European Journal of Neuroscience最新文献

{"title":"Investigating the Contribution of the Imprinted Gene Asb4 to Parental Care","authors":"Rachel-Ann Jones,&nbsp;Matthew J. Higgs,&nbsp;Rosalind M. John,&nbsp;Anthony R. Isles","doi":"10.1111/ejn.70655","DOIUrl":"10.1111/ejn.70655","url":null,"abstract":"<p>Genomic imprinting is a form of epigenetic regulation that leads to expression from one parental allele only and, in animals, is unique to mammals. Imprinted gene expression is predominant in the brain and their roles in neural processes are becoming more appreciated. Recent analyses have indicated an enrichment of imprinted gene expression in the ‘parental hub’ circuitry. Specifically, imprinted genes were over-represented in the transcriptomic profile of galanin positive (Gal⁺) neurons in the medial preoptic area (MPOA) of the hypothalamus. One of those imprinted genes showing enriched expression in Gal⁺ neurons was the maternally expressed <i>Asb4</i>. Here, we propose that <i>Asb4</i> supports normal activation of MPOA Gal⁺ neurons required for parental care. We aim to demonstrate abnormal parental behaviours—such as decreased pup retrieval and impaired nest building—and activity of MPOA Gal⁺ neurons in brain-specific maternal <i>Asb4</i> knockout mice and hypothesis knockout animals will demonstrate a deficient behavioural phenotype in one or more parental behavioural characteristics.</p>","PeriodicalId":11993,"journal":{"name":"European Journal of Neuroscience","volume":"64 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13550800/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905602","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":"Quiescence as an Active and Dynamic Regulator of Neural Stem Cells in Adult Olfactory Neurogenesis","authors":"Jose Manuel Morante-Redolat,&nbsp;Isabel Fariñas","doi":"10.1111/ejn.70671","DOIUrl":"10.1111/ejn.70671","url":null,"abstract":"<p>Adult olfactory neurogenesis depends largely on the persistence of resident quiescent neural stem cells (NSCs) in the ventricular-subventricular zone (V-SVZ) and their capacity to reversibly switch to an activated state to generate new neurons. These cells exhibit reduced cell-cycle and biosynthetic activity while maintaining key signaling and stress-response programs. Rather than representing a uniform condition, quiescence encompasses a continuum of substates, ranging from deep to shallow, each characterized by distinct activation thresholds. The dynamics and reversibility of state transitions are regulated by interactions between NSCs and neighboring cells, the extracellular matrix, and systemic factors, among others. With aging, NSCs progressively shift toward deeper quiescent states that are less permissive to activation, thereby reducing overall neurogenic output. Consequently, quiescence should no longer be regarded as a passive pause in stem cell activity, but an organizing principle that underlies the long-term maintenance and adaptability of adult NSCs. A deeper understanding of how quiescence is established, diversified, and dynamically regulated will be essential for elucidating the principles governing adult olfactory neurogenesis and for harnessing its regenerative potential in aging and disease.</p>","PeriodicalId":11993,"journal":{"name":"European Journal of Neuroscience","volume":"64 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13542941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148887035","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":"Correction to “The Transmitter Release-Site CaV2.2 Channel Cluster is Linked to an Endocytosis Coat Protein Complex”","authors":"","doi":"10.1111/ejn.70674","DOIUrl":"10.1111/ejn.70674","url":null,"abstract":"<p>\u0000 <span>R. Khanna</span>, <span>Q. Li</span>, <span>L. C. Schlichter</span>, and <span>E. F. Stanley</span>, “ <span>The Transmitter Release-Site CaV2.2 Channel Cluster is Linked to an Endocytosis Coat Protein Complex</span>,” <i>European Journal of Neuroscience</i> <span>26</span>, no. <span>3</span> (<span>2007</span>): <span>560</span>–<span>574</span>. https://doi.org/10.1111/j.1460-9568.2007.05681.x.