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学者姓名：陈菲
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Abstract ：
Aggregation of aberrant proteins is a common pathological hallmark in neurodegeneration such as polyglutamine (polyQ) and other repeat-expansion diseases. Here through overexpression of ataxin3 C-terminal polyQ expansion in Drosophila gut enterocytes, we generated an intestinal obstruction model of spinocerebellar ataxia type3 (SCA3) and reported a new role of nuclear-associated endosomes (NAEs)-the delivery of polyQ to the nucleoplasm. In this model, accompanied by the prominently increased RAB5-positive NAEs are abundant nucleoplasmic reticulum enriched with polyQ, abnormal nuclear envelope invagination, significantly reduced endoplasmic reticulum, indicating dysfunctional nucleocytoplasmic trafficking and impaired endomembrane organization. Consistently, Rab5 but not Rab7 RNAi further decreased polyQ-related NAEs, inhibited endomembrane disorganization, and alleviated disease model. Interestingly, autophagic proteins were enriched in polyQ-related NAEs and played non-canonical autophagic roles as genetic manipulation of autophagic molecules exhibited differential impacts on NAEs and SCA3 toxicity. Namely, the down-regulation of Atg1 or Atg12 mitigated while Atg5 RNAi aggravated the disease phenotypes both in Drosophila intestines and compound eyes. Our findings, therefore, provide new mechanistic insights and underscore the fundamental roles of endosome-centered nucleocytoplasmic trafficking and homeostatic endomembrane allocation in the pathogenesis of polyQ diseases.
Keyword ：
Autophagy Autophagy Endosome Endosome Inclusion body Inclusion body Non-canonical role of ATG Non-canonical role of ATG Nucleocytoplasmic trafficking Nucleocytoplasmic trafficking Spinocerebellar ataxia Spinocerebellar ataxia
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| GB/T 7714 | Nan, Yuyu , Chen, Wenfeng , Chen, Fei et al. Endosome mediated nucleocytoplasmic trafficking and endomembrane allocation is crucial to polyglutamine toxicity [J]. | CELL BIOLOGY AND TOXICOLOGY , 2024 , 40 (1) . |
| MLA | Nan, Yuyu et al. "Endosome mediated nucleocytoplasmic trafficking and endomembrane allocation is crucial to polyglutamine toxicity" . | CELL BIOLOGY AND TOXICOLOGY 40 . 1 (2024) . |
| APA | Nan, Yuyu , Chen, Wenfeng , Chen, Fei , Wei, Lili , Zeng, Aiyuan , Lin, Xiaohui et al. Endosome mediated nucleocytoplasmic trafficking and endomembrane allocation is crucial to polyglutamine toxicity . | CELL BIOLOGY AND TOXICOLOGY , 2024 , 40 (1) . |
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Objective We aimed to establish an artificial intelligence (AI) model to identify parathyroid glands during endoscopic approaches and compare it with senior and junior surgeons' visual estimation. Methods A total of 1,700 images of parathyroid glands from 166 endoscopic thyroidectomy videos were labeled. Data from 20 additional full-length videos were used as an independent external cohort. The YOLO V3, Faster R-CNN, and Cascade algorithms were used for deep learning, and the optimal algorithm was selected for independent external cohort analysis. Finally, the identification rate, initial recognition time, and tracking periods of PTAIR (Artificial Intelligence model for Parathyroid gland Recognition), junior surgeons, and senior surgeons were compared. Results The Faster R-CNN algorithm showed the best balance after optimizing the hyperparameters of each algorithm and was updated as PTAIR. The precision, recall rate, and F1 score of the PTAIR were 88.7%, 92.3%, and 90.5%, respectively. In the independent external cohort, the parathyroid identification rates of PTAIR, senior surgeons, and junior surgeons were 96.9%, 87.5%, and 71.9%, respectively. In addition, PTAIR recognized parathyroid glands 3.83 s ahead of the senior surgeons (p = 0.008), with a tracking period 62.82 s longer than the senior surgeons (p = 0.006). Conclusions PTAIR can achieve earlier identification and full-time tracing under a particular training strategy. The identification rate of PTAIR is higher than that of junior surgeons and similar to that of senior surgeons. Such systems may have utility in improving surgical outcomes and also in accelerating the education of junior surgeons. Level of Evidence 3 Laryngoscope, 2022
Keyword ：
artificial intelligence artificial intelligence deep learning deep learning endoscopy endoscopy parathyroid parathyroid thyroidectomy thyroidectomy
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| GB/T 7714 | Wang, Bo , Zheng, Jing , Yu, Jia-Fan et al. Development of Artificial Intelligence for Parathyroid Recognition During Endoscopic Thyroid Surgery [J]. | LARYNGOSCOPE , 2022 , 132 (12) : 2516-2523 . |
