Sung Ok Kim, Hyun Hwangbo, Su Hyun Hong, Yung Hyun Choi
{"title":"Esculetin Attenuates the Migration and Invasion of Human Hepatocellular Carcinoma Cells by Attenuating Matrix Metalloproteinase Activity and Strengthening Tight Junctions.","authors":"Sung Ok Kim, Hyun Hwangbo, Su Hyun Hong, Yung Hyun Choi","doi":"10.15430/JCP.25.014","DOIUrl":"10.15430/JCP.25.014","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a highly malignant liver cancer that metastasizes to various organs. Esculetin, a natural dihydroxy coumarin derivative, has been shown to have a variety of pharmacological properties, including immune-enhancing, antioxidant, and anti-inflammatory effects. Esculetin is also known to have potent anticancer activity; however, studies on its ability to inhibit cancer cell metastasis are relatively rare. In this study, we investigated how esculetin inhibits the migration and invasion of human hepatocellular carcinoma cell lines Hep3B and HepG2, and elucidated the underlying mechanisms. Our results showed that esculetin markedly suppressed the migration and invasion of HCC cells, and this was associated with a decrease in the expression and activity of matrix metalloproteinase (MMP)-9 and MMP-2, and increased expression levels of tissue inhibitors of metalloproteinase (TIMP)-1 and TIMP-2. In addition, esculetin enhanced the tightening of tight junctions by suppressing the expression of claudin family proteins.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"30 2","pages":"111-117"},"PeriodicalIF":2.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Emma Hiscutt, Suzanne Orchard, Rory Wolfe, Victoria Mar
{"title":"Chemoprevention of Keratinocyte Cancers: Could Aspirin Be the Solution?","authors":"Emma Hiscutt, Suzanne Orchard, Rory Wolfe, Victoria Mar","doi":"10.15430/JCP.25.007","DOIUrl":"10.15430/JCP.25.007","url":null,"abstract":"<p><p>Keratinocyte cancer burden is escalating, particularly in older Australian adults, where the incidence was > 6,000/100,000 in persons aged 80 to 84 per year, compared with 26/100,000 in persons aged 20 to 24 per year, in Queensland between 2011 to 2014. Keratinocyte cancers are estimated to account for 25% of all cancer-related hospitalisations and > $1 billion in treatment costs per year in Australlia. This undoubtedly leads to a large strain on the medical system, as well as amplifying patient morbidity and mortality. Those who are immunosuppressed, or with haematological malignancy or a solid organ transplant, are typically at highest risk of developing a keratinocyte cancer; however, older adults, and especially UV exposed Caucasian populations are increasingly requiring treatment for several keratinocyte cancers every year. This has resulted in an acute, urgent need for efficacious, tolerable, safe chemoprevention agents that could decrease keratinocyte cancer burden. Aspirin has been investigated as a chemopreventive agent for many years in other cancers. In this narrative review, the role for aspirin in the chemoprevention of keratinocyte cancers is discussed.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"30 2","pages":"59-74"},"PeriodicalIF":2.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hye Hyeon Lee, Jin-Woo Jeong, Su Hyun Hong, Cheol Park, Byung Woo Kim, Yung Hyun Choi
{"title":"Erratum: Diallyl Trisulfide Suppresses the Production of Lipopolysaccharide-induced Inflammatory Mediators in BV2 Microglia by Decreasing the NF-κB Pathway Activity Associated with Toll-like Receptor 4 and CXCL12/CXCR4 Pathway Blockade.","authors":"Hye Hyeon Lee, Jin-Woo Jeong, Su Hyun Hong, Cheol Park, Byung Woo Kim, Yung Hyun Choi","doi":"10.15430/JCP.18.026r","DOIUrl":"https://doi.org/10.15430/JCP.18.026r","url":null,"abstract":"<p><p>[This corrects the article on p. 134 in vol. 23, PMID: 30370258.].</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"30 2","pages":"118-120"},"PeriodicalIF":2.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226401/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"High-density Lipoprotein Cholesterol and the Development of Extranodal Marginal Zone B-cell Lymphoma of Mucosa-associated Lymphoid Tissue.","authors":"Joon Hyun Cho, Su Youn Nam, Junwoo Jo","doi":"10.15430/JCP.25.006","DOIUrl":"10.15430/JCP.25.006","url":null,"abstract":"<p><p>To date, no studies have examined the effect of high-density lipoprotein cholesterol (HDL-C) on the development of extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma). We investigated, for the first time, the relationship between HDL-C and the risk of MALT lymphoma. In this nationwide population-based cohort study, 4.25 million cancer-free individuals that underwent a National General Health Examination and cancer