{"title":"Novel acetylation-related gene signatures for predicting the prognosis of patients with colorectal cancer.","authors":"Zhuang Jing, Feng Ziwang, Wu Yinhang, Zhou Yani, Chu Jian, Wu Jingwen, Han Shuwen","doi":"10.1007/s13577-022-00720-6","DOIUrl":"10.1007/s13577-022-00720-6","url":null,"abstract":"<p><p>Histone acetylation may affect the tumorigenesis and prognosis of colorectal cancer (CRC). However, there is still a lack of studies exploring the effect of acetylation-related genes on the prognosis of CRC. To explore the role of acetylation-related genes in CRC prognosis using bioinformatics strategies, the expression data and survival information of CRC patients were collected from the Gene Expression Omnibus. The Molecular Signatures Database was used to select acetylation-related genes. Univariate and least absolute shrinkage and selection operator regression analyses were used to screen prognostic genes. Kaplan-Meier curves were plotted for survival analysis. Cibersort and pRRophetics were used to analyze immune infiltration and predict drug sensitivity, respectively. By implementing independent prognostic factors, a nomogram model was constructed. The result showed that a total of 48 prognostic genes which screened from the acetylation-related gene set were mainly enriched in ABC transporters and acetylation/deacetylation-related pathways. Three gene signatures (SDR16C5, MEAF6, and SOX4) were further defined, and a prognostic model was constructed that showed high sensitivity and specificity for predicting CRC prognosis in both training and validation cohorts. Patients with different prognostic risks also presented differential expression of gene signatures, infiltration of activated CD4 memory T cells, and drug sensitivity to bicalutamide, gefitinib, Lenalidomide, and imatinib. The nomogram suggested the potential of a risk score-based model in predicting 1- and 2-year survival in patients with CRC. In conclusion, we proposed three gene signatures from an acetylation-related gene set as potential targets for epigenetic therapy and constructed a prognostic model for CRC.</p>","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1159-1173"},"PeriodicalIF":2.8,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43226151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Establishment and characterization of two novel patient-derived myxoid liposarcoma cell lines.","authors":"Rei Noguchi, Yuki Yoshimatsu, Yooksil Sin, Ryuto Tsuchiya, Takuya Ono, Taro Akiyama, Kaoru Hirabayashi, Iwao Ozawa, Rumi Nakagawa, Kazutaka Kikuta, Tadashi Kondo","doi":"10.1007/s13577-022-00717-1","DOIUrl":"10.1007/s13577-022-00717-1","url":null,"abstract":"<p><p>Myxoid liposarcoma (MLPS) is a lipogenic sarcoma, characterized by myxoid appearance histology and the presence of the FUS-DDIT3 fusion gene. MLPS shows frequent recurrence and poor prognosis after standard treatments, such as surgery. Therefore, novel therapeutic approaches for MLPS are needed. Development of novel treatments requires patient-derived cell lines to study the drug responses and their molecular backgrounds. Presently, only three cell lines of MLPS have been reported, and no line is available from public cell banks. Thus, this study aimed to establish and characterize novel MLPS cell lines. Using surgically resected tumor tissue from two patients with MLPS, two novel lines NCC-MLPS2-C1 and NCC-MLPS3-C1 were established. The presence of FUS-DDIT3 fusion, slow growth, spheroid formation, and invasive capability in these cell lines was confirmed. Growth retardation was monitored for 213 anti-cancer agents using NCC-MLPS2-C1 and NCC-MLPS3-C1 cells, and the results were integrated with the response to treatments in an MLPS cell line, NCC-MLPS1-C1, which was previously established in our laboratory. We found that romidepsin suppressed cell proliferation at considerably low concentrations in all three examined cell lines. NCC-MLPS2-C1 and NCC-MLPS3-C1 cell lines developed here represent a useful tool for basic and preclinical studies of MLPS.</p>","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1279-1289"},"PeriodicalIF":2.8,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41774304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Non-coding RNAs in ferroptotic cancer cell death pathway: meet the new masters.","authors":"Mehdi Rabiee Valashedi, Chia Bamshad, Nima Najafi-Ghalehlou, Amirsadegh Nikoo, Kazuo Tomita, Yoshikazu Kuwahara, Tomoaki Sato, Amaneh Mohammadi Roushandeh, Mehryar Habibi Roudkenar","doi":"10.1007/s13577-022-00699-0","DOIUrl":"10.1007/s13577-022-00699-0","url":null,"abstract":"<p><p>Despite the recent advances in cancer therapy, cancer chemoresistance looms large along with radioresistance, a major challenge in dire need of thorough and minute investigation. Not long ago, cancer cells were reported to have proven refractory to the ferroptotic cell death, a newly discovered form of regulated cell death (RCD), conspicuous enough