\u0000 </p><p>Following publication of this article, it was brought to our attention that the panels in Figure 7A had been previously published by the authors. The earlier publication was cited in the article but not referenced in the corresponding figure caption. The figure caption has been corrected to include the missing citation, as follows:</p><p>\u0000 <b>Figure 7</b>\u0000 </p><p>Differential susceptibility of endocytic proteins coimmunoprecipitated with H-clathrin to an ionic strength challenge. (A) As in Fig. 6A but using anti-H-clathrin for immunoprecipitation. (B) Quantification as in Fig. 6C for H-clathrin immunoprecipitation followed by high ionic-strength challenge using 1150 mm NaCl. Note the low AP180 recovery, the retention of L-intersectin with high NaCl, and the coprecipitation and high ionic-strength resistance of α-adaptin, all of which contrast to findings with CaV2.2 in Fig. 6. (C) Endocytotic proteins liberated by high NaCl from the CaV2.2 complex were coprecipitated by anti-H-clathrin. In this figure we compare endocytic proteins associated with H-clathrin from the entire (Total) synaptosome (lane 1) with those associated with the subset of H-clathrin liberated by high NaCl from the TRS (lanes 2–4). All data are from the same experiment. Thus, lane 1 is simply an IP of H-clathrin from the total synaptosome lysate probed with the indicated antibodies. In lanes 2–4 we first immunoprecipitated the CaV2.2 complex from the synaptosomes and washed the beads thoroughly. The beads were then exposed to 1150 mm NaCl, as above. However, in this case we retained the supernatant to analyse the proteins liberated by the high NaCl, basically to test whether these were shed individually or as part of a subcomplex. H-clathrin was then immunoprecipitated from this supernatant. The captured H-clathrin complex was exposed to a second high-NaCl challenge to analyse its associated proteins. Blots are representative of two independent experiments. (A) reproduced with permission (Khanna et al. <span>2006</span>).</p>","PeriodicalId":11993,"journal":{"name":"European Journal of Neuroscience","volume":"64 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13539460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879724","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":"Centrifugal Effects of Voluntary Movements on Somatosensory and Auditory Evoked Potentials: An Exploratory Study","authors":"Taiki Makibuchi,&nbsp;Sayaka Anazawa,&nbsp;Yudai Hagino,&nbsp;Tomomi Fujimoto,&nbsp;Genta Ochi,&nbsp;Daisuke Sato,&nbsp;Koya Yamashiro","doi":"10.1111/ejn.70654","DOIUrl":"10.1111/ejn.70654","url":null,"abstract":"<div>\u0000 \u0000 <p>Centrifugal mechanisms play a crucial role in supporting sensorimotor integration by modulating sensory processing. Voluntary movements regulate neural activity via centrifugal effects, whereby motor commands from motor areas influence sensory areas. Previous studies have shown that the long-latency somatosensory evoked potentials (SEPs), P100 and N140, increased during stimulus-triggered movement tasks, whereby long-latency auditory evoked potentials (AEPs), N100, were suppressed by self-generated sounds. However, findings were inconsistent regarding stimulus and movement timing. Therefore, the present study was conducted to investigate whether the centrifugal effects differ between somatosensory and auditory modalities. SEPs and AEPs were recorded during movement (button-pressing), attention (stimulus counting), and passive conditions. Difference waveforms were calculated for each modality by subtracting the event-related potentials (ERPs) elicited during attention condition from the ERPs elicited during movement condition. P100, N140, and N1 amplitudes significantly increased during movement compared with attention and/or passive conditions (<i>p</i> &lt; 0.05). Positive components of the difference waveforms were significantly larger in the somatosensory modality than in the auditory modality (<i>p</i> &lt; 0.05). These findings suggest that movement-related modulation may be more pronounced in the SEPs than for AEPs, indicating possible modality-specific differences by centrifugal modulation. However, given the limited electrode coverage, future studies employing high-density EEG will be necessary to clarify whether centrifugal modulation differs across sensory modality.