Free neuropathology最新文献

{"title":"Depletion of nuclear cytoophidia in Alzheimer's disease.","authors":"Alyona Ivanova, David G Munoz, John Woulfe","doi":"10.17879/freeneuropathology-2025-6282","DOIUrl":"10.17879/freeneuropathology-2025-6282","url":null,"abstract":"<p><p>There is considerable evidence for a role for metabolic dysregulation, including disordered purine nucleotide metabolism, in the pathogenesis of Alzheimer's disease (AD). Purine nucleotide synthesis in the brain is regulated with high fidelity to co-ordinate supply with demand. The assembly of some purine biosynthetic enzymes into linear filamentous aggregates called \"cytoophidia\" (Gk. Cellular \"snakes\") represents one post-translational mechanism to regulate enzyme activity. Cytoophidia comprised of the nucleotide biosynthetic enzymes inosine monophosphate dehydrogenase (IMPDH) and phosphoribosyl pyrophosphate synthetase (PRPS) have been described in neuronal nuclei (nuclear cytoophidia; NCs). In light of the involvement of purine nucleotide dysmetabolism in AD, the rationale for this study was to determine whether there are disease-specific qualitative or quantitative alterations in PRPS cytoophidia in the AD brain. Double fluorescence immunostaining for PRPS and the neuronal marker MAP2 was performed on tissue microarrays of cores of temporal cortex extracted from post-mortem tissue blocks from a large cohort of participants with neuropathologically confirmed AD, Lewy body disease (LBD), progressive supranuclear palsy, and corticobasal degeneration, as well as age-matched cognitively unimpaired control participants. The latter group included individuals with substantial beta-amyloid deposition. NCs were significantly reduced in frequency in AD samples relative to those from controls, including those with a high beta-amyloid load, or participants with LBD or 4 repeat tauopathies. Moreover, double staining for PRPS and hyperphosphorylated tau revealed evidence for an association between NCs and neurofibrillary tangles. The results of this study contribute to our understanding of metabolic contributions to AD pathogenesis and provide a novel avenue for future studies. Moreover, because PRPS filamentation is responsive to a variety of drugs and metabolites, they may have implications for the development of biologically rational therapies.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"8"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased frontocortical microvascular raspberry density in frontotemporal lobar degeneration compared to Lewy body disease and control cases: a neuropathological study.","authors":"Henric Ek Olofsson, Elisabet Englund","doi":"10.17879/freeneuropathology-2025-6178","DOIUrl":"10.17879/freeneuropathology-2025-6178","url":null,"abstract":"<p><p><b>Background:</b> Brain raspberries are histologically defined microvascular entities that are highly prevalent in the neocortex. Increased cortical raspberry density occurs in vascular dementia, but also with advancing age. Here, we examined the raspberry density in two neurodegenerative diseases, wherein vascular alterations distinct from conventional vascular risk factors have been indicated: frontotemporal lobar degeneration (FTLD) and Lewy body disease (LBD). <b>Methods:</b> This retrospective study included 283 clinically autopsied individuals: 105 control cases without neurodegenerative disease, 98 FTLD cases (mainly FTLD-tau and FTLD-TDP), and 80 LBD cases (mainly neocortical). The raspberry density was quantified on haematoxylin-eosin-stained tissue sections from the frontal cortex, and the frontocortical atrophy was ranked 0-3. <b>Results:</b> There was a higher raspberry density in the FTLD group compared to both other groups (<i>P</i> ≤ 0.001; Games-Howell post hoc test). The difference between the FTLD and LBD groups remained significant in multiple linear regression models that included age, sex, and either brain weight (<i>P</i> = 0.034) or cortical atrophy (<i>P</i> = 0.012). The difference between the FTLD and control groups remained significant when including age, sex, and brain weight in the model (<i>P</i> = 0.004), while a trend towards significance was demonstrated when including age, sex, and cortical atrophy (<i>P</i> = 0.054). Further analyses of the FTLD group revealed a trend towards a positive correlation between raspberry density and cortical atrophy (<i>P</i> = 0.062; Spearman rank correlation). Comparisons of FTLD subgroups were inconclusive. <b>Conclusion:</b> The frontocortical raspberry density is increased in FTLD. An examination of the raspberry density in relation to a quantitative measure of cortical atrophy is motivated to validate the results. Future studies are needed to determine whether increased raspberry density in FTLD could function as a marker for more widespread vascular alterations, and to elucidate the relation between microvascular alterations and neurodegenerative disease.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"7"},"PeriodicalIF":0.