Core Viewpoint - Jinan University is recruiting outstanding young scholars globally for its Nano Intelligent Manufacturing Research Institute, focusing on advanced materials and biomedical fields to drive scientific innovation and technology transfer from laboratory to industry [2]. Group 1: Research Areas - The research institute invites applications from scholars in various fields, including but not limited to materials science, chemistry, artificial intelligence, nanomedicine, and drug delivery [4][8]. Group 2: Application Requirements - Candidates must have a PhD, be born on or after January 1, 1985, and have at least 36 months of formal teaching or research experience at overseas institutions post-PhD [8]. Group 3: Compensation and Support - The position offers a maximum annual salary of 1 million RMB, a housing allowance up to 3.5 million RMB, and research startup funds ranging from 6 million to 8 million RMB [16]. - Additional support includes assistance in applying for major talent projects and guaranteed student enrollment [16]. Group 4: Application Process - Eligible candidates should send a detailed resume to specified contacts, including personal information, academic background, and research achievements [12].

Core Viewpoint - The research highlights the role of the fungal commensal Kazachstania pintolopesii (Kp) in promoting intestinal repair through its secreted peptide, CD12, marking a significant advancement in understanding gut regeneration mechanisms and positioning gut fungi as potential biotherapeutics for inflammatory and iatrogenic bowel diseases [3][7]. Group 1 - The study confirms that the secreted protein Ygp1 from Kp plays a crucial mediating role in intestinal regeneration [6]. - A 12-amino acid peptide fragment, CD12, derived from Ygp1, is sufficient to promote differentiation of intestinal organoids and accelerate gut healing in mouse models of colitis and chemotherapy-induced damage [6]. - CD12 interacts with mammalian α-enolase (ENO1), increasing YAP1 protein levels and activating regeneration-related transcriptional programs via the Hippo signaling pathway [6]. Group 2 - The research provides a translatable delivery strategy by demonstrating that engineered probiotics expressing CD12 can replicate its therapeutic benefits [6].

撰文丨王聪 编辑丨王多鱼 排版丨水成文 虽然我们对产生 细胞因子 （ Cytokine ） 的细胞特性及其调控机制已有较多了解，但对于响应细胞因子的 细胞类型，仍缺乏系统认知。 2026 年 1 月 7 日，哈佛医学院 Jun R. Huh 团队与麻省理工学院 Gloria B. Choi 团队合作 （博士后 芦广 庆 为论文第一作者） ，在国际顶尖学术期刊 Cell 上发表了题为： In vivo detection of immune responses via cytokine activity labeling 的研究论文。 该研究开发了一种名为 CyCLoP （ Cy tokine- C ellular- Lo cating- P latforms，细胞因子-细胞定位平 台） 的报告系统，可用于可视化、定位并鉴定 对细胞因子作出响应的细胞 。该平台通过将细胞因子结合 所诱导的细胞因子受体 （cytokine receptor） 二聚化事件转化为可遗传追踪的荧光信号， 实现对细胞因 子响应的精准监测 ，为深入理解细胞因子如何在生理与疾病状态下塑造不同的免疫结局提供了强有力工 具。 芦广庆 ，2012 ...

Core Viewpoint - The study highlights the role of hepatic GPR110 in the sex-specific development of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASH), suggesting it as a potential target for female-specific therapies [4][8]. Group 1: Research Findings - GPR110 is identified as a liver-specific G protein-coupled receptor (GPCR) that is closely related to MASH in a sex-specific manner [6]. - The knockout of the Gpr110 gene in liver cells protects female mice from MASH, while having no effect on male mice [6]. - The variant rs937057 T>C of GPR110 is associated with a higher prevalence of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) in women [6]. Group 2: Mechanism of Action - GPR110 couples with Gαs to activate protein kinase A (PKA), which induces phosphorylation of NFAT2, inhibiting its nuclear translocation and transcriptional activity, leading to suppression of Esr1 transcription in liver cells [6][8]. - Reducing Gpr110 expression in liver cells improves the liver pathology in female MASH mice, while knocking down estrogen receptor α (Esr1) negates this improvement [6]. Group 3: Implications for Therapy - The findings suggest that inhibiting GPR110 may represent a gender-specific therapeutic approach for MASH, emphasizing the need for targeted treatments based on sex differences [4][8].

撰文丨王聪 编辑丨王多鱼 排版丨水成文 18 个月大的人类儿童仅通过无意中听到周围人的交流就能学会新词汇。如果能在人类意外的物种身上展示出类似的学习过程，那就表明支持这一过程的社会认知 技能并非人类所独有，而可能在其他物种中进化而来或发展出来，这将为语言相关认知的起源提供宝贵的新见解。 养狗的人可能都知道，狗狗能理解很多词汇，研究也证实了这一观点。除了那些具备普通知识水平的狗狗之外，还有一些狗狗对词汇的理解水平超乎寻常，甚至 能够听懂上百种玩具的名称，这些狗狗被称为" 天才词汇学习犬 "。 近日，匈牙利罗兰大学和维也纳兽医大学的研究人员合作，在国际顶尖学术期刊 Science 上发 表了题为： Dogs with a large vocabulary of object labels learn new labels by overhearing like 1.5-year-old infants 的研究论文。 该研究证明，一些词汇量非常丰富的" 天才词汇学习犬 "能够通过无意中听到主人的交流来学习新词汇。该研究还显示，这些狗狗即使在标签和物体不同时出现的 情况下也能学会新的物体-标签对应关系。 这些结果表明 ...

