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  1. Article ; Online: Flexible light-stimulated artificial synapse based on detached (In,Ga)N thin film for neuromorphic computing.

    Zhang, Qianyi / Hou, Binbin / Zhang, Jianya / Gu, Xiushuo / Huang, Yonglin / Pei, Renjun / Zhao, Yukun

    Nanotechnology

    2024  Volume 35, Issue 23

    Abstract: Because of wide range of applications, the flexible artificial synapse is an indispensable part for next-generation neural morphology computing. In this work, we demonstrate a flexible synaptic device based on a lift-off (In,Ga)N thin film successfully. ... ...

    Abstract Because of wide range of applications, the flexible artificial synapse is an indispensable part for next-generation neural morphology computing. In this work, we demonstrate a flexible synaptic device based on a lift-off (In,Ga)N thin film successfully. The synaptic device can mimic the learning, forgetting, and relearning functions of biological synapses at both flat and bent states. Furthermore, the synaptic device can simulate the transition from short-term memory to long-term memory successfully under different bending conditions. With the high flexibility, the excitatory post-synaptic current of the bent device only shows a slight decrease, leading to the high stability. Based on the experimental conductance for long-term potentiation and depression, the simulated three-layer neural network can achieve a high recognition rate up to 90.2%, indicating that the system comprising of flexible synaptic devices could have a strong learning-memory capability. Therefore, this work has a great potential for the development of wearable intelligence devices and flexible neuromorphic systems.
    MeSH term(s) Synapses ; Neural Networks, Computer ; Wearable Electronic Devices
    Language English
    Publishing date 2024-03-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 1362365-5
    ISSN 1361-6528 ; 0957-4484
    ISSN (online) 1361-6528
    ISSN 0957-4484
    DOI 10.1088/1361-6528/ad2ee3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Engineering non-conservative substrate recognition sites of extradiol dioxygenase: Computation guided design to diversify and accelerate degradation of aromatic compounds.

    Huang, Zihao / Gu, Zhenyu / Abuduwupuer, Xiemuxinuer / Qin, Deyuan / Liu, Yuchen / Guo, Zheng / Gao, Renjun

    International journal of biological macromolecules

    2024  Volume 264, Issue Pt 2, Page(s) 130739

    Abstract: Extradiol dioxygenases (EDOs) catalyzing meta-cleavage of catecholic compounds promise an effective way to detoxify aromatic pollutants. This work reported a novel scenario to engineer our recently identified Type I EDO from Tcu3516 for a broader ... ...

    Abstract Extradiol dioxygenases (EDOs) catalyzing meta-cleavage of catecholic compounds promise an effective way to detoxify aromatic pollutants. This work reported a novel scenario to engineer our recently identified Type I EDO from Tcu3516 for a broader substrate scope and enhanced activity, which was based on 2,3-dihydroxybiphenyl (2,3-DHB)-liganded molecular docking of Tcu3516 and multiple sequence alignment with other 22 Type I EDOs. 11 non-conservative residues of Tcu3516 within 6 Å distance to the 2,3-DHB ligand center were selected as potential hotspots and subjected to semi-rational design using 6 catecholic analogues as substrates; the mutants V186L and V212N returned with progressive evolution in substrate scope and catalytic activity. Both mutants were combined with D285A for construction of double mutants and final triple mutant V186L/V212N/D285A. Except for 2,3-DHB (the mutant V186L/D285A gave the best catalytic performance), the triple mutant prevailed all other 5 catecholic compounds for their degradation; affording the catalytic efficiency k
    MeSH term(s) Molecular Docking Simulation ; Oxygenases/chemistry ; Organic Chemicals ; Sequence Alignment ; Substrate Specificity
    Chemical Substances extradiol dioxygenase (EC 1.14.99.-) ; Oxygenases (EC 1.13.-) ; Organic Chemicals
    Language English
    Publishing date 2024-03-08
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 282732-3
    ISSN 1879-0003 ; 0141-8130
    ISSN (online) 1879-0003
    ISSN 0141-8130
    DOI 10.1016/j.ijbiomac.2024.130739
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Mechanisms of abnormal adult hippocampal neurogenesis in Alzheimer's disease.

    Zhou, Yujuan / Wang, Xu / Liu, Yingying / Gu, Yulu / Gu, Renjun / Zhang, Geng / Lin, Qing

    Frontiers in neuroscience

    2023  Volume 17, Page(s) 1125376

    Abstract: Alzheimer's disease (AD) is a degenerative disease of the central nervous system, the most common type of dementia in old age, which causes progressive loss of cognitive functions such as thoughts, memory, reasoning, behavioral abilities and social ... ...

