Cell Communication and Adhesion最新文献

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Intercellular organelle trafficking by membranous nanotube connections: a possible new role in cellular rejuvenation? 膜状纳米管连接的细胞间细胞器运输:在细胞再生中的可能新作用?
Cell Communication and Adhesion Pub Date : 2012-08-01 Epub Date: 2012-09-04 DOI: 10.3109/15419061.2012.712574
Yi Shan Lim, Bor Luen Tang
{"title":"Intercellular organelle trafficking by membranous nanotube connections: a possible new role in cellular rejuvenation?","authors":"Yi Shan Lim,&nbsp;Bor Luen Tang","doi":"10.3109/15419061.2012.712574","DOIUrl":"https://doi.org/10.3109/15419061.2012.712574","url":null,"abstract":"<p><p>Cells could make actin-based filopodial extensions that connect up with other cells. Such close-ended, actin-based filopodial bridges, or cytonemes, have been observed during developmental and pathological processes. On the other hand, tunneling nanotubes (TNTs) form conduits with open ends that allow transfer of cytoplasmic materials and organelles between cells. The past years have witnessed the description of TNTs in multiple cell types, with a range of interesting physiological and pathophysiological activities. Some hints of the molecular components that drive their formations are now emerging. Recent work has further suggested that TNTs could be important in regenerative transfer of large cellular components, including organelles such as mitochondria and lysosomes between senescing and younger cell types (at least for cells in culture). These findings have intriguing implications in cell biology and regenerative medicine.</p>","PeriodicalId":55269,"journal":{"name":"Cell Communication and Adhesion","volume":"19 3-4","pages":"39-44"},"PeriodicalIF":0.0,"publicationDate":"2012-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419061.2012.712574","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30880363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 16
Pannexin1 and Pannexin3 exhibit distinct localization patterns in human skin appendages and are regulated during keratinocyte differentiation and carcinogenesis. Pannexin1和Pannexin3在人类皮肤附属物中表现出不同的定位模式,并在角化细胞分化和癌变过程中受到调节。
Cell Communication and Adhesion Pub Date : 2012-08-01 Epub Date: 2012-09-04 DOI: 10.3109/15419061.2012.712575
Kyle N Cowan, Stéphanie Langlois, Silvia Penuela, Bryce J Cowan, Dale W Laird
{"title":"Pannexin1 and Pannexin3 exhibit distinct localization patterns in human skin appendages and are regulated during keratinocyte differentiation and carcinogenesis.","authors":"Kyle N Cowan,&nbsp;Stéphanie Langlois,&nbsp;Silvia Penuela,&nbsp;Bryce J Cowan,&nbsp;Dale W Laird","doi":"10.3109/15419061.2012.712575","DOIUrl":"https://doi.org/10.3109/15419061.2012.712575","url":null,"abstract":"<p><p>Having shown that Panx1 and Panx3 are expressed in the epidermis, we investigated their distribution in human skin adnexal structures and skin cancer. Both proteins were found in hair follicles, sebaceous and eccrine glands, as well as blood vessels. Panx1 was detected as punctate or diffuse intracellular labeling, while Panx3 was only observed as diffuse intracellular staining, suggesting different functions. We also identified the Panx3 immunoreactive ~70 kD species modulated during keratinocyte differentiation as Panx3. Since our data indicate that pannexins are regulated during keratinocyte differentiation, we assessed whether their levels are altered under circumstances in which keratinocyte differentiation is compromised. We found that Panx1 and Panx3 levels are highly reduced in human keratinocyte tumors, thus showing for the first time that both pannexins are dysregulated in human cancers. Altogether, these data suggest that Panx1 and Panx3 have distinct and unique functions within the skin in health and disease.</p>","PeriodicalId":55269,"journal":{"name":"Cell Communication and Adhesion","volume":"19 3-4","pages":"45-53"},"PeriodicalIF":0.0,"publicationDate":"2012-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419061.2012.712575","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30879666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 59
