Bone Reports最新文献

{"title":"Unidirectional porous beta-tricalcium phosphate supports three-dimensional osteogenic differentiation of human iPS cells without surface coating","authors":"Akihito Kawai,&nbsp;Yusuke Inagaki,&nbsp;Kensuke Okamura,&nbsp;Yoshinobu Hyakuda,&nbsp;Masakazu Okamoto,&nbsp;Munehiro Ogawa,&nbsp;Akira Kido,&nbsp;Yasuhito Tanaka,&nbsp;Kenji Kawamura","doi":"10.1016/j.bonr.2026.101947","DOIUrl":"10.1016/j.bonr.2026.101947","url":null,"abstract":"<div><div>Beta-tricalcium phosphate (βTCP) is widely used as a bone graft substitute, but it lacks intrinsic osteogenic cells. Human induced pluripotent stem cells (iPSCs) are a promising cell source for bone regeneration; however, the suitability of clinically available, uncoated βTCP as a scaffold for iPSC osteogenic differentiation remains unclear. We compared interconnected porous and unidirectional porous βTCP combined with either negative-pressure or atmospheric-pressure seeding. Metabolic activity was assessed using a CCK-8 assay, and the selected condition was further evaluated by RT-qPCR, scanning electron microscopy, and immunofluorescence staining during osteogenic induction. In vivo osteogenic progression was examined after subcutaneous transplantation into immunodeficient rodents. Negative-pressure seeding was associated with lower metabolic activity, whereas atmospheric-pressure seeding onto unidirectional porous βTCP yielded the highest values among the tested conditions. Under this condition, undifferentiated markers decreased after osteogenic induction, while osteoblast- and osteocyte-related genes showed time-dependent changes consistent with osteogenic lineage progression. Scanning electron microscopy demonstrated cell attachment and three-dimensional extension within the oriented pores, and immunofluorescence staining showed increasing type I collagen deposition during culture. After transplantation, human cell-derived RNA remained detectable, and several osteogenic markers increased over time. These findings indicate that clinically available, uncoated unidirectional porous βTCP can support the survival and osteogenic differentiation of human iPSCs in the absence of additional scaffold coating. This system may provide a simple platform for further studies of iPSC-based bone regenerative strategies.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"30 ","pages":"Article 101947"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148951393","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":"Piezo1-mediated Mechanotransduction in the musculoskeletal system: Signaling networks and therapeutic perspectives","authors":"Hong Zhao,&nbsp;Junyan Huang,&nbsp;Yayi Tan,&nbsp;Shiying Shen,&nbsp;Zehao Ying,&nbsp;Zhengyan Li,&nbsp;Yizhe Xiong,&nbsp;Haiya Ge,&nbsp;Xiang Wang,&nbsp;Hongsheng Zhan,&nbsp;Ying Shen,&nbsp;Guoqing Du","doi":"10.1016/j.bonr.2026.101943","DOIUrl":"10.1016/j.bonr.2026.101943","url":null,"abstract":"<div><div>Mechanical forces are integral to musculoskeletal homeostasis and pathology. Piezo1 is a mechanosensitive ion channel widely expressed in bone, cartilage, muscle, and tendon. It converts mechanical stimuli (tension, compression, shear) into Ca²⁺ influx and downstream signals, regulating proliferation, differentiation, metabolism, inflammation, and apoptosis. This review summarizes Piezo1's structure, gating mechanisms, tissue expression, and functions in the musculoskeletal system, focusing on cartilage degeneration, subchondral bone remodeling, skeletal remodeling, muscle maintenance, and tendon adaptation. Under physiological conditions, Piezo1 contributes to tissue homeostasis; however, under abnormal or sustained loads, excessive Piezo1 activation can disrupt Ca²⁺ balance, amplify inflammation, promote apoptosis, and contribute to pathological remodeling in osteoarthritis, osteoporosis, muscle injury, and tendon degeneration. Preclinical strategies, including chemical agonists/inhibitors, traditional Chinese medicine components, gene-based approaches, and stem-cell-related interventions, have been explored in cell and animal models. Piezo1 is an important mechanosensitive regulator linking mechanical cues to musculoskeletal biology, although its tissue-specific roles, interactions with other mechanosensitive channels, and clinical translational value require further study.