Neurotoxicology and teratology最新文献

{"title":"Environmental factors associated with microcephaly in Africa: A systematic review","authors":"Pelagie Izabayo ,&nbsp;Jean Claude Hakizimana ,&nbsp;Annette Uwineza ,&nbsp;Abdullateef Isiaka Alagbonsi","doi":"10.1016/j.ntt.2025.107577","DOIUrl":"10.1016/j.ntt.2025.107577","url":null,"abstract":"<div><h3>Introduction</h3><div>Microcephaly, a condition characterized by a head circumference below the mean for age and sex, is a significant indicator of impaired fetal brain development. While some environmental factors have been associated with the development of microcephaly in Africa, the available information remains disjointed, making it difficult for healthcare providers and policy makers to translate the information to preventive measures in maternal and child health. This systematic review aims to synthesize primary studies on environmental determinants of microcephaly, focusing on African populations.</div></div><div><h3>Method</h3><div>A systematic literature search was conducted using PubMed, Scopus, AJOL, and Wiley Online Library to identify studies published between 2000 and 2025, focusing on environmental exposures and microcephaly in neonates and infants. Observational and interventional studies in English were included, following PRISMA 2020 guidelines. Data were extracted and tabulated by country, exposure type, study design, and reported outcomes.</div></div><div><h3>Results</h3><div>Sixteen African studies found a multifactorial relationship between environmental exposures and microcephaly. Zika virus infection was a consistent contributor, with maternal febrile illnesses, inadequate antenatal care, HIV exposure, and heavy metal toxicity also linked. Pesticide exposure, particularly to organophosphates and DDT, was associated with neurodevelopmental delays and restricted cranial growth. Ambient air pollution was negatively correlated with neonatal head circumference. Socioeconomic vulnerabilities intensified these environmental risks, especially during epidemic crises like Zika virus outbreaks.</div></div><div><h3>Conclusion</h3><div>Microcephaly in African populations is a multifactorial issue, influenced by emerging infections like ZIKV, chronic environmental exposures, and healthcare gaps. It calls for integrated public health strategies, including surveillance, early prenatal screening, environmental regulation, and region-specific diagnostic standards. Global evidence supports shared biological vulnerability in low-resource settings.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"113 ","pages":"Article 107577"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145794306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is there a glymphatic pathway to environmental risk in neurodevelopmental disorders?","authors":"Maiara de Aguiar da Costa ,&nbsp;Sofia Januário Bolan ,&nbsp;Maria Fernanda Pedro Ebs ,&nbsp;Simone Lespinasse Araújo ,&nbsp;Cristiano Juliano Faller ,&nbsp;Tatiana Barichello ,&nbsp;Michael Aschner ,&nbsp;Jaqueline da Silva Generoso ,&nbsp;Cinara Ludvig Gonçalves","doi":"10.1016/j.ntt.2025.107578","DOIUrl":"10.1016/j.ntt.2025.107578","url":null,"abstract":"<div><div>The glymphatic system (GS) is a glia-dependent perivascular network that mediates cerebrospinal fluid-interstitial fluid exchange and facilitates the clearance of neurometabolites. GS transport is sleep-dependent, with waste elimination heightened during non-rapid eye movement sleep. Emerging evidence links GS dysfunction with neurodevelopmental disorders (NDDs), including autism spectrum disorder, schizophrenia, and attention-deficit/hyperactivity disorder, disorders that frequently co-occur with sleep disturbances. In parallel, multiple environmental toxicants have been associated with adverse neurodevelopment. This study aims to integrate current evidence on the interplay between toxicants, GS dysfunction, and NDDs, highlighting shared biological pathways and exploring potential therapeutic targets. Evidence gaps include the absence of studies directly investigating toxicant effects on GS within NDDs populations, limited longitudinal data across sensitive developmental windows, scarce integration of GS-sensitive imaging, cerebrospinal fuid (CSF) biomarkers, and underassessment of sex differences and exposure mixtures. Translational opportunities span sleep optimization and GS-targeted strategies (e.g., enhancing CSF transport); among pharmacologic candidates, the α2-adrenergic agonist dexmedetomidine shows sedative–anxiolytic, anti-inflammatory, and neuroprotective signals warranting investigation. This narrative review synthesizes current evidence and delineates priorities to test the exposome–glymphatic–neurodevelopment axis.