Core Viewpoint - The article discusses the ambitious vision of creating Artificial Intelligence Virtual Cells (AIVC) to model and predict cellular behavior, leveraging advancements in AI and omics technologies [3][5][7]. Group 1: AI Virtual Cell Development - Multiple research teams are competing to develop AI models for cellular behavior prediction [4]. - The Chan-Zuckerberg Initiative (CZI) plans to invest hundreds of millions over the next decade to create virtual cells [10]. - The development of AI protein structure prediction tools like AlphaFold is contributing to virtual cell projects [10]. Group 2: Current Progress and Challenges - The efforts to create virtual cells are still in the early stages, generating significant interest in academic and industrial labs [8]. - Despite the excitement, some scientists express skepticism about the hype surrounding virtual cells, noting a lack of concrete results and clear success pathways [11]. - Current virtual cell models primarily focus on single-cell RNA sequencing data, which provides snapshots of gene activity and cellular states [16]. Group 3: Data Utilization and Future Directions - CZI plans to release sequencing data from 1 billion cells, while Arc Institute has released data from 100 million cancer cells treated with various drugs [16]. - Researchers are beginning to develop single-cell AI models, with Arc Institute launching its first virtual cell model called "State" [16]. - There is a need for integrating other data forms, such as optical and electron microscopy images, to enhance virtual cell models [17]. Group 4: Definition and Consensus - The concept of virtual cells lacks a clear definition, and there is no consensus among researchers on what constitutes a virtual cell [18]. - Stephen Quake emphasizes that the transition to using virtual cell models in biology will take time, as both the models and the scientists are not yet fully prepared [19].

Core Viewpoint - The study highlights the impact of gut microbiota dysbiosis induced by brain tumors on the efficacy of immunotherapy, suggesting that dietary supplementation with tryptophan can restore gut microbiota and significantly enhance the immune response through T cell circulation [2][11][14]. Group 1: Research Background - The influence of gut microbiota on various tumors, particularly gastrointestinal tumors, is recognized, but its effects on brain tumors remain largely unexplored [2][6]. - Glioblastoma (GBM) is known for its poor prognosis and limited survival rate improvements despite various treatments, attributed to unique characteristics of the tumor microenvironment [4][5]. Group 2: Research Findings - The research utilized a GBM mouse model and employed 16S rRNA sequencing to analyze changes in gut microbiota during tumor progression, finding that tryptophan supplementation could reverse these changes [9]. - Tryptophan supplementation not only restored gut microbiota balance but also significantly improved survival rates in mouse models and enhanced the effectiveness of immunotherapy [9][13]. Group 3: Key Microbial Insights - Among the gut bacteria responding positively to tryptophan, Duncaniella dubosii emerged as a key contributor to the immune modulation effects of tryptophan [10][13]. - The study emphasizes the potential of targeting gut microbiota modulation to improve cancer immunotherapy outcomes, particularly through mechanisms involving T cell regulation [14].

Core Viewpoint - The study highlights the role of senescent macrophages in inducing ferroptosis in skeletal muscle, which accelerates muscle atrophy related to osteoarthritis (OA) [3][8][10]. Group 1: Osteoarthritis and Muscle Atrophy - Osteoarthritis (OA) is characterized by pathological changes including cartilage damage, subchondral bone remodeling, and synovial inflammation, with muscle atrophy being a common manifestation [2]. - Muscle atrophy associated with OA is strongly correlated with knee joint symptoms and the deterioration of joint pathology [2]. Group 2: Mechanisms of Muscle Atrophy - Senescent macrophages induce ferroptosis in skeletal muscle, leading to quadriceps atrophy associated with OA [3][8]. - The mechanism involves iron overload in senescent macrophages causing mitochondrial damage in muscle cells, which reduces aspartate metabolites and inhibits the mTORC1-HMGCR signaling pathway, ultimately decreasing endogenous coenzyme Q10 (CoQ10) synthesis [3][10]. Group 3: Role of CoQ10 - CoQ10 is crucial for maintaining muscle integrity and quality, with its levels positively correlating with antioxidant capacity, muscle mass, strength, and endurance in OA patients [6]. - Exogenous supplementation of CoQ10 has been shown to alleviate muscle atrophy by inhibiting ferroptosis, significantly increasing quadriceps mass and reducing pathological damage to OA joints [10].

