Neurobiology of Disease最新文献

{"title":"Expression of concern: \"Sestrin2 induced by hypoxia inducible factor1 alpha protects the blood-brain barrier via inhibiting VEGF after severe hypoxic-ischemic injury in neonatal rats\" [NEUROBIOL DIS, Volume 95 (2016) Pages 111-121].","authors":"","doi":"10.1016/j.nbd.2025.106948","DOIUrl":"https://doi.org/10.1016/j.nbd.2025.106948","url":null,"abstract":"","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"212 ","pages":"106948"},"PeriodicalIF":5.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nusinersen corrects L-arginine deficiency in the cerebrospinal fluid of patients with severe spinal muscular atrophy","authors":"Amber Hassan ,&nbsp;Raffaella di Vito ,&nbsp;Anna Caretto ,&nbsp;Tommaso Nuzzo ,&nbsp;Adele D'Amico ,&nbsp;Chiara Panicucci ,&nbsp;Claudio Bruno ,&nbsp;Enrico Bertini ,&nbsp;Alessandro Vercelli ,&nbsp;Marina Boido ,&nbsp;Francesco Errico ,&nbsp;Livio Pellizzoni ,&nbsp;Alessandro Usiello","doi":"10.1016/j.nbd.2025.107046","DOIUrl":"10.1016/j.nbd.2025.107046","url":null,"abstract":"<div><div>Spinal Muscular Atrophy (SMA) is a progressive neuromuscular disorder caused by homozygous loss of the <em>survival motor neuron 1</em> (<em>SMN1</em>) gene, leading to reduced SMN protein expression. Increasing evidence implicates neurotransmission deficits in the pathophysiology of SMA. In particular, alterations in neuroactive amino acids involved in glutamatergic neurotransmission have recently been identified in both the cerebrospinal fluid (CSF) of SMApatients and the spinal cord of SMNΔ7 mouse models. L-arginine, a precursor of nitric oxide, plays a critical role in glutamatergic receptor signalling, influencing neurotransmitter release, synaptic plasticity, and neuroprotection. However, it remains unclear whether SMN deficiency affects L-arginine metabolism in SMA. To address this, we used high-performance liquid chromatography to investigate whether SMN deficiency alters L-arginine homeostasis in the central nervous system of SMNΔ7 mice and in the CSF of SMA patients with varying disease severity, both before and after treatment with the SMN-inducing therapy Nusinersen. Notably, we observed significantly reduced L-arginine levels in the brainstem and spinal cord of symptomatic SMA mice compared to age-matched wild-type littermates. Consistent with these findings, we revealed lower L-arginine levels in severe SMA1 patients compared to milder SMA2 and SMA3 patients and healthy controls, enhancing the translational strength of our findings. Importantly, Nusinersen-mediated SMN upregulation fully restored L-arginine homeostasis in the CSF of severe SMA1 patients. In conclusion, our results demonstrate a dysregulation of L-arginine in SMA and highlight a role for SMN-enhancing therapies in restoring neurochemical alterations observed in patients with this neurodegenerative disease.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"214 ","pages":"Article 107046"},"PeriodicalIF":5.6,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Choroid plexus enlargement correlated with motor dysfunction in spinocerebellar ataxia type 3","authors":"Zhiming Zhen ,&nbsp;Peiling Ou ,&nbsp;Yonghua Huang ,&nbsp;Lihua Deng (1) ,&nbsp;Yue Chen ,&nbsp;He Liu ,&nbsp;Yanqiu Hua ,&nbsp;Wei Chen ,&nbsp;Huafu Chen ,&nbsp;Peiyu Huang ,&nbsp;Zhentao Zuo ,&nbsp;Chen Liu","doi":"10.1016/j.nbd.2025.107044","DOIUrl":"10.1016/j.nbd.2025.107044","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate Choroid plexus (CP) structural changes using multimodal MRI, and assess the correlation between CP damage and motor dysfunction in SCA3 patients.</div></div><div><h3>Methods</h3><div>We prospectively recruited 64 SCA3 patients and 50 age- and sex-matched healthy controls (HCs). CP volume (CPV) and other brain regions were measured using FreeSurfer 7.3, while free-water (FW) imaging metrics were analyzed with FSL. We compared the differences in CPV and FW imaging metrics among the pre-symptomatic SCA3 group, symptomatic SCA3 group, and HC group. Partial correlation, structural equation modeling, and multivariate regression explored the relationships among CPV, CAG repeats, brain structures, and motor scales.