Experimental Neurology最新文献

{"title":"ZFHX3 silencing alleviates ischemic stroke by suppressing pericyte contraction and calcium influx through inhibiting WNK3 expression","authors":"Jing Qiu ,&nbsp;Yi-Han Wang ,&nbsp;Hui-Sheng Chen","doi":"10.1016/j.expneurol.2025.115363","DOIUrl":"10.1016/j.expneurol.2025.115363","url":null,"abstract":"<div><div>Zinc finger homeobox 3 (ZFHX3), a zinc finger homeodomain transcription factor, has been implicated in various brain disorders. However, its molecular mechanism in ischemic stroke remains unknown. In this study, we employed a transient middle cerebral artery occlusion/reperfusion (tMCAO/R) model in C57BL/6 mice and subjected mouse primary pericytes to oxygen-glucose deprivation/reoxygenation (OGD/R) treatment. The results revealed a significant upregulation of ZFHX3 expression in tMCAO/R mice <em>in vivo</em>. ZFHX3 knockdown exacerbated ischemic stroke outcomes, as evidenced by increased cerebral infarction volume, elevated risk of brain hemorrhage, aggravated development of cerebral edema, and worsened blood-brain barrier damage in mice with tMCAO/R. Furthermore, ZFHX3 knockdown inhibited calcium influx thereby attenuating pericyte contraction in mice tMCAO/R model. <em>In vitro</em> studies demonstrated that ZFHX3 knockdown significantly upregulated WNK lysine deficient protein kinase 3 (WNK3) expression in OGD/R-treated pericytes. Conversely, WNK3 knockdown relieved ZFHX3 inhibition-induced pericyte contraction in OGD/R-treated pericytes. In conclusion, our study demonstrates that ZFHX3 silencing may confer neuroprotection in ischemic stroke by suppressing pericyte contraction and calcium influx through inhibition of WNK3 expression. These findings position ZFHX3 as a potential therapeutic candidate for the treatment of ischemic stroke.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115363"},"PeriodicalIF":4.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The chronic aftermath of recurrent intimate partner violence-related brain injuries: Insights from rat models of traumatic brain injury and non-fatal strangulation","authors":"Mujun Sun ,&nbsp;Josh Allen ,&nbsp;Tamara L. Baker ,&nbsp;Gershon Spitz ,&nbsp;Soniya Xavier ,&nbsp;Natasha T. Lee ,&nbsp;Richelle Mychasiuk ,&nbsp;Sarah J. Spencer ,&nbsp;Stuart J. McDonald ,&nbsp;David K. Wright ,&nbsp;Sandy R. Shultz","doi":"10.1016/j.expneurol.2025.115368","DOIUrl":"10.1016/j.expneurol.2025.115368","url":null,"abstract":"<div><div>Intimate partner violence (IPV) is a serious global health concern that primarily affects women. Traumatic brain injury (TBI; e.g., concussion) and non-fatal strangulation (NFS) are common forms of IPV-related brain injuries which often occur in combination and are highly repetitive in nature. While our understanding of the consequences of repetitive TBI (rTBI) has improved due to research in sport and military settings, little is known about the repercussions of repetitive NFS (rNFS) or rTBI+rNFS. We recently developed the first rat model of NFS and found that rats exposed to a single TBI + NFS event had exacerbated deficits and pathophysiology than the injuries in isolation. In the current study we utilized these models to investigate the more clinically relevant setting of recurrent IPV-related brain injuries. Female Sprague-Dawley rats were assigned to repeated sham, rTBI, rNFS, and rTBI+rNFS groups. The rats received five exposures to their injury regime, with each exposure 24 h apart, followed by a 12-week recovery before behavioral testing and ex vivo MRI. Only rTBI+rNFS rats had persisting social deficits, while both groups with rTBI had cognitive deficits and anhedonia. Advanced diffusion MRI analysis found that the rTBI+rNFS rats had reduced fiber density and cross-section, an indication of reduced white matter integrity, compared to all other groups. Tensor-based morphometry and region of interest MRI analysis revealed that both groups with rTBI had brain areas with a statistically significant reduction in volume. These findings indicate that rTBI+rNFS results in worse social deficits and white matter damage and provides further evidence that IPV-related brain injuries can result in long-term debilitating consequences.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115368"},"PeriodicalIF":4.