Cells最新文献

{"title":"ODAD4-Related Primary Ciliary Dyskinesia: Report of Five Cases and a Founder Variant in Quebec.","authors":"Marie-Hélène Bourassa, Guillaume Sillon, Shuizi Ding, Maurizio Chioccioli, Monkol Lek, Kaiyue Ma, Alejandro Mejia-Garcia, Simon Gravel, Donald C Vinh, Michael R Knowles, Margaret W Leigh, Stephanie D Davis, Thomas Ferkol, Kenneth N Olivier, Elizabeth N Schecterman, Weining Yin, Patrick R Sears, Martina Gentzsch, Susan E Boyles, William D Bennett, Kirby L Zeman, Lawrence E Ostrowski, Maimoona A Zariwala, Adam J Shapiro","doi":"10.3390/cells14181460","DOIUrl":"10.3390/cells14181460","url":null,"abstract":"<p><p>Pathogenic variants in <i>ODAD4</i> are an ultra-rare cause of primary ciliary dyskinesia (PCD). Previously reported cases display classic disease phenotypes, including chronic oto-sino-pulmonary disease and development of bronchiectasis by adulthood. We report five individuals with PCD harboring biallelic <i>ODAD4</i> variants (median age 14, range 3-41 years). Participants underwent standardized PCD diagnostic evaluations. Three individuals shared the novel homozygous <i>ODAD4</i> genotype [NM_031421.5: c.245delA, p.(Lys82Argfs*29)], and genealogy analysis highly suggests a founder effect in French-Canadians from two regions of Quebec. All five participants had normal pulmonary function values. Two Quebec participants lacked radiographic pneumonias or bronchiectasis (ages 14 and 38 years) despite life-long suppurative respiratory symptoms, low nasal nitric oxide levels, and outer dynein arm defects on electron microscopy. Reverse transcription polymerase chain reaction of the c.245delA variant showed abnormal splicing with in-frame skipping of exon 2, allowing expression of a mildly shortened mRNA product. However, functional analysis showed overall static cilia, absence of ODAD4 protein on Western blot, and absence of in vivo mucociliary clearance. The reason for a milder pulmonary phenotype with the c.245delA variant in <i>ODAD4</i> remains unclear, but regional screening for this variant in Quebec may identify more cases and enhance understanding of this mild form of PCD.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468610/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Backwards Approach to GD2 Immunofluorescence in Human Neuroblastoma Tissue Samples: From Staining to Slicing.","authors":"Sara Peggion, Clara Volz, Magdalena Trochimiuk, Isabelle Ariane Bley, Júlia Ramos, Konrad Reinshagen, Laia Pagerols Raluy","doi":"10.3390/cells14181462","DOIUrl":"10.3390/cells14181462","url":null,"abstract":"<p><strong>Background: </strong>The disialoganglioside GD2, located at the plasma membrane, is selectively overexpressed in various solid tumors, where it contributes to tumor growth and the development of an aggressive tumor phenotype. Thus, over the last two decades GD2 has been gaining importance both as a tumor marker and a therapy target. In neuroblastoma, anti-GD2 monoclonal antibodies and CAR T-cells have become an integral part of the multimodal treatment for relapsed or refractory high-risk cases, which continue to associate with poor prognosis. GD2 characterization in neuroblastoma is well established for bone marrow aspirates and biopsies, but remains challenging in tumoral tissue samples, mostly due to epitope loss upon fixation.</p><p><strong>Aims: </strong>The aim of our work was to assess a new protocol by staining GD2 in tissue specimens prior to fixation.</p><p><strong>Methods: </strong>Positive controls were tissue specimens from patients with histologically confirmed neuroblastoma and GD2 expression in bone marrow aspirate (<i>n</i> = 5). Nephroblastoma or Hodgkin lymphoma samples were considered as negative controls (<i>n</i> = 5). Tissue staining was performed prior to fixation with either anti-GD2 antibody or isotype control, followed by secondary antibody staining and subsequent paraffinization. To examine GD2 staining before and after paraffinization, fluorescence images were acquired using 3D and 2D immunofluorescence microscopy techniques respectively.</p><p><strong>Results: </strong>GD2 signal was detected in all positive controls, while absent in all negative controls. After fixation, paraffinization and slicing no relevant signal loss was observed. Nevertheless, sufficient staining of 3D specimens required long incubation times, which led to increased cytolysis of the unfixed tissue.</p><p><strong>Conclusions: </strong>We were able to establish and validate a novel protocol to reliably perform immunostaining of the membrane antigen GD2 in unfixed, primary neuroblastoma tissue. Although including few limitations, this staining workflow enables relatively quick assessment of GD2 status and thus, might represent a relevant diagnostic tool within the framework of tumor staging and precision medicine.