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"113 ","pages":"Article 107578"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145743465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sevoflurane induced hippocampal neuron cell injury via the miR-132-5p/BDNF axis and further caused cognitive impairment in rats","authors":"Junbo Peng ,&nbsp;Xiaoxiao Dai ,&nbsp;Guohai Chu","doi":"10.1016/j.ntt.2025.107567","DOIUrl":"10.1016/j.ntt.2025.107567","url":null,"abstract":"<div><h3>Background</h3><div>Sevoflurane (Sevo) could cause cognitive dysfunction in patients. MiR-132-5p is associated with nervous system functions. Therefore, this study explored the role of miR-132-5p in Sevo-induced cognitive impairment. This study aimed to provide useful information on preventing Sevo-induced cognitive impairment.</div></div><div><h3>Methods</h3><div>Sprague-Dawley rats and HT22 cells were involved in this study. A Sevo-treated rat model was constructed by making the rat inhale 2 % Sevo for 5 h. A Morris water maze (MWM) assay was conducted to assess the cognitive ability of rats. The qRT-PCR was used to measure miRNA and gene expression. Western Blot was used to measure protein expression. The oxidative stress status was measured using antioxidant activity assay. The flow cytometry was applied for the cell apoptosis assay. The mechanism was investigated using dual luciferase reporter assay.</div></div><div><h3>Results</h3><div>Sevo impaired the cognitive function of rats. Sevo-treatment upregulated miR-132-5p in rat hippocampal tissues, and miR-132-5p further downregulated BDNF. MiR-132-5p mediated the effect of Sevo on rat cognitive functions. MiR-132-5p affected rat cognitive functions by downregulating BDNF. In hippocampal neuron cells, Sevo-treatment upregulated miR-132-5p, and miR-132-5p downregulated BDNF. MiR-132-5p mediated the disrupting effect of Sevo on hippocampal neuron cells. MiR-132-5p caused hippocampal neuron cell damage by downregulating BDNF.</div></div><div><h3>Conclusion</h3><div>Sevo could induce rat cognitive impairments. Sevo-treatment upregulated miR-132-5p and miR-132-5p could downregulate BDNF expression in hippocampal tissues and neuron cells. MiR-132-5p mediated the disrupting effect of Sevo on hippocampal neuron cells and cognitive functions. MiR-132-5p caused hippocampal neuron cell injury and cognitive dysfunction by downregulating BDNF.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107567"},"PeriodicalIF":2.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145391693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The association of preconception and prenatal cannabis and tobacco exposure with autism symptoms in offspring: A population-based longitudinal study","authors":"Kim N. Cajachagua-Torres ,&nbsp;Olga D. Boer ,&nbsp;Anneke Louwerse ,&nbsp;Akhgar Ghassabian ,&nbsp;Irwin K.M. Reiss ,&nbsp;Vincent W.V. Jaddoe ,&nbsp;Hanan El Marroun","doi":"10.1016/j.ntt.2025.107561","DOIUrl":"10.1016/j.ntt.2025.107561","url":null,"abstract":"<div><div>Prenatal cannabis and tobacco exposure is associated with attention and behavior problems in children, while associations with autism symptoms remain unclear. We prospectively examined whether parental cannabis and tobacco use during pregnancy were associated with childhood autism symptoms. Information on parental cannabis and tobacco use was assessed using questionnaires, and maternal cannabis metabolites were detected via urinalysis. We measured autistic symptoms using two mother-reported instruments: Child Behavior Checklist (CBCL) at ages 1.5, 3, and 6; and Social Responsiveness Scale (SRS) at 6 years (<em>n</em> = 4380). Linear mixed models were used to examine the association between parental cannabis and tobacco use and CBCL autism symptoms across childhood. Linear regression was used for SRS autism symptoms. Maternal cannabis use before, but not during, pregnancy was associated with higher CBCL autism symptoms across childhood (β: 0.33, 95 % CI: 0.02, 0.63). Paternal cannabis use was linked to higher CBCL autism symptoms across childhood (β: 0.27, 95 % CI: 0.05, 0.50), explained by maternal psychopathology; no association was found with SRS autism symptoms. Excluding cannabis users, children whose mothers used tobacco throughout pregnancy had more SRS autism symptoms (β: 0.03, 95 % CI: 0.003, 0.05), not CBCL; no association was found with paternal tobacco use.</div><div>Our results suggest that maternal and paternal cannabis use is not associated with offspring autism symptoms, although preconception use is associated with autism symptoms across childhood. In contrast, maternal continued tobacco use during pregnancy was associated with autism symptoms, but not paternal use, suggesting possible intrauterine programming rather than family-based factors.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107561"},"PeriodicalIF":2.