Neuropathology最新文献

{"title":"Blood-brain barrier dysfunction in multiple system atrophy: A human postmortem study.","authors":"Ramil Gabdulkhaev, Hiroshi Shimizu, Masato Kanazawa, Yasuko Kuroha, Arika Hasegawa, Jiro Idezuka, Kazuki Tainaka, Osamu Onodera, Akiyoshi Kakita","doi":"10.1111/neup.13021","DOIUrl":"10.1111/neup.13021","url":null,"abstract":"<p><p>Multiple system atrophy (MSA) is a rare neurodegenerative disease characterized by an accumulation of phosphorylated α-synuclein (p-αsyn) in oligodendrocytes in the form of glial cytoplasmic inclusions (GCIs). In MSA, not only mature oligodendrocytes but also oligodendrocyte precursor cells (OPCs) are affected. The latter play an important role in remyelination by differentiating into mature oligodendrocytes, as well as maintaining the blood-brain barrier (BBB) by promoting the expression of tight junction proteins. We have hypothesized that in MSA, the BBB is impaired as a result of aberrant interactions between affected OPCs and the cerebral vasculature. To verify this hypothesis, we conducted a neuropathological examination of postmortem brains from MSA patients and control subjects, focusing on the primary motor area, one of the main regions affected in MSA. Using double immunofluorescence, we quantified the expression of tight junction protein claudin-5 in capillary endothelial cells and found that it was significantly lower in MSA than in controls in both the gray matter and white matter. Furthermore, a significantly higher amount of fibrinogen was extravasated into the brain parenchyma in MSA patients than in controls. In addition, leakage of IgG was detected almost specifically in MSA brain parenchyma, as visualized in three dimensions by combining techniques of chemical tissue clearing and light sheet microscopy. Finally, we confirmed accumulation of p-αsyn-positive GCIs along the cerebral vasculature within OPCs. These results suggest that BBB dysfunction and associated fibrinogen extravasation are constant findings in MSA, presumably triggered by the deposition of p-αsyn in perivascular OPCs.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"210-222"},"PeriodicalIF":1.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813781","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":"Solitary fibrous tumor of the central nervous system with epithelioid neuroendocrine \"Transdedifferentiation\": A case report and review of the literatures.","authors":"Shazia Bokhari, Michael J Hwang, X Robert Zhang, Meenakshi B Bhattacharjee, Hidehiro Takei","doi":"10.1111/neup.13022","DOIUrl":"10.1111/neup.13022","url":null,"abstract":"<p><p>Solitary fibrous tumors (SFTs) of the central nervous system (CNS) are rare mesenchymal tumors characterized by a fusion of the NGFI-A-binding protein 2 (NAB2) gene and the signal transducer and activator of transcription 6 (STAT6) gene, immunohistochemically resulting in nuclear expression of STAT6 - an immunohistochemical hallmark essential for diagnosis, as outlined in the fifth edition of the World Health Organization Classification of Tumors. Dedifferentiation, where low-grade tumors transform into high-grade forms, has been observed in SFTs, with documented cases involving sarcomatous or rarely epithelial transformations. We report the first case of a CNS SFT exhibiting \"transdedifferentiation\" into epithelioid neuroendocrine differentiation. A 36-year-old woman presented with worsening frontal headaches and vision deterioration due to an 8.2-cm frontal tumor with skull erosion. Histologically, the tumor consisted of predominantly high-grade undifferentiated epithelioid round cells that expressed STAT6, along with multifocal synaptophysin and chromogranin A positivity, and occasional cytokeratin and claudin-4 reactivity, resembling large cell neuroendocrine carcinoma. A minor bland spindle cell component with STAT 6 immunoreactivity was also noted. This case highlights the rare occurrence of neuroendocrine \"transdedifferentiation\" in CNS SFTs. This case highlights the importance of recognizing dedifferentiation in CSF SFTs, which often correlates with aggressive tumor behavior and poor prognosis. Given the rarity of neuroendocrine \"transdedifferentiation,\" this case adds valuable insight into the diverse dedifferentiation patterns seen in CNS SFTs, emphasizing the need for accurate diagnosis to guide appropriate treatment strategies.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"248-256"},"PeriodicalIF":1.