Frontiers in Cellular Neuroscience最新文献

{"title":"Paving the way for better ototoxicity assessments in cisplatin therapy using more reliable animal models.","authors":"Vijayprakash Manickam, Marisa Zallocchi","doi":"10.3389/fncel.2025.1552051","DOIUrl":"10.3389/fncel.2025.1552051","url":null,"abstract":"<p><p>Cisplatin-induced hearing loss is a common and irreversible side effect affecting a significant proportion of cancer patients. While various strategies to mitigate this toxicity have been explored, there remains a critical need for effective treatments. A major challenge in developing new therapies is the lack of reliable animal models that accurately replicate the clinical use of cisplatin in humans, which typically involves multiple cycles of low-dose administration. Traditional models using high doses of cisplatin have resulted in high mortality and variable hearing loss, complicating the assessment of potential treatments. To address this, a multi-cycle model using lower cisplatin doses in mice was developed, providing hearing loss without mortality. However, variability in outcomes across different research groups persisted. In the present study, we optimize the multi-cycle model of cisplatin-induced ototoxicity by using clinical-grade cisplatin rather than laboratory-grade formulations. The use of clinical cisplatin ensures greater consistency, reliability, and relevance to human treatment protocols, as it adheres to the rigorous quality standards required for patient use. This new administration protocol will minimize variability across research laboratories and more accurately mimic the dosing regimens typically administered to cancer patients. Additionally, we have enhanced a zebrafish model for high-throughput screening of potential therapeutics, further improving the consistency of results. These improvements to the animal models are critical for accelerating the discovery and testing of therapies to prevent cisplatin-induced hearing loss, supporting the development of effective treatments for cancer patients undergoing cisplatin chemotherapy.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1552051"},"PeriodicalIF":4.2,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11919870/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acetoacetate, a ketone body, attenuates neuronal bursts in acutely-induced epileptiform slices of the mouse hippocampus.","authors":"Hao Wen, Nagisa Sada, Tsuyoshi Inoue","doi":"10.3389/fncel.2025.1551700","DOIUrl":"10.3389/fncel.2025.1551700","url":null,"abstract":"<p><p>The ketogenic diet increases ketone bodies (β-hydroxybutyrate and acetoacetate) in the brain, and ameliorates epileptic seizures <i>in vivo</i>. However, ketone bodies exert weak or no effects on electrical activity in rodent hippocampal slices. Especially, it remains unclear what kinds of conditions are required to strengthen the actions of ketone bodies in hippocampal slices. In the present study, we examined the effects of acetoacetate on hippocampal pyramidal cells in normal slices and epileptiform slices of mice. By using patch-clamp recordings from CA1 pyramidal cells, we first confirmed that acetoacetate did not change the membrane potentials and intrinsic properties of pyramidal cells in normal slices. However, we found that acetoacetate weakened spontaneous epileptiform bursts in pyramidal cells of epileptiform slices, which were acutely induced by applying convulsants to normal slices. Interestingly, acetoacetate did not change the frequency of the epileptiform bursts, but attenuated individual epileptiform bursts. We finally examined the effects of acetoacetate on excitatory synaptic barrages during epileptiform activity, and found that acetoacetate weakened epileptiform bursts by reducing synchronous synaptic inputs. These results show that acetoacetate attenuated neuronal bursts in epileptiform slices, but did not affect neuronal activity in normal slices, which leads to seizure-selective actions of ketone bodies.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1551700"},"PeriodicalIF":4.2,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11919829/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of DPP6 dysregulation in neuropathology: from synaptic regulation to disease mechanisms.","authors":"Xuan-Yan Ding, Jean de Dieu Habimana, Zhi-Yuan Li","doi":"10.3389/fncel.2025.1547495","DOIUrl":"10.3389/fncel.2025.1547495","url":null,"abstract":"<p><p>As a transmembrane protein, DPP6 modulates the function and properties of ion channels, playing a crucial role in various tissues, particularly in the brain. DPP6 interacts with potassium channel Kv4.2 (KCND2), enhancing its membrane expression and channel kinetics. Potassium ion channels are critical in progressing action potential formation and synaptic plasticity. Therefore, dysfunction of DPP6 can lead to significant health consequences. Abnormal DPP6 expression has been identified in several diseases, such as amyotrophic lateral sclerosis (ALS), autism spectrum disorder (ASD), spinal bulbar muscular atrophy (SBMA), and idiopathic ventricular fibrillation. Recent research has indicated a connection between DPP6 and Alzheimer's disease as well. The most common symptoms resulting from DPP6 dysregulation are mental deficiency and muscle wastage. Notably, these symptoms do not always occur at the same time. Besides genetic factors, environmental factors also undoubtedly play a role in diseases related to DPP6 dysregulation. However, it remains unclear how the expression of DPP6 gets regulated. This review aims to summarize the associations between DPP6 and neurological diseases, offering insights as well as proposing hypotheses to elucidate the underlying mechanisms of DPP6 dysregulation.