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  1. AU="Xiong, Yinyi"
  2. AU="Larciprete, R"
  3. AU="Camila Mugnai Vieira"
  4. AU="Michael Sjöström"
  5. AU="Bouchau, Robin"
  6. AU="Shahabi Rabori, Venus"
  7. AU="Jeronimo, Matthew"
  8. AU="Misra, Maitreyi"
  9. AU="Liu, Xuping"
  10. AU="Corinna Lüneburg"
  11. AU="Clement, Lionel C"
  12. AU="Parkhill, Julian"
  13. AU="Wiita, Arun P"
  14. AU=Lubrano Riccardo
  15. AU=Biggs Andrew
  16. AU="Lian, Kejian"
  17. AU="Almutairi, Abdulrahman"
  18. AU="Cosculluela-Pueyo, Rafaél"
  19. AU="Gehrs, Teresa"
  20. AU="Munir, Atif"
  21. AU="Ou, Ya-Nan"
  22. AU=Brown James E AU=Brown James E
  23. AU="Wang, Zhongmin"
  24. AU="Lemieux, Audrée"
  25. AU="Abdelhameed, Mohamed F"
  26. AU="Schaible, Lonnie M"
  27. AU="Yazie, Taklo Simeneh Yazie"
  28. AU="Jude Orumuah Agbugui"
  29. AU="Kruse, Robert L"
  30. AU="Shyama Nandakumar"
  31. AU="Gelb, M"
  32. AU="Gasparini, L"
  33. AU="Ulvila, J"
  34. AU="Länsimies, Helena"

Suchergebnis

Treffer 1 - 5 von insgesamt 5

Suchoptionen

  1. Artikel: Understanding the Modulatory Effects of Cannabidiol on Alzheimer's Disease.

    Xiong, Yinyi / Lim, Chae-Seok

    Brain sciences

    2021  Band 11, Heft 9

    Abstract: Alzheimer's disease (AD), the most common neurodegenerative disease, is characterized by progressive cognitive impairment. The deposition of amyloid beta (Aβ) and hyperphosphorylated tau is considered the hallmark of AD pathology. Many therapeutic ... ...

    Abstract Alzheimer's disease (AD), the most common neurodegenerative disease, is characterized by progressive cognitive impairment. The deposition of amyloid beta (Aβ) and hyperphosphorylated tau is considered the hallmark of AD pathology. Many therapeutic approaches such as Food and Drug Administration-approved cholinesterase inhibitors and
    Sprache Englisch
    Erscheinungsdatum 2021-09-14
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2651993-8
    ISSN 2076-3425
    ISSN 2076-3425
    DOI 10.3390/brainsci11091211
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Emerging role of mesenchymal stem cells-derived extracellular vesicles in vascular dementia.

    Liu, Ziying / Cheng, Lin / Zhang, Lushun / Shen, Chunxiao / Wei, Shufei / Wang, Liangliang / Qiu, Yuemin / Li, Chuan / Xiong, Yinyi / Zhang, Xiaorong

    Frontiers in aging neuroscience

    2024  Band 16, Seite(n) 1329357

    Abstract: Vascular dementia (VD) is a prevalent cognitive disorder among the elderly. Its pathological mechanism encompasses neuronal damage, synaptic dysfunction, vascular abnormalities, neuroinflammation, and oxidative stress, among others. In recent years, ... ...

    Abstract Vascular dementia (VD) is a prevalent cognitive disorder among the elderly. Its pathological mechanism encompasses neuronal damage, synaptic dysfunction, vascular abnormalities, neuroinflammation, and oxidative stress, among others. In recent years, extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs) have garnered significant attention as an emerging therapeutic strategy. Current research indicates that MSC-derived extracellular vesicles (MSC-EVs) play a pivotal role in both the diagnosis and treatment of VD. Thus, this article delves into the recent advancements of MSC-EVs in VD, discussing the mechanisms by which EVs influence the pathophysiological processes of VD. These mechanisms form the theoretical foundation for their neuroprotective effect in VD treatment. Additionally, the article highlights the potential applications of EVs in VD diagnosis. In conclusion, MSC-EVs present a promising innovative treatment strategy for VD. With rigorous research and ongoing innovation, this concept can transition into practical clinical treatment, providing more effective options for VD patients.
    Sprache Englisch
    Erscheinungsdatum 2024-02-08
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2558898-9
    ISSN 1663-4365
    ISSN 1663-4365
    DOI 10.3389/fnagi.2024.1329357
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Epidermal growth factor receptor promotes high-fructose nonalcoholic fatty liver disease by inducing mitochondrial fission in zebrafish.

