Molecular medicine reports最新文献

{"title":"Potential of resveratrol in the treatment of systemic lupus erythematosus (Review).","authors":"Rongxiu Huo, Yanting Yang, Xiaocong Huo, Danli Meng, Rongjun Huang, Yang Yang, Jinying Lin, Yijia Huang, Xia Zhu, Chengcheng Wei, Xinxiang Huang","doi":"10.3892/mmr.2024.13306","DOIUrl":"10.3892/mmr.2024.13306","url":null,"abstract":"<p><p>Systemic lupus erythematosus (SLE) is a multi‑system chronic autoimmune disease with a complex occurrence and development process, associated with immune disorders, uncertain prognosis, and treatment modalities which vary by patient and disease activity. At present, the clinical treatment of SLE mainly focuses on hormones and immunosuppressants. In recent years, the research on new treatment strategies for SLE has been booming, and strong preclinical results and clinical research have promoted the development of numerous drugs (such as rituximab and orencia), but numerous of these drugs have failed to achieve effectiveness in clinical trials, and there are some adverse reactions. Recent evidence suggests that resveratrol (RSV) has the effect of ameliorating immune disorders by inhibiting overactivation of immune cells. In the present review, advances in research on the protective effects and potential mechanisms of RSV against SLE are summarized and the potential potency of RSV and its use as a promising therapeutic option for the treatment of SLE are highlighted.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11350626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] miR‑4306 inhibits the malignant behaviors of colorectal cancer by regulating lncRNA FoxD2‑AS1.","authors":"Jinjun Ye, Jidong Liu, Tao Tang, Le Xin, Xing Bao, Yukuang Yan","doi":"10.3892/mmr.2024.13299","DOIUrl":"10.3892/mmr.2024.13299","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the colony formation assay data shown in Fig. 5F on p. 7 were strikingly similar to data appearing in different form in several other articles written by different authors at different research institutes, which had already been published prior to the  submission of this article to the journal. In addition, possible anomalies were noted regarding the appearance of the western blots in the paper. Owing to the fact that the contentious data in the above article had already been published prior to its submission to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 24: 723, 2021; DOI: 10.3892/mmr.2021.12362].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11332320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141917163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Diospyros lotus</i> leaf extract and its main component myricitrin inhibit itch‑related IL‑6 and IL‑31 by suppressing microglial inflammation and microglial‑mediated astrocyte activation.","authors":"Jae Young Shin, Byoung Ok Cho, Ji Hyeon Park, Eun Seo Kang, Jang Ho Kim, Hun Yong Ha, Young-Soo Kim, Seon Il Jang","doi":"10.3892/mmr.2024.13303","DOIUrl":"10.3892/mmr.2024.13303","url":null,"abstract":"<p><p><i>Diospyros lotus</i> has been traditionally used in Asia for medicinal purposes, exhibiting a broad spectrum of pharmacological effects including antioxidant, neuroprotective and anti‑inflammatory properties. While the anti‑itch effect of <i>D. lotus</i> leaves has been reported, studies on the detailed mechanism of action in microglia and astrocytes, which are members of the central nervous system, have yet to be revealed. The present study aimed to investigate effects of <i>D. lotus</i> leaf extract (DLE) and its main component myricitrin (MC) on itch‑related cytokines and signaling pathways in lipopolysaccharide (LPS)‑stimulated microglia. The effect of DLE and MC on activation of astrocyte stimulated by microglia was also examined. Cytokine production was evaluated through reverse transcription PCR and western blot analysis. Signaling pathway was analyzed by performing western blotting and immunofluorescence staining. The effect of microglia on astrocytes activation was evaluated via western blotting for receptors, signaling molecules and itch mediators and confirmed through gene silencing using short interfering RNA. DLE and MC suppressed the production of itch‑related cytokine IL‑6 and IL‑31 in LPS‑stimulated microglia. These inhibitory