Core Viewpoint - Myocardial infarction (MI) is a leading cause of heart disease globally, and while treatment for acute MI has improved, the prevalence of heart failure (HF) resulting from MI has increased, presenting a significant public health issue [2] Group 1: Research Development - A collaborative study by teams from Columbia University and UCLA developed an IL-4 loaded microneedle patch (IL4 MP-MN) that induces a macrophage-mediated pro-repair microenvironment, promoting cardiac repair in rodent and porcine models of MI [3][8] - The IL4 MP-MN patch continuously releases IL-4, which not only encourages myocardial cell proliferation but also effectively suppresses endothelial inflammatory signaling [8][9] Group 2: Mechanism and Design - The study addresses the challenge of delivering IL-4 locally and minimally invasively to damaged myocardium by encapsulating IL-4 in PLGA microparticles and integrating them into a hyaluronic acid hydrogel-based microneedle patch [6][8] - This design features biocompatibility, adjustable drug release kinetics, and controlled release, allowing for targeted diffusion of IL-4 to the damaged myocardium [6][8] Group 3: Experimental Results - Experimental results in rat and pig models of MI demonstrated that the microneedle patch significantly improved ventricular contractile function and maintained myocardial tissue integrity, indicating strong safety and efficacy for clinical translation [8][13] - The patch induces a macrophage-associated pro-repair microenvironment and prompts myocardial cells to re-enter the cell cycle [13]

Core Viewpoint - The source of dietary fat significantly influences anti-tumor immunity in obese individuals, with animal fats impairing immune response and promoting tumor growth, while plant fats do not have this negative effect [5][7][9]. Group 1: Research Findings - A study published in Nature Metabolism indicates that high-fat diets based on animal fats (lard, beef tallow, or butter) weaken anti-tumor immunity in obese mice and accelerate tumor growth [5][7]. - In contrast, high-fat diets based on plant oils (coconut oil, palm oil, or olive oil) do not exhibit this detrimental effect, with palm oil even enhancing anti-tumor immunity and slowing tumor growth in obese mice [5][7][9]. - The research highlights that the metabolic byproducts of animal fats, particularly long-chain acylcarnitines, strongly inhibit NK and CTL cells, leading to impaired immune function [9]. Group 2: Implications for Cancer Treatment - The findings suggest that dietary modifications, such as replacing animal fats with plant oils, could be beneficial for obese cancer patients undergoing treatment, potentially lowering their cancer risk [5][6][9]. - The study emphasizes the importance of dietary fat composition in maintaining a healthy immune system and improving treatment outcomes for obese individuals with cancer [9].

Core Viewpoint - The research highlights the effectiveness and safety of AAV-mediated gene therapy for patients with DFNB9, a type of autosomal recessive deafness, demonstrating significant improvements in hearing recovery and language perception abilities [3][4][9]. Group 1: Clinical Research Findings - The study published in The Lancet and Nature Medicine confirms the positive outcomes of gene therapy for DFNB9 patients, showing robust hearing recovery and improvements in auditory processing [3][4]. - A longitudinal analysis of auditory characteristics post-gene therapy revealed significant changes in auditory brainstem response (ABR) and auditory steady-state response (ASSR), indicating reliable objective tools for assessing hearing recovery [7][13]. Group 2: Key Metrics and Results - All participants exhibited clear ABR V waves within 13 weeks post-treatment, with some showing ABR I and III waves by week 52, indicating positive changes in the auditory pathway [11]. - The latency of ABR V wave at 85 dB stimulus intensity decreased significantly from 9.220 milliseconds at 4 weeks to 8.190 milliseconds at 52 weeks, with an upward trend in V wave amplitude [11]. - A significant correlation was found between the thresholds of PTA, ABR, and ASSR within the 0.5-4 kHz frequency range, enhancing the understanding of the relationship between these auditory assessments [11][13]. Group 3: Implications for Future Research - The study emphasizes the importance of understanding the physiological mechanisms behind hearing recovery, including synaptic vesicle release in inner ear hair cells and central auditory pathway neuroplasticity [3][9]. - Ongoing clinical trials (ChiCTR2200063181) aim to further explore the auditory characteristics post-gene therapy, which is crucial for optimizing monitoring and evaluation strategies for hearing recovery in DFNB9 patients [9][10].

