Genes and Environment最新文献

{"title":"Current status and challenges of breast cancer prevention~DNA methylation would lead to groundbreaking progress in breast cancer prevention~","authors":"T. Tsukioki, Seema A. Khan, Tadahiko Shien","doi":"10.1186/s41021-023-00287-0","DOIUrl":"https://doi.org/10.1186/s41021-023-00287-0","url":null,"abstract":"","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" 50","pages":""},"PeriodicalIF":1.7,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138612463","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 Malaysian Society of Toxicology: from establishment to evolution, a promising future!","authors":"N. Kamaludin, Firdaus Kamarulzaman, Rozaini Abdullah, Kok Meng Chan, Salmaan H. Inayat-Hussain","doi":"10.1186/s41021-023-00290-5","DOIUrl":"https://doi.org/10.1186/s41021-023-00290-5","url":null,"abstract":"","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"101 38","pages":""},"PeriodicalIF":1.7,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138609158","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":"Detection of EGFR gene polymorphisms in non-small cell lung cancer Egyptian patients: a case-control study.","authors":"Omali Y El-Khawaga, Mohammed F Al-Azzawy, Afaf M ElSaid, Sherif Refaat, Aliaa N El-Dawa","doi":"10.1186/s41021-023-00289-y","DOIUrl":"10.1186/s41021-023-00289-y","url":null,"abstract":"<p><strong>Background: </strong>Non-Small Cell Lung Cancer displays several genetic mutations including epidermal growth factor receptor. This study's objective was to determine if the EGFR exon19 rs121913438 and exon21 rs121434568 variations play a role in NSCLC susceptibility.</p><p><strong>Methods: </strong>Case-control research was done at the Mansoura university oncology center including 124 NSCLC patients, and 124 healthy volunteers. blood was used to obtain genomic DNA. ARMS-PCR was used to genotype single-nucleotide polymorphisms.</p><p><strong>Results: </strong>Molecular study for EGFR exon 19 del. showed NSCLC cases were significantly associated with a higher proportion of heterozygous WD, WD + DD dominant genotypes, and mutant D allele, (p < 0.05 for each), with a risk to develop NSCLC. also, NSCLC cases were significantly associated with a higher proportion of heterozygous TG, TG + GG dominant genotype, G mutant allele, (p < 0.05 for each), with a risk to develop LC (OR > 1 for each). regarding the two EGFR mutations, TTF1 staining was significantly associated with WD + DD genotypes for EGFR exon 19 del But not EGFR exon 21. No substantial differences were found among all studied cases with CK7 or napsin A Tumor cytochemistry.</p><p><strong>Conclusions: </strong>The WD heterozygous genotype and D allele in exon 19 del. mutation as well as the TG heterozygous and G allele in exon 21 substitution mutation in EGFR gene are strongly associated with the development of advanced-NSCLC in the Egyptians.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"45 1","pages":"32"},"PeriodicalIF":1.7,"publicationDate":"2023-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10680232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138440615","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":"Risk assessment of aflatoxin B₁ in herbal medicines and plant food supplements marketed in Malaysia using margin of exposure and RISK21 approaches.","authors":"Siti Soleha Ab Dullah, Mohd Redzwan Sabran, Ab Hamid Hasiah, Rozaini Abdullah","doi":"10.1186/s41021-023-00286-1","DOIUrl":"10.1186/s41021-023-00286-1","url":null,"abstract":"<p><p>Aflatoxin B₁ (AFB₁) is a mycotoxin produced by several species of Aspergillus fungi which can cause liver cancer in animals and humans. This study aims to perform the risk assessment of AFB₁ in herbal medicines and plant food supplements (PFS) in Malaysian market. A total of 31 herbal medicines and PFS were purchased through online platforms and over the counter using a targeted sampling strategy. Of 31 samples analysed using the ELISA method, 25 (80.6%) were contaminated with AFB₁ at levels ranged from 0.275 to 13.941 μg/kg. The Benchmark Dose Lower Confidence level of 10 (BMDL₁₀) of 63.46 ng/kg bw/day and the estimated dietary intake of the adult population ranged from 0.006 to 10.456 ng/kg bw/day were used to calculate the Margin of Exposure (MOE). The MOEs for 24 (96%) out of the 25 positive samples were lower than 10,000. The RISK21 matrix revealed that AFB₁ exposure levels from herbal medicines and PFS differed greatly over the world. The calculated population risk of acquiring liver cancer from AFB₁ exposure ranged from 0 to 0.261 cancers/100,000 populations/year and accounted for an estimated percentage of liver cancer incidence ranged from 0.002 to 4.149%. This study revealed a moderate risk of liver cancer attributable to AFB₁ from herbal medicine and PFS among Malaysian populations and emphasised an urgency for risk management actions.