Connective Tissue Research最新文献

{"title":"A biphasic calcium phosphate/acylated methacrylate gelatin composite hydrogel promotes osteogenesis and bone repair.","authors":"Ren-Jie Xu,&nbsp;Jin-Jin Ma,&nbsp;Xiao Yu,&nbsp;Xiao-Qiang Zhou,&nbsp;Jing-Yu Zhang,&nbsp;Ya-Dong Li,&nbsp;Hui-Lin Yang,&nbsp;Saijilafu,&nbsp;Guang-Xiang Chen","doi":"10.1080/03008207.2023.2212067","DOIUrl":"https://doi.org/10.1080/03008207.2023.2212067","url":null,"abstract":"<p><strong>Purpose/aim: </strong>Bone defects caused by trauma, tumors, congenital malformation, or inflammation are very common in orthopedics. In recent years, mimicking the composition and structure of natural bone tissue has become a hot topic in biomaterial research, with the aim of developing an ideal biomaterial for bone defect transplantation. Here, the feasibility of a biphasic calcium phosphate (BCP)/acylated methacrylate gelatin (GelMA) composite hydrogel to repair bone defects was evaluated in vitro and in rats.</p><p><strong>Materials and methods: </strong>The biocompatibility of a biphasic calcium phosphate (BCP)/acylated methacrylate gelatin (GelMA) composite hydrogel was evaluated by cytoskeleton staining, live/dead cell staining and cell proliferation assays. The in vitro osteogenic activities of the composite hydrogel were evaluated by alkaline phosphatase and alizarin red staining, as well as osteogenic gene expression analysis at both transcript and protein levels. The in vivo bone repair activities were evaluated using the rat skull defect model.</p><p><strong>Results: </strong>The BCP/GelMA composite hydrogel displayed excellent biocompatibility and promoted osteogenesis of bone marrow mesenchymal stem cells in vitro. In addition, the BCP/GelMA composite hydrogel markedly promoted new bone formation in the rat skull-defect model.</p><p><strong>Conclusions: </strong>BCP/GelMA composite hydrogel may be an effective artificial material for bone tissue engineering.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"64 5","pages":"445-456"},"PeriodicalIF":2.9,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10072337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tenogenic differentiation of human tendon-derived stem cells induced by long non-coding RNA LINCMD1 via miR-342-3p/EGR1 axis.","authors":"Feng Qu,&nbsp;Xuezhen Shen,&nbsp;Ketao Wang,&nbsp;Chengyi Sun,&nbsp;Pengfei Li","doi":"10.1080/03008207.2023.2217258","DOIUrl":"https://doi.org/10.1080/03008207.2023.2217258","url":null,"abstract":"<p><strong>Background: </strong>Tendon-derived stem cells (TDSCs) are proposed as a potential cell-seed for the treatment of tendon injury due to their tenogenic differentiation potential. In this work, we defined the action of long non-coding RNA (lncRNA) muscle differentiation 1 (LINCMD1) in tenogenic differentiation of human TDSCs (hTDSCs).</p><p><strong>Methods: </strong>Quantitative real-time PCR (qRT-PCR) was used to assess the levels of LINCMD1, microRNA (miR)-342-3p, and early growth response-1 (EGR1) mRNA. Cell proliferation was detected by the XTT colorimetric assay. Protein expression was quantified by western blot. hTDSCs were grown in an osteogenic medium to induce osteogenic differentiation, and the extent of osteogenic differentiation was assessed by Alizarin Red Staining (ARS). The activity of alkaline phosphatase (ALP) was measured by the ALP Activity Assay Kit. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to evaluate the direct relationship between miR-342-3p and LINCMD1 or EGR1.</p><p><strong>Results: </strong>Our results showed that enforced expression of LINCMD1 or suppression of miR-342-3p accelerated the proliferation and tenogenic differentiation and reduced osteogenic differentiation of hTDSCs. LINCMD1 regulated miR-342-3p expression by binding to miR-342-3p. EGR1 was identified as a direct and functional target of miR-342-3p, and knockdown of EGR1 reversed the effects of miR-342-3p suppression on cell proliferation and tenogenic and osteogenic differentiation. Furthermore, the miR-342-3p/EGR1 axis mediated the regulation of LINCMD1 on hTDSC proliferation and tenogenic and osteogenic differentiation.