Journal of neurogenetics最新文献

{"title":"A quick and versatile protocol for the 3D visualization of transgene expression across the whole body of larval <i>Drosophila</i>.","authors":"Oliver Kobler,&nbsp;Aliće Weiglein,&nbsp;Kathrin Hartung,&nbsp;Yi-Chun Chen,&nbsp;Bertram Gerber,&nbsp;Ulrich Thomas","doi":"10.1080/01677063.2021.1892096","DOIUrl":"https://doi.org/10.1080/01677063.2021.1892096","url":null,"abstract":"<p><p>Larval <i>Drosophila</i> are used as a genetically accessible study case in many areas of biological research. Here we report a fast, robust and user-friendly procedure for the whole-body multi-fluorescence imaging of <i>Drosophila</i> larvae; the protocol has been optimized specifically for larvae by systematically tackling the pitfalls associated with clearing this small but cuticularized organism. Tests on various fluorescent proteins reveal that the recently introduced monomeric infrared fluorescent protein (mIFP) is particularly suitable for our approach. This approach comprises an effective, low-cost clearing protocol with minimal handling time and reduced toxicity in the reagents employed. It combines a success rate high enough to allow for small-scale screening approaches and a resolution sufficient for cellular-level analyses with light sheet and confocal microscopy. Given that publications and database documentations typically specify expression patterns of transgenic driver lines only within a given organ system of interest, the present procedure should be versatile enough to extend such documentation systematically to the whole body. As examples, the expression patterns of transgenic driver lines covering the majority of neurons, or subsets of chemosensory, central brain or motor neurons, are documented in the context of whole larval body volumes (using nsyb-Gal4, IR76b-Gal4, APL-Gal4 and mushroom body Kenyon cells, or OK371-Gal4, respectively). Notably, the presented protocol allows for triple-color fluorescence imaging with near-infrared, red and yellow fluorescent proteins.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":" ","pages":"306-319"},"PeriodicalIF":1.9,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/01677063.2021.1892096","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25451945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conditioned courtship suppression in <i>Drosophila melanogaster</i>.","authors":"Nicholas Raun,&nbsp;Spencer Jones,&nbsp;Jamie M Kramer","doi":"10.1080/01677063.2021.1873323","DOIUrl":"https://doi.org/10.1080/01677063.2021.1873323","url":null,"abstract":"<p><p><i>Drosophila melanogaster</i> males reduce courtship behaviour after mating failure. In the lab, such conditioned courtship suppression, aka 'courtship conditioning', serves as a complex learning and memory assay. Interestingly, variations in the courtship conditioning assay can establish different types of memory. Here, we review research investigating the underlying cellular and molecular mechanisms that allow male flies to form memories of previous mating failures.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":" ","pages":"154-167"},"PeriodicalIF":1.9,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/01677063.2021.1873323","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25317301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Women in science: a daughter's perspective.","authors":"H Moriah Sokolowski","doi":"10.1080/01677063.2021.1940168","DOIUrl":"https://doi.org/10.1080/01677063.2021.1940168","url":null,"abstract":"<p><p>In the first grade, in one of my first classes, my teacher read us a story about a scientist. To my utter shock, the scientist was a man. After the story, I asked the teacher, 'can men be scientists?' She looked at me, bewildered, and replied: 'of course, anyone can be a scientist.' It was not until later that my teacher learned that my mother is a scientist, and the only scientists I had ever met were women, like me.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":" ","pages":"101-103"},"PeriodicalIF":1.9,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/01677063.2021.1940168","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39252510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of mGluR1-LTD following cocaine exposure accumulates Ca²⁺-permeable AMPA receptors and facilitates synaptic potentiation in the prefrontal cortex.","authors":"Hongyu Ruan,&nbsp;Wei-Dong Yao","doi":"10.1080/01677063.2021.1931180","DOIUrl":"https://doi.org/10.1080/01677063.2021.1931180","url":null,"abstract":"<p><p>Addiction results from drug-elicited alterations of synaptic plasticity mechanisms in dopaminergic reward circuits. Impaired metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD) and accumulation of synaptic Ca²⁺-permeable AMPA receptors (CP-AMPARs) following drug exposure have emerged as important mechanisms underlying drug craving and relapse. Here we show that repeated cocaine exposure in vivo causes