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"45 1","pages":"31"},"PeriodicalIF":1.7,"publicationDate":"2023-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10666461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138295012","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":"Detection of in vivo mutagenicity in rat liver samples using error-corrected sequencing techniques.","authors":"Kazuki Izawa, Masataka Tsuda, Takayoshi Suzuki, Masamitsu Honma, Kei-Ichi Sugiyama","doi":"10.1186/s41021-023-00288-z","DOIUrl":"10.1186/s41021-023-00288-z","url":null,"abstract":"<p><strong>Background: </strong>Mutagenicity, the ability of chemical agents to cause mutations and potentially lead to cancer, is a critical aspect of substance safety assessment for protecting human health and the environment. Metabolic enzymes activate multiple mutagens in living organisms, thus in vivo animal models provide highly important information for evaluating mutagenicity in human. Rats are considered suitable models as they share a similar metabolic pathway with humans for processing toxic chemical and exhibit higher responsiveness to chemical carcinogens than mice. To assess mutagenicity in rats, transgenic rodents (TGRs) are widely used for in vivo gene mutation assays. However, such assays are labor-intensive and could only detect transgene mutations inserted into the genome. Therefore, introducing a technology to directly detect in vivo mutagenicity in rats would be necessary. The next-generation sequencing (NGS) based error-corrected sequencing technique is a promising approach for such purposes.</p><p><strong>Results: </strong>We investigated the applicability of paired-end and complementary consensus sequencing (PECC-Seq), an error-corrected sequencing technique, for detecting in vivo mutagenicity in the rat liver samples. PECC-Seq allows for the direct detection of ultra-rare somatic mutations in the genomic DNA without being constrained by the genomic locus, tissue, or organism. We tested PECC-Seq feasibility in rats treated with diethylnitrosamine (DEN), a mutagenic compound. Interestingly, the mutation and mutant frequencies between PECC-Seq and the TGR assay displayed a promising correlation. Our results also demonstrated that PECC-Seq could successfully detect the A:T > T:A mutation in rat liver samples, consistent with the TGR assay. Furthermore, we calculated the trinucleotide mutation frequency and proved that PECC-Seq accurately identified the DEN treatment-induced mutational signatures.</p><p><strong>Conclusions: </strong>Our study provides the first evidence of using PECC-Seq for in vivo mutagenicity detection in rat liver samples. This approach could provide a valuable alternative to conventional TGR assays as it is labor- and time-efficient and eliminates the need for transgenic rodents. Error-corrected sequencing techniques, such as PECC-Seq, represent promising approaches for enhancing mutagenicity assessment and advancing regulatory science.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"45 1","pages":"30"},"PeriodicalIF":1.7,"publicationDate":"2023-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10664353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138295011","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":"In vivo mutagenicity assessment of orally treated tert-butyl hydroperoxide in the liver and glandular stomach of MutaMouse.","authors":"Yasumasa Murata, Kenichiro Suzuki, Yoshiyuki Shigeta, Takako Iso, Nozomu Hirose, Takaaki Umano, Katsuyoshi Horibata, Kei-Ichi Sugiyama, Akihiko Hirose, Kenichi Masumura, Mariko Matsumoto","doi":"10.1186/s41021-023-00285-2","DOIUrl":"10.1186/s41021-023-00285-2","url":null,"abstract":"<p><strong>Background: </strong>tert-Butyl hydroperoxide (TBHP; CAS 75-91-2), a hydroperoxide, is mainly used as a polymerization initiator to produce polyethylene, polyvinyl chloride, and unsaturated polyester. It is a high-production chemical, widely used in industrial countries, including Japan. TBHP is also used as an additive for the manufacturing of food utensils, containers, and packaging (UCP). Therefore, there could be consumer exposure through oral intake of TBHP eluted from UCPs. TBHP was investigated in various in vitro and in vivo genotoxicity assays. In Ames tests, some positive results were reported with and/or without metabolic activation. As for the mouse lymphoma assay, the positive result was reported, regardless of the presence or absence of metabolic activation enzymes. The results of some chromosomal aberrations test and comet assay in vitro also demonstrated the genotoxic positive results. On the other hand, in in vivo tests, there are negative results in the bone marrow micronucleus test of TBHP-administered mice by single intravenous injection and the bone marrow chromosomal aberration test using rats exposed to TBHP for 5 days by inhalation. Also, about dominant lethal tests, the genotoxic positive results appeared. In contrast, there is little information about in vivo mutagenicity and no information about carcinogenicity by oral exposure.