</div></div><div><h3>Results</h3><div>CPV, FW, and Freewater-corrected Anisotropy (FAt) were significantly increased in symptomatic SCA3 patients compared to HCs and pre-symptomatic patients. CPV was positively correlated with CAG repeats, CSF volume, motor impairment and negatively correlated with cerebellar and brainstem volumes. Structural equation modeling revealed that CPV mediated the effect of CAG repeats on motor function by influencing CSF volume. CP and brainstem volumes were independent predictors of motor function and could distinguish pre-symptomatic from symptomatic patients.</div></div><div><h3>Interpretation</h3><div>This study first demonstrates that CP enlargement is a novel biomarker of motor dysfunction in SCA3. The CP may be involved in the pathogenesis of SCA3 by affecting CSF circulation and brain homeostasis. Targeting the CP could be a potential therapeutic strategy for SCA3.</div><div>Clinical trials registration</div><div>[<span><span>www.ClinicalTrials.gov</span><svg><path></path></svg></span>], identifier [ChiCTR1800019901].</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"214 ","pages":"Article 107044"},"PeriodicalIF":5.6,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cortical map remodeling in the intact hemisphere and functional recovery after focal lesion to the primary somatosensory cortex","authors":"Justine Facchini,&nbsp;Christian Xerri,&nbsp;Abdessadek El Ahmadi,&nbsp;Isabelle Watabe,&nbsp;Nicolas Catz,&nbsp;Yoh'i Zennou-Azogui","doi":"10.1016/j.nbd.2025.107043","DOIUrl":"10.1016/j.nbd.2025.107043","url":null,"abstract":"<div><div>After injury to the primary somatosensory cortex (S1), most studies have focused on perilesional remodeling and its role in functional recovery. In contrast, alterations within the contralesional cortex remain poorly understood, even though the interhemispheric communication is disrupted by the lesion. Using electrophysiological mapping, we investigated in rats the time-course of cutaneous map remodeling in the intact hemisphere following unilateral focal damage to the forepaw area in S1 along with behavioral assessment of sensorimotor deficits. Cortical maps showed a representational dedifferentiation inducing a degradation of the somatotopic organization, starting immediately after the lesion and worsening until the end of the 14th day post-injury. These changes were underpinned by a dramatic enlargement of cutaneous receptive fields accompanied by an increase in neuronal sensitivity. Strong impairment of tactile sensitivity and sensorimotor adjustments was shown for the forepaw contralateral to the injured hemisphere, that gradually abated from the 2nd to the 7th week. Interestingly, deficits of fine sensorimotor adjustments were also observed in the “non-paretic” forepaw. They were less pronounced than in the “paretic” limb but evolved with a similar time course of recovery. A substantial restoration of somatotopic organization occurred gradually, in parallel with the functional recovery. Immediate post-lesion effects suggest an altered interhemispheric interplay and highlight the critical role of hemispheric cross influences in maintaining fine somatotopic organization of cutaneous maps in each hemisphere. S1 map normalization in intact cortex paralleling functional recovery may reflect compensatory mechanisms reorganizing interhemispheric communication and shaping cortical neurons' responses.