</p>\u0000 </div>","PeriodicalId":11993,"journal":{"name":"European Journal of Neuroscience","volume":"64 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effects of Anxiety and Cognitive Load on Freezing of Gait in Parkinson's Disease.","authors":"Demi Zoetewei, Moran Gilat, Nicholas D'Cruz, Jan Cornelis, Jordan Bedime Songue Njiki, Rick C Helmich, Pieter Ginis, Alice Nieuwboer","doi":"10.1111/ejn.70678","DOIUrl":"10.1111/ejn.70678","url":null,"abstract":"<p><p>It is currently unclear whether anxiety, cognitive load, or their combination modulates freezing of gait differently and whether people with Parkinson's disease and freezing of gait (freezers) suffer from stronger threat responsiveness than nonfreezing groups. Therefore, we investigated 28 freezers, 19 nonfreezers, and 19 healthy age-matched controls, who completed a freezing-provoking protocol under different conditions. State anxiety was generated via a threat of shock or a threat of freezing paradigm. Cognitive load was imposed via a dual task. The primary outcome was the freezing ratio, derived from wearable sensors. Stress was monitored by self-reported and physiological markers. Freezers had worse cognition and more severe motor symptoms than nonfreezers yet a similar trait anxiety and threat response compared with both nonfreezing groups. Anxiety and cognitive load tended to increase the freezing ratio across groups. When combined, anxiety and cognitive load showed no surplus effects. Compared with the threat of shock, the threat of freezing had less impact on the freezing ratio, and although it induced less perceived stress, it generated higher physiological stress responses. In conclusion, freezers showed overall comparable levels of trait anxiety and a similar threat response as nonfreezers and healthy controls. Anxiety and cognitive load each tended to increase the freezing ratio, but their combined effect seemed to plateau. The threat of freezing had a smaller effect than the threat of shock as the former may not have diverted the attention away from walking to the same degree as the latter, although this explanation remains speculative.</p>","PeriodicalId":11993,"journal":{"name":"European Journal of Neuroscience","volume":"64 5","pages":"e70678"},"PeriodicalIF":2.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13564402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148943966","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":"Childhood Trauma and Frontoparietal Network Connectivity During Working Memory Task Performance in Individuals With Schizophrenia and Healthy Participants.","authors":"Aoife Warren, David Mothersill, Emma Corley, Derek W Morris, Brian Hallahan, Declan P McKernan, Colm McDonald, Gary Donohoe","doi":"10.1111/ejn.70675","DOIUrl":"10.1111/ejn.70675","url":null,"abstract":"<p><p>Schizophrenia is associated with altered frontoparietal connectivity, which supports higher-order cognition, including working memory. Childhood trauma has been linked to altered functional connectivity and reduced cognitive performance in individuals with schizophrenia and controls. Prior evidence suggests that trauma-related default mode dysconnectivity mediates the association between trauma and cognition. We hypothesised that childhood trauma would be associated with altered frontoparietal connectivity during a working memory task and that such connectivity changes would mediate the relationship between trauma and working memory. Childhood trauma, working memory and fMRI data were collected from individuals with schizophrenia or schizoaffective disorder (n = 38) and controls (n = 128). fMRI data were preprocessed in CONN, and seed-based connectivity analyses were performed for four frontoparietal seeds (bilateral dorsolateral prefrontal and posterior parietal cortices). Connectivity was contrasted across (a) diagnosis and (b) trauma severity. Moderated mediation analyses tested the associations between trauma, connectivity and working memory, with diagnosis as a moderator. Across all participants, higher physical neglect severity predicted poorer working memory performance. Stronger inverse connectivity between left dorsolateral prefrontal and frontal medial cortices predicted better working memory performance. As expected, patients showed widespread frontoparietal dysconnectivity relative to controls, but no differences in frontoparietal connectivity were observed across trauma severity groups. Frontoparietal connectivity did not mediate the association between trauma and working memory, although diagnosis moderated both the trauma-connectivity and connectivity-cognition associations. We conclude that, unlike previous evidence suggesting a mediating role for the default mode network, frontoparietal connectivity did not mediate the trauma-cognition association, possibly suggesting the unique significance of default mode network dysconnectivity in linking trauma to cognition in psychosis.