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spike Timing-Dependent Plasticity at Layer 2/3 Horizontal Connections Between Neighboring Columns During Synapse Formation Before the Critical Period in the Developing Barrel Cortex.","authors":"Chiaki Itami, Fumitaka Kimura","doi":"10.3390/cells14181459","DOIUrl":"10.3390/cells14181459","url":null,"abstract":"<p><p>The Hebbian type of spike timing-dependent plasticity (STDP) with long-term potentiation and depression (LTP and LTD) plays a crucial role at layer 4 (L4) to L2/3 synapses in deprivation-induced map plasticity. In addition, plasticity at the L2/3 horizontal connection is suggested to play an additional role in map plasticity, especially for \"spared whisker response potentiation.\" Unimodal STDP with only LTP, or all-LTP STDP drives circuit formation at thalamocortical, as well as L4-L2/3 synapse before the critical period. Here, we first show that the L2/3 horizontal connections exhibit all-LTP STDP when axons are extending during synapse formation before the critical period. LTP-STDP induced by pre-post timing was mediated by NMDA-R because APV blocked the induction. In addition, PKA signaling was involved because PKI 6-22 blocked the induction. However, LTP-STDP induced by post-pre timing was not mediated by NMDA-R, because APV could not block its induction. Nevertheless, PKA signaling was also involved in its induction because PKI 6-22 blocked the induction. Our finding indicates that PKA signaling plays an important role in all-LTP STDP during synaptic formation at the L2/3-L2/3 connection between neighboring columns with a distinct source of Ca²⁺ influx in the developing mouse barrel cortex.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468516/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expansion Microscopy of the Enteric Nervous System: A Feasibility Study.","authors":"Xin Xu, Wenchuan Zhang, Menachem Hanani","doi":"10.3390/cells14181463","DOIUrl":"10.3390/cells14181463","url":null,"abstract":"<p><p>Expansion microscopy (ExM) enables conventional light microscopes to achieve nanoscale resolution by physically enlarging biological specimens. While ExM has been widely applied in neurobiology, it has not been adapted for the enteric nervous system (ENS). Here, we provide a detailed and reproducible protocol for applying ExM to mouse colonic ENS tissue. The procedure includes preparation of the external muscle layers with the myenteric plexus, histochemical staining for NADPH-diaphorase, immunostaining for glial fibrillary acidic protein (GFAP), anchoring of biomolecules, gelation, proteinase K digestion, and isotropic expansion in a swellable polymer matrix. Step-by-step instructions, required reagents, and critical parameters are described to ensure robustness and reproducibility. Using this protocol, tissues expand 3-5-fold, allowing neuronal somata, fibers, and glial cell processes to be clearly visualized by standard brightfield or fluorescence microscopy. The tissue architecture is preserved, with distortion in the X-Y plane of about 7%. This protocol provides a reliable framework for high-resolution structural analysis of the ENS and can be readily adapted to other peripheral tissues.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468614/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NUP214 in Acute Myeloid Leukemia.","authors":"Øystein Bruserud, Håkon Reikvam","doi":"10.3390/cells14181461","DOIUrl":"10.3390/cells14181461","url":null,"abstract":"<p><p>Nucleoporin 214 (NUP214) is a component of the nucleopore molecular complex, but in addition to this role in nucleocytoplasmic transport it is also involved in the regulation of gene transcription/translation, intracellular signaling, cell cycle progression and programmed cell death. Several uncommon translocations associated with acute myeloid leukemia (AML) involve the <i>NUP214</i> gene, and the corresponding fusion proteins are involved in leukemic transformation. First, the t(6;9) translocation encodes the DEK-NUP214 fusion protein; this translocation is seen in 1-2% of AML patients and is associated with an adverse prognosis that is improved by allogeneic stem cell transplantation. Second, the <i>SET-NUP214</i> fusion gene is less common in AML and is formed either by del(9)(q34.11q34.13) or a balanced t(9;9)(q34;q34). This AML variant shows several biological similarities with the <i>DEK-NUP214</i> variant, but the possible prognostic impact of this fusion protein is not known. Finally, the <i>NUP214-ABL1</i> and especially the <i>NUP214-SQSTM1</i> fusions are very uncommon, and only a few case reports have been published. In this article, we review the functions of the genes/proteins formed by these fusion genes, the available studies of molecular mechanisms and biological functions for each fusion protein, the characteristics of the corresponding AML cells, the clinical characteristics of these patients and the possible prognostic impact of the fusion genes/proteins.