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"214 ","pages":"Article 107043"},"PeriodicalIF":5.6,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From cell death to neurological disease: Unraveling the role of copper","authors":"Qiqi Gao,&nbsp;Yu Chen,&nbsp;Wei Hu,&nbsp;Tong Lou,&nbsp;Yu Fang,&nbsp;Zhenlang Lin,&nbsp;Wei Lin","doi":"10.1016/j.nbd.2025.107042","DOIUrl":"10.1016/j.nbd.2025.107042","url":null,"abstract":"<div><div>Copper, a transition metal, plays a crucial role in various physiological processes within the human body. Its homeostasis is vital for maintaining normal cellular function and facilitating optimal performance of the nervous system. To regulate this homeostasis, cells employ sophisticated regulatory mechanisms that govern intracellular copper levels, allowing an adequate supply of copper ions to participate in essential biological functions such as mitochondrial energy production, antioxidant defense, and extracellular matrix stability. Cuproptosis, which was first systematically described in 2022 as a novel form of programmed cell death, involves molecular mechanisms characterized by oxidative stress activation, inhibition of the ubiquitin-proteasome system, and aggregation of lipoacylated proteins. This cascade can compromise mitochondrial function and ultimately result in cell death. In this review, we summarize current knowledge regarding copper metabolism, cuproptosis mechanism, copper-associated cell death, and copper-associated neurological diseases. Importantly, we sought to enhance the current understanding of copper's influence on cellular processes and disease states while advancing clinical approaches for treating these conditions.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"214 ","pages":"Article 107042"},"PeriodicalIF":5.1,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144704680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cross-sectional associations of plasma vitamin D with plasma phosphorylated tau-181 and plasma neurofilament light chain in older adults with memory complaints","authors":"Claudie Hooper ,&nbsp;Emmanuel González ,&nbsp;Nicola Coley ,&nbsp;Bruno Vellas ,&nbsp;Sophie Guyonnet ,&nbsp;for the MAPT/IHU HealthAge Open Science group","doi":"10.1016/j.nbd.2025.107041","DOIUrl":"10.1016/j.nbd.2025.107041","url":null,"abstract":"<div><h3>Background</h3><div>Lack of vitamin D is associated with cognitive decline and Alzheimer's disease. Therefore, we examined the relationship between plasma 25 hydroxyvitamin D [25(OH)D] and plasma phosphorylated-tau 181 (p-tau 181) and neurofilament light chain (NfL) in older adults with memory complaints.</div></div><div><h3>Methods</h3><div>This is a cross-sectional analysis of ‘Multidomain Alzheimer Preventive Trial’ baseline data. Subjects were 519 French community-dwelling adults aged 70⁺ years at risk of dementia with baseline data on plasma 25(OH)D and plasma p-tau 181 and 311 individuals with baseline data on plasma 25(OH)D and plasma NfL. Plasma 25(OH)D, p-tau 181 and NfL were measured using high-sensitivity immune-based assays and associations were explored using adjusted regression analyses.</div></div><div><h3>Results</h3><div>Subjects had a mean (SD) age of 75.2 years (4.3) and 67.6 % were female. The mean (SD) plasma 25(OH)D concentration was 23.5 ng/ml (11.3). The mean (SD) concentrations of plasma p-tau 181 and plasma NfL were 9.9 pg/ml (4.5) and 81.1 pg/ml (34.1) respectively. We did not find significant cross-sectional associations between baseline plasma 25(OH)D and plasma p-tau 181 (Model 3: β-coefficient, 0.0003, 95 % CI: −0.0036, 0.0042, <em>p</em> = 0.879) or plasma 25(OH)D and plasma NfL (Model 3: β-coefficient, −0.0012, 95 % CI: −0.0055, 0.0032, <em>p</em> = 0.599). Age, cognitive status, sex, cardiovascular risk or <em>apolipoprotein</em> ε4 genotype did not modify these non-significant associations.</div></div><div><h3>Conclusions</h3><div>These findings provide evidence that plasma 25(OH)D is not associated with plasma p-tau 181 or plasma NfL in older adults with heightened dementia risk. Longitudinal replication studies are essential to validate these cross-sectional results.