</p>","PeriodicalId":11993,"journal":{"name":"European Journal of Neuroscience","volume":"64 5","pages":"e70675"},"PeriodicalIF":2.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13572810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963261","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":"Human iPSC-Derived Brain Organoids: A Disease-Oriented Evaluation of Modeling Fidelity.","authors":"Bishwa R Pokharel, Abigail Dickerson, Sanjana G Shenoy, Mira S Ramasamy, Niska Majumdar, Paul P Cook, Shaw M Akula","doi":"10.1111/ejn.70687","DOIUrl":"10.1111/ejn.70687","url":null,"abstract":"<p><p>Two-dimensional (2D) cell culture systems and conventional animal models have been crucial in the study of central nervous system (CNS) pathology. However, they are limited in their abilities to elucidate human-specific neurobiology and disease etiology. Human induced pluripotent stem cell (iPSC)-derived brain organoids have emerged as a complementary platform that offers a three-dimensional (3D) structure and human-specific environment. They exhibit cellular heterogeneity, apical-basal polarity, and the ability to perform tissue-specific functions such as absorption, secretion, and electrophysiological activity. This review critically evaluates the use of iPSC-derived brain organoids as a disease-focused approach to study neuroinflammation, neurodegeneration, infection, and aging. Organoids provide a model for early pathogenic events, cellular interactions, and human-specific responses, providing insights into disease hallmarks such as tau and amyloid pathology, the vulnerability of dopaminergic neurons, and host-pathogen interactions. However, they are limited by developmental immaturity, inadequate systemic integration, and heterogeneity across models, which hinders their ability to represent late-stage disease progression and human level physiology. Therefore, their primary use lies in modeling human-specific early disease mechanisms, while integration with animal models and in vitro systems is crucial for progressing translational neuroscience.</p>","PeriodicalId":11993,"journal":{"name":"European Journal of Neuroscience","volume":"64 5","pages":"e70687"},"PeriodicalIF":2.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13574550/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148967226","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":"Chronic Noise Exposure Induces Anxiety-Like Behavior and Enhances the Excitability of Dorsal Raphe Serotonergic Neurons in Mice","authors":"Quan Yuan,&nbsp;Si-Xin Wang,&nbsp;Zheng-Quan Tang","doi":"10.1111/ejn.70653","DOIUrl":"https://doi.org/10.1111/ejn.70653","url":null,"abstract":"<div>\u0000 \u0000 <p>This study demonstrates that chronic noise exposure induces anxiety-like behaviors in mice, as consistently observed across three classical behavioral paradigms. Electrophysiological recordings showed that chronic noise exposure is associated with increased intrinsic excitability of serotonergic (5-HT) neurons in the dorsal raphe nucleus (DRN), characterized by a depolarized resting membrane potential, increased spontaneous firing frequency, reduced rheobase, and elevated input resistance. In addition, chronic noise exposure was associated with enhanced excitatory synaptic input onto DRN 5-HTergic neurons, as reflected by an increase in the frequency, but not the amplitude, of both spontaneous and miniature excitatory postsynaptic currents. In contrast, neither intrinsic excitability nor excitatory synaptic transmission of local DRN GABAergic neurons was significantly altered. Furthermore, pharmacological blockade of AMPA and NMDA receptors indicated that the increased excitability of DRN 5-HTergic neurons cannot be fully explained by enhanced excitatory synaptic input alone, suggesting a potential contribution of intrinsic membrane mechanisms. Together, these findings provide correlational evidence that chronic noise exposure is associated with functional alterations in DRN 5-HTergic neurons and may represent a potential neural correlate of noise-related anxiety-like behavior.