Molecular Brain最新文献_第4页

Visualization of the existence of growth hormone secretagogue receptor in the rat nucleus accumbens. 大鼠脑核中生长激素分泌受体的可视化。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-06-13 DOI: 10.1186/s13041-024-01109-2

Seohyeon Lee, Wen Ting Cai, Hyung Shin Yoon, Jeong-Hoon Kim

引用次数: 0

Adolescent chemogenetic activation of dopaminergic neurons leads to reversible decreases in amphetamine-induced stereotypic behavior. 青春期化学基因激活多巴胺能神经元会导致苯丙胺诱导的刻板行为可逆性减少。

IF 3.6 3区医学

Molecular Brain Pub Date : 2024-06-11 DOI: 10.1186/s13041-024-01110-9

Muhammad O Chohan, Amy B Lewandowski, Rebecca N Siegel, Kally C O'Reilly, Jeremy Veenstra-VanderWeele

{"title":"Adolescent chemogenetic activation of dopaminergic neurons leads to reversible decreases in amphetamine-induced stereotypic behavior.","authors":"Muhammad O Chohan, Amy B Lewandowski, Rebecca N Siegel, Kally C O'Reilly, Jeremy Veenstra-VanderWeele","doi":"10.1186/s13041-024-01110-9","DOIUrl":"10.1186/s13041-024-01110-9","url":null,"abstract":"Chronic perturbations of neuronal activity can evoke homeostatic and new setpoints for neurotransmission. Using chemogenetics to probe the relationship between neuronal cell types and behavior, we recently found reversible decreases in dopamine (DA) transmission, basal behavior, and amphetamine (AMPH) response following repeated stimulation of DA neurons in adult mice. It is unclear, however, whether altering DA neuronal activity via chemogenetics early in development leads to behavioral phenotypes that are reversible, as alterations of neuronal activity during developmentally sensitive periods might be expected to induce persistent effects on behavior. To examine the impact of developmental perturbation of DA neuron activity on basal and AMPH behavior, we expressed excitatory hM3D(Gq) in postnatal DA neurons in TH-Cre and WT mice. Basal and CNO- or AMPH-induced locomotion and stereotypy was evaluated in a longitudinal design, with clozapine N-oxide (CNO, 1.0 mg/kg) administered across adolescence (postnatal days 15-47). Repeated CNO administration did not impact basal behavior and only minimally reduced AMPH-induced hyperlocomotor response in adolescent TH-CrehM3Dq mice relative to WThM3Dq littermate controls. Following repeated CNO administration, however, AMPH-induced stereotypic behavior robustly decreased in adolescent TH-CrehM3Dq mice relative to controls. A two-month CNO washout period rescued the diminished AMPH-induced stereotypic behavior. Our findings indicate that the homeostatic compensations that take place in response to chronic hM3D(Gq) stimulation during adolescence are temporary and are dependent on ongoing chemogenetic stimulation.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11165814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141301056","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}

引用次数: 0

Exploration of new space elicits phosphorylation of GluA1(Ser831) and S6K and expression of Arc in the hippocampus in vivo as in long-term potentiation. 探索新空间会引起 GluA1（Ser831）和 S6K 的磷酸化，以及体内海马中 Arc 的表达，这与长期电位一样。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-06-10 DOI: 10.1186/s13041-024-01100-x