    Abstract Alzheimer's disease (AD) is a degenerative disease of the central nervous system, the most common type of dementia in old age, which causes progressive loss of cognitive functions such as thoughts, memory, reasoning, behavioral abilities and social skills, affecting the daily life of patients. The dentate gyrus of the hippocampus is a key area for learning and memory functions, and an important site of adult hippocampal neurogenesis (AHN) in normal mammals. AHN mainly consists of the proliferation, differentiation, survival and maturation of newborn neurons and occurs throughout adulthood, but the level of AHN decreases with age. In AD, the AHN will be affected to different degrees at different times, and its exact molecular mechanisms are increasingly elucidated. In this review, we summarize the changes of AHN in AD and its alteration mechanism, which will help lay the foundation for further research on the pathogenesis and diagnostic and therapeutic approaches of AD.
    Language English
    Publishing date 2023-02-15
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2411902-7
    ISSN 1662-453X ; 1662-4548
    ISSN (online) 1662-453X
    ISSN 1662-4548
    DOI 10.3389/fnins.2023.1125376
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Signaling pathways of oxidative stress response: the potential therapeutic targets in gastric cancer.

    Liu, Yingying / Shi, Yu / Han, Ruiqin / Liu, Chaoge / Qin, Xiaogang / Li, Pengfei / Gu, Renjun

    Frontiers in immunology

    2023  Volume 14, Page(s) 1139589

    Abstract: Gastric cancer is one of the top causes of cancer-related death globally. Although novel treatment strategies have been developed, attempts to eradicate gastric cancer have been proven insufficient. Oxidative stress is continually produced and ... ...

    Abstract Gastric cancer is one of the top causes of cancer-related death globally. Although novel treatment strategies have been developed, attempts to eradicate gastric cancer have been proven insufficient. Oxidative stress is continually produced and continually present in the human body. Increasing evidences show that oxidative stress contributes significantly to the development of gastric cancer, either through initiation, promotion, and progression of cancer cells or causing cell death. As a result, the purpose of this article is to review the role of oxidative stress response and the subsequent signaling pathways as well as potential oxidative stress-related therapeutic targets in gastric cancer. Understanding the pathophysiology of gastric cancer and developing new therapies for gastric cancer depends on more researches focusing on the potential contributors to oxidative stress and gastric carcinogenesis.
    MeSH term(s) Humans ; Stomach Neoplasms/drug therapy ; Stomach Neoplasms/metabolism ; Oxidative Stress ; Carcinogenesis ; Signal Transduction ; Cell Death
    Language English
    Publishing date 2023-04-18
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1139589
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The role of intestinal immune cells and matrix metalloproteinases in inflammatory bowel disease.

    Mei, Kun / Chen, Zilu / Wang, Qin / Luo, Yi / Huang, Yan / Wang, Bin / Gu, Renjun

    Frontiers in immunology

    2023  Volume 13, Page(s) 1067950

    Abstract: Inflammatory bowel disease (IBD) has become globally intractable. MMPs play a key role in many inflammatory diseases. However, little is known about the role of MMPs in IBD. In this study, IBD expression profiles were screened from public Gene Expression ...

    Abstract Inflammatory bowel disease (IBD) has become globally intractable. MMPs play a key role in many inflammatory diseases. However, little is known about the role of MMPs in IBD. In this study, IBD expression profiles were screened from public Gene Expression Omnibus datasets. Functional enrichment analysis revealed that IBD-related specific functions were associated with immune pathways. Five MMPS-related disease markers, namely MMP-9, CD160, PTGDS, SLC26A8, and TLR5, were selected by machine learning and the correlation between each marker and immune cells was evaluated. We then induced colitis in C57 mice using sodium dextran sulfate and validated model construction through HE staining of the mouse colon. WB and immunofluorescence experiments confirmed that the expression levels of MMP-9, PTGDS, SLC26A8, and CD160 in colitis were significantly increased, whereas that of TLR5 were decreased. Flow cytometry analysis revealed that MMPs regulate intestinal inflammation and immunity mainly through CD8 in colitis. Our findings reveal that MMPs play a crucial role in the pathogenesis of IBD and are related to the infiltration of immune cells, suggesting that MMPs may promote the development of IBD by activating immune infiltration and the immune response. This study provides insights for further studies on the occurrence and development of IBD.
    MeSH term(s) Animals ; Mice ; Matrix Metalloproteinase 9 ; Toll-Like Receptor 5 ; Inflammatory Bowel Diseases ; Colitis ; Matrix Metalloproteinases/metabolism
    Chemical Substances Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Toll-Like Receptor 5 ; Matrix Metalloproteinases (EC 3.4.24.-)
    Language English
    Publishing date 2023-01-17
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.1067950
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Magnoflorine Ameliorates Collagen-Induced Arthritis by Suppressing the Inflammation Response via the NF-κB/MAPK Signaling Pathways.