transient but complete loss of mGluR1- and mTOR (mammalian target of rapamycin)-dependent LTD in layer 5 pyramidal neurons of mouse prefrontal cortex (PFC), a major dopaminergic target in the reward circuitry. This mGluR1-LTD impairment was prevented by in vivo administration of an mGluR1 positive allosteric modulator (PAM) and rescued by inhibition of dopamine D1 receptors, suggesting that impaired mGluR1 tone and excessive D1 signaling underlie this LTD deficit. Concurrently, CP-AMPARs were generated, indicated by increased sensitivity to the CP-AMPAR inhibitor Naspm and rectification of synaptic AMPAR currents, which were reversed by PAM in cocaine-exposed mice. Finally, these CP-AMPARs mediate an abnormal spike-timing-dependent long-term potentiation enabled by cocaine exposure. Our findings reveal a mechanism by which cocaine impairs LTD and remodels synaptic AMPARs to influence Hebbian plasticity in the PFC. Failure to undergo LTD may prevent the reversal of drug-potentiated brain circuits to their baseline states, perpetuating addictive behaviors.HIGHLIGHTSA mGluR1- and mTOR-dependent LTD is present in the mouse medial prefrontal cortex.Repeated cocaine exposure <i>in vivo</i> temporally but completely abolishes prefrontal mGluR1-LTD.Impaired mGluR1 function and excessive D1 DA signaling likely underlie cocaine impairment of mGluR1-LTD.Ca²⁺-permeable AMPA receptors are generated by cocaine exposure, likely resulting from mGluR1-LTD impairment, and contribute to a cocaine-induced extended spike timing LTP.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"35 4","pages":"358-369"},"PeriodicalIF":1.9,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/01677063.2021.1931180","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10441038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Forty years of foraging research: a legacy of scientists trained and influenced by Marla Sokolowski.","authors":"Ina Anreiter,&nbsp;Jeffrey S Dason","doi":"10.1080/01677063.2021.1960518","DOIUrl":"https://doi.org/10.1080/01677063.2021.1960518","url":null,"abstract":"Figure 1. Marla Sokolowski. A, as a graduate student at the University of Toronto in 1978. B, at York University (Assistant Professor) in 1987. C, with John Heddle, receiving the Young Scientist Award from the Genetics Society of Canada, 1993. D, with Allen Sokolowski (husband), 1985. E, at York University (Full Professor), circa 1994. F, at University of Toronto St. George campus (University Professor), 2011. G, at Moriah Sokolowski’s (daughter) wedding, 2019.","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":" ","pages":"341-350"},"PeriodicalIF":1.9,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39433962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spontaneous motor-behavior abnormalities in two <i>Drosophila</i> models of neurodevelopmental disorders.","authors":"David R Andrew,&nbsp;Mariah E Moe,&nbsp;Dailu Chen,&nbsp;Judith A Tello,&nbsp;Rachel L Doser,&nbsp;William E Conner,&nbsp;Jaswinder K Ghuman,&nbsp;Linda L Restifo","doi":"10.1080/01677063.2020.1833005","DOIUrl":"https://doi.org/10.1080/01677063.2020.1833005","url":null,"abstract":"<p><p>Mutations in hundreds of genes cause neurodevelopmental disorders with abnormal motor behavior alongside cognitive deficits. Boys with fragile X syndrome (FXS), a leading monogenic cause of intellectual disability, often display repetitive behaviors, a core feature of autism. By direct observation and manual analysis, we characterized spontaneous-motor-behavior phenotypes of <i>Drosophila dfmr1</i> mutants, an established model for FXS. We recorded individual 1-day-old adult flies, with mature nervous systems and prior to the onset of aging, in small arenas. We scored behavior using open-source video-annotation software to generate continuous activity timelines, which were represented graphically and quantitatively. Young <i>dfmr1</i> mutants spent excessive time grooming, with increased bout number and duration; both were rescued by transgenic wild-type <i>dfmr1⁺</i>. By two grooming-pattern measures, <i>dfmr1</i>-mutant flies showed elevated repetitions consistent with perseveration, which is common in FXS. In addition, the mutant flies display a preference for grooming posterior body structures, and an increased rate of grooming transitions from one site to another. We raise the possibility that courtship and circadian rhythm defects, previously reported for <i>dfmr1</i> mutants, are complicated by excessive grooming. We also observed significantly increased grooming in <i>CASK</i> mutants, despite their dramatically decreased walking phenotype. The mutant flies, a model for human <i>CASK</i>-related neurodevelopmental disorders, displayed consistently elevated grooming indices throughout the assay, but transient locomotory activation immediately after placement in the arena. Based on published data identifying FMRP-target transcripts and functional analyses of mutations causing human genetic neurodevelopmental disorders, we propose the following proteins as candidate mediators of excessive repetitive behaviors in FXS: CaMKIIα, NMDA receptor subunits 2A and 2B, NLGN3, and SHANK3. Together, these fly-mutant phenotypes and mechanistic insights provide starting points for drug discovery to identify compounds that reduce dysfunctional repetitive behaviors.