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1547495"},"PeriodicalIF":4.2,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920134/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morphology and connectivity of retinal horizontal cells in two avian species.","authors":"Anja Günther, Vaishnavi Balaji, Bo Leberecht, Julia J Forst, Alexander Y Rotov, Tobias Woldt, Dinora Abdulazhanova, Henrik Mouritsen, Karin Dedek","doi":"10.3389/fncel.2025.1558605","DOIUrl":"10.3389/fncel.2025.1558605","url":null,"abstract":"<p><p>In the outer vertebrate retina, the visual signal is separated into intensity and wavelength information. In birds, seven types of photoreceptors (one rod, four single cones, and two members of the double cone) mediate signals to >20 types of second-order neurons, the bipolar cells and horizontal cells. Horizontal cells contribute to color and contrast processing by providing feedback signals to photoreceptors and feedforward signals to bipolar cells. In fish, reptiles, and amphibians they either encode intensity or show color-opponent responses. Yet, for the bird retina, the number of horizontal cell types is not fully resolved and even more importantly, the synapses between photoreceptors and horizontal cells have never been quantified for any bird species. With a combination of light microscopy and serial EM reconstructions, we found four different types of horizontal cells in two distantly related species, the domestic chicken and the European robin. In agreement with some earlier studies, we confirmed two highly abundant cell types (H1, H2) and two rare cell types (H3, H4), of which H1 is an axon-bearing cell, whereas H2-H4 are axonless. H1 cells made chemical synapses with one type of bipolar cell and an interplexiform amacrine cell at their soma. Dendritic contacts of H1-H4 cells to photoreceptors were type-specific and similar to the turtle retina, which confirms the high degree of evolutionary conservation in the vertebrate outer retina. Our data further suggests that H1 and potentially H2 cells may encode intensity, whereas H3 and H4 may represent color opponent horizontal cells which may contribute to the birds' superb color and/or high acuity vision.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1558605"},"PeriodicalIF":4.2,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11914121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A dual role for pleiotrophin in modulating inflammation and myelination in the presence of chondroitin sulfate proteoglycans after nervous system injury.","authors":"Somnath J Gupta, Matthew A Churchward, Kathryn G Todd, Ian R Winship","doi":"10.3389/fncel.2025.1549433","DOIUrl":"10.3389/fncel.2025.1549433","url":null,"abstract":"<p><p>Chondroitin sulfate proteoglycans (CSPGs), key components of the extracellular matrix and the glial scar that forms around central nervous system (CNS) injuries, are recognized for hindering neuronal regeneration. We previously demonstrated the potential of pleiotrophin (PTN) to induce neurite outgrowth even in the presence of inhibitory CSPGs. The effects of PTN on microglia and oligodendrocytes are not well described. Here, we examined how PTN administration alters the differentiation of oligodendrocyte precursor cells (OPCs) into mature oligodendrocytes in the presence of CSPGs using <i>in vitro</i> cell culture model. Moreover, we explored the effects of PTN on the inflammatory activity of microglia with and without inflammatory stimulation (IFN-<i>γ</i>) in a CSPG-rich environment. The data showed that the CSPG matrix inhibited the differentiation of OPCs into mature oligodendrocytes. PTN induced dose-dependent differentiation of OPCs into mature oligodendrocytes, with an optimal effect at 10 nM PTN. Moreover, PTN modified the immunological response of microglia in the presence of CSPGs, with reduced proinflammatory activity that was further reduced by PTN administration, in contrast to the increased release of matrix metalloproteinases (MMP 9). However, when IFN-<i>γ</i>-activated microglia were treated with PTN, proinflammatory signaling was stimulated at higher PTN concentrations (10 nM and 100 nM). Overall, our results indicate that PTN can overcome the inhibitory effect of CSPGs on the differentiation of OPCs into oligodendrocytes and can modulate inflammation mediated by CSPGs from microglia. Collectively, these findings demonstrate that PTN can effectively counteract the inhibitory effects of CSPGs on the differentiation of OPCs into mature oligodendrocytes while also modulating microglial responses to reduce proinflammatory activity and increase MMP-9 release. Thus, PTN has great potential to improve remyelination and neuroprotective strategies in the treatment of demyelinating diseases or any injury.