Research最新文献

{"title":"Astrocytic BDNF Modulates Sensitivity to Stress-Induced Anxiety-Like Behaviors.","authors":"Wei-Peng Li, Gui-Yu Liu, Shi-Yun Wang, Jiao Hu, Wen-Juan Ji, Jun-Ming Zhu, Qing-Yu Chang, Tian-Yi Li, Guo-Rong Wei, Jian-Qing Shang, Hong-Zhan Li, Fu-Hua Peng, Yun-Yan Zhao, Xiao-Hong Su, Wei Xie","doi":"10.34133/research.0818","DOIUrl":"10.34133/research.0818","url":null,"abstract":"<p><p>Chronic stress exposure is a potent risk factor for anxiety, disrupting adaptive responses and increasing vulnerability. Astrocytes, as essential regulators of synaptic function and neuroimmune homeostasis, are implicated in mood regulation and neuropsychiatric pathogenesis. However, the precise molecular mechanisms of astrocytes involved in stress-induced anxiety remain poorly understood. In this study, we reveal a pivotal role of astrocytic brain-derived neurotrophic factor (BDNF) in modulating anxiety sensitivity through coordinated regulation with hippocampal CA1 neurons. Chronic restraint stress induces anxiety-like behaviors and disrupts presynaptic glutamatergic transmission in hippocampal CA1 neurons, with astrocytes potentially playing a central regulatory role in a Ca²⁺-dependent manner. Pharmacological manipulation confirms the involvement of BDNF/TrkB signaling, while knockdown of astrocytic BDNF further impairs synaptic function and exacerbates stress-induced anxiety. Transcriptomic analysis suggests interferon-related signaling pathways as potential downstream effectors, amplifying anxiety sensitivity through altered astrocytic activation and neuroimmune dynamics. Our study provides critical mechanistic insights into astrocytic regulation of anxiety sensitivity and highlights astrocytic BDNF as a promising therapeutic target for stress-related anxiety disorders.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0818"},"PeriodicalIF":10.7,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144800120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual Roles of SIRT7 Inhibition by Oroxylin A Reprogram HSCs Fate: PRMT5 Succinylation-Driven Senescence and Ecto-Calreticulin-Dependent NK Cell Immune Clearance in Liver Fibrosis.","authors":"Junrui Wang, Haoyuan Tian, Yuanyuan Gao, Xinran Qiu, Zhengyang Bao, Danli Zhao, Feng Zhang, Zili Zhang, Feixia Wang, Shizhong Zheng, Haibo Cheng, Jiangjuan Shao","doi":"10.34133/research.0808","DOIUrl":"10.34133/research.0808","url":null,"abstract":"<p><p>Activation of hepatic stellate cells (HSCs) represents a central pathological event in liver fibrogenesis, and targeted clearance of activated HSCs is considered to be a promising therapeutic strategy. However, our understanding of the underlying molecular mechanisms is limited. Here, we report that Oroxylin A (OA) inhibited the activation of HSCs by inhibiting the dual roles of Sirtuin 7 (SIRT7). Single-cell transcriptome sequencing analysis and bioinformatics analysis were employed to identify critical pathways, followed by validation through molecular assays including Western blotting, immunofluorescence, and co-immunoprecipitation. In human samples, animal models, and primary cultures, the translational relevance of molecular discoveries was heightened. OA binds to the Gln299 and Asp305 residues of SIRT7, triggering a dual regulatory program in hepatic fibrosis. OA suppresses SIRT7, triggering succinylation-dependent proteasomal degradation of protein arginine methyltransferase 5 (PRMT5). This cascade attenuated symmetric dimethylation of cyclic GMP-AMP synthase (cGAS), thereby activating the cGAS-stimulator of interferon genes (STING) signaling and promoting HSC senescence. Concurrently, OA-elicited SIRT7 inhibition promotes externalized calreticulin (ecto-CRT) expression, thereby enhancing natural killer (NK) cell recognition and targeted elimination of activated HSCs. However, enzymatically dead mutant SIRT7 (H187Y) also suppressed ecto-CRT expression promoted by OA, showing that it is independent of its desuccinylase activity. Our findings reveal a dual regulatory mechanism whereby SIRT7 inhibition by OA coordinates PRMT5 degradation-mediated cellular senescence and ecto-CRT-dependent NK cell immune clearance of HSCs. This work establishes SIRT7 as a pivotal therapeutic target and provides mechanistic insights for developing antifibrotic strategies.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0808"},"PeriodicalIF":10.7,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329212/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144800121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Arachidonic Acid Metabolism Down-Regulation-Mediated Tumor Necrosis Factor Signaling Contributes to Cutaneous Fibrosis and Skull Hyperplasia in Goldfish Hoods.","authors":"Liang-Liang Li, Qi-Lin Xu, Wen-Jing Yi, Di-Di Ma, Hui Jin, De-Zheng Fu, Xiao-Li Yang, Yang Wang, Zhi Li, Zhong-Wei Wang, Xi-Yin Li, Meng Lu, Xiao-Juan Zhang, Li Zhou, Jian-Fang Gui, Peng Yu","doi":"10.34133/research.0786","DOIUrl":"10.34133/research.0786","url":null,"abstract":"<p><p>Goldfish (<i>Carassius auratus</i>) are renowned as a premier