Neuropathology最新文献

{"title":"Transferrin Receptor 1 Overexpression Drives Proliferation and Ferroptosis Sensitivity in Glioblastoma: A Potential Therapeutic Vulnerability.","authors":"Minakshi M Behera, Suvendu Purkait, Amit Ghosh, Mukund N Sable, Rabi Narayan Sahu, Gaurav Chhabra","doi":"10.1111/neup.70056","DOIUrl":"https://doi.org/10.1111/neup.70056","url":null,"abstract":"<p><p>Glioblastoma (GBM) is an aggressive CNS malignancy with extensive tumor growth and invasion. Highly proliferating cells require an increased intracellular iron concentration to maintain cell metabolism. We assessed the expression of transferrin receptor 1 (TFR1), the principal iron transporter, in GBM and ascertained its clinicopathological significance, implication in pathobiology, and therapeutic potential. Ninety-four cases of adult-type hemispheric GBM were included, along with 60 cases of IDH-mutant astrocytic and oligodendroglial tumors (grade 2-4) for comparison. The protein and mRNA expression were assessed by immunohistochemistry and qRT-PCR, respectively. We used U87MG and LN229 cell lines for in vitro analysis. TFR1 expression was significantly higher in GBM than in other IDH-mutant/lower-grade diffuse gliomas at mRNA and protein level. The non-tumor brain was negative on immunohistochemistry, and strong immunoreactivity was present only in GBM, indicating its diagnostic significance. SiRNA-mediated knockdown of TFR1 was associated with reduced cell survival, proliferation, migration, invasion, and increased apoptosis in vitro. Ferroptosis induction by RSL3/FIN56 led to increased TFR1 expression and ROS generation. The pro-ferroptotic effect of these drugs could be reversed by TFR1 knockdown. Hence, TFR1 appears to be crucially implicated in the cell survival and proliferation and ferroptosis sensitivity of malignant cells. Temozolomide in combination with siRNA-mediated gene silencing showed a significantly higher antitumor effect than the drug or silencing alone. This may be one of the important therapeutic vulnerabilities of GBM. High TFR1 expression was associated with shorter overall survival in all gliomas together but not in GBM separately.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":"46 2","pages":"e70056"},"PeriodicalIF":1.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147618782","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":"DNA Virus Detection in Olfactory Neuroblastomas Using Targeted Enrichment NGS.","authors":"Maria K Jauhiainen, Outi I Mielonen, Aaro Haapaniemi, Maria Söderlund-Venermo, Jaana Hagström, Maria F Perdomo, Saku T Sinkkonen, Antti A Mäkitie","doi":"10.1111/neup.70055","DOIUrl":"10.1111/neup.70055","url":null,"abstract":"<p><p>A variety of malignancies can be found in the sinonasal tract including the nasal cavity, paranasal sinuses, and skull base. Many of these are attributed to viruses, for example, carcinomas with the presence of transcriptionally active high-risk human papillomavirus, as well as Epstein-Barr virus associated malignant lymphoepithelial carcinoma and haematolymphoid neoplasias. Olfactory neuroblastoma (ONB) is a rare malignant tumor of the olfactory fossa with an unknown etiology. We present the first comprehensive virus study of ONB. By targeted next-generation sequencing for 41 DNA viruses, we investigated the presence of papillomaviruses, herpesviruses, polyomaviruses, and parvoviruses, among others, in 12 ONBs. In addition, herpesvirus presence was evaluated by qPCR. Low-risk HPV6 was detected in one sample. Human endogenous retroviruses were positive in all samples, supporting successful library preparation and sequencing, considered as an internal quality control. No other virus findings were observed. The present broad-scale virus study did not reveal abundant presence of viral DNA in ONB suggesting a limited viral role in its etiology. Nevertheless, our cohort exhibited a finding of low-risk HPV, which has been associated with increased risk of cancer progression of inverted sinonasal papilloma in the same anatomic site advocating for further research. Trial Registration: §31/07.03.2019.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":"46 2","pages":"e70055"},"PeriodicalIF":1.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13011989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504350","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":"An Autopsy Case of a Patient With Corticobasal Degeneration and a History of Acute Restlessness and Stupor.","authors":"Saori Shimizu, Yuji Saitoh, Masashi Mizutani, Terunori Sano, Naoko Satake, Noriko Sato, Masaki Takao","doi":"10.1111/neup.70057","DOIUrl":"10.1111/neup.70057","url":null,"abstract":"<p><p>Some patients with corticobasal degeneration (CBD) present with neuropsychiatric symptoms, including frontal lobe symptoms. However, stupor is rarely reported. Here, we report a case of acute restlessness at onset, which was clinically diagnosed as frontotemporal dementia (FTD) but was found to be CBD at autopsy. A 71-year-old woman with COVID-19 presented to our hospital. At the