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1549433"},"PeriodicalIF":4.2,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 Bmal1 impairs the glutamatergic light input to the SCN in mice.","authors":"Hüseyin Korkmaz, Max Anstötz, Tim Wellinghof, Benedetta Fazari, Angelika Hallenberger, Ann Kathrin Bergmann, Elena Niggetiedt, Fatma Delâl Güven, Federica Tundo-Lavalle, Fathima Faiba A Purath, Kevin Bochinsky, Lothar Gremer, Dieter Willbold, Charlotte von Gall, Amira A H Ali","doi":"10.3389/fncel.2025.1538985","DOIUrl":"10.3389/fncel.2025.1538985","url":null,"abstract":"<p><strong>Introduction: </strong>Glutamate represents the dominant neurotransmitter that conveys the light information to the brain, including the suprachiasmatic nucleus (SCN), the central pacemaker for the circadian system. The neuronal and astrocytic glutamate transporters are crucial for maintaining efficient glutamatergic signaling. In the SCN, glutamatergic nerve terminals from the retina terminate on vasoactive intestinal polypeptide (VIP) neurons, which are essential for circadian functions. To date, little is known about the role of the core circadian clock gene, Bmal1, in glutamatergic neurotransmission of light signal to various brain regions.</p><p><strong>Methods: </strong>The aim of this study was to further elucidate the role of Bmal1 in glutamatergic neurotransmission from the retina to the SCN. We therefore examined the spontaneous rhythmic locomotor activity, neuronal and glial glutamate transporters, as well as the ultrastructure of the synapse between the retinal ganglion cells (RGCs) and the SCN in adult male Bmal1-/- mice.</p><p><strong>Results: </strong>We found that the deletion of Bmal1 affects the light-mediated behavior in mice, decreases the retinal thickness and affects the vesicular glutamate transporters (vGLUT1, 2) in the retina. Within the SCN, the immunoreaction of vGLUT1, 2, glial glutamate transporters (GLAST) and VIP was decreased while the glutamate concentration was elevated. At the ultrastructure level, the presynaptic terminals were enlarged and the distance between the synaptic vesicles and the synaptic cleft was increased, indicative of a decrease in the readily releasable pool at the excitatory synapses in Bmal1-/-.</p><p><strong>Conclusion: </strong>Our data suggests that Bmal1 deletion affects the glutamate transmission in the retina and the SCN and affects the behavioral responses to light.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1538985"},"PeriodicalIF":4.2,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Glial cells in homeostasis, neurodevelopment, and repair.","authors":"Antonio Cibelli, David C Spray, Maria Grazia Mola","doi":"10.3389/fncel.2025.1575105","DOIUrl":"10.3389/fncel.2025.1575105","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1575105"},"PeriodicalIF":4.2,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autism spectrum disorder related phenotypes in a mouse model lacking the neuronal actin binding protein profilin 2.","authors":"Walter Witke, Marina Di Domenico, Laura Maggi, Alessia Di Nardo, Valentin Stein, Pietro Pilo Boyl","doi":"10.3389/fncel.2025.1540989","DOIUrl":"10.3389/fncel.2025.1540989","url":null,"abstract":"<p><strong>Introduction: </strong>Profilin 2 (PFN2) is an actin binding protein highly expressed in the brain that participates in actin dynamics. It has been shown in vitro and in vivo that in neurons it functions both post-synaptically to shape and maintain dendritic arborizations and spine density and plasticity, as well as pre-synaptically to regulate vesicle exocytosis. PFN2 was also found in protein complexes with proteins that have been implicated in or are causative of autism spectrum disorder.</p><p><strong>Methods: </strong>We employ a genetically engineered knock-out mouse line for <i>Pfn2</i> that we previously generated to study the mouse social, vocal and motor behavior in comparison to wild type control littermates. We also study neuronal physiology in the knock-out mouse model by means of cellular and field electrophysiological recordings in cerebellar Purkinje cells and in the Schaffer collaterals. Lastly, we study anatomical features of the cerebellum using immunofluorescence stainings.