Core Viewpoint - Long-term exposure to air pollutants, specifically PM2.5, significantly increases the risk of Lewy body dementia (LBD), highlighting the need for further research on air pollution's role in neurodegenerative diseases and its implications for public health strategies [4][11]. Group 1: Research Findings - A large-scale study involving 56 million individuals indicates a strong association between long-term PM2.5 exposure and hospitalization due to α-synucleinopathies, particularly in patients with LBD compared to those with non-dementia Parkinson's disease [4][7]. - The study demonstrates that α-synuclein plays a critical role in PM2.5-related neurodegenerative diseases, with wild-type mice exposed to PM2.5 for 10 months showing brain atrophy, cognitive deficits, and widespread α-synuclein pathology [8][11]. - PM2.5 exposure induces a pathogenic variant of α-synuclein, termed PM-PFF, which exhibits characteristics similar to those found in human LBD, including accelerated aggregation and increased neurotoxicity [8][11]. Group 2: Mechanisms and Implications - Chronic PM2.5 exposure and PM-PFF inoculation in humanized α-synuclein mice trigger gene expression changes that resemble those in LBD patients, underscoring a specific pathogenic axis for LBD [9][11]. - The findings suggest that PM-PFF could serve as a potential therapeutic target, emphasizing the importance of understanding environmental mechanisms in the pathogenesis of LBD [11].

Core Insights - Stem cells are at the forefront of life sciences research, known for their self-renewal and differentiation capabilities, often referred to as "seeds of life" [1][2] - Ongoing research on stem cells contributes to various fields, including cell therapy, organ replacement, disease gene therapy, and drug development [2] Conference Overview - The conference titled "Stem Cell Biology: From Embryonic Development to Aging and Therapy" will be held from November 19-21, 2025, at Westlake University, Hangzhou, China [3][5] - The event aims to explore the relationship between stem cells and life mechanisms such as development and aging, fostering academic exchange and collaboration among global scientists [3][6] Key Topics - The conference will cover core topics including organ formation, cellular clonality and lineage, tissue repair, cellular reprogramming, and regenerative medicine [7] - A poster presentation session will be included, allowing selected abstracts to be presented orally, along with a "Meet the Editor" segment for deeper engagement with journal editors [7] Registration Details - Registration fees vary based on the timing and participant category, with early bird rates starting at RMB 900 for students and RMB 1500 for external participants [34] - Participants can submit academic posters for evaluation, with specific requirements for size and format [34] Notable Speakers - The conference will feature prominent speakers from various prestigious institutions, including Linda Partridge from University College London and Toshiro Sato from Keio University [9][11]

该论文题为： Agriculture breaks down traditional biogeographic barriers of soil fungi （农业打破了土 壤真菌的传统生物地理屏障 ） ，该论文于 2025 年 8 月 27 日在线发表于 Cell 子刊 One Earth 上， 论 文通讯作者为西北农林科技大学 焦硕 教授和 韦革宏 教授。 撰文丨王聪 编辑丨王多鱼 排版丨水成文 近日， 西北农林科技大学 的一项最新研究登上了 Cell Press 官网头条。 研究团队表示，随着全球粮食需求的增长，农业扩张已成为地球上生物多样性变化最普遍的驱动因素之 一。了解农业如何影响生物多样性对于构建可持续的粮食系统和保护生态系统健康至关重要。虽然农业对 于养活世界至关重要，但它也以我们刚刚开始理解的方式深刻地重塑着自然世界。而通过了解土地利用变 化如何重塑微生物的生物地理分布，我们能够更好地预测集约化农业的生态代价，并为更可持续的土地管 理提供信息。此外，这项研究也为将生物多样性因素纳入农业和保护规划提供了科学基础。 农业扩张和集约化正在重塑生物多样性格局，给维持生态系统功能带来了紧迫挑战。土地利 ...

编辑丨王多鱼 排版丨水成文 行星内部存在 内核 （ inner core， IC） 这一情况在行星演化过程中具有重要意义。然而，对 行星深部结构的探测向来充满挑战，实际上，1936 年科学家通过 地震波首次推测出地球内核的存在，但直到 1980 年代才充分确认这一点。迄今为止，除了地球和月球之外，其他天体的内核尚未得到确认。 2025 年 9 月 3 日，中国科学技术大学 孙道远 教授作为通讯作者， 毕慧星 作为第一作者，在 Nature 期刊发表了题为： Seismic detection of a 600-km solid inner core in Mars 的研究论文 。 研究团队通过深入分析美国 NASA"洞察号" （InSight） 火星探测 器记录的火震 （火星上的地震） 数据， 首次确证 火星 内部存在一个半径约 600 千米的 固态 内核 ，并揭示其主要成分构成可能是富含轻元素的结晶铁镍合金。 该研究是首次在地球以外的行星中确认了固态内核的存在，证实了火星与地球相似的核幔分异结构。 对类地行星而言， 固态内核 的存在对其核心成分与热演化过程以及行星磁场历史具有重要影响。 对于火星而言，其具有 ...

