Brain最新文献

{"title":"Reduced brain oxygen response to spreading depolarization predicts worse outcome in ischaemic stroke.","authors":"Nils Hecht, Daisy Haddad, Konrad Neumann, Leonie Schumm, Nora F Dengler, Lars Wessels, Patrick Dömer, Simeon Helgers, Franziska Meinert, Sebastian Major, Coline L Lemale, Jens P Dreier, Peter Vajkoczy, Johannes Woitzik","doi":"10.1093/brain/awae376","DOIUrl":"10.1093/brain/awae376","url":null,"abstract":"<p><p>Spreading depolarization (SD) describes a propagating neuronal mass depolarization within the cerebral cortex that represents a mediator of infarct development and strongly stimulates the metabolic rate of O2 consumption. Here, we investigated the influence of spreading depolarization on brain tissue partial pressure of O2 (ptiO2) within the peri-infarct tissue of patients suffering malignant hemispheric stroke. This prospective observational trial included 25 patients with malignant hemispheric stroke that underwent decompressive hemicraniectomy followed by subdural placement of electrodes for electrocorticography (ECoG) and neighbouring implantation of a ptiO2 probe within the peri-infarcted cortex. Continuous side-by-side ECoG + ptiO2 recordings were obtained for 3-6 days postoperatively and analysed for the occurrence of SD-independent and SD-coupled ptiO2 changes, radiological findings, as well as their association with clinical outcome at 6 months. During the combined ECoG + ptiO2 monitoring period of 2604 h and among 1022 SDs, 483 (47%) SD-coupled ptiO2 variations were identified as biphasic (59%), hypoxic (36%) or hyperoxic (5%) ptiO2 responses that differed significantly (P < 0.0001). Among the remaining 538/1022 (53%) SDs, no SD-coupled ptiO2 response was detected, which we categorized as 'No response'. The overall infarct progression was 1.7% (interquartile range -2.5-10.9). SD characteristics regarding type, duration and frequency, as well as SD-independent baseline ptiO2 had no association with outcome. In contrast, a high occurrence rate and amplitude of SD-coupled variations in ptiO2 were associated with improved outcome at 6 months (occurrence: r = -0.62, P = 0.035; amplitude: r = -0.57, P = 0.024; Spearman correlation). In conclusion, an absent or reduced ptiO2 response to SD could indicate tissue-at-risk and help direct targeted treatment strategies in ischaemic stroke, which is further evidence that not all SDs are the same but tissue responses coupled to SD such as ptiO2 contain prognostic information. In particular, a lack of SD-coupled ptiO2 variations appears to be a predictor of worse outcome in large hemispheric stroke.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":"1924-1935"},"PeriodicalIF":10.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12129726/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combinatorial approaches increasing neuronal activity accelerate recovery after spinal cord injury.","authors":"Bing Chen, Siddharth Gaikwad, Robert H Powell, Hang Jin Jo, Allison B Kessler, David Chen, Charles J Heckman, Linda Jones, James D Guest, Jonathan R Wolpaw, Martin Oudega, Andrew R Blight, Monica A Perez","doi":"10.1093/brain/awaf099","DOIUrl":"10.1093/brain/awaf099","url":null,"abstract":"<p><p>Combinatorial approaches targeting multiple aspects of spinal cord injury (SCI) pathophysiology are needed to maximize functional recovery. We hypothesized that enhancing neuronal activity-by strengthening corticospinal synapses through Hebbian stimulation and increasing neuronal transmission with 4-aminopyridine (4-AP), a potassium blocker-could accelerate locomotor recovery in individuals with chronic SCI. Participants were randomly assigned to receive 10 mg of 4-AP or placebo, where both groups followed with 60 min of Hebbian stimulation targeting corticospinal-motor neuronal synapses supplying leg muscles involved in locomotion and 60 min of standard exercise rehabilitation for 40 sessions over 8-14 weeks. During Hebbian stimulation, 720 paired pulses were delivered to elicit corticospinal action potentials via electrical stimulation of the thoracic spine, ensuring volleys reached the spinal cord 1-2 ms before motor neurons were retrogradely activated through bilateral electrical stimulation of the femoral, common peroneal, and posterior tibial nerves (targeting the quadriceps femoris, tibialis anterior and soleus muscles, respectively). Results showed that participants who received 4-AP exhibited significantly greater improvements in walking speed and endurance, corticospinal excitability, and light touch sensation compared to those who received the placebo. The minimal clinically important difference in walking speed and endurance was achieved after 20 sessions in the 4-AP group, but was not consistently reached in the placebo group. Although walking continued to improve in both groups over the course of 40 sessions, the 4-AP group demonstrated significantly greater progress. Improvement in the 4-AP group was still present approximately 12 months later. These findings suggest that 4-AP represents a strategy to potentiate and accelerate Hebbian stimulation effects on motor recovery in individuals with chronic SCI.