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144549538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aromatase inhibition modulates intrinsic properties and excitability of hippocampal CA1 pyramidal cells in the APP/PS1 mouse model of Alzheimer's disease","authors":"Alexander R. French ,&nbsp;Catherine A. Christian-Hinman","doi":"10.1016/j.expneurol.2025.115365","DOIUrl":"10.1016/j.expneurol.2025.115365","url":null,"abstract":"<div><div>Changes in the hippocampus stemming from heightened neuronal excitability contribute to memory loss in AD. In this context the role of estradiol, the primary estrogen in the brain, is mixed as it generally supports cognition but is also pro-convulsive. In addition to circulating ovarian estradiol in females, neurons in both males and females, including many of those in the hippocampus, express the enzyme aromatase, which converts testosterone to estradiol. Previous studies suggest that aromatase inhibition modulates hippocampal function and excitability, demonstrating actions of local neuroestradiol. However, how the role of estradiol in regulating hippocampal excitability changes in the context of AD is unknown. Here we investigated whether inhibition of aromatase modifies hippocampal CA1 pyramidal cell intrinsic excitability in the APP/PS1 mouse model of AD, which is prone to hyperexcitability and seizures. Mice at 11–14 weeks old received daily injections of the aromatase inhibitor letrozole or vehicle for 7 days. 24 h after the final injection, acute slices through the dorsal hippocampus were prepared and the response function of CA1 pyramidal cells to injected current was measured using whole-cell patch-clamp electrophysiology. CA1 pyramidal cells in vehicle-treated gonad-intact APP/PS1 mice showed increased excitability compared to those in wild-type counterparts, and this difference was reversed by letrozole. Furthermore, the effects of APP/PS1 genotype and of letrozole in females were abolished after ovariectomy. Overall, these results suggest that estradiol plays a complex role in regulating hippocampal excitability in AD.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115365"},"PeriodicalIF":4.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144522883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redefining the data landscape in experimental neurological research - Transparency, integration, and insight.","authors":"R Vavrek, A Keller, J R Huie, K Fouad","doi":"10.1016/j.expneurol.2025.115362","DOIUrl":"10.1016/j.expneurol.2025.115362","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":" ","pages":"115362"},"PeriodicalIF":4.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"MAPK signaling pathway in spinal cord injury: Mechanisms and therapeutic potential\" [Experimental Neurology 383 (2025) 115043].","authors":"Fei-Xiang Lin, Hou-Yun Gu, Wei He","doi":"10.1016/j.expneurol.2025.115353","DOIUrl":"https://doi.org/10.1016/j.expneurol.2025.115353","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":" ","pages":"115353"},"PeriodicalIF":4.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144511757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-specific proteomic analysis of epileptic brain tissues from Pten knockout mice and human refractory epilepsy","authors":"Yibo Li ,&nbsp;Zahra Sadri ,&nbsp;Katherine J. Blandin ,&nbsp;David A. Narvaiz ,&nbsp;Uma K. Aryal ,&nbsp;Joaquin N. Lugo ,&nbsp;Nicholas P. Poolos ,&nbsp;Amy L. Brewster","doi":"10.1016/j.expneurol.2025.115361","DOIUrl":"10.1016/j.expneurol.2025.115361","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Rationale&lt;/h3&gt;&lt;div&gt;Epilepsy presents significant sex-based disparities in prevalence and manifestation. Epidemiological studies reveal that epilepsy is more prevalent in males, with lesional types being more common, whereas idiopathic generalized epilepsies are more frequently observed in females. These differences stress the importance of considering sex-specific factors in epilepsy diagnosis, treatment, and mechanistic research using preclinical models. To elucidate potential molecular differences that could explain these disparities and inform personalized treatment strategies, we conducted a proteomic analysis of epileptic brain tissues from both an experimental mouse model of genetic epilepsy and humans with drug-resistant epilepsy (DRE).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;We employed mass spectrometry-based proteomic analysis on brain tissues from DRE patients and the &lt;em&gt;Pten&lt;/em&gt; knockout (KO) mouse model of genetic epilepsy with focal cortical dysplasia. Mouse samples included hippocampi from adult wild-type (WT) and &lt;em&gt;Pten&lt;/em&gt; KO mice (4–5 per group and sex). Human samples included the temporal cortex from 12 DRE adult patients (7 males, 5 females) and 5 non-epileptic (NE) controls (2 males, 3 females). Brain biopsies were collected with patients' informed consent under approved IRB protocols (Indiana University Health Biorepository). Proteomic profiles were analyzed using principal component analysis (PCA) along with volcano plots to identify significant changes in protein expression. The enrichment analysis of differentially expressed proteins was conducted by Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genomes (KEGG) pathway.