    Li, Li / Xiong, Yinyi / Cao, Wa / Chen, Zhiyin / He, Ling / Tong, Mingfu / Zhang, Le / Wu, Moxin

    Biochemical and biophysical research communications

    2023  Band 652, Seite(n) 112–120

    Abstract: Mitochondrial function has a pivotal role in the pathogenesis of NAFLD. Mitochondrial dynamics is a foundational activity underlying the maintenance of mitochondrial function in bioenergetics, the maintenance of MtDNA, calcium homeostasis, reactive ... ...

    Abstract Mitochondrial function has a pivotal role in the pathogenesis of NAFLD. Mitochondrial dynamics is a foundational activity underlying the maintenance of mitochondrial function in bioenergetics, the maintenance of MtDNA, calcium homeostasis, reactive oxygen species metabolism, and quality control. Loss of mitochondrial plasticity in terms of functions, morphology and dynamics may also be the critical switch from NAFLD/NASH to HCC. However, the cause of mitochondrial fission in NAFLD remains unclear. Recent studies have reported that EGFR can bind to Mfn1 and interfere with its polymerization. In this study, we investigated whether EGFR binds to Mfn1 in NAFLD, and whether reducing their binding can improve NAFLD in zebrafish model. Our results demonstrated that EGFR was activated in hepatocytes from high fructose (HF)-induced NAFLD zebrafish and interfered with Mfn1 polymerization, leading to reduction of MtDNA. Suppression of EGFR activation or mitochondrial translocation significantly improved mitochondrial morphology and increased mitochondrial DNA, ultimately preventing hepatic steatosis. In conclusion, these results suggest that EGFR binding to Mfn1 plays an important role in NAFLD zebrafish model and that inhibition of their binding could be a potential therapeutic target.
    Mesh-Begriff(e) Animals ; Non-alcoholic Fatty Liver Disease/metabolism ; Zebrafish ; Mitochondrial Dynamics ; Carcinoma, Hepatocellular/pathology ; Fructose/metabolism ; Liver Neoplasms/pathology ; ErbB Receptors/metabolism ; DNA, Mitochondrial/metabolism ; Liver/metabolism
    Chemische Substanzen Fructose (30237-26-4) ; ErbB Receptors (EC 2.7.10.1) ; DNA, Mitochondrial
    Sprache Englisch
    Erscheinungsdatum 2023-02-20
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2023.02.051
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 116: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Artikel ; Online: Generation of a Novel Transgenic Zebrafish for Studying Adipocyte Development and Metabolic Control.

    Mao, Yousheng / Hong, Kwang-Heum / Liao, Weifang / Li, Li / Kim, Seong-Jin / Xiong, Yinyi / Nam, In-Koo / Choe, Seong-Kyu / Kwak, Seong-Ae

    International journal of molecular sciences

    2021  Band 22, Heft 8

    Abstract: Zebrafish have become a popular animal model for studying various biological processes and human diseases. The metabolic pathways and players conserved among zebrafish and mammals facilitate the use of zebrafish to understand the pathological mechanisms ... ...