| MLA | Wang, Bo et al. "Development of Artificial Intelligence for Parathyroid Recognition During Endoscopic Thyroid Surgery" . | LARYNGOSCOPE 132 . 12 (2022) : 2516-2523 . |
| APA | Wang, Bo , Zheng, Jing , Yu, Jia-Fan , Lin, Si-Ying , Yan, Shou-Yi , Zhang, Li-Yong et al. Development of Artificial Intelligence for Parathyroid Recognition During Endoscopic Thyroid Surgery . | LARYNGOSCOPE , 2022 , 132 (12) , 2516-2523 . |
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Biological pattern formation ensures that tissues and organs develop in the correct place and orientation within the body. A great deal has been learned about cell and tissue staining techniques, and today's microscopes can capture digital images. A light microscope is an essential tool in biology and medicine. Analyzing the generated images will involve the creation of unique analytical techniques. Digital images of the material before and after deformation can be compared to assess how much strain and displacement the material responds. Furthermore, this article proposes Development Biology Patterns using Digital Image Technology (DBP-DIT) to cell image data in 2D, 3D, and time sequences. Engineered materials with high stiffness may now be characterized via digital image correlation. The proposed method of analyzing the mechanical characteristics of skin under various situations, such as one direction of stress and temperatures in the hundreds of degrees Celsius, is achievable using digital image correlation. A DBP-DIT approach to biological tissue modeling is based on digital image correlation (DIC) measurements to forecast the displacement field under unknown loading scenarios without presupposing a particular constitutive model form or owning knowledge of the material microstructure. A data-driven approach to modeling biological materials can be more successful than classical constitutive modeling if adequate data coverage and advice from partial physics constraints are available. The proposed procedures include a wide range of biological objectives, experimental designs, and laboratory preferences. The experimental results show that the proposed DBP-DIT achieves a high accuracy ratio of 99,3%, a sensitivity ratio of 98.7%, a specificity ratio of 98.6%, a probability index of 97.8%, a balanced classification ratio of 97.5%, and a low error rate of 38.6%.
Keyword ：
biology patterns biology patterns data-driven data-driven digital image correlation digital image correlation medicine medicine microscopes microscopes
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| GB/T 7714 | Ni, Shiwei , Chen, Fei , Chen, Guolong et al. Mathematical model and genomics construction of developmental biology patterns using digital image technology [J]. | FRONTIERS IN GENETICS , 2022 , 13 . |
| MLA | Ni, Shiwei et al. "Mathematical model and genomics construction of developmental biology patterns using digital image technology" . | FRONTIERS IN GENETICS 13 (2022) . |
| APA | Ni, Shiwei , Chen, Fei , Chen, Guolong , Yang, Yufeng . Mathematical model and genomics construction of developmental biology patterns using digital image technology . | FRONTIERS IN GENETICS , 2022 , 13 . |
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Background: Alzheimer's disease (AD) is a common cause of dementia among elderly people. Hyperphosphorylation and aggregation of tau correlates with the clinical progression of AD; therefore, therapies targeting the aggregation of tau may have potential applications for anti-AD drug development. Several inhibitors of tau aggregation, including small molecules and antibodies, have been found to decrease the aggregation of tau and the corresponding pathology. Objective: To screen one kind of single-chain variable fragment (scFv) antibody which could inhibit the aggregation of tau and ameliorate its cytotoxicity. Methods/Results: Using phosphorylated tau (pTau) as an antigen, we obtained a scFv antibody via the screening of a high-capacity phage antibody library. Biochemical analysis revealed that this scFv antibody (scFv T1) had a strong ability to inhibit pTau aggregation both in dilute solutions and under conditions of macromolecular crowding. ScFv T1 could also depolymerize preformed pTau aggregates in vitro. Furthermore, scFv T1 was found to be able to inhibit the cytotoxicity of extracellular pTau aggregates and ameliorate tau-mediated toxicity when coexpressed with a hTauR406W mutant in the eye of transgenic Drosophila flies. Conclusion: This scFv T1 antibody may be a potential new therapeutic agent against AD. Our methods can be used to develop novel strategies against protein aggregation for the treatment of neurodegenerative diseases.
