Molecular Psychiatry最新文献

{"title":"Gesture deficits in psychosis and the combination of group psychotherapy and transcranial magnetic stimulation: A randomized clinical trial.","authors":"Sebastian Walther, Lydia Maderthaner, Victoria Chapellier, Sofie von Känel, Daniel R Müller, Stephan Bohlhalter, Mischa Baer, Anastasia Pavlidou","doi":"10.1038/s41380-025-03303-7","DOIUrl":"https://doi.org/10.1038/s41380-025-03303-7","url":null,"abstract":"<p><p>Hand gesture deficits are common in schizophrenia predicting poor social functioning with no treatment currently available. We used 10-sessions of repetitive transcranial magnetic stimulation (rTMS; 2-weeks) over the right inferior parietal lobe (IPL) in combination with 16-sessions of social cognitive remediation group therapy (SCRT; 8-weeks) to examine improvements in hand gesture performance in schizophrenia. In this 3-arm, double-blind, randomized, sham-controlled trial, 89 patients were randomized and 73 received at least one session of rTMS/SCRT: 19 patients were allocated to the real rTMS + real SCRT treatment, 26 to the sham rTMS + real SCRT treatment, and 28 to sham SCRT treatment. Hand gesture performance along with socio-cognitive and functional assessments were examined at 2-weeks, 8-weeks, and 32-weeks follow-up. Of 73 patients analyzed, (57% male), 53 completed the intervention and week-8 assessments. At week-8 no difference in overall hand gesture performance accuracy was observed across treatments. However, at week-32 follow-up the real rTMS + real group SCRT treatment showed significant improvements in novel unlearned gestures (F_{(6, 210)} = 2.2; p-value = 0.04), and significant gains in social functioning/personal performance at week-8 and sustained at week-32 follow-up (all F-values > 2.6; all p-values < 0.05). No treatment effects were found for overall hand gesture performance accuracy. However, improvements in secondary outcomes such as novel unlearned gestures and social/personal functioning hold promise for testing optimized rTMS + group SCRT combinations. Future studies should explore the neural effects of rTMS over right IPL + group SCRT.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145251960","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":"Genome-wide meta-analyses of cross substance use disorders in diverse populations.","authors":"Dongbing Lai, Michael Zhang, Nick Green, Marco Abreu, Tae-Hwi Schwantes-An, Clarissa C Parker, Shanshan Zhang, Fulai Jin, Anna Sun, Pengyue Zhang, Howard J Edenberg, Yunlong Liu, Tatiana Foroud","doi":"10.1038/s41380-025-03294-5","DOIUrl":"https://doi.org/10.1038/s41380-025-03294-5","url":null,"abstract":"<p><p>Substance use disorders (SUDs, including alcohol, cannabis, opioids, and tobacco) represent significant public health challenges. The estimated heritability of SUDs is ~50% and many individuals experience multiple SUDs concurrently. Studies have demonstrated the existence of genes shared across multiple SUDs, and identifying these SUD-shared genes is critical to developing novel prevention and treatment strategies. Here, we conducted the largest cross SUD meta-analysis to date to identify SUD-shared genes using samples genetically similar to 1000 Genomes Project European (1kg-EUR-like), African (1kg-AFR-like), and American mixed (1kg-AMR-like) populations. We defined variants that had the same direction of effects across different SUDs (i.e., concordant variants) as SUD-shared. In total, we identified 220 loci, including 40 novel loci that were not reported as SUD-associated in previous genome-wide association studies. Through gene-based analyses, gene mapping, and gene prioritization, we identified 785 SUD-shared genes. These genes are highly expressed in the amygdala, cortex, hippocampus, hypothalamus, and thalamus; and are primarily highly expressed in neuronal cells, suggesting that more brain regions may be involved in SUDs than previously reported. Concordant variants explained 56-96% of the SNP-heritability of each SUD in the 1kg-EUR-like sample. Furthermore, the top 10% of individuals in the 1kg-EUR-like and 1kg-AMR-like samples with the highest polygenic scores had odds ratios ranging from 1.95-2.87 to develop SUDs, and these polygenic scores could potentially be used to identify high-risk individuals. Lastly, using a real-world dataset, we identified seven SUD-shared genes targeting drugs that may be repurposed for treating SUDs, particularly in those suffering from comorbid SUDs.