Core Insights - On October 15, 2025, a total of 22 papers were published in the prestigious journal Nature, with several authored by Chinese scholars, highlighting the significant contributions of Chinese researchers in various scientific fields [2][4][6][9][12][21][22][24]. Group 1: Research Contributions - Zhang Zhenhua from RWTH Aachen University published a paper on "Deaminative cross-coupling of amines by boryl radical β-scission," focusing on a novel reaction mechanism involving boryl radicals [2]. - A collaborative work by Xu Minyu from National University of Singapore and Zhang Xinglong from Chinese University of Hong Kong discussed "Photocatalytic oxygen-atom transmutation of oxetanes," presenting advancements in photocatalysis [4]. - A team from Shanghai Jiao Tong University, Fudan University, and Nanjing University of Science and Technology introduced "Tin-based perovskite solar cells with a homogeneous buried interface," contributing to solar energy technology [6]. - The Taiwan Precision Medicine Initiative was highlighted in a paper by researchers from Academia Sinica, providing a cohort for large-scale studies in precision medicine [9]. - A study on "Population-specific polygenic risk scores for people of Han Chinese ancestry" was published by researchers from Academia Sinica, focusing on genetic risk assessment [12]. Group 2: Environmental and Material Science - Lin Yucheng from Rutgers University published a paper on "Modern sea-level rise breaks 4,000-year stability in southeastern China," addressing significant environmental changes [17]. - Research on "Patchy nanoparticles by atomic stencilling" was conducted by Chen Qian from the University of Illinois, exploring innovative methods in nanotechnology [19]. - A study on "A conserved H3K14ub-driven H3K9me3 for chromatin compartmentalization" was published by researchers from East China Normal University and the Chinese Academy of Sciences, contributing to the understanding of chromatin biology [21]. - Tsinghua University’s Fang Lu published a paper on "Integrated lithium niobate photonics for sub-ångström snapshot spectroscopy," advancing photonic technologies [22]. - Chen Chi-Fang from UC Berkeley introduced "Efficient quantum thermal simulation," focusing on quantum computing applications [24].

Core Insights - Stroke is the second leading cause of death globally and a major factor in long-term disability, with its rising incidence closely linked to population aging [3] - Post-Stroke Emotional Disorder (PSED) significantly impacts patient recovery and quality of life, increasing the risk of stroke recurrence and mortality [3] Research Findings - A study published in the journal Neuron identified the role of Lcn2 from neutrophil extracellular traps (NETs) in the development of PSED, highlighting the interaction between the peripheral immune system and the central nervous system [4] - The research indicates that NETs in serum are a significant feature of PSED, controlled by the permeability of the blood-brain barrier (BBB) [6][7] - The study suggests that the release of Lcn2 protein from NETs promotes the proliferation of astrocytes, which is a core mechanism of PSED [6][7] - Transcranial direct current stimulation (tDCS) can alleviate PSED by reducing the release of Lcn2 [6][7] Implications - The findings illustrate a unique peripheral-central immune interaction pattern following BBB damage, emphasizing the potential of non-invasive stimulation in reshaping the neuroimmune environment [9]

Core Viewpoint - The article emphasizes the importance of the Fourth Protein Science and Antibody Discovery Symposium, focusing on protein innovation and accelerating industry development, scheduled for November 21, 2025, in Shanghai Zhangjiang [4][21]. Group 1: Event Overview - The symposium aims to create a high-quality platform for early-stage research, emphasizing technology implementation and data exchange [5]. - The event will feature a main forum and two sub-forums focusing on autoimmune and tumor drug development, as well as complex antibodies and protein engineering [5][6]. - Key topics include trends in emerging targets, next-generation tumor immunology, and various strategies for antibody drug development [5][6]. Group 2: Participants and Contributions - The symposium will gather experts from leading companies, including CSOs, CTOs, and R&D directors, to share the latest research findings and practical experiences [7]. - The event is free for pharmaceutical companies and research institutions, with a focus on scientists and relevant R&D personnel [23]. Group 3: Organizers and Collaborators - The symposium is initiated by WuXi Biologics and supported by partners such as GENEWIZ, ACROBiosystems, and Agilent [21]. - The collaboration aims to enhance the scientific community's engagement and foster innovation in biopharmaceutical research [21][24].