screening in 2010 were enrolled and followed until the end of 2017. Subjects were classified into 5 groups based on HDL-C levels (< 30, 30-39, 40-49, 50-59, or ≥ 60 mg/dL). MALT lymphoma was diagnosed in 1,119 of the 4.25 million study subjects during the follow-up period. Subjects with the lowest HDL-C level (< 30 mg/dL) had a higher risk of MALT lymphoma (adjusted hazard ratio [aHR] 1.79, 95% CI 1.08-2.96) than those with a HDL-C level of 40 to 49 mg/dL, whereas those with the highest HDL-C level (≥ 60 mg/dL) had a lower risk of MALT lymphoma (aHR 0.84, 95% CI 0.71-0.99). Sensitivity analyses, excluding individuals who were diagnosed with MALT lymphoma within 2-year of follow-up, also revealed similar association. In subgroup analysis, the hazardous effect of low HDL-C on MALT lymphoma development was significant in females (aHR 2.31, 95% CI 1.13-4.72) but not in males. An unfavorable effect of low HDL-C on MALT lymphoma was significant in never smokers (aHR 2.20, 95% CI 1.19-4.05) but not in smokers. In conclusion, a low HDL-C level was found to be associated with an increased risk of MALT lymphoma particularly in females or never smokers.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"30 2","pages":"89-96"},"PeriodicalIF":2.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226400/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Seyed Vahid Ahmadi Tabatabaei, Ali Akbar Haghdoost, Seyyed Mohammad Alavi, Milad Rajabzadeh-Dehkordi, Hamid Ghalandari, Moein Askarpour
{"title":"Fruit and Vegetable Intake in Relation to Lung Cancer Risk: A Systematic Review and Dose-response Meta-analysis of Prospective Cohort Studies.","authors":"Seyed Vahid Ahmadi Tabatabaei, Ali Akbar Haghdoost, Seyyed Mohammad Alavi, Milad Rajabzadeh-Dehkordi, Hamid Ghalandari, Moein Askarpour","doi":"10.15430/JCP.25.009","DOIUrl":"10.15430/JCP.25.009","url":null,"abstract":"<p><p>The objective of this study was to consolidate the mounting evidence related to the association between fruit and vegetable intake and lung cancer risk by conducting a systematic review of prospective studies and a dose-response meta-analysis. A systematic search was conducted on major online databases (PubMed, Scopus, and Web of Science) from inception up to January 2024. The exposures included daily intake of total fruits and vegetables (FVs), vegetables, fruits, and their subclasses (including cruciferous and green leafy vegetables, and citrus fruits). The main outcome was lung cancer and its subclasses (incidence and mortality). Out of 31,819 records initially retrieved, 41 eligible studies were included. Significant inverse associations were observed between lung cancer and daily consumption of total FVs (risk ratios [RR]: 0.81, 95% CI: 0.74-0.90), vegetables (RR: 0.87, 95% CI: 0.83-0.91), fruits (RR: 0.78, 95% CI: 0.72-0.85), cruciferous vegetables (RR: 0.82, 95% CI: 0.75-0.91), green leafy vegetables (RR: 0.85, 95% CI: 0.76-0.94), and citrus fruits (RR: 0.80, 95% CI: 0.73-0.88). Non-linear dose-response associations were observed regarding lung cancer and all of the exposures, except for cruciferous vegetables. The consumption of FVs may decrease the risk of lung cancer incidence and mortality. The type of lung cancer, biological sex of individuals, and smoking status can alter this association.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"30 2","pages":"75-88"},"PeriodicalIF":2.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226403/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sevelamer Ameliorates Early Cirrhosis and Inhibits Its Progression towards Hepatocellular Carcinoma in a Diethylnitrosamine-induced Rat Model.","authors":"Ze-Ning Chen, Yang-Feng Lv, Zhi-Xing Liu, Rui Zhao, Zhi-Qiang Deng, Mei-Diao Kang, Zi-Qiang Liao, Fan-Kun Zhou, Qing-Rong Liang, Qun Tang","doi":"10.15430/JCP.25.003","DOIUrl":"10.15430/JCP.25.003","url":null,"abstract":"<p><p>Cirrhosis has a very high morbidity and mortality and partially progressed into hepatocellular carcinoma (HCC). Sevelamer is an oral phosphate binder to treat hyperphosphatemia. Here, we investigated the contribution of sevelamer to the remission of cirrhosis, and further the prevention of HCC. Diethylnitrosamine (DEN)-treated rats, developing the sequential stage of cirrhosis to HCC, were used to identify the therapeutic and preventive effects via transient elastography, hematological biochemistry, and pathological examination. Ultrasound image and transient elastography are indicative of the occurrence of cirrhosis characterized by the pseudolobular formation and higher stiffness after DEN exposure, and few nodules and lower stiffness values were observed in the control and sevelamer treated group. Hematological biochemistry