</p><p><strong>Conclusion: </strong>Our study suggests the induction of LINCMD1 in tenogenic differentiation of hTDSCs through miR-342-3p/EGR1 axis.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"64 5","pages":"479-490"},"PeriodicalIF":2.9,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10130003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Notch1 is a marker for <i>in situ</i> resting osteocytes in a 3-dimensional gel culture model.","authors":"Ying-Hui Zhou,&nbsp;Jia-Yu Zhu,&nbsp;Yue Guo,&nbsp;Hao-Neng Tang,&nbsp;Fang Wang,&nbsp;Junaid Iqbal,&nbsp;Hui-Xuan Wu,&nbsp;Nan Hu,&nbsp;Fen Xiao,&nbsp;Ting Wang,&nbsp;Long Li,&nbsp;Hou-De Zhou","doi":"10.1080/03008207.2023.2217271","DOIUrl":"https://doi.org/10.1080/03008207.2023.2217271","url":null,"abstract":"<p><strong>Purpose: </strong>Osteocytes <i>in</i> <i>vivo</i> exhibit different functional states, but no specific marker to distinguish these is currently available.</p><p><strong>Materials and methods: </strong>To simulate the differentiation process of pre-osteoblasts to osteocytes <i>in</i> <i>vitro</i>, MC3T3-E1 cells were cultured on type I collagen gel and a three-dimensional (3D) culture system was established. The Notch expression of osteocyte-like cells in 3D culture system was compared with that of <i>in situ</i> osteocytes in bone tissues.</p><p><strong>Results: </strong>Immunohistochemistry demonstrated that Notch1 was not detected in \"resting\" <i>in</i> <i>situ</i> osteocytes, but was detected in normal cultured osteocyte-like cell line MLO-Y4. Osteocytes obtained from conventional osteogenic-induced osteoblasts and long-term cultured MLO-Y4 cells could not replicate the Notch1 expression pattern from <i>in</i> <i>situ</i> osteocytes. From day 14-35 of osteogenic induction, osteoblasts in 3D culture system gradually migrated into the gel to form canaliculus-like structures similar to bone canaliculus. On day 35, stellate-shaped osteocyte-like cells were observed, and expression of DMP1 and SOST, but not Runx2, was detected. Notch1 was not detected by immunohistochemistry, and <i>Notch1</i> mRNA level was not significantly different from that of <i>in</i> <i>situ</i> osteocytes. In MC3T3-E1 cells, down-regulation of <i>Notch2</i> increased <i>Notch1</i>, Notch downstream genes (<i>β-catenin</i> and <i>Nfatc1</i>), and <i>Dmp1</i>. In MLO-Y4 cells, Notch2 decreased after <i>Notch1</i> siRNA transfection. Downregulation of <i>Notch1</i> or <i>Notch2</i> decreased <i>Nfatc1</i>, <i>β-catenin</i>, and <i>Dmp1</i>, and increased <i>Sost</i>.</p><p><strong>Conclusions: </strong>We established \"resting state\" osteocytes using an <i>in</i> <i>vitro</i> 3D model. Notch1 can be a useful marker to help differentiate the functional states of osteocytes (activated vs. resting state).</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"64 5","pages":"491-504"},"PeriodicalIF":2.9,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10449885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LPS-induced inflammation potentiates dental pulp stem cell odontogenic differentiation through C5aR and p38.","authors":"Ji-Hyun Kim, Muhammad Irfan, Md Akil Hossain, Susie Shin, Anne George, Seung Chung","doi":"10.1080/03008207.2023.2218944","DOIUrl":"10.1080/03008207.2023.2218944","url":null,"abstract":"<p><strong>Aim: </strong>Inflammation is a complex host response to harmful infection or injury, and it seems to play a crucial role in tissue regeneration both positively and negatively. We have previously demonstrated that the activation of the complement C5a pathway affects dentin-pulp regeneration. However, limited information is available to understand the role of the complement C5a system related to inflammation-mediated dentinogenesis. The aim of this study was to determine the role of complement C5a receptor (C5aR) in regulating lipopolysaccharide (LPS)-induced odontogenic differentiation of dental pulp stem cells (DPSCs).