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142838491","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":"A glioneuronal tumor with neurocytic rosettes harboring FGFR1 internal tandem duplication - A report of a unique case.","authors":"Jiri Soukup, Nikola Hajkova, Veronika Hajkova, Marian Svajdler, David Netuka, Martin Majovsky","doi":"10.1111/neup.13018","DOIUrl":"10.1111/neup.13018","url":null,"abstract":"<p><p>Rosette-forming glioneuronal tumors (RGNTs) with FGFR1 tyrosine kinase domain internal tandem duplication (FGFR1 ITD) is exceedingly rare, with only a few cases reported in the literature. Hereby we present a case of a tumor with RGNT morphology occurring in area of septum pellucidum of 43-year-old male. The tumor showed FGFR1 ITD, no PIK3CA, PIK3R1 or NF1 alterations and inconclusive methylation profile with match for class of \"low-grade glial/glioneuronal/neuroepithelial tumors\". No areas characteristic of dysembryoplastic neuroepithelial tumor were identified. A brief review of literature on discrepancies between morphological diagnosis of RGNT and molecular profile of the entity is provided.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"234-240"},"PeriodicalIF":1.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716666","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":"Utilizing quantitative susceptibility mapping to differentiate primary lateral sclerosis from progressive supranuclear palsy: A case report.","authors":"Hiroaki Sekiya, Ryota Satoh, Farwa Ali, Dennis W Dickson, Jennifer L Whitwell, Keith A Josephs","doi":"10.1111/neup.13015","DOIUrl":"10.1111/neup.13015","url":null,"abstract":"<p><p>We report a patient who presented clinically with progressive supranuclear palsy (PSP) but was pathologically diagnosed as having primary lateral sclerosis (PLS) with magnetic resonance imaging (MRI) with a quantitative susceptibility mapping (QSM) protocol. A 70-year-old man was clinically diagnosed with PSP due to early falls and unresponsiveness to levodopa therapy. Postmortem pathological examination revealed mild loss of Betz cells, gliosis, and transactive response DNA binding protein of 43 kDa (TDP-43)-positive inclusions in the motor cortex, leading to the pathological diagnosis of PLS. To explore methods for differentiating PLS from PSP, ante-mortem QSM images were visually and quantitatively assessed for abnormal increases in magnetic susceptibility in the motor cortex. Prussian blue and Luxol fast blue combined with periodic acid-Schiff staining were also performed to understand the source of the susceptibility increases. QSM showed clear hyperintense signals in the motor cortex. Magnetic susceptibility in the motor cortex was higher in the PLS patient (Z = 4.7, p < 0.001) compared to normal controls and pathologically diagnosed PSP patients. Pathological examination of the region showed intracortical myelin loss, as well as iron deposition. Underlying pathological processes for the increased magnetic susceptibility include not only iron deposition but also intracortical myelin. Our case suggests that QSM is a potential tool to differentiate PLS from PSP, providing insights for accurate diagnosis and enhancing clinical decision-making.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"223-227"},"PeriodicalIF":1.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12085713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142668626","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":"Alzheimer's Disease With Cardiac Transthyretin Amyloidosis: A Clinicopathological Study of Autopsy Cases.","authors":"Yasuo Sugita, Takuya Furuta, Kenji Takahashi, Koichi Higaki, Yoshiro Koda, Shin-Ichiro Mori, Shoko Hongo, Hideomi Hamasaki, Akiyoshi Kakita, Mitsuharu Ueda, Keisuke Kitagawa","doi":"10.1111/neup.70011","DOIUrl":"https://doi.org/10.1111/neup.70011","url":null,"abstract":"<p><p>The relationship between Alzheimer's disease and cardiac transthyretin amyloidosis (ATTR) has been reported epidemiologically. However, the details of its clinicopathological characteristics are unclear. To clarify the pathogenesis of Alzheimer's disease combined with cardiac ATTR, 50 autopsy cases of Alzheimer's disease with cardiac hypertrophy were examined. Transthyretin amyloid deposition was studied by immunostaining in cases where amyloid deposition was suspected in various organs by HE staining. ATTR in systemic organs was also examined. The pathological diagnosis of Alzheimer's disease was done based on the National Institute on Aging and Alzheimer's Association (NIA-AA) guidelines. Cerebral amyloid angiopathy (CAA) was rated on a 3-point scale according to the Vonsattel scale. The pathological diagnosis of cardiac ATTR was done using a 3-point scale based on previously published findings on amyloid amounts. Six out of 50 patients were found to have cardiac ATTR by immunostaining and protein mass analysis of myocardial tissue. The sex distribution of the six patients was two males (Cases 3 and 6) and four females (Cases 1, 2, 4, and 5), and their ages were 97, 89, 91, 104, 86, and 77 years in Cases 1-6, respectively. In Cases 1-6, the NIAA score/CAA assessment/ATTR stages were intermediate/severe/G3, intermediate/moderate/G3, high/severe/G3, high/severe/G2, high/severe/G2, and intermediate/moderate/G2, respectively. Cases 1-5 also had cerebral infarction. In all cases, Transthyretin amyloid deposition was seen mainly in the vessel walls of various organs throughout the body. In the heart, transthyretin amyloid deposition was observed in the myocardial vessel walls and between myocardial fibers. On autopsy, cardiogenic cerebral infarction or heart failure was considered to be the main cause of death in Cases 1-5. These results indicate that Alzheimer's disease could be regarded as a systemic disease rather than just a localized disease presenting with dementia.