Core Viewpoint - Perovskite solar cells (PSC) are recognized as a key direction for next-generation photovoltaic technology due to their high efficiency, low cost, and solution processing capabilities. The development of self-assembled molecules (SAM) is crucial for enhancing the performance of PSCs [2]. Group 1: Research Breakthroughs - A significant breakthrough was achieved in the design of new organic self-assembled molecules, resulting in the first development of a highly efficient, stable, and well-dispersed self-assembled molecular material with dual radical characteristics [2][5]. - The research team successfully designed a dual radical self-assembled monolayer to facilitate hole transport within the monolayer [4]. Group 2: Performance Metrics - The small-area devices based on the new material achieved a power conversion efficiency of 26.3%, while micro-modules (10.05 cm²) reached an efficiency of 23.6%. The perovskite-silicon tandem cells (1 cm²) exceeded 34.2% efficiency, certified by the National Renewable Energy Laboratory (NREL) [7]. - The developed materials and devices exhibited excellent stability, maintaining over 97% performance retention after 2000 hours of operation at 45°C, significantly surpassing traditional materials and devices [8]. Group 3: Implications for Industry - This research provides a new molecular design paradigm to address the conductivity, stability, and large-area processing challenges in perovskite solar cells, injecting core driving forces for the industrialization of next-generation efficient and stable photovoltaic components [8].

Core Viewpoint - MD Anderson Cancer Center is recruiting postdoctoral researchers to advance cutting-edge single-cell multi-omics technologies and explore molecular regulatory networks in cancer development and drug resistance [3][8]. Group 1: Research Focus - The laboratory aims to develop single-cell multi-omics technologies, investigate the epigenetic regulatory mechanisms of cancer cell plasticity, and understand the epigenetic basis of individualized drug responses [3]. - The research group is led by Dr. Zhang Bingjie, who has a strong background in epigenomics and single-cell multi-omics [2]. Group 2: Institutional Overview - MD Anderson Cancer Center is a leading cancer treatment and research institution, consistently ranked as the top cancer specialty by U.S. News & World Report, located in Houston, Texas [8]. - The center has conducted over 1,680 clinical trials in 2024, with 22 drugs approved by the FDA and research funding amounting to $1.1 billion [8]. Group 3: Application Requirements - The position is for two postdoctoral researchers in genomics and tumor biology, requiring a Ph.D. in relevant biological fields [9][10]. - Candidates with backgrounds in tumor biology, genomics, and computational biology are preferred, along with strong communication and teamwork skills [10][11].

浙江大学医学院姜东课题组诚聘专职研究员和博士后 浙江大学医学院 姜东 课题组，现公开招聘 专职研究员 和 博士后 ，欢迎相关背景的优秀申请者 加入 我们 的团队 ！ 实验室简介 姜东 ，浙江大学医学院 " 百人计划 " 研究员、博士生导师、浙江大学医学院附属第二医院 / 经血管植入器 械全国重点实验室研究员。 2014 年毕业于厦门大学获学士学位， 2019 年毕业于清华大学获博士学位， 并继续在清华大学完成博士后研究， 2025 年全职加入浙江大学 ，实验室位于浙江大学紫金港校区 。姜东 一直致力于 迁移体 （ migrasome ） 的生物学功能与机制研究，全程参与并系统推进了迁移体生物学的建 立与发展。博士 / 博后期间首次建立了迁移体研究的动物模型，开发了哺乳动物迁移体活体成像技术平台 等一系列体内迁移体研究的方法和系统，解析了迁移体在胚胎发育、凝血、肿瘤和免疫中的生理病理功 能，揭示了迁移体介导的时空特异性信号传递、信号梯度形成及细胞间通讯的新机制，开创了体内迁移体 研究的范式。相关研究工作 以第一（含共同）作者 发表在 Nature Cell Biology ( 2019 cover , 2024 ...