Core Viewpoint - The research highlights a novel biological signaling axis between nerves and cancer cells, revealing that cancer cells can hijack mitochondria from neurons to enhance their metastatic capabilities, thus providing new therapeutic targets for cancer treatment [4][5][6]. Group 1: Research Findings - The study published in Nature identifies that cancer cells utilize tubular structures to steal mitochondria from neurons, which helps them withstand stress during metastasis [4][5]. - The research team observed a universal phenomenon of mitochondrial transfer between neurons and cancer cells, confirming that cancer cells with stolen mitochondria generate more energy [11][12]. - Experiments showed that cancer cells that had acquired mitochondria from neurons had a significantly higher survival rate when subjected to stress conditions, indicating the importance of mitochondrial transfer in cancer metastasis [12]. Group 2: Implications for Cancer Treatment - The findings suggest a need for further investigation into the mechanisms of nerve-cancer cell mitochondrial transfer and the development of targeted therapies to prevent cancer metastasis [15]. - The research provides a compelling metabolic explanation for the observed dependency of cancer cells on the nervous system, which could apply to a broader range of cancers [15].

Core Viewpoint - The study indicates that optogenetic vagal nerve stimulation (VNS) can alleviate heart failure (HF) by limiting the generation of monocyte-derived inflammatory CCRL2+ macrophages [2][3][4]. Summary by Sections Mechanism of Action - The research demonstrates that VNS reduces the proportion of CCRL2+ macrophages, which are derived from myeloid monocytes and exhibit unique tumor necrosis factor alpha (TNF-α) cytokine responses, hypertrophic, and fibrotic characteristics [4]. - The elimination of CCRL2+ macrophages can prevent cardiac remodeling and heart failure [4]. Key Findings - The study confirms a positive correlation between CCRL2+ macrophages and TNF-α responsive proteins in the human heart with cardiac remodeling and dysfunction [5]. - Activation of the α7 nicotinic acetylcholine receptor (α7nAChR) plays a crucial role in the cardiac protective effects mediated by VNS, as it inhibits the response of CCRL2+ macrophages to TNF-α by increasing the expression of the transcription factor NRF2 [4][5]. Therapeutic Implications - Overall, the results suggest that the vagus nerve-immune axis can regulate heart failure and represents a promising therapeutic target [6].

其中，NJU120-1 是一种厚度仅约 8 纳米的 纳米片 ，相当于 1.5 个晶胞，而 NJU120-2 是一种尺寸为 50×250 纳米的 纳米棒 。 通过利用 微晶电子衍射 （MicroED） 技术平台 快速确定结构，研究团队揭示了这两种纳米沸石的 多维孔道结构， 极大地加速了对这些物质的合成优化，它们 最大自由球体直径高达 1.2 纳米，再加上纳米级的形态，使得能够对大分子进行 催化裂化 （FCC） 反应， 展现出优异的重油转化率和轻质燃料 （汽油、柴油和 液化石油气） 选择性 ，其性能均媲美甚至超越现有的超大孔沸石和工业沸石。 编辑丨王多鱼 排版丨水成文 具有超大孔道和纳米尺寸、能够处理大分子的稳定沸石，需求量很大，但一直难以生产。它们复杂的结构和纳米级的晶体尺寸给采用传统 X 射线衍射技术进行的 分析带来了挑战，导致材料开发效率低下。 2025 年 6 月 26 日 ， 南京大学 黎建 研究员、 中国石化石油化工科学研究院 林伟 研究员 、香港理工大学 林聪 研究员 作为共同通讯作者 （ 南京大学 博士生 马超 、博士生 章正汉 、硕士生 张梦迪 为共同第一作者 ） ，在国际顶尖学术期刊 Scie ...

编辑丨王多鱼 排版丨水成文 生命的 DNA 由四种碱基 A、T、C、G 组成，它们每 3 个组成一组密码子，共计 64 组密码子，这些密码子利用对应的 20 种天然氨基酸合成蛋白质 。 在此基础 上对密码子进行扩展，有望 从底层改写生命法则，乃至发展出全新治疗方法。 TGA、 TAA 和 TAG 为 终止密码子 ，它们本身不对应任何氨基酸，只代表蛋白质合成时的终止信号； 此前的 密码子扩展 （ codon-expansion ） 技术， 通过 将终止密码子重新指定为"空白"密码子 ，为利用 非天然氨基酸 （ncAA） 编码提供了一种通用方法；然而，对于细胞转录本而言，它并非完全与翻译终止过程相 互独立，因此，这种在 DNA 层面的密码子扩展可能存在持续的 终止密码子通读威胁，并可能产生不可预测的错误。 2025 年 6 月 25 日，北京大学 陈鹏 团队和 伊成器 团队 （ 博士研究生 刘江乐 、博士后 闫学青 、博士研究生 乌浩 为共同第一作者 ） 合作，在国际顶尖学术 期刊 Nature 上 发表题为： RNA codon expansion via programmable pseudouridine ...

