ASN NEURO最新文献

{"title":"Galectin-3 in the Lateral Ventricle Regulates Immune Functions.","authors":"Luana Campos Soares, Hana Bernhardova, Francis G Szele","doi":"10.1080/17590914.2026.2622750","DOIUrl":"10.1080/17590914.2026.2622750","url":null,"abstract":"<p><p>Galectin-3 (Gal-3) is a protein expressed by glia that belongs to an ancient family. Gal-3 recognises molecular patterns on pathogens due to the high degree of its binding specificity with carbohydrate recognition domains. Thus, in sponges as well as other invertebrates, galectins are an important component of the primitive innate immune system. Whereas Gal-3's function in driving mammalian inflammation is well known, its function in warding off bacterial and viral infections is not well appreciated. One route of brain infection is via the cerebrospinal fluid brain interface (CSFBI) which is primarily composed of ependymal cells (EC). ECs express high levels of Gal-3, and their motile cilia are compromised in Gal-3 KOs. In this mini-review, we discuss fundamentally important potential roles of Gal-3 in pathogen recognition at the CSFBI and suggest avenues of further study.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2622750"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12885407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myelin <i>g</i> Ratios: The Model Is in the Details.","authors":"Alexander Gow","doi":"10.1080/17590914.2025.2612034","DOIUrl":"10.1080/17590914.2025.2612034","url":null,"abstract":"<p><p>In contemporary myelin biology, there is a growing trend to prioritize faster, more convenient methodologies for evaluating white matter structure over quality of the analysis. This shift is often accompanied by less attention to the mechanistic foundations of the methods in preclinical and clinical research. To address such worrisome trends, the current article assesses three approaches for estimating the myelin <i>g</i> ratio from electron microscopy data, which is the gold standard approach to measure the impacts of neuropathology and treatment strategies on white matter integrity. Of the mathematical models examined, two are consistent with and equivalent to the linear relation defined by the axon versus fiber diameter plot (the principal data). The final model is the canonical almost universally accepted approach to measuring <i>g</i> ratios. This model is demonstrated to be internally inconsistent and discordant with the axon versus fiber diameter relation and can lead to inaccurate conclusions about myelin integrity. Furthermore, the increasing interest in non-invasive neuroimaging approaches to measure <i>g</i> ratios clinically in both physiologic and pathophysiologic studies necessitates calibration with electron microscopy-derived <i>g</i> ratios. In this vein, mathematical models applicable to these methodologies are concordant; thus, magnetic resonance imaging holds significant promise for accurate determination of myelin integrity in patients. On the other hand, the metrics measurable by this voxel-based technology may preclude application to gray matter myelin and perhaps limit its use to linearly-organized white matter tracts.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2612034"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12802999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145958267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-Synaptic Mechanism of Ocular Dominance Plasticity.","authors":"Maxwell K Foote, William C Huffman, Erin N Santos, Philip R Lee, Michal Jarnik, Wei Li, Juan S Bonifacino, R Douglas Fields","doi":"10.1080/17590914.2026.2616376","DOIUrl":"10.1080/17590914.2026.2616376","url":null,"abstract":"<p><p>Classic experiments showing that monocular visual disruption alters synaptic connections to binocular neurons established the fundamental concept of synaptic plasticity. Synaptic inputs that are activated coincidently with postsynaptic action potential firing are strengthened, and inputs from cells firing before or after the postsynaptic action potential are weakened. An implicit assumption, however, is that the speed of impulse transmission is not altered by visual deprivation. If so, spike time arrival at binocular neurons would be affected, thereby inducing synaptic plasticity. This possibility is tested here in adult mice by monocular eyelid suture and monocular action potential inhibition in retinal axons. The results show that spike time arrival in visual cortex is altered by monocular visual disruption in association with morphological changes in myelin (nodes of Ranvier) on axons in optic nerve and optic tract. This non-synaptic mechanism of ocular dominance plasticity, mediated by myelin-forming cells, supplements and may drive synaptic plasticity.