Molecular Brain最新文献

{"title":"Oligomer logic of memory molecules.","authors":"Jerry W Rudy","doi":"10.1186/s13041-026-01307-0","DOIUrl":"https://doi.org/10.1186/s13041-026-01307-0","url":null,"abstract":"<p><p>It has been 40 years since Francis Crick [1] noted the problem molecular turnover poses for maintaining memories and offered a general solution. The solution requires that the critical molecules must be replaced without altering the overall structure of the complex. It is timely then that Todd Sacktor's group [2] has identified critical intermolecular interactions that satisfy Crick's requirement. Sacktor's early work identified the continuously active kinase, protein kinase Mzeta (PKMzeta) as a critical molecule for maintaining localized postsynaptic AMPA receptors that support long-term potentiation (LTP) and memory. More recent work revealed that PKMzeta forms heterodimers with the scaffolding protein KIBRA (KIbra BRAin) and preventing dimerization erased both LTP and memory. Even so, dimers degrade too fast to support long-lasting memories. Based on biophysical modeling, Sacktor's group with Harel Shouval reasoned that if KIBRA-PKMzeta heterodimers interact to form oligomers (such as hexamers), they can survive molecular turnover because as a dimer degrades it can be replaced by another. AlphaFold 3 predicted a site where the small molecule inhibitor, zeta-stat, would bind and disrupt oligomer formation. If so, then infusing zeta-stat into the hippocampus should erase long-term memory. This predicted outcome was observed. Thus, Crick's solution has been achieved. Oligomers formed from KIBRA-PKMzeta dimers allow degraded individual molecules to be replaced one at a time while maintaining their overall structure. This permits a continuous presence of PKMzeta where it interacts with AMPA receptors (through GluA2 subunits) and other molecules to ensure long-term memories endure.</p>","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":"19 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"VPS13B maintains lysosomal homeostasis through regulation of TFEB.","authors":"Soo-Kyeong Lee, Semin Park, Min-Young Yeom, Jin-A Lee","doi":"10.1186/s13041-026-01309-y","DOIUrl":"https://doi.org/10.1186/s13041-026-01309-y","url":null,"abstract":"<p><p>Cohen syndrome (CS) is a rare autosomal recessive neurodevelopmental disorder characterized by intellectual disability, microcephaly, retinal dystrophy, and neutropenia. We previously demonstrated that VPS13B mediates phosphatidylinositol 4-phosphate (PI4P) transport to promote mitochondrial fission. Here, we identify VPS13B as a regulator of lysosomal homeostasis. VPS13B knockout (KO) HeLa cells exhibited aberrant lysosomal distribution and reduction in LAMP1-positive lysosomes. Bulk RNA sequencing revealed coordinated downregulation of lysosome-related genes, including genes required for acidification and lysosome biogenesis, which was confirmed by quantitative RT-PCR. Consistent with these transcriptional changes, VPS13B KO significantly reduced the abundance of LysoTracker-positive acidic compartments. Induced neurons derived from CS patient iPSCs recapitulated the loss of acidic lysosomal compartments, supporting disease relevance. Mechanistically, VPS13B KO altered TFEB mRNA levels and modestly increased the basal nuclear-to-cytoplasmic (N/C) ratio of endogenous TFEB, but blunted its further increase upon Torin1 treatment. Together, these findings identify VPS13B as a regulator of lysosomal homeostasis and provide insight into how VPS13B deficiency may contribute to Cohen syndrome pathology.</p>","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An alternative inhibitory avoidance task for studying hippocampus-dependent spatial aversive memory in mice.","authors":"Haiyan Wang, Masanori Nomoto, Emi Murayama, Kaori Yamada-Nomoto, Kaoru Inokuchi","doi":"10.1186/s13041-026-01308-z","DOIUrl":"https://doi.org/10.1186/s13041-026-01308-z","url":null,"abstract":"<p><p>In natural environments, animals must navigate to goals while avoiding　potential danger, making adaptive route choice crucial for survival. However, behavioral tasks for quantitatively evaluating avoidance through route choice during spatial navigation remain limited in mice, and the neural mechanisms underlying experience-dependent updating of route choice remain incompletely understood. Here, we established an air puff-based alternative inhibitory avoidance (AIA) task in mice to examine how aversive experience modifies a previously learned route preference. Water-restricted mice were first trained for 3 consecutive days to prefer a short path for obtaining water reward. They were then trained to avoid this preferred short path by receiving an air puff at its center when they passed through it. Mice that received only 3 air puffs showed lower avoidance behavior at the 6-h memory test. In contrast, mice that continued to receive air puffs until they rarely selected the short path during training showed significantly stronger avoidance at the 6-h test, and this avoidance was also observed at the 24-h test. We next examined whether hippocampal activity is required for retrieval of aversive memory in the AIA task. Chemogenetic suppression of hippocampal activity 30 min before the 6-h test impaired retrieval of aversive memory. Together, these results indicate that the AIA task provides a useful behavioral paradigm for assessing experience-dependent changes in route choice based on aversive events in mice, and that retrieval of this spatial aversive memory depends on hippocampal activity.