Intercellular calcium waves in primary cultured rat mesenteric smooth muscle cells are mediated by connexin43. 原代培养的大鼠肠系膜平滑肌细胞中的细胞间钙波是由 connexin43 介导的。
Cell Communication and Adhesion Pub Date : 2012-04-01 DOI: 10.3109/15419061.2012.690792
Nadia Halidi, Florian Alonso, Janis M Burt, Jean-Louis Bény, Jacques-Antoine Haefliger, Jean-Jacques Meister
{"title":"Intercellular calcium waves in primary cultured rat mesenteric smooth muscle cells are mediated by connexin43.","authors":"Nadia Halidi, Florian Alonso, Janis M Burt, Jean-Louis Bény, Jacques-Antoine Haefliger, Jean-Jacques Meister","doi":"10.3109/15419061.2012.690792","DOIUrl":"10.3109/15419061.2012.690792","url":null,"abstract":"<p><p>Intercellular Ca(2+) wave propagation between vascular smooth muscle cells (SMCs) is associated with the propagation of contraction along the vessel. Here, we characterize the involvement of gap junctions (GJs) in Ca(2+) wave propagation between SMCs at the cellular level. Gap junctional communication was assessed by the propagation of intercellular Ca(2+) waves and the transfer of Lucifer Yellow in A7r5 cells, primary rat mesenteric SMCs (pSMCs), and 6B5N cells, a clone of A7r5 cells expressing higher connexin43 (Cx43) to Cx40 ratio. Mechanical stimulation induced an intracellular Ca(2+) wave in pSMC and 6B5N cells that propagated to neighboring cells, whereas Ca(2+) waves in A7r5 cells failed to progress to neighboring cells. We demonstrate that Cx43 forms the functional GJs that are involved in mediating intercellular Ca(2+) waves and that co-expression of Cx40 with Cx43, depending on their expression ratio, may interfere with Cx43 GJ formation, thus altering junctional communication.</p>","PeriodicalId":55269,"journal":{"name":"Cell Communication and Adhesion","volume":"19 2","pages":"25-37"},"PeriodicalIF":0.0,"publicationDate":"2012-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419061.2012.690792","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30650267","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}
引用次数: 10
3D coupling of fibronectin fibril arrangement with topology of ventral plasma membrane. 纤维连接蛋白原纤维排列与腹侧质膜拓扑结构的三维耦合。
Cell Communication and Adhesion Pub Date : 2012-04-01 Epub Date: 2012-03-12 DOI: 10.3109/15419061.2012.665968
Hiroaki Hirata, Chwee Teck Lim, Hidetake Miyata
{"title":"3D coupling of fibronectin fibril arrangement with topology of ventral plasma membrane.","authors":"Hiroaki Hirata,&nbsp;Chwee Teck Lim,&nbsp;Hidetake Miyata","doi":"10.3109/15419061.2012.665968","DOIUrl":"https://doi.org/10.3109/15419061.2012.665968","url":null,"abstract":"<p><p>Interaction of integrins with extracellular matrices is essential for cell adhesion to substrata. Ventral surfaces of fibroblasts adhering to flat substrata are not flat but have uneven 3D topology. However, spatial relationship between the topology of the ventral cell surface and arrangement of extracellular matrix fibrils remains unclear. Here, we report a novel and simple method based on total internal reflection fluorescence microscopy to quantify the distance between the ventral plasma membrane and the glass substratum. We observe that the distance varies from < 25 nm at focal adhesions to 40-50 nm at close contacts and > 80 nm in other regions. Furthermore, by applying this novel method, we show that fibronectin fibrils are also separated from the substratum in regions where the ventral cell surface-substratum distance is > 80 nm. Our results reveal that fibronectin fibrils are not simply adsorbed to the glass substratum but follow the ventral cell surface topology.</p>","PeriodicalId":55269,"journal":{"name":"Cell Communication and Adhesion","volume":" ","pages":"17-23"},"PeriodicalIF":0.0,"publicationDate":"2012-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419061.2012.665968","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40155766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
