Towards Strengthening Deep Learning-based Side Channel Attacks with Mixup

In recent years, various deep learning techniques have been exploited in side channel attacks, with the anticipation of obtaining more appreciable attack results. Most of them concentrate on improving network architectures or putting forward novel algorithms, assuming that there are adequate profiling traces available to train an appropriate neural network. However, in practical scenarios, profiling traces are probably insufficient, which makes the network learn deficiently and compromises attack performance. In this paper, we investigate a kind of data augmentation technique, called mixup, and first propose to exploit it in deep-learning based side channel attacks, for the purpose of expanding the profiling set and facilitating the chances of mounting a successful attack. We perform Correlation Power Analysis for generated traces and original traces, and discover that there exists consistency between them regarding leakage information. Our experiments show that mixup is truly capable of enhancing attack performance especially for insufficient profiling traces. Specifically, when the size of the training set is decreased to 30% of the original set, mixup can significantly reduce acquired attacking traces. We test three mixup parameter values and conclude that generally all of them can bring about improvements. Besides, we compare three leakage models and unexpectedly find that least significant bit model, which is less frequently used in previous works, actually surpasses prevalent identity model and hamming weight model in terms of attack results

Effects of typhoons on surface seawater pCO(2) and air-sea CO2 fluxes in the Northern South China Sea

Author Posting. © American Geophysical Union, 2020. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research: Oceans 125(8), (2020): e2020JC016258, doi:10.1029/2020JC016258.This study assessed the effects of typhoons on sea surface pCO2 and CO2 flux in the northern South China Sea (SCS). During the passage of three major typhoons from May to August 2013, sea surface pCO2, surface seawater temperature (SST), and other meteorological parameters were continuously measured on a moored buoy. Surface water in the region was a source of CO2 to the atmosphere with large variations ranging from hours to months. SST was the primary factor controlling the variation of surface pCO2 through most of the time period. Typhoons are seen to impact surface pCO2 in three steps: first by cooling, thus decreasing surface pCO2, and then by causing vertical mixing that brings up deep, high‐CO2 water, and lastly triggering net uptake of CO2 due to the nutrients brought up in this deep water. The typhoons of this study primarily impacted air‐sea CO2 flux via increasing wind speeds. The mean CO2 flux during a typhoon ranged from 3.6 to 5.4 times the pretyphoon mean flux. The magnitude of the CO2 flux during typhoons was strongly inversely correlated with the typhoon center distance. The effect of typhoons accounted for 22% of the total CO2 flux in the study period, during which typhoons occurred only 9% of the time. It was estimated that typhoons enhanced annual CO2 efflux by 23–56% in the northern SCS during the last decade. As such, tropical cyclones may play a large and increasingly important role in controlling CO2 fluxes in a warmer and stormier ocean of the future.This study was supported by the Marine Public Welfare Project of China (Grant 200905012), the Scientific Research Fund of the Second Institute of Oceanography of China (Grant JT1502), the Global Change and Air‐Sea Interaction project of China (Grant GASI‐03‐01‐02‐02), and the National Natural Sciences Foundation of China (Grant 91128212).2021-02-0

Hybrid Representation Learning for Cognitive Diagnosis in Late-Life Depression Over 5 Years with Structural MRI

Late-life depression (LLD) is a highly prevalent mood disorder occurring in older adults and is frequently accompanied by cognitive impairment (CI). Studies have shown that LLD may increase the risk of Alzheimer's disease (AD). However, the heterogeneity of presentation of geriatric depression suggests that multiple biological mechanisms may underlie it. Current biological research on LLD progression incorporates machine learning that combines neuroimaging data with clinical observations. There are few studies on incident cognitive diagnostic outcomes in LLD based on structural MRI (sMRI). In this paper, we describe the development of a hybrid representation learning (HRL) framework for predicting cognitive diagnosis over 5 years based on T1-weighted sMRI data. Specifically, we first extract prediction-oriented MRI features via a deep neural network, and then integrate them with handcrafted MRI features via a Transformer encoder for cognitive diagnosis prediction. Two tasks are investigated in this work, including (1) identifying cognitively normal subjects with LLD and never-depressed older healthy subjects, and (2) identifying LLD subjects who developed CI (or even AD) and those who stayed cognitively normal over five years. To the best of our knowledge, this is among the first attempts to study the complex heterogeneous progression of LLD based on task-oriented and handcrafted MRI features. We validate the proposed HRL on 294 subjects with T1-weighted MRIs from two clinically harmonized studies. Experimental results suggest that the HRL outperforms several classical machine learning and state-of-the-art deep learning methods in LLD identification and prediction tasks

