Inhalation Toxicology最新文献

{"title":"Exposure to tungsten particles via inhalation triggers early toxicity marker expression in the rat brain.","authors":"Léo Macé, Chloé Brizais, Florence Bachelot, Annabelle Manoury, Sébastien Thomé, Céline Gloaguen, Imène Garali, Victor Magneron, Virginie Monceau, Amandine Sache, Frédéric Voyer, Christelle Elie, Laurence Roy, François Gensdarmes, Dmitry Klokov, Michelle L Block, Chrystelle Ibanez","doi":"10.1080/08958378.2024.2349895","DOIUrl":"https://doi.org/10.1080/08958378.2024.2349895","url":null,"abstract":"<p><strong>Objective: </strong>Our work is focused on tungsten, considered as an emerging contaminant. Its environmental dispersion is partly due to mining and military activities. Exposure scenario can also be occupational, in areas such as the hard metal industry and specific nuclear facilities. Our study investigated the cerebral effects induced by the inhalation of tungsten particles.</p><p><strong>Methods: </strong>Inhalation exposure campaigns were carried out at two different concentrations (5 and 80 mg/m³) in single and repeated modes (4 consecutive days) in adult rats within a nose-only inhalation chamber. Processes involved in brain toxicity were investigated 24 h after exposure.</p><p><strong>Results and discussion: </strong>Site-specific effects in terms of neuroanatomy and concentration-dependent changes in specific cellular actors were observed. Results obtained in the olfactory bulb suggest a potential early effect on the survival of microglial cells. Depending on the mode of exposure, these cells showed a decrease in density accompanied by an increase in an apoptotic marker. An abnormal phenotype of the nuclei of mature neurons, suggesting neuronal suffering, was also observed in the frontal cortex, and can be linked to the involvement of oxidative stress. The differential effects observed according to exposure patterns could involve two components: local (brain-specific) and/or systemic. Indeed, tungsten, in addition to being found in the lungs and kidneys, was present in the brain of animals exposed to the high concentration.</p><p><strong>Conclusion: </strong>Our data question the perceived innocuity of tungsten relative to other metals and raise hypotheses regarding possible adaptive or neurotoxic mechanisms that could ultimately alter neuronal integrity.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":"36 4","pages":"261-274"},"PeriodicalIF":2.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247871","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":"Sinomenine attenuates bleomycin-induced pulmonary fibrosis, inflammation, and oxidative stress by inhibiting TLR4/NLRP3/TGFβ signaling.","authors":"Yijue Liu, Hong Chen, Yan Wu, Fen Ai, Wei Li, Huan Peng, Feng Gui, Bo Yu, Zhen Chen","doi":"10.1080/08958378.2024.2335193","DOIUrl":"10.1080/08958378.2024.2335193","url":null,"abstract":"<p><strong>Objective: </strong>The present work concentrated on validating whether sinomenine alleviates bleomycin (BLM)-induced pulmonary fibrosis, inflammation, and oxidative stress.</p><p><strong>Methods: </strong>A rat model of pulmonary fibrosis was constructed through intratracheal injection with 5 mg/kg BLM, and the effects of 30 mg/kg sinomenine on pulmonary inflammation, fibrosis, apoptosis, and 4-hydroxynonenal density were evaluated by hematoxylin and eosin staining, Masson's trichrome staining, TUNEL staining, and immunohistochemistry. Hydroxyproline content and concentrations of inflammatory cytokines and oxidative stress markers were detected using corresponding kits. MRC-5 cells were treated <i>with</i> 10 ng/ml PDGF, and the effects of 1 mM sinomenine on cell proliferation were assessed by EdU assays. The mRNA expression of inflammatory cytokines and the protein levels of collagens, fibrosis markers, and key markers involved in the TLR4/NLRP3/TGFβ signaling were tested with RT-qPCR and immunoblotting analysis.</p><p><strong>Results: </strong>Sinomenine attenuated pulmonary fibrosis and inflammation while reducing hydroxyproline content and the protein expression of collagens and fibrosis markers in BLM-induced pulmonary fibrosis rats. Sinomenine reduced apoptosis in lung samples of BLM-challenged rats by increasing Bcl-2 and reducing Bax and cleaved caspase-3 protein expression. In addition, sinomenine alleviated inflammatory response and oxidative stress in rats with pulmonary fibrosis induced by BLM. Moreover, sinomenine inhibited the TLR4/NLRP3/TGFβ signaling pathway in lung tissues of BLM-stimulated rats. Furthermore, TLR4 inhibitor, TAK-242, attenuated PDGF-induced fibroblast proliferation and collagen synthesis in MRC-5 cells.</p><p><strong>Conclusion: </strong>Sinomenine attenuates BLM-caused pulmonary fibrosis, inflammation, and oxidative stress by inhibiting the TLR4/NLRP3/TGFβ signaling, indicating that sinomenine might become a therapeutic candidate to treat pulmonary fibrosis.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"217-227"},"PeriodicalIF":2.