Core Viewpoint - The recent research on Ruddlesden-Popper structured double-layer nickelate La3Ni2O7 reveals its potential as a superconductor material, achieving a superconducting transition temperature (Tc) of approximately 80 K under pressures exceeding 14 GPa, while challenges remain in synthesizing high-quality single crystals without high-pressure oxygen growth conditions [2][4]. Group 1 - A study published in the journal Nature reports the observation of bulk superconductivity up to 96 K in pressurized nickelate single crystals synthesized at ambient pressure, breaking key limitations in the crystal growth of nickelate superconductors [4][9]. - The research team confirmed the high uniformity and excellent crystal quality of La2SmNi2O7-δ single crystals grown using a flux method, demonstrating clear bulk superconductivity, including zero-resistance phenomena at 21 GPa with a maximum onset Tc of 92 K and a maximum zero-resistance temperature of 73 K [7][9]. - The study indicates that both monoclinic and tetragonal crystal structures can support the superconductivity of the double-layer nickelate, with a correlation found between higher Tc under pressure and greater in-plane lattice distortion at ambient pressure [8][9]. Group 2 - The research provides effective pathways for achieving higher Tc in superconducting materials by elucidating the crystal structure characteristics of the superconducting state [9].

Core Viewpoint - Obesity is identified as a chronic metabolic disease characterized by excessive fat accumulation and is a major global public health concern, with nearly 50% of the adult population estimated to be overweight, leading to various non-communicable diseases [2] Group 1: Chronic Inflammation and Obesity - Chronic inflammation in adipose tissue is a key link between obesity and several chronic diseases, including type 2 diabetes, non-alcoholic fatty liver disease, and cardiovascular diseases [7] - The interaction between adipocytes and resident immune cells in adipose tissue plays a crucial regulatory role in this pathological process, although the underlying mechanisms remain largely unclear [7] Group 2: Research Findings - A recent study published in Signal Transduction and Targeted Therapy reveals that hypertrophic adipocytes mediate inflammation through a β2-microglobulin (B2M)-dependent mechanism, activating resident CD8+ T cells and macrophages in adipose tissue [4][5] - The study emphasizes the potential of targeting B2M in adipocytes as a therapeutic strategy for obesity-related chronic inflammation and metabolic disorders [5] Group 3: Mechanisms of Action - The research indicates that during obesity, the expression of B2M in hypertrophic adipocytes is upregulated, which not only activates CD8+ T cells but also promotes iron overload and ferroptosis in adipocytes, leading to M1 polarization of macrophages [7] - Specific knockout of B2M in adipocytes effectively inhibits the activation and accumulation of CD8+ T cells, as well as iron-induced cell death and M1 polarization, preventing obesity and related inflammation and metabolic disorders induced by a high-fat diet [7] Group 4: Correlation with Human Data - Bioinformatics analysis of human adipose tissue transcriptome data shows a strong correlation between B2M levels and obesity, with significantly elevated B2M expression found in adipocytes isolated from obese patients [9] - Overall, the findings highlight the critical role of adipocytes in obesity-related chronic inflammation and metabolic disorders through a B2M-dependent mechanism [9]

Core Viewpoint - A new study published in the journal Nature challenges the long-held belief that economic inequality significantly impacts subjective well-being and mental health, suggesting that the direct effects are negligible [2][4]. Group 1: Study Findings - The research conducted by the University of Lausanne analyzed 168 studies involving over 11.38 million participants, finding no significant correlation between economic inequality and subjective well-being [2][4]. - Initial analyses indicated a potential harmful effect of economic inequality on mental health, but further investigation revealed that this was largely influenced by "publication bias," where studies with significant findings are more likely to be published [4][8]. Group 2: Key Conditions for Impact - The study identified two critical conditions under which economic inequality may affect mental health and well-being: 1. Economic inequality impacts mental health primarily in low-income groups, where it correlates with poorer mental health outcomes due to heightened awareness of resource scarcity [11]. 2. The effect on happiness is influenced by inflation; during high inflation periods, economic inequality decreases life satisfaction, while in low inflation environments, it may even enhance happiness as people perceive inequality as a sign of economic mobility [11]. Group 3: Policy Implications - The findings suggest that policymakers should focus on reducing absolute poverty rather than merely addressing income disparity, controlling inflation to stabilize livelihoods, and providing targeted psychological support for low-income groups [15]. - The research emphasizes that economic inequality may act more as a catalyst rather than a direct cause of mental health issues, highlighting the need for nuanced policy interventions that address poverty and economic instability [15].

