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10. adVAE: A self-adversarial variational autoencoder with Gaussian anomaly prior knowledge for anomaly detection

Author

Wang, Xuhong, Du, Ying, Lin, Shijie, Cui, Ping, Shen, Yuntian, and Yang, Yupu

Subjects
Computer Science - Machine Learning, Computer Science - Artificial Intelligence, Statistics - Machine Learning
Abstract

Recently, deep generative models have become increasingly popular in unsupervised anomaly detection. However, deep generative models aim at recovering the data distribution rather than detecting anomalies. Besides, deep generative models have the risk of overfitting training samples, which has disastrous effects on anomaly detection performance. To solve the above two problems, we propose a Self-adversarial Variational Autoencoder with a Gaussian anomaly prior assumption. We assume that both the anomalous and the normal prior distribution are Gaussian and have overlaps in the latent space. Therefore, a Gaussian transformer net T is trained to synthesize anomalous but near-normal latent variables. Keeping the original training objective of Variational Autoencoder, besides, the generator G tries to distinguish between the normal latent variables and the anomalous ones synthesized by T, and the encoder E is trained to discriminate whether the output of G is real. These new objectives we added not only give both G and E the ability to discriminate but also introduce additional regularization to prevent overfitting. Compared with the SOTA baselines, the proposed model achieves significant improvements in extensive experiments. Datasets and our model are available at a Github repository., Comment: This paper has been accepted by Knowledge-based Systems

Published
2019
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11. hBMSC-EVs alleviate weightlessness-induced skeletal muscle atrophy by suppressing oxidative stress and inflammation.

Author

Chang, Mengyuan, Liu, Ruiqi, Chen, Bingqian, Xu, Jin, Wang, Wei, Ji, Yanan, Gao, Zihui, Liu, Boya, Yao, Xinlei, Sun, Hualin, Xu, Feng, and Shen, Yuntian

Subjects
MUSCULAR atrophy, MYOSITIS, MESENCHYMAL stem cells, SIRTUINS, WESTERN immunoblotting, PROTEOLYSIS, AUTOPHAGY, HINDLIMB, SOLEUS muscle
Abstract

Background: Muscle disuse and offloading in microgravity are likely the primary factors mediating spaceflight-induced muscle atrophy, for which there is currently no effective treatment other than exercise. Extracellular vesicles derived from bone marrow mesenchymal stem cells (BMSC-EVs) possess anti-inflammatory and antioxidant properties, offering a potential strategy for combating weightless muscular atrophy. Methods: In this study, human BMSCs-EVs (hBMSC-EVs) were isolated using super-centrifugation and characterized. C2C12 myotube nutrition-deprivation and mice tail suspension models were established. Subsequently, the diameter of C2C12 myotubes, Soleus mass, cross-sectional area (CSA) of muscle fibers, and grip strength in mice were assessed to investigate the impact of hBMSC-EVs on muscle atrophy. Immunostaining, transmission electron microscopy observation, and western blot analysis were employed to assess the impact of hBMSC-EVs on muscle fiber types, ROS levels, inflammation, ubiquitin–proteasome system activity, and autophagy lysosome pathway activation in skeletal muscle atrophy. Results: The active hBMSC-EVs can be internalized by C2C12 myotubes and skeletal muscle. hBMSC-EVs can effectively reduce C2C12 myotube atrophy caused by nutritional deprivation, with a concentration of 10 × 108 particles/mL showing the best effect (P < 0.001). Additionally, hBMSC-EVs can down-regulate the protein levels associated with UPS and oxidative stress. Moreover, intravenous administration of hBMSC-EVs at a concentration of 1 × 1010 particles/mL can effectively reverse the reduction in soleus mass (P < 0.001), CSA (P < 0.01), and grip strength (P < 0.001) in mice caused by weightlessness. They demonstrate the ability to inhibit protein degradation mediated by UPS and autophagy lysosome pathway, along with the suppression of oxidative stress and inflammatory responses. Furthermore, hBMSC-EVs impede the transition of slow muscle fibers to fast muscle fibers via upregulation of Sirt1 and PGC-1α protein levels. Conclusions: Our findings indicate that hBMSC-EVs are capable of inhibiting excessive activation of the UPS and autophagy lysosome pathway, suppressing oxidative stress and inflammatory response, reversing muscle fiber type transformation, effectively delaying hindlimb unloading-induced muscle atrophy and enhancing muscle function. Our study has further advanced the understanding of the molecular mechanism underlying muscle atrophy in weightlessness and has demonstrated the protective effect of hBMSC-EVs on muscle atrophy. [ABSTRACT FROM AUTHOR]