Core Viewpoint - The research reveals the dynamic nature of the membrane-associated periodic skeleton (MPS) in neurons, indicating that it undergoes continuous disassembly and reassembly cycles regulated by calcium signaling, which is crucial for various neuronal functions [3][5][8]. Group 1: MPS Structure and Function - The MPS consists of actin filaments forming a periodic lattice structure, which is essential for multiple neuronal functions, providing mechanical support and serving as a signaling platform [2][5]. - The MPS is highly ordered and conserved across different neuron types and species, highlighting its fundamental role in neuronal activity [2][5]. Group 2: Dynamic Characteristics of MPS - The study demonstrates that even in the absence of external stimuli, specific regions of the MPS spontaneously undergo continuous disassembly and reassembly cycles [5][6]. - Calcium ion influx activates protein kinase C (PKC), leading to the phosphorylation of actin capping proteins, which decreases the stability of actin rings and promotes MPS disassembly [6][8]. Group 3: Mechanisms of MPS Remodeling - The remodeling of MPS is driven by a cascade of enzymatic reactions triggered by calcium signaling, involving calpain-mediated spectrin degradation and the replacement of capping proteins by formin [6][8]. - Enhanced neuronal activity increases the dynamic nature of MPS, significantly promoting axonal endocytosis, which is essential for various cellular processes [6][8]. Group 4: Implications and Future Research - The dynamic properties of MPS not only facilitate endocytosis but may also support other physiological processes requiring membrane contact or deformation [8]. - Understanding the interaction mechanisms between MPS remodeling and neuronal activity remains a critical scientific question that needs further exploration [8].

Core Viewpoint - The study highlights the significant impact of respiratory viral infections, such as influenza and SARS-CoV-2, on the awakening and proliferation of dormant disseminated cancer cells (DCC) in the lungs, which may lead to increased cancer-related mortality and metastasis risk [3][14][15]. Group 1: Research Findings - Influenza and SARS-CoV-2 infections can cause dormant DCC in the lungs to awaken, leading to rapid proliferation and metastasis [3][4]. - The research indicates that the presence of interleukin-6 (IL-6) is crucial for the reactivation of DCC, as its levels increase following viral infection [9][12]. - CD4+ T cells play a necessary role in maintaining the awakened state of DCC, although they are not required to initiate this process [12][14]. Group 2: Clinical Implications - The study found that cancer patients infected with SARS-CoV-2 have a significantly higher risk of cancer-related death and lung metastasis compared to those who are not infected [14][15]. - The findings suggest a potential link between respiratory infections and the recurrence of metastatic cancer, emphasizing the need for further exploration in this area [4][15]. Group 3: Mechanisms of Action - The research demonstrated that CD4+ T cells limit the ability of CD8+ T cells to control DCC growth, indicating a complex interplay between different immune cell types in the context of viral infections and cancer [12][14]. - The study also explored the role of inflammation caused by respiratory infections in influencing dormant cancer cells, which had not been a primary focus in previous research [7][8].

Core Viewpoint - The research on Alzheimer's disease (AD) has shifted focus from the traditional view of amyloid-beta (Aβ) accumulation and tau protein tangles as the primary causes of dementia, highlighting the role of dysfunctional microglia and chronic neuroinflammation in disease progression [2][3]. Group 1: Research Findings - Recent studies indicate that abnormal protein deposition is a pathological feature of AD rather than its causative mechanism, emphasizing the harmful effects of these proteins on disease progression [2]. - The study published by Xu Peisheng's team at the University of South Carolina introduces a ceria nanocluster-based therapy that targets activated microglia and reduces Aβ deposition [3][4]. Group 2: Innovative Treatment Approach - The developed brain-targeted ceria nanoparticles (T-CeNP) effectively penetrate the blood-brain barrier (BBB) and alleviate neuroinflammation while reducing Aβ accumulation [4][6]. - T-CeNP operates through a triple-function mechanism: it crosses the BBB via RAGE-targeting peptides, regulates pathological processes by enhancing microglial phagocytosis of Aβ, and exhibits multi-pathway synergistic effects in AD mouse models [6][7]. Group 3: Implications for Future Research - The study's findings suggest that T-CeNP can effectively block the pathological cascade of Alzheimer's disease by modulating the neuroinflammatory microenvironment and amyloid metabolism, providing a new paradigm for multi-target therapies in neurodegenerative diseases [9].

Core Viewpoint - The research indicates that dietary galactose can reprogram hepatocytes to produce insulin-like growth factor binding protein-1 (IGFBP-1), which prevents T cell exhaustion and stimulates antitumor immune responses [2][3][5]. Group 1: Research Findings - High galactose diets promote hepatocytes to produce IGFBP-1, inhibiting T cell exhaustion dependent on insulin-like growth factor-1 (IGF-1) signaling [5]. - The absence of IGF-1 receptor (IGF-1R) in T cells enhances antitumor CD8+ T cell responses and prevents T cell exhaustion, demonstrating a phenotype associated with high galactose feeding [5]. - Galactose in the circulatory system reprograms hepatocyte metabolism, inhibiting mTORC1 activity and inducing IGFBP-1 production to enhance CD8+ T cell function [5]. Group 2: Clinical Observations - In cancer patients, those with higher plasma levels of IGFBP-1 exhibited reduced T cell exhaustion and enhanced T cell responses in tumor tissues [5]. - These findings suggest that dietary galactose can specifically stimulate robust antitumor CD8+ T cell responses, providing new insights for developing more effective cancer immunotherapies [5].