ornamental fish in the world. Especially, the hood, a distinctive cephalic skin protrusion, is a highly sought-after feature for its endearing aesthetics. Despite a longstanding hypothesis that the hood is a type of tumor, the details of their composition, structure, and the mechanism of its formation have remained enigmatic. In this study, we attempted to demystify the morphogenetic mechanism of hood development by providing a detailed analysis of the hood's architectural and compositional attributes, complemented by multi-omics changes across its developmental stages. Our results were also validated through dual-luciferase reporter assays and cytological evaluations in vitro and in vivo. We uncovered a 4-layered complex structure (stratum compactum, stratum spongiosum, stratum adventitia, and epithelial cell layer), with the hood's protrusions mainly resulting from marked collagen accumulation in the stratum spongiosum and epithelial cell proliferation, suggesting that the goldfish hood belongs to a cutaneous fibrosis. Furthermore, we found that the down-regulation of arachidonic acid metabolism triggers an inflammatory response, culminating in the dysregulation of the tumor necrosis factor (TNF) pathway, which in turn enhances collagen deposition and epithelial cell proliferation-central to hood morphogenesis. During post-formation process, the aberrant TNF pathway expression and collagen accumulation inhibit osteoclast differentiation, promoting the irregular proliferation of the skull and the formation of bony protrusions that support hood attachment. Our findings not only shed light on the molecular mechanism underlying cutaneous fibrosis in goldfish but also offer potential parallels to analogous conditions in humans.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0786"},"PeriodicalIF":10.7,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12327030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Three-Dimensional Curved Workflow-Based Optical Coherence Tomography Angiography for Enhancing Atopic Dermatitis Theranostics.","authors":"Junwei Li, Yunrui Zhang, Ying Huang, Ronghui Li, Kun Wang, Dongbei Guo, Zicheng Huang, Youliang Yao, Yunxin Xue, Guibo Sun, Cheng Jiang, Leyun Wang, Chenzhong Li, Qingliang Zhao","doi":"10.34133/research.0778","DOIUrl":"10.34133/research.0778","url":null,"abstract":"<p><p>Optical coherence tomography angiography (OCTA) is a major advancement in imaging, offering high-resolution microvascular volumetric images crucial for diagnosing and studying dermatological diseases. However, current data analysis and clinical evaluation criteria primarily rely on 2-dimensional (2D) imaging results, resulting in imprecise diagnoses due to the substantial loss of 3D curved structures and microvascular details. To address this issue, we propose a high-fidelity 3D curved processing workflow that integrates an artificial neural network (ANN) with a 3D denoising algorithm based on the curvelet transform and optimal orientation flow (OOF). This innovative workflow enables precise 3D segmentation and accurate quantification of dermal layer microvasculature in atopic dermatitis (AD) in vivo. Furthermore, the use of 3D multiparametric microvasculature quantitative metrics establishes a robust framework for assessing the efficacy of AD treatments in 3D images. Our study results demonstrate that skin structure imaging and the dynamic evolution of 3D microvasculature align with observed pathological changes. Compared to traditional 2D analysis, the maximum variation rate of 3D curved multiparametric information is approximately 10%. Consequently, our research marks a significant advancement in the accurate quantification of microvasculature in AD development and theranostics, paving the way for the clinical application of OCTA in dermatology.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0778"},"PeriodicalIF":10.7,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12327028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artificial Intelligence of Things in Hydrogen Sensing: Toward Optic and Intelligent System.","authors":"Jianxiong Zhu, Yifan Zhan, Xijie Ni, Yuze Gao","doi":"10.34133/research.0750","DOIUrl":"10.34133/research.0750","url":null,"abstract":"<p><p>Hydrogen sensing is of increasing importance in conjunction with the development and expanded utilization of hydrogen as an energy carrier or chemical reactant. This study focuses nanoscale hydrogen sensors that incorporate nanohybrid structural innovations to fabricate various systems, thereby enhancing detection efficiency and accuracy. Concurrently, advancements in optical hydrogen sensing and next-generation hybrid functional mechanisms have provided greater precision and universality with the aid of artificial intelligence of things (AIoT). For instance, optical hydrogen sensors offer high sensitivity and accurate gas detection with strong immunity to electromagnetic interference. Beyond optics, emerging models of next-generation composite multifunctional detection mechanisms provide operational advantages in hydrogen sensing, such as self-powering and long-range capabilities. In addition, the continual advancements in machine learning methods provide a feasible solution for data processing in hydrogen sensing applications through their integration with AIoT. This paper not only highlights the application of machine learning to enhance hydrogen sensor detection but also underscores its potential to improve the accuracy of future detection systems. In summary, these advances in nanohybrid structures, optical sensing, hybrid functional mechanisms, and machine learning integration represent strides in improving the performance, reliability, and versatility of hydrogen sensors, offering promising solutions for diverse hydrogen-related applications.