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"30 ","pages":"Article 101943"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148854423","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":"Orthopaedic diagnostic pitfalls in fibroblast growth factor 23-mediated hypophosphatemic rickets/osteomalacia in fibrous dysplasia/McCune-Albright syndrome: Two burosumab-treated cases","authors":"Tomoo Nakagawa,&nbsp;Jungo Imanishi,&nbsp;Ayako Koda,&nbsp;Taisuke Matsuyama,&nbsp;Kenji Sato,&nbsp;Asako Yamamoto,&nbsp;Kentaro Matsui,&nbsp;Yoshinobu Watanabe,&nbsp;Hirotaka Kawano","doi":"10.1016/j.bonr.2026.101945","DOIUrl":"10.1016/j.bonr.2026.101945","url":null,"abstract":"<div><div>Fibrous dysplasia/McCune-Albright syndrome (FD/MAS) can obscure fibroblast growth factor 23 (FGF23)-mediated hypophosphatemic rickets/osteomalacia. We report two FD/MAS patients with recurrent fractures, hypophosphatemia, elevated FGF23, and serial imaging showing overlooked rachitic changes years before diagnosis. Burosumab improved serum phosphate levels after dose adjustment and was associated with mobility gains in Case 1 and increased growth velocity with physeal normalization in Case 2. Age-appropriate phosphate assessment and FGF23 testing are warranted when orthopaedic findings suggest impaired mineralization.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"30 ","pages":"Article 101945"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148951390","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":"Children with unilateral spastic cerebral palsy have smaller and weaker tibias in the spastic limb compared to the non-spastic limb","authors":"Jessica L. Stockhausen,&nbsp;Julio Carballido-Gamio,&nbsp;Dana Carpenter,&nbsp;Jason T. Rhodes,&nbsp;David R. Howell,&nbsp;Sayan De,&nbsp;Patrick M. Carry,&nbsp;Christine M. Swanson,&nbsp;Kellen T. Krajewski","doi":"10.1016/j.bonr.2026.101946","DOIUrl":"10.1016/j.bonr.2026.101946","url":null,"abstract":"<div><div>Cerebral palsy (CP) is associated with poor bone architecture. It is unclear if abnormal bone architecture is localized to the area affected by spasticity and whether these deficiencies are dependent on physical activity. This study aimed to examine differences in tibial bone architecture between the spastic and non-spastic limbs in children with unilateral spastic CP and the association between physical activity habits with spastic limb bone architecture. Twenty-four ambulatory children with CP (13 females, 11 males; 7.8 ± 1.7 years) completed bilateral high-resolution peripheral quantitative computed tomography (HR-pQCT) at the distal tibia metaphysis. The frequency of participation (FPS), bone specific physical activity questionnaire (BPAQ), and dynamic participation survey (DPS) were used to assess physical activity habits. Differences between limb architecture were assessed with paired <em>t</em>-tests. Linear regressions were performed on FPS/BPAQ/DPS scores with each HR-pQCT outcome separately. HR-pQCT data without significant motion artifacts were available for eighteen participants. The spastic limb had less total area (<em>p</em> = 0.013, 95%CI 4.87–35.13mm²), trabecular area (<em>p</em> = 0.035, 95%CI 1.22–29.96mm²), cortical area (<em>p</em> = 0.008, 95%CI 1.35–7.63mm²), cortical perimeter (<em>p</em> = 0.012, 95%CI 0.52–3.60 mm), cortical thickness (<em>p</em> = 0.046, 95%CI 0.001–0.112 mm), stiffness (<em>p</em> = 0.012, 95%CI 2065-13,429 N/mm), and failure load (<em>p</em> = 0.008, 95%CI 128-747 N) than the non-spastic limb. Only BPAQ was associated with limb length (<em>p</em> = 0.011, R = -0.584). The distal tibia metaphysis of the spastic limb had similar bone density but was smaller and weaker compared to the non-spastic limb. Differences in bone geometry likely accounted for between-limb differences in estimated bone strength.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"30 ","pages":"Article 101946"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148951389","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":"Blockade of NLRP3 alleviates systemic lupus erythematosus-induced osteoporosis through dual modulation of osteogenesis and osteoclastogenesis","authors":"Feifu Deng,&nbsp;Yuting Liao,&nbsp;Weixiong Guo,&nbsp;Xiangxin Zhong,&nbsp;Xiang Gao,&nbsp;Ahmad,&nbsp;Yanzhi Liu,&nbsp;Jinsong Wei","doi":"10.1016/j.bonr.2026.101942","DOIUrl":"10.1016/j.bonr.2026.101942","url":null,"abstract":"<div><div>Systemic lupus erythematosus (SLE) is a chronic autoimmune disease frequently associated with accelerated bone loss and osteoporosis. Emerging evidence implicates the NLRP3 inflammasome as a pivotal mediator of inflammation-driven bone remodeling dysregulation in SLE. This study investigates the therapeutic potential of targeting NLRP3 inhibition for SLE treatment using both a synthetic NLRP3 inhibitor (MCC950) and a natural NLRP3 inhibitor—oridonin, for its potential clinical translation.</div><div>Using a combination of <em>in vitro</em> and <em>in vivo</em> approaches, we demonstrate that NLRP3 activation by lipopolysaccharide (LPS) promotes osteoclast differentiation and inhibits osteogenic differentiation through distinct molecular mechanisms. In RAW264.7 macrophages, LPS-induced NLRP3 activation upregulates autophagy-related genes (LC3B, p62) and osteoclastogenesis- related genes (TRAF6, c-Jun, NFATc1), which are effectively suppressed by MCC950 intervention. In mesenchymal stem cells, LPS exposure impairs osteogenic differentiation by reducing Runx2 and OCN gene expression while increasing pyroptosis-related genes (GSDMD, Caspase-11), these effects that are significantly ameliorated by oridonin intervention.