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"214 ","pages":"Article 107041"},"PeriodicalIF":5.1,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144696976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiple sclerosis lesions exhibit sex-specific steroid changes","authors":"Sabina Luchetti ,&nbsp;Matthew R.J. Mason ,&nbsp;Philippe Liere ,&nbsp;Antoine Pianos ,&nbsp;Sara Cossu ,&nbsp;Marloes Hofstee ,&nbsp;Arja Sluiter ,&nbsp;Adelia ,&nbsp;Jackelien van Scheppingen ,&nbsp;Eleonora Aronica ,&nbsp;Michael Schumacher ,&nbsp;Inge Huitinga","doi":"10.1016/j.nbd.2025.107040","DOIUrl":"10.1016/j.nbd.2025.107040","url":null,"abstract":"<div><div>Sex differences in disease susceptibility and progression in multiple sclerosis (MS) indicate hormonal influences. We previously found sex differences in steroidogenic enzyme expression in mixed active/inactive (mixed) and inactive lesions, suggesting increased synthesis and signalling of progesterone in females and of estradiol (E2) in males. Here we measured steroid levels in mixed and inactive MS lesions (14 males, 16 females) and control donor white matter (10 males, 10 females) by gas chromatography–mass spectrometry (GC/MS). In mixed and inactive lesions, we found a female-specific increase in the production of the neuroactive steroid allopregnanolone, and a reduction in testosterone metabolites and the precursor androgen dehydroepiandrosterone (DHEA). In males, however, most steroids remained unchanged, although the weakly neuroactive 5α-DHDOC was increased. No significant differences were found in steroid levels in remyelinating MS lesions (6 males, 6 females) and control donor white matter (8 males, 7 females). However, higher gene expression of steroid receptors and of the steroidogenic enzyme AKR1C3 persisted in these remyelinated lesions in females. In vitro<em>,</em> we found that E2, and to a lesser degree progesterone and testosterone, had mostly beneficial effects on cytokine expression in primary microglia isolated from MS donors but not from controls; and on neuroprotective gene (APOE, BDNF, GLT1, IGF1, LIF) expression in human fetal astrocytes, but only under inflammatory conditions. Sex-specific changes in the levels of steroids, their metabolizing enzymes, their receptors, and the actions of steroids on glial neuroinflammatory responses may contribute to the sex differences in MS disease progression and lesion resolution.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"214 ","pages":"Article 107040"},"PeriodicalIF":5.1,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144702925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Age-related cerebral amyloid angiopathy accumulation in the APPSw mouse model is associated with perivascular inflammation and brain-wide vascular and inflammatory gene and protein changes” [213, 107013]","authors":"Katelynn E. Krick ,&nbsp;Erica M. Weekman ,&nbsp;Sherika N. Johnson ,&nbsp;Tiffany L. Sudduth ,&nbsp;Colin B. Rogers ,&nbsp;Emma J. Nicolaysen ,&nbsp;Maureen T. Kleinhenz ,&nbsp;Donna M. Wilcock","doi":"10.1016/j.nbd.2025.107033","DOIUrl":"10.1016/j.nbd.2025.107033","url":null,"abstract":"","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"214 ","pages":"Article 107033"},"PeriodicalIF":5.6,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144691067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network-wide modulation of synaptic plasticity and spike patterns in motor circuits after pallidal deep brain stimulation in a dystonia model","authors":"Denise Franz ,&nbsp;Fabiana Santana Kragelund ,&nbsp;Marco Heerdegen ,&nbsp;Stefanie Perl ,&nbsp;Anika Lüttig ,&nbsp;Franz Veit Plocksties ,&nbsp;Henning Bathel ,&nbsp;Angelika Richter ,&nbsp;Rüdiger Köhling","doi":"10.1016/j.nbd.2025.107037","DOIUrl":"10.1016/j.nbd.2025.107037","url":null,"abstract":"<div><h3>Aims</h3><div>We aimed to investigate the functional network effects of long-term deep brain stimulation (DBS) of the globus pallidus pars interna (GPi) on synaptic activity in motor thalamic and motor cortical neurons in an animal model of generalised dystonia (dt^sz hamster) with a focus on understanding the underlying mechanisms of GPi-DBS in modulating neural activity.