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244794","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":"Differential effect of cannabis use and antipsychotic medication on extracellular free-water in the brain of individuals with early psychosis and controls.","authors":"Laura Martínez-Sadurní, Marta Barrera-Conde, Patricia Robledo, Emma Veza-Estevez, Jordi Garcia-Quintana, Anna Mané, Alba Toll, Amira Trabsa, Tyler A Lesh, Cameron S Carter, Daniel Bergé","doi":"10.1038/s41380-025-03287-4","DOIUrl":"https://doi.org/10.1038/s41380-025-03287-4","url":null,"abstract":"<p><p>Inflammatory changes have been widely reported in psychosis. Cannabis use has been consistently related to increased risk of psychosis, earlier onset, higher rates of relapse and poorer treatment response. However, it is unclear how cannabis use interacts with brain inflammatory changes in psychosis. In this cross-sectional study we used diffusion imaging to measure extracellular free water in the brain (FW), a measure that has been associated with inflammation, in 62 individuals with recent onset psychosis (ROP) and 38 controls, with and without cannabis use. Past cannabis use was associated with lower FW in controls, and conversely, to elevated FW in ROP. This group x past cannabis use interaction was found significant in average GM (p = 0.049), and in cortical regions, including the temporal lobe expanding to parietal regions (TFCE p-FWE < 0.05). Within ROP, antipsychotic exposure was related to lower FW in gray matter and white matter only in the non-cannabis users, with no significant association in cannabis users (p interaction in WM = 0.005, in GM = 0.073). Our results demonstrate a differential effect of cannabis use on FW, a surrogate marker of neuroinflammatory processes and suggest that past cannabis use may influence the effects of antipsychotic medication on the brain. However, given the cross-sectional design and moderate sample size, causal interpretations are limited, and further longitudinal studies are warranted.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244802","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":"Role of telomere length and telomerase activity in accelerated cellular aging and major depressive disorder: a systematic review.","authors":"Samantha Wai Sam Au Young, Chuin Hau Teo, Ishwar S Parhar, Tomoko Soga","doi":"10.1038/s41380-025-03296-3","DOIUrl":"https://doi.org/10.1038/s41380-025-03296-3","url":null,"abstract":"<p><p>Recent research has increasingly focused on understanding the relationship between cellular aging and mental health, particularly Major Depressive Disorder (MDD). Telomeres, protective structures at the end of chromosomes, and telomerase, an enzyme responsible for their maintenance, have emerged as potential markers of cellular aging and targets for therapeutic interventions in MDD. This review synthesizes findings from 30 studies conducted over the past 15 years, examining alterations in telomere length (TL) and telomerase activity (TA) in individuals with MDD compared to healthy controls. Most studies reported shorter TL in MDD patients, particularly in cases of chronic or severe depression, determined by the duration of illness or illness episode and by measurements of depression severity (e.g. HAM-D, BDI, etc.), suggesting an association between MDD and accelerated cellular aging. Elevated TA was also observed in MDD, with potential implications for treatment response. However, conflicting findings and methodological variations highlight the complexity of the relationship between TL, TA, and MDD, warranting further research. Additionally, studies investigating other biomarkers of cellular aging, such as mitochondrial DNA, provide further insights into the pathophysiology of MDD. Studies on brain cells reveal regional variations in telomere dynamics, suggesting a nuanced relationship between depression and cellular aging across different brain regions. While evidence suggests a potential reversibility of TL alterations in MDD, further research is needed to elucidate underlying mechanisms and develop targeted interventions. Overall, this review underscores the importance of understanding cellular aging processes in MDD and their potential implications for diagnosis, treatment, and the development of novel therapeutic strategies.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145239277","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":"Cortical 5-HT_2A receptors in depression and suicide: a systematic review and meta-analysis of in vivo and post-mortem imaging studies.","authors":"George E Chapman, George Turner, Alexander P Noar, Tommaso Barba, Rayyan Zafar, Robert A McCutcheon, David Erritzoe","doi":"10.1038/s41380-025-03233-4","DOIUrl":"https://doi.org/10.1038/s41380-025-03233-4","url":null,"abstract":"<p><strong>Introduction: </strong>Major depressive disorder (MDD) is a leading cause of suicide and disability. Better understanding changes to serotonin_2A receptors (5-HT_2ARs) in MDD and suicide may help to improve treatments. We systematically reviewed and meta-analysed positron emission tomography (PET), single photon emission computed tomography (SPECT) and post-mortem radioligand binding studies of cortical 5-HT_2ARs in MDD and suicide.</p><p><strong>Methods: </strong>Databases were searched from inception to August/September 2024. Binding data were extracted and pooled before random-effects meta-analyses of mean difference (Hedges' g) and variance were undertaken. Simple linear regression was performed to investigate the relationship between receptor binding and depression severity at baseline in PET and SPECT studies. We also assessed study quality and tested for evidence of publication bias.