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Form and Function of Retinal Ganglion Cells in Diabetes.","authors":"Alistair J Barber","doi":"10.3390/cells14181455","DOIUrl":"10.3390/cells14181455","url":null,"abstract":"<p><p>This review examines how diabetes affects the ganglion cells of the retina, including the axons that make up the optic nerve. Links between established changes in the morphology of retinal ganglion cells (RGCs) and vision loss, as well as other functions, such as the pupillary light reflex, are considered. RGC morphology and function are significantly altered in both animal models and humans with diabetes. Diabetes affects all parts of the RGC, including the dendrites, the cell body, the axons making up the nerve fiber layer, and the optic nerve. Subtypes of RGCs appear to be affected differently by diabetes, and the morphology and electrophysiological output are more significantly affected in ON-RGCs than in OFF cells, which may explain part of the mechanism underlying the widely documented diabetes-induced reduction in contrast sensitivity. Furthermore, the morphology of the specialized light-sensitive melanopsin-containing RGCs also appears to be affected by diabetes, which may explain deficits in circadian rhythm and the pupillary light reflex. Potential therapeutic approaches aimed at protecting RGCs in diabetes are also discussed. Overall, strong evidence supports the conclusion that diabetes impacts the form and function of RGCs and their axons within the optic nerve, resulting in deficient regulation of circadian rhythms and the pupillary light reflex, in addition to vision.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulation of SELENOI Is Associated with TDP-43 Neuropathology in Amyotrophic Lateral Sclerosis.","authors":"Finula I Isik, Jasmin Galper, Russell Pickford, Nicolas Dzamko, YuHong Fu, Woojin Scott Kim","doi":"10.3390/cells14181457","DOIUrl":"10.3390/cells14181457","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis (ALS), also known as motor neuron disease, is characterized by progressive degeneration of motor neurons and accumulation of TAR DNA-binding protein 43 (TDP-43) in the brain. Increasing evidence indicates that aberration in lipid synthesis or regulation underlies neuronal dysfunction and degeneration. Phosphatidylethanolmine (PE) is an abundant phospholipid in the brain and is synthesized by the SELENOI gene. SELENOI is important in motor neuron development and function, as demonstrated in hereditary spastic paraplegia, a neurological disorder in which SELENOI is mutated. Despite this, virtually nothing was known about SELENOI in the context of ALS neuropathology. We therefore undertook a comprehensive assessment of PE in ALS brain tissues, using sophisticated liquid chromatography-mass spectrometry, and investigated how SELENOI regulates TDP-43 expression. PE levels were significantly decreased in the disease-affected motor cortex of ALS compared to controls and were inversely associated with disease duration. In contrast, PE levels were unaltered in the disease-unaffected cerebellum. Consistent with this, SELENOI expression was dysregulated only in the motor cortex of ALS. The correlation between SELENOI and TDP-43 was also lost in the motor cortex of ALS. A knockdown of SELENOI expression in neuronal cells caused an upregulation of TDP-43 expression. When put together, these results suggest that SELENOI dysregulation may contribute to TDP-43 pathology in ALS brain. Our study has provided new insights into an unrecognized pathway in ALS brain and revealed new targets for controlling TDP-43 pathology in ALS brain.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12469239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>ATHB1</i> Interacts with Hormone-Related Gene Regulatory Networks Involved in Biotic and Abiotic Stress Responses in <i>Arabidopsis</i>.","authors":"Valentina Forte, Sabrina Lucchetti, Andrea Ciolfi, Barbara Felici, Marco Possenti, Fabio D'Orso, Giorgio Morelli, Simona Baima","doi":"10.3390/cells14181456","DOIUrl":"10.3390/cells14181456","url":null,"abstract":"<p><p>ATHB1, an <i>Arabidopsis thaliana</i> homeodomain-leucine zipper (HD-Zip) transcription factor, is involved in the control of leaf development and hypocotyl elongation under short-day conditions. As growth adaptation to environmental conditions is essential for plant resilience, we investigated the role of <i>ATHB1</i> in the interaction between transcriptional regulatory networks and hormone signaling pathways. We found that wounding, flooding and ethylene induce <i>ATHB1</i> expression. In addition, we found that the ethylene signal transduction pathway is also involved in