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140876291","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":"Celastrol reduces lung inflammation induced by multiwalled carbon nanotubes in mice <i>via</i> NF-κb-signaling pathway.","authors":"Tao-Lin Qing, Xuan-Yao Jiang, Jin-Feng Li, Qi Shen, Xin-Yi Zhao, Li-Jun Ren, Xiao-Yu Dai, Ji-Qian-Zhu Zhang, Wen-Jing Shi, Xiao-Fang Zhang, Bin Zhang, Lang Yan, Ji-Kuai Chen, Jiang-Bo Zhu","doi":"10.1080/08958378.2024.2351098","DOIUrl":"10.1080/08958378.2024.2351098","url":null,"abstract":"<p><p>Multiwalled carbon nanotubes (MWCNTs) have numerous applications in the field of carbon nanomaterials. However, the associated toxicity concerns have increased significantly because of their widespread use. The inhalation of MWCNTs can lead to nanoparticle deposition in the lung tissue, causing inflammation and health risks. In this study, celastrol, a natural plant medicine with potent anti-inflammatory properties, effectively reduced the number of inflammatory cells, including white blood cells, neutrophils, and lymphocytes, and levels of inflammatory cytokines, such as IL-1β, IL-6, and TNF-α, in mice lungs exposed to MWCNTs. Moreover, celastrol inhibited the activation of the NF-κB-signaling pathway. This study confirmed these findings by demonstrating comparable reductions in inflammation upon exposure to MWCNTs in mice with the deletion of NF-κB (P50^-/-). These results indicate the utility of celastrol as a promising pharmacological agent for preventing MWCNT-induced lung tissue inflammation.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":"36 4","pages":"275-281"},"PeriodicalIF":2.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247870","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":"The role of membrane transporters in the absorption of atrazine following nasal exposure.","authors":"Wisam Al Bakri, Maureen D Donovan","doi":"10.1080/08958378.2024.2348165","DOIUrl":"10.1080/08958378.2024.2348165","url":null,"abstract":"<p><strong>Objective: </strong>The purpose of these studies was to investigate the uptake of atrazine across the nasal mucosa to determine whether direct transport to the brain through the olfactory epithelium is likely to occur. These studies were undertaken to provide important new information about the potential for the enhanced neurotoxicity of herbicides following nasal inhalation.</p><p><strong>Materials and methods: </strong>Transport of atrazine from aqueous solution and from commercial atrazine-containing herbicide products was assessed using excised nasal mucosal tissues. The permeation rate and the role of membrane transporters in the uptake of atrazine across the nasal mucosa were also investigated. Histological examination of the nasal tissues was conducted to assess the effects of commercial atrazine-containing products on nasal tissue morphology.</p><p><strong>Results: </strong>Atrazine showed high flux across both nasal respiratory and olfactory tissues, and efflux transporters were found to play an essential role in limiting its uptake at low exposure concentrations. Commercial atrazine-containing herbicide products showed remarkably high transfer across the nasal tissues, and histological evaluation showed significant changes in the morphology of the nasal epithelium following exposure to the herbicide products.</p><p><strong>Discussion: </strong>Lipophilic herbicides such as atrazine can freely permeate across the nasal mucosa despite the activity of efflux transporters. The adjuvant compounds in commercial herbicide products disrupt the nasal mucosa's epithelial barrier, resulting in even greater atrazine permeation across the tissues. The properties of the herbicide itself and those of the formulated products play crucial roles in the potential for the enhanced neurotoxicity of herbicides following nasal inhalation.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"250-260"},"PeriodicalIF":2.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140912148","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":"Notoginsenoside R1 restrains the proliferation and migration of airway smooth muscle cells isolated from rats with chronic obstructive pulmonary disease.","authors":"Xiaoyong Li, Kai Chen, Xuefei Shi, Shunli Dong, Yi Chen, Bin Wang","doi":"10.1080/08958378.2024.2319708","DOIUrl":"10.1080/08958378.2024.2319708","url":null,"abstract":"<p><strong>Objective: </strong>Chronic obstructive pulmonary disease (COPD) is a common disorder that is characterized by systemic and lung inflammation. Notoginsenoside R1 (NGR1) displays anti-inflammatory properties in numerous diseases. We aimed to explore the function and mechanism of NGR1 in COPD.</p><p><strong>Materials and methods: </strong>COPD rats were established through cigarette smoke exposure, lipopolysaccharide injection, and cold stimulation. Rat airway smooth muscle cells (ASMCs) were separated and identified. Then, ASMCs were treated with NGR1 (25 or 50 μM) and cigarette smoke extract (CSE). Thereafter, the vitality, proliferation, and migration of ASMCs were measured. Additionally, cell cycle, inflammation-related factors, α-SMA, and PI3K/AKT pathway-related marker expressions of the ASMCs were also detected. Molecular docking experiments were conducted to explore the interaction of NGR1 to PI3K, TGF-β, p65, and AKT. Moreover, 740 Y-P (a PI3K/Akt pathway agonist) were used to validate the mechanism of NGR1 on COPD.