L.H.D. Le , A.M. Feidler , L. Calcines Rodriguez , M. Cealie , E. Plunk , H. Li , K. Kara-Pabani , C. Lamantia , M.K. O’Banion , A.K. Majewska
{"title":"Noradrenergic signaling controls Alzheimer’s disease pathology via activation of microglial β2 adrenergic receptors","authors":"L.H.D. Le , A.M. Feidler , L. Calcines Rodriguez , M. Cealie , E. Plunk , H. Li , K. Kara-Pabani , C. Lamantia , M.K. O’Banion , A.K. Majewska","doi":"10.1016/j.bbi.2025.04.022","DOIUrl":"10.1016/j.bbi.2025.04.022","url":null,"abstract":"<div><div>Norepinephrine (NE) is a potent anti-inflammatory agent in the brain. In Alzheimer’s disease (AD), the loss of NE signaling heightens neuroinflammation and exacerbates amyloid pathology. NE inhibits surveillance activity of microglia, the brain’s resident immune cells, via their β2 adrenergic receptors (β2ARs). Here, we investigate the role of microglial β2AR signaling in AD pathology in the 5xFAD mouse model of AD. We found that loss of cortical NE projections preceded the degeneration of NE-producing neurons and that microglia in 5xFAD mice, especially those microglia that were associated with plaques, significantly downregulated β2AR expression early in amyloid pathology. Importantly, dampening microglial β2AR signaling worsened plaque load and the associated neuritic damage, while stimulating microglial β2AR signaling attenuated amyloid pathology. Our results suggest that microglial β2AR could be explored as a potential therapeutic target to modify AD pathology.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"128 ","pages":"Pages 307-322"},"PeriodicalIF":8.8,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143843629","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":"Traveling to the brain: Intestinal dendritic cells as early mediator of gut microbiota − innate immune system Axis","authors":"Stefano Farioli Vecchioli","doi":"10.1016/j.bbi.2025.04.023","DOIUrl":"10.1016/j.bbi.2025.04.023","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"128 ","pages":"Pages 305-306"},"PeriodicalIF":8.8,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143843631","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":"PNIRS Society Announcements","authors":"","doi":"10.1016/S0889-1591(25)00142-4","DOIUrl":"10.1016/S0889-1591(25)00142-4","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"126 ","pages":"Pages iv-v"},"PeriodicalIF":8.8,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143828165","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}
Canal Maria Pilar , Acutain Maria Florencia , Nini Karen Agustina , Munner Mariana , Caruso Ornella , De Tomas-Liorio Anna , Badollati Adelina , Baez María Verónica
{"title":"Inducing elevated glucose levels in vitro: A model to simulate prediabetes (preDBT) states in primary cultures","authors":"Canal Maria Pilar , Acutain Maria Florencia , Nini Karen Agustina , Munner Mariana , Caruso Ornella , De Tomas-Liorio Anna , Badollati Adelina , Baez María Verónica","doi":"10.1016/j.bbi.2025.04.019","DOIUrl":"10.1016/j.bbi.2025.04.019","url":null,"abstract":"<div><div>There is increasing evidence suggesting a relationship between prediabetes (preDBT, the early stage of Type 2 Diabetes or DBT2) and neurodegenerative disorders (NDDs) such as Alzheimer’s disease. The preDBT stage, characterized by impaired fasting glucose (IFG), may represent an early risk factor for cognitive decline and the onset of NDDs. However, the underlying mechanisms connecting preDBT to cognitive impairment and neurodegeneration remain poorly understood. This study aims to explore the effects of IFG on central nervous system (CNS) cells by developing an in vitro model of preDBT using sera from individuals with IFG. Our results demonstrate that exposure of astrocyte-neuron mixed cultures to IFG sera induced hyperglycemia, increased oxidative levels and astrogliosis that would lead to cognitive impairment observed in the analyzed cohort, as evidenced by a battery of cognitive tests. These findings suggest that the early stages of preDBT may trigger changes in CNS cells that correlate with cognitive decline. The study underscores the importance of early diagnosis and intervention in preDBT to prevent progression to DBT2 and associated NDDs.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"128 ","pages":"Pages 323-335"},"PeriodicalIF":8.8,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143843630","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}
Tatum A. Jolink , Mallory J. Feldman , Natalie M. Antenucci , Megan N. Cardenas , Taylor N. West , Zev M. Nakamura , Keely A. Muscatell