Longitudinal associations of concurrent falls and fear of falling with functional limitations differ by living alone or not

BackgroundFalls and fear of falling (FOF) are independent risk factors for functional limitations in older adults. However, the combined effect of falls and FOF on functional limitations and the moderating role of living alone or not is unclear. We aimed to examine (1) the independent and combined effect of falls and FOF on functional limitations in older adults and (2) whether living alone moderates these associations.MethodsWe used data from the National Health and Aging Trends Study (NHATS) and included 5,950 U.S. community-dwelling older adults aged 65 and older from Round 1 (Year 2011) and Round 2 (Year 2012). Falls and FOF were ascertained by asking participants whether they had any falls in the last year and whether they had worried about falling in the previous month at R1. Assessed functional limitations included any difficulties with mobility, self-care, or household activities at R2. Poisson regression models were used to examine the longitudinal associations of falls and FOF with functional limitations and the moderation effects of baseline living alone.ResultsOf the 5,950 participants, 16.3% had falls only; 14.3% had FOF only; 14.3% had both, and 55.1% had neither at baseline. In the adjusted model, those who experienced concurrent falls and FOF in R1 had a higher risk of functional limitations at R2 than those with neither (Mobility: Incidence risk ratio [IRR] = 1.34, 95% CI: 1.24–1.45; Self-care: IRR = 1.18, 95% CI: 1.11–1.26; Household: IRR = 1.20, 95% CI: 1.11–1.30). Moreover, living alone significantly moderated the longitudinal associations of concurrent falls and FOF with mobility activity limitations.ConclusionThe findings suggest that strategies to improve falls and FOF together could potentially help prevent functional limitations. Older adults who live with others and have falls or FOF should receive interventions to promote their mobility activities

NEDD4L facilitates granulosa cell ferroptosis by promoting GPX4 ubiquitination and degradation

Background: Polycystic ovary syndrome (PCOS) is an androgen disorder and ovarian dysfunction disease in women of reproductive age. The cell death of granulosa cells (GCs) plays an important role in the development of PCOS. However, the mechanism of GC death is still unclear. Methods: In the current study, NEDD4L was found to be elevated in PCOS GEO (Gene Expression Omnibus) databases and mouse models. The cell viability was analyzed by CCK-8 and FDA staining. The expression of ferroptosis markers was assessed by ELISA and immunofluorescence. The direct interaction of GPX4 and NEDD4L was verified by co-immunoprecipitation assay. Result: Functionally, results from CCK-8 and FDA staining demonstrated that NEDD4L inhibited the cell viability of KGN cells and NEDD4L increased the levels of iron, malonyldialdehyde, and reactive oxygen species and decreased glutathione levels. Moreover, the cell death of KGN induced by NEDD4L was blocked by ferroptosis inhibitor, suggesting that NEDD4L regulates KGN cell ferroptosis. Mechanistically, NEDD4L directly interacts with GPX4 and promotes GPX4 ubiquitination and degradation. Conclusion: Taken together, our study indicated that NEDD4L facilitates GC ferroptosis by promoting GPX4 ubiquitination and degradation and contributes to the development of PCOS

Replication of British Rheumatoid Arthritis Susceptibility Loci in Two Unrelated Chinese Population Groups