</p>","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147817729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive protein synthesis inhibition impairs natural and artificial memory recall.","authors":"Yeonjun Kim, Ilgang Hong, Bong-Kiun Kaang","doi":"10.1186/s13041-026-01305-2","DOIUrl":"https://doi.org/10.1186/s13041-026-01305-2","url":null,"abstract":"<p><p>Protein synthesis is critical for long-lasting memory formation and synaptic plasticity. However, whether protein synthesis is required for artificially evoked memory retrieval remains debated. To address this, we used a translation-inhibitor cocktail (CKT; anisomycin and cycloheximide) to achieve a more comprehensive blockade of protein synthesis compared to more commonly used anisomycin alone (ANI). When administered immediately after memory acquisition, ANI impaired natural recall while still showing preserved artificial recall. In contrast, CKT treatment showed significant impairment in both natural and artificial recall. Together, these results provide additional evidence that de novo protein synthesis is required for both natural and artificial memory recall.</p>","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impaired phrenic nerve axon development and diaphragm neuromuscular junction formation in embryonic Cyfip2-null mice.","authors":"Su Yeon Kim, Jun Young Oh, U Suk Kim, Ruiying Ma, Yoonhee Kim, Kihoon Han","doi":"10.1186/s13041-026-01301-6","DOIUrl":"10.1186/s13041-026-01301-6","url":null,"abstract":"<p><p>Pathogenic variants in CYFIP2 cause developmental and epileptic encephalopathy 65 (DEE65) and have been predominantly investigated in the context of central nervous system dysfunction. However, emerging clinical evidence suggests that peripheral nervous system (PNS) involvement may also contribute to disease manifestations. To explore this possibility, we examined the role of CYFIP2 in the development of the phrenic neuromuscular system, which is essential for neonatal respiration. Because conventional Cyfip2-null (Cyfip2^-/-) mice exhibit perinatal lethality, we analyzed phrenic nerve axon development and diaphragm neuromuscular junction (NMJ) formation in embryonic mice. At embryonic day 16.5, Cyfip2^-/- embryos displayed significantly reduced phrenic nerve axon length and branching compared to wild-type controls. Postsynaptic acetylcholine receptor (AChR) clustering in Cyfip2^-/- diaphragms showed spatial heterogeneity: sparse regions exhibited a significant increase in endplate bandwidth, whereas dense regions showed a decreasing trend. Further analysis using synaptophysin and α-bungarotoxin labeling revealed reduced pre- and post-synaptic puncta density and decreased colocalization, despite preserved puncta intensity and volume, indicating impaired synaptic organization. Together, these findings demonstrate that CYFIP2 is required for proper phrenic nerve innervation and NMJ organization during embryonic development. This study extends the functional scope of CYFIP2 to the PNS and establishes the diaphragm as a tractable model for investigating peripheral mechanisms underlying CYFIP2-associated neurodevelopmental disorders.</p>","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":"19 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13130780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome-wide mapping of stress-responsive lncRNA, uc.104, reveals the chromatin-mediated regulation of stress and plasticity-related genes in the hippocampus of chronic restraint rats.","authors":"Anuj K Verma, Bhaskar Roy, Kevin Prall, Ellie Hulwi, Yogesh Dwivedi","doi":"10.1186/s13041-026-01304-3","DOIUrl":"https://doi.org/10.1186/s13041-026-01304-3","url":null,"abstract":"<p><p>Chronic stress significantly impacts hippocampal function through transcriptional and epigenetic mechanisms. While the roles of lncRNAs in stress-related transcriptional and epigenetic regulation have recently been recognized, their genome-wide functions controlling the transcriptional network remain largely unclear. Evidence indicates that the lncRNA uc.104 is involved in stress responses; however, its genome-wide chromatin interactions and gene regulatory effects are yet to be explored. To examine this, we combined chromatin isolation by RNA purification sequencing (ChIRP-seq) and RNA sequencing (RNA-seq) in the hippocampus from handled control and chronic restraint stress (CRS) rats. ChIRP-seq identified 6,664 uc.104 binding peaks under CRS, including 6,517 enriched and 149 reduced. Many peaks were mapped to intronic and promoter-proximal regions of protein-coding genes. Integration of ChIRP-seq with RNA-seq data