{"title":"Effects of a mild inflammatory challenge on cytokines and sickness behavior: A randomized controlled trial using the influenza vaccine","authors":"Tatum A. Jolink , Mallory J. Feldman , Natalie M. Antenucci , Megan N. Cardenas , Taylor N. West , Zev M. Nakamura , Keely A. Muscatell","doi":"10.1016/j.bbi.2025.04.018","DOIUrl":"10.1016/j.bbi.2025.04.018","url":null,"abstract":"<div><div>The influenza vaccine has reliably been associated with mild, within-person increases in inflammation. However, the field lacks rigorous experimental work comparing the effects of the influenza vaccine to a placebo control on changes in plasma inflammatory cytokines and self-reported sickness behavior. In a double-blind, randomized, placebo-controlled trial, 102 participants received either the influenza vaccine or saline placebo. Four cytokines were measured in plasma 24-hours following injection; participants also reported on psychosocial outcomes, specifically sickness behavior, positive/negative affect, sleep, and subjective social disconnection. All cytokines—IL-6, IL-10, TNF-α, IFN-γ—were significantly increased in the influenza vaccine condition compared to placebo. None of the psychosocial outcomes differed by condition. This study fills a gap in the literature by presenting critical causal evidence that the influenza vaccine leads to elevated levels of four inflammatory cytokines, compared to placebo control. However, a more robust increase in inflammation or a larger sample size may be necessary to observe differences in self-reported sickness behavior and other psychosocial outcomes.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"128 ","pages":"Pages 429-439"},"PeriodicalIF":8.8,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874412","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}
Ruth M. Barrientos , Michael V. Baratta , Matthew G. Frank
{"title":"Dr. Steven F. Maier: A fearless scientist, a rigorous mentor, and a legacy of excellence","authors":"Ruth M. Barrientos , Michael V. Baratta , Matthew G. Frank","doi":"10.1016/j.bbi.2025.04.021","DOIUrl":"10.1016/j.bbi.2025.04.021","url":null,"abstract":"<div><div>For more than 40 years, Dr. Steven F. Maier has shaped the field of psychoneuroimmunology through innovative research, influential mentorship, and dedicated service to the scientific community. As he concludes his tenure as Associate Editor of Brain, Behavior, and Immunity, this tribute reflects on his most transformative scientific contributions—from conceptualizing learned helplessness to uncovering the neural and immune mechanisms linking stress to disease vulnerability. Drawing from our experiences as longtime mentees and later colleagues, we also share reflections on his unique mentoring style, unwavering commitment to scientific rigor, and enduring influence on the field.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"128 ","pages":"Pages 303-304"},"PeriodicalIF":8.8,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143839753","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}
Sara A. Norton , Aaron J. Gorelik , Sarah E. Paul , Emma C. Johnson , David AA Baranger , Jayne L Siudzinski , Zhaolong Adrian Li , Erin Bondy , Hailey Modi , Nicole R. Karcher , Tamara Hershey , Alexander S. Hatoum , Arpana Agrawal , Ryan Bogdan
{"title":"A Phenome-Wide association study (PheWAS) of genetic risk for C-reactive protein in children of European Ancestry: Results from the ABCD study","authors":"Sara A. Norton , Aaron J. Gorelik , Sarah E. Paul , Emma C. Johnson , David AA Baranger , Jayne L Siudzinski , Zhaolong Adrian Li , Erin Bondy , Hailey Modi , Nicole R. Karcher , Tamara Hershey , Alexander S. Hatoum , Arpana Agrawal , Ryan Bogdan","doi":"10.1016/j.bbi.2025.04.012","DOIUrl":"10.1016/j.bbi.2025.04.012","url":null,"abstract":"<div><h3>Background</h3><div>C-reactive protein (CRP) is a moderately heritable marker of systemic inflammation that is associated with adverse physical and mental health outcomes. Identifying factors associated with genetic liability to elevated CRP in childhood may inform our understanding of variability in CRP that could be targeted to prevent and/or delay the onset of related health outcomes.</div></div><div><h3>Methods</h3><div>We conducted a phenome-wide association study (PheWAS) of genetic risk for elevated CRP (i.e. CRP polygenic risk score [PRS]) among children genetically similar to European ancestry reference populations (median analytic n = 5,509, range = 120–5,556) from the Adolescent Brain and Cognitive Development<sup>SM</sup> (ABCD) Study baseline assessment. Associations between CRP PRS and 2,377 psychosocial and neuroimaging phenotypes were estimated using independent mixed effects models nested by recruitment site (or scanner) and family, with ancestral genomic principal components (n = 10), age, and sex, as well as global brain metrics (when relevant) included as fixed effect covariates. <em>Post hoc</em> analyses examined whether: (1) covarying for measured body mass index (BMI) or removing the shared genetic architecture between CRP and BMI altered phenotypic associations, (2) sex moderated CRP PRS associations, and (3) associations were unconfounded by assortative mating or passive gene-environment correlations (using <em>within-family</em> analyses). Multiple testing was adjusted for using Bonferroni and false discovery rate (FDR) correction.