age of 62, she had suddenly become restless and confused without any preceding motor or psychiatric symptoms. She was treated with psychotropic drugs but subsequently entered stupor and was admitted to a psychiatric hospital. Magnetic resonance imaging showed mild atrophy of the frontal lobe. Single-photon emission computed tomography showed decreased blood flow in the frontal lobe, and the patient was clinically diagnosed with FTD. At the age of 71, she was transferred to our hospital from a psychiatric hospital for COVID-19 treatment. Upon transfer to our hospital, the patient presented with akinetic mutism. The patient died of respiratory failure 10 days after the onset of COVID-19. Immunostaining with AT8 and RD4 antibodies revealed astrocytic plaques, pretangles, coiled bodies, and threads, predominantly in the frontal lobes and basal ganglia. Other pathologies include accumulation of pTDP43 in the basal ganglia, thalamus, and frontal lobes. Argyrophilic grains were observed in the amygdala and the hippocampus, which corresponded to Saito stage 2. Other neurodegenerative proteins, such as amyloid β or α-synuclein, were not observed. The patient was pathologically diagnosed with CBD. We present a rare autopsy case involving a patient with CBD who presented with acute psychiatric symptoms and stupor. The psychiatric symptoms were characterized by agitation and fear-related behavior, which differ from the disinhibition and antisocial behavior typically associated with frontal lobe symptoms. Further autopsies are needed to examine the extent of tau pathology spread and accumulation to better understand the psychiatric symptoms of CBD.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":"46 2","pages":"e70057"},"PeriodicalIF":1.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147691335","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":"Pleiotrophin/Midkine Pathway Is Dysregulated in a TDP-43^A315T Mouse Model of Amyotrophic Lateral Sclerosis (ALS).","authors":"Paloma Martínez-Alesón, Cristina Benito-Casado, Carmen María Fernández-Martos, María José Polanco Mora","doi":"10.1111/neup.70044","DOIUrl":"10.1111/neup.70044","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease (MND) characterized by progressive degeneration of both upper and lower motor neurons, along with skeletal muscles innervated by them. The identification of key molecules involved in disease pathology remains crucial for ALS, as no curative treatment is currently available. Pleiotrophin (PTN) and midkine (MK) are closely related, heparin-binding cytokines with overlapping effects. These molecules have been shown to be neuroprotective by modulating neuroinflammation, supporting neuronal survival, growth, and differentiation, and enhancing synaptic strength and plasticity. Despite their reported neuroprotective properties, the involvement of PTN and MK signaling in ALS has not been previously investigated. In this study, we characterized the expression of the PTN/MK pathway in the lumbar spinal cords (SCs) of TDP-43^A315T mice across different disease stages. We report a significant upregulation of Ptn, Mdk, and its receptor protein tyrosine phosphatase zeta (Ptprz1) mRNA levels at end-stage of disease in the lumbar SC of TDP-43^A315T mice compared with age-matched wild-type littermates. Protein levels of PTN and MK were also upregulated at end-stage of disease. By immunofluorescence analysis, we also observed an upregulation of the immunostaining of both cytokines in neurons, astrocytes, microglia, and pericytes-like structures at end-stage of disease in the SC of TDP-43^A315T mice. These findings open a new avenue to further study the potential role of the PTN/MK signaling axis in the pathogenesis of ALS. Trial Registration: Animal Ethics Committee of the Hospital Nacional de Parapléjicos in Toledo (Spain): Approval No. 26/OH 2018.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":"46 1","pages":"e70044"},"PeriodicalIF":1.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12851830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146093055","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":"Phospho-MLKL Upregulation in Immune-Mediated Necrotizing Myopathy: Implications for Disease Pathophysiology and Diagnosis.","authors":"Mingshi Gao, Nachuan Cheng, Dongyue Yue, Zhangyang Wang, Bochen Zhu, Chong Yan, Jie Song, Chong Sun, Jianying Xi, Sushan Luo, Yanyin Zhao, Chongbo Zhao, Wenhua Zhu","doi":"10.1111/neup.70046","DOIUrl":"https://doi.org/10.1111/neup.70046","url":null,"abstract":"<p><p>Immune-mediated necrotizing myopathy (IMNM) is a subtype of idiopathic inflammatory myopathies (IIMs) characterized by severe muscle weakness and refractory response to immunotherapy. Recent studies proposed a role for necroptosis in IMNM-associated myonecrosis. This study aims to investigate the potential diagnostic value of phospho-mixed lineage kinase domain-like protein (pMLKL), the executive molecule of necroptosis, for IMNM. Sero-positive and -negative IMNM patients and various myopathies with myonecrosis diagnosed