effects were mediated through the blockade of NF‑κB, MAPK and JAK/STAT pathways. In astrocytes, stimulation by microglia promoted the expression of itch‑related molecules such as oncostatin M receptor, interleukin 31 receptor a, inositol 1,4,5‑trisphosphate receptor 1, lipocalin‑2 (LCN2), STAT3 and glial fibrillary acidic protein. However, DLE and MC significantly inhibited these receptors. Additionally, astrocytes stimulated by microglia with IL‑6, IL‑31, or both genes silenced did not show activation of LCN2 or STAT3. The findings of the present study demonstrated that DLE and MC could suppress pruritic activity in astrocytes induced by microglia‑derived IL‑6 and IL‑31. This suggested the potential of DLE and MC as functional materials capable of alleviating pruritus.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11338241/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141917164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Liraglutide protects renal mesangial cells against hyperglycemia‑mediated mitochondrial apoptosis by activating the ERK‑Yap signaling pathway and upregulating Sirt3 expression.","authors":"Jian Li, Nan Li, Shuangtong Yan, Yanhui Lu, Xinyu Miao, Zhaoyan Gu, Yinghong Shao","doi":"10.3892/mmr.2024.13310","DOIUrl":"10.3892/mmr.2024.13310","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the TUNEL assay data shown in Fig. 1C on p. 2853 and Fig. 5H on p. 2857 were strikingly similar to data that had already been published in different form in different articles written by different authors at different research institutes, or were submitted for publication at around the same time (a number of of which have now been retracted). Owing to the fact that the contentious data in the above article had already been published, or were already under consideration for publication, prior to its submission to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 19: 2849‑2860, 2019; DOI: 10.3892/mmr.2019.9946].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11350627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] SFRP2 modulates non‑small cell lung cancer A549 cell apoptosis and metastasis by regulating mitochondrial fission via Wnt pathways.","authors":"Peng Li, Shu Zhao, Yi Hu","doi":"10.3892/mmr.2024.13305","DOIUrl":"10.3892/mmr.2024.13305","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the JC1‑stained cellular images shown in Fig. 2C on p. 1928 were strikingly similar to data that had already been published in different form in another article written by different authors at different research institutes [Yao S and Yan W: Overexpression of Mst1 reduces gastric cancer cell viability by repressing the AMPK‑Sirt3 pathway and activating mitochondrial fission. Onco Targets Ther 11: 8465‑8479, 2019]. Owing to the fact that the contentious data in the above article had already been published prior to its submission to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 20: 1925‑1932, 2019; DOI: 10.3892/mmr.2019.10393].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11338225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adiponectin receptor 1 regulates endometrial receptivity via the adenosine monophosphate‑activated protein kinase/E‑cadherin pathway.","authors":"Bolor-Erdene Sarankhuu, Hye Jin Jeon, Da-Un Jeong, Seok-Rae Park, Tae-Hyun Kim, Sung Ki Lee, Ae Ra Han, Seong-Lan Yu, Jaeku Kang","doi":"10.3892/mmr.2024.13308","DOIUrl":"10.3892/mmr.2024.13308","url":null,"abstract":"<p><p>Endometrial receptivity is essential for successful embryo implantation and pregnancy initiation and is regulated via various signaling pathways. Adiponectin, an important adipokine, may be a potential regulator of reproductive system functions. The aim of the present study was to elucidate the regulatory role of adiponectin receptor 1 (ADIPOR1) in endometrial receptivity. The endometrial receptivity between RL95‑2 and AN3CA cell lines was confirmed using an <i>in vitro</i> JAr spheroid attachment model. 