CNS-Net: Conservative Novelty Synthesizing Network for Malware Recognition in an Open-set Scenario

We study the challenging task of malware recognition on both known and novel unknown malware families, called malware open-set recognition (MOSR). Previous works usually assume the malware families are known to the classifier in a close-set scenario, i.e., testing families are the subset or at most identical to training families. However, novel unknown malware families frequently emerge in real-world applications, and as such, require to recognize malware instances in an open-set scenario, i.e., some unknown families are also included in the test-set, which has been rarely and non-thoroughly investigated in the cyber-security domain. One practical solution for MOSR may consider jointly classifying known and detecting unknown malware families by a single classifier (e.g., neural network) from the variance of the predicted probability distribution on known families. However, conventional well-trained classifiers usually tend to obtain overly high recognition probabilities in the outputs, especially when the instance feature distributions are similar to each other, e.g., unknown v.s. known malware families, and thus dramatically degrades the recognition on novel unknown malware families. In this paper, we propose a novel model that can conservatively synthesize malware instances to mimic unknown malware families and support a more robust training of the classifier. Moreover, we also build a new large-scale malware dataset, named MAL-100, to fill the gap of lacking large open-set malware benchmark dataset. Experimental results on two widely used malware datasets and our MAL-100 demonstrate the effectiveness of our model compared with other representative methods.Comment: 16 pages, 8 figure

De novo transcriptome sequencing and comprehensive analysis of the drought-responsive genes in the desert plant Cynanchum komarovii

The figure of an agarose gel with PCR products. (TIFF 11899 kb

De novo sequencing and comparative transcriptome analysis of white petals and red labella in Phalaenopsis for discovery of genes related to flower color and floral differentation

Phalaenopsis is one of the world’s most popular and important epiphytic monopodial orchids. The extraordinary floral diversity of Phalaenopsis is a reflection of its evolutionary success. As a consequence of this diversity, and of the complexity of flower color development in Phalaenopsis, this species is a valuable research material for developmental biology studies. Nevertheless, research on the molecular mechanisms underlying flower color and floral organ formation in Phalaenopsis is still in the early phases. In this study, we generated large amounts of data from Phalaenopsis flowers by combining Illumina sequencing with differentially expressed gene (DEG) analysis. We obtained 37 723 and 34 020 unigenes from petals and labella, respectively. A total of 2736 DEGs were identified, and the functions of many DEGs were annotated by BLAST-searching against several public databases. We mapped 837 up-regulated DEGs (432 from petals and 405 from labella) to 102 Kyoto Encyclopedia of Genes and Genomes pathways. Almost all pathways were represented in both petals (102 pathways) and labella (99 pathways). DEGs involved in energy metabolism were significantly differentially distributed between labella and petals, and various DEGs related to flower color and floral differentiation were found in the two organs. Interestingly, we also identified genes encoding several key enzymes involved in carotenoid synthesis. These genes were differentially expressed between petals and labella, suggesting that carotenoids may influence Phalaenopsis flower color. We thus conclude that a combination of anthocyanins and/or carotenoids determine flower color formation in Phalaenopsis. These results broaden our understanding of the mechanisms controlling flower color and floral organ differentiation in Phalaenopsis and other orchids

Roles of circRNA dysregulation in esophageal squamous cell carcinoma tumor microenvironment

Esophageal squamous cell carcinoma (ESCC) is the most prevalent histological esophageal cancer characterized by advanced diagnosis, metastasis, resistance to treatment, and frequent recurrence. In recent years, numerous human disorders such as ESCC, have been linked to abnormal expression of circular RNAs (circRNAs), suggesting that they are fundamental to the intricate system of gene regulation that governs ESCC formation. The tumor microenvironment (TME), referring to the area surrounding the tumor cells, is composed of multiple components, including stromal cells, immune cells, the vascular system, extracellular matrix (ECM), and numerous signaling molecules. In this review, we briefly described the biological purposes and mechanisms of aberrant circRNA expression in the TME of ESCC, including the immune microenvironment, angiogenesis, epithelial-to-mesenchymal transition, hypoxia, metabolism, and radiotherapy resistance. As in-depth research into the processes of circRNAs in the TME of ESCC continues, circRNAs are promising therapeutic targets or delivery systems for cancer therapy and diagnostic and prognostic indicators for ESCC

De novo sequencing and comparative transcriptome analysis of white petals and red labella in Phalaenopsis for discovery of genes related to flower color and floral differentation