</p><p><strong>Results: </strong>We show that PFN2 deficiency reproduces a number of autistic-like phenotypes in the mouse, such as social behavior impairment, stereotypic behavior, altered vocal communication, and deficits in motor performance and coordination. Our studies correlate the behavioral phenotypes with increased excitation/inhibition ratio in the brain, due to brain-wide hyperactivity of glutamatergic neurons and increased glutamate release not compensated by enhanced GABAergic neurotransmission. Consequently, lack of PFN2 caused seizures behavior and age-dependent loss of cerebellar Purkinje cells, comorbidities observed in a subset of autistic patients, which can be attributed to the effect of excessive glutamatergic neurotransmission.</p><p><strong>Discussion: </strong>Our data directly link altered pre-synaptic actin dynamics to autism spectrum disorder in the mouse model and support the hypothesis that synaptic dysfunctions that asymmetrically increase the excitatory drive in neuronal circuits can lead to autistic-like phenotypes. Our findings inspire to consider novel potential pathways for therapeutic approaches in ASD.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1540989"},"PeriodicalIF":4.2,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GABAergic integration of transient and persistent neurons in the developing mouse somatosensory cortex.","authors":"Ahd Abusaada, Federico De Rosa, Heiko J Luhmann, Werner Kilb, Anne Sinning","doi":"10.3389/fncel.2025.1556174","DOIUrl":"10.3389/fncel.2025.1556174","url":null,"abstract":"<p><p>GABA is an essential element in the function of neocortical circuits. The origin, migration and mechanisms of synaptogenesis of GABAergic neurons have been intensively studied. However, little information is available when GABAergic synapses are formed within the different cortical layers, neuronal cell types and subcellular compartments. To quantify the distribution of GABAergic synapses in the immature somatosensory mouse cortex, GABAergic synapses were identified by spatially coincident immunoprofiles for the pre- and postsynaptic markers vGAT and gephyrin at postnatal days (P)0-12. Between P0-5, GABAergic synapses are mainly restricted to the marginal zone, while at later developmental stages a more homogenous distribution is obtained. Cajal-Retzius neurons represent a major target of GABAergic synapses in the marginal zone with a homogeneous synapse distribution along the dendrite. The number of GABAergic synapses per pyramidal neuron increases substantially between P0 and P12, with a stable density and distribution in basal dendrites. In contrast, along apical dendrites synapses accumulate to more proximal positions after P8. Overall, the results of this study demonstrate that early GABAergic synaptogenesis is characterized by a consistent increase in the density of synapses with first a stringent overrepresentation in the marginal zone and a delayed establishment of perisomatic synapses in pyramidal neurons.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1556174"},"PeriodicalIF":4.2,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intrinsic retinoic acid synthesis is required for oligodendrocyte progenitor expansion during CNS remyelination.","authors":"Sonia E Nanescu, Natacha M Wathieu, Lauren Rosko, David S Cha, Mahesh N Kumar, Rafal T Olszewski, Joan Reger, Maryna Baydyuk, Alisha N Dua, Wojciech Krezel, Violetta Zujovic, Jeffrey K Huang","doi":"10.3389/fncel.2025.1550139","DOIUrl":"10.3389/fncel.2025.1550139","url":null,"abstract":"<p><p>Myelin regeneration (remyelination) in the CNS depends on the recruitment, proliferation and differentiation of oligodendrocyte precursor cells (OPCs) at demyelinated lesions. However, despite the presence of OPCs, very few oligodendrocytes and myelin are regenerated in chronic multiple sclerosis (MS) lesions for reasons that remain poorly understood. Here, using a spontaneous remyelination model in mice, we found that retinaldehyde dehydrogenase 2 (Raldh2), a rate-limiting enzyme for retinoic acid (RA) synthesis, is upregulated in OPCs and in a subpopulation of microglia/macrophages during remyelination. Tamoxifen induced deletion of Raldh2 globally, or conditionally in OPCs, resulted in significantly fewer proliferating OPCs in lesions, leading to decreased oligodendrocyte numbers and myelin density. Moreover, induced deletion of Raldh2 globally also resulted in increased microglia/macrophage density in lesions. Further, exogenous RA delivery into lesions significantly increased oligodendrocyte lineage cells, while also decreasing proinflammatory microglia/macrophages, with no significant effect on anti-inflammatory microglia/macrophages. Postmortem MS brain sections revealed Raldh2 was absent in the majority of OPCs in chronic inactive lesions compared to the other lesion types. These results suggest that Raldh2 upregulation in lesions is critical for OPC proliferation during remyelination, and reveal that the failure to regenerate sufficient oligodendrocytes and myelin in chronic MS lesions may arise from impaired OPC expansion due to the failure to intrinsically synthesize RA.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1550139"},"PeriodicalIF":4.2,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11891161/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}