</p><p><strong>Results: </strong>NGR1 inhibited the proliferation and migration, but caused cell cycle arrest for CSE-triggered ASMCs. Furthermore, NGR1 not only decreased IL-1β, IL-6, IL-8, and TNF-α contents, but also reduced α-SMA expression in CSE-stimulated ASMCs. Moreover, NGR1restrainedTGF-β1 expression, PI3K, p65, and AKT phosphorylation in CSE-stimulated ASMCs. Molecular docking experiments showed NGR1 exhibited a strong binding ability to PI3K, TGF-β1, p65, and AKT. Notably, the effects of NGR1 on the proliferation and migration of CSE-induced ASMCs were reversed by 740 Y-P.</p><p><strong>Conclusions: </strong>NGR1 can restrain the proliferation and migration of CSE-induced ASMCs, indicating that NGR1 may be a therapeutic candidate for treating COPD.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"145-157"},"PeriodicalIF":2.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139971733","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":"Short-term hyperoxia induced mitochondrial respiratory chain complexes dysfunction and oxidative stress in lung of rats.","authors":"Leonardo Tenfen, Richard Simon Machado, Khiany Mathias, Natalia Piacentini, Larissa Joaquim, Sandra Bonfante, Lucineia Gainski Danielski, Nicole Alessandra Engel, Mariella Reinol da Silva, Gislaine Tezza Rezin, Rafaella Willig de Quadros, Fernanda Frederico Gava, Fabricia Petronilho","doi":"10.1080/08958378.2024.2322497","DOIUrl":"10.1080/08958378.2024.2322497","url":null,"abstract":"<p><strong>Background: </strong>Oxygen therapy is an alternative for many patients with hypoxemia. However, this practice can be dangerous as oxygen is closely associated with the development of oxidative stress.</p><p><strong>Methods: </strong>Male Wistar rats were exposed to hyperoxia with a 40% fraction of inspired oxygen (FIO₂) and hyperoxia (FIO₂ = 60%) for 120 min. Blood and lung tissue samples were collected for gas, oxidative stress, and inflammatory analyses.</p><p><strong>Results: </strong>Hyperoxia (FIO₂ = 60%) increased PaCO₂ and PaO₂, decreased blood pH and caused thrombocytopenia and lymphocytosis. In lung tissue, neutrophil infiltration, nitric oxide concentration, carbonyl protein formation and the activity of complexes I and II of the mitochondrial respiratory chain increased. FIO₂ = 60% decreased SOD activity and caused several histologic changes.</p><p><strong>Conclusion: </strong>In conclusion, we have experimentally demonstrated that short-term exposure to high FIO₂ can cause oxidative stress in the lung.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"174-188"},"PeriodicalIF":2.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140049376","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":"Biological effects of diesel exhaust inhalation. III cardiovascular function.","authors":"Kristine Krajnak, Hong Kan, Janet A Thompson, Walter McKinney, Stacey Waugh, Tim South, Dru Burns, Ryan Lebouf, Jared Cumpston, Theresa Boots, Jeffrey S Fedan","doi":"10.1080/08958378.2024.2327364","DOIUrl":"10.1080/08958378.2024.2327364","url":null,"abstract":"<p><strong>Objective: </strong>Inhalation of diesel exhaust (DE) has been shown to be an occupational hazard in the transportation, mining, and gas and oil industries. DE also contributes to air pollution, and therefore, is a health hazard to the general public. Because of its effects on human health, changes have been made to diesel engines to reduce both the amounts of particulate matter and volatile fumes they generate. The goal of the current study was to examine the effects of inhalation of diesel exhaust.</p><p><strong>Materials and methods: </strong>The study presented here specifically examines the effects of exposure to 0.2 and 1.0 mg/m³ DE or filtered air (6h/d for 4 d) on measures of peripheral and cardio-vascular function, and biomarkers of heart and kidney dysfunction in male rats. A Tier 2 engine used in oil and gas fracking operations was used to generate the diesel exhaust.</p><p><strong>Results: </strong>Exposure to 0.2 mg/m³ DE resulted in an increase in blood pressure 1d following the last exposure, and increases in dobutamine-induced cardiac output and stroke volume 1 and 27d after exposure. Changes in peripheral vascular responses to norepinephrine and acetylcholine were minimal as were changes in transcript expression in the heart and kidney. Exposure to 1.0 mg/m³ DE did not result in major changes in blood pressure, measures of cardiac function, peripheral vascular function or transcript expression.