Core Insights - On September 3, 2025, a total of 27 papers were published in the prestigious journal Nature, with 8 of them authored by Chinese scholars, highlighting the significant contribution of Chinese researchers to global scientific discourse [3][5][7][8][10][11][13][15]. Group 1: Research Contributions - The paper titled "Cas9 senses CRISPR RNA abundance to regulate CRISPR spacer acquisition" was published by researchers from the University of Michigan, with Zhang Yan and Hou Zhonggang as co-corresponding authors and Zhou Xufei as the first author [3]. - The study "Divergent evolutionary strategies pre-empt tissue collision in gastrulation" was authored by Yu-Chiun Wang from RIKEN, showcasing innovative evolutionary strategies [5]. - "Single-cell transcriptomic and genomic changes in the ageing human brain" was published by researchers from the University of Massachusetts Medical School, with Wang Zhiping and Tianxiong Yu as co-first authors [7]. - The research "Spatial joint profiling of DNA methylome and transcriptome in tissues" was conducted by scholars from the University of Pennsylvania, with Yanxiang Deng and Wanding Zhou as co-corresponding authors [8]. - The paper "3D-printed micro ion trap technology for quantum information applications" was co-authored by Shuqi Xu from UC Berkeley and Xiaoxing Xia from Lawrence Livermore National Laboratory [10]. - "Supervised learning in DNA neural networks" was published by Lulu Qian from Caltech, contributing to advancements in neural network applications [11]. - The study "PICALM Alzheimer's risk allele causes aberrant lipid droplets in microglia" was authored by researchers from the Endeavor Health Research Center and the University of Chicago, with Jubao Duan as the corresponding author [13]. - The research "Seismic detection of a 600-km solid inner core in Mars" was led by Professor Sun Daoyuan from the University of Science and Technology of China, marking a significant advancement in planetary science [15].

Core Viewpoint - The research identifies a metabolic vulnerability in glioblastoma, revealing that the tumor relies on "stealing" serine from its environment for rapid growth, which can be targeted for treatment [4][8]. Group 1: Research Findings - Glioblastoma is the most common and aggressive primary malignant brain tumor in adults, with standard treatments including surgery, radiotherapy, and temozolomide chemotherapy, but it often recurs, leading to a high mortality rate within 1-2 years post-diagnosis [3]. - The study published in Nature highlights that glioblastoma tumors can utilize serine from their surroundings instead of synthesizing it, presenting a critical metabolic weakness [4][8]. - By feeding glioblastoma mouse models a diet lacking serine, researchers observed a slowdown in tumor growth and spread, extending survival time [4][8]. Group 2: Metabolic Mechanism - The research team analyzed samples from eight glioblastoma patients and found that tumors utilize glucose from the environment to synthesize essential components like DNA, facilitating aggressive growth [6][7]. - In healthy brain tissue, glucose is metabolized for the tricarboxylic acid (TCA) cycle and converted into serine, while glioblastoma bypasses serine synthesis by "stealing" it, allowing glucose to be redirected for synthesizing nucleotides necessary for cancer cell proliferation [7][8]. Group 3: Clinical Implications - The study suggests that the reliance on serine presents a targetable metabolic vulnerability, and the team plans to conduct clinical trials on a serine-restricted diet for patients, which, while not curative, could provide additional time for some patients [8].

Core Viewpoint - The study identifies mitochondrial dysfunction as a potential mechanism for autism-related social deficits through the elevation of H₂S levels and subsequent sulfhydration of synaptic proteins [3][6]. Group 1: Research Findings - Mitochondrial dysfunction leads to increased H₂S levels, which mediates the sulfhydration of the synaptic protein mGluR5, potentially contributing to social deficits associated with autism [3][6]. - The research focused on the anterior cingulate cortex (ACC) and found that overexpression of cystathionine β-synthase (CBS) in wild-type mice impaired synaptic transmission and social function, while its knockdown effectively restored these functions in two autism mouse models [4][6]. - Significant changes in the sulfhydration of synaptic proteins were observed in Shank3b−/− ACC, confirming excessive sulfhydration of mGluR5 in both autism mouse models [4][6]. Group 2: Implications and Mechanisms - The study suggests that excessive H₂S and the sulfhydration of synaptic proteins may be underlying mechanisms for social function impairments in autism [6][7]. - Reducing the intake of sulfur-containing amino acids improved social dysfunction in Shank3b−/− and Fmr1−/y mice, as well as synaptic defects in corresponding human neurons [4][7].