    Abstract Zebrafish have become a popular animal model for studying various biological processes and human diseases. The metabolic pathways and players conserved among zebrafish and mammals facilitate the use of zebrafish to understand the pathological mechanisms underlying various metabolic disorders in humans. Adipocytes play an important role in metabolic homeostasis, and zebrafish adipocytes have been characterized. However, a versatile and reliable zebrafish model for long-term monitoring of adipose tissues has not been reported. In this study, we generated stable transgenic zebrafish expressing enhanced green fluorescent protein (EGFP) in adipocytes. The transgenic zebrafish harbored adipose tissues that could be detected using GFP fluorescence and the morphology of single adipocyte could be investigated in vivo. In addition, we demonstrated the applicability of this model to the long-term in vivo imaging of adipose tissue development and regulation based on nutrition. The transgenic zebrafish established in this study may serve as an excellent tool to advance the characterization of white adipose tissue in zebrafish, thereby aiding the development of therapeutic interventions to treat metabolic diseases in humans.
    Mesh-Begriff(e) Adipocytes/cytology ; Adipocytes/metabolism ; Adipose Tissue/metabolism ; Animal Nutritional Physiological Phenomena ; Animals ; Animals, Genetically Modified ; Cell Shape ; Green Fluorescent Proteins/metabolism ; Larva/genetics ; Larva/metabolism ; Promoter Regions, Genetic/genetics ; Transgenes ; Zebrafish/genetics ; Zebrafish/metabolism ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
    Chemische Substanzen Zebrafish Proteins ; enhanced green fluorescent protein ; Green Fluorescent Proteins (147336-22-9)
    Sprache Englisch
    Erscheinungsdatum 2021-04-13
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22083994
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Dysfunction of NMDA receptors in neuronal models of an autism spectrum disorder patient with a DSCAM mutation and in Dscam-knockout mice.

    Lim, Chae-Seok / Kim, Min Jung / Choi, Ja Eun / Islam, Md Ariful / Lee, You-Kyung / Xiong, Yinyi / Shim, Kyu-Won / Yang, Jung-Eun / Lee, Ro Un / Lee, Jiah / Park, Pojeong / Kwak, Ji-Hye / Seo, Hyunhyo / Kim, Chul Hoon / Lee, Jae-Hyung / Lee, Yong-Seok / Hwang, Su-Kyeong / Lee, Kyungmin / Lee, Jin-A /
    Kaang, Bong-Kiun

    Molecular psychiatry

    2021  Band 26, Heft 12, Seite(n) 7538–7549

    Abstract: Heterogeneity in the etiopathology of autism spectrum disorders (ASD) limits the development of generic remedies, requires individualistic and patient-specific research. Recent progress in human-induced pluripotent stem cell (iPSC) technology provides a ... ...

    Abstract Heterogeneity in the etiopathology of autism spectrum disorders (ASD) limits the development of generic remedies, requires individualistic and patient-specific research. Recent progress in human-induced pluripotent stem cell (iPSC) technology provides a novel platform for modeling ASDs for studying complex neuronal phenotypes. In this study, we generated telencephalic induced neuronal (iN) cells from iPSCs derived from an ASD patient with a heterozygous point mutation in the DSCAM gene. The mRNA of DSCAM and the density of DSCAM in dendrites were significantly decreased in ASD compared to control iN cells. RNA sequencing analysis revealed that several synaptic function-related genes including NMDA receptor subunits were downregulated in ASD iN cells. Moreover, NMDA receptor (R)-mediated currents were significantly reduced in ASD compared to control iN cells. Normal NMDA-R-mediated current levels were rescued by expressing wild-type DSCAM in ASD iN cells, and reduced currents were observed by truncated DSCAM expression in control iN cells. shRNA-mediated DSCAM knockdown in control iN cells resulted in the downregulation of an NMDA-R subunit, which was rescued by the overexpression of shRNA-resistant DSCAM. Furthermore, DSCAM was co-localized with NMDA-R components in the dendritic spines of iN cells whereas their co-localizations were significantly reduced in ASD iN cells. Levels of phospho-ERK1/2 were significantly lower in ASD iN cells, suggesting a potential mechanism. A neural stem cell-specific Dscam heterozygous knockout mouse model, showing deficits in social interaction and social memory with reduced NMDA-R currents. These data suggest that DSCAM mutation causes pathological symptoms of ASD by dysregulating NMDA-R function.
    Mesh-Begriff(e) Animals ; Autism Spectrum Disorder/metabolism ; Cell Adhesion Molecules/genetics ; Humans ; Mice ; Mice, Knockout ; Mutation/genetics ; Neurons/metabolism ; Receptors, N-Methyl-D-Aspartate/genetics ; Receptors, N-Methyl-D-Aspartate/metabolism
    Chemische Substanzen Cell Adhesion Molecules ; DSCAM protein, human ; Dscam protein, mouse ; Receptors, N-Methyl-D-Aspartate
    Sprache Englisch
    Erscheinungsdatum 2021-07-12
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-021-01216-9
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 4812: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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