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0750"},"PeriodicalIF":10.7,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12327029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NMDA Receptors Coordinate Metabolic Reprogramming and Mitophagy in Schwann Cells to Promote Peripheral Nerve Regeneration.","authors":"Fangzhen Shan, Xiaoying Yao, Qingqing Zhang, Ruolin Li, Lingmeng Kong, Qian Zheng, Nannan Zhang, Yuzhong Wang","doi":"10.34133/research.0825","DOIUrl":"10.34133/research.0825","url":null,"abstract":"<p><p>Schwann cells (SCs) are indispensable for peripheral nerve regeneration, yet the mechanisms enabling their metabolic adaptation to meet the energetic demands of axonal repair remain elusive. Here, we identify <i>N</i>-methyl-D-aspartate (NMDA) receptors as central regulators of SC metabolic plasticity. In a mouse model of acute motor axonal neuropathy, nerve injury led to a marked decrease in NMDA receptor expression on SC. Functional studies revealed that NMDA receptors mediate calcium influx to drive glycolysis and oxidative phosphorylation via the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin and hypoxia-inducible factor-1α/c-Myc pathways, ensuring adenosine triphosphate production for axonal repair. Simultaneously, NMDA receptors orchestrate ataxia telangiectasia-mutated and Rad3-related protein-autophagy related 13-dependent mitophagy to clear reactive oxygen species-damaged mitochondria, maintaining metabolic efficiency during energy stress. Targeted metabolomics, Seahorse flux, and molecular pathological analysis revealed NMDA receptor-dependent remodeling of glucose metabolism, tricarboxylic acid cycle, nucleotide synthesis, and mitochondrial ultrastructure in SC. NMDA receptor deficiency disrupts energy metabolism and impairs axonal survival following sciatic nerve injury, resulting in aggravated neurological deficits and hindered nerve regeneration. Crucially, NMDA receptor activation rescued axonal integrity and motor function in mice with acute motor axonal neuropathy, underscoring their therapeutic potential. Our findings establish NMDA receptors as dual regulators of SC energy metabolism and mitochondrial quality control, providing a novel strategy to enhance glia-axonal metabolic coupling in peripheral neuropathies.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0825"},"PeriodicalIF":10.7,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12322490/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144789849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Task-Related Controllability of Functional Connectome During a Working Memory Task in Schizophrenia, Bipolar Disorder, and Major Depressive Disorder.","authors":"Jun Yang, Zhening Liu, Feiwen Wang, Wenjian Tan, Danqing Huang, Xuan Ouyang, Haojuan Tao, Guowei Wu, Yunzhi Pan, Jie Yang, Lena Palaniyappan","doi":"10.34133/research.0792","DOIUrl":"10.34133/research.0792","url":null,"abstract":"<p><p>Working memory (WM) deficit is a prominent and common cognitive impairment in major psychiatric disorders (MPDs). Altered control of brain state transitions may underlie the neural basis of WM deficit. We investigate whether shared and illness-specific alterations in controllability underlie WM deficits in MPDs. We examined functional magnetic resonance imaging data during an <i>n</i>-back WM task from 105 patients with schizophrenia (SZ), 67 with bipolar disorder (BD), 51 with major depressive disorder (MDD), and 80 healthy controls (HCs). We calculated each brain region's capacity to steer transitions to connectomic states with less input (average controllability) and to difficult-to-reach states with high input (modal controllability). The effect of altered controllability on clinical and cognitive characteristics and their likely genetic and neurotransmitter basis were investigated. All MPDs demonstrated a common but graded pattern of reduced modal controllability within the frontoparietal network compared to HC, with SZ showing the most pronounced impairment. Relative to BD and MDD, SZ exhibited the broadest profile of reduced average and modal controllability across the cortex, particularly in sensory, default mode, and salience networks. The affected brain regions preferentially expressed genes that determine synaptic biology and chemoarchitecture involving glutamate/γ-aminobutyric acid (GABA) and monoamine [dopamine and 5-hydroxytryptamine (5-HT)] neurotransmitter systems. A graded, transdiagnostic reduction in the influence of the sensory networks and triple network system in implementing state transitions underlies WM deficits in MPDs. This deficit, especially pronounced in SZ, has its likely basis in synaptic biology and in glutamate/GABA and monoamine (dopamine and 5-HT) neurotransmitters.