Published
2025
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20. Potential Therapeutic Strategies for Skeletal Muscle Atrophy

Author

Huang, Li, primary, Li, Ming, additional, Deng, Chunyan, additional, Qiu, Jiayi, additional, Wang, Kexin, additional, Chang, Mengyuan, additional, Zhou, Songlin, additional, Gu, Yun, additional, Shen, Yuntian, additional, Wang, Wei, additional, Huang, Ziwei, additional, and Sun, Hualin, additional

Published
2022
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25. Inflammation: Roles in Skeletal Muscle Atrophy

Author

Ji, Yanan, primary, Li, Ming, additional, Chang, Mengyuan, additional, Liu, Ruiqi, additional, Qiu, Jiayi, additional, Wang, Kexin, additional, Deng, Chunyan, additional, Shen, Yuntian, additional, Zhu, Jianwei, additional, Wang, Wei, additional, Xu, Lingchi, additional, and Sun, Hualin, additional

Published
2022
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28. Additional file 2 of Anti-IgLON5 antibodies cause progressive behavioral and neuropathological changes in mice

Author

Ni, You, Feng, Yifan, Shen, Dingding, Chen, Ming, Zhu, Xiaona, Zhou, Qinming, Gao, Yining, Liu, Jun, Zhang, Qi, Shen, Yuntian, Peng, Lisheng, Zeng, Zike, Yin, Dou, Hu, Ji, and Chen, Sheng

Abstract

Additional file 2: Fig. S1. Clinical information of an anti-IgLON5 disease patient. Related to Figure 1. (A) Representative images of cell-based assays showing anti-IgLON5 antibodies in the serum from the patient but not in the serum from a healthy control. Scale bar=20μm. (B) The cranial 18F-FDG PET-MR image of the patient upon first admission. The standardized uptake value ratios (SUVR) of the left thalamus, right thalamus, and left temporal lobe are 1.12, 0.97, and 0.91, respectively. The cranial 18F-FDG PET-MR of the patient upon the second admission. The SUVRs of the bilateral thalamus and left temporal lobe are lower than they are 18 months ago (left thalamus, 0.97; right thalamus, 0.82; left temporal lobe, 0.70). (C) Immunoprecipitation results show the presence of these antibodies in patient but their absence in control serum. (D) Timeline of symptoms.

Published
2022
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29. Additional file 5 of Anti-IgLON5 antibodies cause progressive behavioral and neuropathological changes in mice

Author

Ni, You, Feng, Yifan, Shen, Dingding, Chen, Ming, Zhu, Xiaona, Zhou, Qinming, Gao, Yining, Liu, Jun, Zhang, Qi, Shen, Yuntian, Peng, Lisheng, Zeng, Zike, Yin, Dou, Hu, Ji, and Chen, Sheng

Subjects
nervous system
Abstract

Additional file 5: Fig. S4. Anti-IgLON5 antibodies reduce associated neurotransmitters. Related to Figure 6. (A) Concentration of Glu in the hippocampus of control and anti-IgLON5 IgG group (n=3 per group, t=2.822, df=4, p=0.0477, unpaired t-test). (B) Concentration of GABA in the hippocampus of control and anti-IgLON5 IgG group. (C) Concentration of NE in the hippocampus of control and anti-IgLON5 IgG group. (D) Cultures treated with anti-IgLON5 IgG showed a decrease in PSD-95. Scale bar=25μm.

