Cell biology international reports最新文献

{"title":"Analysis of SPATA19 gene expression during male germ cells development, lessons from in vivo and in vitro study","authors":"Seyedmehdi Nourashrafeddin,&nbsp;Reza Ebrahimzadeh-Vesal,&nbsp;Mohammad Miryounesi,&nbsp;Mahmoud Aarabi,&nbsp;Nosratollah Zarghami,&nbsp;Mohammad Hosein Modarressi,&nbsp;Mohammad Nouri","doi":"10.1002/cbi3.10010","DOIUrl":"10.1002/cbi3.10010","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>Spermatogenesis-associated-19 (<i>SPATA19</i>) is a novel spermatogenesis related gene that has important biological functions in reproduction. However, the expression aspects of <i>SPATA19</i> gene are not yet well understood. We analysed <i>SPATA19</i> gene expression during mouse testis development in vivo (5, 15 and 25 days old mouse testis), in parallel with mouse embryonic stem cells (ESCs) differentiation into male germ-like cells in vitro (5, 11, 19 and 27 days after differentiation), as well as Sertoli cell, mouse embryonic fibroblasts (MEF), and NIH3T3 cancerous cell line. We cultured transgenic mouse ESCs line C57BL/6J expressing Stra8-EGFP in ESC's medium and induced their differentiation by retinoic acid (RA) treatment, and meiotic cells were then sorted by FACS. RT-PCR and real-time PCR were used for analysis of <i>SPATA19</i> mRNA expression. The expression of <i>SPATA19</i> mRNA is increased during mouse testis development in vivo and it is highest in 25-days-old mouse testis. <i>SPATA19</i> is also expressed most highly in mouse ESC-derived germ-like cells after 27 days of RA induction and NIH3T3 cell line but no expression was found in mouse ESC and Sertoli cell line. These findings demonstrate that the expression of <i>SPATA19</i> increases during male germ cells development. We also suggest an additional possible role for <i>SPATA19</i> in male germ cell differentiation and tumourigenic process.</p>\u0000 </section>\u0000 </div>","PeriodicalId":75683,"journal":{"name":"Cell biology international reports","volume":"21 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2013-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/cbi3.10010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51264366","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":"Matrix metalloproteinases and collective cell migration in 24 h primary zebrafish explant cultures: MMP13 plays an inhibitory role and MMP14 may respond to stretch during reepithelialisation","authors":"Timothy M. McDonald,&nbsp;Adam J. Sumner,&nbsp;Jonazary F. Reyes,&nbsp;Agnes S. Pascual,&nbsp;Chandana K. Uppalapati,&nbsp;Kimbal E. Cooper,&nbsp;Kathryn J. Leyva,&nbsp;Elizabeth E. Hull","doi":"10.1002/cbi3.10006","DOIUrl":"10.1002/cbi3.10006","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>Zebrafish keratocytes collectively migrate rapidly when established in explant cultures but little is known about the signals that initiate motility or the signal transduction pathways that result in an epithelial to mesenchymal transition. Matrix metalloproteinases (MMPs) are strong candidates for playing a role in this regulation and have previously not been analysed in this wound healing model system. Results presented here document a rapid and dramatic rise in MMP14a, MMP2, MMP9 and MMP13a mRNA levels over time. In a motility assay, a broad-spectrum MMP inhibitor and an inhibitor specific for MMP2 and MMP9 significantly decrease cell migration in a dose dependent manner but treatment with an MMP13 specific inhibitor significantly increases cell sheet area. Immunofluorescence staining with an antibody specific for the catalytic domain of MMP14 indicates that activated MMP14 protein is highly expressed on cells at the leading edge of a sheet compared with follower cells in the centre of the sheet, and is augmented further in leader cells that are stretched, thus likely in the process of detaching from the cell sheet. These data are consistent with a model in which active MMP14 at the leading edge of cell sheets in explant cultures triggers activation of MMP2 and/or MMP9, thus creating promigratory signal(s) that outweigh the inhibitory role of targets cleaved by MMP13. Taken together, these data suggest that MMPs play an important but complex role in regulating the collective cell migration of zebrafish keratocytes and provide support for the relevance of using zebrafish as a model for human disease.