNA and is required for telomere integrity

Efficient and faithful replication of telomeric DNA is critical for maintaining genome integrity. The G-quadruplex (G4) structure arising in the repetitive TTAGGG sequence is thought to stall replication forks, impairing efficient telomere replication and leading to telomere instabilities. However, pathways modulating telomeric G4 are poorly understood, and it is unclear whether defects in these pathways contribute to genome instabilities in vivo. Here, we report that mammalian DNA2 helicase/nuclease recognizes and cleaves telomeric G4 in vitro. Consistent with DNA2’s role in removing G4, DNA2 deficiency in mouse cells leads to telomere replication defects, elevating the levels of fragile telomeres (FTs) and sister telomere associations (STAs). Such telomere defects are enhanced by stabilizers of G4. Moreover, DNA2 deficiency induces telomere DNA damage and chromosome segregation errors, resulting in tetraploidy and aneuploidy. Consequently, DNA2-deficient mice develop aneuploidy-associated cancers containing dysfunctional telomeres. Collectively, our genetic, cytological, and biochemical results suggest that mammalian DNA2 reduces replication stress at telomeres, thereby preserving genome stability and suppressing cancer development, and that this may involve, at least in part, nucleolytic processing of telomeric G4

Repeated Loading Model for Elastic-Plastic Contact of Geomaterial

A new nonlinear hysteretic model with considering the loading, unloading, and reloading processes is developed based on Drucker—Prager yield criterion and finite-element analysis. This model can be used for multiple repeated elastic—plastic normal direction contact problems between two identical spherical geomaterials. After examining the influence of material properties, strain hardening, and loading histories, we found that the hysteretic phenomena (represented by residual displacement and plastic work) become weak after the first cycle, and the subsequent cycles step into elastic shakedown state eventually. A critical number of cycles can be used to estimate the state of ratchetting, plastic shakedown, as well as elastic shakedown. It also found that the subsequent curves will be stiffer than the previous ones, especially when the yield strength is high and ratchetting effect is not strong. This new model can be used for a wide range of geomaterials under different loading levels, and it can also be extended to describe the constitutive behavior of spheres under earthquake as well as aftershocks

Multi-ancestry study of blood lipid levels identifies four loci interacting with physical activity.

Many genetic loci affect circulating lipid levels, but it remains unknown whether lifestyle factors, such as physical activity, modify these genetic effects. To identify lipid loci interacting with physical activity, we performed genome-wide analyses of circulating HDL cholesterol, LDL cholesterol, and triglyceride levels in up to 120,979 individuals of European, African, Asian, Hispanic, and Brazilian ancestry, with follow-up of suggestive associations in an additional 131,012 individuals. We find four loci, in/near CLASP1, LHX1, SNTA1, and CNTNAP2, that are associated with circulating lipid levels through interaction with physical activity; higher levels of physical activity enhance the HDL cholesterol-increasing effects of the CLASP1, LHX1, and SNTA1 loci and attenuate the LDL cholesterol-increasing effect of the CNTNAP2 locus. The CLASP1, LHX1, and SNTA1 regions harbor genes linked to muscle function and lipid metabolism. Our results elucidate the role of physical activity interactions in the genetic contribution to blood lipid levels