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2616376"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12826708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146008680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of Fatty Acid Oxidation by Neural Stem and Progenitor Cells Increases Proliferation but Does Not Improve Long-Term Neurogenesis After Mild Traumatic Brain Injury.","authors":"Javier Allende Labastida, Regina F Fernandez, Tiffany Chu, Noelle Puleo, Maria Shishikura, Michael J Wolfgang, Joseph Scafidi, Susanna Scafidi","doi":"10.1080/17590914.2025.2610198","DOIUrl":"10.1080/17590914.2025.2610198","url":null,"abstract":"<p><p>Neurogenesis in the dentate gyrus of the hippocampus is a conserved and highly regulated process throughout the lifespan. Hippocampal neural stem and progenitor cells (NSPCs) can either transition into an activated proliferative state or remain quiescent. Accumulating data suggests that mitochondrial fatty acid β-oxidation is important in maintaining NSPCs quiescence under normal physiological conditions; however, the contribution of this pathway in NSPCs following brain injury remains unknown. While severe traumatic brain injury (TBI) is characterized by increased NSPCs proliferation in the hippocampus, the extent of this proliferative response after mild TBI, the most prevalent form of TBI, has not been fully delineated. Using closed head injury as a model of mild TBI and a brain-specific knockout mouse of carnitine palmitoyltransferase 2 (CPT2; an obligate gene in mitochondrial fatty acid β-oxidation), we investigated the role of fatty acid oxidation in hippocampal NSPCs proliferation in naïve and injured male and female mice. Our results show that loss of CPT2 in the brain does not affect hippocampal proliferation in naïve mice. Furthermore, mild TBI upregulates proliferation at day 3 post-injury, and is further increased only in male CPT2-deficient mice. Despite the post-injury increase in hippocampal NSPCs proliferation in CPT2^B-/- mice, long-term neurogenesis remained unchanged. Together, these data provides a new insight into the metabolic regulation of NSPCs neurogenesis in the hippocampus following mild traumatic brain injury.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2610198"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12818800/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145997010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Membrane Molecular Species Remodeling as a Signature of ω-3 Fatty Acid Action in Cultured Neural Cells.","authors":"Kyndall R Nicholas, Hennrique Taborda Ribas, Kevin D Browne, Kamryn R Purpura, Peining Xu, Ashika Mani, Elizabeth N Krizman, Clementina Mesaros, D Kacy Cullen","doi":"10.1080/17590914.2026.2644959","DOIUrl":"10.1080/17590914.2026.2644959","url":null,"abstract":"<p><p>Omega-3 polyunsaturated fatty acids (ω3 PUFAs) are critical structural components of neuronal membranes, yet the molecular specificity of their incorporation within neural cells remains incompletely defined. We integrated untargeted and targeted lipidomics with lipid ontology analysis and coarse-grained membrane simulations to characterize remodeling in primary rat cortical neurons and neuron-astrocyte co-cultures following supplementation with docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), or docosapentaenoic acid (DPA). Each ω3 PUFA produced a distinct lipidomic signature. DHA showed the most consistent incorporation, selectively enriching phosphatidylethanolamine (PE) species-particularly PE(18:0/22:6) and PE(18:1/22:6)-associated with membrane curvature and organelle organization. Ontology analysis linked DHA supplementation to intrinsic curvature-related membrane features, and membrane simulations demonstrated enhanced collective bilayer bending without substantial changes in overall membrane thickness. EPA preferentially increased EPA-containing PE species without elevating DHA levels, whereas DPA effects were variable and culture-dependent, indicating selective metabolic handling of individual ω3 species. Differences between neurons and neuron-astrocyte co-cultures underscore the importance of cellular context in ω3-driven remodeling. By resolving ω3 incorporation at molecular species resolution and linking compositional changes to predicted membrane behavior, this study provides a structural framework for understanding how dietary ω3 fatty acids may influence neuronal membrane organization and cellular resilience.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2644959"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13007425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MyeliMetric: A Python-Based Toolbox for Standardized G-Ratio Analysis of Axon-Myelin Integrity.","authors":"Intakhar Ahmad, Farjana Sultana Chowdhury, Anne I Boullerne, Alexander Gow, Douglas L Feinstein","doi":"10.1080/17590914.2025.2603411","DOIUrl":"10.1080/17590914.2025.2603411","url":null,"abstract":"<p><p>The g-ratio, defined as the ratio of an axon's diameter to the total fiber diameter (axon plus myelin), is a key metric for assessing myelin integrity and axonal conduction velocity in both the central and peripheral nervous systems. Deviations from the physiological range often signal underlying pathology. Despite its diagnostic importance, there is currently no standardized, open-source tool for g-ratio analysis from post-segmented electron microscopy images. To address this gap, we developed MyeliMetric, a Python-based, user-friendly toolbox that streamlines g-ratio data preprocessing and integrates biologically informed validation, requiring minimal statistical expertise to operate without introducing common analytical errors. It is built on the principle that g-ratios exhibit relative consistency