revealed 1,839 differentially expressed genes associated with uc.104 binding sites, with 106 high-confidence overlaps. Several genes (Gabra3, Htr7, Irs1, Gpr37, Clu, Hspa1b, Ppp3r2, Nfasc, Pcdhac2, and Cysltr2) identified as regulatory targets of uc.104, have been directly implicated in stress responses, synaptic plasticity, and neuroinflammation. Gene ontology and Synapse GO (SynGO) analyses revealed significant enrichment for processes involving dendritic spine formation, synapse organization, and pre- and postsynaptic signaling. Protein-protein interaction analysis identified hub genes, including EGFR, CDC42, IGF1R, CTNNB1, CALM1, CALM3, POLR2A, MDM2, TBP, and CSNK1E, several of which have been linked to stress-responsive pathways. Together, our findings reveal that uc.104 binding to chromatin near stress- and synapse-related genes may act as a regulator of stress-responsive transcriptional networks in the hippocampus. By linking uc.104 occupancy to stress and synaptic responsive genes, this study highlights uc.104 as a potential mediator of stress-induced hippocampal malfunctions.</p>","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147723428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thalamic homeostatic transcriptomic signatures are altered in a mouse model of cholestatic liver injury and are mitigated by systemic TNF neutralization.","authors":"Wagdi Almishri, Jeff F Dunn, Mark G Swain","doi":"10.1186/s13041-026-01302-5","DOIUrl":"10.1186/s13041-026-01302-5","url":null,"abstract":"<p><p>Cholestatic liver diseases (CLD), including PBC and PSC, are frequently associated with debilitating sickness‑behavior symptoms such as fatigue, cognitive impairment, and anxiety/depression, which have poorly defined etiology and limited treatment options, substantially reducing quality of life. Across immune‑mediated diseases, thalamic changes have been well documented and found to correlate with a number of theses symptoms. Changes in thalamic structure and neural connectivity have been previously identified in PBC patients by us and other groups. These changes include findings indicating reduced tissue neuronal density and myelination, decreased thalamic size, and changes in functional neural connectivity between the thalamus and basal ganglia and cortical behavior-regulating areas that correlated with symptom severity. These observations implicate altered thalamic structure and function in the genesis of CLD-related sickness‑behavior symptoms. Therefore, we used a well characterized mouse model of CLD due to bile duct ligation (BDL) to mechanistically examine how CLD impacts thalamic structure and function. BDL mice showed reduced thalamic volume compared to sham-ligated controls, as determined by MRI, and an altered thalamic RNA-seq transcriptomic signature with predicted molecular activity consistent with inhibition of cellular growth, proliferation, neurite formation, neural function, and myelination, as well as enhanced apoptosis. Additionally, BDL was associated with changes in gene expression for key thalamic nervous system signaling pathways that regulate neurotransmission and behavior. We have previously demonstrated that systemic TNF is a key regulator of liver-to-brain communication and the development of adverse behavioral symptoms in BDL mice. Therefore, we administered anti-TNF antibody to neutralize systemic TNF in BDL mice and determined the impact on thalamic transcriptomic changes. TNF neutralization attenuated BDL-associated thalamic transcriptomic changes and enhanced gene expression in pathways regulating neurotransmission, cell proliferation, and those associated with neuron survival, although myelination pathways remained unaltered. We show that reduced thalamic volume in BDL mice is associated with transcriptomic alterations suggesting inhibition of structural machinery and dysfunction of neural signaling; findings that are significantly attenuated after systemic TNF neutralization. Our findings suggest that TNF inhibition may represent a potential novel approach to attenuate thalamic changes in CLD.</p>","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147717327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered ECM deposition and cell adhesion signaling in a human cortical organoid model of fragile X syndrome.","authors":"Sapir Havusha-Laufer, Venkat Raghavan Krishnaswamy, Noy Krugliak-Shechter, Anjana Shenoy, Maayan Karlinski Zur, Liron Kuznitsov-Yanovsky, Inna Solomonov, Jacob H Hanna, Irit Sagi, Dalit Ben Yosef","doi":"10.1186/s13041-026-01280-8","DOIUrl":"https://doi.org/10.1186/s13041-026-01280-8","url":null,"abstract":"<p><p>Fragile X Syndrome (FXS) is the most common inherited intellectual disability, and the most common monogenic cause of autism spectrum disorder (ASD). It is caused by epigenetic silencing of the FMR1 gene leading to the loss of FMRP, an RNA-binding protein that regulates local mRNA translation in neuronal dendrites, crucial for synapse development. Three-dimensional (3D) brain organoid models derived through in vitro differentiation of pluripotent stem cells offer a powerful