Bone Reports最新文献

{"title":"Deep phenotyping of an ATDC5 in-vitro cartilage model system","authors":"Anna Klawonn ,&nbsp;Stefan Tholen ,&nbsp;Ilona Skatulla ,&nbsp;Chiara M. Schröder ,&nbsp;Sebastian J. Arnold ,&nbsp;Oliver Schilling ,&nbsp;Miriam Schmidts","doi":"10.1016/j.bonr.2026.101924","DOIUrl":"10.1016/j.bonr.2026.101924","url":null,"abstract":"<div><div>Cartilage is characterized by a highly specialized extracellular matrix (ECM) secreted by chondrocytes and limited self-regenerative capacity. In vivo investigations of chondrogenesis are limited by difficult and traumatic access, especially in humans. While it is known for decades that disturbances of chondrocyte differentiation and changed cartilage ECM composition cause severe skeletal phenotypes in vertebrates, a detailed molecular understanding of chondrogenesis and cartilage ECM formation is still missing, especially in the context of human genetic skeletal diseases.</div><div>ATDC5 cells, derived from AT805 mouse teratocarcinoma cells, have been used in the past to model chondrogenic differentiation, however, most studies have investigated few major cellular differentiation markers only so that the composition of the secreted ECM as well as effects on the ATDC5 transcriptome upon differentiation are still unclear. Here, we performed time-resolved transcriptomic and ECM proteomic analyses of differentiating ATDC5 cells. Both datasets confirmed the formation of a cartilage-like matrix with increasing expression of key chondrocyte genes over the course of differentiation. ECM proteomics further revealed a number of ECM components not previously reported in ATDC5 cells or the secreted ECM, encompassing collagens, proteoglycans, glycoproteins and other secreted factors. Overall, our findings provide a more detailed molecular characterization of ATDC5 chondrogenesis and highlight the potential of this model system for ECM-focused studies.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"29 ","pages":"Article 101924"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148184301","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":"The dinitrothiophenol SN-2 reduces osteoclastogenesis and estrogen deficiency-induced bone loss by inhibiting TRAF6 auto-ubiquitination","authors":"Jian Lu ,&nbsp;Huang suo Wang ,&nbsp;Jun Wang ,&nbsp;Tao Fan ,&nbsp;Jianbin Hu ,&nbsp;Baotong Xun ,&nbsp;Xiaodong Jia ,&nbsp;Haoyu Feng ,&nbsp;Haishan Guan ,&nbsp;Yongwen Qiao ,&nbsp;Feng Gao","doi":"10.1016/j.bonr.2026.101923","DOIUrl":"10.1016/j.bonr.2026.101923","url":null,"abstract":"<div><div>Post-menopausal osteoporosis is characterized by overactive bone resorption in response to estrogen withdrawal. As Receptor Activator of NF-κB ligand (RANKL)-induced auto-ubiquitination of TNF receptor-associated factor 6 (TRAF6) on its K124 residue promotes osteoclastogenesis, inhibiting TRAF6^K124 auto-ubiquitination may be a promising therapeutic strategy for post-menopausal osteoporosis. We investigated the impact of the synthetic dinitrothiophenol SN-2 (4-(Dimethylamino)-2,6-bis[[N-[2-[(2-nitrophenyl)dithio]-ethyl]amino]methyl]pyridine) on TRAF6^K124 auto-ubiquitination, osteoclast generation, and osteoporotic bone loss. <em>In vitro</em>, SN-2 inhibited RANKL-induced osteoclast differentiation and osteoclast marker expression in a dose-dependent manner. SN-2 also inhibited RANKL-induced F-actin ring formation and bone resorption <em>in vitro</em>. SN-2 suppressed RANKL-induced TRAF6^K124 auto-ubiquitination (TRAF6-Ub), TRAF6's binding to Transforming Growth Factor Beta-Activated Kinase 1 (TAK1), and TAK1 phosphorylation, thereby inhibiting downstream NF-κB and c-Jun N-terminal Kinase (JNK) signaling pathways critical to osteoclast differentiation. In an ovariectomized mouse model of osteoporosis, SN-2 ameliorated estrogen-deficiency-induced bone loss, improved femoral biomechanical parameters, and inhibited osteoclastogenesis <em>in vivo</em>. SN-2 may show promise as a therapeutic agent in treating bone disorders characterized by RANKL signaling over-activation and excessive bone resorption.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"29 ","pages":"Article 101923"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148241769","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":"Development of a large porcine model of osteogenesis imperfecta type I","authors":"Maria E. Aguirre-Flores ,&nbsp;Leah E. Tokach ,&nbsp;Eric Cheang ,&nbsp;Gregory Trahan ,&nbsp;Dennis A. Webster ,&nbsp;Adrienne L. Watson ,&nbsp;Daniel F. Carlson ,&nbsp;David R. Deyle","doi":"10.1016/j.bonr.2026.101897","DOIUrl":"10.1016/j.bonr.2026.101897","url":null,"abstract":"<div><div>Osteogenesis imperfecta (OI) comprises a group of disorders that lead to bone fragility. The most common forms are caused by pathogenic variants in COL1A1 and COL1A2. There are many different animal models OI from zebrafish to dogs, with murine models being the most used model. In this brief study, we describe the successful generation of the first large animal porcine model of OI Type I carrying a clinically relevant pathogenic variant, c.757C&gt;T (p.Arg253Ter). These pigs exhibited classic features of OI Type I including blue sclera, low bone mass, and bone fragility. This model is more genetically and physiologically similar to humans and will be useful in studying the skeletal and extra-skeletal symptoms associated with OI.