</p><p><strong>Results: </strong>We conducted in vivo gene mutation assay using MutaMice according to the OECD Guidelines for the Testing of Chemicals No. 488 to investigate in vivo mutagenicity of TBHP through oral exposure. After repeated dosing for 28 days, there were no significant differences in the mutant frequencies (MFs) of the liver and glandular stomach up to 300 mg/kg/day (close to the maximum tolerable dose (MTD)). The positive and negative controls produced the expected responses.</p><p><strong>Conclusions: </strong>These findings show that orally administrated TBHP is not mutagenic in the mouse liver and glandular stomach under these experimental conditions.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"45 1","pages":"29"},"PeriodicalIF":1.7,"publicationDate":"2023-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10662197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138290778","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":"Genoprotective potential of Macaranga species phytochemical compounds on HT-29 human colorectal adenocarcinoma cell line.","authors":"Ee Ling Siew,&nbsp;Lishantini Pearanpan,&nbsp;Zhafri Zamkhuri,&nbsp;Fariza Juliana Nordin,&nbsp;Theng Choon Ooi,&nbsp;Kok Meng Chan,&nbsp;Aisyah Salihah Kamarozaman,&nbsp;Norizan Ahmat,&nbsp;Nor Fadilah Rajab","doi":"10.1186/s41021-023-00282-5","DOIUrl":"10.1186/s41021-023-00282-5","url":null,"abstract":"<p><strong>Background: </strong>The species of genus Macaranga are widely found in Malaysian secondary forests and has been used as an alternative for treating varieties of illness. Studies have shown that the medicinal properties of this genus contain anti-inflammatory, antioxidant, and anti-cancer effects. This study aimed to determine the cytotoxicity of six isolated phytochemicals from Macaranga heynei (M. heynei), Macaranga lowii and Shorea leprosula on HT-29 human colorectal adenocarcinoma cell lines.</p><p><strong>Results: </strong>One out of six isolated phytochemical compounds, identified as \"Laevifolin A\", showed a cytotoxicity with an IC₅₀ value of 21.2 µM following 48 h treatment as detected using Sulforhodamine B (SRB) assay. Additionally, no induction of apoptosis and oxidative stress were observed on Laevifolin A treated HT-29 cells as determined using Annexin V-FITC/PI assay and dihydroethidine (HE) staining, respectively. Additionally, no damage to the DNA were observed as measured using the Alkaline Comet assay. Further investigation on menadione-induced oxidative DNA damage showed the genoprotective potential of Laevifolin A on HT-29 cells.</p><p><strong>Conclusions: </strong>In conclusion, this study indicated that only one compound (Laevifolin A) that extracted from M. heynei has the cytotoxicity potential to be developed as an anticancer agent in human colorectal adenocarcinoma. However, besides exhibiting cytotoxic effect, the compound also exhibits genoprotective capability that warrant further investigation.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"45 1","pages":"28"},"PeriodicalIF":1.7,"publicationDate":"2023-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10614388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71411950","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":"LncRNA PVT1 induces apoptosis and inflammatory response of bronchial epithelial cells by regulating miR-30b-5p/BCL2L11 axis in COPD.","authors":"Taoli Fu, Hui Tian, Hui Rong, Ping Ai, Xiaoping Li","doi":"10.1186/s41021-023-00283-4","DOIUrl":"10.1186/s41021-023-00283-4","url":null,"abstract":"<p><strong>Background: </strong>Chronic obstructive pulmonary disease (COPD) is a serious health burden worldwide with high mortality. LncRNA plasmacytoma variant translocation 1 (PVT1) has been illustrated to serve as a biomarker for COPD progression. Nonetheless, its specific functions and mechanisms in COPD are unclarified.</p><p><strong>Methods: </strong>Cigarette smoke extract (CSE) was utilized to stimulate 16HBE cells, and cigarette smoke combining with lipopolysaccharide (LPS) was employed to induce COPD in rats. Western blotting and RT-qPCR were utilized for measuring protein and RNA levels. Flow cytometry was implemented for detecting cell apoptosis. Concentrations of inflammatory factors TNF-α and IFN-γ were examined using ELISA. Luciferase reporter assay was utilized for verifying the interaction between molecules. Hematoxylin-eosin staining was performed for histological analysis of rat lung tissues.</p><p><strong>Results: </strong>PVT1 was highly expressed in CSE-stimulated 16HBE cells and the lungs of COPD rats. PVT1 depletion restored the viability, restrained apoptosis and hindered inflammatory cytokine production in 16HBE cells under CSE treatment and alleviated pathological damages in COPD rats. PVT1 bound to miR-30b-5p and miR-30b-5p targeted BCL2 like 11 (BCL2L11). Overexpressing BCL2L11 offset the above effects mediated by PVT1 in CSE-triggered 16HBE cells.</p><p><strong>Conclusion: </strong>PVT1 enhances apoptosis and inflammation of 16HBE cells under CSE stimulation by modulating miR-30b-5p/BCL2L11 axis.