Core Viewpoint - The study reveals a signaling axis involving visceral adipose tissue-derived extracellular vesicles (VAT-EV) that promotes pancreatic cancer development and resistance to immune checkpoint blockade therapy in obese patients, suggesting potential new therapeutic strategies for obesity-related cancers [4][7]. Group 1: Research Findings - The research identifies that VAT-EV from obese patients facilitates communication with pancreatic ductal adenocarcinoma (PDAC) tissues [4]. - PDAC cells can internalize VAT-EV, leading to the stabilization of ribonuclease Rnaset2b and the production of free pseudouridine [4][5]. - Pseudouridine activates mast cells by increasing reactive oxygen species (ROS) and reducing H3K27me3 modifications, creating an immunosuppressive tumor microenvironment that promotes cancer progression [4][5]. Group 2: Implications for Therapy - Targeting the VAT-EV-CTSA-pseudouridine-mast cell signaling pathway could enhance the efficacy of immune checkpoint blockade therapy for PDAC [5][7]. - The study provides hope for developing new treatment strategies for obesity-related cancers by elucidating the molecular mechanisms linking obesity and cancer [7].

撰文丨王聪 编辑丨王多鱼 排版丨水成文 据估计，全球范围内约有 3.25 亿 人慢性感染了 乙型肝炎病毒 （HBV） ，尽管已有有效疫苗，HBV 仍导致了每年近 100 万人死亡。HBV 的慢性感染会对肝细 胞造成长期损伤，使感染者面临进展性肝病风险，近一半的 肝细胞癌 是因为 HBV 慢性感染所致。 目前，针对慢性乙型肝炎病毒 （HBV） 感染的治疗方法效果不佳，原因是高循环水平的乙型肝炎表面抗原 （HBsAg） 导致了免疫耗竭。 2025 年 12 月 1 日， 悦康药业 宋更申 团队在 Nature 子刊 Nature Communications 上发表了题为： An RNA interference therapeutic potentially achieves functional cure of chronic hepatitis B virus infection 的研究论文。 该研究表明，靶向 乙型肝炎病毒 S 区的 siRNA 药物 KC13-M2G2 ，有望实现慢性乙型肝炎病毒感染的功能性治愈。 这种名为 KC13-M2G2 的 siRNA 制剂在体外对所有乙型肝炎病毒 （HBV） 基 ...

撰文丨王聪 编辑丨王多鱼 排版丨水成文 热胁迫 （ Heat stress） 会触发细胞膜脂质重塑，然而这是否作为植物感知高温的信号，以及此类物 理信号如何被解码成生物学信号，目前仍不清楚。 2025 年 12 月 2 日， 上海交通大学农业与生物学院 林尤舜 团队、 中国科学院分子植物科学卓越创新中 心 林鸿宣 团队及广州医科大学/ 广州国家实验室 李亦学 团队合作，在国际顶尖学术期刊 Cell 上发表了题 为： A stepwise decoding mechanism for heat sensing in plants connects lipid remodeling to a nuclear signaling cascade 的研究论文。 该研究揭示了植物感知高温并启动防御反应的完整分子通路： DGK7 在质膜上 响应热胁迫，将二酰甘油转 化为 磷脂酸，MdPDE1 感知磷脂酸后进入细胞核，通过降解 cAMP 调控基因表达， TT2 通过抑制 DGK7 活性实现信号通路的负反馈调节。进一步田间试验证实，通过调控该通路可精准设计水稻的耐高温性，为 应对全球变暖下的粮食安全提供了新的育种策略。 在这 ...

Core Viewpoint - The article discusses the launch of a new research journal, Chem Circularity, by Cell Press, focusing on advancing circular development solutions and transforming linear processes into sustainable closed-loop systems [1][2][3]. Group 1: Journal Overview - Chem Circularity aims to publish cutting-edge research that emphasizes reduction, redesign, reuse, and recycling, moving beyond just end-of-life recycling to source reduction and product redesign [2][4]. - The journal is positioned as a top-tier interdisciplinary platform, welcoming research from various fields such as chemistry, engineering, materials science, biotechnology, environmental science, business, and policy [4][5]. Group 2: Editorial Vision - The inaugural editor, Dr. Michelle Muzzio, emphasizes the journal's mission to connect foundational technologies with systemic thinking in circular economy research [7][10]. - The journal seeks to create a dedicated space for researchers to address fundamental questions about moving away from fossil fuels and minimizing waste [10][11]. Group 3: Unique Features - Chem Circularity introduces a new article type called "Closing the Loop," which showcases collaborations between academia and industry to optimize processes and accelerate innovation [16]. - The journal will require research articles, reviews, and perspectives to include a "context & scale" section, allowing authors to explain how their work fits into broader circular economy frameworks [15][16]. Group 4: Future Aspirations - The journal aims to publish impactful research that resonates with both the public and policymakers, fostering a deeper understanding of circular economy issues across various disciplines [17][22]. - There is a high expectation for the journal's quality, with an initial target impact factor of over 10 [22].