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":"1911-1923"},"PeriodicalIF":10.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Snatches of time. Fragments.","authors":"Matthew Butler","doi":"10.1093/brain/awaf166","DOIUrl":"10.1093/brain/awaf166","url":null,"abstract":"","PeriodicalId":9063,"journal":{"name":"Brain","volume":"148 6","pages":"1847-1849"},"PeriodicalIF":10.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12129727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply: Overstating harms can have consequences.","authors":"Michael Benatar, Christopher J McDermott, Martin R Turner, Ruben P A van Eijk","doi":"10.1093/brain/awaf047","DOIUrl":"10.1093/brain/awaf047","url":null,"abstract":"","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":"e54"},"PeriodicalIF":10.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Harnessing psychedelics for stroke recovery: therapeutic potential and mechanisms.","authors":"Yuefeng Yang, Yibo Wang, Xiaohui Wang","doi":"10.1093/brain/awaf093","DOIUrl":"10.1093/brain/awaf093","url":null,"abstract":"","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":"1862-1865"},"PeriodicalIF":10.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impaired reward sensitivity in Parkinson's depression is unresponsive to dopamine treatment.","authors":"Harry Costello, Yumeya Yamamori, Karel Kieslich, Mackenzie Murphy, Kamilla Bobyreva, Anette-Eleonore Schrag, Robert Howard, Jonathan P Roiser","doi":"10.1093/brain/awaf098","DOIUrl":"10.1093/brain/awaf098","url":null,"abstract":"<p><p>Willingness to exert effort for a given goal is dependent on the magnitude of the potential rewards and effort costs of an action. Such effort-based decision making is an essential component of motivation, in which the dopaminergic system plays a key role. Depression in Parkinson's disease (PD) is common, disabling and has poor outcomes. Motivational symptoms such as apathy and anhedonia are prominent in PD depression and related to dopaminergic loss. We hypothesized that dopamine-dependent disruption in effort-based decision making contributes to depression in PD. In the present study, an effort-based decision-making task was administered to 62 patients with PD, with and without depression, ON and OFF their dopaminergic medication across two sessions, as well as to 34 patients with depression and 29 matched controls on a single occasion. During the task, on each trial, participants decided whether to accept or reject offers of different levels of monetary reward in return for exerting varying levels of physical effort via grip force, measured using individually calibrated dynamometers. The primary outcome variable was choice (accept/decline offer), analysed using both logistic mixed-effects modelling and a computational model which dissected the individual contributions of reward and effort on depression and dopamine state in PD. We found PD depression was characterized by lower acceptance of offers, driven by markedly lower incentivization by reward (reward sensitivity), compared to all other groups. Within-subjects analysis of the effect of dopamine medication revealed that, although dopamine treatment improves reward sensitivity in non-depressed PD patients, this therapeutic effect is not present in PD patients with depression. These findings suggest that disrupted effort-based decision making, unresponsive to dopamine, contributes to PD depression. This highlights reward sensitivity as a key mechanism and treatment target for PD depression that potentially requires non-dopaminergic therapies.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":"2122-2134"},"PeriodicalIF":10.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12129732/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143655808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serotonergic dysfunction in patients with impulse control disorders in Parkinson's disease.","authors":"Stéphane Prange, Elise Metereau, Hélène Klinger, Marine Huddlestone, Melinda De Oliveira, Sandra Duperrier, Pierre Courault, Jérôme Redoute, Léon Tremblay, Véronique Sgambato, Sophie Lancelot, Stéphane Thobois","doi":"10.1093/brain/awaf087","DOIUrl":"10.1093/brain/awaf087","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Impulse control disorders (ICDs) are frequent and particularly distressing neuropsychiatric symptoms in patients with Parkinson's disease, which are related to impaired behavioural inhibition. Multiple PET imaging studies indicate that striatal dopaminergic abnormalities contribute to hyperdopaminergic functioning in Parkinson's disease patients with ICD (PDICD+) and to the dysregulation of the limbic fronto-striatal networks, which are critical for reward-related decision impulsivity. However, the serotonergic system is central to response inhibition and plays a critical role in neuropsychiatric symptoms