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"35 1","pages":"1-22"},"PeriodicalIF":1.9,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/01677063.2020.1833005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38583553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"De novo mutation in <i>SLC25A22</i> gene: expansion of the clinical and electroencephalographic phenotype.","authors":"Antonio Gennaro Nicotera,&nbsp;Daniela Dicanio,&nbsp;Erica Pironti,&nbsp;Maria Bonsignore,&nbsp;Anna Cafeo,&nbsp;Stephanie Efthymiou,&nbsp;Patrizia Mondello,&nbsp;Vincenzo Salpietro,&nbsp;Henry Houlden,&nbsp;Gabriella Di Rosa","doi":"10.1080/01677063.2021.1892094","DOIUrl":"https://doi.org/10.1080/01677063.2021.1892094","url":null,"abstract":"<p><p>The <i>SLC25A22</i> (Solute Carrier Family 25, Member 22) gene encodes for a mitochondrial glutamate/H⁺ symporter and is involved in the mitochondrial transport of metabolites across the mitochondrial membrane. We hereby report a 12-year-old girl presenting with early-onset epileptic encephalopathy, hypotonia, and global developmental delay. Whole exome sequencing identified a novel homozygous missense mutation in <i>SLC25A22</i> gene (c.97A>G; p.Lys33Glu), as the likely cause of the disease. The phenotype of our patient and EEG recordings do not completely overlap with the phenotypes previously described, leading to a new and more complex form of disease associated with <i>SLC25A22</i> variants, characterized by dyskinetic movements and oculogyric crisis.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"35 2","pages":"67-73"},"PeriodicalIF":1.9,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/01677063.2021.1892094","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25563588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Change in gene expression levels of GABA, glutamate and neurosteroid pathways due to acoustic trauma in the cochlea.","authors":"Meltem Cerrah Gunes,&nbsp;Murat Salih Gunes,&nbsp;Alperen Vural,&nbsp;Fatma Aybuga,&nbsp;Arslan Bayram,&nbsp;Keziban Korkmaz Bayram,&nbsp;Mehmet Ilhan Sahin,&nbsp;Muhammet Ensar Dogan,&nbsp;Sevda Yesim Ozdemir,&nbsp;Yusuf Ozkul","doi":"10.1080/01677063.2021.1904922","DOIUrl":"https://doi.org/10.1080/01677063.2021.1904922","url":null,"abstract":"<p><p>The characteristic feature of noise-induced hearing loss (NIHL) is the loss or malfunction of the outer hair cells (OHC) and the inner hair cells (IHC) of the cochlea. 90-95% of the spiral ganglion neurons, forming the cell bodies of cochlear nerve, synapse with the IHCs. Glutamate is the most potent excitatory neurotransmitter for IHC-auditory nerve synapses. Excessive release of glutamate in response to acoustic trauma (AT), may cause excitotoxicity by causing damage to the spiral ganglion neurons (SGN) or loss of the spiral ganglion dendrites, post-synaptic to the IHCs. Another neurotransmitter, GABA, plays an important role in the processing of acoustic stimuli and central regulation after peripheral injury, so it is potentially related to the regulation of hearing function and sensitivity after noise. The aim of this study is to evaluate the effect of AT on the expressions of glutamate excitotoxicity, GABA inhibition and neurosteroid synthesis genes.We exposed 24 BALB/c mice to AT. Controls were sacrificed without exposure to noise, Post-AT(1) and Post-AT(15) were sacrificed on the 1st and 15th day, respectively, after noise exposure. The expressions of various genes playing roles in glutamate, GABA and neurosteroid pathways were compared between groups by real-time PCR.Expressions of <i>Cyp11a1</i>, <i>Gls</i>, <i>Gabra1</i>, <i>Grin2b</i>, <i>Sult1a1</i>, <i>Gad1,</i> and <i>Slc1a2</i> genes in Post-AT(15) mice were significantly decreased in comparison to control and Post-AT(1) mice. No significant differences in the expression of <i>Slc6a1</i> and <i>Slc17a8</i> genes was detected.These findings support the possible role of balance between glutamate excitotoxicity and GABA inhibition is disturbed during the post AT days and also the synthesis of some neurosteroids such as pregnenolone sulfate may be important in this balance.