across varying axon diameters in healthy conditions. To rigorously assess this relationship, MyeliMetric implements a binning strategy that groups axons into biologically relevant diameter cohorts, enabling the detection of size-dependent deviations in g-ratio distributions. This approach addresses common limitations in conventional analyses, including insufficient sampling, pseudo-replication, and artifacts such as misleading regression slopes. Validation using both synthetic and published datasets from rodent models of demyelination demonstrated the tool's accuracy, reproducibility, and biological relevance. Synthetic data yielded expected outcomes, and in experimental models, MyeliMetric reliably detected reductions in myelin thickness through g-ratio shifts while minimizing artifacts, thereby providing biologically meaningful insights. It is available on GitHub: https://github.com/Intakhar-Ahmad/NeuroMyelin-G-Ratio-Analysis-Toolkit.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2603411"},"PeriodicalIF":3.7,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12818378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145809330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Demystifying The Myelin <i>g</i> Ratio: Its Origin, Derivation and Interpretation.","authors":"Alexander Gow","doi":"10.1080/17590914.2025.2542166","DOIUrl":"10.1080/17590914.2025.2542166","url":null,"abstract":"<p><p>Most studies involving myelin <i>g</i> ratios over the past 120 years assume this metric enumerates differences in myelin thickness (larger <i>g</i> ratio = thinner myelin) with axon or fiber diameter. And, moreover, such changes are directly correlated with internodal function (conduction velocity). However, such assumptions are warranted only in the absence of experimental errors and artifacts (i.e. under theoretical conditions). In reality, <i>g</i> ratios can easily under- or overestimate the rate of change for this relation in excess of 10%, especially for small caliber fibers. Typical analyses of myelin internodes rely on an explicit mathematical model, <math><mi>g</mi><mi> </mi><mtext>ratio</mtext><mo>=</mo><mrow><mfrac><mrow><mrow><msub><mrow><mi>D</mi></mrow><mrow><mi>A</mi></mrow></msub></mrow></mrow><mrow><mrow><msub><mrow><mi>D</mi></mrow><mrow><mi>F</mi></mrow></msub></mrow></mrow></mfrac></mrow><mtext>,</mtext></math> where D_A is axon diameter and D_F is fiber diameter (myelin plus axon). Shown recently and herein, this model approximates normal physiological conditions only when the axon-fiber diameter relation is directly proportional, whence it is concordant with the axomyelin unit model. However, in transient or non-steady states (development/aging, disease or myelin plasticity) with linear but not directly proportional relations, <i>g</i> ratios may not accurately describe myelin structure. Acceptance of this counterintuitive assertion is predicated on a detailed understanding of the <i>g</i> ratio - its origins, properties and the biology represented - which has been heretofore unexplored. In light of such <i>g</i> ratio limitations, and toward consistency with experimental data, two more reliable metrics are proposed, the myelin <i>g_c</i> ratio and the <i>g'</i> cline. But irrespective which of metric is preferred , the analysis herein shows that the axon-to-fiber diameter ratio under normal physiological conditions is a constant for all fiber diameters.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2542166"},"PeriodicalIF":3.7,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12360196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144862091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the Myelin <i>g</i> Ratio from First Principles, Its Derivation, Uses and Artifacts.","authors":"Alexander Gow","doi":"10.1080/17590914.2024.2445624","DOIUrl":"10.1080/17590914.2024.2445624","url":null,"abstract":"<p><p>In light of the increasing importance for measuring myelin <i>g</i> ratios - the ratio of axon-to-fiber (axon + myelin) diameters in myelin internodes - to understand normal physiology, disease states, repair mechanisms and myelin plasticity, there is urgent need to minimize processing and statistical artifacts in current methodologies. Many contemporary studies fall prey to a variety of artifacts, reducing study outcome robustness and slowing development of novel therapeutics. Underlying causes stem from a lack of understanding of the myelin <i>g</i> ratio, which has persisted more than a century. An extended exploratory data analysis from first principles (the axon-fiber diameter relation) is presented herein and has major consequences for interpreting published <i>g</i> ratio studies. Indeed, a model of the myelin internode naturally emerges because of (1) the strong positive correlation between axon and fiber diameters and (2) the demonstration that the relation between these variables is one of direct proportionality. From this model, a robust framework for data analysis, interpretation and understanding allows specific predictions about myelin internode structure under normal physiological conditions. Further, the model establishes that a regression fit to <i>g</i> ratio plots has zero slope, and it identifies the underlying causes of several data processing artifacts that can be mitigated by plotting <i>g</i> ratios against fiber diameter (not axon diameter). Hypothesis testing can then be used for extending the model and evaluating myelin internodal properties under pathophysiological conditions (forthcoming). For without a statistical model as anchor, hypothesis testing is aimless like a rudderless ship on the ocean.