</p><p><strong>Results: </strong>Data on 556 MDD patients or suicide victims and 526 controls from 31 studies were included. Cortical 5-HT_2AR binding was significantly lower in living MDD patients, who had not taken antidepressants for between one week and forever, than controls in frontal, prefrontal, cingulate, anterior cingulate and, upon sensitivity analysis, temporal cortex (Hedges' g = -0.40 to -0.57). In frontal and cingulate regions, binding effect size correlated with depression severity at baseline. There was study-level evidence of lower regional binding in never-medicated MDD patients than controls which, upon exploratory meta-analysis, reached significance in anterior cingulate cortex. Most PET or SPECT studies were of good or fair quality. The results of most post-mortem analyses were negative and included studies were of variable quality. There was limited evidence of publication bias.</p><p><strong>Conclusion: </strong>In vivo 5-HT_2AR binding is reduced in MDD in frontal, cingulate and temporal cortex. This finding is based mainly on studies that used antagonist or inverse agonist radiotracers.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145239258","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":"Correction: Developing an individualized treatment rule for Veterans with major depressive disorder using electronic health records.","authors":"Nur Hani Zainal, Robert M Bossarte, Sarah M Gildea, Irving Hwang, Chris J Kennedy, Howard Liu, Lucinda B Leung, Alex Luedtke, Brian P Marx, Maria V Petukhova, Edward P Post, Eric L Ross, Nancy A Sampson, Erik Sverdrup, Brett Turner, Stefan Wager, Ronald C Kessler","doi":"10.1038/s41380-025-03299-0","DOIUrl":"https://doi.org/10.1038/s41380-025-03299-0","url":null,"abstract":"","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145239275","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":"A novel lncRNA FAM151B-DT regulates degradation of aggregation prone proteins.","authors":"Arun Renganathan, Miguel A Minaya, Matthew Broder, Isabel Alfradique-Dunham, Rebecca L Miller, Dhruva D Dhavale, Michelle Moritz, Reshma Bhagat, Jacob Marsh, Anthony Verbeck, Grant Galasso, Emma Starr, David A Agard, Paul T Kotzbauer, Carlos Cruchaga, Celeste M Karch","doi":"10.1038/s41380-025-03277-6","DOIUrl":"https://doi.org/10.1038/s41380-025-03277-6","url":null,"abstract":"<p><p>Neurodegenerative diseases share common features of protein aggregation along with other pleiotropic traits, including shifts in transcriptional patterns, neuroinflammation, disruption in synaptic signaling, mitochondrial dysfunction, oxidative stress, and impaired clearance mechanisms like autophagy. However, key regulators of these pleiotropic traits have yet to be identified. Here, we used transcriptomics, mass spectrometry, and biochemical assays to define the role of a novel lncRNA on tau pathophysiology. We discovered a long non-coding RNA (lncRNA), FAM151B-DT, that is reduced in a stem cell model of frontotemporal lobar dementia with tau inclusions (FTLD-tau) and in brains from FTLD-tau, progressive supranuclear palsy, Alzheimer's disease, and Parkinson's disease patients. We show that silencing FAM151B-DT in vitro is sufficient to enhance tau and α-synuclein aggregation. To begin to understand the mechanism by which FAM151B-DT mediates tau aggregation and contributes to several neurodegenerative diseases, we deeply characterized this novel lncRNA and found that FAM151B-DT resides in the cytoplasm where it interacts with tau, α-synuclein, HSC70, and other proteins involved in protein homeostasis. When silenced, FAM151B-DT blocks autophagy, leading to the accumulation of tau and α-synuclein. Importantly, we discovered that increasing FAM151B-DT expression is sufficient to promote autophagic clearance of phosphorylated tau and α-synuclein, and reduce tau and α-synuclein aggregation. Overall, these findings pave the way for further exploration of FAM151B-DT as a promising molecular target for several neurodegenerative diseases.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145239296","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":"Regulation of stress susceptibility by chromatin-binding protein PHF6 in the pituitary intermediate lobe.","authors":"Bing Liu, Jingjie Wang, Xiaohua Wu, Linhua Gan, Jingjing Sun, Guangzhong Wang, Qian Li, Ju Huang","doi":"10.1038/s41380-025-03300-w","DOIUrl":"https://doi.org/10.1038/s41380-025-03300-w","url":null,"abstract":"<p><p>The pituitary intermediate lobe (IL) is a surprisingly understudied pituitary region. Here, we find that chromatin-binding protein PHF6 is enriched in the pituitary IL and plays a crucial role in regulating stress susceptibility in mice. Conditional knockout of Phf6 in PHF6-positive IL cells (^ILPHF6 cells) significantly reduces acute stress-induced anxiety-like behaviors and chronic stress-induced depression-like behaviors by impairing cellular activation and the release of stress-related hormones. Mechanistically, conditional knockout of Phf6 in the pituitary IL cells downregulates the calcium channel β3 subunit and suppresses transcription of stress-responsive genes. Chemogenetic inhibition of ^ILPHF6 cells reduces stress susceptibility, whereas activation of these cells increases anxiety-like behaviors. Circuit tracing demonstrates that ^ILPHF6 cells receive direct synaptic inputs from CRH-expressing neurons in the hypothalamus paraventricular nucleus (PVN), positioning ^ILPHF6 cells as a crucial interface between neural stress signals and endocrine output. These findings reveal a previously unknown mechanism in the regulation of stress susceptibility that operates through anxiogenic ^ILPHF6 cells, providing a perspective for understanding how stress susceptibility is molecularly tuned.