</p>\u0000 </section>\u0000 </div>","PeriodicalId":75683,"journal":{"name":"Cell biology international reports","volume":"20 2","pages":"24-36"},"PeriodicalIF":0.0,"publicationDate":"2013-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/cbi3.10006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51264253","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":"Spatiotemporal changes in Cx30 and Cx43 expression during neuronal differentiation of P19 EC and NT2/D1 cells","authors":"Carthur K. Wan,&nbsp;Simon J. O'Carroll,&nbsp;Sue-Ling Kim,&nbsp;Colin R. Green,&nbsp;Louise F. B. Nicholson","doi":"10.1002/cbi3.10005","DOIUrl":"10.1002/cbi3.10005","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>While connexins (Cxs) are thought to be involved in differentiation, their expression and role has yet to be fully elucidated. We investigated the temporal expression of Cx30, Cx36 and Cx43 in two in vitro models of neuronal differentiation: human NT2/D1 and murine P19 cells, and the spatial localisation of Cx30 and Cx43 in these models.</p>\u0000 \u0000 <p>A temporal Cx43 downregulation was confirmed in both cell lines during RA-induced neuronal differentiation using RT-PCR (<i>P</i> &lt; 0.05) preceding an increase in neuronal doublecortin protein. RT-PCR showed Cx36 was upregulated twofold in NT2/D1 cells (<i>P</i> &lt; 0.05) and sixfold in P19 cells (<i>P</i> &lt; 0.001) during neuronal differentiation. Cx30 exhibited a transient peak in expression midway through the timecourse of differentiation increasing threefold in NT2/D1 cells (<i>P</i> &lt; 0.001) and eightfold in P19 cells (<i>P</i> &lt; 0.01).</p>\u0000 \u0000 <p>Qualitative immunocytochemistry was used to examine spatiotemporal patterns of Cx protein distribution alongside neuronal differentiation markers. The temporal immunolabelling pattern was similar to that seen using RT-PCR. Cx43 was observed intracellularly and on cell surfaces, while Cx30 was seen as puncta. Spatially Cx43 was seen on doublecortin-negative cells, which may indicate Cx43 downregulation is requisite for differentiation in these models. Conversely, Cx30 puncta were observed on doublecortin-positive and -negative cells in NT2/D1 cells and examination of the Cx30 peak showed puncta also localized to nestin-positive cells, with few puncta on MAP2-positive cells. In P19 cells Cx30 was localized on clusters of cells surrounded by MAP2- and doublecortin-positive processes. The expression pattern of Cx30 indicates a role in neuronal differentiation; the nature of that role warrants future investigation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":75683,"journal":{"name":"Cell biology international reports","volume":"20 2","pages":"13-23"},"PeriodicalIF":0.0,"publicationDate":"2013-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/cbi3.10005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32906293","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":"Activation of kinase phosphorylation by heat-shift and mild heat-shock","authors":"Pamela Petrocchi,&nbsp;Stefania Quaresima,&nbsp;Patrizia Maria Mongiardi,&nbsp;Cinzia Severini,&nbsp;Roberta Possenti","doi":"10.1042/CBR20100002","DOIUrl":"10.1042/CBR20100002","url":null,"abstract":"<p>Most cells activate intracellular signalling to recover from heat damage. An increase of temperature, known as HS (heat shock), induces two major signalling events: the transcriptional induction of HSPs (heat-shock proteins) and the activation of the MAPK (mitogen-activated protein kinase) cascade. We performed the present study to examine the effects of HS, induced by different experimental conditions, on various kinases [ERK (extracellular-signal-regulated kinase), JNK (c-Jun N-terminal kinase), p38, Akt, AMPK (AMP-activated protein