RAS signalling in the colorectum in health and disease. 结直肠中RAS信号在健康和疾病中的作用
Cell Communication and Adhesion Pub Date : 2012-02-01 Epub Date: 2012-01-10 DOI: 10.3109/15419061.2011.649380
George Poulogiannis, Feijun Luo, Mark J Arends
{"title":"RAS signalling in the colorectum in health and disease.","authors":"George Poulogiannis,&nbsp;Feijun Luo,&nbsp;Mark J Arends","doi":"10.3109/15419061.2011.649380","DOIUrl":"https://doi.org/10.3109/15419061.2011.649380","url":null,"abstract":"<p><p>RAS proteins act as molecular switches between several homeostatic inputs and signal transduction pathways that regulate important cellular processes including cell growth, differentiation and survival. Activating mutations change the function of normal proto-oncogenic RAS proteins to oncogenic RAS proteins that trigger a wide range of downstream effectors altering expression of transcription factors that together stimulate cell proliferation and modulate apoptosis and differentiation. RAS genes are amongst the most frequently mutated genes in human cancers, in particular KRAS is mutated in 40-50% of colorectal cancers. Mutation of this gene has a significant impact on treatment management and patients' survival, particularly in relation to anti-EGFR therapy, which is only effective in KRAS wild-type cases. Here, we discuss the regulation of KRAS signalling in the colorectum, some of the post-transcriptional and post-translational modifications that control its activity, the mutations and other DNA alterations that are found in this tumour type and the implications that they have for disease progression and current drug treatments.</p>","PeriodicalId":55269,"journal":{"name":"Cell Communication and Adhesion","volume":"19 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2012-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419061.2011.649380","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30377522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 21
γ-Secretase-dependent cleavage of E-cadherin by staurosporine in breast cancer cells. staurosporine在乳腺癌细胞中裂解e-钙粘蛋白的γ-分泌酶依赖性作用。
Cell Communication and Adhesion Pub Date : 2012-02-01 Epub Date: 2012-03-08 DOI: 10.3109/15419061.2012.665969
Chul Bae Yoo, Sang-Moon Yun, Chulman Jo, Young Ho Koh
{"title":"γ-Secretase-dependent cleavage of E-cadherin by staurosporine in breast cancer cells.","authors":"Chul Bae Yoo,&nbsp;Sang-Moon Yun,&nbsp;Chulman Jo,&nbsp;Young Ho Koh","doi":"10.3109/15419061.2012.665969","DOIUrl":"https://doi.org/10.3109/15419061.2012.665969","url":null,"abstract":"<p><p>E-cadherin is a transmembrane protein that serves as a cell adhesion molecule component of the adherens junction. We previously showed that cadmium induced γ-secretase-dependent E-cadherin cleavage via oxidative stress. In this study, we report that staurosporine (STS)-induced apoptosis induces caspase-2 and/or -8-dependent E-cadherin cleavage. STS increased γ-secretase-dependent cleavage of E-cadherin in breast cancer cells through caspase activation. The ability of the γ-secretase inhibitor DAPT and the caspase inhibitor zVAD-FMK to block E-cadherin cleavage provided support for these results. The cleavage of E-cadherin was blocked by caspase-2 and -8 inhibitors. Immunofluorescence analysis confirmed that, along with the disappearance of E-cadherin staining at the cell surface, the E-cadherin cytoplasmic domain accumulated in the cytosol. In the presence of an inhibitor of γ-secretase or caspase, the cleavage of E-cadherin was partially blocked. Our findings suggest that activation of caspase-2/-8 stimulated the disruption of cadherin-mediated cell-cell contacts in apoptotic cells via γ-secretase activation.</p>","PeriodicalId":55269,"journal":{"name":"Cell Communication and Adhesion","volume":" ","pages":"11-6"},"PeriodicalIF":0.0,"publicationDate":"2012-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419061.2012.665969","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40150486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 14