Roberta Cagnetta, Jean-Claude Lacaille, Nahum Sonenberg

{"title":"Exploration of new space elicits phosphorylation of GluA1(Ser831) and S6K and expression of Arc in the hippocampus in vivo as in long-term potentiation.","authors":"Roberta Cagnetta, Jean-Claude Lacaille, Nahum Sonenberg","doi":"10.1186/s13041-024-01100-x","DOIUrl":"10.1186/s13041-024-01100-x","url":null,"abstract":"The brain responds to experience through modulation of synaptic transmission, that is synaptic plasticity. An increase in the strength of synaptic transmission is manifested as long-term potentiation (LTP), while a decrease in the strength of synaptic transmission is expressed as long-term depression (LTD). Most of the studies of synaptic plasticity have been carried out by induction via electrophysiological stimulation. It is largely unknown in which behavioural tasks such synaptic plasticity occurs. Moreover, some stimuli can induce both LTP and LTD, thus making it difficult to separately study the different forms of synaptic plasticity. Two studies have shown that an aversive memory task - inhibitory avoidance learning and contextual fear conditioning - physiologically and selectively induce LTP and an LTP-like molecular change, respectively, in the hippocampus in vivo. Here, we show that a non-aversive behavioural task - exploration of new space - physiologically and selectively elicits a biochemical change in the hippocampus that is a hallmark of LTP. Specifically, we found that exploration of new space induces an increase in the phosphorylation of GluA1(Ser831), without affecting the phosphorylation of GluA1(Ser845), which are biomarkers of early-LTP and not NMDAR-mediated LTD. We also show that exploration of new space engenders the phosphorylation of the translational regulator S6K and the expression of Arc, which are features of electrophysiologically-induced late-LTP in the hippocampus. Therefore, our results show that exploration of new space is a novel non-aversive behavioural paradigm that elicits molecular changes in vivo that are analogous to those occurring during early- and late-LTP, but not during NMDAR-mediated LTD.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11165848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141301084","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}

引用次数: 0

Globus pallidus is not independent from striatal direct pathway neurons: an up-to-date review. 苍白球并非独立于纹状体直接通路神经元：最新综述。

IF 3.6 3区医学

Molecular Brain Pub Date : 2024-06-07 DOI: 10.1186/s13041-024-01107-4

Fumino Fujiyama, Fuyuki Karube, Yasuharu Hirai

{"title":"Globus pallidus is not independent from striatal direct pathway neurons: an up-to-date review.","authors":"Fumino Fujiyama, Fuyuki Karube, Yasuharu Hirai","doi":"10.1186/s13041-024-01107-4","DOIUrl":"10.1186/s13041-024-01107-4","url":null,"abstract":"Striatal projection neurons, which are classified into two groups-direct and indirect pathway neurons, play a pivotal role in our understanding of the brain's functionality. Conventional models propose that these two pathways operate independently and have contrasting functions, akin to an \"accelerator\" and \"brake\" in a vehicle. This analogy further elucidates how the depletion of dopamine neurons in Parkinson's disease can result in bradykinesia. However, the question arises: are these direct and indirect pathways truly autonomous? Despite being distinct types of neurons, their interdependence cannot be overlooked. Single-neuron tracing studies employing membrane-targeting signals have shown that the majority of direct pathway neurons terminate not only in the output nuclei, but also in the external segment of the globus pallidus (GP in rodents), a relay nucleus of the indirect pathway. Recent studies have unveiled the existence of arkypallidal neurons, which project solely to the striatum, in addition to prototypic neurons. This raises the question of which type of GP neurons receive these striatal axon collaterals. Our morphological and electrophysiological experiments showed that the striatal direct pathway neurons may affect prototypic neurons via the action of substance P on neurokinin-1 receptors. Conversely, another research group has reported that direct pathway neurons inhibit arkypallidal neurons via GABA. Regardless of the neurotransmitter involved, it can be concluded that the GP is not entirely independent of direct pathway neurons. This review article underscores the intricate interplay between different neuronal pathways and challenges the traditional understanding of their independence.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11157709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141288331","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}

引用次数: 0

TDP43 interacts with MLH1 and MSH6 proteins in a DNA damage-inducible manner TDP43 以 DNA 损伤诱导的方式与 MLH1 和 MSH6 蛋白相互作用

IF 3.6 3区医学

Molecular Brain Pub Date : 2024-06-05 DOI: 10.1186/s13041-024-01108-3

Vincent E. Provasek, Manohar Kodavati, Brandon Kim, Joy Mitra, Muralidhar L. Hegde