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"28 ","pages":"Article 101897"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022354","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":"Selective deletion of the membrane-bound isoform of CSF1 in vivo augments the anabolic response to PTH without impairing bone resorption","authors":"Gang-Qing Yao,&nbsp;Meiling Zhu,&nbsp;Karl Insogna","doi":"10.1016/j.bonr.2025.101896","DOIUrl":"10.1016/j.bonr.2025.101896","url":null,"abstract":"<div><div>Single daily doses of parathyroid hormone (PTH) are an established anabolic therapy for osteoporosis. The actions of PTH in bone are modulated by interactions between osteoblasts and osteoclasts. Colony-stimulating factor 1 (CSF1) exists in both soluble (sCSF1) and membrane-bound (mCSF1) isoforms, with distinct roles in skeletal remodeling identified for each isoform. To investigate the specific role of mCSF1 in PTH-induced bone anabolism, we treated mCSF1 knockout (KO) and wild-type (WT) mice with single daily doses of hPTH (1–34) for 4 weeks. Both genotypes exhibited increased bone mineral density and trabecular bone volume in response to PTH, but KO mice demonstrated significantly greater bone density gains. Histomorphometric analysis demonstrated enhanced osteoblast activity in KO mice, with no significant differences in osteoclast numbers or in the bone resorption marker carboxyterminal cross-linked telopeptide of type 1 collagen (serum CTx), compared to WT. These findings indicate that mCSF1 constrains the anabolic effects of PTH, likely by modulating osteoblast activity, and that its absence enhances bone formation without disrupting resorptive processes. Targeting mCSF1 may therefore represent a strategy to amplify the skeletal benefits of anabolic therapies without impairing bone turnover.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"28 ","pages":"Article 101896"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022355","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":"Intelligent identification of osteoporosis on hip X-rays using vision transformer","authors":"Wei Huang ,&nbsp;Pin Pan ,&nbsp;Kunpeng Liu ,&nbsp;Yang Xu ,&nbsp;Shuyi Cheng ,&nbsp;Hanyang Wang ,&nbsp;Longxu Han ,&nbsp;Yinyu Qi ,&nbsp;Lu Ren ,&nbsp;Jianjun Chu","doi":"10.1016/j.bonr.2026.101898","DOIUrl":"10.1016/j.bonr.2026.101898","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to develop and evaluate a deep learning model based on the Vision Transformer (ViT) architecture for the automatic classification of hip X-ray images into three categories: normal bone mass, osteopenia, and osteoporosis. The goal was to explore the model's potential for early screening and auxiliary diagnosis of osteoporosis.</div></div><div><h3>Methods</h3><div>A total of 3016 hip anteroposterior X-ray images were retrospectively collected from Hefei Hospital Affiliated to Anhui Medical University and affiliated community clinics. After standard preprocessing and extraction of proximal femur regions of interest (ROI), the dataset was split into training and internal validation sets in an 8:2 ratio. A pretrained ViT model was fine-tuned for the three-class classification task and compared with conventional convolutional neural networks (ResNet50 and InceptionV3). Performance was assessed using accuracy, area under the ROC curve (AUC), sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV). Additionally, the model was further validated using an external dataset to assess its generalizability.</div></div><div><h3>Results</h3><div>On the internal validation set, the ViT model achieved an overall classification accuracy of 97.0%. The AUCs for osteoporosis, osteopenia, and normal bone mass were 99.6%, 99.4%, and 99.9%, respectively. The PPV were 96.9%, 94.1% and 100%;The NPV were 97.9%, 98.5% and 99.2%. On the external validation set, the ViT model achieved an overall classification accuracy of 89.4%. The AUCs for osteoporosis, osteopenia, and normal bone mass were 96.5%, 91.6%, and 98.4%, respectively. The PPV were 83.5%, 90.2% and 91.3%;The NPV were 94.5%, 91.3% and 96.4%. The model demonstrated high sensitivity, specificity, PPV, and NPV across all classes, and outperformed both ResNet50 and InceptionV3 in overall diagnostic performance and classification stability.