Group 1 - The article introduces Professor Song Zhenju, who holds multiple prestigious positions in emergency medicine and clinical research, including Director of the Emergency Department at Fudan University Zhongshan Hospital and Vice President of the same hospital [1] - Professor Song has led numerous national and provincial research projects, published extensively in high-impact journals, and holds multiple patents, indicating a strong research background and contributions to the field [1] Group 2 - The research directions focus on Acute Respiratory Distress Syndrome (ARDS) mechanisms and interventions, organ damage from sepsis, and mechanisms and interventions for acute poisoning [6] Group 3 - Recruitment is open for postdoctoral positions in fields such as Clinical Medicine, Life Sciences, Biology, Biomedical Engineering, and Pharmacy [3] - Candidates must be under 35 years old, have a strong academic background, and have published at least one SCI paper [5] Group 4 - Compensation will follow national and Fudan University standards, with additional rewards for outstanding performance during the contract period [7] Group 5 - Applicants are required to submit a detailed CV, proof of doctoral degree, and 1-3 representative papers [8] - Contact information for applications is provided, with specific instructions for email subject lines [9][10]

Core Viewpoint - The article discusses the advancements in in vivo CAR-T cell therapy, particularly focusing on a new type of lipid nanoparticle (LNP) that does not require antibody modification, which enhances the delivery of circRNA-based CAR-T cells for treating inflammatory aging diseases [1][2][3][5]. Group 1: In Vivo CAR-T Therapy Advantages - In vivo CAR-T therapy, based on mRNA, offers significant advantages over traditional ex vivo CAR-T therapy, especially in treating inflammatory aging diseases [6][14]. - The transient expression of in vivo CAR-T cells may be beneficial for inflammatory aging, contrasting with its potential drawbacks in solid tumor treatments [6][14]. Group 2: Research Innovations - The research team developed a novel type of LNP inspired by cardiolipin, which enhances T cell targeting without the need for antibody modification [8][15]. - The study demonstrated that the CAMP lipid increases the stiffness and phase separation of LNPs, improving T cell uptake [9][15]. Group 3: CircRNA Utilization - The research utilized circRNA to modify CAR mRNA, enhancing its stability and reducing cytotoxicity, which prolongs CAR protein expression in vivo [10][15]. - The encapsulation of CAR mRNA targeting uPAR in PL40-LNP provides a proof of concept for treating liver fibrosis and rheumatoid arthritis [11][12]. Group 4: Clinical Implications - The study highlights the potential of non-antibody targeting strategies in developing in vivo CAR-T therapies for clearing senescent cells associated with inflammatory aging diseases [17].

Core Viewpoint - The article announces the recruitment of postdoctoral researchers and PhD students by Dr. Ronghui Li's research group at the National University of Singapore, focusing on somatic reprogramming and stem cell development for drug screening and regenerative medicine [2][4]. Group 1: Research Focus - The main research directions include the simulation of organoid or embryonic development using stem cells to produce functional tissues or cells [3] - Editing and precise regulation of multicellular organoid or embryonic systems [3] - Cell reprogramming to restore and enhance engineered cell functions for improved therapeutic applications [3] Group 2: Recruitment Details - The group is open to recruiting postdoctoral researchers, PhD students, and outstanding undergraduate or intern candidates, including those funded by CSC [4] - Interested candidates are encouraged to send their resumes to the provided email address, with specific subject line instructions [4] - The article also mentions the establishment of professional communication groups to facilitate research dissemination and collaboration [7]

Core Viewpoint - The article discusses the impact of systemic inflammation on the aging of muscle stem cells (MuSC) and highlights a mechanism linking chronic inflammation to stem cell aging and ferroptosis, suggesting potential therapeutic strategies to combat age-related muscle degeneration [4][11][13]. Group 1: Mechanism of Aging and Inflammation - Systemic inflammation induces epigenetic erosion, promoting ferroptosis in muscle stem cells, while long-term suppression of systemic inflammation can effectively prevent ferroptosis and maintain muscle stem cell numbers [4][11]. - The study reveals that age-related inflammation decreases H4K20 monomethylation levels in MuSCs, disrupting their quiescent state and leading to ferroptosis [11]. - Inflammation signals downregulate the enzyme Kmt5a, which is responsible for H4K20me1 accumulation, resulting in the epigenetic silencing of genes that counteract ferroptosis [11]. Group 2: Impact on Muscle Regeneration - Aging is characterized by a decline in muscle mass, strength, and regenerative capacity, leading to decreased quality of life in the elderly [7]. - Muscle stem cells play a crucial role in muscle repair and maintenance, but their function significantly declines with age due to both intrinsic changes and external factors like inflammation [7][8]. - Chronic systemic inflammation is one of the most important external factors leading to stem cell aging, as it inhibits muscle regeneration [8][9]. Group 3: Research Findings and Implications - The research emphasizes that aging cells are a major contributor to age-related inflammation in the muscle stem cell microenvironment, impairing their regenerative capacity [9]. - Long-term suppression of inflammation starting at middle age (12 months in mice) can restore muscle vitality and promote functional recovery [11][13]. - These findings reveal an epigenetic switch linking chronic inflammation to muscle stem cell aging and ferroptosis, providing potential therapeutic strategies against age-related muscle degeneration [13].