kinase) and PKC (protein kinase C)]. We investigated by Western blot analysis the phosphorylation of MAPK as a measure of cellular responsiveness to heat shift (37°C) and mild HS (40°C) in different cell lines. The results of the study indicate that every cell line responded to heat shift, and to a greater extent to HS, increasing ERK and JNK phosphorylation, whereas variable effects on activation or inhibition of PKC, AMPK, Akt and p38 were observed. Besides the implications of intracellular signalling activated by heat variations, these data may be of technical relevance, indicating possible sources of error due to different experimental temperature conditions.</p>","PeriodicalId":75683,"journal":{"name":"Cell biology international reports","volume":"17 1","pages":"9-12"},"PeriodicalIF":0.0,"publicationDate":"2013-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/CBR20100002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31022037","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":"Fluid shear stress-induced cytosolic calcium signalling and degranulation dynamics in mast cells","authors":"Fei Wei,&nbsp;Xiaomin Shi,&nbsp;Jiyao Chen,&nbsp;Luwei Zhou","doi":"10.1042/CBR20120004","DOIUrl":"10.1042/CBR20120004","url":null,"abstract":"<p>A mast cell line (rat basophilic leukaemia cells, RBL-2H3) was used <i>in vitro</i> to study cellular responses to fluid shear stress generated by a rotating rotor in a cell dish. The [Ca²⁺]_c (cytosolic calcium concentration) in mast cells was detected by confocal fluorescence microscopy after Fluo-3/AM (acetoxymethyl ester) staining. Cytosolic calcium fluorescence intensity oscillated, pulsed, or steadily increased after the application of a weak, moderate or strong fluid shear stress respectively. From a mathematical model, we reproduced a change in [Ca²⁺]_c under different levels of fluid shear stress in mast cells. The model calculation confirmed another experimental observation, specifically, that the degranulation rate increases with shear stress and reaches certain steady values. Since mast cells can react clearly and quickly and obviously to mechanical stimuli, calcium signalling and degranulation dynamics could be one of the mechanisms of acupuncture and massage therapies.</p>","PeriodicalId":75683,"journal":{"name":"Cell biology international reports","volume":"19 2","pages":"45-51"},"PeriodicalIF":0.0,"publicationDate":"2013-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/CBR20120004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58439102","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":"Reversible conversion of epithelial and mesenchymal phenotypes in SV40 large T antigen-immortalized rat liver cell lines","authors":"Takato Takenouchi,&nbsp;Miyako Yoshioka,&nbsp;Noriko Yamanaka,&nbsp;Hiroshi Kitani","doi":"10.1042/CBR20100001","DOIUrl":"10.1042/CBR20100001","url":null,"abstract":"<p>EMT (epithelial—mesenchymal transition) is a key process in the development of liver fibrosis. This process is also essential for liver morphogenesis in embryonic development. To study the cellular and molecular basis of EMT, we established two phenotypically different SV40 large T antigen-immortalized cell lines from rat hepatocytes. The first cell line, which had an epithelial morphology and was established in DMEM (Dulbecco's modified Eagle's medium)/Ham's F-12 (DF)-based medium (RL/DF cells), expressed CK18 (cytokeratin 18), a marker of parenchymal hepatocytes. The other, a mesenchymal-like cell line established in DMEM-based medium (RL/DMEM cells), expressed αSMA (α-smooth muscle actin), a marker of hepatic myofibroblasts. Epithelial RL/DF cells underwent phenotypic changes, such as increased expression of αSMA, when the culture medium was switched to DMEM-based medium. In contrast, mesenchymal RL/DMEM cells were induced to express the epithelial marker CK18 with a concomitant decrease in αSMA expression when the culture medium was replaced with DF-based medium. These cell lines may provide novel <i>in vitro</i> models for the study of the conversion between epithelial and mesenchymal phenotypes during EMT in liver fibrosis and morphogenesis.