</div></div><div><h3>Conclusion</h3><div>The ViT-based deep learning model showed excellent performance in classifying bone mineral density using hip X-rays, with high accuracy and generalizability. Relying on routine X-ray images, this method provides a cost-effective and efficient tool for osteoporosis screening, with strong potential for clinical implementation in primary care settings.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"28 ","pages":"Article 101898"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146023103","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":"Rapid fracture healing of the greater tuberosity fragment after shoulder hemiarthroplasty in a patient with daily abaloparatide injection: A case report","authors":"Itsuo Joko ,&nbsp;Mio Uchida ,&nbsp;Masahito Hino ,&nbsp;Shunsuke Miyaoka ,&nbsp;Manabu Tanaka ,&nbsp;Kazuo Kasuga ,&nbsp;Nobuyuki Shimojo ,&nbsp;Shigeharu Uchiyama","doi":"10.1016/j.bonr.2026.101899","DOIUrl":"10.1016/j.bonr.2026.101899","url":null,"abstract":"<div><div>We report a case of a 64-year-old woman who developed a 4-parts shoulder fracture-dislocation with peripheral nerve injury by the displaced fragment, during abaloparatide treatment. Following shoulder hemiarthroplasty, bone union at the greater tuberosity was achieved on postoperative day 16, with remodelling completed at 6 months postoperatively. This course was exceptionally favourable. Factors potentially contributing to the early bone union progression may include the coincidental administration of abaloparatide prior to trauma and the presence of peripheral nerve injury.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"28 ","pages":"Article 101899"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022353","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":"The effect of spaceflight on tissues of the spinal column","authors":"Joanna Veres ,&nbsp;Eduardo A.C. Almeida ,&nbsp;Jeannie Bailey ,&nbsp;Grace D. O'Connell","doi":"10.1016/j.bonr.2025.101895","DOIUrl":"10.1016/j.bonr.2025.101895","url":null,"abstract":"<div><div>The unique mechanical unloading induced by spaceflight is associated with a very high incidence rate of chronic back pain and general degradation of tissues associated with the spinal column (i.e., bone, skeletal muscle, intervertebral disc, and cartilage). Despite the well documented phenomena of spinal damage following microgravity conditions, there is not a clear timeline of the pathways that leads to bulk tissue damage and back pain. This is both due to the majority of work in the field focusing on assessing the impact of microgravity on a single component or tissue, as well as in doing so at a narrow scale (e.g., genetic, cellular, morphologic, etc.). This review paper surveyed the literature to assemble a multiscale timeline for the pathway of degeneration due to mechanical unloading for key tissues of the spinal column. In doing so, we aim to clarify the cascading, multiscale, degenerative pathway caused by spaceflight conditions that manifest into bulk tissue atrophy and pain. This work also covers potential avenues of investigation to mitigate the deleterious effects of prolonged mechanical unloading on the spine.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"28 ","pages":"Article 101895"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073558","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":"Erythropoietin and bone health: Single high-dose administration triggers bone loss in mice","authors":"Anton Gorodov ,&nbsp;Albert Kolomansky ,&nbsp;Lior Lezerovich ,&nbsp;Michelle Piper ,&nbsp;Nathalie Ben-Califa ,&nbsp;Yankel Gabet ,&nbsp;Drorit Neumann","doi":"10.1016/j.bonr.2025.101889","DOIUrl":"10.1016/j.bonr.2025.101889","url":null,"abstract":"<div><div>Erythropoietin (EPO) is a key regulator of erythropoiesis, and it is mainly used to treat anemia. However, it is also administered prophylactically to non-anemic patients in certain clinical settings and is known to be used illicitly by athletes. The effect of EPO is controversial but emerging evidence indicates that EPO treatment induces bone loss in healthy mice. Here, we investigated the immediate and short-term skeletal effects of a single high-dose EPO injection in young mature (9 weeks) female mice. Cellular and molecular markers of bone turnover were evaluated at multiple time points post-injection. EPO administration led to a rapid increase in macrophage colony-stimulating factor (M-CSF) levels within the bone marrow (BM) microenvironment and in the serum, accompanied by an increase in BM CD115-positive cells and osteoclast precursors, as assessed by flow cytometry. This early cellular response to EPO was followed by an increase in tartrate-resistant acid phosphatase 5b (TRAP5b) and a decrease in procollagen type 1 N-terminal propeptide (P1NP), as determined by serum ELISA analyses, suggesting increased osteoclast numbers and decreased bone formation, respectively. Micro-computed tomography (μCT) revealed a significant reduction in trabecular bone volume. These findings demonstrate that even a single high-dose EPO injection disrupts bone homeostasis and induces significant bone loss through early modulation of the BM niche and osteoclastogenic pathways. Our results have important clinical implications for the prophylactic use of EPO and highlight potential skeletal risks.