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11884261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143574782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Capillary basal lamina in human brain and spinal cord has fibrillar collagen type I and type III: Ignorance may not be bliss.","authors":"Wen-Lang Lin, Dennis W Dickson","doi":"10.17879/freeneuropathology-2025-6159","DOIUrl":"10.17879/freeneuropathology-2025-6159","url":null,"abstract":"<p><p>The capillary basal lamina (BL) located between the endothelial cell, pericyte and perivascular astrocyte plays important roles in normal and diseased central nervous system (CNS). Using immunohistochemistry (IHC), electron microscopy (EM) and post-embedding immunogold EM (IEM), we studied capillary BL in biopsy and autopsy tissues of human CNS from cases with and without significant brain pathology and aged from 4 days to 49 years. In all cases, IHC showed, in the BL of microvessels, immunoreactivity for collagen types I, III, IV, VI and fibronectin. EM revealed fusion of the BL of capillary endothelial cells or pericyte with perivascular astrocyte BL, which was focally split, resulting in expanded spaces bordered by BL and containing striated fibrils. There was no significant thickening of fused or split BL. IEM showed localization of collagen I and III to banded fibrils, and of collagen IV to split and fused BL. These characteristic ultrastructural findings in human capillary BL were not found in normal or transgenic mice. Our observations of fibrillar collagen in young individuals complement previous observations of similar findings in older individuals. This raises the possibility that fibrillar collagen in human vascular BL plays a significant role in CNS capillary physiology and pathophysiology. The species-specific differences in capillary morphology between humans and mice might have relevance to poor correlations between benefits of immunotherapy and drug treatment in mice compared with human.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"6"},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11862662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143517622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel KDM2A::YAP1 fusion in a pediatric supratentorial CNS neoplasm resembling a tumor with BCOR internal tandem duplication.","authors":"Arnault Tauziède-Espariat, Alice Métais, Dorian Bochaton, Euphrasie Servant, Guillaume Chotard, Mégane Le Quang, Benjamin Bonhomme, Nathalène Truffaux, Volodia Dangouloff-Ros, Nathalie Boddaert, Lauren Hasty, Edouard Gimbert, Pascale Varlet","doi":"10.17879/freeneuropathology-2025-6152","DOIUrl":"10.17879/freeneuropathology-2025-6152","url":null,"abstract":"","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11862909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143517620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preservation of cellular structure via immersion fixation in brain banking.","authors":"Macy Garrood, Emma L Thorn, Adam Goldstein, Allison Sowa, William Janssen, Alyssa Wilson, Claudia S López, Raakhee Shankar, Erin S Stempinski, Kurt Farrell, John F Crary, Andrew T McKenzie","doi":"10.17879/freeneuropathology-2025-6104","DOIUrl":"10.17879/freeneuropathology-2025-6104","url":null,"abstract":"<p><p>Immersing the brain in a solution containing formaldehyde is a commonly used method for preserving the structure of human brain tissue in brain banking. However, there are questions about the quality of preservation using this method, as formaldehyde takes a relatively long period of time to penetrate a large organ such as the human brain. As a result, there is a critical need to determine whether immersion fixation is an adequate initial preservation method. To address this, we present exploratory histologic findings from our brain bank following the immersion fixation of hemi-sectioned brain specimens under refrigeration. Using light microscopy, we found that there was no significant change in the size of pericellular or perivascular rarefaction areas based on the postmortem interval (PMI) or on the progression from the outer (frontal cortex) to the inner (striatum) brain regions. Additionally, we did not identify any significant number of ghost cells - a state of late-stage cellular necrosis - in the light micrographs analyzed. Using transmission electron microscopy of tissue from the frontal cortex, we found that synapses could still be visualized, but there was vacuolization and variable degrees of myelin disbanding identified. Using serial section transmission electron microscopy, we found that identified synapses could be traced from one section to the next. Using serial block face scanning electron microscopy, we also found that myelinated axons on 2D images can be traced with high fidelity from one image to the next, even at PMIs of up to 27 hours. Collectively, our data corroborate previous findings that immersion fixation is effective for prevention of cellular necrosis and for visualizing many ultrastructural features in at least the surface areas of the brain. However, how structural preservation quality should best be assessed in brain banking is an open question that depends on the intended research applications.