{"title":"RETRACTION: Development of an Experimental Animal Model for Lower Back Pain by Percutaneous Injury-Induced Lumbar Facet Joint Osteoarthritis","authors":"","doi":"10.1002/jcp.31455","DOIUrl":"10.1002/jcp.31455","url":null,"abstract":"<p><b>RETRACTION</b>: J.-S. Kim, K. Ahmadinia, X. Li, J. L. Hamilton, S. Andrews, C. A. Haralampus, G. Xiao, H.-M. Sohn, J.-W. You, Y.-S. Seo, G. S. Stein, A. J. Van Wijnen, S.-G. Kim, and H.-J. Im, “Development of an Experimental Animal Model for Lower Back Pain by Percutaneous Injury-Induced Lumbar Facet Joint Osteoarthritis,” <i>Journal of Cellular Physiology</i> 230, no. 11 (2015): 2837-2847, https://doi.org/10.1002/jcp.25015.</p><p>The above article, published online on 9 April 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has occurred due to concerns related to the data presented in the article raised by the Office of Research Compliance at Rush University Medical Center following an investigation jointly conducted by Rush University and the Jesse Brown Veterans Affairs Medical Center (JBVAMC). Specifically, the journal has been made aware of discrepancies in the reported sample sizes for each of the three experimental groups in Figure 4A, with the indicated numbers exceeding the actual sample sizes. Additionally, image elements of the experimental data in Figure 7A and B were found to have been used by the same author(s) for publication elsewhere in a different scientific context. The corresponding author, Dr. Hee-Jeong Im Sampen, has been informed of the decision to retract but did not agree with it, as she is confident that any errors in the publication do not impact the reliability of the paper's findings. She also advised the editors that she stands ready to cooperate fully to make any necessary corrections. However, the article is retracted as the editors lost trust in the accuracy of the data and consider the conclusions invalid.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"239 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31455","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiaoling Chen, An Wenting, Huang Zhiqing, Gang Jia, Hua Zhao
{"title":"Taurine reduces glycolysis of pig skeletal muscle by inhibiting HIF-1α signaling","authors":"Xiaoling Chen, An Wenting, Huang Zhiqing, Gang Jia, Hua Zhao","doi":"10.1002/jcp.31461","DOIUrl":"10.1002/jcp.31461","url":null,"abstract":"<p>The aim of this study was to investigate the effect of taurine on skeletal muscle glycolysis in pigs. The results showed that dietary supplementation of taurine significantly reduced the activities of hexokinase (HK), phosphofructose kinase (PFK), and pyruvate kinase (PK) in finishing pigs. Meanwhile, taurine reduced the protein and mRNA expression levels of hypoxia inducible factor 1α (HIF-1α) and the mRNA expression of glycolytic enzyme related genes (such as HK type II, HK Ⅱ; pyruvate kinase M2, PKM2; lactate dehydrogenase A, LDHA). In addition, taurine reduced the expression of HIF-1α, lactate content, and the expression of glycolysis related genes in porcine myotubes. These results suggest that taurine may regulate glycolysis in skeletal muscle of finishing pigs through the HIF-1α signaling pathway. To further investigate the mechanism by which taurine affects skeletal glycolysis, HIF-1α activator dimethyloxalyl glycine (DMOG) was used to treat porcine myotubes, our results showed that DMOG significantly increased the protein and mRNA expression levels of HIF-1α, lactate content, and glycolytic enzyme (HK, PFK, PK, and LDH) activity, but taurine treatment significantly inhibited this effect. Taken together, these results of in vivo and in vitro experiments revealed that taurine reduces skeletal muscle glycolysis by inhibiting HIF-1α signaling.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"RETRACTION: PNU-74654 enhances the antiproliferative effects of 5-FU in breast cancer and antagonizes thrombin-induced cell growth via the Wnt pathway","authors":"","doi":"10.1002/jcp.31462","DOIUrl":"10.1002/jcp.31462","url":null,"abstract":"<p><b>RETRACTION</b>: F. Rahmani, F. Amerizadeh, S. M. Hassanian, M. Hashemzehi, S.-N. Nasiri, H. Fiuji, G. A. Ferns, M. Khazaei, and A. Avan, “PNU-74654 Enhances the Antiproliferative Effects of 5-FU in Breast Cancer and Antagonizes Thrombin-induced Cell Growth via the Wnt Pathway,” <i>Journal of Cellular Physiology</i> 234, no. 8 (2019): 14123-14132, https://doi.org/10.1002/jcp.28104.