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145183780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydrogen activated the Nrf2/HO pathway to alleviate the cognitive decline in PD Drosophila after long-term sevoflurane exposure","authors":"Ming Li ,&nbsp;Bo Ma ,&nbsp;Si Liang ,&nbsp;Xuanyi Pan ,&nbsp;Jingyi Xie ,&nbsp;Hongjie Wang ,&nbsp;Jiguang Guo","doi":"10.1016/j.ntt.2025.107560","DOIUrl":"10.1016/j.ntt.2025.107560","url":null,"abstract":"<div><div>The demand for surgical and anesthetic care in patients with Parkinson's disease (PD) is projected to increase, because PD is the fastest-growing neurological disorder. Sevoflurane, the most commonly used volatile anesthetic, is neurotoxic to human and animal neonatal brains. Moreover, sevoflurane-based anesthesia can induce postoperative delirium (POD) in patients with PD. Therefore, our study was aimed at finding an effective treatment for sevoflurane-induced neurotoxicity in patients with PD by using a PD-POD <em>Drosophila</em> model. The small gas, hydrogen (H₂), was found to ameliorate learning and memory impairment, and increase the lifespan of PD flies, after long-term sevoflurane exposure. The performance index of the PD-POD flies increased by 30 % after H₂ inhalation. Moreover, H₂ inhalation decreased oxidative stress levels in PD fly brains, and increased electron transport chain and OXPHOS efficiency, as well as ATP synthesis, thus indicating enhanced mitochondrial function. In addition, PD flies with H₂ inhalation after sevoflurane exposure showed increased nuclear levels of Nrf2 and expression of its downstream target HO. Therefore, H₂ might exert antioxidant effects by activating the Nrf2/HO pathway, thereby decreasing oxidative stress levels and apoptosis in PD fly brains after long-term sevoflurane treatment. Inhalation of H₂ is likely to be an effective and convenient method to alleviate the neurotoxicity effects or POD caused by long-term sevoflurane exposure.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107560"},"PeriodicalIF":2.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145252292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Organophosphorus compounds and neurological conditions: Dr. Jekyll and Mr. Hyde","authors":"Eugenio Aztiria ,&nbsp;Carlos Javier Baier","doi":"10.1016/j.ntt.2025.107563","DOIUrl":"10.1016/j.ntt.2025.107563","url":null,"abstract":"<div><div>This article reviews the use, toxicology, and neurological effects of organophosphates (OPs) used as pharmacological agents. OPs, a versatile chemical family, have been applied in many sectors but pose significant risks, particularly to the nervous system. In the first part of this review, we discuss the toxicological effects of OPs, particularly their inhibition of the acetylcholinesterase (AChE) enzyme, leading to severe neurological impairments. Indeed, prolonged exposure to these chemicals can trigger neuroinflammation, oxidative stress, and changes in neurotransmitter systems, resulting in cognitive deficits, neuropsychiatric disorders, and, potentially, neurodegeneration. In the second part, we address the therapeutic potential of these chemicals, focusing mainly on their effects on the central nervous system (CNS). Some naturally occurring compounds, like citicoline, have shown neuroprotective properties, while synthetic OPs such as bisphosphonates and their derivatives are being explored to treat some mental conditions. However, the high toxicity and side effects of some of them, whether in the short or long term, may limit their use in clinical settings. Overall, there is a call for better animal models and continued research to develop safer therapeutic options.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107563"},"PeriodicalIF":2.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential cognitive, behavioral, and neurochemical responses to acute chlorpyrifos exposure in normotensive compared to hypertensive adult rats","authors":"Gabriel Gavazza Noé ,&nbsp;Larissa de Jesus Corrêa ,&nbsp;Janne Ketly da Silva Oliveira ,&nbsp;Karoline de Oliveira Sant'Anna ,&nbsp;Vitor Sampaio Minassa ,&nbsp;Andrew Vieira Aitken ,&nbsp;Karla Nivea Sampaio ,&nbsp;Vanessa Beijamini","doi":"10.1016/j.ntt.2025.107565","DOIUrl":"10.1016/j.ntt.2025.107565","url":null,"abstract":"<div><div>Clinical and preclinical evidence points to a bilateral association between cardiovascular diseases (CVD) and mental disorders such as anxiety and depression. We previously reported that exposure to organophosphate (OP) compounds, such as chlorpyrifos (CPF), promotes cardiovascular damage and behavioral alterations in normotensive rats. Also, spontaneously hypertensive rats (SHR), a well-established rodent model of hypertension, exhibit more severe symptoms of acute CPF toxicosis and higher mortality rates, likely due to lower plasma butyrylcholinesterase (BuChE) activity. The potential role of pre-existing hypertension in increasing susceptibility to acute OP toxicity, particularly in relation to psychiatric disorders, remains an open question. Given this, we investigated whether SHR are more susceptible than normotensive Wistar rats to the damage caused by acute CPF exposure on innate (elevated plus maze, EPM; light-dark transition, LDT; and open field tests) and learned (contextual fear conditioning) anxiety-like behaviors. A single dose of CPF (20 mg/kg) induced an anxiolytic-like behavior in SHR exposed to the EPM and no effect in Wistar rats. CPF acute intoxication increased fear expression in both strains, but impaired memory extinction only in Wistar rats. CPF inhibited BuChE in Wistar at all tested doses (10, 20 and 30 mg/kg), whereas inhibition occurred only at the highest dose in SHR. CPF also decreased acetylcholinesterase (AChE) activity in the hippocampus and prefrontal cortex of both strains. In summary, acute intoxication with CPF induces strain-dependent behavioral changes. SHRs intoxicated with CPF may not be the most suitable model for studying anxiety susceptibility to OP intoxication in previously hypertensive rats.