</div></div><div><h3>Results</h3><div>Nine phenotypes were positively associated with CRP PRS after multiple testing correction: five weight- and eating-related phenotypes (e.g. BMI, overeating), three phenotypes related to caregiver somatic problems (e.g. caregiver somatic complaints), as well as weekday video watching (all <em>p</em>s = 1.2 x 10<sup>-7</sup> − 2.5 x 10<sup>-4</sup>, all <em>p<sub>FDR</sub></em>s = 0.0002–0.05). No neuroimaging phenotypes were associated with CRP PRS (all <em>p</em>s = 0.0003–0.998; all <em>p<sub>FDR</sub></em>s = 0.08–0.998) after correction for multiple testing. Eating and weight-related phenotypes remained associated with CRP PRS in within-family analyses. Covarying for BMI resulted in largely consistent results, and sex did not moderate any CRP PRS associations. Removing the shared genetic variance between CRP and BMI attenuated all relationships; associations with weekday video watching, caregiver somatic problems and caregiver report that the child is overweight remained significant while associations with waist circumference, weight, and caregiver report that child overeats did not.</div></div><div><h3>Discussion</h3><div>Genetic liability to elevated CRP is associated with higher weight, eating, and weekday video watching during childhood as well as caregiver somatic problems. These associations were consistent with direct genetic effects (i.","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"128 ","pages":"Pages 487-496"},"PeriodicalIF":8.8,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143886590","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}
Wenyue Gong , Qinghua Zhai , Yiwen Wang , Azi Shen , Yinghong Huang , Kaiyu Shi , Yingying Huang , Moxuan Song , Rui Yan , Zhijian Yao , Qing Lu
{"title":"Glymphatic function and choroid plexus volume is associated with systemic inflammation and oxidative stress in major depressive disorder","authors":"Wenyue Gong , Qinghua Zhai , Yiwen Wang , Azi Shen , Yinghong Huang , Kaiyu Shi , Yingying Huang , Moxuan Song , Rui Yan , Zhijian Yao , Qing Lu","doi":"10.1016/j.bbi.2025.04.008","DOIUrl":"10.1016/j.bbi.2025.04.008","url":null,"abstract":"<div><h3>Background</h3><div>Inflammatory processes were recognized as key factors in the pathophysiology of major depressive disorder (MDD). The choroid plexus (ChP) and glymphatic system played central roles in immune interactions between the brain and periphery. However, their specific roles in MDD and their relationship with systemic inflammation and oxidative stress remained unclear.</div></div><div><h3>Methods</h3><div>This study finally included 665 MDD patients and 338 healthy controls. Clinical data and MRI scans were collected, and some patients also underwent blood routine and biochemical tests. ChP volume was manually segmented, and the diffusion tensor imaging along the perivascular space (DTI-ALPS) index, reflecting glymphatic function, was obtained through the FSL pipeline. The differences in these dices between groups were compared, and their associations with systemic inflammation and oxidative stress were analyzed.</div></div><div><h3>Results</h3><div>MDD patients showed increased ChP volume (total: <em>d</em> = 0.316, <em>p</em> < 0.001; left: <em>d</em> = 0.317, <em>p</em> < 0.001; right: <em>d</em> = 0.268, <em>p</em> = 0.003) and decreased DTI-ALPS index (<em>d</em> = −0.144, <em>p</em> = 0.022), with a negative correlation between them (<em>ρ</em> = −0.135, <em>p <</em> 0.001). In MDD patients, lower DTI-ALPS index was correlated with higher LHR (<em>ρ</em> = −0.107, <em>p</em> = 0.025) and MHR (<em>ρ</em> = −0.126, <em>p</em> = 0.008). Larger right ChP volume was associated with higher MLR (<em>ρ</em> = 0.107, <em>p</em> = 0.009), SIRI (<em>ρ</em> = 0.086, <em>p</em> = 0.036), PIV (<em>ρ</em> = 0.086, <em>p</em> = 0.036), MHR (<em>ρ</em> = 0.136, <em>p</em> = 0.004), and PHR (<em>ρ</em> = 0.126, <em>p</em> = 0.008), while larger total ChP volume was correlated with higher MHR (<em>ρ</em> = 0.097, <em>p</em> = 0.042) and PHR (<em>ρ</em> = 0.114, <em>p</em> = 0.017).</div></div><div><h3>Conclusion</h3><div>MDD appeared to be accompanied by an increase in ChP volume and a decrease in glymphatic function, and these changes were related to systemic inflammation and oxidative stress.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"128 ","pages":"Pages 266-275"},"PeriodicalIF":8.8,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143824058","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}
Lusi Zhang , Chengmin Yang , Wenjing Zhang , Su Lui , Jeffrey R. Bishop