</p><p><strong>Discussion and conclusions: </strong>Based on the results of this study, we suggest that exposure to DE generated by a Tier 2 compliant diesel engine generates acute effects on biomarkers indicative of cardiovascular dysfunction. Recovery occurs quickly with most measures of vascular/cardiovascular function returning to baseline levels by 7d following exposure.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"189-204"},"PeriodicalIF":2.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11099779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140093817","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":"Evaluation of neural reflex activation as a potential mode of action for respiratory and cardiovascular effects of fine particulate matter.","authors":"Robyn L Prueitt, Cassandra J Meakin, Nicholas L Drury, Julie E Goodman","doi":"10.1080/08958378.2024.2324033","DOIUrl":"10.1080/08958378.2024.2324033","url":null,"abstract":"<p><strong>Objectives: </strong>Mortality from respiratory and cardiovascular health conditions contributes largely to the total mortality that has been associated with exposure to PM_2.5 in epidemiology studies. A mode of action (MoA) for these underlying morbidities has not been established, but it has been proposed that some effects of PM_2.5 occur through activation of neural reflexes.</p><p><strong>Materials and methods: </strong>We critically reviewed the experimental studies of PM_2.5 (including ambient PM_2.5, diesel exhaust particles, concentrated ambient particles, diesel exhaust, and cigarette smoke) and neural reflex activation, and applied the principles of the International Programme on Chemical Safety (IPCS) MoA/human relevance framework to assess whether they support a biologically plausible and human-relevant MoA by which PM_2.5 could contribute to cardiovascular and respiratory causes of death. We also considered whether the evidence from these studies supports a non-threshold MoA that operates at low, human-relevant PM_2.5 exposure concentrations.</p><p><strong>Results and discussion: </strong>We found that the proposed MoA of neural reflex activation is biologically plausible for PM_2.5-induced respiratory effects at high exposure levels used in experimental studies, but further studies are needed to fill important data gaps regarding the relevance of this MoA to humans at lower PM_2.5 exposure levels. A role for the proposed MoA in PM_2.5-induced cardiovascular effects is plausible for some effects but not others.</p><p><strong>Conclusions: </strong>Further studies are needed to determine whether neural reflex activation is the MoA by which PM_2.5 could cause either respiratory or cardiovascular morbidities in humans, particularly at the ambient concentrations associated with total mortality in epidemiology studies.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"125-144"},"PeriodicalIF":2.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140131359","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":"Elongated particulate burden in an individual who died of mesothelioma and had an occupational history as a talc \"mucker\".","authors":"Ronald F Dodson, Jacqueline Moline, Carlos D Salinas, Lee W Poye","doi":"10.1080/08958378.2024.2329935","DOIUrl":"10.1080/08958378.2024.2329935","url":null,"abstract":"<p><strong>Introduction: </strong>Tissue from a 77-year-old man diagnosed with mesothelioma was referred with a request for identification of the presence of fibrous structures in tissue samples. The individual's work history including working as a \"mucker\" at a specific \"industrial\" talc mine.</p><p><strong>Methods: </strong>Ferruginous bodies in the tissue digests as well as asbestos fibers were found. A bulk sample of a talc containing product from that mine was also analyzed.</p><p><strong>Discussions/conclusions: </strong>The correlation between the unique asbestos mineral/fibrous content of the talc to which he was exposed and findings of the same type of asbestos found in his lung is discussed. The type of asbestos found (tremolite) is a \"non-commercial\" type of asbestos that has been identified in some talc deposits. Tremolite, like all forms of asbestos is a causative agent for mesothelioma-the disease from which this individual suffered.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"205-216"},"PeriodicalIF":2.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140158025","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":"Inhalation exposure to toxic heavy metals in nail salon technicians and health risk assessment using Monte Carlo simulation","authors":"Zohreh Mohebian, Fatemeh Paridokht, Sara Karimi Zeverdegani, Farzaneh Mohammadi","doi":"10.1080/08958378.2024.2315124","DOIUrl":"https://doi.org/10.1080/08958378.2024.2315124","url":null,"abstract":"Nail salons offer a developing and diverse occupation for many women, especially the new generation. Due to the increasing apprehension surrounding heavy metals in dust caused by filing nails conta...","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":"1 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139968178","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}