Published
2022
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30. Additional file 4 of Anti-IgLON5 antibodies cause progressive behavioral and neuropathological changes in mice

Author

Ni, You, Feng, Yifan, Shen, Dingding, Chen, Ming, Zhu, Xiaona, Zhou, Qinming, Gao, Yining, Liu, Jun, Zhang, Qi, Shen, Yuntian, Peng, Lisheng, Zeng, Zike, Yin, Dou, Hu, Ji, and Chen, Sheng

Abstract

Additional file 4: Fig. S3. The lower magnification views of Fig.4 E and G. Related to Figure 4. (A) The lower magnification views of Fig.4 E and G have provided. In the representative pictures of NeuN expression in the hippocampus on day 7 (left), the black rectangles that appear at the corners of these images are areas that are not scanned by the confocal microscope. Because it is outside the target area, the analysis result is not affected. The white box area is the area we present in the results. Scale bars = 100µm.

Published
2022
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31. Additional file 6 of Anti-IgLON5 antibodies cause progressive behavioral and neuropathological changes in mice

Author

Ni, You, Feng, Yifan, Shen, Dingding, Chen, Ming, Zhu, Xiaona, Zhou, Qinming, Gao, Yining, Liu, Jun, Zhang, Qi, Shen, Yuntian, Peng, Lisheng, Zeng, Zike, Yin, Dou, Hu, Ji, and Chen, Sheng

Abstract

Additional file 6: Fig. S5. Anti-IgLON5 antibodies reduce cell surface synaptic proteins. Related to Figure 6. (A) Immunoblot analysis of NMDAR1, PSD-95, and Synaptophysin expression in brains of anti-IgLON5 IgG and control-IgG treated mice. (B) Immunoblot analysis of NMDAR1, PSD-95, and Synaptophysin expression in cultures exposed to anti-IgLON5 IgG and control-IgG. (C) QRT-PCR results of related inflammatory markers and chemokines: TGF-β, IL-6, IL-1β, TNF-α, CXCL16, CXCR6, CCL5, CCL12, CXCL13 (TGF-β: n=3 per group, t=5.739, df=4, p=0.0046, unpaired t-test; CCL5: n=3 per group, t=18.49, df=4, p

Published
2022
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32. Additional file 3 of Anti-IgLON5 antibodies cause progressive behavioral and neuropathological changes in mice

Author

Ni, You, Feng, Yifan, Shen, Dingding, Chen, Ming, Zhu, Xiaona, Zhou, Qinming, Gao, Yining, Liu, Jun, Zhang, Qi, Shen, Yuntian, Peng, Lisheng, Zeng, Zike, Yin, Dou, Hu, Ji, and Chen, Sheng

Abstract

Additional file 3: Fig. S2. Minor pathogenicity dose of anti-IgLON5 IgG and Metabolism in mice. Related to Figure 2. (A) We diluted the patient's IgG by 10-fold and 100-fold with PBS respectively (0.23mg/ml and 0.023mg/ml). The novel object recognition index of 1/10 anti-IgLON5 IgG injected mice is lower than healthy control IgG-injected mice at Day 7 (n=6 per group, p=0.0419, one-way ANOVA with Tukey’s post-hoc test). (B) In the Y-maze, there is a reduced discrimination rate in 1/10 anti-IgLON5 IgG injected mice than the other two groups at Day 7 (Control-IgG vs. 1/10 anti-IgLON5 IgG: n=6 per group, p=0.001, one-way ANOVA with Tukey’s post-hoc test; 1/10 anti-IgLON5 IgG vs. 1/100 anti-IgLON5 IgG: n=6 per group, p=0.0097, one-way ANOVA with Tukey’s post-hoc test). (C) Body weights were tested every 2 days after final injection at the same time period and recorded again 30 days after the injection (Day 8: p=0.0193, unpaired t-test; Day 15: p=0.0406, unpaired t-test). (D) Rectal body temperature was measured every 2 days after final injection and recorded again 30 days after the injection. (E) Food intake were measured once every 2 days after final injection at the same time and recorded again 30 days after the injection (Day 13: p=0.0059, unpaired t-test). (F) Water intake were measured once every 2 days after final injection at the same time and recorded again 30 days after the injection (Day 13: p=0.0208, unpaired t-test). For (C)–(F), n=6 per group. *p < 0.05, **p < 0.01, ***p < 0.001 vs control IgG group

