Core Insights - The research published by the team from USC Keck School of Medicine demonstrates the successful construction of human kidney organoids with complex three-dimensional structures, which replicate most physiological functions of the kidney and produce urine-like fluids after transplantation [3][4]. Group 1: Research Findings - The study introduces kidney progenitor assembloids (KPA) derived from human pluripotent stem cells (hPSC), which exhibit significant advancements in cellular complexity and maturity, successfully mimicking the self-assembly process of kidney progenitor cells observed in vivo [4][5]. - The KPA model allows for high-fidelity disease modeling, specifically creating a model for autosomal dominant polycystic kidney disease (ADPKD), which replicates cystic phenotypes and the molecular and cellular characteristics of the disease [5][7]. Group 2: Implications and Applications - This innovative platform for kidney organoids opens new avenues for high-fidelity disease modeling and lays a solid foundation for regenerative medicine in the field of nephrology, with significant implications for drug development and disease simulation [3][7].

Core Insights - The article discusses a recent study from Northeast Agricultural University published in Cell Host & Microbe, highlighting the role of common mycorrhizal networks (CMN) in enhancing plant disease resistance through alterations in the rhizosphere microbiome assembly [5][6]. Group 1: Research Findings - The study demonstrates that CMN mediates inter-plant communication, regulating the assembly of rhizosphere microbiomes [7]. - Arbuscular mycorrhizal fungi (AMF) transfer jasmonic acid from pathogen-infected donor plants to healthy receptor plants [7]. - The transfer of jasmonic acid alters the root exudates of receptor plants, leading to changes in their rhizosphere microbiome [7]. Group 2: Mechanism of Action - Pathogen infection in donor plants triggers the transfer of jasmonic acid through CMN, activating the defense mechanisms in receptor plants [9]. - This process results in changes to the composition of root exudates, which in turn recruits beneficial microorganisms that suppress pathogen infections [9]. - The study outlines a complete pathway by which CMN enhances plant disease resistance, providing new insights for agricultural biocontrol strategies [9].

Core Insights - On September 17, 2025, a total of 24 papers were published in the prestigious journal Nature, with 10 of them authored by Chinese scholars, highlighting the significant contribution of Chinese researchers to global scientific advancements [2][5][7][9][12][14][16][18][21]. Group 1: Research Contributions - A paper titled "Toughened self-assembled monolayers for durable perovskite solar cells" was co-authored by scholars from Hong Kong City University and the Chinese Academy of Sciences, focusing on enhancing the durability of perovskite solar cells [2]. - Another significant paper, "A movable long-term implantable soft microfibre for dynamic bioelectronics," was published by researchers from the Chinese Academy of Sciences and Donghua University, contributing to the field of bioelectronics [5]. - The paper "Atomic-scale imaging of frequency-dependent phonon anisotropy" was authored by researchers from the University of California, Irvine, providing insights into phonon behavior at the atomic level [7]. - A study titled "Covariation mass spectrometry uncovers a protein that controls cysteine catabolism" was led by a researcher from Dana-Farber Cancer Institute, revealing important findings in protein metabolism [9]. - The research "A room temperature rechargeable all-solid-state hydride ion battery" was published by scholars from the Dalian Institute of Physical Chemistry, focusing on advancements in battery technology [12]. - A paper on "High-density soft bioelectronic fibres for multimodal sensing and stimulation" was authored by researchers from Stanford University, contributing to the development of bioelectronic devices [14]. - The study "DeepSeek-R1 incentivizes reasoning in LLMs through reinforcement learning" was published by DeepSeek, exploring advancements in large language models [16]. - A paper titled "Structural basis for mTORC1 activation on the lysosomal membrane" was authored by researchers from the University of California, Berkeley, providing insights into cellular signaling mechanisms [17]. - The research "Peroxisomal metabolism of branched fatty acids regulates energy homeostasis" was published by scholars from Washington University in St. Louis, contributing to the understanding of metabolic processes [18]. - A study on "Delta-type glutamate receptors are ligand-gated ion channels" was published by Johns Hopkins University, enhancing knowledge in neurobiology [21].

Core Viewpoint - The article discusses the discovery of Lac-Phe, a metabolite produced during intense exercise, which suppresses appetite and aids in weight loss without adverse side effects [2][3][10]. Group 1: Research Findings - Lac-Phe is identified as the most significantly increased metabolite in the blood after intense exercise, observed in mice, humans, and racehorses [6]. - The recent study published in Nature Metabolism reveals that Lac-Phe inhibits AgRP neurons, which are responsible for stimulating hunger, thereby reducing food intake [3][10]. - The mechanism by which Lac-Phe suppresses appetite involves the activation of ATP-sensitive potassium channels (K ATP) on AgRP neurons, leading to hyperpolarization and reduced activity of these neurons [11]. Group 2: Implications for Weight Management - The findings provide insights into how exercise naturally lowers appetite and improves metabolism, suggesting potential new targets for obesity treatment [12]. - The research indicates that both metformin and exercise may utilize the same pathway through Lac-Phe to achieve appetite suppression and weight loss [8].