{"title":"TDP43 interacts with MLH1 and MSH6 proteins in a DNA damage-inducible manner","authors":"Vincent E. Provasek, Manohar Kodavati, Brandon Kim, Joy Mitra, Muralidhar L. Hegde","doi":"10.1186/s13041-024-01108-3","DOIUrl":"https://doi.org/10.1186/s13041-024-01108-3","url":null,"abstract":"Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that affects the motor neuron. One aspect of the neuropathology involved in ALS includes increased genomic damage and impaired DNA repair capability. The TAR-DNA binding protein 43 (TDP43) has been associated with both sporadic and familial forms of ALS, and is typically observed as cytosolic mislocalization of protein aggregates, termed TDP43 proteinopathy. TDP43 is a ubiquitous RNA/DNA binding protein with functional implications in a wide range of disease processes, including the repair of DNA double-strand breaks (DSBs). While TDP43 is widely known to regulate RNA metabolism, our lab has reported it also functions directly at the protein level to facilitate DNA repair. Here, we show that the TDP43 protein interacts with DNA mismatch repair (MMR) proteins MLH1 and MSH6 in a DNA damage-inducible manner. We utilized differentiated SH-SY5Y neuronal cultures to identify this inducible relationship using complementary approaches of proximity ligation assay (PLA) and co-immunoprecipitation (CoIP) assay. We observed that signals of TDP43 interaction with MLH1 and MSH6 increased significantly following a 2 h treatment of 10 μM methylmethanesulfonate (MMS), a DNA alkylating agent used to induce MMR repair. Likewise, we observed this effect was abolished in cell lines treated with siRNA directed against TDP43. Finally, we demonstrated these protein interactions were significantly increased in lumbar spinal cord samples of ALS-affected patients compared to age-matched controls. These results will inform our future studies to understand the mechanisms and consequences of this TDP43-MMR interaction in the context of ALS-affected neurons.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141258831","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}

引用次数: 0

Dendritic spine head diameter is reduced in the prefrontal cortex of progranulin haploinsufficient mice 单倍体基因缺陷小鼠前额叶皮层树突棘头直径减小

IF 3.6 3区医学

Molecular Brain Pub Date : 2024-06-05 DOI: 10.1186/s13041-024-01095-5

Anna K. Cook, Kelsey M. Greathouse, Phaedra N. Manuel, Noelle H. Cooper, Juliana M. Eberhardt, Cameron D. Freeman, Audrey J. Weber, Jeremy H. Herskowitz, Andrew E. Arrant

{"title":"Dendritic spine head diameter is reduced in the prefrontal cortex of progranulin haploinsufficient mice","authors":"Anna K. Cook, Kelsey M. Greathouse, Phaedra N. Manuel, Noelle H. Cooper, Juliana M. Eberhardt, Cameron D. Freeman, Audrey J. Weber, Jeremy H. Herskowitz, Andrew E. Arrant","doi":"10.1186/s13041-024-01095-5","DOIUrl":"https://doi.org/10.1186/s13041-024-01095-5","url":null,"abstract":"Loss-of-function mutations in the progranulin (GRN) gene are an autosomal dominant cause of Frontotemporal Dementia (FTD). These mutations typically result in haploinsufficiency of the progranulin protein. Grn+/– mice provide a model for progranulin haploinsufficiency and develop FTD-like behavioral abnormalities by 9–10 months of age. In previous work, we demonstrated that Grn+/– mice develop a low dominance phenotype in the tube test that is associated with reduced dendritic arborization of layer II/III pyramidal neurons in the prelimbic region of the medial prefrontal cortex (mPFC), a region key for social dominance behavior in the tube test assay. In this study, we investigated whether progranulin haploinsufficiency induced changes in dendritic spine density and morphology. Individual layer II/III pyramidal neurons in the prelimbic mPFC of 9–10 month old wild-type or Grn+/– mice were targeted for iontophoretic microinjection of fluorescent dye, followed by high-resolution confocal microscopy and 3D reconstruction for morphometry analysis. Dendritic spine density in Grn+/– mice was comparable to wild-type littermates, but the apical dendrites in Grn+/– mice had a shift in the proportion of spine types, with fewer stubby spines and more thin spines. Additionally, apical dendrites of Grn+/– mice had longer spines and smaller thin spine head diameter in comparison to wild-type littermates. These changes in spine morphology may contribute to altered circuit-level activity and social dominance deficits in Grn+/– mice.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141258859","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}