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;PCA revealed distinct clustering of brain proteomes between epilepsy and control cases in both human and mice, with 390 proteins showing significant differences in human and 437 proteins in mouse samples. These proteins are primarily associated with ion channels, synaptic processes, and neuronal energy regulation. In the mouse model, males have more pronounced proteomic changes than females, with enrichment in metabolic pathways and VEGF signaling pathway, indicating a more severe vascular permeability impairment in males. In human DRE cases, 118 proteins were significantly changed by comparing epileptic females to males. Pathway analysis revealed changes in metabolic pathways and the HIF-1 signaling pathway, indicating that altered neuronal activity and inflammation may lead to increased oxygen consumption.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;These findings highlight differences between epilepsy and control brain samples in both humans and mice. Sex-specific analysis revealed distinct pathway enrichments between females and males, with males exhibiting a broader range of proteomic alterations. While these observations suggest potential sex-related differences in proteomic profiles, larger studies are needed to further validate these patterns. This","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115361"},"PeriodicalIF":4.6,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144501222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Torin-1 improves cognitive decline by regulating autophagic system and cholesterol metabolism in hepatic encephalopathy","authors":"Yerin Chae ,&nbsp;Yena Cho ,&nbsp;Su Kyoung Lee ,&nbsp;Eunju Go ,&nbsp;Chan Gil Kim ,&nbsp;So Yeong Cheon","doi":"10.1016/j.expneurol.2025.115358","DOIUrl":"10.1016/j.expneurol.2025.115358","url":null,"abstract":"<div><div>Patients with liver diseases, such as liver cirrhosis and liver failure, have a high likelihood of developing hepatic encephalopathy (HE). HE is characterised by neurological impairments ranging from mild cognitive dysfunction to severe coma. Hyperammonaemia, metabolic disruption, and inflammation are recognised as key factors in the onset of HE. Recently, impaired autophagy has also been suggested to contribute to the development of HE. Therefore, in this study, we aimed to examine whether the autophagy inducer torin-1 is effective in reducing signs of HE. In this study, C57BL/6 mice were subjected to bile duct ligation (BDL) for 14 days to establish a model of HE. Liver function and structure were assessed using aspartate aminotransferase, alanine aminotransferase, total bilirubin, and haematoxylin and eosin staining, respectively. Neurological function was evaluated through the elevated plus maze, novel object recognition test, marble-burying test, clasping test, and passive avoidance test. To evaluate the effects of torin-1, it was administrated intraperitoneally to mice daily for 14 days. Changes in autophagy, cholesterol metabolism, and the cytokine/chemokine profile in the cerebral cortex were measured with and without torin-1 treatment. We found that although systemic administration of torin-1 could not reduce the induction of jaundice and liver impairment caused by BDL, it appeared to delay the onset of HE. Torin-1 treatment reduced the BDL-induced elevation in serum cholesterol and ammonia levels. Furthermore, abnormal expression of autophagy- and cholesterol-associated molecules in the cerebral cortex was reduced by torin-1 treatment. Cognitive function was improved in mice undergoing BDL with torin-1 treatment. Conclusively, these findings indicate that the induction of autophagy was found to alleviate the adverse effects seen in HE by regulating cholesterol metabolism in the cerebral cortex. The autophagy inducer torin-1 might be a potential approach to alleviate alterations and symptoms in HE.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115358"},"PeriodicalIF":4.6,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum evaluation of NFL correlates with histological identification of degenerating axons","authors":"Anna F. Fusco ,&nbsp;Sabhya Rana ,&nbsp;Sruti Rayaprolu ,&nbsp;Maya M. MacIntyre ,&nbsp;Marda Jorgensen ,&nbsp;Gerry Shaw ,&nbsp;David D. Fuller","doi":"10.1016/j.expneurol.2025.115360","DOIUrl":"10.1016/j.expneurol.2025.115360","url":null,"abstract":"<div><div>Serum neurofilament light chain (NF-L) is a promising minimally invasive biomarker for axonal degeneration after neurological damage. The current work demonstrates the utility of serum NF-L as a biomarker for the extent of active axonal degeneration in the injured spinal cord. Adult Sprague Dawley rats received a unilateral C4 contusion (150kdyne). Brainstem and spinal cords were harvested, and serum was collected at 1 h, 6 h, 1 day, 3 days, or 10 days post-injury. Serum NF-L and glial fibrillary acid protein (GFAP) were assessed using the Quanterix® Simoa™ assay. Serial spinal cord cross-sections spanning the caudal medulla to the mid-thoracic spinal cord were stained with the NF-L Degenotag™ MCA-6H63 antibody, which specifically detects degenerating axonal profiles. Sections were qualitatively and quantitatively analyzed for the pattern and extent of axonal degeneration. MCA-6H63 staining and serum NF-L levels peaked at 1–3 days post SCI, and then declined. Further, serum NF-L and the number of MCA-6H63 positive axons were highly correlated across time points (R² = 0.739; <em>p</em> &lt; 0.0001). These data support the hypothesis that serum NF-L levels are indicative of the amount of active axonal degeneration in the injured spinal cord and therefore provide a biomarker to monitor degeneration over time post injury.