Core Viewpoint - The article discusses the successful application of in vivo CAR-T cell therapy for treating refractory systemic lupus erythematosus (SLE), highlighting its potential to provide rapid and lasting relief without severe side effects [2][3][14]. Group 1: Research Background - In August 2021, a team from Erlangen-Nuremberg University published a paper in NEJM demonstrating the use of CAR-T cell therapy for systemic lupus erythematosus, leading to rapid and sustained relief for patients [2]. - Traditional CAR-T cell therapy is complex and costly, requiring chemotherapy pretreatment, which can cause serious side effects [2][5]. Group 2: Study Details - A paper published on September 17, 2025, in NEJM presented the first human clinical study using mRNA-LNP based in vivo CAR-T cell therapy for SLE [2]. - The study involved five patients with refractory SLE, showing B cell clearance and reduced disease activity without severe toxic effects [3][8]. Group 3: Technology and Methodology - The in vivo CAR-T cell therapy utilizes engineered lipid nanoparticles (EnC-LNP) to deliver CD19 CAR mRNA directly to CD8+ T cells, generating functional CAR-T cells in situ [5][6]. - HN2301, developed by Hongxin Biotech, successfully transduced CD19 CAR into CD8+ T cells in preclinical studies without significant toxicity [6][10]. Group 4: Treatment Outcomes - After HN2301 infusion, CD8+ CD19 CAR-T cells were detectable within 6 hours, with significant B cell reduction observed in patients receiving higher doses [10]. - No severe cytokine release syndrome or immune effector cell-associated neurotoxicity syndrome was reported, with only mild side effects noted [12][14]. Group 5: Efficacy and Future Directions - All five patients showed a decrease in systemic lupus erythematosus disease activity index scores after three months of treatment, indicating improved disease activity [12][14]. - The findings support the feasibility and effectiveness of in vivo CAR-T cell therapy in autoimmune diseases, although further data is needed to assess long-term efficacy and appropriate dosing for sustained remission [14].

Core Viewpoint - The article discusses the potential of CRISPR activation (CRISPRa) technology in treating SCN2A-related neurodevelopmental disorders, particularly focusing on haploinsufficiency as a common cause of these disorders [3][6][8]. Group 1: Research Findings - SCN2A haploinsufficiency is a leading cause of neurodevelopmental disorders, often resulting in autism, intellectual disability, and in some cases, refractory epilepsy [3]. - A study published in Nature demonstrated that CRISPRa could successfully restore SCN2A levels in a mouse model equivalent to a 10-year-old human, reversing neurodevelopmental disorders [3][6]. - The research team confirmed that restoring Scn2a expression in adolescent mice could rescue related electrophysiological defects [6][8]. Group 2: Methodology - The study utilized adeno-associated virus (AAV) to deliver CRISPRa, correcting intrinsic defects in cortical pyramidal cells, which are primarily responsible for the neurodevelopmental disorders and epilepsy associated with SCN2A haploinsufficiency [6][7]. - Systemic delivery of CRISPRa enabled Scn2a+/− mice to resist chemically induced seizures, indicating the therapeutic potential of this approach [7]. Group 3: Implications and Future Directions - The results suggest that CRISPRa-based therapeutic strategies could effectively rescue SCN2A haploinsufficiency, even when intervention occurs during adolescence [8]. - Regel Therapeutics has obtained licensing from the University of California, San Francisco, to develop therapies targeting SCN2A haploinsufficiency, highlighting the commercial potential of this research [8].

Core Viewpoint - The article emphasizes the importance of Open Access (OA) in accelerating research dissemination and fostering global collaboration, ultimately enhancing scientific innovation and public access to scientific advancements [2]. Group 1: Open Access and Its Benefits - Open Access serves as an "accelerator" for research outcomes to be quickly transformed into real-world solutions and as a "catalyst" for innovation by breaking down knowledge barriers [2]. - Governments, funders, and institutions are increasingly recognizing the value of open research, leading to more funding support for OA initiatives [2]. - Springer Nature has collaborated with various institutions to facilitate the transition to Open Access and has released the "Open Access Journal Handbook and Author Guidelines" to encourage authors to publish OA research [2]. Group 2: Nature Portfolio's Communications Series - The Communications series of journals under Nature Portfolio focuses on publishing high-quality research that provides new insights across various disciplines while ensuring diversity among content, editors, authors, and reviewers [4]. - The series currently includes nine peer-reviewed journals, all of which are Open Access, allowing immediate online access to published articles [12]. - The journals have shown significant performance metrics, with six journals ranked in the Q1 category according to the 2024 Journal Citation Reports, and five journals have seen an increase in their impact factors [12]. Group 3: Journal Performance Metrics - **Communications Biology**: Impact Factor (2024): 5.1, Acceptance Rate: 33.1%, Median Time to First Decision: 11 days [14]. - **Communications Chemistry**: Impact Factor (2024): 6.2, Acceptance Rate: 51.9%, Median Time to First Decision: 7 days [18]. - **Communications Earth & Environment**: Impact Factor (2024): 8.9, Acceptance Rate: 30.8%, Median Time to First Decision: 9 days [22]. - **Communications Materials**: Impact Factor (2024): 9.6, Acceptance Rate: 26.2%, Median Time to First Decision: 4 days [30]. - **Communications Medicine**: Impact Factor (2024): 6.3, Acceptance Rate: 31.1%, Median Time to First Decision: 15 days [34]. - **Communications Physics**: Impact Factor (2024): 5.8, Acceptance Rate: 31.3%, Median Time to First Decision: 9 days [38].