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"45 1","pages":"24"},"PeriodicalIF":2.7,"publicationDate":"2023-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10566077/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41198904","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":"Easily-controllable, helper phage-free single-stranded phagemid production system.","authors":"Tetsuya Suzuki,&nbsp;Hiroyuki Kamiya","doi":"10.1186/s41021-022-00254-1","DOIUrl":"https://doi.org/10.1186/s41021-022-00254-1","url":null,"abstract":"<p><strong>Background: </strong>Single-stranded (ss) DNAs are utilized in various molecular biological and biotechnological applications including the construction of double-stranded DNAs with a DNA lesion, and are commonly prepared by using chimeric phage-plasmids (phagemids) plus M13-derived helper phages. However, the yields of ss DNA with these methods are poorly reproducible, and multiple factors must be optimized.</p><p><strong>Results: </strong>In this report, we describe a new arabinose-inducible ss phagemid production method without helper phage infection. The newly exploited DNA derived from VCSM13 expresses the pII protein, which initiates ss DNA synthesis, under the control of the araBAD promoter. In addition, the packaging signal is deleted in the DNA to reduce the contamination of the phage-derived ss DNA. The phagemid DNA of interest, carrying the M13 origin of replication and the packaging signal, was introduced into bacterial cells maintaining the modified VCSM13 DNA as a plasmid, and the ss phagemid DNA production was induced by arabinose. The DNA recovered from the phage particles had less contamination from VCSM13 DNA, as compared to the conventional method. Moreover, we extended the method to purify the ss DNAs by using an anion-exchange column, to avoid the use of hazardous chemicals.</p><p><strong>Conclusion: </strong>Using this combination of methods, large quantities of phagemid ss DNAs of interest can be consistently obtained.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":"25"},"PeriodicalIF":1.7,"publicationDate":"2022-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9667628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40475955","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":"In vivo genotoxicity assessment of a multiwalled carbon nanotube in a mouse ex vivo culture.","authors":"Katsuyoshi Horibata,&nbsp;Hironao Takasawa,&nbsp;Motoki Hojo,&nbsp;Yuhji Taquahashi,&nbsp;Miyuki Shigano,&nbsp;Satoshi Yokota,&nbsp;Norihiro Kobayashi,&nbsp;Kei-Ichi Sugiyama,&nbsp;Masamitsu Honma,&nbsp;Shuichi Hamada","doi":"10.1186/s41021-022-00253-2","DOIUrl":"https://doi.org/10.1186/s41021-022-00253-2","url":null,"abstract":"<p><strong>Background: </strong>Multiwalled carbon nanotubes (MWCNTs) are suspected lung carcinogens because their shape and size are similar to asbestos. Various MWCNT types are manufactured; however, only MWNT-7 is classified into Group 2B by The International Agency for Research on Cancer. MWNT-7's carcinogenicity is strongly related to inflammatory reactions. On the other hand, inconsistent results on MWNT-7 genotoxicity have been reported. We previously observed no significant differences in both Pig-a (blood) and gpt (lung) mutant frequencies between MWNT-7-intratracheally treated and negative control rats. In this study, to investigate in vivo MWNT-7 genotoxicity on various endpoints, we attempted to develop a lung micronucleus assay through ex vivo culture targeting the cellular fraction of Clara cells and alveolar Type II (AT-II) cells, known as the initiating cells of lung cancer. Using this system, we analyzed the in vivo MWNT-7 genotoxicity induced by both whole-body inhalation exposure and intratracheal instillation. We also conducted an erythrocyte micronucleus assay using the samples obtained from animals under intratracheal instillation to investigate the tissue specificity of MWNT-7 induced genotoxicities.</p><p><strong>Results: </strong> We detected a significant increase in the incidence of micronucleated cells derived from the cellular fraction of Clara cells and AT-II cells in both MWNT-7-treated and positive control groups compared to the negative control group under both whole-body inhalation exposures and intratracheal instillation. Additionally, the erythrocyte micronucleus assay detected a significant increase in the incidence of micronucleated reticulocytes only in the positive control group.</p><p><strong>Conclusions: </strong>Our findings indicated that MWNT-7 was genotoxic in the lungs directly exposed by both the body inhalation and intratracheal instillation but not in the hematopoietic tissue.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":"24"},"PeriodicalIF":1.7,"publicationDate":"2022-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9580184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40337162","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}