to draw attention from scholars in terms of targeting ferroptosis as a prospective therapeutic strategy. However, our knowledge concerning the underlying molecular mechanisms through which cancer cells gain immunity against ferroptosis is still in its infancy. Of late, the implication of non-coding RNAs (ncRNAs), including circular RNAs (circRNAs), microRNAs (miRNAs), and long non-coding RNAs (lncRNAs) in ferroptosis has been disclosed. Nevertheless, precisely explaining the molecular mechanisms behind the contribution of ncRNAs to cancer radio/chemotherapy resistance remains a challenge, requiring further clarification. In this review, we have presented the latest available information on the ways and means of regulating ferroptosis by ncRNAs. Moreover, we have provided important insights about targeting ncRNAs implicated in ferroptosis with the hope of opening up new horizons for overcoming cancer treatment modalities. Though a long path awaits until we make this ambitious dream come true, recent progress in gene therapy, including gene-editing technology will aid us to be optimistic that ncRNAs-based ferroptosis targeting would soon be on stream as a novel therapeutic strategy for treating cancer.</p>","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"972-994"},"PeriodicalIF":2.8,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45540990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human CellPub Date : 2022-07-01Epub Date: 2022-06-02DOI: 10.1007/s13577-022-00721-5
Yuki Yoshimatsu, Rei Noguchi, Yooksil Sin, Ryuto Tsuchiya, Takuya Ono, Taro Akiyama, Jun Sugaya, Naoki Kojima, Akihiko Yoshida, Akira Kawai, Tadashi Kondo
{"title":"Establishment and characterization of NCC-SS5-C1: a novel patient-derived cell line of synovial sarcoma.","authors":"Yuki Yoshimatsu, Rei Noguchi, Yooksil Sin, Ryuto Tsuchiya, Takuya Ono, Taro Akiyama, Jun Sugaya, Naoki Kojima, Akihiko Yoshida, Akira Kawai, Tadashi Kondo","doi":"10.1007/s13577-022-00721-5","DOIUrl":"10.1007/s13577-022-00721-5","url":null,"abstract":"<p><p>Synovial sarcoma (SS) is a rare and aggressive mesenchymal malignancy driven by a unique chromosomal translocation that generates the expression of the SS18:SSX fusion protein. It occurs at almost any anatomical site and most commonly in young adults. The standard curative treatment for primary SS is a wide surgical resection combined with radiotherapy and/or neoadjuvant chemotherapy. The prognosis of SS varies among patients, with the 5 years survival rate ranging from 50 to 60% in adults and 90% in children. Although patient-derived cell lines are a useful resource for the development of new therapies, only a few are available from public cell banks. Therefore, this study aimed to establish and characterize a novel SS cell line. We successfully established a novel cell line, NCC-SS5-C1, harboring an SS18-SSX1 fusion gene. NCC-SS5-C1 cells demonstrated constant growth and invasion ability. We performed integrative drug screening using eight SS cell lines, including NCC-SS5-C1 cells, and examined the response spectrum of existing anticancer agents. We conclude that NCC-SS5-C1 is a useful resource for studying SS.</p>","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1290-1297"},"PeriodicalIF":2.8,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43357557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human CellPub Date : 2022-07-01Epub Date: 2022-05-27DOI: 10.1007/s13577-022-00708-2
Yunlong Cui, Ning Jiang
{"title":"Identification of a seven-gene signature predicting clinical outcome of liver cancer based on tumor mutational burden.","authors":"Yunlong Cui, Ning Jiang","doi":"10.1007/s13577-022-00708-2","DOIUrl":"10.1007/s13577-022-00708-2","url":null,"abstract":"<p><p>The total number of somatic mutations may affect the prognosis of cancer, so we applied bioinformatics methods to investigate the association between the TMB (tumor mutational burden)-related differentially expressed genes (DEGs) and the prognosis of hepatocellular carcinoma (HCC). We calculated the TMB value of the patients with HCC in TCGA database and identified the differentially expressed genes between the high-TMB and low-TMB patients. We performed functional enrichment analysis and LASSO Cox regression analysis of the DEGs, and seven genes were screened to establish a risk score model. A nomogram based on the risk scores was drawn to assess the predictive outcomes compared to the actual outcomes. The expression level of the seven genes was verified in cancer cell lines. Moreover, we explored the difference in immune cells infiltration and immune checkpoints between the high-risk and low-risk groups. The results showed that the DEGs between the high-TMB and low-TMB patients were enriched in extracellular matrix organization. A seven-gene risk score model (PAGE1, CHGA, OGN, MMP7, TRIM55, MAGEA6, and MAGEA12) was established for predicting HCC prognosis. Patients with lower risk scores had longer survival time and lower mortality rate. The nomogram based on risk scores and TNM staging showed good performance and reliability in predicting the clinical outcomes. Significant differences in cell infiltration and checkpoints were found between the high-risk and low-risk groups. Our study demonstrated a seven-gene signature and a nomogram based on the risk score model to predict the prognosis of HCC. Some of the newly identified DEGs may be potential biomarkers or therapeutic targets.