an age-dependent <i>ATHB1</i> expression increase in leaves. Conversely, methyl jasmonate (MeJA) application decreases the <i>ATHB1</i> transcript level. By exploiting mutant and over-expressing (OE) lines, we also found that the ATHB1 level influences plant sensitivity to the inhibitory effect of MeJA treatment on growth. To gain deeper insights into the regulatory pathways affected by <i>ATHB1</i>, we performed a microarray analysis comparing the transcriptome of wild-type and <i>athb1</i> mutant plants following exposure to MeJA. Remarkably, although the response to the MeJA treatment was not impaired in <i>athb1</i>, several genes involved in jasmonate and salycilic acid signaling were already downregulated in <i>athb1</i> seedlings under normal conditions compared to the wild type. Thus, our study suggests that <i>ATHB1</i> may integrate different hormone signaling pathways to influence plant growth under various stress conditions.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocytes and Astrocyte-Derived Extracellular Conduits in Opiate-Mediated Neurological Disorders.","authors":"Sudipta Ray, Souvik Datta, Arnab Saha, Susmita Sil","doi":"10.3390/cells14181454","DOIUrl":"10.3390/cells14181454","url":null,"abstract":"<p><p>Opioid-use disorder (OUD) poses a growing global health crisis, with chronic opioid exposure linked not only to addiction but also to enduring neurological impairments. While traditional research has focused primarily on neuronal alterations, emerging evidence underscores the pivotal role of astrocytes, abundant glial cells in the central nervous system, and their secreted extracellular vesicles (EVs) in opioid-mediated neuropathology. This review delineates the mechanistic roles of astrocytes and astrocyte-derived EVs (ADEVs) across a spectrum of opioids, including morphine, heroin, fentanyl, codeine, tramadol, buprenorphine, and methadone. Opioids disrupt astrocytic homeostasis by impairing glutamate regulation, altering the redox balance, and activating pro-inflammatory signaling pathways. In response, astrocytes release EVs enriched with neurotoxic cargo, including amyloidogenic proteins, cytokines, microRNAs, and long non-coding RNAs, that propagate neuroinflammation, compromise blood-brain barrier (BBB) integrity, and exacerbate synaptic dysfunction. Preclinical models and in vitro studies reveal drug-specific astrocytic responses and ADEV profiles, implicating these vesicles in modulating microglial function, neuroimmune signaling, and neuronal viability. Notably, morphine-induced ADEVs promote amyloidosis and inflammatory signaling, while heroin and fentanyl affect glutamatergic and inflammasome pathways. Even opioids used in therapy, such as buprenorphine and methadone, alter astrocyte morphology and EV cargo, particularly during neurodevelopment. Collectively, these findings advance a neuro-glial paradigm for understanding opioid-induced brain injury and highlight ADEVs as both biomarkers and mediators of neuropathology. Targeting astrocyte-EV signaling pathways represents a promising therapeutic avenue to mitigate long-term neurological consequences of opioid exposure and improve outcomes in OUD.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocytes in Fear Memory Processing: Molecular Mechanisms Across the Amygdala-Hippocampus-Prefrontal Cortex Network.","authors":"Young-Rae Kim, Moonhyung Lee, Man S Kim","doi":"10.3390/cells14181444","DOIUrl":"10.3390/cells14181444","url":null,"abstract":"<p><p>Fear memory is a critical adaptive process that enables organisms to avoid potential threats and survive in complex environments. Traditionally viewed as a neuronal phenomenon, emerging evidence has demonstrated that astrocytes play a fundamental role in fear memory acquisition, consolidation, extinction, and retrieval across the distributed neural network encompassing the amygdala, hippocampus, and prefrontal cortex. This review presents recent advances in our understanding of the molecular mechanisms by which astrocytes modulate fear memory processing within the tripartite circuit. We examine how astrocytes contribute to synaptic plasticity, neurotransmitter regulation, metabolic support, and intercellular communication during the different phases of fear memory processing. Particular emphasis is placed on the region-specific functions of astrocytes, their dynamic interactions with neurons, and their therapeutic implications for treating fear-related disorders such as post-traumatic stress disorder (PTSD) and anxiety disorders. The integration of cutting-edge technologies, including spatial transcriptomics, optogenetics, and chemogenetics, has revealed sophisticated astrocyte-neuron communication mechanisms that challenge the traditional neuron-centric view of memory processing.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}