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115360"},"PeriodicalIF":4.6,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144491268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Complex cognitive and motivational deficits precede motor dysfunction in the zQ175 (190 CAG repeat) Huntington's disease model","authors":"D.J. Harrison ,&nbsp;P. Linehan ,&nbsp;Y. Patel ,&nbsp;Z. Bayram-Weston ,&nbsp;A.E. Rosser ,&nbsp;S.B. Dunnett ,&nbsp;S.P. Brooks ,&nbsp;M.J. Lelos","doi":"10.1016/j.expneurol.2025.115350","DOIUrl":"10.1016/j.expneurol.2025.115350","url":null,"abstract":"<div><div>Huntington's disease (HD) is a progressive, inherited neurodegenerative disorder characterised by motor, cognitive, and neuropsychiatric dysfunction for which several mouse models have been developed. Knock-in models, such as zQ175, retain the genetic context observed in people with HD by introducing CAG repeats into the native huntingtin gene. In this study, we conducted a comprehensive, longitudinal analysis of phenotypic changes in the zQ175 mouse, with a focus on exploring the emergence of complex cognitive processes. Our findings indicate that robust cognitive and motivational deficits precede motor dysfunction in this model, with some apparent sex differences. Specifically, male zQ175 mice were slower to habituate to a novel environment and they showed impaired sensorimotor gating, in comparison to female mice. By 12 weeks old, cognitive deficits were observed in zQ175 mice of both sexes on a Pavlovian classical conditioning task. Reduced motivation to work for reward was identified as early as 27 weeks, while attentional and visuospatial deficits were also detected in the 5-choice serial reaction time task. Implicit learning deficits were identified at 30 weeks. zQ175 mice were hypoactive at ∼24 weeks but became hyperactive by 60 weeks of age. Motor impairments emerged by 24 weeks for females and 48 weeks for males. Thus, we observed a wide range of cognitive deficits (attentional, visuospatial, sensorimotor, instrumental and implicit learning), as well as a gradual progression of motor changes. This detailed phenotypic timeline establishes the face validity of this model insofar as these mice present with complex neuropsychiatric and cognitive impairments that are evident in people with HD.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115350"},"PeriodicalIF":4.6,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144491267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FGFR1 agonists alleviate pathology and cognitive impairment in an Alzheimer's disease mouse model","authors":"Wei-Chien Hung ,&nbsp;Wei-Chun Sun ,&nbsp;Tzu-Ching Su ,&nbsp;Yi-Jung Lee ,&nbsp;Irene Han-Juo Cheng","doi":"10.1016/j.expneurol.2025.115357","DOIUrl":"10.1016/j.expneurol.2025.115357","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is the leading cause of dementia, characterized by the buildup of amyloid plaques and neurofibrillary tangles, which lead to neuronal damage and trigger inflammatory responses in glial cells. The fibroblast growth factor receptor 1 (FGFR1)-mediated signaling pathways support the function of damaged neurons and modulate the inflammatory response. The FGFR1 agonists, including Fibroblast growth factor 1 (FGF1) and FG loop peptide (FGL), have been implicated in multiple disease therapies. However, whether FGFR1 agonists can improve pathology and cognitive function in AD remains unknown. This study showed that administration of FGF1 and FGL to the AD mouse model reversed spatial memory impairment, enhanced neurogenesis, suppressed reactive astrogliosis, and restricted dystrophic neurites. However, only FGF1 treatment reduced the deposition of senile plaque. In microglial culture studies, FGF1 improves the phagocytosis ability of microglia, but this effect is blocked by the FGFR1-specific inhibitor. Together, our findings suggested that FGFR1 agonists alleviate pathological and cognitive impairments in the AD mouse model.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115357"},"PeriodicalIF":4.6,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144495430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}