</p><p>The above article, published online on 11 January 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC.</p><p>The retraction has been agreed due to concerns raised by a third party on the data presented in the article. Specifically, image elements in Figure 1c were previously published by the same author group in a different scientific context. Additionally, the panels representing the histological staining corresponding to the “Control” and “5-FU” groups in Figure 3b were found to originate from the same biological sample. Finally, splicing sites have been detected within Figure 6b. The concerns were not satisfactorily addressed by the authors upon request. Accordingly, retraction is warranted as the editors have lost trust in the data presented in the article and in its conclusions. The corresponding author Majid Khazaei disagrees with the decision of retraction. No confirmation was obtained by the remaining co-authors.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"239 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31462","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anna A. Valyaeva, Maria A. Tikhomirova, Junyi Feng, Anastasia A. Zharikova, Daria M. Potashnikova, Yana R. Musinova, Andrey A. Mironov, Yegor S. Vassetzky, Eugene V. Sheval
{"title":"Compensatory reactions of B cells in response to chronic HIV-1 Tat exposure","authors":"Anna A. Valyaeva, Maria A. Tikhomirova, Junyi Feng, Anastasia A. Zharikova, Daria M. Potashnikova, Yana R. Musinova, Andrey A. Mironov, Yegor S. Vassetzky, Eugene V. Sheval","doi":"10.1002/jcp.31459","DOIUrl":"10.1002/jcp.31459","url":null,"abstract":"<p>Patients infected with human immunodeficiency virus-1 (HIV-1) have an increased incidence of B-cell lymphoma, even though HIV-1 does not infect B cells. The development of B-cell lymphomas appears to be related to the action of the HIV-1 transactivator protein (Tat), which is released from HIV-infected cells and penetrates uninfected B cells, affecting host cell gene expression. Upon chronic HIV-1 infection, Tat acts on the cells for a long time, probably allowing the cells to adapt to the presence of the viral protein. The aim of this work was to identify and study the mechanism of adaptation of cells to prolonged (chronic) exposure to HIV-1 Tat. We performed a comparative analysis of cells expressing Tat under the action of either an inducible promoter or a constitutive promoter, allowing us to model acute and chronic Tat effects, respectively. We found that the acute action of Tat leads to the suppression of cell proliferation, probably due to the downregulation of genes associated with replication and protein synthesis. In the case of chronic action of Tat, cell proliferation was restored and the expression of genes associated with the implementation of protective (antiviral) functions of the cell was increased. Analysis using proteasome inhibitors showed that in the case of chronic action, intense Tat proteolysis occurred, which could be the main mechanism of B-cell adaptation. Thus, B cells have a powerful mechanism to adapt to the entry of HIV-1 Tat, the efficiency of which may determine the frequency of lymphomagenesis in HIV-1-infected patients.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31459","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"RETRACTION: Basic Fibroblast Growth Factor Accelerates Matrix Degradation via a Neuro-endocrine Pathway in Human Adult Articular Chondrocytes","authors":"","doi":"10.1002/jcp.31453","DOIUrl":"10.1002/jcp.31453","url":null,"abstract":"<p><b>RETRACTION:</b> H.-J. Im, X. Li, P. Muddasani, G.-H. Kim, F. Davis, J. Rangan, C. B. Forsyth, M. Ellman, and E. J. Thonar, “Basic Fibroblast Growth Factor Accelerates Matrix Degradation via a Neuro-endocrine Pathway in Human Adult Articular Chondrocytes,” <i>Journal of Cellular Physiology</i> 215, no. 2 (2008): 452-463, https://doi.org/10.1002/jcp.21317.</p><p>The above article, published online on 24 October 2007 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has occurred due to concerns related to the data presented in the article raised by the Office of Research Compliance at Rush University Medical Center following an investigation jointly conducted by Rush University and the Jesse Brown Veterans Affairs Medical Center (JBVAMC). Specifically, image elements of the experimental data in Figure 6 A were found to have been used by the same author(s) for publication elsewhere in a different scientific context. The corresponding author, Dr. Hee-Jeong Im Sampen, has been informed of the decision to retract but did not agree with it, as she is confident that any errors in the publication do not impact the reliability of the paper's findings. She also advised the editors that she stands ready to cooperate fully to make any necessary corrections. However, the article is retracted as the editors lost trust in the accuracy of the data and consider the conclusions invalid.