</p>","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1192-1206"},"PeriodicalIF":2.8,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43199263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ultrasound-targeted microbubble destruction-mediated silencing of FBXO11 suppresses development of pancreatic cancer.","authors":"Jing Xue, Shengjiang Chen, Dongfeng Ge, Xiaozhi Yuan","doi":"10.1007/s13577-022-00700-w","DOIUrl":"10.1007/s13577-022-00700-w","url":null,"abstract":"<p><p>Ultrasound-targeted microbubble destruction (UTMD) has been a promising noninvasive tool for organ- or tissue-specific gene or drug delivery. This study aimed to explore the function of F-box protein 11 (FBXO11), an E3 ubiquitin ligase, in the development of pancreatic cancer (PCa). Differentially expressed genes in PCa were identified using the GSE62452 and GSE28735 datasets, and FBXO11 was significantly highly expressed in PCa. UTMD-mediated FBXO11 silencing significantly suppressed growth activity, epithelial-mesenchymal transition, migration, and invasion while reduced apoptosis of PCa cells in vitro and reduced the growth and metastasis of xenograft tumors in vivo. Importantly, UTMD-mediated sh-FBXO11 showed more pronounced tumor-suppressive effects than direct administration of sh-FBXO11 alone. The potential substrates of FBXO11 as an E3 ubiquitin ligase were predicted using the Ubibrowser. TP53 was predicted and validated as a downstream substrate of FBXO11. FBXO11 induced ubiquitination and degradation of the tumor suppressor protein TP53 to induce PCa progression. In conclusion, this study suggests that silencing of FBXO11, especially that mediated by UTMD, might suppress the malignant biological behaviors of PCa cells and serve as a potential therapeutic strategy for PCa management.</p>","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1174-1191"},"PeriodicalIF":2.8,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48466132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A novel mitochondria-related gene signature for controlling colon cancer cell mitochondrial respiration and proliferation.","authors":"Zhenyu Zhu, Qingsheng Hou, Bishi Wang, Changhao Li, Luguang Liu, Weipeng Gong, Jie Chai, Hongliang Guo","doi":"10.1007/s13577-022-00702-8","DOIUrl":"10.1007/s13577-022-00702-8","url":null,"abstract":"<p><p>Colon cancer cells rely on mitochondrial respiration as major source of energy for supporting their proliferation and invasion, thus promoting colon cancer malignancy and progression. In this study, we comprehensively investigated the prognostic significance of mitochondria-related genes in colon cancer and identified the hub genes that control colon cancer cell mitochondrial respiration and proliferation. We first systematically evaluated the prognostic significance of differentially expressed mitochondria-related genes in colon cancer specimens. Furthermore, a protein-protein interaction network was constructed to explore the hub genes. Eventually, five hub genes were identified, namely, POLG, FASTK, MRPS5, AARS2, and VARS2. Functional analyses showed that all these five hub genes are essential for maintaining mitochondrial respiration and proliferation of colon cancer cells. Mechanistic studies revealed the roles of these five hub genes in modulating mitochondrial DNA expression, that in turn influence mitochondrial respiration. In summary, our study demonstrated that POLG, FASTK, MRPS5, AARS2, and VARS2 may potentially serve as prognostic biomarkers and therapeutic targets for colon cancer.</p>","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1126-1139"},"PeriodicalIF":2.8,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44668966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human CellPub Date : 2022-07-01Epub Date: 2022-05-05DOI: 10.1007/s13577-022-00705-5
Girish K Srivastava, David Rodriguez-Crespo, Ivan Fernandez-Bueno, José Carlos Pastor