    Wang, Lei / Li, Pengfei / Zhou, Yu / Gu, Renjun / Lu, Ge / Zhang, Chunbing

    Journal of inflammation research

    2023  Volume 16, Page(s) 2271–2296

    Abstract: Objective: Magnoflorine (Mag) has been reported to have anxiolytics, anti-cancer, and anti-inflammatory properties. In this study, we aim to investigate the effects of Mag on the rheumatoid arthritis (RA) and explore the underlying mechanism using a ... ...

    Abstract Objective: Magnoflorine (Mag) has been reported to have anxiolytics, anti-cancer, and anti-inflammatory properties. In this study, we aim to investigate the effects of Mag on the rheumatoid arthritis (RA) and explore the underlying mechanism using a collagen-induced arthritis (CIA) mouse model and a lipopolysaccharide (LPS)-stimulated macrophage inflammation model.
    Methods: The in vivo effects of Mag on CIA were studied by inducing CIA in a mouse model using DBA/1J mice followed by treatment with vehicle, methotrexate (MTX, 1 mg/kg/d), and Mag (5 mg/kg/d, 10 mg/kg/d, and 20 mg/kg/d), and the in vitro effects of Mag on macrophages were examined by stimulation of RAW264.7 cells line and peritoneal macrophages (PMs) by LPS in the presence of different concentrations of Mag. Network pharmacology and molecular docking was then performed to predict the the binding ability between Mag and its targets. Inflammatory mediators were assayed by quantitative real-time PCR and enzyme linked immunosorbent assay (ELISA). Signaling pathway changes were subsequently determined by Western blotting and immunohistochemistry (IHC).
    Results: In vivo experiments demonstrated that Mag decreased arthritis severity scores, joints destruction, and macrophages infiltration into the synovial tissues of the CIA mice. Network pharmacology analysis revealed that Mag interacted with TNF-α, IL-6, IL-1β, and MCP-1. Consistent with this, analysis of the serum, synovial tissue of the CIA mice, and the supernatant of the cultured RAW264.7 cells and PMs showed that Mag suppressed the expression of TNF-α, IL-6, IL-1β, MCP-1, iNOS, and IFN-β. Furthermore, Mag attenuated the phosphorylation of p65, IκBα, ERK, JNK, and p38 MAPKs in the synovial tissues of the CIA mice and LPS-stimulated RAW 264.7 cells.
    Conclusion: Mag may exert anti-arthritic and anti-inflammatory effects by inhibiting the activation of NF-κB and MAPK signaling pathways.
    Language English
    Publishing date 2023-05-27
    Publishing country New Zealand
    Document type Journal Article
    ZDB-ID 2494878-0
    ISSN 1178-7031
    ISSN 1178-7031
    DOI 10.2147/JIR.S406298
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  7. Article: Emerging role of substance and energy metabolism associated with neuroendocrine regulation in tumor cells.

    Liu, Yingying / Gu, Renjun / Gao, Murong / Wei, Yangwa / Shi, Yu / Wang, Xu / Gu, Yihuang / Gu, Xin / Zhang, Hongru

    Frontiers in endocrinology

    2023  Volume 14, Page(s) 1126271

    Abstract: Cancer is the second most common cause of mortality in the world. One of the unresolved difficult pathological mechanism issues in malignant tumors is the imbalance of substance and energy metabolism of tumor cells. Cells maintain life through energy ... ...

    Abstract Cancer is the second most common cause of mortality in the world. One of the unresolved difficult pathological mechanism issues in malignant tumors is the imbalance of substance and energy metabolism of tumor cells. Cells maintain life through energy metabolism, and normal cells provide energy through mitochondrial oxidative phosphorylation to generate ATP, while tumor cells demonstrate different energy metabolism. Neuroendocrine control is crucial for tumor cells' consumption of nutrients and energy. As a result, better combinatorial therapeutic approaches will be made possible by knowing the neuroendocrine regulating mechanism of how the neuroendocrine system can fuel cellular metabolism. Here, the basics of metabolic remodeling in tumor cells for nutrients and metabolites are presented, showing how the neuroendocrine system regulates substance and energy metabolic pathways to satisfy tumor cell proliferation and survival requirements. In this context, targeting neuroendocrine regulatory pathways in tumor cell metabolism can beneficially enhance or temper tumor cell metabolism and serve as promising alternatives to available treatments.
    MeSH term(s) Humans ; Energy Metabolism ; Neoplasms/metabolism ; Oxidative Phosphorylation ; Mitochondria/metabolism ; Metabolic Networks and Pathways
    Language English
    Publishing date 2023-03-27
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2023.1126271
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  8. Article: Development of an exosome-related and immune microenvironment prognostic signature in colon adenocarcinoma.