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"239 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31453","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"RETRACTION: Environmental Disruption of Circadian Rhythm Predisposes Mice to Osteoarthritis-Like Changes in Knee Joint","authors":"","doi":"10.1002/jcp.31457","DOIUrl":"10.1002/jcp.31457","url":null,"abstract":"<p><b>RETRACTION:</b> R. Kc, X. Li, R. M. Voigt, M. B. Ellman, K. C. Summa, M. H. Vitaterna, A. Keshavarizian, F. W. Turek, Q.-J. Meng, G. S. Stein, A. J. van Wijnen, D. Chen, C. B. Forsyth, and H.-J. Im, “Environmental Disruption of Circadian Rhythm Predisposes Mice to Osteoarthritis-Like Changes in Knee Joint,” <i>Journal of Cellular Physiology</i> 230, no. 9 (2015): 2174-2183, https://doi.org/10.1002/jcp.24946.</p><p>The above article, published online on 5 February 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has occurred due to concerns related to the data presented in the article raised by the Office of Research Compliance at Rush University Medical Center following an investigation jointly conducted by Rush University and the Jesse Brown Veterans Affairs Medical Center (JBVAMC). Specifically, image elements of the experimental data in Figure 4 A were found to have been used by the same author(s) for publication elsewhere in a different scientific context. The corresponding author, Dr. Hee-Jeong Im Sampen, has been informed of the decision to retract but did not agree with it, as she is confident that any errors in the publication do not impact the reliability of the paper's findings. She also advised the editors that she stands ready to cooperate fully to make any necessary corrections. However, the article is retracted as the editors lost trust in the accuracy of the data and consider the conclusions invalid.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"239 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31457","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zena Wehbe, Maya Wehbe, Ali Al Khatib, Ali H. Dakroub, Gianfranco Pintus, Firas Kobeissy, Ali H. Eid
{"title":"Emerging understandings of the role of exosomes in atherosclerosis","authors":"Zena Wehbe, Maya Wehbe, Ali Al Khatib, Ali H. Dakroub, Gianfranco Pintus, Firas Kobeissy, Ali H. Eid","doi":"10.1002/jcp.31454","DOIUrl":"10.1002/jcp.31454","url":null,"abstract":"<p>Atherosclerosis remains a major contributor to cardiovascular disease, the leading cause of global morbidity and mortality. Despite the elucidation of several molecular, biochemical, and cellular aspects that contribute to the etio-pathogenesis of atherosclerosis, much remains to be understood about the onset and progression of this disease. Emerging evidence supports a role for exosomes in the cellular basis of atherosclerosis. Indeed, exosomes of activated monocytes seem to accentuate a positive feedback loop that promotes recruitment of pro-inflammatory leukocytes. Moreover, in addition to their role in promoting proliferation and invasion of vascular smooth muscle cells, exosomes can also induce neovascularization within lesions and increase endothelial permeability, two important features of fibrous plaques. Depending on their sources and cargo, exosomes can also induce clot formation and contribute to other hallmarks of atherosclerosis. Taken together, it is becoming increasingly evident that a better understanding of exosome biology is integral to elucidating the pathogenesis of atherosclerosis, and may thus provide insight into a potentially new therapeutic target for this disease.