</div></div><div><h3>Methods</h3><div>Whole-cell recordings were performed on motor thalamic and motor cortical neurons from DBS-treated and sham-treated dt^sz hamsters. Spontaneous synaptic activity was pharmacologically characterised and analysed by examining interspike intervals (ISI), postsynaptic current (PSC) frequencies, and discharge rates of spontaneous and evoked action potentials. Oscillatory patterns were also assessed to evaluate potential alterations in cortico-thalamo-cortical loops.</div></div><div><h3>Results</h3><div>The results revealed significant alterations in synaptic activity following long-term GPi-DBS. DBS-treated animals exhibited reduced ISI and increased PSC frequencies compared to sham-treated animals, with increased excitatory input to thalamic and a more clustered (though not more frequent) excitatory input to cortical M1. Fast oscillations were observed in both thalamic and motor cortical neurons, suggesting modulation of cortico-thalamo-cortical loops. While overall discharge rates of spontaneous and evoked action potentials remained unchanged, alterations in synaptic plasticity were noted, including increased PSC amplitudes and changes in inhibitory synaptic currents.</div></div><div><h3>Conclusion and main finding</h3><div>GPi-DBS modulates synaptic plasticity within the motor network by disrupting desynchronised neural activity. The alterations in pre- and postsynaptic mechanisms, including changes in inhibitory synaptic currents and axonal activity, lead to reorganising neuronal firing patterns and synaptic connectivity. These network-wide modulations may underpin the therapeutic effects of GPi-DBS in generalised dystonia.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"214 ","pages":"Article 107037"},"PeriodicalIF":5.6,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144699111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNA helicase maheshvara interacts with TDP-43 and exacerbates neurodegeneration in Drosophila model of amyotrophic lateral sclerosis","authors":"Pranjali Pandey ,&nbsp;Rituparna Das ,&nbsp;Harshita Yadav ,&nbsp;Ashim Mukherjee ,&nbsp;Mousumi Mutsuddi","doi":"10.1016/j.nbd.2025.107036","DOIUrl":"10.1016/j.nbd.2025.107036","url":null,"abstract":"<div><div><em>Drosophila maheshvara</em> (<em>mahe</em>) encodes a conserved DEAD box RNA helicase that regulates various important signaling pathways like Notch and JAK/STAT, pathways that have been functionally implicated in neuronal development. In order to identify novel modulators of <em>mahe</em> as well as to unravel its role in neurodegenerative disorders, a genetic modifier screen using <em>Drosophila</em> models of neurodegenerative disorders was carried out. From this screen, we identified <em>mahe</em> to be a potent modifier of <em>TDP-43</em> mediated proteinopathy in <em>Drosophila</em> model of Amyotrophic Lateral Sclerosis (ALS). We demonstrate that Mahe genetically interacts and associates with cytosolic hyperphosphorylated toxic aggregates of TDP-43 leading to enhanced TDP-43 mediated neurodegenerative phenotype. Increased autophagy, cytoskeletal disruption, and FMRP-mediated translational repression of neuronal target Futsch were observed, potentially contributing to neuronal dysfunction. The current study indicates a strong interaction of <em>mahe</em> and <em>TDP-43</em> (<em>TARDBP</em>) resulting in augmentation of TDP-43 mediated neurodegenerative phenotypes which parallels ALS clinical pathology.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"214 ","pages":"Article 107036"},"PeriodicalIF":5.1,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}