Core Viewpoint - The study presents a novel CXCR4 partial agonist, TFF2-MSA, which enhances the efficacy of cancer immunotherapy by targeting immunosuppressive neutrophils and cancer-driven granulopoiesis, particularly in gastric cancer [2][3][8]. Group 1: Research Findings - TFF2-MSA is identified as a CXCR4 partial agonist that sensitizes gastric cancer mouse models to anti-PD-1 therapy [6]. - TFF2-MSA reduces immunosuppressive neutrophils and cancer-driven granulocyte production [6]. - The combination of TFF2-MSA with anti-PD-1 therapy induces a robust anti-tumor CD8+ T cell response [6]. - In gastric cancer patients, decreased levels of TFF2 are associated with an increase in polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) [6][5]. Group 2: Mechanism of Action - The study demonstrates that TFF2-MSA, when fused with mouse serum albumin (MSA), shows improved stability and effectively inhibits primary tumor growth and distal metastasis in gastric cancer mouse models [4]. - TFF2-MSA selectively reduces Hdc-GFP+ CXCR4high immunosuppressive neutrophils, enhancing the tumor-killing ability of CD8+ T cells mediated by anti-PD-1 [4]. - Unlike CXCR4 antagonists, TFF2-MSA also inhibits bone marrow granulocyte production, contributing to its therapeutic benefits [4]. Group 3: Implications for Cancer Therapy - The research proposes a new strategy that utilizes CXCR4 partial agonism to restore tumor sensitivity to immune checkpoint inhibitors [8].

Core Viewpoint - The article discusses the emergence of Virtual Cells (VC) as a frontier in the intersection of artificial intelligence and biology, aiming to revolutionize life sciences research by predicting cellular responses to disturbances [2][6]. Group 1: Virtual Cell Challenge - The Virtual Cell Challenge was launched by Arc Institute, with sponsorship from NVIDIA, 10x Genomics, and Ultima Genomics, offering cash prizes of $100,000, $50,000, and $25,000 for the top three models that accurately predict cellular responses to genetic disturbances [4]. - The challenge aims to provide a fair and open evaluation framework to identify the best virtual cell models through rigorous testing [2][4]. Group 2: Importance of Virtual Cells - Understanding and predicting cellular responses to disturbances, such as gene knockout or drug treatment, is a core challenge in biological and medical research [6]. - Advances in single-cell sequencing technology and breakthroughs in AI have reignited efforts to develop powerful virtual cell models that can predict responses across different cell types and states [6][20]. Group 3: Challenges in the Field - A significant bottleneck in the field is the lack of standardized evaluation criteria to assess whether a model truly understands cell biology rather than merely memorizing specific patterns in data [10]. - The Virtual Cell Challenge draws inspiration from the success of the CASP competition in protein structure prediction, which has catalyzed advancements in AI tools like AlphaFold [10]. Group 4: Challenge Design - The core task of the challenge is to assess the "cross-environment generalization" ability of models, requiring them to predict gene expression changes in a new cell type based on limited data from known cell types [13]. - A rigorous three-tier evaluation system is established to avoid model bias, focusing on differential expression scores, disturbance differentiation scores, and mean absolute error [14][15]. Group 5: Anticipated Impact - The challenge sets a benchmark for the industry by establishing a rigorous evaluation framework for predicting gene-level disturbance responses, guiding future developments in the field [19]. - It aims to promote data standards and reproducibility in single-cell functional genomics, accelerating the evolution of AI models through community competition and collaboration [19]. - The initiative is expected to gather global research efforts to tackle the challenges of virtual cell modeling, facilitating the transition from laboratory research to practical applications [19]. Group 6: Future Prospects - The first Virtual Cell Challenge focuses on gene disturbance predictions within a single cell type, with plans for future challenges to include combination disturbance predictions and integration of multi-omics data [20]. - The launch of the Virtual Cell Challenge signifies a new phase in AI-enabled life sciences, potentially transforming human understanding and intervention capabilities in biology [20].

Core Viewpoint - A recent study from the University of Science and Technology of China published in the journal Matter indicates that an iron-rich diet enhances the macro strength and toughness of bamboo rat tooth enamel, improving its damage resistance. This research provides new insights for the design of advanced structural materials and offers a novel approach to enhance human tooth enamel [3][6][9]. Group 1 - The study demonstrates that an iron-rich diet can significantly improve the mechanical properties of bamboo rat teeth, specifically their enamel strength and toughness [3][6]. - The research team successfully cultivated bamboo rats with iron-rich incisors and systematically studied the mechanical role of iron in tooth enamel [6][7]. - The findings suggest that the combination of compositional adjustments and graded structural advantages can synergistically enhance strength and toughness, providing new insights for advanced material design [9]. Group 2 - The study highlights the potential of dietary strategies to incorporate ions into the nanoscale structure of human tooth enamel, which could mitigate health risks associated with tooth fractures and cavities [9]. - The research indicates that the additional iron in the enamel of the bamboo rat enhances hardness, wear resistance, and damage resistance due to the aggregation of iron compounds in the intercrystalline domains [7]. - The results emphasize the importance of understanding how trace elements affect macro properties, which remains a relatively unexplored area in the field of biomaterials [5].