</p>\u0000 </div>","PeriodicalId":11993,"journal":{"name":"European Journal of Neuroscience","volume":"64 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148823343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changes in Cerebral Glucose Metabolism at Rest Following Hemicontusive Cervical Spinal Cord Injury in Mice: A Whole-Brain Autoradiographic Study","authors":"Zhuo Wang,&nbsp;Camelia A. Danilov,&nbsp;Dilan Setiya,&nbsp;Daniel P. Holschneider","doi":"10.1111/ejn.70661","DOIUrl":"https://doi.org/10.1111/ejn.70661","url":null,"abstract":"<div>\u0000 \u0000 <p>Spinal cord injury (SCI) disrupts brain-spinal cord communications and results in profound brain reorganization. Here, we apply high-resolution, voxel-based, whole-brain metabolic mapping using the [¹⁴C]-2-deoxyglucose autoradiographic method in adult, female mice to assess functional brain reorganization in a subacute stage (1 week after SCI). Right moderate contusive injury at the cervical 5 level was confirmed by glial fibrillary acidic protein (GFAP) immunohistochemical staining. SCI compared to sham-lesioned animals showed significant motor deficits (grip strength and rotarod) alongside decreases in glucose uptake in sensorimotor regions of the cortex, basal ganglia, and thalamus. In contrast, regions in the limbic system (the amygdala, accumbens nucleus, lateral septum, and hippocampus) and in the cerebellum demonstrated increases in glucose uptake in SCI animals. Most of these effects were noted bilaterally, suggesting functional reorganization involving ascending and descending neural pathways in both hemispheres. In addition, functional metabolic connectivity between the ventral posterolateral thalamic nucleus and primary somatosensory cortex was bilaterally decreased. The current preliminary findings underscore the broadness of brain reorganization in the subacute stage following a unilateral contusive-type SCI. Functional whole-brain metabolic mapping provides a roadmap for future targeted studies examining neuroplastic markers to evaluate new therapeutic strategies.</p>\u0000 </div>","PeriodicalId":11993,"journal":{"name":"European Journal of Neuroscience","volume":"64 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148823322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intracranial Electrical Stimulation of the Superior Temporal Gyrus Evokes Rapid Responses in Human Visual Cortex","authors":"Emily C. Cunningham,&nbsp;David Brang","doi":"10.1111/ejn.70660","DOIUrl":"https://doi.org/10.1111/ejn.70660","url":null,"abstract":"<p>Sounds can alter visual processing even at the earliest stages of the cortical pathway. However, our understanding of how acoustic signals are relayed to visual cortex is limited, particularly with respect to the involvement of different regions of auditory cortex in the most rapid stages of this communication across distinct visual areas. Here, we address this question by examining occipital intracranial responses to direct electrical stimulation of the superior temporal gyrus (STG) in 23 patients with epilepsy. Stimulation of mid- and posterior-STG elicited responses in visual cortex as early as 18 ms after onset, with a distribution that favored lateral occipital cortex, lingual gyrus, and anterior calcarine regions near peripheral V1. Early visual cortex (V1/V2) responded most strongly to stimulation over mid-STG, whereas lateral occipital cortex (near V5/hMT+) exhibited the most robust response to posterior STG stimulation. Responses in visual cortex were organized in a manner similar to that of nonhuman primates, with possible evidence for an exception over the occipital pole. These results support theories that human visual responses to sound are inherited in part from auditory cortex and provide insight into routes through which acoustic information may rapidly facilitate processing of visual input.</p>","PeriodicalId":11993,"journal":{"name":"European Journal of Neuroscience","volume":"64 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/ejn.70660","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148823279","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}