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151381","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":"https://doi.org/10.1111/neup.70010","url":null,"abstract":"","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-05-15","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":"Two Brothers With ADSS1 Myopathy: A Report of Clinical, Radiological, and Autopsy Findings.","authors":"Yuka Hama, Terunori Sano, Yasushi Oya, Chihiro Matsumoto, Yuji Nakayama, Yoshihiko Saito, Aritoshi Iida, Makoto Shibuya, Yuko Saito, Ichizo Nishino, Yuji Takahashi, Masaki Takao","doi":"10.1111/neup.70008","DOIUrl":"https://doi.org/10.1111/neup.70008","url":null,"abstract":"<p><p>ADSS1 myopathy, previously known as adenylosuccinate synthetase-like 1 (ADSSL1) myopathy, is an autosomal recessive muscle disease caused by variants in ADSS1 (adenylosuccinate synthase 1). ADSS1 myopathy is complicated by respiratory muscle weakness or cardiomyopathy as well as limb muscle weakness. We analyzed two siblings with ADSS1 myopathy, both harboring compound heterozygous pathogenic variants (c.781G>A/c.919delA) in ADSS1 and provided details of their phenotypes together with muscle imaging and autopsy findings. Although it was reported that ADSS1 myopathy usually began with lower limb muscle weakness, our cases showed early involvement of the cervical paraspinal muscle, triceps brachii muscle, flexor digitorum superficialis and profundus muscles, rectus abdominis muscle, gluteus maximus and medius muscles, and cardiomyopathy. While a previous study reported that the trunk and hip muscles were relatively spared, atrophy of paraspinal muscles, gluteus medius and maximus muscles, and adductor muscles were observed. Our two siblings allowed for long-term follow-up and will be useful reference cases. We evaluated the frequency of fibers with nemaline bodies in various autopsied muscles and found that the ratio of fibers with nemaline bodies was lower compared to other nemaline myopathies. Postmortem examination revealed, for the first time, nemaline bodies in the diaphragm and myocardium, associated with respiratory failure and cardiomyopathy.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144029897","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 Amyotrophic Lateral Sclerosis With Sudden Death Showed Histological Features of Lewy Body Disease.","authors":"Shunsuke Miyachi, Yuki Oshima, Kazuo Yazaki, Nozomi Futaki, Yusuke Shirai, Zen-Ichi Tanei, Yohei Ikebe, Ikuko Iwata, Hideki Ujiie, Masahiro Onozawa, Satoshi Hirano, Shinya Tanaka, Ichiro Yabe","doi":"10.1111/neup.70009","DOIUrl":"https://doi.org/10.1111/neup.70009","url":null,"abstract":"<p><p>We present the case of an 81-year-old man diagnosed with probable amyotrophic lateral sclerosis (ALS) based on the Updated Awaji criteria. The patient exhibited progressive motor neuron degeneration with muscle weakness, atrophy, and fasciculations primarily in the right lower limb and later extending to the right upper limb. Three months after being referred to a home care clinic, he collapsed in front of his family members and died. An autopsy revealed phosphorylated TDP-43 pathology consistent with ALS, with involvement of the hypoglossal nucleus, facial nerve nucleus, and medulla oblongata. Interestingly, widespread a-synuclein pathology indicative of diffuse neocortical type Lewy body disease (LBD; Braak stage 6) was identified, despite the absence of clinical parkinsonism or dementia with Lewy bodies (DLB) during his lifetime. The presence of autonomic symptoms such as constipation and urinary retention shortly before death may be attributable to a-synuclein pathology affecting the autonomic nervous system. The coexistence of ALS and LBD underscores the clinical challenge of diagnosing overlapping pathologies, as motor symptoms may obscure signs of LBD. Dopamine transporter imaging or MIBG myocardial scintigraphy might aid in identifying preclinical LBD in ALS patients with atypical symptoms. The patient died of respiratory failure due to extensive organizing pneumonia, but the possibility of sudden cardiac arrest could not be excluded. This case highlights the potential for coexisting neurodegenerative pathologies in ALS, emphasizing the importance of comprehensive evaluation when autonomic symptoms or other atypical features are present.