Core Viewpoint - The article discusses the role of the p53 R172H mutation in pancreatic ductal adenocarcinoma (PDAC), highlighting its contribution to creating an immunosuppressive tumor microenvironment and reducing the efficacy of immune checkpoint inhibitors (ICIs) [4][13][15]. Group 1: Background on PDAC - PDAC is a highly aggressive cancer characterized by KRAS gene activation mutations and TP53 gene alterations, with TP53 mutations leading to the loss of tumor suppressor function [2][6]. - Approximately 90% of PDAC cases have KRAS activation mutations, while around 70% exhibit changes in the TP53 tumor suppressor gene, indicating the critical role of p53 in genomic protection [7]. Group 2: Research Findings - A study published by MIT researchers reveals that the common p53 mutation, p53 R172H, occupies enhancers of immunosuppressive chemokines (e.g., Cxcl1), stimulating their expression and establishing an immunosuppressive tumor microenvironment in PDAC [3][4][11]. - The study indicates that knocking out the p53 R172H mutation enhances the efficacy of immune checkpoint inhibitors [13][15]. - Mechanistically, p53 R172H enhances Cxcl1 expression by occupying its distal enhancer, with NF-κB being a crucial cofactor for this process [12][15]. Group 3: Implications for Treatment - The findings suggest that p53 R172H promotes tumor growth by regulating cancer cell-specific gene expression programs that shape the tumor microenvironment, thereby inhibiting anti-tumor immune responses [15][16]. - In mouse models of PDAC, tumors lacking p53 R172H showed fewer T cells and higher levels of myeloid-derived suppressor cells (MDSCs), indicating a more favorable immune environment for tumor growth [15].

Core Insights - Vascular dementia (VaD) accounts for approximately 25% of all dementia cases, making it the second most common type after Alzheimer's disease (AD) [2] - There is a significant overlap between VaD and AD, with 84% of elderly individuals exhibiting features of both conditions, suggesting a potential synergistic effect [2] - Current treatments for VaD are limited and primarily symptomatic, highlighting the urgent need for comprehensive research to identify therapeutic targets [2] Research Findings - A study published in Cell identified the CD39-A3AR signaling pathway as crucial for brain repair in VaD, demonstrating that the A3AR-specific agonist Piclidenoson can promote brain tissue repair and restore memory and gait functions in mouse models [3][11] - The study developed a mouse model that replicates the focal ischemic characteristics of human VaD, addressing the limitations of existing models [8] - The research team constructed a comprehensive VaD interaction network by integrating mouse and human data, identifying conserved signaling pathways altered in VaD [9][10] Mechanisms and Challenges - The understanding of the neurovascular unit (NVU) and its cell-type-specific responses in VaD remains incomplete, which complicates the development of effective therapies [6] - The study emphasizes the need for high-resolution transcriptomic analysis of NVU cells to uncover disease mechanisms and the development of next-generation animal models to bridge the gap between rodent and human pathophysiology [7] Therapeutic Implications - The findings suggest that enhancing CD39-A3AR signaling may aid in the recovery of tissue and behavioral functions in VaD patients, providing a potential new therapeutic target [12][15] - The research indicates that even delayed treatment interventions can be effective, which is critical given that VaD is often diagnosed late [14]

Core Viewpoint - The article discusses the significance of synonymous mutations in genetic research, particularly their role in cucumber domestication through epitranscriptomic regulation, challenging traditional views on these mutations [2][3]. Group 1: Research Findings - The study published in the journal Cell demonstrates that synonymous mutations can regulate important traits in cucumber by altering m6A modifications and mRNA structural conformations [2][3]. - The research identifies two closely linked genes, YTH1 and ACS2, that interact epistatically to influence cucumber fruit length [5][9]. - A specific synonymous mutation, 1287C>T in the ACS2 gene, is identified as a pathogenic mutation that disrupts m6A methylation and alters RNA structure, leading to changes in fruit length [6][9]. Group 2: Genetic Mechanisms - The YTH1 gene encodes an m6A reader protein, while the ACS2 gene encodes a rate-limiting enzyme for ethylene synthesis in plants, both of which are crucial for cucumber domestication [5][9]. - The study reveals that the wild-type cucumber's ACS2 1287C leads to m6A modification and a loose RNA structure, while the cultivated cucumber's ACS2 1287T results in a compact RNA structure, affecting protein levels and fruit length [6][9].