Keyword ：
Aggregation Aggregation Alzheimer's disease Alzheimer's disease Drosophila Drosophila single-chain variable fragment antibody single-chain variable fragment antibody tau tau tauopathy tauopathy toxicity toxicity
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| GB/T 7714 | Li, Sen , Yi, Yushan , Cui, Ke et al. A Single-Chain Variable Fragment Antibody Inhibits Aggregation of Phosphorylated Tau and Ameliorates Tau Toxicity in vitro and in vivo [J]. | JOURNAL OF ALZHEIMERS DISEASE , 2021 , 79 (4) : 1613-1629 . |
| MLA | Li, Sen et al. "A Single-Chain Variable Fragment Antibody Inhibits Aggregation of Phosphorylated Tau and Ameliorates Tau Toxicity in vitro and in vivo" . | JOURNAL OF ALZHEIMERS DISEASE 79 . 4 (2021) : 1613-1629 . |
| APA | Li, Sen , Yi, Yushan , Cui, Ke , Zhang, Yanqiu , Chen, Yange , Han, Dou et al. A Single-Chain Variable Fragment Antibody Inhibits Aggregation of Phosphorylated Tau and Ameliorates Tau Toxicity in vitro and in vivo . | JOURNAL OF ALZHEIMERS DISEASE , 2021 , 79 (4) , 1613-1629 . |
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Reactive oxygen species (ROS) contribute to cellular redox environment and serve as signaling molecules. Excessive ROS can lead to oxidative stress that are involved in a broad spectrum of physiological and pathological conditions. Stem cells have unique ROS regulation while cancer cells frequently show a constitutive oxidative stress that is associated with the invasive phenotype. Antioxidants have been proposed to forestall tumor progression while targeted oxidants have been used to destroy tumor cells. However, the delicate beneficial range of ROS levels for stem cells and tumor cells under distinct contexts remains elusive. Here, we used Drosophila midgut intestinal stem cell (ISCs) as an in vivo model system to tackle this question. The ROS levels of ISCs remained low in comparison to that of differentiated cells and increased with ageing, which was accompanied by elevated proliferation of ISCs in aged Drosophila. Neither upregulation nor downregulation of ROS levels significantly affected ISCs, implicating an intrinsic homeostatic range of ROS in ISCs. Interestingly, we observed similar moderately elevated ROS levels in both tumor-like ISCs induced by Notch (N) depletion and extracellular matrix (ECM)-deprived ISCs induced by p-integrin (mys) depletion. Elevated ROS levels further promoted the proliferation of tumor-like ISCs while reduced ROS levels suppressed the hyperproliferation phenotype; on the other hand, further increased ROS facilitated the survival of ECM-deprived ISCs while reduced ROS exacerbated the loss of ECM-deprived ISCs. However, N- and mys-depleted ISCs, which resembled metastatic tumor cells, harbored even higher ROS levels and were subjected to more severe cell loss, which could be partially prevented by ectopic supply of antioxidant enzymes, implicating a delicate pro-surviving and proliferating range of ROS levels for ISCs. Taken together, our results revealed stem cells can differentially respond to distinct ROS levels under various conditions and suggested that the antioxidant-based intervention of stem cells and tumors should be formulated with caution according to the specific situations.