{"title":"Human leukocyte antigen (HLA) class I and II genetic relationships with brain imaging measures: A systematic review and meta-analysis","authors":"Lusi Zhang , Chengmin Yang , Wenjing Zhang , Su Lui , Jeffrey R. Bishop","doi":"10.1016/j.bbi.2025.04.011","DOIUrl":"10.1016/j.bbi.2025.04.011","url":null,"abstract":"<div><div>This systematic review and <em>meta</em>-analysis synthesizes current evidence on associations between genetic polymorphisms of human leukocyte antigen (HLA) class I and II molecules, which play key roles in antigen presentation and immune response regulation, and brain imaging phenotypes across various neurological and psychiatric conditions. The strongest associations were observed in multiple sclerosis (MS), where HLA-DRB1*15:01 was linked to increased lesion volume and disease progression. Meta-analyses revealed significant pooled effect sizes for both T1 and T2 lesion volumes. Emerging evidence also suggests that variants in HLA class I and II genes contribute to brain structural changes associated with age-related cognitive decline, schizophrenia, and Gulf War illness. Our findings revealed stronger patterns of association between HLA class II polymorphisms with brain imaging implications as compared to class I in neurodegenerative conditions. Considering HLA class II roles in exogenous protein/peptide presentation, this highlights the potential importance of neuroimmune-environmental interactions as contributing factors to disease pathogenesis and progression. Population-based studies from the UK Biobank highlight the potential influence of HLA class I and II genetic polymorphisms on brain structure beyond disease-specific contexts, suggesting broader implications for neurodevelopment and neurodegeneration. Despite these emerging insights, the limited availability of studies using imaging modalities beyond structural MRI, along with inconsistent findings within specific diseases and across conditions, underscores the need for further investigation into the mechanistic contributions of specific genetic variants on impacting brain structural and functional outcomes. Future research should include larger, more diverse study cohorts and employ advanced genotyping technologies to provide a more comprehensive investigations of HLA’s role on brain health across the lifespan.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"128 ","pages":"Pages 336-351"},"PeriodicalIF":8.8,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847959","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}
Lena J. Lee, Jennifer J. Barb, Elisa H. Son, Li Yang, Chantal Gerrard, Gwenyth R. Wallen
{"title":"Factors associated with inflammatory cytokines in family caregivers of allogeneic hematopoietic stem cell transplantation (HSCT) recipients","authors":"Lena J. Lee, Jennifer J. Barb, Elisa H. Son, Li Yang, Chantal Gerrard, Gwenyth R. Wallen","doi":"10.1016/j.bbi.2025.04.013","DOIUrl":"10.1016/j.bbi.2025.04.013","url":null,"abstract":"<div><h3>Background</h3><div>Family caregiving has been proposed as chronic stress that may lead to immune health risks through increased systemic inflammation. Cytokines are key modulators of inflammation via a complex network of interactions. However, most studies examined only a single to a few cytokines to determine whether they correlate with psychobehavioral variables of interest. This study aimed to investigate factors influencing multiple inflammatory cytokines in family caregivers of allogeneic hematopoietic stem cell transplantation (HSCT) recipients.</div></div><div><h3>Methods</h3><div>Baseline data from a randomized controlled clinical trial at the National Institutes of Health Clinical Center were collected from caregivers of allogeneic HSCT recipients. The 20 serum cytokine levels were measured using multiplexed cytokine immunoassays. Multiple linear regression was conducted.</div></div><div><h3>Results</h3><div>Caregivers (N = 45) were 44.6 ± 15.4 years of age; primarily female (87 %), White (66 %), non-Hispanic (82 %), and a spouse/partner of the HSCT recipient (56 %). Caring for HSCT recipients with hematologic malignancy predicted higher IL-12/IL-23p40 than caring for non-malignant HSCT recipients (<em>β</em> = 0.291, <em>p</em> = 0.044). Medication use was associated with higher IL-15 (<em>β</em> = 0.425, <em>p</em> = 0.017). Caregiver BMI overweight (<em>β</em> = 0.342, <em>p</em> = 0.043) or obese (<em>β</em> = 0.411, <em>p</em> = 0.010), taking prescribed medications (<em>β</em> = 0.521, <em>p</em> = 0.007), caregiving 8 to 16 h (<em>β</em> = 0.396, <em>p</em> = 0.027) or more than 16 h per day (<em>β</em> = 0.510, <em>p</em> = 0.006) predicted higher TNF-α than the counterparts.</div></div><div><h3>Discussion</h3><div>These findings suggest inflammatory responses may be associated with providing care to an HSCT recipient, especially in caregivers who take medications, provide more hours of care a day and care for patients with hematologic malignancies. The results highlight a physiological response of stress and bring to light the importance of developing interventions focused on reducing time spent caregiving, such as a respite care program for family caregivers.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"128 ","pages":"Pages 362-369"},"PeriodicalIF":8.8,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143855709","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}