Core Insights - The study indicates that gut microbiota can predict the efficacy of consolidation immunotherapy and chemoradiotherapy toxicity in lung cancer patients [3][9] - The research highlights the dynamic changes in gut microbiota during treatment and its correlation with progression-free survival (PFS) and treatment-related lung toxicity [5][6] Group 1: Research Findings - The research team utilized 16S rRNA sequencing to track the dynamic changes in gut microbiota of stage III lung cancer patients undergoing concurrent chemoradiotherapy (CRT) and consolidation immune checkpoint inhibitors (ICI) [5] - In traditional CRT, the composition of gut microbiota remained unaffected, whereas in CRT combined with ICI, patients with longer PFS exhibited higher baseline gut microbiota diversity, which decreased during treatment [6][9] - The abundance of Akkermansia muciniphila (Akk) increased post-chemoradiotherapy, correlating with extended distant metastasis-free survival in patients receiving CRT combined with ICI [6][10] Group 2: Clinical Implications - The study suggests that the overall clinical benefit of CRT combined with ICI is significantly greater compared to CRT alone for locally advanced lung cancer patients [9] - The dynamic changes in Akkermansia muciniphila serve as a potential prognostic indicator for patient survival outcomes [10] - Distinct gut microbiota characteristics were observed in patients who developed severe lung toxicity post-treatment, indicating a possible predictive marker for treatment-related pneumonia [6][10]

Core Insights - The article discusses the potential of anti-BCMA CAR-T cell therapy in treating progressive multiple sclerosis (PMS), highlighting its effectiveness and safety in clinical trials [4][11]. Group 1: Disease Overview - Progressive multiple sclerosis (PMS) is characterized by chronic inflammation in the central nervous system, leading to brain atrophy and demyelination [3]. - Current treatment options for PMS are limited and often ineffective, posing significant challenges for clinical management [3]. Group 2: Treatment Mechanism - B cells are identified as key drivers of disease progression through various mechanisms, including the production of autoantibodies and inflammatory cytokines [3]. - Existing B cell depletion therapies, such as CD20-targeted monoclonal antibodies, have shown efficacy in treating relapsing forms of multiple sclerosis but are limited in their ability to target plasma cells in the central nervous system due to the blood-brain barrier [3]. Group 3: Clinical Trial Findings - A phase 1 clinical trial involving 5 PMS patients (1 primary, 4 secondary) demonstrated that anti-BCMA CAR-T cell therapy is safe and effective [4]. - The therapy resulted in a significant reduction of plasma cells in the central nervous system and showed sustained expansion of CAR-T cells in cerebrospinal fluid, indicating a unique response in the CNS environment [6][9]. - Patients exhibited notable functional improvements over a follow-up period of up to 9 months, which was not observed in cases treated with anti-CD19 CAR-T cells [6][11]. Group 4: Safety Profile - The therapy was associated with only grade 1 cytokine release syndrome, and all grade 3 or higher cytopenias occurred within 40 days post-infusion [7]. Group 5: Future Implications - The study provides insights into the potential application of anti-BCMA CAR-T cell therapy in clinical management of PMS and suggests further research to evaluate long-term clinical efficacy and durability of treatment [11].