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"35 1","pages":"45-57"},"PeriodicalIF":1.9,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/01677063.2021.1904922","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25568122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Description of clinical features and genetic analysis of one ultra-rare (SPG64) and two common forms (SPG5A and SPG15) of hereditary spastic paraplegia families.","authors":"Mahdieh Pashaei,&nbsp;Atefeh Davarzani,&nbsp;Reza Hajati,&nbsp;Babak Zamani,&nbsp;Shahriar Nafissi,&nbsp;Farzaneh Larti,&nbsp;Yalda Nilipour,&nbsp;Mohammad Rohani,&nbsp;Afagh Alavi","doi":"10.1080/01677063.2021.1895146","DOIUrl":"https://doi.org/10.1080/01677063.2021.1895146","url":null,"abstract":"<p><p>Hereditary spastic paraplegia (HSP) is a clinically and genetically heterogeneous neurodegenerative disorder, characterized by lower-limb spasticity and weakness. To date, more than 82 loci/genes (SPG1-SPG82) have been identified that contribute to the cause of HSP. Despite the use of next-generation sequencing-based methods, genetic-analysis has failed in the finding of causative genes in more than 50% of HSP patients, indicating a more significant heterogeneity and absence of a given phenotype-genotype correlation. Here, we performed whole-exome sequencing (WES) to identify HSP-causing genes in three unrelated-Iranian probands. Candidate variants were detected and confirmed in the probands and co-segregated in the family members. The phenotypic data gathered and compared with earlier cases with the same sub-types of disease. Three novel homozygous variants, c.978delT; p.Q327Kfs*39, c.A1208G; p.D403G and c.3811delT; p.S1271Lfs*44, in known HSP-causing genes including <i>ENTPD1</i>, <i>CYP7B1</i>, and <i>ZFYVE26</i> were identified, respectively. Intra and interfamilial clinical variability were observed among affected individuals. Mutations in <i>CYP7B1</i> and <i>ZFYVE26</i> are relatively common causes of HSP and associated with SPG5A and SPG15, respectively. However, mutations in <i>ENTPD1</i> are related to SPG64 which is an ultra-rare form of HSP. The research affirmed more complexities of phenotypic manifestations and allelic heterogeneity in HSP. Due to these complexities, it is not feasible to show a clear phenotype-genotype correlation in HSP cases. Identification of more families with mutations in HSP-causing genes may help the establishment of this correlation, further understanding of the molecular basis of the disease, and would provide an opportunity for genetic-counseling in these families.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"35 2","pages":"84-94"},"PeriodicalIF":1.9,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/01677063.2021.1895146","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25520610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Compound heterozygous <i>KCTD7</i> variants in progressive myoclonus epilepsy.","authors":"Elizabeth A Burke,&nbsp;Morgan Sturgeon,&nbsp;Diane B Zastrow,&nbsp;Liliana Fernandez,&nbsp;Cameron Prybol,&nbsp;Shruti Marwaha,&nbsp;Edward P Frothingham,&nbsp;Patricia A Ward,&nbsp;Christine M Eng,&nbsp;Laure Fresard,&nbsp;Stephen B Montgomery,&nbsp;Gregory M Enns,&nbsp;Paul G Fisher,&nbsp;Lynne A Wolfe,&nbsp;Brian Harding,&nbsp;Blake Carrington,&nbsp;Kevin Bishop,&nbsp;Raman Sood,&nbsp;Yan Huang,&nbsp;Abdel Elkahloun,&nbsp;Camilo Toro,&nbsp;Alexander G Bassuk,&nbsp;Matthew T Wheeler,&nbsp;Thomas C Markello,&nbsp;William A Gahl,&nbsp;May Christine V Malicdan","doi":"10.1080/01677063.2021.1892095","DOIUrl":"https://doi.org/10.1080/01677063.2021.1892095","url":null,"abstract":"<p><p>KCTD7 is a member of the potassium channel tetramerization domain-containing protein family and has been associated with progressive myoclonic epilepsy (PME), characterized by myoclonus, epilepsy, and neurological deterioration. Here we report four affected individuals from two unrelated families in which we identified <i>KCTD7</i> compound heterozygous single nucleotide variants through exome sequencing. RNAseq was used to detect a non-annotated splicing junction created by a synonymous variant in the second family. Whole-cell patch-clamp analysis of neuroblastoma cells overexpressing the patients' variant alleles demonstrated aberrant potassium regulation. While all four patients experienced many of the common clinical features of PME, they also showed variable phenotypes not previously reported, including dysautonomia, brain pathology findings including a significantly reduced thalamus, and the lack of myoclonic seizures. To gain further insight into the pathogenesis of the disorder, zinc finger nucleases were used to generate <i>kctd7</i> knockout zebrafish. <i>Kctd7</i> homozygous mutants showed global dysregulation of gene expression and increased transcription of <i>c-fos</i>, which has previously been correlated with seizure activity in animal models. Together these findings expand the known phenotypic spectrum of <i>KCTD7</i>-associated PME, report a new animal model for future studies, and contribute valuable insights into the disease.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":"35 2","pages":"74-83"},"PeriodicalIF":1.9,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/01677063.2021.1892095","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38967602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}