</p><p><strong>Material and methods: </strong>Human DPSCs were subjected to LPS-stimulated odontogenic differentiation in dentinogenic media treated with the C5aR agonist and antagonist. A putative downstream pathway of the C5aR was examined using a p38 mitogen-activated protein kinase (p38) inhibitor (SB203580).</p><p><strong>Results: </strong>Our data demonstrated that inflammation induced by the LPS treatment potentiated DPSC odontogenic differentiation and that this is C5aR dependent. C5aR signaling controlled the LPS-stimulated dentinogenesis by regulating the expression of odontogenic lineage markers like dentin sialophosphoprotein (DSPP) and dentin matrix protein 1 (DMP-1). Moreover, the LPS treatment increased the total p38, and the active form of p38 expression, and treatment with SB203580 abolished the LPS-induced DSPP and DMP-1 increase.</p><p><strong>Conclusions: </strong>These data suggest a significant role of C5aR and its putative downstream molecule p38 in the LPS-induced odontogenic DPSCs differentiation. This study highlights the regulatory pathway of complement C5aR/p38 and a possible therapeutic approach for improving the efficiency of dentin regeneration during inflammation.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"64 5","pages":"505-515"},"PeriodicalIF":2.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10524681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10449891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contribution of immune cells to intervertebral disc degeneration and the potential of immunotherapy.","authors":"Hao Xu,&nbsp;Juan Li,&nbsp;Qinming Fei,&nbsp;Libo Jiang","doi":"10.1080/03008207.2023.2212051","DOIUrl":"https://doi.org/10.1080/03008207.2023.2212051","url":null,"abstract":"<p><p>Substantial evidence supports that chronic low back pain is associated with intervertebral disc degeneration (IDD), which is accompanied by decreased cell activity and matrix degradation. The role of immune cells, especially macrophages, in a variety of diseases has been extensively studied; therefore, their role in IDD has naturally attracted widespread scholarly interest. The IVD is considered to be an immunologically-privileged site given the presence of physical and biological barriers that include an avascular microenvironment, a high proteoglycan concentration, high physical pressure, the presence of apoptosis inducers such as Fas ligand, and the presence of notochordal cells. However, during IDD, immune cells with distinct characteristics appear in the IVD. Some of these immune cells release factors that promote the inflammatory response and angiogenesis in the disc and are, therefore, important drivers of IDD. Although some studies have elucidated the role of immune cells, no specific strategies related to systemic immunotherapy have been proposed. Herein, we summarize current knowledge of the presence and role of immune cells in IDD and consider that immunotherapy targeting immune cells may be a novel strategy for alleviating IDD symptoms.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"64 5","pages":"413-427"},"PeriodicalIF":2.9,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10077417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retinoic acid inhibits the pyroptosis of degenerated nucleus pulposus cells by activating Sirt1-SOD2 signaling.","authors":"Peng-Fei Li,&nbsp;Fei Xiong,&nbsp;Hong-Yuan Xing,&nbsp;Shao-Jun Hu,&nbsp;Ning Zhang","doi":"10.1080/03008207.2023.2192286","DOIUrl":"https://doi.org/10.1080/03008207.2023.2192286","url":null,"abstract":"<p><strong>Aim: </strong>Intervertebral disc (IVD) degeneration is a common disease initiated by the degeneration of the nucleus pulposus (NP). The pyroptosis of degenerated NP cells (dNPCs) plays an important role in NP degeneration. The purpose of this study is to identify a feasible solution that can inhibit NP cell pyroptosis to therapy the degeneration of the intervertebral disc.