Core Viewpoint - The article discusses the development and capabilities of DeepSeek-R1, a reasoning model that significantly reduces computational costs while enhancing reasoning abilities in large language models (LLMs) through pure reinforcement learning [1][2]. Group 1: Model Development and Training - DeepSeek-R1 was launched by a startup in Hangzhou, China, on January 20, 2025, and has gained global attention for its strong reasoning capabilities and low computational requirements [1]. - The training cost for DeepSeek-R1 was only $294,000, which is significantly lower than similar models that often cost tens of millions [2]. - The model employs a pure reinforcement learning approach, minimizing reliance on human-annotated reasoning paths, which allows for more autonomous exploration of reasoning capabilities [6][10]. Group 2: Performance and Capabilities - DeepSeek-R1-Zero, a precursor to DeepSeek-R1, demonstrated remarkable performance improvements in reasoning tasks, achieving an average pass@1 score of 77.9% in the American Mathematics Invitational Exam (AIME) 2024, up from 15.6% [17]. - The model also excelled in programming competitions and graduate-level problems in biology, physics, and chemistry, showcasing its versatility [19]. - The research indicates that advanced reasoning behaviors, such as self-validation and reflection, emerged organically during the reinforcement learning process [29]. Group 3: Challenges and Limitations - Despite its strengths, DeepSeek-R1-Zero faces challenges such as poor readability and language mixing issues, particularly when responding in both English and Chinese [21]. - The model's performance in broader domains like writing and open-domain Q&A remains limited due to its focus on reasoning tasks during training [22]. - The article highlights potential ethical risks associated with enhanced reasoning capabilities, including vulnerability to jailbreak attacks and the generation of dangerous content [27][28].

撰文丨王聪 编辑丨王多鱼 排版丨水成文 慢性肾病 （CKD） 已成为全球性的健康危机，其患病率不断上升，并对患者的生活质量和死亡率产生深远影响。在 CKD 的诸多严重并发症中，与 心血管疾病 （CVD） 的关联尤为突出，CVD 导致的死亡占 CKD 患者死亡总数的一半以上，心力衰竭 （HF） 更是其中导致死亡的主要因素。 尽管在理解 CKD 肾功能障碍的病理生理学方面取得了重大进展，但 CKD 患者的心血管并发症发病率的上升凸显了我们知识上的重大空白，尤其是关于肾功能障 碍与心脏疾病之间关联机制的认识不足。这些空白突显了迫切需要新的预测性生物标志物和更有效的治疗靶点来减轻这些并发症。 心力衰竭 （HF） 在 慢性肾病 （CKD） 患者中极为常见，并与肠道微生物群的变化有关，但其潜在机制目前尚不清楚，这给诊断和治疗带来了困难。 2025 年 9 月 16 日，南方医科大学周宏伟、李壮团队联合哈尔滨医科大学第一附属医院李悦团队，在 Cell 子刊 Cell Host & Microbe 上发表了题为： Gut Microbiota-Derived Indole Sulfate Promotes Heart Fai ...

Core Viewpoint - The study published by the team from the University of Chicago identifies a specific mutation in the PICALM gene that leads to the accumulation of harmful lipid droplets in microglia, resulting in impaired phagocytic function and increased risk of late-onset Alzheimer's disease (LOAD) [2][3][7]. Group 1: Research Findings - The research utilized a functional genome-wide association study (GWAS) approach to identify potential LOAD risk mutations in neurons, astrocytes, and microglia derived from human induced pluripotent stem cells (iPSCs) [5]. - The study revealed 26 functional risk mutations specific to LOAD, most of which are present in microglia [5]. - The LOAD risk allele rs10792832 in the PICALM gene reduces the binding of the transcription factor PU.1 and the expression of PICALM, impairing the uptake of β-amyloid (Aβ) and neurofibrillary debris [5]. Group 2: Mechanism of Action - The research elucidates that the selective susceptibility of microglia to LOAD is mediated through the accumulation of harmful lipid droplets at the PICALM gene locus [7]. - Microglia carrying the PICALM risk allele show enrichment in transcriptional pathways related to cholesterol synthesis and lipid droplet formation [5]. - Genetic and pharmacological interventions in microglia confirmed the causal relationship between reduced PICALM expression, lipid droplet accumulation, and impaired phagocytic function [5]. Group 3: Implications for Clinical Interventions - This study provides a critical neurobiological basis for developing new clinical intervention strategies for Alzheimer's disease [7].