293T cells were transfected with control or short hairpin (sh)ADIPOR1 vectors and RL95‑2 cells were transduced with lentiviral particles targeting <i>ADIPOR1</i>. Reverse transcription‑quantitative PCR and immunoblot assays were also performed. <i>ADIPOR1</i> was consistently upregulated in the endometrium during the mid‑secretory phase compared with that in the proliferative phase and in receptive RL95‑2 cells compared with that in non‑receptive AN3CA cells. Stable cell lines with diminished <i>ADIPOR1</i> expression caused by shRNA showed reduced E‑cadherin expression and attenuated <i>in vitro</i> endometrial receptivity. ADIPOR1 regulated AMP‑activated protein kinase (AMPK) activity in endometrial epithelial cells. Regulation of AMPK activity via dorsomorphin and 5‑aminoimidazole‑4‑carboxamide ribonucleotide affected E‑cadherin expression and <i>in vitro</i> endometrial receptivity. The ADIPOR1/AMPK/E‑cadherin axis is vital to endometrial receptivity. These findings can help improve fertility treatments and outcomes.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11350624/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Imatinib‑ and ponatinib‑mediated cardiotoxicity in zebrafish embryos and H9c2 cardiomyoblasts.","authors":"Zain Z Zakaria, Muna Suleiman, Fatiha M Benslimane, Mashael Al-Badr, Siveen Sivaraman, Hesham M Korashy, Fareed Ahmad, Shahab Uddin, Fatima Mraiche, Huseyin C Yalcin","doi":"10.3892/mmr.2024.13311","DOIUrl":"10.3892/mmr.2024.13311","url":null,"abstract":"<p><p>Tyrosine kinase inhibitors (TKIs) offer targeted therapy for cancers but can cause severe cardiotoxicities. Determining their dose‑dependent impact on cardiac function is required to optimize therapy and minimize adverse effects. The dose‑dependent cardiotoxic effects of two TKIs, imatinib and ponatinib, were assessed <i>in vitro</i> using H9c2 cardiomyoblasts and <i>in vivo</i> using zebrafish embryos. <i>In vitro</i>, H9c2 cardiomyocyte viability, apoptosis, size, and surface area were evaluated to assess the impact on cellular health. <i>In vivo</i>, zebrafish embryos were analyzed for heart rate, blood flow velocity, and morphological malformations to determine functional and structural changes. Additionally, reverse transcription‑quantitative PCR (RT‑qPCR) was employed to measure the gene expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), established markers of cardiac injury. This comprehensive approach, utilizing both <i>in vitro</i> and <i>in vivo</i> models alongside functional and molecular analyses, provides a robust assessment of the potential cardiotoxic effects. TKI exposure decreased viability and surface area in H9c2 cells in a dose‑dependent manner. Similarly, zebrafish embryos exposed to TKIs exhibited dose‑dependent heart malformation. Both TKIs upregulated ANP and BNP expression, indicating heart injury. The present study demonstrated dose‑dependent cardiotoxic effects of imatinib and ponatinib in H9c2 cells and zebrafish models. These findings emphasize the importance of tailoring TKI dosage to minimize cardiac risks while maintaining therapeutic efficacy. Future research should explore the underlying mechanisms and potential mitigation strategies of TKI‑induced cardiotoxicities.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11350628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Corrigendum] Alcohol extracts from <i>Anemone flaccida</i> Fr. Schmidt treat rheumatoid arthritis via inhibition of synovial hyperplasia and angiogenesis.","authors":"Qi Rao, Xin Zhao, Fenghua Wu, Xiaohong Guo, Yundan Xu, He Yu, Dayong Cai, Gang Zhao","doi":"10.3892/mmr.2024.13302","DOIUrl":"10.3892/mmr.2024.13302","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, the authors drew to the attention of the Editorial Office that they had assembled the data shown for the cell migration assay experiments in Fig. 4F (on p. 8), incorrectly; essentially, the 'Control' data panel had inadvertently been copied across for the '10 μg/ml' data panel. The revised version of Fig. 4, showing the correct data panel for the '10 μg/ml' experiment in Fig. 4F,  is shown on the next page. Note that the replacement of the erroneous data does not affect either the results or the conclusions reported in this paper, and all the authors agree to the publication of this Corrigendum. The authors are grateful to the Editor of <i>Molecular Medicine Reports</i> for granting them this opportunity to publish a Corrigendum, and apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 27: 88, 2023; DOI: 10.3892/mmr.2023.12975].