showed that indicators of liver fibrosis (serum hyaluronic acid and type III precollagen) and serum tumor biomarkers (VEGF-α, α-L-fucosidase) were also simultaneously reversed. Pathological examination showed that hepatic steatosis, inflammation, and fibrotic deposits were remarkably alleviated after sevelamer administration. The pharmacology of sevelamer might be attributable to rebalance of oxidative stress as assessed by determination of the total reactive oxygen specie, malondialdehyde and antioxidant enzymes, to modulation of inflammation as evidenced by decreased interleukin (IL)-1β, IL-4, IL-6 and TNFα levels, and to inhibition of angiogenesis as measured by microvessel density. Our findings confirm that sevelamer reverses cirrhosis and prevents its deterioration to in the DEN-induced rat HCC model.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"30 2","pages":"97-110"},"PeriodicalIF":2.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jae Young Jang, Nayoung Kim, Ryoung Hee Nam, Eun Hye Kim, Chin-Hee Song, Sungchan Ha, Jieun Lee
{"title":"Establishment of an Organoid Culture Model Derived from Small Intestinal Epithelium of C57BL/6 Mice and Its Benefits over Tissues.","authors":"Jae Young Jang, Nayoung Kim, Ryoung Hee Nam, Eun Hye Kim, Chin-Hee Song, Sungchan Ha, Jieun Lee","doi":"10.15430/JCP.25.008","DOIUrl":"10.15430/JCP.25.008","url":null,"abstract":"<p><p>This study aimed to establish an organoid culture model using small intestine tissues from male and female C57BL/6 mice and to compare it with rat organoid cultures derived from frozen tissues. Crypts were isolated from the small intestines of eight-week-old male and female mice and cultured in 3D extracellular matrix with Wnt, R-spondin, and Noggin. In addition, small intestine tissues from sixteen-week-old F344 rats were preserved in a storage solution immediately post-sacrifice and stored at -80°C before being transferred to a nitrogen tank. Upon thawing, crypts from frozen rat tissues failed to develop into organoids due to structural damage, suggesting the need for fresh tissues or optimized preservation methods. In contrast, mouse-derived organoids showed viability for 7 days, with distinct morphological changes and clear differentiation by Day 7. Quantitative real-time PCR analysis revealed that Lgr5, a stem cell marker, showed significantly higher expression in organoids than in tissues, confirming the successful establishment of the organoid culture. Among epithelial markers, the antimicrobial enzyme Lyz1 was more highly expressed in organoids, while Muc2, a key goblet cell marker, was more highly expressed in male tissues. The enterocyte marker Alp exhibited higher expression in male organoids compared to females, with no sex differences in tissues. These findings highlight sex-specific differences in gene expression related to small intestine differentiation and demonstrate the challenges in organoid culture from frozen rat tissues. The results suggest the importance of immediate tissue processing or improved preservation methods for successful organoid cultures.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"30 1","pages":"12-23"},"PeriodicalIF":2.5,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11973465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Impact of Early Testing and Analysis of Germline Genetic Mutation in Patients with Breast Cancer: A Single Institution Experience.","authors":"Maha Zafar, Manaswini Krishnakumar, Aswanth Reddy","doi":"10.15430/JCP.25.001","DOIUrl":"10.15430/JCP.25.001","url":null,"abstract":"<p><p>Breast cancer is the most common cancer among women worldwide, with germline mutations in high-penetrance genes like BRCA1 and BRCA2, and moderate-penetrance genes such as CHEK2 and ATM contributing majorly to the onset of the same. Universal germline genetic testing offers an avenue to improve early identification and develop appropriate management guidelines. Our retrospective cohort study analyzed data from 525 newly diagnosed breast cancer patients at Mercy Hospital Fort Smith from January 2020 to December 2023. Patients underwent germline genetic testing using next-generation sequencing panels irrespective of family history of cancer. Details on patient demographics, clinical characteristics, and genetic test results were collected and analyzed. The median age at diagnosis of patients was 66, with invasive ductal carcinoma (IDC) being the major subtype (66%). CHEK2 mutations were the most common pathogenic mutations (9 patients), followed by BRCA1 and MUTYH (6 each). Pathogenic mutations were more prevalent in patients over 60 years (63%). Germline mutations were identified more frequently in IDC than in ductal carcinoma in situ. Among patients with germline mutations, there was a significant drift toward mastectomy over breast-conserving surgery. Universal germline genetic testing identified pathogenic mutations in a significant proportion of breast cancer patients, especially among the older patient population. The findings further emphasize the importance of integrating universal genetic testing into routine care to guide surgical and risk-reduction management protocols effectively. Further research is needed to regularize genetic testing in similar patients.