Core Insights - The research identifies a conserved mechanism for the formation of pericentric heterochromatin driven by H3K14ub-dependent SUV39H compartmentalization, revealing new insights into the mechanisms of heterochromatin formation, maintenance, and genetic stability in mammalian cells [3][7]. Group 1: Mechanism and Findings - The study discovered that G2E3 is a specific E3 ubiquitin ligase that recognizes H3K14ub, localized in pericentric heterochromatin regions, and enhances SUV39H-mediated H3K9me3, driving the localization of SUV39H and H3K9me3 in these regions [6][7]. - G2E3 is highly expressed during the G2/M phase and catalyzes H3K14ub, which lays the foundation for the sequential recruitment of SUV39H and HP1 proteins [7]. - The absence of G2E3 leads to the disruption of pericentric heterochromatin structure and abnormal accumulation of SUV39H and H3K9me3 in euchromatin regions, resulting in widespread transcriptional repression [7]. Group 2: Implications - The findings highlight the critical role of H3K14ub-dependent SUV39H compartmentalization in the correct partitioning of heterochromatin and euchromatin, as well as in the transcriptional regulation of euchromatin [7]. - This research addresses the molecular mechanisms underlying the formation and dynamic maintenance of mammalian heterochromatin, providing a new paradigm for epigenetic regulation [7].

Core Viewpoint - The research focuses on developing a novel totipotent-like cell-based embryo model that can continuously replicate mouse embryogenesis from zygotic genome activation to gastrulation, providing a powerful platform for studying early mammalian embryonic development [4][12]. Group 1: Research Background - The team from Peking University has been dedicated to the study of chemical small molecules regulating early stem cell developmental potential, establishing extended pluripotent stem cells (EPS cells) in 2017 and totipotent potential stem cells (TPS cells) in 2022, which exhibit significant application potential in constructing embryo models [3][5]. - Current models primarily focus on specific developmental stages, highlighting the need for a continuous in vitro model that replicates the complete developmental trajectory of mouse embryos from pre-implantation to post-implantation [2][3]. Group 2: Methodology and Findings - The research developed a new system for inducing and maintaining mouse totipotent stem cells, successfully constructing an embryo model that simulates mouse embryonic development from E1.5 to E7.5, showing early organogenesis signs [5][12]. - A novel small molecule combination was identified to efficiently induce EPS cells to establish a totipotent network within 48 hours, significantly enhancing cell proliferation rates to match early embryonic cleavage cycles [7][8]. - The model successfully replicated key developmental events, including zygotic genome activation, lineage specification, blastocyst formation, and the establishment of embryonic axes, validated through immunofluorescence and single-cell transcriptomic analysis [8][10]. Group 3: Implications and Future Directions - The model demonstrated the ability to respond to developmental perturbations similarly to natural embryos, indicating its potential for exploring regulatory mechanisms of early embryonic development [10][12]. - Notably, some E7.5-like structures could further develop into morphologically similar E8.5 embryos, showcasing early organogenesis features, thus advancing the understanding of early life formation [12]. - This research not only establishes an efficient method for inducing mouse totipotent stem cells but also provides a new platform for in-depth studies of early embryonic development, moving closer to the ultimate goal of constructing complete living organisms using early stem cells [12].

Core Viewpoint - T cell exhaustion is a unique state of T cell dysfunction that occurs during chronic antigen stimulation, significantly impacting immune responses in chronic infections and cancer [5][6]. Group 1: Mechanisms of T Cell Exhaustion - T cell exhaustion is characterized by impaired effector functions, reduced proliferation, and sustained expression of inhibitory receptors such as PD1, LAG3, and TIM3 [5]. - The development of T cell exhaustion is coordinated by complex interactions among transcriptional, epigenetic, and environmental factors, with transcription factors like NFAT, TOX, and NR4A1 playing crucial roles [5][12]. - Recent studies have identified a unique cell population known as exhausted T cell precursors (Tpex), which retain proliferative capacity and respond to immune checkpoint blockade therapy, providing insights for potential therapeutic strategies [5][6]. Group 2: Environmental Regulation of T Cell Exhaustion - The microenvironment significantly influences CD8⁺ T cell exhaustion, with various cytokines and metabolites modulating T cell function and fate [10][14]. - Understanding the environmental signals that drive or limit T cell exhaustion is essential for rejuvenating T cell responses in chronic diseases and enhancing the effectiveness of immunotherapy [6][14]. Group 3: Therapeutic Implications - The review highlights the importance of understanding the regulatory factors of T cell exhaustion to develop and improve immunotherapies targeting these pathways for cancer and chronic infections [14]. - By elucidating the mechanisms that guide the fate and function of different exhausted T cell subsets, the research provides critical references for developing targeted immunotherapies [14].