</div><div>In an SLE murine model (MRL/lpr mice), 12 weeks of NLRP3 inhibition with either MCC950 or oridonin both restore bone microstructure, enhance trabecular bone density, improve biomechanical properties, and normalize serum biomarkers of bone turnover.</div><div>This study provides compelling evidence that targeting NLRP3 signaling represents a promising therapeutic strategy for SLE-associated osteoporosis. The osteogenic effect of oridonin, a naturally occurring compound with established clinical safety, highlights its potential as a promising agent for treating bone loss in SLE patients. These findings underscore the importance of inflammasome targeting in managing SLE-induced bone remodeling disorders.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"30 ","pages":"Article 101942"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148853994","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":"A novel PTH1R missense variant in a patient with early-onset primary hyperparathyroidism","authors":"Conghui Cao,&nbsp;Xiaoli Wang","doi":"10.1016/j.bonr.2026.101948","DOIUrl":"10.1016/j.bonr.2026.101948","url":null,"abstract":"<div><div>We report a 30-year-old male with early-onset primary hyperparathyroidism (PHPT) and incidental papillary thyroid carcinoma. Biochemical tests showed hypercalcemia, hypophosphatemia, elevated PTH and normal renal function. Planar ⁹⁹ᵐTc-MIBI scintigraphy projected a parathyroid lesion to the left thyroid inferior pole, while surgery revealed an ectopic solitary parathyroid adenoma in the left upper mediastinum; serum calcium, phosphate and PTH normalized two months postoperatively. Whole-exome sequencing detected a novel heterozygous PTH1R variant c.982G &gt; A (p.Gly328Ser), classified as a variant of uncertain significance by ACMG/AMP criteria. The identical variant was identified in the proband's father, whose annual routine calcium and phosphorus tests remained persistently normal, so he declined additional parathyroid-related biochemical testing. Unlike previously reported PTH1R mutations linked to skeletal/dental defects, this patient presented isolated PHPT without skeletal or dental abnormalities. Neither classic loss-of-function nor canonical gain-of-function mechanisms fully explain this unique phenotype, and no in vitro functional data are available to validate variant pathogenicity. This case expands the phenotypic spectrum of PTH1R-related disorders and offers a new genetic clue for early-onset PHPT. Further functional experiments and long-term family follow-up are needed to verify the clinical relevance of this variant.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"30 ","pages":"Article 101948"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148951391","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":"Artificial intelligence and machine learning in bone research","authors":"Mustafa Unal,&nbsp;Karl J. Lewis,&nbsp;Cheryl L. Ackert-Bicknell,&nbsp;Jeffry S. Nyman","doi":"10.1016/j.bonr.2026.101922","DOIUrl":"10.1016/j.bonr.2026.101922","url":null,"abstract":"","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"30 ","pages":"Article 101922"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148995108","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":"Burosumab improves alkaline phosphatase and rickets severity in X-linked hypophosphatemia: 3-year SUNFLOWER analysis","authors":"Keiichi Ozono,&nbsp;Hee Gyung Kang,&nbsp;Noriyuki Namba,&nbsp;Nobuaki Ito,&nbsp;Takuo Kubota,&nbsp;Ayumi Shintani,&nbsp;Ryota Kawai,&nbsp;Osamu Miyazaki,&nbsp;Masanori Kanematsu,&nbsp;Haruka Ishii,&nbsp;Toshimi Michigami","doi":"10.1016/j.bonr.2026.101944","DOIUrl":"10.1016/j.bonr.2026.101944","url":null,"abstract":"<div><div>SUNFLOWER is a 10-year longitudinal observational cohort study of patients with X-linked hypophosphatemia (XLH) in Japan and South Korea. This report describes the 3-year cut-off of SUNFLOWER, including data from 1 year of burosumab administration (burosumab-treated group) and 1 year after providing informed consent (non-burosumab-treated group). The real-world effectiveness of burosumab and the associations between bone metabolism markers and quality of life (QoL)/patient-reported outcomes (PROs) and rickets severity scores (RSS)/height over 1 year in burosumab-treated patients with XLH were assessed. As burosumab had not been launched in South Korea at the time of cut-off, data from South Korea were not available. The main outcome measures were changes in serum parameters, and correlations between alkaline phosphatase (ALP) levels and RSS and height (children), and between ALP (children) or bone-specific ALP (BALP; adults) levels and QoL/PROs and motor functions. In total, 146 patients were enrolled, including 69 (47.3%) children and 77 (52.7%) adults. After 1 year of treatment, burosumab-treated patients (43 [62.3%] children, 29 [37.7%] adults) had improved serum phosphate levels, 1,25-dihydroxyvitamin D, and ALP/BALP compared with pre-treatment levels. In children, RSS changes significantly correlated with ALP changes (correlation coefficient: 0.806, <em>p</em> &lt; 0.001), but height changes did not show significant correlation. There were no significant correlations between changes in ALP/BALP and QoL/PRO assessments or motor function. In conclusion, decreased ALP correlated with an improvement in rickets severity score in Japanese children with XLH, suggesting that ALP may be a useful marker for monitoring both the severity and improvement of rickets/osteomalacia.