以下文章来源于CellPress全科学 ，作者Cell Press 传统上， 免疫系统 被视为宿主的防御系统，主要任务是识别病原体等外来元素，以及由自身组织编码的 蛋白质突变，因此人们认为免疫系统的唯一终极目的，是修复受损或受威胁状态，恢复到功能正常的静息 但近年来，研究界逐渐认识到，免疫系统的功能超越了这一范畴，还包括在无扰动状态下维持器官和组织 的正常功能。本次会议将呈现这一概念领域的洞见。欢迎大家参会，共同探索免疫功能的多重作用。 会议详情 这场研讨会将围绕五大前沿议题展开 ： 会议详情： CellPress全科学 . 1974年，我们出版了首本旗舰期刊《细胞》。如今，CellPress已发展为拥有60多本期刊的全科学领域国 际前沿学术出版社。我们坚信，科学的力量将永远造福人类。 与上海市免疫学研究所、上海交通大学医学院合作 会议时间： 2026年5月11-13日 会议地点： 中国上海 手机端： 扫描二维码，查看会议详情 电脑端： 使用Chrome浏览器打开链接 https://www.cell-symposia.com/immune-homeostasis-2026/index.html 会议组织者 ...

撰文丨王聪 编辑丨王多鱼 排版丨水成文 染色体外 DNA （extrachromosomal DNA，ecDNA） 是编码癌基因和有助于肿瘤适应性的染色体外遗传元件，是一种大小可达兆碱基对 （Mb） 的环状 DNA， 它们存在于超过 505 的癌症中，驱动癌基因扩增、肿瘤内遗传异质性、肿瘤快速进化以及治疗耐药性，与癌症患者的不良预后密切相关。 ecDNA 是基因组不稳定性的一种主要形式，它驱动基因组重排，并通过非孟德尔遗传方式迅速选择出适应性增强的变异，从而导致患者预后不良。晚期和转移性 肿瘤表现出更多的 ecDNA 拷贝数和结构复杂性，其中在 ecDNA 扩增的癌基因位点内结构变异负担尤其高，这突显了由 ecDNA 驱动的基因组不稳定性在侵袭性 癌症进展中的作用。鉴于存在 ecDNA 的肿瘤的高恶性程度以及高发性，亟待阐明其特异的分子机制以研发新的诊断与治疗方法。 2026 年 1 月 7 日，斯坦福大学 张元豪 教授 （现为安进公司高级研发副总裁兼首席科学家） 和 Paul S. Mischel 教授作为共同通讯作者 （ Hyerim Yi 、 张书 为论文共同第一作者） ，在国际顶尖学术期刊 Cell ...

Core Viewpoint - Dendritic cell vaccines have potential in cancer immunotherapy, but their success has been limited due to unidentified mechanisms of induced tolerance [2][3]. Group 1: Research Findings - A study published by Professor Kang Yibin's team at Princeton University identified that dendritic cells express ALDH1A2 and secrete retinoic acid (RA), which inhibits dendritic cell activity [3][6]. - The research developed a small molecule inhibitor, KyA33, that effectively targets ALDH1A2, reducing RA production and enhancing the efficacy of antitumor dendritic cell vaccines [3][6]. - The study demonstrated the unique role of the ALDH1A2-RA signaling axis in regulating dendritic cell function and proposed KyA33 as a potential drug for cancer immunotherapy [6].

Core Viewpoint - The article discusses the promising advancements in regulatory T cell (Treg) biology and their potential clinical applications in treating immune-related diseases, emphasizing the shift from immune suppression to immune tolerance as a therapeutic strategy [2][4][5][8]. Group 1: Treg Cell Biology and Clinical Applications - Treg cells, defined by FOXP3 expression, play a crucial role as natural suppressors of autoreactive immune responses, with research over the past 30 years highlighting their importance [2][3]. - Recent clinical trials have demonstrated the feasibility and safety of enhancing or transferring Treg cells, showing encouraging results in various immune-related diseases [5][8]. - The article outlines key findings in Treg biology and clinical applications, including promising results from low-dose IL-2 treatment in amyotrophic lateral sclerosis (ALS) and the effectiveness of adoptive Treg cell transfer in preventing graft-versus-host disease (GvHD) [5][7]. Group 2: Challenges and Future Directions - A significant challenge remains in translating Treg cell biology discoveries into effective therapies for human diseases [4][8]. - The article emphasizes the need for further research to clarify dose sensitivity mechanisms and develop targeted therapies for Treg cells [7][8]. - The concept of "tolerance-by-design" is proposed as a potential paradigm shift in treating autoimmune and inflammatory diseases, similar to the impact of immune checkpoint inhibitors and CAR-T cells in oncology [19].

Core Viewpoint - The article discusses the discovery of a novel membraneless organelle called Lipid-induced granule (LIG) in hepatocytes, which is induced by lipid accumulation and has implications for understanding liver fibrosis and potential intervention targets for fatty liver disease [3][9]. Group 1: Discovery and Characteristics of LIG - A new type of membraneless organelle, named Lipid-induced granule (LIG), has been identified in hepatocytes, revealing its characteristics, formation, and function [3]. - LIG is formed through the liquid-liquid phase separation (LLPS) of the DDX49 protein, which is induced by lipid metabolites, particularly arachidonic acid [10]. Group 2: Mechanism of Action - LIG plays a role in inhibiting the progression of metabolic dysfunction-associated fatty liver disease (MASLD) by feedback inhibition of the pro-fibrotic liver factor TIMP2 [10]. - The mechanism involves the recruitment of m5C-modified Timp2 mRNA and its reader YBX1 to LIG, which suppresses the translation of Timp2 mRNA, thereby inhibiting liver fibrosis [7][10]. Group 3: Clinical Relevance - The presence of LIG has been identified in human MASLD livers, and its abundance is negatively correlated with the progression of fibrosis [8]. - The global prevalence of MASLD is estimated to be 30% among adults, with its severe form, MASH, leading to liver fibrosis and significant health risks [6].