tool to dissect the underlying mechanisms of neurodevelopmental disorders. Here, we generated human FXS and control organoids using isogenic human embryonic stem cell clones with and without the FXS mutation. Our results show that mature FXS cortical brain organoids can be derived by inhibiting the TGFβ and Wnt pathways. Moreover, expression analyses including immunofluorescence, qRT-PCR, proteomics and western blotting reveal altered levels of neuronal markers and ECM deposition along with modulated downstream signaling molecules. Interestingly, in silico analysis of proteomics revealed several altered pathways, such as cell adhesion, regulation of neurogenesis and cell cycle that are implicated in FXS. Collectively, our unique FXS-organoids derived from isogenic hESC lines may serve as a model for studying the pathology of FXS disorder and for developing therapeutical intervention.</p>","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147691028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FCHO1 fine-tunes synaptic vesicle endocytosis in an activity-dependent manner.","authors":"Hyun Jung Lee, Wongyoung Lee, Sung Hyun Kim","doi":"10.1186/s13041-026-01295-1","DOIUrl":"https://doi.org/10.1186/s13041-026-01295-1","url":null,"abstract":"<p><p>Synaptic vesicle (SV) recycling is critical for sustaining neurotransmission. Although FCHO1, a protein containing both an F-BAR domain and a μ-homology (μ-HD) domain, is recognized as a nucleator of clathrin-mediated endocytosis in non-neuronal systems, its physiological role at synapses remains unclear. Here, we investigated the function of FCHO1 in SV endocytosis at central synapses using a combination of shRNA-mediated knockdown and pHluorin-based live imaging. Within defined stimulation paradigms (25-300 action potentials at 10 Hz), depletion of FCHO1 markedly slowed endocytic kinetics across all stimulation intensities and was fully rescued by re-expression of an shRNA-resistant construct. Domain-specific functional analyses revealed stimulation-strength-dependent functional requirements. The F-BAR domain was sufficient to support vesicle retrieval under low stimulation conditions, whereas the μ-homology domain (μ-HD) became essential as stimulation strength increased. These findings support a model in which FCHO1 operates as a demand-sensitive scaffold within the endocytic pathway, with distinct structural domains differentially required as neural activity and consequently endocytic load escalates. Our results establish FCHO1 as a critical regulator of SV endocytosis and suggest that multidomain endocytic proteins may scale their functional contributions according to the magnitude of neuronal activation.</p>","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147628160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hippocampal transcriptome profiling in a 22q11.2 deletion syndrome mouse model: comparison with human schizophrenia.","authors":"Hinano Yonemaru, Takaaki Ozawa, Takatoshi Hikida","doi":"10.1186/s13041-026-01300-7","DOIUrl":"https://doi.org/10.1186/s13041-026-01300-7","url":null,"abstract":"<p><p>22q11.2 deletion syndrome (22q11.2DS) confers one of the highest genetic risks for schizophrenia, yet the molecular mechanisms remain incompletely understood. We performed comprehensive RNA sequencing of the dorsal hippocampus in Df1/+ mice, a 22q11.2DS model, integrating behavioral assessment and cross-species comparison with human schizophrenia postmortem data. Df1/+ mice exhibited selective contextual fear memory impairment without gross locomotor deficits. Transcriptomic analysis using integrated over-representation and gene set enrichment approaches revealed upregulation of synaptic signaling pathways, including glutamatergic and GABAergic neurotransmission, alongside downregulation of translational machinery and ribosomal proteins. Top upregulated pathways included \"regulation of postsynaptic membrane potential\" and \"postsynapse organization,\" featuring glutamatergic receptors, voltage-gated channels, and synaptic adhesion molecules. Downregulated pathways centered on protein synthesis, including cytoplasmic translation and ribosome biogenesis. Cross-species comparison with human schizophrenia hippocampus revealed limited but directionally consistent gene-level overlap, with 21 of 23 shared differentially expressed genes showing concordant regulation. \"Regulation of postsynaptic membrane potential\" was the pathway significantly enriched across both species and analytical methods, encompassing both excitatory and inhibitory receptor subunits and synaptic regulators. Concordantly downregulated genes spanned glial markers and extracellular matrix components. These findings reveal a molecular signature of enhanced synaptic gene expression coupled with reduced translational capacity and glial support, with cross-species correspondence supporting the model's translational relevance and highlighting excitatory-inhibitory imbalance as a shared mechanism in hippocampal dysfunction underlying schizophrenia.</p>","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}