</p><p><strong>Methods: </strong>Cell viability and proliferation were quantified by Cell Counting Kit-8 assay. The measurement of cellular reactive oxygen species (ROS) was detected by 2,7-Dichlorodi-hydrofluorescein diacetate. The death of cells was analyzed by the Terminal Deoxynucleotidyl Transferase-mediated dUTP Nick-End Labeling (TUNEL) method of fluorescence analysis. The pyroptosis of cells was assessed by flow cytometry analyses. The contents of sulfate glycosaminoglycans were detected by a blyscan assay kit.</p><p><strong>Result: </strong>In this study, we determined the effects of retinoic acid (RA) on dNPCs and investigated the underlying mechanism of RA-mediated pyroptosis in dNPCs. We also verified the effects of RA on IVD degeneration in vivo. Our results demonstrated that RA significantly increased the proliferation and the protein expression of sox9, aggrecan, and collagen II of dNPCs. Pyroptosis-related proteins and the pyroptosis rate of dNPCs were significantly decreased by RA. We found that Sirt1-SOD2 signaling was activated, while ROS generation and TXNIP/NLRP3 signaling in dNPCs were inhibited after the addition of RA. Furthermore, RA also recovered the structure of NP and increased the contents of sulfated glycosaminoglycans and collagen in vivo.</p><p><strong>Conclusion: </strong>Our study demonstrated that RA could inhibit the pyroptosis and increase the extracellular matrix synthesis function of dNPCs and verified that RA has a protective effect on IVD degeneration.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"64 4","pages":"337-349"},"PeriodicalIF":2.9,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9751525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulation of metalloproteinases in spinal ligament degeneration.","authors":"Chao Wang,&nbsp;Ziran Wei,&nbsp;Tengbo Yu,&nbsp;Lu Zhang","doi":"10.1080/03008207.2022.2160327","DOIUrl":"https://doi.org/10.1080/03008207.2022.2160327","url":null,"abstract":"<p><strong>Purpose: </strong>Degenerative changes in the spinal ligaments, such as hypertrophy or ossification, are important pathophysiological mechanisms of secondary spinal stenosis and neurological compression. Extracellular matrix (ECM) remodeling is one of the major pathological changes in ligament degeneration, and in this remodeling, ECM proteinase-mediated degradation of elastin and collagen plays a vital role. Zinc-dependent endopeptidases, including matrix metalloproteinases (MMPs), a disintegrin and metalloproteinases (ADAMs), and ADAMs with thrombospondin-1 motifs (ADAMTSs) are key factors in ECM remodeling. This review aims to elucidate the underlying mechanisms of these metalloproteinases in the initiation and progression of spinal ligament degeneration.</p><p><strong>Methods: </strong>We clarify current literature on the dysregulation of MMPs/ADAMs/ADAMTS and their endogenous inhibitors in degenerative spinal ligament diseases. In addition, some instructive information was excavated from the raw data of the relevant high-throughput analysis.</p><p><strong>Results and conclusions: </strong>The dysregulation of metalloproteinases and their endogenous inhibitors may affect ligament degeneration by involving several interrelated processes, represented by ECM degradation, fibroblast proliferation, and osteogenic differentiation. Antagonists of the key targets of the processes may in turn ease ligament degeneration.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"64 4","pages":"310-322"},"PeriodicalIF":2.9,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9748313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zinc finger E-box binding homebox 2 alleviated experimental osteoarthritis in rats.","authors":"Gao-Feng Zhao,&nbsp;Le-Bin Huang","doi":"10.1080/03008207.2023.2186133","DOIUrl":"https://doi.org/10.1080/03008207.2023.2186133","url":null,"abstract":"<p><strong>Aims: </strong>Osteoarthritis (OA) is a chronic inflammatory disease, characterized by degradation of extracellular matrix, apoptosis of chondrocytes and inflammation in articular cartilage. Zinc finger E-box binding homebox 2 (ZEB2), a transcription repressor, has been demonstrated with anti-inflammatory role in some cells. The analysis from GEO data reveals that ZEB2 expression is upregulated in articular cartilage of OA patients and experimental OA rodents. This study aims to confirm the function of ZEB2 in OA process.