引用次数: 0

Chronic unpredictable stress induces autophagic death of adult hippocampal neural stem cells. 慢性不可预测压力诱导成体海马神经干细胞自噬死亡

IF 3.6 3区医学

Molecular Brain Pub Date : 2024-06-03 DOI: 10.1186/s13041-024-01105-6

Seongwon Choe, Hyeonjeong Jeong, Jieun Choi, Seong-Woon Yu

引用次数: 0

Hypothalamic protein profiling from mice subjected to social defeat stress. 社会挫败应激小鼠下丘脑蛋白质图谱分析

IF 3.6 3区医学

Molecular Brain Pub Date : 2024-05-27 DOI: 10.1186/s13041-024-01096-4

Shiladitya Mitra, Ghantasala S Sameer Kumar, Anumita Samanta, Mathias V Schmidt, Suman S Thakur

{"title":"Hypothalamic protein profiling from mice subjected to social defeat stress.","authors":"Shiladitya Mitra, Ghantasala S Sameer Kumar, Anumita Samanta, Mathias V Schmidt, Suman S Thakur","doi":"10.1186/s13041-024-01096-4","DOIUrl":"10.1186/s13041-024-01096-4","url":null,"abstract":"The Hypothalmic-Pituitary-Adrenal axis also known as the HPA axis is central to stress response. It also acts as the relay center between the body and the brain. We analysed hypothalamic proteome from mice subjected to chronic social defeat paradigm using iTRAQ based quantitative proteomics to identify changes associated with stress response. We identified greater than 2000 proteins after processing our samples analysed through Q-Exactive (Thermo) and Orbitrap Velos (Thermo) at 5% FDR. Analysis of data procured from the runs showed that the proteins whose levels were affected belonged primarily to mitochondrial and metabolic processes, translation, complement pathway among others. We also found increased levels of fibrinogen, myelin basic protein (MBP) and neurofilaments (NEFL, NEFM, NEFH) in the hypothalamus from socially defeated mice. Interestingly, research indicates that these proteins are upregulated in blood and CSF of subjects exposed to trauma and stress. Since hypothalamus secreted proteins can be found in blood and CSF, their utility as biomarkers in depression holds an impressive probability and should be validated in clinical samples.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11131206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141158287","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}

引用次数: 0

S100 proteins: a new frontier in fibromyalgia research. S100 蛋白：纤维肌痛研究的新前沿。

IF 3.6 3区医学

Molecular Brain Pub Date : 2024-05-26 DOI: 10.1186/s13041-024-01102-9

María Teresa Vega-Ramírez, Enrique Becerril-Villanueva, José Luis Maldonado-García, Lenin Pavón, Gilberto Pérez-Sánchez