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2445624"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11877616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143031981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Statistically-Robust Model of the Axomyelin Unit under Normal Physiologic Conditions with Application to Disease States.","authors":"Alexander Gow, Jeffrey L Dupree, Douglas L Feinstein, Anne Boullerne","doi":"10.1080/17590914.2024.2447336","DOIUrl":"10.1080/17590914.2024.2447336","url":null,"abstract":"<p><p>Despite tremendous progress in characterizing the myriad cellular structures in the nervous system, a full appreciation of the interdependent and intricate interactions between these structures is as yet unfulfilled. Indeed, few more so than the interaction between the myelin internode and its ensheathed axon. More than a half-century after the ultrastructural characterization of this axomyelin unit, we lack a reliable understanding of the physiological properties, the significance and consequence of pathobiological processes, and the means to gauge success or failure of interventions designed to mitigate disease. Herein, we highlight shortcomings in the most common statistical procedures used to characterize the myelin <i>g</i> ratio, with particular emphasis on the underlying principles of simple linear regression. These shortcomings lead to insensitive detection and/or ambiguous interpretation of normal physiology, disease mechanisms and remedial methodologies. To address these problems, we syndicate insights from early seminal myelin studies and use a statistical model of the axomyelin unit that is established in Gow (2025). Herein, we develop and demonstrate a statistically-robust analysis pipeline with which to examine and interpret axomyelin physiology and pathobiology in two disease states, experimental autoimmune encephalomyelitis and the <i>rumpshaker</i> mouse model of leukodystrophy. On a cautionary note, our pipeline is a relatively simple and streamlined approach that is not necessarily a panacea for all <i>g</i> ratio analyses. Rather, it approximates a minimum effort needed to elucidate departures from normal physiology and to determine if more comprehensive studies may lead to deeper insights.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2447336"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11974466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of Oligodendrocyte Lineage Cell Progression with Cre-Mediated RiboTag Reporter Lines.","authors":"George S Melchor, Maya S Shah, Zeeba Manavi, Lauren M Rosko, Jingwen Hu, Haiyang Wang, Maryna Baydyuk, Jeffrey K Huang","doi":"10.1080/17590914.2025.2513885","DOIUrl":"10.1080/17590914.2025.2513885","url":null,"abstract":"<p><p>Cre-reporter strategies in transgenic mice are widely used to assess the specificity of gene promoter activities, and for fate-mapping studies during development and under injury conditions. The ribosome tagging strategy, RiboTag, is a transgenic approach, in which a hemagglutinin (HA) tag fused to the endogenous ribosomal protein, RPL22, is expressed through the Cre/loxP system. To profile RiboTag reporter expression in oligodendrocyte lineage cells (OLCs), we generated NG2^Cre:Rpl22^HA, Pdgfra^CreERT:Rpl22^HA, and Plp^CreERT:Rpl22^HA mice. We found that NG2^Cre:Rpl22^HA displayed strong HA reporter expression in OLCs and neuronal subpopulations in the postnatal CNS. Tamoxifen administration into Pdgfra^CreERT:Rpl22^HA and Plp^CreERT:Rpl22^HA mice led to widespread HA reporter expression in oligodendrocyte precursor cells (OPCs) and oligodendrocytes, respectively, throughout the brain and spinal cord. Following focal demyelinating injury, Pdgfra^CreERT:Rpl22^HA mice exhibited HA labeling in OPCs, with a gradual increase in oligodendrocyte labeling during remyelination. In contrast, Plp^CreERT:Rpl22^HA exhibited oligodendrocyte labeling in lesions and throughout the CNS parenchyma, presenting a challenge in distinguishing newly generated oligodendrocytes during remyelination from pre-existing oligodendrocytes. Notably, HA expression was induced in oligodendrocytes, but not OPCs in demyelinated lesions of Plp^CreERT:Rpl22^HA mice even when the demyelinating injury was conducted several days after tamoxifen had cleared. This suggests a potential regulation of gene expression in OPCs in demyelinated lesions, in which Rpl22^HA translation may be prevented until oligodendrocyte differentiation occurs. Overall, the RiboTag reporter demonstrates high sensitivity and stability, and its potential application should be carefully considered in relation to the experimental model, timeline in which it will be used, and cell tracking conditions.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2513885"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12169044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}