    Cui, Guoliang / Wang, Can / Liu, Jinhui / Shon, Kinyu / Gu, Renjun / Chang, Cheng / Ren, Lang / Wei, Fei / Sun, Zhiguang

    Frontiers in genetics

    2022  Volume 13, Page(s) 995644

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2022-09-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606823-0
    ISSN 1664-8021
    ISSN 1664-8021
    DOI 10.3389/fgene.2022.995644
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  9. Article ; Online: Ginseng adjuvant therapy on COVID-19: A protocol for systematic review and meta-analysis.

    Shi, Hang / Xia, Yawen / Gu, Renjun / Yu, Shuang

    Medicine

    2021  Volume 100, Issue 43, Page(s) e27586

    Abstract: Background: Corona virus disease 2019 (COVID-19) is spreading fast and it brings great pressure to the social economy. Many reports revealed that ginseng can develop immunity for respiratory disease, but there is no evidence to prove its effects on ... ...

    Abstract Background: Corona virus disease 2019 (COVID-19) is spreading fast and it brings great pressure to the social economy. Many reports revealed that ginseng can develop immunity for respiratory disease, but there is no evidence to prove its effects on COVID-19. This protocol of systematic review and meta-analysis will clarify the safety and effectiveness of ginseng adjuvant therapy on COVID-19 patients.
    Methods: Different databases (Web of Science, Cochrane Library, PubMed, Chinese Biomedical Literature Database, Chinese National Knowledge Infrastructure, Chinese Scientific Journal Database, Wan fang Database, ClinicalTrials, World Health Organization Trials, and Chinese Clinical Trial Registry) will be retrieved to search related articles according to pre-defined inclusion and exclusion criteria. Clinical recovery time and effective rates will be assessed as the primary outcomes and any changes of patient's condition will be considered as the secondary outcomes. Subgroup analysis and sensitivity analysis will be conducted to explore sources of heterogeneity. Endnote X9.3 will be used to manage data screening. The statistical analysis will be completed by RevMan5.3 and Stata/SE 15.1 software.
    Results: This study will assess the effects and safety for ginseng adjuvant therapy on COVID-19 patients.
    Conclusion: The discussion will be considered to determine whether sufficient evidence exists to prove the effects of ginseng adjuvant therapy for COVID-19 patients.
    Systematic review registration: PROSPERO (ID: CRD42021277843).
    MeSH term(s) COVID-19/therapy ; Chemotherapy, Adjuvant/methods ; Humans ; Panax ; Randomized Controlled Trials as Topic ; Research Design ; SARS-CoV-2 ; Meta-Analysis as Topic ; Systematic Review as Topic
    Language English
    Publishing date 2021-10-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80184-7
    ISSN 1536-5964 ; 0025-7974
    ISSN (online) 1536-5964
    ISSN 0025-7974
    DOI 10.1097/MD.0000000000027586
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  10. Article ; Online: Cancer-associated fibroblast-targeted nanodrugs reshape colorectal tumor microenvironments to suppress tumor proliferation, metastasis and improve drug penetration.

    Shen, Wenqi / Yao, Ping-An / Li, Wenjing / Gu, Changji / Gao, Tian / Cao, Yi / Wang, Zheng / Pei, Renjun / Xing, Chungen

    Journal of materials chemistry. B

    2023  Volume 11, Issue 9, Page(s) 1871–1880

    Abstract: Cancer-associated fibroblasts (CAFs) produce a critical tumor-promoting effect by cellular crosstalk with cancer cells and remodel the extracellular matrix (ECM) to form a protective physical barrier. The simple elimination of CAFs is not sufficient to ... ...

    Abstract Cancer-associated fibroblasts (CAFs) produce a critical tumor-promoting effect by cellular crosstalk with cancer cells and remodel the extracellular matrix (ECM) to form a protective physical barrier. The simple elimination of CAFs is not sufficient to govern the CAF-shaped aggressive tumor microenvironment (TME) because of the complexity of tumors. Herein, a CAF-targeted poly (lactic-
    MeSH term(s) Humans ; Cancer-Associated Fibroblasts/metabolism ; Cancer-Associated Fibroblasts/pathology ; Tumor Microenvironment ; Colorectal Neoplasms/pathology ; RNA, Small Interfering/pharmacology ; Cell Proliferation ; Nanoparticles/therapeutic use
    Chemical Substances RNA, Small Interfering
    Language English
    Publishing date 2023-03-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2702241-9
    ISSN 2050-7518 ; 2050-750X
    ISSN (online) 2050-7518
    ISSN 2050-750X
    DOI 10.1039/d2tb02253b
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