Keyword ：
Drosophila Drosophila Integrin Integrin Intestinal stem cell Intestinal stem cell Notch Notch Reactive oxygen species Reactive oxygen species Tumor Tumor
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| GB/T 7714 | Chen, Fei , Su, Run , Ni, Shiwei et al. Context-dependent responses of Drosophila intestinal stem cells to intracellular reactive oxygen species [J]. | REDOX BIOLOGY , 2021 , 39 . |
| MLA | Chen, Fei et al. "Context-dependent responses of Drosophila intestinal stem cells to intracellular reactive oxygen species" . | REDOX BIOLOGY 39 (2021) . |
| APA | Chen, Fei , Su, Run , Ni, Shiwei , Liu, Yan , Huang, Jiexiang , Li, Gege et al. Context-dependent responses of Drosophila intestinal stem cells to intracellular reactive oxygen species . | REDOX BIOLOGY , 2021 , 39 . |
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How complex interactions of genetic, environmental factors and aging jointly contribute to dopaminergic degeneration in Parkinson's disease (PD) is largely unclear. Here, we applied frequent gene co-expression analysis on human patientsubstantia nigra-specific microarray datasets to identify potential novel disease-related genes. In vivoDrosophilastudies validated two of 32 candidate genes, a chromatin-remodeling factor SMARCA4 and a biliverdin reductase BLVRA. Inhibition of SMARCA4 was able to prevent aging-dependent dopaminergic degeneration not only caused by overexpression of BLVRA but also in four most commonDrosophilaPD models. Furthermore, down-regulation of SMARCA4 specifically in the dopaminergic neurons prevented shortening of life span caused by alpha-synuclein and LRRK2. Mechanistically, aberrant SMARCA4 and BLVRA converged on elevated ERK-ETS activity, attenuation of which by either genetic or pharmacological manipulation effectively suppressed dopaminergic degeneration inDrosophilain vivo. Down-regulation of SMARCA4 or drug inhibition of MEK/ERK also mitigated mitochondrial defects inPINK1(a PD-associated gene)-deficient human cells. Our findings underscore the important role of epigenetic regulators and implicate a common signaling axis for therapeutic intervention in normal aging and a broad range of age-related disorders including PD.
Keyword ：
aging aging Brahma Brahma Drosophila Drosophila MAPK-ERK-ETS signaling MAPK-ERK-ETS signaling neurodegeneration neurodegeneration Parkinson's disease Parkinson's disease SMARCA4 SMARCA4
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| GB/T 7714 | Sun, Ling , Zhang, Jie , Chen, Wenfeng et al. Attenuation of epigenetic regulator SMARCA4 and ERK-ETS signaling suppresses aging-related dopaminergic degeneration [J]. | AGING CELL , 2020 , 19 (9) . |
| MLA | Sun, Ling et al. "Attenuation of epigenetic regulator SMARCA4 and ERK-ETS signaling suppresses aging-related dopaminergic degeneration" . | AGING CELL 19 . 9 (2020) . |
| APA | Sun, Ling , Zhang, Jie , Chen, Wenfeng , Chen, Yun , Zhang, Xiaohui , Yang, Mingjuan et al. Attenuation of epigenetic regulator SMARCA4 and ERK-ETS signaling suppresses aging-related dopaminergic degeneration . | AGING CELL , 2020 , 19 (9) . |
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Aberrant mitophagy has been implicated in a broad spectrum of disorders. PINK1, Parkin, and ubiquitin have pivotal roles in priming mitophagy. However, the entire regulatory landscape and the precise control mechanisms of mitophagy remain to be elucidated. Here, we uncover fundamental mitophagy regulation involving PINK1 and a non-canonical role of the mitochondrial Tu translation elongation factor (TUFm). The mitochondrion-cytosol dual-localized TUFm interacts with PINK1 biochemically and genetically, which is an evolutionarily conserved Parkin-independent route toward mitophagy. A PINK1-dependent TUFm phosphoswitch at Ser222 determines conversion from activating to suppressing mitophagy. PINK1 modulates differential translocation of TUFm because p-S222-TUFm is restricted predominantly to the cytosol, where it inhibits-mitophagy by impeding Atg5-Atg12 formation. The self-antagonizing feature of PINK1/TUFm is critical for the robustness of mitophagy regulation, achieved by the unique kinetic parameters of p-S222-TUFm, p-S65-ubiquitin, and their common kinase PINK1. Our findings provide new mechanistic insights into mitophagy and mitophagy-associated disorders.
