Publications by authors named "Ruiwei Ye"

This review seeks to elucidate the therapeutic potential of tumor necrosis factor receptor 1 (TNFR1) and enhance our comprehension of its role in disease mechanisms. As a critical cell-surface receptor, TNFR1 regulates key signaling pathways, such as nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK), which are associated with pro-inflammatory responses and cell death. The intricate regulatory mechanisms of TNFR1 signaling and its involvement in various diseases, including inflammatory disorders, infectious diseases, cancer, and metabolic syndromes, have attracted increasing scholarly attention.

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Cancer is the leading cause of death worldwide, accounting for nearly 10 million deaths every year. Immune checkpoint blockade approaches have changed the therapeutic landscape for many tumor types. However, current immune checkpoint inhibitors PD-1 or CTLA-4 are far from satisfactory, due to high immune-related adverse event incident (up to 60%) and the inefficiency in cases of "cold" tumor microenvironment.

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Article Synopsis
  • Immune-related adverse events, especially colitis, hinder the progress of immune checkpoint therapies, leading researchers to explore strategies like blocking TNF-α and modifying gut microbiota.
  • A mouse model demonstrated that combining Infliximab with DICB reduced colitis and improved therapeutic effectiveness, while also revealing changes in gut microbiota linked to the condition.
  • The study indicates that a complex feedback loop involving DICB, TNF-α, and gut microbiota plays a crucial role in irAE-colitis, with Infliximab showing promise in treating its toxicity.
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Overexpression of tumor necrosis factor-α (TNF-α) is implicated in many inflammatory diseases, including septic shock, hepatitis, asthma, insulin resistance and autoimmune diseases, such as rheumatoid arthritis and Crohn's disease. The TNF-α signaling pathway is a valuable target, and anti-TNF-α drugs are successfully used to treat autoimmune and inflammatory diseases. Here, we study anti-inflammatory activity of an anti-TNF-α peptide (SN1-13, DEFHLELHLYQSW).

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Predator-prey arms races are ideal models for studying the natural selection and adaptive evolution that drive the formation of biological diversity. For venomous snakes, venom is a key bridge linking snakes with their prey, but whether and how venom evolves under the selection of diet remains unclear. Here, we focused on two closely related sea snakes, Hydrophis cyanocinctus and Hydrophis curtus, which show significant differences in prey preferences.

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Inhibiting TNF-α-mediated acute inflammation is an effective treatment against inflammatory bowel disease. In this study, TNF-α-based T7 phage display library screening combined with in vitro and in vivo assays was applied. A lead peptide, pep2 (ACHAWAPTR, = 5.

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Background: The application of multi-omics technologies provides a new perspective to solve three main problems including species identification, toxin screening and effective antagonist conformation in the studies of marine toxic jellyfish.

Methods: A series of transcriptome-proteome based analysis accompanied with toxicity evaluations were performed for the ornamental jellyfish Phacellophora camtschatica.

Results: Through combined morphological observation and Cytochrome c oxidase subunit Ⅰ (CO1) molecular alignment, the sample jellyfish was identified as P.

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Background: We successfully captured a kind of gelatinous organism DA-6 from Antarctic water, extracted its total RNAs and proteins, and performed species identification through a combination of transcriptomics and proteomics in this study.

Methods: The gelatinous organism DA-6 was captured 200 m underwater in Antarctica. Total RNA was extracted to construct the transcriptome and the proteins were identified by LC-MS/MS.

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