in Huashan Hospital during October 2020 to October 2022 were enrolled in this study. Comprehensive immunohistochemical staining including pMLKL was performed. The spatial distribution of pMLKL was assessed by qualitative and semi-quantitative scoring. Upregulation of pMLKL on sarcolemma was seen in both IIMs and non-IIMs (nIIMs) with distinct spatial patterns and varying positive rates. In IMNM and nIIM, it radiates outward from the center of myonecrosis and is upregulated on the surrounding non-necrotic myofibers, while in dermatomyositis, it is extensively upregulated around microinfarcts but not expressed within them. IMNM patients showed a 93.48% pMLKL expression rate, surpassing other IIMs (50%) and nIIMs (47.9%) (p < 0.0001). The concurrent upregulation and colocalization of pMLKL, MHC-I, and MAC on non-necrotic myofibers lack consistency. The frequent upregulation of pMLKL in IMNM suggests a potential correlation between necroptosis and the etiology as well as progression of IMNM. Nevertheless, its upregulated expression across diverse myopathic conditions attenuates its efficacy as a diagnostic myopathological biomarker for IMNM.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":"46 1","pages":"e70046"},"PeriodicalIF":1.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100301","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":"An Autopsy Case of ALS Which Clinically Presented Sporadic Adult-Onset Lower Motor Neuron Disease and Genetically Had p. Leu127Ser (L126S) Variant in SOD1 and SMN2 Deletion.","authors":"Kimiko Inoue, Harutoshi Fujimura, Kayo Ueda, Hisahide Nishio, Hiroya Naruse, Yuishin Izumi","doi":"10.1111/neup.70032","DOIUrl":"10.1111/neup.70032","url":null,"abstract":"<p><p>Herein, we report an autopsy case of sporadic amyotrophic lateral sclerosis (ALS) with a p. L127S (L126S) SOD1 variant, SMN2 deletion and one hybrid SMN. A 43-year-old Japanese man noticed muscle weakness in his left lower extremity. At the age of 51, his muscle strength was moderately diminished in the upper extremities and severely in the lower extremities with hyporeflexia. At the age of 55, he started noninvasive intermittent ventilation (NIV) during nighttime. At the age of 57, he developed dysphagia and died of pneumonia. The total clinical course was 14 years and 8 months (13 years 9 months until NIV). Pathologically we found severe loss of lower motor neurons, moderate neuronal loss in Clarke's nuclei and mild grumose degeneration of the dentate nucleus. The primary motor cortex was well preserved and the pyramidal tracts showed vague myelin pallor in the lumbar cord. There were a few conglomerate hyaline inclusions (CHIs) that were negative for Bodian staining. Immunohistochemically, CHIs were positive for phosphorylated neurofilament (pNF) and were stained with Uq and SOD1 to varying degrees. Some CHIs contained granular-like components positive for p62. A post-mortem genetic test revealed that the patient had 2 copies of SMN1, 0 copies of SMN2, and one hybrid gene with exon 1 to 7 of SMN2 and SMN1 exon 8. Additional gene research elucidated a heterozygous SOD1 p. Leu127Ser (L126S) mutation. Compared to previous reports of ALS with the same mutation, the distribution of degenerative lesions was similar. It has been suggested that SMN2 deletion may not be directly implicated in lower motor neuron pathology, but further research is needed to confirm this. Further accumulation of cases is necessary to determine the effect of SMN2 on SOD1-ALS.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":"45 6","pages":"e70032"},"PeriodicalIF":1.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145523913","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":"MYB Alterations in Angiocentric Gliomas.","authors":"Isabela Peña Pino, A Yohan Alexander, Sanjay Dhawan, Samuel W Cramer, William E Butler, Darby Bedell, Liam L Chen, Andrew S Venteicher","doi":"10.1111/neup.70036","DOIUrl":"10.1111/neup.70036","url":null,"abstract":"<p><p>We performed a systematic review of the literature to better define the scope of MYB alterations in angiocentric glioma and their associated clinical characteristics, as well as to include a novel MYB mutation in an angiocentric glioma case. We also review MYB alterations in the context of oncologic disease. Following PRISMA guidelines, we searched PubMed and Web of Science for relevant literature from 2010 to October 2024. Included articles reported original data on human subjects with angiocentric glioma and a detected MYB mutation. We include one additional angiocentric glioma case showcasing a novel MYB mutation. A total of 14 studies met the inclusion criteria, with a total of 114 patients with individual data for pooled analysis. The mean age was 10.3 years (SD ±9.7 years); 60% of patients were male. MYB::QKI was the most common fusion in 68% of patients. Other MYB mutations included MYB rearrangements, MYB::ESR1, MYB::PCDHGA1, MYB::LOC105378099, and MYB::MMP16. The most common anatomical location was in the cerebral cortex in 68% of patients. MYB fusions in other relevant neuro-oncologic diseases highlight the importance of MYB fusions in adenoid cystic carcinomas, which frequently occur at the skull base, head and neck, and breast. In conclusion, we characterize the breadth of angiocentric glioma patterns in terms of demographics, anatomic location, and MYB fusion patterns. The updated molecular diagnosis of angiocentric glioma as of 2021 warrants continued exploration of the scope of MYB oncogene fusions as drivers of prognosis and targets for future therapies.