Core Viewpoint - The research reveals that cancer cells hijack iron-rich macrophages in the bone marrow to promote bone metastasis and anemia, opening new avenues for therapies to mitigate both bone metastasis and associated severe anemia [3][12]. Group 1: Mechanism of Cancer Metastasis - Cancer cells effectively "hijack" a specific type of macrophage, known as VCAM1+ CD163+ CCR3+ macrophages, which are responsible for recycling iron in the bone, depriving red blood cells of the iron needed for maturation [5][10]. - The study indicates that the hijacking of these macrophages not only leads to a lack of iron necessary for red blood cell development but also supports tumor growth in the bone [9][10]. Group 2: Implications for Anemia - The cancer cells' action results in the red blood cells being in an immature state, leading to anemia due to insufficient healthy red blood cell production [9][10]. - Tumor cells simulate red blood cells to adapt to the hypoxic environment of the bone tissue, utilizing the stolen iron to produce hemoglobin, which is crucial for oxygen transport [9][12]. Group 3: Research Significance - This research shifts the focus from solely studying cancer cells ("seeds") to understanding the surrounding microenvironment ("soil") that facilitates cancer metastasis [7][8]. - The findings have broader implications beyond metastatic breast cancer, potentially extending to other major cancer types, highlighting the importance of the tumor's manipulation of its environment [12].

Core Viewpoint - The research reveals a conserved BBM-BAR1 regulatory module that can directly drive the fate reprogramming of microspores from gametophyte development to embryogenesis, providing a revolutionary new method for efficient in vivo haploid induction in various crops, overcoming the long-standing technical bottleneck of stress treatment [9]. Group 1 - The study demonstrates that stress treatment induces the specific expression of the transcription factor BABY BOOM (BBM) in microspores, which is sufficient to induce fate change and embryogenesis in tobacco and rice microspores, indicating BBM as a key regulatory factor in stress-induced reprogramming [5][6]. - BAR1 (BBM-activated Androgenesis Regulator 1) is identified as a new downstream effector of BBM, capable of independently initiating the embryogenesis process in microspores, similar to the role of BBM in promoting fate reprogramming [5][7]. Group 2 - Ectopic expression of BBM in microspores can trigger in vivo male gametophyte development within anthers [7]. - The expression of BBM and BAR1 can replace the need for stress treatment in inducing male gametophyte development [7]. - The conserved BBM-BAR1 module enables efficient in vivo haploid induction across various crops [7].

Core Viewpoint - The study highlights the role of the metabolite Xylulose 5-phosphate (Xu5P) in enhancing the sustained antitumor activity of SLC35E2+ exhausted CD8+ T effector cells, suggesting dietary interventions as a potential treatment for metastatic cancer [3][8]. Group 1: Research Findings - Xu5P promotes the sustained antitumor activity of SLC35E2+ CD8+ exhausted precursor T cells, and its supplementation or consumption of Xu5P-rich foods can synergize with anti-PD-1 therapy to significantly enhance antitumor immune responses [3][7]. - The study identifies Xylulose kinase (XYLB) as a tumor suppressor that generates Xu5P, which enhances the cytotoxicity of CD8+ T cells and inhibits tumor colonization in the lungs [6][8]. - Clinical data indicate that elevated levels of XYLB or increased Xu5P in the blood correlate with enhanced CD8+ T cell efficacy and reduced tumor metastasis [7][8]. Group 2: Mechanism of Action - CD8+ T cells express SLC35E2, which is essential for the transport of Xu5P, thereby maintaining energy/redox homeostasis through the pentose phosphate pathway and glycolysis [7][8]. - Xu5P promotes the generation of SLC35E2+ CD8+ exhausted precursor T cells by mediating TET3-driven DNA demethylation of the Tcf7 promoter, enhancing CD8+ T cell responses [7][8]. - Supplementation with Xu5P or dietary plans rich in Xu5P shows synergistic effects with anti-PD-1 therapy, significantly boosting antitumor immune responses [6][8].