Biology subjects

Liu, S.-C.

Publications and source records attributed to Liu, S.-C..

4 recordsLinked to original sources

bioRxiv2025

Comparative Analysis of Phytochemical Constituents of Ginkgo Biloba Flowers and Leaves, and Evaluation of Their Biological Activities

BackgroundsGinkgo biloba L. has attracted much attention for its unique chemical composition and pharmacological properties, and most of the research focused on Ginkgo biloba leaves (GBL). Our preliminary research found that Ginkgo biloba flowers (GBF) were superior to GBL in terms of anti-radiation activity, but the underlying cause of this discrepancy in activity remains elusive. ObjectivesThe aim of this study was to systematically compare the chemical and nutritional composition of Ginkgo biloba flowers and leaves, to further elucidate the material basis of the medicinal and nutritional value of Ginkgo biloba flowers, and to conduct further comparative studies on the anti-ferroptosis activity and anti-radiation activity of the two. MethodsIn this study, the chemical constituents of GBF and GBL were identified by UPLC-Q-orbitrap HRMS, and the contents of amino acids, fatty acids, inorganic elements, purines, and ceramides of both were determined. Meanwhile, the anti-iron death activity and anti-radiation activity of GBF and GBL were comparatively studied by cellular experiments. ResultsThe results showed that the content of chemical components such as flavonoids and other nutrients such as amino acids, fatty acids, and ceramides were richer in GBF than in GBL, and GBF was indeed superior to GBL in terms of anti-radiation and anti-ferroptosis activity. ConclusionThrough in-depth analyses of the chemical and nutritional compositions of Ginkgo biloba flowers and leaves, the present study reveals the possible material basis for the stronger activity of GBF and provides theoretical support for its application in nutraceuticals and pharmaceuticals, especially in the development of functional nutraceuticals and anti-radiation drugs with higher health benefits.

biochemistry↗

bioRxiv2024

Epstein-Barr viral product-containing exosome facilitates LIF-associated immunosuppressive polarization of macrophage in nasopharyngeal carcinoma

Epstein-Barr virus (EBV)-associated nasopharyngeal carcinoma (NPC) is characterized by a highly infiltrated, yet immunosuppressive, tumor microenvironment (TME) in which tumor-associated macrophages (TAMs) play a central role in tumor progression. In this study, we identified exosome-mediated delivery of the EBV oncoprotein LMP1, which acts via induction of leukemia inhibitory factor (LIF), as a key mechanism driving immunosuppressive macrophage polarization. Immunohistochemistry revealed that, in addition to tumor cells, LIF is primarily expressed by stromal TAMs and correlates with poor prognosis. We demonstrated that LMP1-containing exosomes are internalized by macrophages, leading to NF-{kappa}B-dependent upregulation of LIF and polarization toward an immunosuppressive M2d-like phenotype. These macrophages exhibit impaired anti-tumor activity and promote tumor proliferation and vascular dissemination in a LIF-dependent manner. Single-cell transcriptomic analyses of exosome-treated NPC biopsies revealed transcriptional reprogramming across tumor, myeloid, and lymphoid compartments impacting epithelial-mesenchymal transition (EMT); extracellular matrix (ECM) remodeling in tumor cells; immunosuppressive signaling (e.g., CD163 anti-inflammatory and VEGF signaling in macrophages); and enrichment of immune checkpoints and pathways, including PD-1, TGF{beta}-SMAD, and NF-{kappa}B-associated pathways in T cells. Exosome treatment increased expansion of CCL18+-TAMs and expression of CTLA4 in regulatory T cells and exhausted T cells. Immunohistochemistry further confirmed a positive correlation between expression of LIF and CTLA4 in NPC tumors and an inverse correlation between LIF and GZMB/CD8A. These findings define an exosome-driven LMP1-LIF axis that orchestrates immune suppression in NPC and suggest potential targets for restoring anti-tumor immunity.

cancer biology↗

bioRxiv2024

Real-time control of a hearing instrument with EEG-based attention decoding

Enhancing speech perception in everyday noisy acoustic environments remains an outstanding challenge for hearing aids. Speech separation technology is improving rapidly, but hearing devices cannot fully exploit this advance without knowing which sound sources the user wants to hear. Even with high-quality source separation, the hearing aid must know which speech streams to enhance and which to suppress. Advances in EEG-based decoding of auditory attention raise the potential of neurosteering, in which a hearing instrument selectively enhances the sound sources that a hearing-impaired listener is focusing their attention on. Here, we present and discuss a real-time brain-computer interface (BCI) system that combines a stimulus-response model based on canonical correlation analysis (CCA) for real-time EEG attention decoding, coupled with a multi-microphone hardware platform enabling low-latency real-time speech separation through spatial beamforming. We provide an overview of the system and its various components, discuss prospects and limitations of the technology, and illustrate its application with case studies of listeners steering acoustic feedback of competing speech streams via real-time attention decoding. A software implementation code of the system is publicly available for further research and explorations.

neuroscience↗

bioRxiv2024

Allelic DNA synthesis followed by template switching underlies BRCA1-linked tandem duplication

Microhomology-mediated short tandem duplication (TD) is among specific mutational signatures associated with BRCA1-deficient tumors. Several mechanisms have been proposed for its generation, but may not be applicable in repeat-less regions of the human genome. We thus developed a repeat-less TD reporter and a PCR-based site-specific TD assay to analyze short TDs induced by one-ended DNA double strand breaks (DSBs) converted from DNA nicks in Brca1-deficient cells. We found that short TDs induced by DNA nicks are significantly stimulated in Brca1-deficient cells. Analysis of TD products revealed that the TD formation is partly mediated by template switching of displaced nascent strand after allelic DNA synthesis. This suggests either allelic DNA synthesis or the strand annealing step of allelic break-induced replication might be more easily aborted in Brca1-deficient cells, thus promoting TD. Neither depletion of Rad51 or Brca2 nor inactivation of the Brca1 coiled-coil domain stimulated nick-induced TD, indicating that RAD51 loading by BRCA1 is dispensable for BRCA1-mediated TD suppression. These results together provide novel insights into the mechanisms underlying BRCA1-linked TD formation in cancer.

cancer biology↗