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| GB/T 7714 | Lin, Jingjing , Chen, Kai , Chen, Wenfeng et al. Paradoxical Mitophagy Regulation by PINK1 and TUFm [J]. | MOLECULAR CELL , 2020 , 80 (4) : 607-, . |
| MLA | Lin, Jingjing et al. "Paradoxical Mitophagy Regulation by PINK1 and TUFm" . | MOLECULAR CELL 80 . 4 (2020) : 607-, . |
| APA | Lin, Jingjing , Chen, Kai , Chen, Wenfeng , Yao, Yizhou , Ni, Shiwei , Ye, Meina et al. Paradoxical Mitophagy Regulation by PINK1 and TUFm . | MOLECULAR CELL , 2020 , 80 (4) , 607-, . |
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MicroRNAs (miRNAs) are post-transcriptional regulators of gene expression that target mRNAs for translational repression or cleavage. The present study was conducted to identify differentially expressed miRNAs in primary tumor tissues of rectal carcinoma (RC) that may be associated with heterochrony hepatic metastasis (HHM). Samples were collected exclusively from patients with RC but not colon cancer (CC); Next-generation high-throughput sequencing technology and bioinformatics tools were used to profile and analyze small RNAs and their corresponding targets in primary tumor tissues with HHM (n=2) or without metastases (non-metastatic, NM; n=2). A total of 24 known miRNAs were identified to be differentially expressed (P< 0.01; absolute value of log(2)-fold change >= 1). Hsa-let-7e-5p exhibited the most significant elevation in tissues with HHM (log(2)-fold change=2.62). By combining online informatics resources and previous mRNA sequencing data, it was identified that 54 validated target genes of let-7e were downregulated in primary tumor tissues with HHM. A number of these target genes have been demonstrated to be directly involved in tumor metastasis (including MYC proto-oncogene, bHLH transcription factor, high-mobility group AT-Hook 2, peptidase inhibitor 3, KIT proto-oncogene receptor tyrosine kinase, Jun proto-oncogene, AP-1 transcription factor subunit and ribonuclease T2), or have physiological associations to immunity (including C-C motif chemokine receptor 4 and cluster of differentiation 40 ligand) and cellular metabolism (including peroxisome proliferator-activated receptor gamma, coactivator 1 alpha). Next, 14 target genes were selected for reverse transcription-quantitative polymerase chain reaction analysis in non-sequenced samples, and the downregulation of 10 target genes in RC samples with HHM was confirmed. In addition, it was demonstrated that hsa-let-7e-5p stimulated colorectal cancer cell migration in vitro. The miRNA hsa-let-7e-5p may serve as a potential biomarker for rectal carcinoma-associated HHM, facilitating the identification of patients with RC who are at risk of developing HHM.