</p>","PeriodicalId":75683,"journal":{"name":"Cell biology international reports","volume":"17 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2013-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/CBR20100001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31022036","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":"Isolation and characterization of equine amnion mesenchymal stem cells","authors":"Alessandra Coli,&nbsp;Francesca Nocchi,&nbsp;Roberta Lamanna,&nbsp;Mariacarla Iorio,&nbsp;Simone Lapi,&nbsp;Patrizia Urciuoli,&nbsp;Fabrizio Scatena,&nbsp;Elisabetta Giannessi,&nbsp;Maria Rita Stornelli,&nbsp;Simona Passeri","doi":"10.1042/CBR20110004","DOIUrl":"10.1042/CBR20110004","url":null,"abstract":"<p>The amnion is a particular tissue whose cells show features of multipotent stem cells proposed for use in cellular therapy and regenerative medicine. From equine amnion collected after the foal birth we have isolated MSCs (mesenchymal stem cells), namely EAMSCs (equine amnion mesenchymal stem cells), from the mesoblastic layer. The cells were grown in α-MEM (α-modified minimum essential medium) and the effect of EGF (epidermal growth factor) supplementation was evaluated. To assess the growth kinetic of EAMSCs we have taken into account some parameters [PD (population doubling), fold increase and DT (doubling time)]. The differentiation in chondrogenic, adipogenic and osteogenic types of cells and their epitope expression by a cytofluorimetric study have been reported. EGF supplementation of the culture medium resulted in a significant increase in PD growth parameter and in the formation of bone nodules for the osteogenic differentiation. By immunohistochemistry the amnion tissue shows a positivity for the c-Kit (cluster tyrosine-protein kinase), CD105 and Oct-4 (octamer-binding transcription factor 4) antigens that confirmed the presence of MSCs with embryonic phenotype.</p>","PeriodicalId":75683,"journal":{"name":"Cell biology international reports","volume":"18 1","pages":"23-29"},"PeriodicalIF":0.0,"publicationDate":"2013-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/CBR20110004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31025287","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":"Effect of 60 Hz electromagnetic fields on the activity of hsp70 promoter: an in vivo study","authors":"Rodríguez-De Abraham O. la Fuente,&nbsp;Juan M. Alcocer-González,&nbsp;J. Antonio Heredia-Rojas,&nbsp;Cristina Rodríguez-Padilla,&nbsp;Laura E. Rodríguez-Flores,&nbsp;Martha A. Santoyo-Stephano,&nbsp;Esperanza Castañeda-Garza,&nbsp;Reyes S. Tamëz-Guerra","doi":"10.1042/CBR20110010","DOIUrl":"10.1042/CBR20110010","url":null,"abstract":"<p>Exposure to EMFs (electromagnetic fields) results in a number of important biological changes, including modification of genetic expression. We have investigated the effect of 60 Hz sinusoidal EMFs at a magnetic flux density of 80 μT on the expression of the luciferase gene contained in a plasmid labelled as pEMF (EMF plasmid). This gene construct contains the specific sequences for the induction of hsp70 (heat-shock protein 70) expression by EMFs, as well as the reporter for the luciferase gene. The pEMF vector was electrotransferred into quadriceps muscles of BALB/c mice that were later exposed to EMFs. Increased luciferase expression was observed in mice exposed to EMFs 2 h daily for 7 days compared with controls (<i>P</i>&lt;0.05). These data along with other reports in the literature suggest that EMFs can have far-reaching effects on the genome.