in PD, but its role remains undetermined in PDICD. We hypothesized that PDICD+ patients exhibit serotonergic dysfunction within the cortico-striato-pallido-thalamic circuits involved in the inhibitory control of behaviour and decided to investigate the pre- and postsynaptic serotonergic innervation using two highly specific PET tracers for the serotonin transporter (SERT) using 11C-3-amino-4-(2-dimethylaminomethylphenylsulfanyl)-benzonitrile (11C-DASB) and the 5-HT2A receptor using 18F-altanserin. In this prospective, case-control, double-tracer PET study, we recruited 15 PDICD+ patients, 15 PDICD- patients and 15 healthy controls, matched for age and sex, and compared the availability of 11C-DASB and 18F-altanserin using permutation-based analysis. PDICD+ patients had one (n = 9) or multiple ICDs (n = 6), consisting of hypersexuality (n = 8), compulsive eating (n = 6), compulsive shopping (n = 5) and pathological gambling (n = 4), and were characterized by greater choice impulsivity (impaired delay discounting for monetary rewards) and greater urgency with more severe depressive and anxious symptoms. We demonstrate that PDICD+ patients had greater 11C-DASB binding in the posterior putamen and pallidum in comparison to PDICD- patients, corresponding to relatively preserved presynaptic SERT availability within the subcortical sensorimotor network involved in response inhibition. In addition, cortical 18F-altanserin binding was greater in PDICD+ patients in the bilateral supplementary motor area, precentral gyrus and right dorsolateral prefrontal cortex, involving the sensorimotor and associative networks which regulate behavioural inhibition. Furthermore, we show that pre- and postsynaptic serotonergic dysfunction subserving action versus decision impulsivity in patients with Parkinson's disease specifically followed the distinctive functional organization of the sensorimotor and associative fronto-striatal networks. Altogether, we demonstrate that serotonergic dysfunction related to ICDs in Parkinson's disease specifically involve the sensorimotor and associative cortico-striato-pallido-thalamic circuits involved in inhibitory control. Thus, serotonergic dysfunction contributes to the mechanisms related to the vulnerability and development of ICDs in patients with Parkinson's disease, beyond the known dopaminergic abnormalities in the limb","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":"2108-2121"},"PeriodicalIF":10.6,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12129733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The parasagittal dural space of the human brain","authors":"Manus J Donahue, Colin D McKnight, Daniel O Claassen, Kilian Hett","doi":"10.1093/brain/awaf204","DOIUrl":"https://doi.org/10.1093/brain/awaf204","url":null,"abstract":"The historical understanding of cerebrospinal fluid (CSF) production and flow comprises CSF production primarily in the choroid plexus of the 1st-3rd ventricles, flow through the aqueduct of Sylvius en route to the 4th ventricle, circulation around the subarachnoid space, and ultimately resorption into the blood circulation through arachnoid granulations. Since the discovery of a perivascular CSF clearance system in 2012 and in 2015 of lymphatic vessels localized to the dura mater of mice, there has been a growing interest in characterizing the structure and function of the tissues surrounding the dural sinuses, or the parasagittal dural (PSD) space. This work is now being pursued with increasing frequency to understand how the PSD space may relate to impaired neurofluid egress or neuroimmune function, with the intent of further informing our understanding of neurodegenerative proteinopathies and associated therapeutic avenues in disease. This review summarizes (i) our current understanding of neurofluid (comprised of CSF and interstitial fluid) circulation within the brain, as well as the (ii) anatomy and (iii) function of the PSD space in the context of neurofluid circulation and neuroimmune surveillance. With this context in place, we report on recent (iv) abilities to quantify the PSD volume and function in humans, (v) large-scale studies of PSD evolution across the human lifespan, and (vi) evidence for PSD structural variation in the setting of neurodegenerative disease.