Phalaenopsis is one of the world’s most popular and important epiphytic monopodial orchids. The extraordinary floral diversity of Phalaenopsis is a reflection of its evolutionary success. As a consequence of this diversity, and of the complexity of flower color development in Phalaenopsis, this species is a valuable research material for developmental biology studies. Nevertheless, research on the molecular mechanisms underlying flower color and floral organ formation in Phalaenopsis is still in the early phases. In this study, we generated large amounts of data from Phalaenopsis flowers by combining Illumina sequencing with differentially expressed gene (DEG) analysis. We obtained 37 723 and 34 020 unigenes from petals and labella, respectively. A total of 2736 DEGs were identified, and the functions of many DEGs were annotated by BLAST-searching against several public databases. We mapped 837 up-regulated DEGs (432 from petals and 405 from labella) to 102 Kyoto Encyclopedia of Genes and Genomes pathways. Almost all pathways were represented in both petals (102 pathways) and labella (99 pathways). DEGs involved in energy metabolism were significantly differentially distributed between labella and petals, and various DEGs related to flower color and floral differentiation were found in the two organs. Interestingly, we also identified genes encoding several key enzymes involved in carotenoid synthesis. These genes were differentially expressed between petals and labella, suggesting that carotenoids may influence Phalaenopsis flower color. We thus conclude that a combination of anthocyanins and/or carotenoids determine flower color formation in Phalaenopsis. These results broaden our understanding of the mechanisms controlling flower color and floral organ differentiation in Phalaenopsis and other orchids

The identities of insulin signaling pathway are affected by overexpression of Tau and its phosphorylation form

IntroductionHyperphosphorylated Tau formed neurofibrillary tangles was one of the major neuropathological hallmarks of Alzheimer’s disease (AD). Dysfunctional insulin signaling in brain is involved in AD. However, the effect of Tau pathology on brain insulin resistance remains unclear. This study explored the effects of overexpressing wild-type Tau (WTau) or Tau with pseudo-phosphorylation at AT8 residues (PTau) on the insulin signaling pathway (ISP).Methods293T cells or SY5Y cells overexpressing WTau or PTau were treated with or without insulin. The elements in ISP or the regulators of IPS were analyzed by immunoblotting, immunofluorescent staining and co-immunoprecipitation. Akt inhibitor MK2206 was used for evaluating the insulin signaling to downstream of mTOR in Tau overexpressing cells. The effects of anti-aging drug lonafarnib on ISP in WTau or PTau cells were also analyzed with immunoblotting. Considering lonafarnib is an inhibitor of FTase, the states of Rhes, one of FTase substrate in WTau or PTau cells were analyzed by drug affinity responsive target stability (DARTS) assay and the cellular thermal shift assay (CETSA).ResultsWTau or PTau overexpression in cells upregulated basal activity of elements in ISP in general. However, overexpression of WTau or PTau suppressed the ISP signaling transmission responses induced by insulin simulation, appearing relative higher response of IRS-1 phosphorylation at tyrosine 612 (IRS-1 p612) in upstream IPS, but a lower phosphorylation response of downstream IPS including mTOR, and its targets 4EPB1 and S6. This dysregulation of insulin evoked signaling transmission was more obvious in PTau cells. Suppressing Akt with MK2206 could compromise the levels of p-S6 and p-mTOR in WTau or PTau cells. Moreover, the changes of phosphatases detected in WTau and PTau cells may be related to ISP dysfunction. In addition, the effects of lonafarnib on the ISP in SY5Y cells with WTau and PTau overexpression were tested, which showed that lonafarnib treatment resulted in reducing the active levels of ISP elements in PTau cells but not in WTau cells. The differential effects are probably due to Tau phosphorylation modulating lonafarnib-induced alterations in Rhes, as revealed by DARTS assay.Conclusion and discussionOverexpression of Tau or Tau with pseudo-phosphorylation at AT8 residues could cause an upregulation of the basal/tonic ISP, but a suppression of insulin induced the phasic activation of ISP. This dysfunction of ISP was more obvious in cells overexpressing pseudo-phosphorylated Tau. These results implied that the dysfunction of ISP caused by Tau overexpression might impair the physiological fluctuation of neuronal functions in AD. The different effects of lonafarnib on ISP between WTau and PTau cells, indicating that Tau phosphorylation mediates an additional effect on ISP. This study provided a potential linkage of abnormal expression and phosphorylation of Tau to the ISP dysfunction in AD