Keyword ：
heterochrony hepatic metastasis heterochrony hepatic metastasis microRNA hsa-let-7e-5p microRNA hsa-let-7e-5p next-generation sequencing next-generation sequencing rectal carcinoma rectal carcinoma
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| GB/T 7714 | Chen, Wenfeng , Lin, Guosheng , Yao, Yizhou et al. MicroRNA hsa-let-7e-5p as a potential prognosis marker for rectal carcinoma with liver metastases [J]. | ONCOLOGY LETTERS , 2018 , 15 (5) : 6913-6924 . |
| MLA | Chen, Wenfeng et al. "MicroRNA hsa-let-7e-5p as a potential prognosis marker for rectal carcinoma with liver metastases" . | ONCOLOGY LETTERS 15 . 5 (2018) : 6913-6924 . |
| APA | Chen, Wenfeng , Lin, Guosheng , Yao, Yizhou , Chen, Jishen , Shui, Hanli , Yang, Qinghai et al. MicroRNA hsa-let-7e-5p as a potential prognosis marker for rectal carcinoma with liver metastases . | ONCOLOGY LETTERS , 2018 , 15 (5) , 6913-6924 . |
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Mitophagy is the selective degradation of mitochondria by autophagy, which is an important mitochondrial quality and quantity control process. During Drosophila metamorphosis, the degradation of midgut involves a large change in length and organization, which is mediated by autophagy. Here we noticed a cell-type specific mitochondria] clearance process that occurs in enterocytes (ECs), while most mitochondria remain in intestinal stem cells (ISCs) during metamorphosis. Although PINK]/PARKIN represent the canonical pathway for the elimination of impaired mitochondria in varied pathological conditions, their roles in developmental processes or normal physiological conditions have been less studied. To examine the potential contribution of PINK1 in developmental processes, we monitored the dynamic expression pattern of PINKI in the midgut development by taking advantage of a newly CRISPR/Cas9 generated knock-in fly strain expressing PINK1-mCherry fusion protein that presumably recapitulates the endogenous expression pattern of PINK1. We disclosed a spatiotemporal correlation between the expression pattern of PINKI and the mitochondrial clearance or persistence in ECs or ISCs respectively. By mosaic genetic analysis, we then demonstrated that PINK1 and PARKIN function epistatically to mediate the specific timely removal of mitochondria, and are involved in global autophagy in ECs during Drosophila midgut metamorphosis, with kinase-dead PINKI exerting dominant negative effects. Taken together, our studies concluded that the PINK1/PARKIN is crucial for timely cell-type specific mitophagy under physiological conditions and demonstrated again that Drosophila midgut metamorphosis might serve as an elegant in vivo model to study autophagy. (C) 2016 Elsevier Inc. All rights reserved.
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| GB/T 7714 | Liu, Yan , Lin, Jingjing , Zhang, Minjie et al. PINK1 is required for timely cell-type specific mitochondrial clearance during Drosophila midgut metamorphosis [J]. | DEVELOPMENTAL BIOLOGY , 2016 , 419 (2) : 357-372 . |
| MLA | Liu, Yan et al. "PINK1 is required for timely cell-type specific mitochondrial clearance during Drosophila midgut metamorphosis" . | DEVELOPMENTAL BIOLOGY 419 . 2 (2016) : 357-372 . |
| APA | Liu, Yan , Lin, Jingjing , Zhang, Minjie , Chen, Kai , Yang, Shengxi , Wang, Qun et al. PINK1 is required for timely cell-type specific mitochondrial clearance during Drosophila midgut metamorphosis . | DEVELOPMENTAL BIOLOGY , 2016 , 419 (2) , 357-372 . |
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色素细胞是动物体内产生色素的一类特化细胞,不仅为动物提供不同的体表颜色及斑纹,还具有防止生物体免受紫外线伤害等功能.本研究概述了色素细胞的分布、发育分化以及这一过程中受到的基因调控,并概述了干细胞分化为黑色素细胞的研究进展.
Keyword ：
干细胞 干细胞 色素斑图 色素斑图 色素细胞 色素细胞
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| GB/T 7714 | 林翔 , 周桂炫 , 陈菲 et al. 色素细胞发育分化的分子调控机制 [J]. | 福州大学学报（自然科学版） , 2011 , 39 (5) : 649-657 . |
| MLA | 林翔 et al. "色素细胞发育分化的分子调控机制" . | 福州大学学报（自然科学版） 39 . 5 (2011) : 649-657 . |
| APA | 林翔 , 周桂炫 , 陈菲 , 黄炜娟 , 乐志操 . 色素细胞发育分化的分子调控机制 . | 福州大学学报（自然科学版） , 2011 , 39 (5) , 649-657 . |
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