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"35 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mild behavioural impairment-apathy and core Alzheimer’s disease cerebrospinal fluid biomarkers","authors":"Daniella Vellone, Rebeca Leon, Zahra Goodarzi, Nils D Forkert, Eric E Smith, Zahinoor Ismail","doi":"10.1093/brain/awaf194","DOIUrl":"https://doi.org/10.1093/brain/awaf194","url":null,"abstract":"Apathy is a common neuropsychiatric symptom (NPS) in Alzheimer’s disease (AD) but can emerge earlier in prodromal and even preclinical stages as part of mild behavioural impairment (MBI-apathy), a syndrome defined by emergent and persistent NPS. In dementia, apathy is associated with higher morbidity, mortality, and caregiver distress. However, the significance of MBI-apathy in dementia-free persons, including its associations with AD biomarkers, remains unclear. This study aimed to determine whether MBI-apathy is associated with biomarker evidence of amyloid beta (Aβ) and tau (phosphorylated [p-tau], total [t-tau]) in CSF. Because MBI predicts incident dementia better than NPS without MBI, we aimed to determine the association between apathy and AD biomarkers when it occurred as part of the MBI syndrome and when it did not. Dementia-free participants with mild cognitive impairment (MCI) or normal cognition from the Alzheimer’s Disease Neuroimaging Initiative were stratified by NPS status – MBI-apathy, non-apathy MBI, non-MBI NPS, and no-NPS – based on the Neuropsychiatric Inventory (NPI) or NPI-Questionnaire (NPI-Q). Linear regressions modelled cross-sectional associations between NPS status (predictor) and CSF biomarker ratios (Aβ42/Aβ40, p-tau181/Aβ42, and t-tau/Aβ42; primary outcomes) and levels (Aβ40, Aβ42, p-tau181, t-tau; exploratory outcomes), adjusting for age, sex, Apolipoprotein E4, education, Mini Mental State Examination, and NPI version. Hierarchical linear mixed-effects (LME) models assessed longitudinal associations over two years incorporating random intercepts and slopes to account for repeated measures. Fixed effects included NPS status, all covariates from the linear regression model, as well as an interaction term between NPS status and time. Among 477 participants (176 cognitively normal), 52 had MBI-apathy. Primary cross-sectional analyses showed that, compared to the no-NPS group, MBI-apathy was associated with higher CSF p-tau181/Aβ42 (11.25% [2.56% – 20.68%]; adjusted p = 0.018) and t-tau181/Aβ42 (10.26% [2.42% – 18.70%]; adjusted p = 0.018). Exploratory analyses revealed that MBI-apathy was associated with higher CSF p-tau181 (5.98% [0.50% – 11.77%]; p = 0.032). Primary LMEs showed that MBI-apathy was associated with higher CSF p-tau181/Aβ42 (11.34% [2.55% – 20.88%]; adjusted p = 0.022) and t-tau181/Aβ42 (10.34% [2.41–18.88%]; adjusted p = 0.022) over two years. Exploratory LMEs revealed that MBI-apathy was associated with higher CSF p-tau181 (6.03% [0.56% – 11.81%]; p = 0.032) and t-tau (4.96% [0.07% – 10.09%]; p = 0.049) over two years. MBI-apathy was significantly associated with core AD biomarkers cross-sectionally and longitudinally, over two years, underscoring its relevance as a marker of AD pathological burden. An overall MBI composite score may reflect a broader spectrum of pathology and warrants further investigation.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"52 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biallelic LGI1 and ADAM23 variants cause hippocampal epileptic encephalopathy via the LGI1–ADAM22/23 pathway","authors":"Yoko Hirano, Yuri Miyazaki, Daisuke Ishikawa, Hiroki Inahashi, Zuhair Nasser Al-Hassnan, Giovanni Zifarelli, Peter Bauer, Javeria Raza Alvi, Tipu Sultan, Michelle L Thompson, Abdullah Sezer, Bahadır Konuşkan, Razan S Hajir, Ayman W El-Hattab, Stephanie Efthymiou, Ayuki Ishida, Norihiko Yokoi, Hans-Christian Kornau, Dietmar Schmitz, Harald Prüss, Henry Houlden, Yuji Ikegaya, Yuko Fukata, Masaki Fukata, Reza Maroofian","doi":"10.1093/brain/awaf202","DOIUrl":"https://doi.org/10.1093/brain/awaf202","url":null,"abstract":"Monoallelic pathogenic variants in LGI1 cause autosomal dominant epilepsy with auditory features with onset in childhood/adolescence. LGI1 is a secreted neuronal protein, functions as a ligand for ADAM22/23, and regulates excitatory synaptic transmission and neuronal excitability in the brain. While biallelic ADAM22 variants cause developmental and epileptic encephalopathy (DEE), the whole picture of LGI1–ADAM22/23 pathway-related diseases remains incompletely understood. Through international genetic data sharing, we identified the first ultra-rare biallelic LGI1 variants in six individuals from four consanguineous families. Affected individuals presented DEE with neonatal/infantile-onset epilepsy (6/6), global developmental delay/intellectual disability (6/6), and infant/premature death (5/6). Brain MRI showed mild cerebral atrophy in a subset of patients (3/6). Functional analyses revealed that all LGI1 variants result in reduced secretion and ADAM22-binding. Residual LGI1 function levels correlated with clinical severity, ranging from infantile lethality to intermediate phenotypes. Further, we observed epileptic discharges from the isolated whole hippocampus of Lgi1–/– knockout mice, experimentally modelling the hippocampal origin of LGI1-related epilepsy. Automated behavioural analysis of a mouse model for ADAM22-related DEE revealed its impaired cognitive function. Furthermore, we report the first ADAM23 variant associated with lethal neonatal-onset epilepsy and myopathy. Collectively, this study defines the LGI1–ADAM22/23 pathway-related disease spectrum.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"12 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}