{"title":"Factors influencing mesenchymal stromal cells in in vitro cellular models to study retinal pigment epithelial cell rescue.","authors":"Girish K Srivastava, David Rodriguez-Crespo, Ivan Fernandez-Bueno, José Carlos Pastor","doi":"10.1007/s13577-022-00705-5","DOIUrl":"10.1007/s13577-022-00705-5","url":null,"abstract":"<p><p>Mesenchymal stromal cells (MSC) stop or slow retinal pigment epithelium (RPE) and neuroretina (NR) degeneration by paracrine activity in oxidative stress-induced retinal degenerative diseases. However, it is mandatory to develop adequate in vitro models that allow testing new treatment strategies against oxidative stress before performing in vivo studies. The viable double- and triple-layered setups are composed of separate layers of NR, MSC, and RPE (NR-MSC-RPE, NR-RPE, MSC-RPE) partially mimic in vivo retinal conditions. In this study, the paracrine neuroprotective effect of each setup's microenvironment on hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-stressed was compared with unstressed RPE cells. RPE cell proliferation viability was assessed on day 1, 3, and 6 using Alamar Blue® (10%), MTT (10%) and a cell viability/cytotoxicity assay kit followed by data analysis. The results showed that RPE cells, highly viable (> 90%) in mixed medium of DMEM and neurobasal A (1:1), lost 50% viability on exposure to 400 µM of H<sub>2</sub>O<sub>2</sub> (P < 0.05). The unexposed groups differed significantly from exposed groups for RPE cell growth (RPE and [Formula: see text]RPE (P < 0.0001), NR-MSC-RPE, and NR-MSC-[Formula: see text]RPE (P < 0.05), NR-RPE and NR-[Formula: see text]RPE (P < 0.01), and MSC-RPE and MSC-[Formula: see text]RPE (P < 0.01). NR-[Formula: see text]RPE and NR-RPE supported RPE cell proliferation viability better than other setups (P < 0.01) and RPE cells proliferated 0.49-fold more in NR-MSC-[Formula: see text]RPE than NR-MSC-RPE. Thus, NR and MSC presence improved significantly each setup's microenvironment for cell rescue, nevertheless, each setup also showed limitations for its use as an in vitro study tool. Health of microenvironment of such setups depends on many factors including cell-secreted trophic factors.</p>","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1005-1015"},"PeriodicalIF":2.8,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47223689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human CellPub Date : 2022-07-01Epub Date: 2022-05-21DOI: 10.1007/s13577-022-00715-3
Atika Al Saqri, Shika Hanif Malgundkar, Fatima Al Kindi, Ishita Gupta, Mansour Al Moundhri, Yahya Tamimi
{"title":"SOCS3 gene silencing does not occur through methylation and mutations in gastric cancer.","authors":"Atika Al Saqri, Shika Hanif Malgundkar, Fatima Al Kindi, Ishita Gupta, Mansour Al Moundhri, Yahya Tamimi","doi":"10.1007/s13577-022-00715-3","DOIUrl":"10.1007/s13577-022-00715-3","url":null,"abstract":"<p><p>Gastric cancer (GC) is ranked the third leading cause of cancer-related deaths worldwide. Mutations and epigenetic alterations in several essential genes, including p53, KRAS, PIK3CA, FAT4 and ARID1A, are often reported. Furthermore, loss of SOCS3 expression was reported in GC, suggesting its tumor suppressor role. To assess the mutational and methylation status of SOCS3, we performed gene panel exome sequencing on 47 human GC samples. The SOCS3 gene was rarely mutated, suggesting alternative regulation mechanisms, such as promoter hypermethylation and/or long non-coding RNAs (lncRNAs). We first explored SOCS3 promoter methylation status in 44 human GC samples by methylation-specific PCR (MS-PCR). Thirteen out of forty-four patients (29.5%) displayed a methylation pattern. Then, to see whether SOCS3 expression is silenced by CpG methylation, we examined publicly available databases (cbioportal and The Cancer Genome Atlas (TCGA)). The analysis revealed β values lower than 0.1, indicating hypo-methylation in healthy and GC samples. Moreover, moderate methylation (β < 0.4) and high methylation (β > 0.4) did not affect the free survival, suggesting that methylation is unlikely to be the mechanism ruling SOCS3 silencing in GC. Next, to assess the regulatory effects of lncRNAs on SOCS3, we silenced the AC125807.2-lncRNA and quantified the SOCS3 gene expression in AGS and NCI-N87 gastric cancer cell line. SOCS3 was found to be downregulated following AC125807.2-lncRNA silencing in AGS cells, suggesting the potential implication of lncRNA AC125807.2 in SOCS3 regulation. However, in NCI-N87 cells, there was no significant change in SOCS3 expression. In conclusion, neither mutations nor hypermethylation was associated with the SOCS3 downregulation in GC, and alternative mechanisms, including non-coding RNAs-mediated gene silencing, may be proposed.</p>","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1114-1125"},"PeriodicalIF":2.8,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45541994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Increased neuropilin-1 expression by COVID-19: a possible cause of long-term neurological complications and progression of primary brain tumors.","authors":"Hamidreza Zalpoor, Hooriyeh Shapourian, Abdullatif Akbari, Shaghayegh Shahveh, Leila Haghshenas","doi":"10.1007/s13577-022-00716-2","DOIUrl":"10.1007/s13577-022-00716-2","url":null,"abstract":"","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1301-1303"},"PeriodicalIF":4.3,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9084541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43427481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}