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145239223","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":"Effect sizes of APOE e4 on the same general cognitive ability test taken by the same people from age 11 to age 90: The Lothian Birth Cohorts 1921 and 1936.","authors":"Ian J Deary, Sarah E Harris, Tom C Russ, Simon R Cox, Janie Corley","doi":"10.1038/s41380-025-03274-9","DOIUrl":"https://doi.org/10.1038/s41380-025-03274-9","url":null,"abstract":"<p><p>Variation in the gene for apolipoprotein E (APOE) is one of the few variables that is associated with individual differences in age-related cognitive decline in humans. Therefore, it is important to understand the conditions that affect the strength of its effect. Here we examine how the effect size of APOE variation (possession of one or more e4 alleles) on a test of general cognitive ability changes with age from 11-90 years. The data are from the Lothian Birth Cohorts of 1936 and 1921 who took the same cognitive test (the Moray House Test No. 12) at, respectively, ages 11 (N = 954), 70 (N = 1001), 76 (N = 636), 79 (N = 471), and 11 (N = 483), 79 (N = 533), 87 (N = 198), 90 (N = 120). The standardised absolute effect of APOE e4 on general cognitive ability was about zero at ages 11 (beta < 0.05) and 70 (beta ≤ 0.025) and increased linearly to beta = 0.30 (p < 0.001) at age 90. The effect sizes were minimally affected by adjusting for medical conditions (hypertension, diabetes, cardiovascular disease, stroke). However, the results were less robust to removing those participants who developed dementia; effect sizes were reduced by about a third to a half, and were largely non-significant. The results suggest that the negative effect of APOE e4 on cognitive functioning becomes greater with age; this urges more work to understand the mechanisms by which e4 status renders the older person's brain increasingly vulnerable to cognitive decline and dementia.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145239291","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":"Connectome-based markers predict the sub-types of frontotemporal dementia.","authors":"Xinglin Zeng, Jiangshan He, Kaixi Zhang, Shiyang Xu, Xiaoluan Xia, Zhen Yuan","doi":"10.1038/s41380-025-03290-9","DOIUrl":"https://doi.org/10.1038/s41380-025-03290-9","url":null,"abstract":"<p><p>Frontotemporal dementia (FTD) presents a complex spectrum of neurodegenerative disorders, encompassing distinct subtypes with varied clinical manifestations. This study investigates alterations in brain module organization associated with FTD subtypes using connectome analysis, aiming to identify potential biomarkers and enhance subtype prediction. Resting-state functional magnetic resonance imaging data were obtained from 41 individuals with behavioral variant frontotemporal dementia (BV-FTD), 32 with semantic variant frontotemporal dementia (SV-FTD), 28 with progressive non-fluent aphasia frontotemporal dementia (PNFA-FTD), and 94 healthy controls. Individual functional brain networks were constructed at the voxel level and binarized based on density thresholds. Modular segregation index (MSI) and participation coefficient (PC) were calculated to assess module integrity and identify regions with altered nodal properties. The relationship between modular measures and clinical scores was examined, and machine learning models were developed for subtype prediction. Both BV-FTD and SV-FTD groups exhibited decreased MSI in the subcortical module (SUB), default mode network (DMN), and ventral attention network (VAN) compared to healthy controls. Additionally, BV-FTD specifically displayed disrupted frontoparietal network (FPN) integrity compared to other FTD subtypes and controls. All FTD subtypes showed increased PC values in the insular region and reduced connections between the insular and VAN/FPN compared to controls. Moreover, significant associations between specific network alterations and clinical variables were observed. Machine learning models utilizing these matrices achieved high performance in differentiating FTD subtypes. This pilot study reveals diverse brain module organization across FTD subtypes, shedding light on both shared and distinct neurobiological underpinnings of the disorder.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145239273","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}