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ethionine-induced S-adenosylmethionine deficiency suppressed H3K27me3 and cell differentiation during neural tube development in mice","authors":"Li Zhang, Xiaona Zhang, Yurong Liu, Kaixin Wei, Huijing Ma, Li Xia, Rui Cao, Yuqing Sun, Ronghua Zheng, Xiuwei Wang, Bingmei Chang","doi":"10.1002/jcp.31452","DOIUrl":"10.1002/jcp.31452","url":null,"abstract":"<p>S-adenosylmethionine (SAM) as a major methyl donor plays a key role in methylation modification in vivo, and its disorder was closely related to neural tube defects (NTDs). However, the exact mechanism between SAM deficiency and NTDs remained unclearly. Hence, we investigated the association between histone methylation modification and cell differentiation in NTDs mice induced by SAM deficiency. The levels of SAM and SAH (S-adenosylhomocysteine) were determined by enzyme linked immunosorbent assay (ELISA). The level of histone methylation, β-catenin were analyzed by Western blot, reversing transcription and quantitative PCR (RT-qPCR) and immunofluorescence. The results showed that the incidence rate of NTDs induced by ethionine were 46.2%. Post treatment of ethionine combined with SAM, the incidence rate of NTDs was reduced to 26.2%. The level of SAM was significantly decreased (<i>p</i> < 0.05) and a reduction in the SAM/SAH ratio was observed after entionine treatment. The SAM deficiency caused the reduction of H3K27me3 modifications and the elevated UTX activity (<i>p</i> < 0.05), and inhibited the expressions of β-catenin. The differentiations of NSCs into neurons and oligodendrocytes were inhibited under SAM deficiency (<i>p</i> < 0.05). These results indicated that the SAM deficiency led to reduce H3K27me3 modifications, prevented the β-catenin signaling pathway and NSCs differentiation, which provided an understanding of the novel function of epigenetic regulation in NTDs.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"RETRACTION: Circular RNA Circ_0001946 Acts As a Competing Endogenous RNA to Inhibit Glioblastoma Progression by Modulating miR-671-5p and CDR1","authors":"","doi":"10.1002/jcp.31408","DOIUrl":"10.1002/jcp.31408","url":null,"abstract":"<p><b>RETRACTION:</b> X. Li and H. Diao, “Circular RNA Circ_0001946 Acts as a Competing Endogenous RNA to Inhibit Glioblastoma Progression by Modulating miR-671-5p and CDR1,” <i>Journal of Cellular Physiology</i> 234, no. 8 (2019): 13807-13819, https://doi.org/10.1002/jcp.28061.</p><p>The above article, published online on 21 January 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Alexander Hutchison; and Wiley Periodicals LLC. The retraction has been agreed due to several instances of overlaps within and between images in Figures 4e, 4 g, 6e and 6 g, which should represent different cell types and experimental conditions. The authors were invited to comment on the concerns raised but did not respond. The editors consider the results and conclusion reported in this article unreliable.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"239 10","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31408","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Joel Nieto-Felipe, Alvaro Macias-Díaz, Vanesa Jimenez-Velarde, Jose J. Lopez, Gines M. Salido, Tarik Smani, Isaac Jardin, Juan A. Rosado
{"title":"Feedback modulation of Orai1α and Orai1β protein content mediated by STIM proteins","authors":"Joel Nieto-Felipe, Alvaro Macias-Díaz, Vanesa Jimenez-Velarde, Jose J. Lopez, Gines M. Salido, Tarik Smani, Isaac Jardin, Juan A. Rosado","doi":"10.1002/jcp.31450","DOIUrl":"10.1002/jcp.31450","url":null,"abstract":"<p>Store-operated Ca<sup>2+</sup> entry is a mechanism controlled by the filling state of the intracellular Ca<sup>2+</sup> stores, predominantly the endoplasmic reticulum (ER), where ER-resident proteins STIM1 and STIM2 orchestrate the activation of Orai channels in the plasma membrane, and Orai1 playing a predominant role. Two forms of Orai1, Orai1α and Orai1β, have been identified, which arises the question whether they are equally regulated by STIM proteins. We demonstrate that STIM1 preferentially activates Orai1α over STIM2, yet both STIM proteins similarly activate Orai1β. Under resting conditions, there is a pronounced association between STIM2 and Orai1α. STIM1 and STIM2 are also shown to influence the protein levels of the Orai1 variants, independently of Ca<sup>2+</sup> influx, via lysosomal degradation. Interestingly, Orai1α and Orai1β appear to selectively regulate the protein level of STIM1, but not STIM2. These observations offer crucial insights into the regulatory dynamics between STIM proteins and Orai1 variants, enhancing our understanding of the intricate processes that fine-tune intracellular Ca<sup>2+</sup> signaling.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}