Core Viewpoint - The article discusses a groundbreaking research on AI-designed insulin receptor agonists that offer improved efficacy and safety for diabetes treatment compared to traditional insulin therapies [3][10]. Group 1: Research Background - Insulin has been a cornerstone in diabetes treatment since its discovery, but it has limitations such as complex production, strict storage conditions, and potential cancer risks [2]. - The insulin receptor acts as a "lock" that insulin "unlocks," initiating two main signaling pathways: one for metabolic regulation (AKT pathway) and another for cell growth (MAPK pathway) [2]. Group 2: Research Findings - Researchers from Washington University and Texas Southwestern Medical Center developed AI-designed insulin receptor agonists that outperform traditional insulin in lowering blood sugar and can precisely regulate signaling pathways, avoiding cancer cell proliferation [3][5]. - The new insulin receptor agonists exhibit remarkable properties, including enhanced thermal stability, remaining stable at 95°C, and precise signal regulation through adjustable linkers [7]. Group 3: Experimental Results - In mouse models, the AI-designed agonist RF-409 demonstrated superior blood sugar-lowering effects, requiring only half the dosage of insulin for the same effect and maintaining low blood sugar levels for up to 6 hours [7][8]. - These agonists can activate mutated insulin receptors in insulin-resistant patients, providing new treatment hope for rare genetic diabetes [8]. Group 4: Implications and Future Directions - The specificity of these agonists allows them to activate normal and mutated insulin receptors while avoiding activation of cancer cell receptors, significantly reducing potential cancer risks associated with traditional insulin therapy [8][10]. - The research lays the groundwork for developing safer and more effective next-generation diabetes treatments, with the founding of Lila Biologics aimed at utilizing AI protein design for breakthrough therapies [10][11].

Core Viewpoint - The research indicates that oral administration of clinical safe doses of Vitamin C can significantly delay ovarian aging in primates, revealing its protective mechanism through the activation of the NRF2 signaling pathway [2][4][5]. Group 1: Research Background - Ovarian aging plays a critical role in women's reproductive health, impacting treatment strategies and quality of life [3]. - Previous studies by Liu Guanghui's team have established that Vitamin C can delay cellular aging and has been linked to a significant decline in antioxidant capacity during ovarian aging in primates [3]. Group 2: Key Findings - A 3.3-year intervention study on middle-aged crab-eating macaques demonstrated that oral Vitamin C can reduce key aging biomarkers, including oxidative stress and follicle depletion [4]. - The study constructed a primate ovarian single-cell transcriptome aging clock, showing that Vitamin C can make oocyte biological age younger by an average of 1.35 years and somatic cell biological age younger by 5.66 years, particularly in granulosa, endothelial, and stromal cells [4]. - Vitamin C effectively reverses aging and inflammation-related phenotypes in endothelial cells, making their biological age nearly 7 years younger [4]. Group 3: Mechanism of Action - The effect of Vitamin C in delaying ovarian aging is partially mediated through the NRF2 pathway, which plays multiple protective roles in human ovarian cells, including delaying aging, inhibiting inflammation, maintaining chromatin stability, and enhancing mitochondrial function [5]. Group 4: Implications - This research validates the concept of using a single compound to delay ovarian aging in primate models and highlights the potential of Vitamin C in developing interventions for human ovarian aging [8].