</p><p><strong>Material and methods: </strong>The experimental OA was induced by anterior cruciate ligament transaction (ACLT) in rats, and the adenovirus loaded with ZEB2 coding sequence was intra-articularly injected into rats (1 × 10 PFU). The primary articular chondrocytes were stimulated by interleukin-1β (IL-1β) (10 ng/ml) to mimic the osteoarthritic injury, and transfected with the adenovirus carrying ZEB2 coding or silencing sequence. The apoptosis, content of extracellular matrix, inflammation, and the activity of NFκB signaling in chondrocytes and cartilage were determined.</p><p><strong>Results: </strong>ZEB2 was highly expressed in osteoarthritic cartilage tissues and IL-1β-treated chondrocytes. The overexpression of ZEB2 restrained ACLT- or IL-1β administration-induced apoptosis, matrix degradation and inflammation in vivo or in vitro, evidenced by changed levels of cleaved caspase-3/PARP, collagen-II, aggrecan, matrix metalloproteinase 3/13, tumor necrosis factor-α and interleukin-6. Additionally, the phosphorylation of NFκB p65, IκBα and IKKα/β, and the nuclear translocation of p65 was blocked by ZEB2, implying inactivation of this signaling.</p><p><strong>Conclusions: </strong>ZEB2 mitigated osteoarthritic symptoms in rats and chondrocytes, and NFκB signaling might be involved. These findings may provide novel insights for clinical treatment of OA.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"64 4","pages":"323-336"},"PeriodicalIF":2.9,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9757423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ovariectomy with simulated vaginal delivery to establish a rat model for pelvic organ prolapse.","authors":"Tao Guo,&nbsp;Zhe Du,&nbsp;Xiu-Qi Wang,&nbsp;Jing-He Lang,&nbsp;Zhi-Jing Sun","doi":"10.1080/03008207.2023.2199091","DOIUrl":"https://doi.org/10.1080/03008207.2023.2199091","url":null,"abstract":"<p><p>The widespread prevalence of Pelvic Organ Prolapse (POP) and the paucity of ongoing treatments prompted us to develop a unique rat model combining ovariectomy and simulated vaginal delivery. We hypothesized that the tissue changes caused by low hormone levels and mechanical stretch could complement each other. Thus, the combined model can potentially mimic the collagen metabolism of vaginal wall tissue as well as mechanical stretch properties to complement disease progression in POP. Ovariectomy with sequential simulated vaginal delivery was performed on rats in the modeling group. Sham surgeries were performed as control. At 2, 4, and 12 weeks after modeling, the vaginal tissues of rats were evaluated by Masson's trichrome staining, Picro-Sirius red staining, immunohistochemistry, western blotting, and uniaxial tensile tests. Compared to the control group, the vaginal tissues of the model rats showed an atrophic epithelial layer and loose collagen fibers. The smooth muscle fibers were ruptured, smaller in diameter, and disorganized. The ratio of collagen type I/III significantly increased, but the contents of both Collagen I and III decreased. The expression of metalloproteinases 2 and 9 in the tissues increased, and the expression of tissue inhibitors of metalloproteinases 1 and 2 decreased. The tangent modulus of the tissues was significantly increased in the model rats. We verified a novel method to establish a pelvic organ prolapse model in rats. This approach combined the advantages of low hormone levels and mechanical stretch effects.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"64 4","pages":"376-388"},"PeriodicalIF":2.9,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10125886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A tribute to doctor Arthur Veis.","authors":"Elizabeth Lux","doi":"10.1080/03008207.2023.2213502","DOIUrl":"10.1080/03008207.2023.2213502","url":null,"abstract":"","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"64 4","pages":"307-309"},"PeriodicalIF":2.9,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9740327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}