</p>","PeriodicalId":75683,"journal":{"name":"Cell biology international reports","volume":"19 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2013-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/CBR20110010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31025845","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":"Marine sponge depsipeptide increases gap junction length in HTC cells transfected with Cx43–GFP","authors":"Marisa Rangel,&nbsp;Marisa Ionta,&nbsp;Cristina Sandra Pfister,&nbsp;Adolpho Sant'Anna Raphael Ferreira,&nbsp;Maria Glaucia Machado-Santelli","doi":"10.1042/CBR20100003","DOIUrl":"10.1042/CBR20100003","url":null,"abstract":"<p>Connexins are membrane proteins that form GJ (gap junction) channels between adjacent cells. Cx43 (connexin 43), the most widely expressed member of the connexin family, has a rapid turnover rate, and its degradation involves both the lysosomal and ubiquitin—proteasome pathway. The goal of this work was to study the effects of geodiamolides, natural peptides from marine sponge that normally are involved with microfilament disruption, on connexin assembly or degradation in the plasma membrane. HTC (hepatocarcinoma cells) expressing Cx43–GFP (green fluorescent protein) were submitted to treatment with 200 nM geodiamolides A, B, H and I for 2 and 4 h. Microfilament distribution and the presence and size of GJ plaques were evaluated by laser scanning confocal microscopy. Among the four peptides tested, only Geo H (geodiamolide H) statistically enhanced the length of GJ plaques. Geodiamolide A also showed activity in the GJ plaque size; however, its effect was less pronounced. Treatment with Geo H could interfere with the delivery of connexins to the degradation structures, similar to proteasomal pathways, keeping the connexins assembled and accumulating GJ plaques. Further experiments, with the cells treated with Geo H, using the fungal antibiotic BFA (brefeldin A), were performed in order to uncouple events leading to GJ assembly from those related to GJ removal, since BFA is known to block protein trafficking within a fused ER (endoplasmic reticulum)/Golgi compartment. GJ plaques were drastically reduced after BFA/Geo H treatment, thus indicating that Geo H affects mainly the delivery pathway of Cx43 protein.</p>","PeriodicalId":75683,"journal":{"name":"Cell biology international reports","volume":"17 1","pages":"13-18"},"PeriodicalIF":0.0,"publicationDate":"2013-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/CBR20100003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31020779","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":"Down-regulation of TERE1/UBIAD1 activated Ras—MAPK signalling and induced cell proliferation","authors":"Yanzhi Xia,&nbsp;Xiong Wei,&nbsp;Shimin Wu,&nbsp;Bo Wang,&nbsp;Ximing Wang,&nbsp;Ling Hong","doi":"10.1042/CBR20100005","DOIUrl":"10.1042/CBR20100005","url":null,"abstract":"<p>TERE1/UBIAD1 is involved in SCCD (Schnyder crystalline corneal dystrophy) and multiple human cancers. So far, the molecular mechanism of TERE1/UBIAD1 in tumourigenesis is unclear. Here, the expression levels of hTERT and TERE1/UBIAD1 in pathologically proven Chinese TCC (transitional cell carcinoma) samples were measured. It was found that decreased TERE1/UBIAD1 expression is closely related to both an increased hTERT expression and activation of Ras—MAPK signalling. Chemically modified TERE1 siRNA oligos were used to knock down TERE1 expression in human L02 cells. Cells transfected with TERE1 siRNA oligos underwent significant cell proliferation. When the levels of hTERT expression and ERK phosphorylation were measured, it was found that both of them increased in the above transfected cells, suggesting the activation of Ras—MAPK signalling. Addition of the MEK inhibitor U0126 into the transfected L02 cells described above inhibited ERK phosphorylation and hTERT expression. Our result is the initial demonstration that down-regulation of TERE1 activates Ras—MAPK signalling and induces subsequent cell proliferation. TERE1 might be a new negative regulator of Ras—MAPK signalling, which plays a pivotal role in the cell proliferation of multiple human cancers.</p>","PeriodicalId":75683,"journal":{"name":"Cell biology international reports","volume":"17 1","pages":"19-26"},"PeriodicalIF":0.0,"publicationDate":"2013-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/CBR20100005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31020780","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}