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107565"},"PeriodicalIF":2.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145346303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Introduction to developmental outcomes of neuroinflammatory insults","authors":"Laura M. Carlson ,&nbsp;G. Jean Harry ,&nbsp;Kelly Carstens","doi":"10.1016/j.ntt.2025.107566","DOIUrl":"10.1016/j.ntt.2025.107566","url":null,"abstract":"","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107566"},"PeriodicalIF":2.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145459216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing replicability and power estimates of behavioral performance of control rats across standardized pre-clinical and toxicology studies","authors":"Kathryn S. Konrad ,&nbsp;Laura Betz ,&nbsp;Sandra McBride ,&nbsp;Keith R. Shockley ,&nbsp;Georgia Roberts ,&nbsp;Helen Cunny ,&nbsp;G. Jean Harry","doi":"10.1016/j.ntt.2025.107562","DOIUrl":"10.1016/j.ntt.2025.107562","url":null,"abstract":"<div><div>Behavioral assays are critical in evaluating impacts on nervous system function in rodents due to genetic or environmental factors and are frequently incorporated into regulatory decision-making studies. Despite numerous sources of guidance for such studies, results across behavioral assays are reputed to be highly variable with questionable replicability. Behavioral data obtained from control rats within four contract laboratory studies were used to evaluate replicability across studies, calculate the level of statistical power, and estimate the number of animals required for a specific effect size. For the three behaviors evaluated here (motor activity, acoustic startle response, and learning and memory), control rats from all studies showed the expected pattern of behavior, e.g., open field acclimation, startle habituation, % prepulse inhibition (PPI) over pre-pulse intensities, and acquisition and goal quadrant preference in the Morris Water Maze (MWM). For selected representative individual endpoints, power analyses were conducted to evaluate sample size requirements. Across all endpoints, a drop in power occurred as differences between two groups became smaller. Power analysis of multiple representative endpoints suggested that a sample size of 20 may detect a 30 % effect with 80 % power. Sample size requirements changed with the effect size, and achieving 80 % power with a 20 % effect size generally required a sample size of 30 rats. While the behavioral performance was replicated over the Study Cohorts, power analyses suggested a need for moderation of expectations regarding detectable differences if decisions relied on single endpoints or small effect sizes. Reporting results from a low powered study can have significant and wide-ranging impacts, including undermining confidence in data interpretation, misleading future research, and failing to adhere to the ethical framework of the 3 R's.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107562"},"PeriodicalIF":2.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal corticosteroid use and offspring neurological outcomes","authors":"Yun Yan ,&nbsp;Junyi Wang ,&nbsp;Xiaoping Lei","doi":"10.1016/j.ntt.2025.107564","DOIUrl":"10.1016/j.ntt.2025.107564","url":null,"abstract":"<div><div>Prenatal use of synthetic corticosteroids has been widely applied in preventing respiratory distress syndrome in preterm infants. In recent years, research has begun to focus on the effects of Antenatal Corticosteroids(ACS) on the short-term and long-term neurological development of offspring. This review summarizes the direct and potential effects of ACS on offspring neurological outcomes, including cognitive function, behavioral problems, and neurodevelopmental disorders. Studies have shown that prenatal corticosteroid exposure may be associated with improved short-term neurological outcomes in extremely preterm infants. However, the benefits on near- and long-term outcomes in late preterm and full-term infants remain inconclusive and controversial due to a lack of robust evidence. This article explores the potential effects of exposure timing and different dosages on offspring neurological outcomes, and emphasizes the need for further research to optimize the indications for ACS use. This will ensure its benefits in preterm complications while minimizing its potential negative impact on offspring neurodevelopment.</div></div>","PeriodicalId":19144,"journal":{"name":"Neurotoxicology and teratology","volume":"112 ","pages":"Article 107564"},"PeriodicalIF":2.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145337338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}