Invariant Feature Learning for Generalized Long-Tailed Classification

Existing long-tailed classification (LT) methods only focus on tackling the class-wise imbalance that head classes have more samples than tail classes, but overlook the attribute-wise imbalance. In fact, even if the class is balanced, samples within each class may still be long-tailed due to the varying attributes. Note that the latter is fundamentally more ubiquitous and challenging than the former because attributes are not just implicit for most datasets, but also combinatorially complex, thus prohibitively expensive to be balanced. Therefore, we introduce a novel research problem: Generalized Long-Tailed classification (GLT), to jointly consider both kinds of imbalances. By "generalized", we mean that a GLT method should naturally solve the traditional LT, but not vice versa. Not surprisingly, we find that most class-wise LT methods degenerate in our proposed two benchmarks: ImageNet-GLT and MSCOCO-GLT. We argue that it is because they over-emphasize the adjustment of class distribution while neglecting to learn attribute-invariant features. To this end, we propose an Invariant Feature Learning (IFL) method as the first strong baseline for GLT. IFL first discovers environments with divergent intra-class distributions from the imperfect predictions and then learns invariant features across them. Promisingly, as an improved feature backbone, IFL boosts all the LT line-up: one/two-stage re-balance, augmentation, and ensemble. Codes and benchmarks are available on Github: https://github.com/KaihuaTang/Generalized-Long-Tailed-Benchmarks.pytorchComment: Accepted to ECCV 2022. Codes and benchmarks are available on Github: https://github.com/KaihuaTang/Generalized-Long-Tailed-Benchmarks.pytorc

Knockdown of Brm and Baf170, Components of Chromatin Remodeling Complex, Facilitates Reprogramming of Somatic Cells

© Copyright 2015, Mary Ann Liebert, Inc. 2015. The SWI/SNF (SWItch/Sucrose NonFermentable or BAF, Brg/Brahma-associated factors) complexes are epigenetic modifiers of chromatin structure and undergo progressive changes in subunit composition during cellular differentiation. For example, in embryonic stem cells, esBAF contains Brg1 and Baf155, while their homologs, Brm and Baf170, are present in BAF of somatic cells. In this study, we sought to determine whether Brm and Baf170 play any roles in induced pluripotent stem cell (iPSC) reprogramming by using shRNA-mediated knockdown studies in the mouse model. We found that knocking down Brm during early, mid, and late stages (days 3, 6, and 9 after initial iPSC induction) and knocking down Baf170 during late-stage (day 9) reprogramming improve the numbers of iPSC colonies formed. We further showed that inhibition of these somatic BAF components also promotes complete reprogramming of partially reprogrammed somatic cells (pre-iPSCs). Finally, we found that the expression of Brm and Baf170 during reprogramming was regulated by Jak/Stat3 activity. Taken together, these data suggest that inhibiting somatic BAF improves complete reprogramming by facilitating the activation of the pluripotency circuitry

FADE: Enabling Federated Adversarial Training on Heterogeneous Resource-Constrained Edge Devices

Federated adversarial training can effectively complement adversarial robustness into the privacy-preserving federated learning systems. However, the high demand for memory capacity and computing power makes large-scale federated adversarial training infeasible on resource-constrained edge devices. Few previous studies in federated adversarial training have tried to tackle both memory and computational constraints simultaneously. In this paper, we propose a new framework named Federated Adversarial Decoupled Learning (FADE) to enable AT on heterogeneous resource-constrained edge devices. FADE differentially decouples the entire model into small modules to fit into the resource budget of each device, and each device only needs to perform AT on a single module in each communication round. We also propose an auxiliary weight decay to alleviate objective inconsistency and achieve better accuracy-robustness balance in FADE. FADE offers theoretical guarantees for convergence and adversarial robustness, and our experimental results show that FADE can significantly reduce the consumption of memory and computing power while maintaining accuracy and robustness.Comment: Preprint versio

Transcriptome of Small Regulatory RNAs in the Development of the Zoonotic Parasite Trichinella spiralis

BACKGROUND: Trichinella spiralis is a parasite with unique features. It is a multicellular organism but with an intracellular parasitization and development stage. T. spiralis is the helminthic pathogen that causes zoonotic trichinellosis and afflicts more than 10 million people worldwide, whereas the parasite's biology, especially the developmental regulation is largely unknown. In other organisms, small non-coding RNAs, such as microRNAs (miRNA) and small interfering RNAs (siRNA) execute post-transcriptional regulation by translational repression or mRNA degradation, and a large number of miRNAs have been identified in diverse species. In T. spiralis, the profile of small non-coding RNAs and their function remains poorly understood. METHODOLOGY AND PRINCIPAL FINDINGS: Here, the transcriptional profiles of miRNA and siRNA in three developmental stages of T. spiralis in the rat host were investigated, and compared by high-throughput cDNA sequencing technique ("RNA-seq"). 5,443,641 unique sequence tags were obtained. Of these, 21 represented conserved miRNAs related to 13 previously identified metazoan miRNA families and 213 were novel miRNAs so far unique to T. spiralis. Some of these miRNAs exhibited stage-specific expression. Expression of miRNAs was confirmed in three stages of the life cycle by qRT-PCR and northern blot analysis. In addition, endogenous siRNAs (endo-siRNAs) were found mainly derived from natural antisense transcripts (NAT) and transposable elements (TE) in the parasite. CONCLUSIONS AND SIGNIFICANCE: We provide evidence for the presence of miRNAs and endo-siRNAs in T. spiralis. The miRNAs accounted for the major proportion of the small regulatory RNA population of T. spiralis, while fewer endogenous siRNAs were found. The finding of stage-specific expression patterns of the miRNAs in different developmental stages of T. spiralis suggests that miRNAs may play important roles in parasite development. Our data provide a basis for further understanding of the molecular regulation and functional evolution of miRNAs in parasitic nematodes

The anti-resection activity of the X protein encoded by Hepatitis Virus B

Chronic infection of hepatitis virus B (HBV) is associated with an increased incidence of hepatocellular carcinoma (HCC). HBV encodes an oncoprotein (HBx) that is crucial for viral replication and interferes with multiple cellular activities including gene expression, histone modifications and genomic stability. To date, it remains unclear how disruption of these activities contributes to hepatocarcinogenesis. Here, we report that HBV exhibits a novel anti‐resection activity by disrupting DNA end resection, thus impairing the initial steps of homologous recombination (HR). This anti‐resection activity occurs in primary human hepatocytes (PHHs) undergoing a natural viral infection‐replication cycle, as well as in cells with integrated HBV genomes. Among the seven HBV‐encoded proteins, we identified HBx as the sole viral factor that inhibits resection. By disrupting an evolutionarily conserved Cullin4A‐DDB1‐RING type of E3 ligase, CRL4WDR70, via its H‐box, we show that HBx inhibits H2B monoubiquitylation at lysine 120 (uH2B) at double strand breaks, thus reducing the efficiency of long‐range resection. We further show that directly impairing H2B monoubiquitylation elicited tumorigenesis upon engraftment of deficient cells in athymic mice, confirming that the impairment of CRL4WDR70 function by HBx is sufficient to promote carcinogenesis. Finally, we demonstrated that lack of H2B monoubiquitylation is manifest in human HBV‐associated HCC (HBVHCC) when compared with HBV‐free HCC, implying corresponding defects of epigenetic regulation and end resection. We conclude that the anti‐resection activity of HBx induces an HR defect and genome instability and contributes to tumorigenesis of host hepatocytes