Progranulin stimulated by LPA promotes the migration of aggressive breast cancer cells. LPA刺激的前颗粒蛋白促进侵袭性乳腺癌细胞的迁移。
Cell Communication and Adhesion Pub Date : 2011-12-01 Epub Date: 2011-12-19 DOI: 10.3109/15419061.2011.641042
Muthulekha Swamydas, Do Nguyen, Lauren D Allen, Jill Eddy, Didier Dréau
{"title":"Progranulin stimulated by LPA promotes the migration of aggressive breast cancer cells.","authors":"Muthulekha Swamydas,&nbsp;Do Nguyen,&nbsp;Lauren D Allen,&nbsp;Jill Eddy,&nbsp;Didier Dréau","doi":"10.3109/15419061.2011.641042","DOIUrl":"https://doi.org/10.3109/15419061.2011.641042","url":null,"abstract":"<p><p>Activator and inhibitor roles for the 88-kDa-secreted glycoprotein progranulin (PGRN) have been demonstrated in ovarian cancer cells. Here, we investigated the effects of PGRN in breast cancer migration. Testing MCF7, MDA-MB-453, and MDA-MB-231 human breast cancer cells and the MCF10A breast epithelial cell line, we demonstrate that LPA-induced PGRN stimulation led to a significant increase in cell invasion of MDA-MB-453 and MDA-MB-231 cells only (p<0.05). Moreover, incubation with an anti-PGRN antibody, an inhibitor of the ERK pathway (PD98059) or both in combination inhibited the ability of MDA-MB-231 cells to invade. Furthermore, the expression of focal adhesion kinases promoted by LPA-induced PGRN was also inhibited by PD98059 alone or in combination with an anti-PGRN antibody (p<0.05). Taken together, these results suggest that the LPA activation of PGRN involving the ERK pathway is critical to promote MDA-MB-231 breast cancer cell invasion.</p>","PeriodicalId":55269,"journal":{"name":"Cell Communication and Adhesion","volume":"18 6","pages":"119-30"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419061.2011.641042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30331378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 30
E-cadherin and the cytoskeletal network in colorectal cancer development and metastasis. e -钙粘蛋白和细胞骨架网络在结直肠癌发展和转移中的作用。
Cell Communication and Adhesion Pub Date : 2011-12-01 Epub Date: 2011-12-19 DOI: 10.3109/15419061.2011.636465
Andrea Buda, Massimo Pignatelli
{"title":"E-cadherin and the cytoskeletal network in colorectal cancer development and metastasis.","authors":"Andrea Buda,&nbsp;Massimo Pignatelli","doi":"10.3109/15419061.2011.636465","DOIUrl":"https://doi.org/10.3109/15419061.2011.636465","url":null,"abstract":"<p><p>Abnormalities in the expression and functional activity of cell adhesion molecules are implicated in the development and progression of the majority of colorectal cancers (CRC). Cell-cell adhesion molecule E-cadherin regulates cell polarity, differentiation, proliferation and migration through its intimate association to the actin cytoskeletal network. During colorectal carcinogenesis changes in intercellular adhesion and dynamic rearrangements in the actin cytoskeleton result in altered signalling and migration with loss of contact inhibition. The adenomatous polyposis coli (APC) protein, besides its established role in the β catenin/Wnt signalling pathway, can coordinate microtubule and actin organization during cell migration. The actin-bundling protein Fascin promotes cell motility and is overexpressed in CRC. Based on recent molecular and pathological studies, this review focusses on the role of these molecules sharing the common feature of being associated with the cytoskeletal network during colorectal carcinogenesis and metastasis. The potential use of these molecules as prognostic markers and/or therapeutic targets will also be discussed.</p>","PeriodicalId":55269,"journal":{"name":"Cell Communication and Adhesion","volume":"18 6","pages":"133-43"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419061.2011.636465","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30331269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 62
Vascular endothelial growth factor receptors and the therapeutic targeting of angiogenesis in cancer: where do we go from here? 血管内皮生长因子受体和肿瘤血管生成的治疗靶点:我们将何去何从?
