Neuropathology最新文献

{"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":1.3,"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":"Atypical Histopathological Findings in an Epilepsy Surgery Case of Sturge-Weber Syndrome With Coexisting Developmental Venous Anomaly.","authors":"Jumpei Abe, Tomonori Ono, Ryoko Honda, Shiro Miura, Masahiro Ito, Yasuji Yoshida, Hajime Miyata","doi":"10.1111/neup.70045","DOIUrl":"10.1111/neup.70045","url":null,"abstract":"<p><p>Leptomeningeal angiomatosis (LMA) in Sturge-Weber syndrome (SWS) typically presents with cortical calcifications on computed tomography (CT) scans and is often accompanied by enlarged, low-signal deep medullary veins seen on susceptibility-weighted magnetic resonance imaging (MRI) that lack flow-void signs on T2-weighted MRI. However, subcortical calcifications on CT and concurrent developmental venous anomaly (DVA), visible as deep medullary veins with prominent flow-void signs on T2-weighted MRI, are uncommon. We describe atypical clinicopathological features in a surgical case of a 6-year-old female patient with SWS, who had early-onset intractable epilepsy due to LMA, complicated by subcortical calcifications and DVA on neuroimaging. Presurgical MRI revealed a hypoplastic left frontal lobe covered with an LMA, and a DVA extending from the ipsilateral frontal periventricular white matter to the deep middle cerebral vein. She underwent resection of the left central and prefrontal regions and remained seizure-free postoperatively. Histopathology confirmed the presence of an LMA, dilated veins in the subcortical white matter, focal microscopic polymicrogyria, and cortical pseudolaminar sclerosis consistent with focal cortical dysplasia type IIIc. Four atypical findings were observed: (1) absent or minimal cortical calcifications; (2) clearly defined areas of fibrillary gliosis bordered by a linear band of prominent calcifications, encasing non-dilated veins in the subcortical white matter; (3) a localized cortical venous malformation; and (4) subarachnoid arterial abnormalities, including fibromuscular intimal thickening, internal elastic lamina degeneration, irregular medial thickness, and segmental medial losses replaced by dense calcifications. These findings, considered in the context of the intrinsic cerebral venous system, suggest that the non-dilated white matter veins encased by calcified gliosis represent superficial medullary veins, while the dilated veins correspond with deep medullary veins draining into the DVA. The latter possibly serve as collateral venous drainage pathways, compensating for abnormal cortical and subarachnoid venous development. The observed arterial abnormalities likely reflect secondary regressive changes.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":"46 1","pages":"e70045"},"PeriodicalIF":1.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146065625","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":"Immunohistochemical Analysis of Tom20 in Choroid Plexus Epithelial Cells From Elderly Brains With Neurodegenerative Diseases.","authors":"Ryuta Murakami, Yoichi Chiba, Yumi Miyai, Koichi Matsumoto, Keiji Wakamatsu, Yuko Saito, Manato Hara, Shigeo Murayama, Masaki Ueno","doi":"10.1111/neup.70042","DOIUrl":"10.1111/neup.70042","url":null,"abstract":"<p><p>The choroid plexus (CP) contributes to cerebrospinal fluid (CSF) production and regulation of circadian rhythm. Recently, many neuroimaging studies have reported enlarged CP volumes in patients with neurodegenerative diseases, including Alzheimer's disease (AD). While previous morphometric analysis revealed age-related enlargement of CP epithelial cells, the metabolic significance of such morphological changes including eosinophilic enlarged changes remains unclear. In this study, we investigated mitochondrial alterations in CP epithelial cells using immunohistochemistry for Tom20, a marker of the mitochondrial outer membrane. Temporal lobes, including CP, in patients with AD, vascular dementia, Parkinson's disease, and multiple system atrophy, and neuropathologically unremarkable controls were examined. Quantitative image analysis was performed using AI-assisted segmentation (cellpose) and Python-based processing (OpenCV, NumPy, and Pandas). Cell area and the proportion of Tom20-positive pixels (brown ratio) were measured in 13 090 epithelial cells from 20 cases, and data were analyzed using Spearman's rank correlation. The brown ratio was positively correlated with cell area. Enlarged epithelial cells frequently exhibited strong Tom20 immunoreactivity. These findings suggest that cellular enlargement in the CP epithelium is accompanied by increased mitochondrial content, highlighting a potential metabolic response in neurodegenerative brains.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":"46 1","pages":"e70042"},"PeriodicalIF":1.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12823287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146019160","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":"Malignant Craniopharyngioma With Features Resembling Ghost Cell Odontogenic Carcinoma: A Case Report and Histopathology Literature Review.","authors":"Sompon Apornvirat, Pitchayanant Laemad, Bhannaporn Limsuksrikul, Phirasit Chaijitrawan, Putch Phairintr, Raywat Noiphithak","doi":"10.1111/neup.70043","DOIUrl":"10.1111/neup.70043","url":null,"abstract":"<p><p>Malignant transformation of craniopharyngioma is an exceptionally rare and poorly characterized phenomenon. We report a case of a 15-year-old girl who developed symptom recurrence 9 years after undergoing surgery and radiotherapy for adamantinomatous craniopharyngioma. Histology revealed malignant areas comprising highly proliferative basaloid cells with abrupt transitions into ghost cells, resembling ghost cell odontogenic carcinoma. We conducted a literature review and pooled case analysis of 45 cases, which showed a median benign-to-malignant latency of 10 years and a median overall survival of 9 months. The majority of benign diagnoses were adamantinomatous type. Prior radiotherapy was noted in 27 cases (60%). Histological findings of malignant components were reported as unspecified malignant transformation in 20 cases (44.4%), squamous cell carcinoma (SCC) in 16 cases (35.6%), odontogenic-type carcinomas in 5 cases (11.1%), and other types in 4 cases (8.9%). Immunohistochemical analyses showed consistent positivity for pan-cytokeratin, p63, and p40 in all cases performed. The p53 and Ki-67 also consistently exhibited increased or abnormal expression. Due to the overlapping histological and immunohistochemical features of odontogenic-type carcinomas and SCC, careful assessment is recommended when diagnosing recurrent CPs.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":"46 1","pages":"e70043"},"PeriodicalIF":1.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145998682","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":"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":"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":1.3,"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}