Core Viewpoint - Nanjing University is expanding its Suzhou campus by recruiting global leaders for three new engineering schools, focusing on automation, biomedical engineering, and advanced manufacturing, aiming to enhance its academic and industrial resources [3][4]. Group 1: Recruitment and Responsibilities - The university is seeking deans for the School of Robotics and Automation, School of Biomedical Engineering, and School of Mechanical and Advanced Manufacturing [3]. - Responsibilities include overseeing the establishment and development of the schools, including strategic planning and execution [5]. Group 2: Candidate Requirements - Candidates should have a strong academic reputation internationally, administrative experience, and leadership skills, aligning with the university's values [6]. - Proficiency in Mandarin and/or English is required, along with a passion for higher education and research [6]. Group 3: Benefits and Application Process - The position offers globally competitive and negotiable salary and benefits, including support for team building and access to world-class facilities [7]. - Interested applicants should submit their resumes via email, detailing their academic and professional background [8]. Group 4: About Suzhou - Suzhou is a historical city known for its advanced manufacturing, biotechnology, and information technology sectors, making it a hub for high-tech enterprises and research institutions [9]. - The city combines urban vibrancy with natural tranquility, offering a rich cultural experience [9]. Group 5: Strategic Goals - The university aims to recruit top faculty, design talent development programs, and enhance industry-academia collaboration [11]. - Strengthening international partnerships is also a key goal to elevate the university's global reputation [11].

编辑丨王多鱼 排版丨水成文 近日，南京大学发布招聘启事，面向全球招聘 医学院 和 生命科学学院 院长 。医学院前任院长为 张峻峰 教授 （目前任中国海洋大学校长） ，生命科学学院现 任院长为 张辰宇 教授。 福利待遇 ： 具有全球竞争力且可协商的薪资和福利待遇。充足的人员配备支持和启动资金，以促进团队建设。可使用世界一流的教学和研究设施、专用实验室以及高性能共 享设备平台。有资格获得住房及搬迁补助、VIP 医疗服务以及子女入读顶级附属学校的机会。 南京大学医学院 历史悠久，声名远扬，其历史可追溯至 1925 年，医学院现有教授 142 名，副教授 207 名，并拥有多个世界知名的研究平台，例如国家慢性肾 病临床医学研究中心、国家基因工程小鼠资源中心以及教育部模式动物与疾病研究重点实验室。 南京大学生命科学学院 起源 于 1914 年，是中国首个大学生物系， 也是国内最早致力于生命科学研究与教育的机构之一。生命科学学院现有 53 名教授和 47 名 副教授。此外，学院还拥有多个国家级和省级研究平台，其中包括国家药用植物生物技术重点实验室。 应聘要求 ： 对高等教育和研究充满热情，遵守中国职业道德和法律。 在国际 ...

Core Viewpoint - The collaboration between Fudan University and Seoul National University Hospital has led to significant advancements in gene therapy for hereditary hearing loss, specifically targeting the MPZL2 gene mutation prevalent in East Asian populations, offering potential precision treatment strategies for genetic hearing loss [3][8][19]. Group 1: Research Findings - The study published in Nature Communications demonstrates that a flexible adenine base editor (ABE) can rescue hearing loss in a humanized MPZL2 mouse model with an East Asian founder mutation [3][8]. - Approximately 4.3 billion people globally suffer from disabling hearing loss, with 26 million being congenital cases, highlighting the urgent need for effective treatments [6]. - The MPZL2 gene mutation is identified as a significant cause of autosomal recessive non-syndromic hearing loss, with specific mutations like c.220C>T being common in East Asian populations [7][8]. Group 2: Gene Therapy Innovations - The research team developed a PAM-flexible ABE variant that minimizes off-target effects and successfully restored hearing in mutant mice for at least 20 weeks [9][11]. - The dual-AAV delivery system was utilized to correct abnormal gene expression and restore the integrity of the inner ear structure in the mouse model [11][21]. - The team has previously achieved significant milestones in gene therapy for congenital hearing loss, including the first-in-human clinical trial for OTOF gene therapy, which has shown promising results in restoring hearing and speech [20][24]. Group 3: Future Implications - The advancements in gene therapy for hearing loss could pave the way for treatments of other genetic disorders, enhancing confidence in the application of ABE technology [11][29]. - The research findings have been recognized in top medical journals, indicating a paradigm shift in the treatment of hearing loss and the potential for broader applications in genetic diseases [24][29].