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0792"},"PeriodicalIF":10.7,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12324819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144789852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advanced Nanomaterial Platforms for Targeted Therapy of Myocardial Ischemia-Reperfusion Injury.","authors":"Hanxi Wang, Li Li, Lihan Luo, Yuqi Cheng, Feng Zhou, ShuangJun Zhao, Yang Li, Yuzhu Yang, Qianqian Zhou, Hanyun Niu, Jiannan He, Cao Zhang, Jian Guo, Longguang Tang, Jianhong Xu","doi":"10.34133/research.0822","DOIUrl":"10.34133/research.0822","url":null,"abstract":"<p><p>Ischemic heart disease (IHD) remains a major global health challenge due to its persistently high incidence and mortality rates. Although early thrombolytic or interventional therapy reduces infarct size, myocardial ischemia-reperfusion injury (MIRI) often occurs when restoring blood flow to ischemic myocardium, paradoxically causing cardiomyocyte death. Unlike conventional cardioprotective agents, bioengineered nanomaterials enable targeted drug delivery to ischemic cardiomyocytes through tunable physicochemical properties. This improves therapeutic efficacy while reducing systemic exposure, providing innovative strategies for MIRI treatment. This review summarizes recent advances in nanomaterial-based MIRI therapies and critically evaluates their clinical translation potential, highlighting both opportunities and challenges.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0822"},"PeriodicalIF":10.7,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12324810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144789737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Dual Nature of Cellular Senescence: From Aging Signature to Regenerative Catalyst.","authors":"Peng Li, Yi Yang, Xiang Qin, Juan Liao","doi":"10.34133/research.0830","DOIUrl":"10.34133/research.0830","url":null,"abstract":"<p><p>This perspective critically examines the paradigm-shifting findings regarding cellular senescence's dual role in tissue biology, particularly focusing on its unexpected regenerative potential in hair growth. While cellular senescence has traditionally been viewed as a detrimental process associated with aging and tissue dysfunction, research has revealed its surprising beneficial effects on tissue regeneration. We analyze the groundbreaking discovery that senescent melanocytes can stimulate hair follicle stem cells through the osteopontin-CD44 signaling pathway, challenging the conventional understanding of senescence. This perspective also evaluates the implications of this finding for both basic research and therapeutic applications, suggesting that cellular senescence represents a complex, context-dependent phenomenon rather than a uniformly detrimental process. We discuss how this new perspective necessitates a more nuanced approach to senescence-targeted therapies and opens novel therapeutic possibilities for hair loss treatment. This analysis underscores the importance of understanding senescent cell heterogeneity and their diverse functions in tissue homeostasis, which could lead to more precise therapeutic strategies in regenerative medicine.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0830"},"PeriodicalIF":10.7,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144789853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Two-Dimensional Metals Over, Inside, or Beneath Templates.","authors":"Jinbo Pang, Shuye Zhang, Yufeng Hao, Hong Liu, Mark H Rummeli, Weijia Zhou, Rafael G Mendes","doi":"10.34133/research.0790","DOIUrl":"10.34133/research.0790","url":null,"abstract":"<p><p>Two-dimensional (2D) metals have drawn great attention because of their extraordinary properties, especially in applications that favor van der Waals interaction. The development of advanced characterization tools has facilitated the understanding of formation or growth mechanisms of 2D metals. In this perspective, we discuss 5 common approaches to obtaining 2D metals, including, (top down) van der Waals squeezing and selective extraction, and (bottom up) electron beam-induced growth, self-assembly, and graphene-templated wet chemistry growth. The future opportunities are proposed in the summary section. Furthermore, challenges and problems such as thermodynamic stability and scalability in 2D material growth are proposed for the community to tackle.</p>","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0790"},"PeriodicalIF":10.7,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12322969/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144789854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}