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11338228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141917162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Indole‑3‑propionic acid alleviates intestinal epithelial cell injury via regulation of the TLR4/NF‑κB pathway to improve intestinal barrier function.","authors":"Ying Chen, Yu Li, Xiaojuan Li, Qingqing Fang, Feng Li, Shiyao Chen, Weichang Chen","doi":"10.3892/mmr.2024.13313","DOIUrl":"10.3892/mmr.2024.13313","url":null,"abstract":"<p><p>Indole‑3‑propionic acid (IPA), a product of <i>Clostridium sporogenes</i> metabolism, has been shown to improve intestinal barrier function. In the present study, in vitro experiments using NCM460 human colonic epithelial cells were performed to investigate how IPA alleviates lipopolysaccharide (LPS)‑induced intestinal epithelial cell injury, with the aim of improving intestinal barrier function. In addition, the underlying mechanism was explored. NCM460 cell viability and apoptosis were measured using the Cell Counting Kit‑8 assay and flow cytometry, respectively. The integrity of the intestinal epithelial barrier was evaluated by measuring transepithelial electrical resistance (TEER). The underlying molecular mechanism was explored using western blotting, immunofluorescence staining, a dual luciferase reporter gene assay and quantitative PCR. The results showed that 10 µg/ml LPS induced the most prominent decrease in cell viability after 24 h of treatment. By contrast, IPA effectively inhibited LPS‑induced apoptosis in the intestinal epithelial cells. Additionally, >0.5 mM IPA improved intestinal barrier function by increasing TEER and upregulating the expression of tight junction proteins (zonula occludens‑1, claudin‑1 and occludin). Furthermore, IPA inhibited the release of pro‑inflammatory cytokines (IL‑1β, IL‑6 and TNF‑α) in a dose‑dependent manner and this was achieved via regulation of the Toll‑like receptor 4 (TLR4)/myeloid differentiation factor 88/NF‑κB and TLR4/TRIF/NF‑κB pathways. In conclusion, IPA may alleviate LPS‑induced inflammatory injury in human colonic epithelial cells. Taken together, these results suggest that IPA may be a potential therapeutic approach for the management of diseases characterized by LPS‑induced intestinal epithelial cell injury and intestinal barrier dysfunction.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11350629/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role and mechanism of action of miR‑92a in endothelial cell autophagy.","authors":"Weili Cao, Boxin Zhao, Lin Gui, Xueyuan Sun, Zhiyong Zhang, Lijuan Huang","doi":"10.3892/mmr.2024.13296","DOIUrl":"10.3892/mmr.2024.13296","url":null,"abstract":"<p><p>Although microRNAs (miRNAs/miRs) serve a significant role in the autophagy of vascular endothelial cells (ECs), the effect of miR‑92a on the autophagy of ECs is currently unclear. Therefore, the present study aimed to investigate the impact of miR‑92a on autophagy in ECs and the underlying molecular processes that control this biological activity. Firstly, an autophagy model of EA.hy926 cells was generated via treatment with the autophagy inducer rapamycin (rapa‑EA.hy926 cells). The expression levels of miR‑92a were then detected by reverse transcription‑quantitative PCR, and the effect of miR‑92a expression on the autophagic activity of rapa‑EA.hy926 cells was studied by overexpressing or inhibiting miR‑92a. The level of autophagy was evaluated by western blot analysis, immunofluorescence staining and transmission electron microscopy. Dual‑luciferase reporter assays were used to confirm the interaction between miR‑92a and FOXO3. The results demonstrated that the expression levels of miR‑92a were decreased in the rapa‑EA.hy926 cell autophagy model. Furthermore, overexpression and inhibition of miR‑92a revealed that upregulation of miR‑92a in these cells inhibited autophagy, whereas miR‑92a knockdown promoted it. It was also confirmed that miR‑92a directly bound to the 3'‑untranslated region of the autophagy‑related gene FOXO3 and reduced its expression. In conclusion, the present study suggested that miR‑92a inhibits autophagy activity in EA.hy926 cells by targeting FOXO3.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11304162/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141759867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}