Previous genome-wide association study by WTCCC identified many susceptibility loci of common autoimmune diseases in British, including rheumatoid arthritis (RA). Because of the genetic heterogeneity of RA, it is necessary to replicate these susceptibility loci in other populations. Here, three SNPs with strong RA association signal in the British were analyzed in Han Chinese, and two SNPs (rs6457617 and rs11761231) were genotyped in the test cohort firstly. The rs6457617 was significantly associated with RA in the test cohort. The individuals bearing the homozygous genotype CC had 0.39-fold risk than these bearing the wild-type genotype TT ( = 0.004, OR 0.39, [95% CI 0.21-0.74]). And the protective effect of allele C was confirmed in another validation cohort with 1514 samples ( / = 5.9 × 10 −10 , OR 0.34, [95% CI 0.24-0.48]). The rs6457617 can be used as a tagSNP of HLA-DQA1 * 03 which encoded MHC-II chain. Since MHC restriction is important for primary T-cells in positive selection and negative selection stages, MHC protein polymorphisms may be implicated in shaping the T-cell repertoire, including the emergence of a T-cell clone involved in the inflammatory arthritis

Replication of British Rheumatoid Arthritis Susceptibility Loci in Two Unrelated Chinese Population Groups

Previous genome-wide association study by WTCCC identified many susceptibility loci of common autoimmune diseases in British, including rheumatoid arthritis (RA). Because of the genetic heterogeneity of RA, it is necessary to replicate these susceptibility loci in other populations. Here, three SNPs with strong RA association signal in the British were analyzed in Han Chinese, and two SNPs (rs6457617 and rs11761231) were genotyped in the test cohort firstly. The rs6457617 was significantly associated with RA in the test cohort. The individuals bearing the homozygous genotype CC had 0.39-fold risk than these bearing the wild-type genotype TT (P=0.004, OR 0.39, [95% CI 0.21–0.74]). And the protective effect of allele C was confirmed in another validation cohort with 1514 samples (Pgenotye CC/TT=5.9   ×  10−10, OR 0.34, [95% CI 0.24–0.48]). The rs6457617 can be used as a tagSNP of HLA-DQA1*03 which encoded MHC-II α chain. Since MHC restriction is important for primary T-cells in positive selection and negative selection stages, MHC protein polymorphisms may be implicated in shaping the T-cell repertoire, including the emergence of a T-cell clone involved in the inflammatory arthritis

Galectin-9 contributes to the pathogenesis of atopic dermatitis via T cell immunoglobulin mucin-3

BackgroundAtopic dermatitis (AD), a common type 2 inflammatory disease, is driven by T helper (TH) 2/TH22polarization and cytokines.Galectin-9 (Gal-9), via its receptor T cell immunoglobulin- and mucin-domain-containing molecule-3 (TIM-3), can promote TH2/TH22 immunity. The relevance of this in AD is largely unclear.ObjectivesTo characterize the role of TIM-3 and Gal-9 in the pathogenesis of AD and underlying mechanisms.MethodsWe assessed the expression of Gal-9 and TIM-3 in 30 AD patients, to compare them with those of 30 healthy controls (HC) and to explore possible links with disease features including AD activity (SCORAD), IgE levels, and circulating eosinophils and B cells. We also determined the effects of Gal-9 on T cells from the AD patients.ResultsOur AD patients had markedly higher levels of serum Gal-9 and circulating TIM-3-expressing TH1 and TH17 cells than HC. Gal-9 and TIM-3 were linked to high disease activity, IgE levels, and circulating eosinophils and/or B cells. The rates of circulating TIM-3-positive CD4+ cells were positively correlated with rates of TH2/TH22 cells and negatively correlated with rates of TH1/TH17 cells. Gal-9 inhibited the proliferation and induced the apoptosis of T cells in patients with AD, especially in those with severe AD.ConclusionOur findings suggest thatGal-9, via TIM-3, contributes to the pathogenesis of AD by augmenting TH2/TH22 polarization through the downregulation of TH1/TH17immunity. This makes Gal-9 and TIM-3 interesting to explore further, as possible drivers of disease and targets of novel AD treatment