{"title":"S100 proteins: a new frontier in fibromyalgia research.","authors":"María Teresa Vega-Ramírez, Enrique Becerril-Villanueva, José Luis Maldonado-García, Lenin Pavón, Gilberto Pérez-Sánchez","doi":"10.1186/s13041-024-01102-9","DOIUrl":"10.1186/s13041-024-01102-9","url":null,"abstract":"Fibromyalgia (FM) is a chronic condition that causes widespread pain, fatigue, and other symptoms that significantly affect quality of life. The underlying mechanisms of fibromyalgia involve both the immune system and the central nervous system. It has been proposed that changes in multiple ascending and descending pathways in the central nervous system may contribute to increased pain sensitivity in individuals with this condition. Recent research has identified S100 proteins as a new area of interest in fibromyalgia studies. These proteins are a group of small molecular weight proteins involved in inflammation and various functions inside and outside of cells, and they may play a critical role in the development and progression of FM. Although S100B has been the most studied in FM patients, other studies have reported that S100A7, S100A8, S100A9, and S100A12 may also be useful as potential biomarkers or for a deeper understanding of FM pathophysiology. The potential role of S100 proteins in the pathophysiology of fibromyalgia could be mediated by RAGE and TLR4, which signal through JNK, ERK, and p38 to activate AP-1 and NF-κB and induce the release of proinflammatory cytokines, thereby producing the inflammation, fatigue, and chronic pain characteristic of fibromyalgia. To gain new perspectives on targeted therapeutic approaches, it is crucial to understand how S100 proteins could impact the pathophysiology of fibromyalgia. This review examines the potential role of S100 proteins in fibromyalgia and their impact on improving our comprehension of the condition, as well as facilitating further research on this interesting topic.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11129469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141154091","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}

引用次数: 0

A novel mouse model for investigating α-synuclein aggregates in oligodendrocytes: implications for the glial cytoplasmic inclusions in multiple system atrophy. 研究少突胶质细胞中α-突触核蛋白聚集体的新型小鼠模型：对多发性系统萎缩中胶质细胞质内含物的影响。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-05-24 DOI: 10.1186/s13041-024-01104-7

Tomoyuki Ishimoto, Miki Oono, Seiji Kaji, Takashi Ayaki, Katsuya Nishida, Itaru Funakawa, Takakuni Maki, Shu-Ichi Matsuzawa, Ryosuke Takahashi, Hodaka Yamakado

{"title":"A novel mouse model for investigating α-synuclein aggregates in oligodendrocytes: implications for the glial cytoplasmic inclusions in multiple system atrophy.","authors":"Tomoyuki Ishimoto, Miki Oono, Seiji Kaji, Takashi Ayaki, Katsuya Nishida, Itaru Funakawa, Takakuni Maki, Shu-Ichi Matsuzawa, Ryosuke Takahashi, Hodaka Yamakado","doi":"10.1186/s13041-024-01104-7","DOIUrl":"10.1186/s13041-024-01104-7","url":null,"abstract":"The aggregated alpha-synuclein (αsyn) in oligodendrocytes (OLGs) is one of the pathological hallmarks in multiple system atrophy (MSA). We have previously reported that αsyn accumulates not only in neurons but also in OLGs long after the administration of αsyn preformed fibrils (PFFs) in mice. However, detailed spatial and temporal analysis of oligodendroglial αsyn aggregates was technically difficult due to the background neuronal αsyn aggregates. The aim of this study is to create a novel mouse that easily enables sensitive and specific detection of αsyn aggregates in OLGs and the comparable analysis of the cellular tropism of αsyn aggregates in MSA brains. To this end, we generated transgenic (Tg) mice expressing human αsyn-green fluorescent protein (GFP) fusion proteins in OLGs under the control of the 2', 3'-cyclic nucleotide 3'-phosphodiesterase (CNP) promoter (CNP-SNCAGFP Tg mice). Injection of αsyn PFFs in these mice induced distinct GFP-positive aggregates in the processes of OLGs as early as one month post-inoculation (mpi), and their number and size increased in a centripetal manner. Moreover, MSA-brain homogenates (BH) induced significantly more oligodendroglial αsyn aggregates than neuronal αsyn aggregates compared to DLB-BH in CNP-SNCAGFP Tg mice, suggestive of their potential tropism of αsyn seeds for OLGs. In conclusion, CNP-SNCAGFP Tg mice are useful for studying the development and tropism of αsyn aggregates in OLGs and could contribute to the development of therapeutics targeting αsyn aggregates in OLGs.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11127389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141093765","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}

引用次数: 0