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":"45 6","pages":"e70036"},"PeriodicalIF":1.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145557551","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":"Embryonal tumor with multilayered rosettes, DICER1-mutated, showing histologically unique neuronal differentiation after chemoradiotherapy.","authors":"Ayako Yamazaki, Chikako Kiyotani, Kimikazu Matsumoto, Takako Yoshioka, Hideaki Yokoo, Junko Hirato, Sumihito Nobusawa","doi":"10.1111/neup.13027","DOIUrl":"10.1111/neup.13027","url":null,"abstract":"<p><p>Embryonal tumors with multilayered rosettes (ETMRs) are rare and highly aggressive embryonal central nervous system tumors that predominantly affect infants younger than 3 years old. These tumors typically have a C19MC alteration (ETMR, C19MC-altered) or, more rarely, a DICER1 mutation (ETMR, DICER1-mutated). Post-chemotherapeutic or post-chemoradiotherapeutic histological changes of C19MC-altered ETMRs, such as maturation or loss of histological characteristics of ETMR have been described in several reports. However, histological changes of recurrent DICER1-mutated ETMRs have not been reported to date. Herein, we report a case of DICER1-mutated ETMR with unique post-treatment morphological changes, including both maturation and loss of histological characteristics. Although pathological examination of tissue from the first resection revealed typical ETMR histology, the recurrent tumor after chemoradiotherapy was composed predominantly of a primitive embryonal component without multilayered rosettes or neuropil-like areas. Furthermore, the recurrent tumor contained a component composed of unique tumor cells with oval eccentric nuclei and eosinophilic cytoplasm demonstrating a neuronal immunohistohemical phenotype. No mitotic figures were found in the component. Molecular analysis identified a mutation in the DICER1 RNase IIIb domain in the primary tumor and the primitive embryonal component of the recurrent tumor, but not in the unique neuronal area.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"e13027"},"PeriodicalIF":1.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142983751","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":"Astroblastoma With MN1::BEND2 Fusion Showing an Atypical Signal Pattern in MN1 Break-Apart FISH: A Potential Diagnostic Pitfall.","authors":"Takahiro Shirakura, Noriaki Sakamoto, Yasuhito Arai, Natsuko Hama, Hiroyoshi Kino, Haruna Okuno, Ayako Yamazaki, Nozomi Matsumura, Hideaki Yokoo, Tatsuhiro Shibata, Sumihito Nobusawa, Eiichi Ishikawa","doi":"10.1111/neup.70010","DOIUrl":"10.1111/neup.70010","url":null,"abstract":"","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"e70010"},"PeriodicalIF":1.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079163","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":"An autopsy case of coexisting spinal and bulbar muscular atrophy and multiple system atrophy.","authors":"Motoki Miura, Hiroshi Shintaku, Yoshiyuki Numasawa, Kokoro Ozaki, Tadashi Kanouchi, Kinya Ishikawa, Takanori Yokota","doi":"10.1111/neup.13031","DOIUrl":"10.1111/neup.13031","url":null,"abstract":"<p><p>Here, we report an autopsy case of concurrent spinal and bulbar muscular atrophy (SBMA) and multiple system atrophy (MSA). A 55-year-old man presented with weakness, atrophy, and fasciculation of the tongue and the proximal parts of all limbs. The patient gradually developed severe orthostatic hypotension, urinary retention, and cerebellar ataxia; however, no parkinsonism was observed. The patient succumbed to sudden death during sleep. The autopsy revealed widespread and abundant α-synuclein-positive glial cytoplasmic inclusions in the central nervous system, indicative of MSA. Neuronal loss was also observed in the substantia nigra and locus coeruleus. Consequently, the patient was diagnosed with MSA. Additionally, immunostaining for the monoclonal 1C2 antibody revealed positive neurons in the medulla oblongata and spinal cord, supporting the additional diagnosis of SBMA. Genetic analysis revealed an expansion of 41 CAG repeats in the androgen receptor (AR) gene (normal range: 12-38), confirming the diagnosis of SBMA. Altogether, concurrent SBMA and MSA were diagnosed based on the autopsy findings, making this the first reported case of such coexistence in the Japanese and English literature.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"e13031"},"PeriodicalIF":1.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143365303","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}