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"4"},"PeriodicalIF":0.0,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11795511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Parkinsonism associated with prolonged unresponsive wakefulness syndrome after blunt head injury: a clinico-pathological study.","authors":"Kurt A Jellinger","doi":"10.17879/freeneuropathology-2025-5982","DOIUrl":"10.17879/freeneuropathology-2025-5982","url":null,"abstract":"<p><p><b>Objective:</b> Survival after traumatic brain injury (TBI) and posttraumatic parkinsonian-like symptoms is increasing, in particular in those patients developing during disease course an unresponsive wakefulness syndrome (UWS) previously termed persistent vegetative state. <b>Material & methods:</b> 100 patients with disorders of consciousness after a blunt TBI ranging from deep coma to defective states / minimal cognitive state survived between 12 and 900 days. 15 patients developed parkinsonian symptoms, which were correlated with their neuropathological changes. <b>Results:</b> The patients, surviving either UWS recovery (n = 10) or defective minimally conscious state (MCS) (n = 5), clinically presented with severe (n = 7), moderate (n = 5), or mild (n = 3) parkinsonian symptoms mainly comprising symmetrical rigidity, amimia, hypo- / akinesia and convergence disorder, which in six patients were associated with unilateral or bilateral resting tremor. Following levodopa treatment, 11 patients showed mild to moderate improvement and four patients almost complete improvement of UWS, parkinsonism or both. Neuropathology revealed in most cases supratentorial traumatic lesions such as contusions, cerebral hemorrhages and diffuse white matter lesions. In addition to lesions in the basal ganglia and hippocampus, all cases displayed older lesions in the dorsolateral or lateral parts of the pons and in lower midbrain with various involvement of substantia nigra. The periaqueductal gray and upper midbrain tegmentum were however preserved. The pattern of brainstem lesions correlated with the sequelae of transtentorial shifting due to increased intracranial pressure. <b>Conclusions:</b> These and other rare observations following blunt TBI confirm the importance of the pattern of secondary brainstem lesions for the development and prognosis of UWS and rare parkinson-like symptoms.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143191411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cryopreservation of brain cell structure: a review.","authors":"Andrew T McKenzie, Emma L Thorn, Oge Nnadi, Borys Wróbel, Emil Kendziorra, Kurt Farrell, John F Crary","doi":"10.17879/freeneuropathology-2024-5883","DOIUrl":"10.17879/freeneuropathology-2024-5883","url":null,"abstract":"<p><p>Cryopreservation, the preservation of tissues at subzero temperatures, is a mainstay of brain banking that allows for the storage of brain tissue without the use of chemical fixatives. This is particularly important for molecular studies that are incompatible with tissue fixation. However, brain tissue is vulnerable to various forms of damage during the cryopreservation process, in particular due to the phase transition of water from a liquid to a solid state with the formation of ice crystals, which can disrupt cellular morphology. There is a critical need to characterize the effects of cryopreservation on brain cell structure at the microscopic level. In this review, we conducted a comprehensive literature search, identifying 97 studies that yielded 146 distinct observations of the effects of cryopreservation on neurohistology. We classified the reviewed studies into three main categories: cryofixation, freezing, and cryopreservation with cryoprotectants. Cryofixation techniques enable vitrification and excellent ultrastructural preservation of thin tissue samples but are limited in terms of the depth of tissue that can be preserved without ice artifacts. Freezing methods, particularly when applied to brain slices, can achieve rapid cooling rates that result in minimal ice artifacts detectable by light microscopy. Cryoprotectant-based approaches have the potential to reduce ice damage and achieve vitrification. For thin tissue samples, immersion in cryoprotectants has been found to be effective for structural preservation. However, for larger samples or the entire brain, perfusion of cryoprotectants is necessary to perform rapid distribution, and this has a more limited evidence base. In conclusion, while current cryopreservation methods can provide sufficient quality for some downstream applications, there is a need for improved techniques that enable the cryopreservation of larger brain tissue samples while maintaining excellent structural preservation.