</div></div><div><h3>Clinical trial registration</h3><div><span><span>NCT03745521</span><svg><path></path></svg></span> and UMIN000031605.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"30 ","pages":"Article 101944"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148951269","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":"The natural history of osteogenesis imperfecta: a systematic review","authors":"Davide Gatti ,&nbsp;Samantha Prince ,&nbsp;Ogün Sazova ,&nbsp;Clive Whitcher ,&nbsp;Antoinette Randet ,&nbsp;Matthew Carter ,&nbsp;Maria Rapoport ,&nbsp;Oliver Semler","doi":"10.1016/j.bonr.2026.101927","DOIUrl":"10.1016/j.bonr.2026.101927","url":null,"abstract":"<div><div>Osteogenesis imperfecta (OI) is a rare, heritable condition characterised by bone fragility, varied manifestations, and phenotypic heterogeneity. Understanding its natural history is essential for anticipating clinical needs. This systematic review collated literature on OI's natural history, focussing on diagnosis, signs, symptoms, and events (SSEs), and mortality.</div><div>MEDLINE, Embase, and Embase Conference Abstracts were searched on March 24, 2024. Longitudinal (≥5 years follow-up) and cross-sectional studies which analysed outcomes by age were included, irrespective of interventions, due to treatment variability in OI.</div><div>Sixty-six studies were included. Age of diagnosis varied widely; severe OI was typically diagnosed in early childhood, whereas milder types showed greater variability. SSEs manifest across ages. Some SSEs progress rapidly in childhood (e.g. scoliosis and bone deformities), whereas others (e.g. cardiac, ocular, auditory, and joint issues) emerge in adulthood, often earlier and more commonly than in the general population. Severe phenotypes may be associated with earlier onset and greater symptom severity than milder types. Fractures may be most frequent during childhood and adolescence but continue into adulthood, with limb fractures most reported. Aging, pregnancy, and menopause may increase the risk of hip, spine, and femur fractures. Life expectancy appears reduced by an average 9.5 years in men and 7.1 in women versus the general population. Leading causes of mortality include OI-related complications, cardiovascular and respiratory issues, and fracture-related trauma.</div><div>The heterogeneous, progressive nature of SSEs supports the need for tailored, multidisciplinary long-term care. However, substantial evidence gaps and methodological inconsistencies limit comparability, highlighting the need for further evidence.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"29 ","pages":"Article 101927"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148183673","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}

{"title":"Fibrin, from blood to bone: a review","authors":"Hamza Danguir ,&nbsp;Lisa Reiniche ,&nbsp;Khalil El Mabrouk ,&nbsp;Maxime Ducret ,&nbsp;Meriame Bricha ,&nbsp;Mourad Bekhouche","doi":"10.1016/j.bonr.2026.101925","DOIUrl":"10.1016/j.bonr.2026.101925","url":null,"abstract":"<div><div>Fibrin is principally involved in blood coagulation and hemostasis. Its structure, abundance and turnover are reciprocally related to blood flow. Decreased abundance of fibrin in afibrinogenemic or hemophilic patients leads to bone disorders such as bone cysts or hemarthroses. Fibrin accumulation in growing children with chronic disease leads to osteoarthritis and physeal disruption. Despite its clear role in bone disorders; the underlying mechanisms are not clearly understood. Bone formation and hemostasis is mediated by osteocyte mechanosensitivity involving plasma membrane disruption, calcium signaling cascade. Fibrin is related to mechanotransduction in platelets and recently in mitochondrial mechanosensing in macrophages, however its role in bone mechanobiology is not elucidated. This review underlines the link of fibrin and bone pathophysiology and emphasizes the gap of knowledge between fibrin function during healing and mechanobiology of bone homeostasis. This review proposed an original perspective to better understand bone loss, repair and formation, that could open the path to further investigations to adapt innovative therapeutic strategies.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"29 ","pages":"Article 101925"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148183674","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}