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"30 1","pages":"41-46"},"PeriodicalIF":2.5,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11973463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hyejin Lee, Hyerim Jang, Jeongyeon Kim, Seoyeon Maeng, Jihye Kim
{"title":"Bladder Cancer Medication Bacillus Calmette-Guérin-Cell Wall Skeleton Focusing on Alternatives and Developments to Limitations.","authors":"Hyejin Lee, Hyerim Jang, Jeongyeon Kim, Seoyeon Maeng, Jihye Kim","doi":"10.15430/JCP.25.002","DOIUrl":"10.15430/JCP.25.002","url":null,"abstract":"<p><p>Bacillus Calmette-Guérin (BCG) serves as an anticancer drug for bladder cancer by enhancing the innate immune response and facilitating the expression of beta-defensin-2/-3. BCG is significantly more effective than other treatment modalities; however, it has limitations due to the nonspecific secretion of immune proteins such as interleukin-2 (IL-2) and IFN-γ, necessitating frequent injections that result in toxicity. The newly developed BCG-cell wall skeleton (BCG-CWS) is intended to address the non-specificity and the requirement for repeated treatments associated with BCG. BCG-CWS stimulates antigen-presenting cells by secreting cytokines such as IL-12, using an adjuvant to enhance the immune response and synergize with it to provoke a potent immune reaction. Nevertheless, BCG-CWS encounters issues related to cellular uptake due to the substantial molecular weight of the drug. To meet this challenge, various strategies such as the introduction of R8 protein, the liposome evaporated via an emulsified lipid method, and nanoparticle formulation have been employed which can enhance targeted drug delivery, though issues related to particle size remain unresolved. This paper aims to discuss future perspectives by examining the mechanisms and challenges of BCG-CWS.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"30 1","pages":"1-6"},"PeriodicalIF":2.5,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11973459/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mitochondrial Ribosomal Protein S17 Silencing Inhibits Proliferation and Invasiveness of Lung Cancer Cells.","authors":"Woo Rin Lee, Kook Sun Ha","doi":"10.15430/JCP.24.023","DOIUrl":"10.15430/JCP.24.023","url":null,"abstract":"<p><p>Chromosomal alterations are frequent events in lung cancer progression. Although gains and losses of chromosomal position have been reported, the association between copy number alteration and lung cancer patient survival has not been extensively investigated. In this study, we performed a meta-analysis of public cBioPortal datasets spanning 25 lung cancer studies to identify putative cancer driver genes with copy number alterations associated with overall patient survival. Ten copy-number altered genes enriched in deceased lung cancer patients were identified. Seven of these putative driver genes were located in the 7p11.2 chromosomal location, and two were in the 9p21.3 cytoband. Among these genes, the mitochondrial ribosomal protein S17 (MRPS17) amplification was significantly associated with a lower patient survival rate (<i>P</i> = 1.47e-7). To investigate the functional role of MRPS17, small interfering RNA-mediated knockdown was performed in two non-small cell lung cancer cell lines, A549 and NCI-H460. MRPS17 knockdown significantly reduced cell proliferation, migration, invasion, and anchorage-independent growth in both cell lines. Furthermore, knockdown of MRPS17 decreased the activation of the phosphatidylinositol 3-kinase/protein kinase B signaling pathway, suggesting its role in driving lung cancer progression through this critical oncogenic pathway. Our findings highlight MRPS17 as a potential cancer therapy target and a prognostic biomarker that may improve the survival rates of lung cancer patients. Future studies should explore its inhibition as a therapeutic strategy as well as elucidate its molecular mechanisms in cancer progression.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"30 1","pages":"47-55"},"PeriodicalIF":2.5,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11973458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}