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"5 ","pages":"35"},"PeriodicalIF":0.0,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753176/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel FUS::BEND2 fusion expanding the molecular spectrum of astroblastomas.","authors":"Arnault Tauziède-Espariat, Benjamin Bonhomme, Nathalène Truffaux, Volodia Dangouloff-Ros, Nathalie Boddaert, Kévin Beccaria, Lauren Hasty, Alice Métais, Pascale Varlet","doi":"10.17879/freeneuropathology-2024-5983","DOIUrl":"10.17879/freeneuropathology-2024-5983","url":null,"abstract":"","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"5 ","pages":"34"},"PeriodicalIF":0.0,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adult glioblastoma with Lynch syndrome-associated mismatch repair deficiency forms a distinct high-risk molecular subgroup.","authors":"Maria-Magdalena Georgescu","doi":"10.17879/freeneuropathology-2024-5892","DOIUrl":"10.17879/freeneuropathology-2024-5892","url":null,"abstract":"<p><p>Glioblastoma is the most frequent and malignant primary brain tumor. Although the survival is generally dismal for glioblastoma patients, risk stratification and the identification of high-risk subgroups is important for prompt and aggressive management. The G1-G7 molecular subgroup classification based on the MAPK pathway activation has offered for the first time a non-redundant, all-inclusive classification of adult glioblastoma. Five patients from the large, 218-patient, prospective cohort showed germline mutations in mismatch repair (MMR) genes (Lynch syndrome) and a significantly worse median survival of 3.25 months post-surgery than those from the G1/EGFR and G3/NF1 major subgroups, or from the rest of the cohort adjusted for age. These rare tumors were assigned to a new subgroup, G3/MMR, a G3/NF1 subgroup spin-off, as they generally show genomic alterations leading to RAS activation, such as <i>NF1</i> and <i>PTPN11</i> mutations. An integrated clinical, histologic and molecular analysis of the G3/MMR tumors showed distinct characteristics as compared to other glioblastomas, including those with iatrogenic high tumor mutation burden (TMB), warranting a separate subgroup. Prior history of cancer, midline location or multifocality, presence of multinucleated giant cells (MGCs), positive p53 and MMR immunohistochemistry, and specific molecular characteristics, including high TMB, <i>MSH2</i>/<i>MSH6</i> alterations, biallelic <i>TP53</i> Arg mutations and co-occurring <i>PIK3CA</i> p.R88Q and <i>PTEN</i> alterations, alert to this high-risk G3/MMR subgroup. The MGCs and p53 immunohistochemistry analysis in G1-G7 subgroups showed that one in 7 tumors with these characteristics is a G3/MMR glioblastoma. The FDA-approved first-line therapy for many advanced solid tumors consists of nivolumab-ipilimumab immune checkpoint inhibitors. One G3/MMR patient received this regimen and survived much longer than the rest, setting a proof-of-principle example for the treatment of these very aggressive G3/MMR glioblastomas.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"5 ","pages":"32"},"PeriodicalIF":0.0,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11745196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropathology in 1984: a deadly shot into the heart of Europe.","authors":"Herbert Budka","doi":"10.17879/freeneuropathology-2024-5976","DOIUrl":"10.17879/freeneuropathology-2024-5976","url":null,"abstract":"<p><p>Just 40 years ago, Europe was divided into the Eastern communist bloc, which included the Czechoslovak Socialist Republic (ČSSR) and was dominated by the now historical Soviet Union, and the Western bloc comprising democracies such as Austria. The Iron Curtain, a heavily guarded and deadly border zone, separated the two blocs and constrained, in prison style, the populations of the Eastern bloc. The present neuropathological article relates the sad fate of František Faktor, a 33 years-old Czech who was shot by ČSSR border guards when attempting to flee to Austria at the border between <i>Česke Velenice</i> and <i>Gmünd</i>. František Faktor was found dead on November 5^th, 1984, on Austrian soil some 500 meters from the border. ČSSR authorities claimed that he was shot when still within their territory, then ran some 900 meters to the other side of the border and died there. Neuropathology demonstrated a gunshot injury of the spinal canal, with transverse lesioning of the spinal cord predominating at Th10 that must have resulted in immediate paraplegia. This finding proved that ČSSR border guards had shot on Austrian territory, resulting in a major diplomatic <i>éclat</i> between both countries. After the implosion of the communist governments of the Eastern bloc in 1989, relations between Czechia and Austria started to normalise. By now, the <i>Gmünd/Česke Velenice</i> region has developed an exemplary good local neighbourhood and the former border has become virtually irrelevant. Attempts to bring justice have started in Czechia as well as other countries behind the past Iron Curtain, and some former Czechoslovak officials held responsible for border killings were legally prosecuted. The present article demonstrates how a small medico-scientific discipline such as neuropathology can contribute to assess critical political events in our world. \"Who controls the past controls the future:who controls the present controls the past.\"- George Orwell (1903-1950), Nineteen Eighty-Four (1984) [1].</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"5 ","pages":"33"},"PeriodicalIF":0.0,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11748761/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}