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144036399","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":"A DRPLA-Affected Family: Clinical Course and Autopsy Findings in a Long-Surviving Case.","authors":"Yoko Mochizuki, Akira Arakawa, Miho Osako, Tomoyasu Matsubara, Tomio Arai, Yuko Saito","doi":"10.1111/neup.70007","DOIUrl":"https://doi.org/10.1111/neup.70007","url":null,"abstract":"<p><p>A long-surviving older sister and her younger brother, both with a juvenile type of DRPLA, were autopsied. They had 69 and 77 CAG repeats in the atrophin-1 gene (ATN1), respectively. The older sister developed intellectual disability at the age of 10 years, followed by epilepsy, and survived for 40 years supported by tube feeding and tracheostomy with laryngeal closure without signs of anoxia and malnutrition. As the disease progressed, brain CT revealed a progressive skull thickening alongside brain atrophy. The younger brother, who had developmental delay at the age of 3 years, died of status epilepticus aged 24 years. Their father developed cerebellar ataxia at 56 years old when his daughter was 27 years old, and the expanded allele had 63 CAG repeats in ATN1. His clinical course was characterized by the sudden onset of severe psychiatric symptoms and choreatic movement. He died of aspiration pneumonia and suffered from malignant lymphoma aged 72 years. Neuropathological examination of this older sister with extended survival of DRPLA revealed a thickened skull, atrophic brainstem and cerebellum, and a thin spinal cord. We found neuronal loss and gliosis across a wide range of brain regions in addition to severe degeneration of the dentatorubral and pallidoluysian systems along with regions previously reported to exhibit polyglutamine pathology. In contrast, some regions previously reported to exhibit polyglutamine pathology remained preserved. The cerebellar cortex showed three-layer degeneration, and changes in the cerebral white matter appeared to correspond to lesions in the cerebral cortex.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144037996","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":"Solitary subependymal giant cell astrocytoma lacking TSC1/2 mutations and TTF-1 expression: A potential diagnostic pitfall.","authors":"Davide Mulone, Andrea Mafficini, Evelina Miele, Francesco Sala, Valeria Barresi","doi":"10.1111/neup.13013","DOIUrl":"10.1111/neup.13013","url":null,"abstract":"<p><p>Subependymal giant cell astrocytoma (SEGA) is a rare, low-grade glioma typically associated with tuberous sclerosis (TS) and mutations in the TSC1 or TSC2 genes. It is characterized by an intraventricular location, an expansive growth pattern, and the expression of glial and neural markers. TTF-1 expression is considered a sensitive marker of SEGA, likely reflecting its origin from progenitor cells in the caudothalamic groove. We report a case of SEGA with unusual immunohistochemical and molecular features in a 20-year-old man with no signs or family history of TS. The tumor was located in the anterior horn of the right ventricle and obstructed the foramen of Monro. Histologically, it exhibited an expansive growth pattern and was composed of cells with ovoid nuclei and abundant eosinophilic cytoplasm. Immunohistochemically, the tumor cells were positive for GFAP and S-100 protein, weakly positive for SOX2, focally positive for synaptophysin, and negative for TTF-1, neurofilament protein, NeuN, EMA, chromogranin, and BCOR. Scattered OLIG2-positive neoplastic cells were also observed. Molecular analysis revealed no pathogenic mutations or copy number variations in the analyzed 174 genes, including TSC1/2, except for a variant of unknown significance in BAP1. The histopathological features and immunohistochemical profile suggested SEGA, despite the absence of TTF-1 expression and TSC1/2 mutations. The diagnosis was confirmed by DNA methylation profiling, which assigned the tumor to the methylation class \"subependymal giant cell astrocytoma with TSC1/TSC2 alterations\" with a calibrated score of 0.95. This case highlights the potential diagnostic pitfall of SEGA lacking TTF-1 expression and emphasizes the importance of considering this entity in the differential diagnosis of intraventricular tumors, even in the absence of TS and characteristic molecular alterations. The existence of TTF-1 negative SEGAs reveals that these tumors might also derive from TTF-1 negative cells in the subpendymal region.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"167-173"},"PeriodicalIF":1.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11962586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142568316","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}