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Sökning: WFRF:(Zhou Junhua) > (2021)

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1.
  • He, Mingshu, et al. (författare)
  • Deep-Feature-Based Autoencoder Network for Few-Shot Malicious Traffic Detection
  • 2021
  • Ingår i: Security and Communication Networks. - : Hindawi Limited. - 1939-0114 .- 1939-0122. ; 2021
  • Tidskriftsartikel (refereegranskat)abstract
    • With the increase of Internet visits and connections, it is becoming essential and arduous to protect the networks and different devices of the Internet of Things (IoT) from malicious attacks. The intrusion detection systems (IDSs) based on supervised machine learning (ML) methods require a large number of labeled samples. However, the number of abnormal behaviors is far less than that of normal behaviors, let alone that the shots of malicious behavior samples which can be intercepted as training dataset are actually limited. Consequently, it is a key research topic to conduct the anomaly detection for the small number of abnormal behavior samples. This paper proposes an anomaly detection model with a few abnormal samples to solve the problem in few-shot detection based on convolutional neural networks (CNN) and autoencoder (AE). This model mainly consists of the CNN-based supervised pretraining module and the AE-based data reconstruction module. Only a few abnormal samples are utilized to the pretrain module to build the structure of extracting deep features. The data reconstruction module simply chooses the deep features of normal samples as training data. There also exist some effective attention mechanisms in the pretraining module. Through the pretraining of small samples, the accuracy of abnormal detection is improved compared with merely training normal samples with AE. The simulation results prove that this solution can solve the above problems occurring in network behavior anomaly detection. In comparison to the original AE model and other clustering methods, the proposed model advances the detection results in a visible way.
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2.
  • Zhou, Junhua, et al. (författare)
  • Somatic mutations of GNA11 and GNAQ in CTNNB1-mutant aldosterone-producing adenomas presenting in puberty, pregnancy or menopause
  • 2021
  • Ingår i: Nature Genetics. - : Springer Nature. - 1061-4036 .- 1546-1718. ; 53:9, s. 1360-1372
  • Tidskriftsartikel (refereegranskat)abstract
    • Sequence analysis identifies gain-of-function somatic mutations in GNA11 or GNAQ in CTNNB1-mutant aldosterone-producing adenomas. Most patients with these mutations presented during puberty, pregnancy or menopause, with elevated LHCGR expression. Most aldosterone-producing adenomas (APAs) have gain-of-function somatic mutations of ion channels or transporters. However, their frequency in aldosterone-producing cell clusters of normal adrenal gland suggests a requirement for codriver mutations in APAs. Here we identified gain-of-function mutations in both CTNNB1 and GNA11 by whole-exome sequencing of 3/41 APAs. Further sequencing of known CTNNB1-mutant APAs led to a total of 16 of 27 (59%) with a somatic p.Gln209His, p.Gln209Pro or p.Gln209Leu mutation of GNA11 or GNAQ. Solitary GNA11 mutations were found in hyperplastic zona glomerulosa adjacent to double-mutant APAs. Nine of ten patients in our UK/Irish cohort presented in puberty, pregnancy or menopause. Among multiple transcripts upregulated more than tenfold in double-mutant APAs was LHCGR, the receptor for luteinizing or pregnancy hormone (human chorionic gonadotropin). Transfections of adrenocortical cells demonstrated additive effects of GNA11 and CTNNB1 mutations on aldosterone secretion and expression of genes upregulated in double-mutant APAs. In adrenal cortex, GNA11/Q mutations appear clinically silent without a codriver mutation of CTNNB1.
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