Cell Communication and Adhesion Pub Date : 2011-10-01 Epub Date: 2011-10-24 DOI: 10.3109/15419061.2011.619673
David Bruce, Peng H Tan
{"title":"Vascular endothelial growth factor receptors and the therapeutic targeting of angiogenesis in cancer: where do we go from here?","authors":"David Bruce,&nbsp;Peng H Tan","doi":"10.3109/15419061.2011.619673","DOIUrl":"https://doi.org/10.3109/15419061.2011.619673","url":null,"abstract":"<p><p>Abstract Vascular Endothelial Growth Factor receptors (VEGFRs), the interactions with their ligands and the subsequent signalling pathways are known to play a vital role in tumour angiogenesis. Initial clinical trials of VEGFR inhibitors were disappointing but over the past decade some therapies have been successfully brought to market. At present, VEGFR inhibitors appear to be most promising as adjuvants to conventional chemotherapy. However, several interacting signalling molecules and downstream pathways have recently been shown to interact with VEGFR signalling and provide promising novel targets, such as the platelet-derived growth factor (PDGF), epithelial growth factor (EGF), human epithelial receptor-2, (HER-2) Tie-2 and oestrogen receptors. Elucidation of this web of signalling pathways may identify new therapeutic strategies which may be used in combination with VEGFR inhibitors to augment the efficacy of anti-angiogenic cancer treatments. This review assesses the role of modulating VEGFR activity in cancer and systematically examines current evidence and trials in this area.</p>","PeriodicalId":55269,"journal":{"name":"Cell Communication and Adhesion","volume":"18 5","pages":"85-103"},"PeriodicalIF":0.0,"publicationDate":"2011-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419061.2011.619673","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30224367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 24
Gap junctions mediate STAT5-independent β-casein expression in CID-9 mammary epithelial cells. 间隙连接介导CID-9乳腺上皮细胞中stat5非依赖性β-酪蛋白的表达。
Cell Communication and Adhesion Pub Date : 2011-10-01 Epub Date: 2011-12-05 DOI: 10.3109/15419061.2011.639468
Rabih S Talhouk, Antoine A Khalil, Rachid Bajjani, Gilbert J Rahme, Marwan E El-Sabban
{"title":"Gap junctions mediate STAT5-independent β-casein expression in CID-9 mammary epithelial cells.","authors":"Rabih S Talhouk,&nbsp;Antoine A Khalil,&nbsp;Rachid Bajjani,&nbsp;Gilbert J Rahme,&nbsp;Marwan E El-Sabban","doi":"10.3109/15419061.2011.639468","DOIUrl":"https://doi.org/10.3109/15419061.2011.639468","url":null,"abstract":"<p><p>Crosstalk between gap junction intracellular communication (GJIC), STAT5 and OCT-1 in gap junction (GJ)-dependent β-casein expression was investigated. CID-9 mammary cells plated with prolactin on non-adherent substratum (poly-HEMA) expressed β-casein independent of STAT5 only in the presence of the GJIC inducer, cAMP. Nuclear STAT5 levels were not detectable. By contrast, cells on EHS-drip expressed β-casein in a STAT5-dependent manner and nuclear STAT5 levels were up-regulated. A 75 kDa OCT-1 isoform was detected in conditions that induced β-casein expression regardless of substratum. Interestingly, 40 and 28 kDa OCT-1 isoforms were induced in cells on polyHEMA with cAMP. Electrophoretic mobility shift assays (EMSA) for OCT-1 revealed two band shifts in cells on polyHEMA with cAMP and on EHS-drip, which were repressed by the GJIC inhibitor, 18α-GA. These studies demonstrated that mammary cells on polyHEMA expressed β-casein in response to prolactin in a pathway that involves GJIC and OCT-1 and is independent of STAT5 nuclear translocation.</p>","PeriodicalId":55269,"journal":{"name":"Cell Communication and Adhesion","volume":"18 5","pages":"104-16"},"PeriodicalIF":0.0,"publicationDate":"2011-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419061.2011.639468","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30303639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
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