Core Viewpoint - Lung cancer is the most common cancer globally and a leading cause of cancer-related deaths. Radiation therapy (RT) is an effective method for controlling local tumors in lung cancer, but its long-term benefits are often compromised by radioresistance, leading to tumor recurrence. The development of targeted therapies has significantly improved the prognosis for lung cancer patients, particularly those with non-small cell lung cancer (NSCLC). However, inherent and acquired resistance to targeted drugs remains a challenge, and the complex interactions between targeted therapies and radiation therapy are a research focus. Therefore, understanding the molecular mechanisms of radioresistance in lung cancer and exploring the combination of targeted therapy with radiation therapy is urgent [1][4]. Group 1 - The study published by researchers from Sichuan University West China Hospital identifies the JMJD6/EHF signaling axis as a potential therapeutic target to overcome radioresistance in non-small cell lung cancer [2][3]. - The research aims to explore new mechanisms of tumor metastasis following radiation therapy in NSCLC patients and to enhance the durability of radiation therapy's efficacy [5]. - The study utilized human NSCLC tissue arrays, whole transcriptome sequencing, CUT&Tag sequencing, and single-cell RNA sequencing to identify gene expression changes induced by radiation therapy [5]. Group 2 - Results indicate that radiation therapy upregulates the expression of JMJD6 in NSCLC tissues, and high expression of JMJD6 is associated with reduced overall survival [5]. - This upregulation activates EHF and leads to the demethylation of H4R3me2s, subsequently transcribing pluripotency factor genes. The JMJD6/EHF signaling axis plays a critical role in the metastasis of NSCLC, potentially mediated through TGF-β/SMAD and AKT/ERK signaling pathways [5]. - These findings suggest that JMJD6 may serve as a potential therapeutic target against tumor metastasis following radiation therapy in non-small cell lung cancer [5].

撰文丨王聪 编辑丨王多鱼 排版丨水成文 艾滋病 （AIDS） 是 获得性免疫缺陷综合征 的简称，由感染 HIV 病毒引起。HIV 是一种能攻击人体免疫系统的病毒，它把人体免疫系统中重要的 CD4 + T 细胞 作为主要攻击目标，大量破坏该细胞，经过数年、甚至长达十年或更长的潜伏期后发展成艾滋病病人，使人体丧失免疫功能，因抵抗力极度下降会出现多种感 染，后期常常发生恶性肿瘤，以至全身衰竭而死亡。 据估计，自艾滋病流行以来，全世界累计感染患者高达 8800万，造成了数千万人死亡。然而，起劲仍未研发出有效的 艾滋病疫苗，现有的 抗逆转录病毒药物 （ART） 也只能抑制病毒，不能清除 HIV 病毒或治愈艾滋病。 迄今为止，全世界只有 6 位艾滋病患者被宣布"治愈"，分别是—— 分别是 " 柏林病人 "、" 伦敦病人 "、 " 杜塞尔多夫病人 "、 " 纽约病人 "、" 希望之城病人 "和" 日内瓦病人 "。 早在 1996 年， 邓宏魁 等人发现了 CCR5 是 HIV-1 病毒入侵人类 T 细胞的主要受体。有极少数人因为携带了罕见的 CCR5 Δ32/ Δ32 基因纯合突变，导致不 会感染艾滋病。长期以来，携带 C ...

Core Viewpoint - The emergence of GLP-1 receptor agonists, such as Semaglutide developed by Novo Nordisk, marks a new era in safe and effective weight loss, initially intended for type 2 diabetes treatment but showing significant weight reduction effects in non-diabetic patients [2][3]. Group 1: GLP-1 Receptor Agonists - GLP-1 receptor agonists primarily reduce caloric intake, potentially mediated by activating GLP-1 receptors in the central nervous system, leading to significant weight loss [2]. - These drugs are generally considered safe but may cause gastrointestinal side effects, including nausea, vomiting, and diarrhea [2]. - A major challenge with GLP-1 receptor agonists is the difficulty in maintaining weight loss long-term due to metabolic adaptation, which reduces energy expenditure and can lead to weight regain upon discontinuation [2]. Group 2: NN501 Development - A new peptide analog, NN501, developed by researchers from the University of Manchester and Novo Nordisk, shows weight loss effects comparable to Semaglutide but operates through a different mechanism, primarily increasing energy expenditure via sustained fatty acid oxidation rather than reducing food intake [3][5]. - NN501 does not produce significant gastrointestinal side effects or muscle loss, and weight rebound after discontinuation is less pronounced compared to GLP-1 receptor agonists [5][7]. - This new treatment could serve as a viable alternative or complementary therapy for obesity management [7].