Published
2022
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36. Potential Therapeutic Strategies for Skeletal Muscle Atrophy.

Author

Huang, Li, Li, Ming, Deng, Chunyan, Qiu, Jiayi, Wang, Kexin, Chang, Mengyuan, Zhou, Songlin, Gu, Yun, Shen, Yuntian, Wang, Wei, Huang, Ziwei, and Sun, Hualin

Subjects
MUSCULAR atrophy, SKELETAL muscle, NANOMEDICINE, LASER therapy, PROTEOLYSIS, ELECTRIC stimulation, PHOTOBIOMODULATION therapy, STEM cell treatment, EXERCISE therapy
Abstract

The maintenance of muscle homeostasis is vital for life and health. Skeletal muscle atrophy not only seriously reduces people's quality of life and increases morbidity and mortality, but also causes a huge socioeconomic burden. To date, no effective treatment has been developed for skeletal muscle atrophy owing to an incomplete understanding of its molecular mechanisms. Exercise therapy is the most effective treatment for skeletal muscle atrophy. Unfortunately, it is not suitable for all patients, such as fractured patients and bedridden patients with nerve damage. Therefore, understanding the molecular mechanism of skeletal muscle atrophy is crucial for developing new therapies for skeletal muscle atrophy. In this review, PubMed was systematically screened for articles that appeared in the past 5 years about potential therapeutic strategies for skeletal muscle atrophy. Herein, we summarize the roles of inflammation, oxidative stress, ubiquitin-proteasome system, autophagic-lysosomal pathway, caspases, and calpains in skeletal muscle atrophy and systematically expound the potential drug targets and therapeutic progress against skeletal muscle atrophy. This review focuses on current treatments and strategies for skeletal muscle atrophy, including drug treatment (active substances of traditional Chinese medicine, chemical drugs, antioxidants, enzyme and enzyme inhibitors, hormone drugs, etc.), gene therapy, stem cell and exosome therapy (muscle-derived stem cells, non-myogenic stem cells, and exosomes), cytokine therapy, physical therapy (electroacupuncture, electrical stimulation, optogenetic technology, heat therapy, and low-level laser therapy), nutrition support (protein, essential amino acids, creatine, β-hydroxy-β-methylbutyrate, and vitamin D), and other therapies (biomaterial adjuvant therapy, intestinal microbial regulation, and oxygen supplementation). Considering many treatments have been developed for skeletal muscle atrophy, we propose a combination of proper treatments for individual needs, which may yield better treatment outcomes. [ABSTRACT FROM AUTHOR]

Published
2023
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50. Cardiac arrest and resuscitation activates the hypothalamic-pituitary-adrenal axis and results in severe immunosuppression

Author

Zhao, Qiang, primary, Shen, Yuntian, additional, Li, Ran, additional, Wu, Jiangbo, additional, Lyu, Jingjun, additional, Jiang, Maorong, additional, Lu, Liping, additional, Zhu, Minghua, additional, Wang, Wei, additional, Wang, Zhuoran, additional, Liu, Qiang, additional, Hoffmann, Ulrike, additional, Karhausen, Jörn, additional, Sheng, Huaxin, additional, Zhang, Weiguo, additional, and Yang, Wei, additional

Published
2020
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