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"28 ","pages":"Article 101889"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145665310","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":"Post-translational modifications of collagen type I in osteogenesis imperfecta: Systematic review and meta-analysis","authors":"Priyesh Patel ,&nbsp;Sirion Aksornthong ,&nbsp;Svetlana V. Komarova","doi":"10.1016/j.bonr.2025.101894","DOIUrl":"10.1016/j.bonr.2025.101894","url":null,"abstract":"<div><div>Osteogenesis imperfecta (OI) is a rare genetic disorder most often caused by mutations in genes that encode collagen type I. OI collagen-I differs from healthy collagen-I due to the underlying mutation and altered post-translational modifications (PTMs). The objective of this study was to use knowledge synthesis to quantify the levels of selected PTMs, hydroxylysine (HYL), hydroxyproline (HYP) and glycosylation (GLY) in OI collagen-I. A systematic search in Medline, Ovid and Web of Science, identified 701 studies reporting on PTM outcomes for OI patients with collagen-I mutation. We excluded animal studies, and reports for OI patients with mutations other than in collagen-I. After screening, we included 36 qualitative studies and 25 quantitative studies for meta-analysis. All qualitative studies reported that OI collagen-I was overmodified. Meta-analysis of studies with quantitative data was performed using normalized mean difference as a study-level effect size and a random-effects model with the Hunter and Smith with sample size correction. The hydroxylysine dataset included 150 patients across 20 studies and had an effect size of 0.33 (confidence interval (CI) 0.21, 0.45). HYL levels were higher in bone-derived collagen-I than in fibroblast- or dentine-derived. The hydroxyproline dataset included 141 patients across 17 studies and had an effect size of 0.00 (CI: −0.02, 0.02). The glycosylation dataset included 17 patients across 5 studies and had an effect size of 0.55 (CI: 0.38, 0.71). Patients with the most severe form of OI (type 2) had the highest levels of collagen-I HYL and GLY. Our study provides new insights into collagen-I pathophysiology in OI, generating new hypotheses regarding the role of PTM in mediating disease presentation in different tissues and overall severity.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"28 ","pages":"Article 101894"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145788336","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":"Effectiveness of romosozumab following prior raloxifene treatment in primary osteoporosis: An observational study","authors":"Kazuaki Mineta ,&nbsp;Toshihiko Nishisho ,&nbsp;Masahiko Okada ,&nbsp;Mitsuhiro Kamada ,&nbsp;Koichi Sairyo","doi":"10.1016/j.bonr.2026.101900","DOIUrl":"10.1016/j.bonr.2026.101900","url":null,"abstract":"<div><div>Romosozumab is an anti-sclerostin antibody that increases bone formation and decreases bone resorption. It has been available for patients at high risk of osteoporotic fractures in Japan since 2019. The aim of this study was to clarify the clinical effectiveness and safety of romosozumab following previous treatment with raloxifene. The study had an observational pre–post design and included 62 women with primary osteoporosis. Romosozumab 210 mg was administered subcutaneously every 4 weeks for 12 months in patients who had been previously treated with raloxifene (raloxifene group, <em>n</em> = 12) and in those who were treatment-naïve (treatment-naïve group, <em>n</em> = 50). The incidence of new fractures, safety, and changes in bone mineral density (BMD) and bone turnover markers (BTMs) were recorded. No new fractures occurred in either group. Ten patients (16.1%) in the treatment-naïve group discontinued romosozumab for the following reasons: non-serious adverse events (<em>n</em> = 2, 3.2%), a change to another hospital (<em>n</em> = 1, 1.6%), self-discontinuation (<em>n</em> = 5, 8.1%), and financial constraints (<em>n</em> = 2, 3.2%). The percent changes in spine BMD and total hip BMD at 12 months were respectively +13.5% and + 4.9% in the treatment-naïve group and + 16.0% and + 3.4%, respectively, in the raloxifene group. We did not detect significant differences in the changes in BTMs according to whether there was previous treatment with raloxifene. Prior raloxifene treatment may be well tolerated and may not affect increases in BMD, changes in BTMs, and fracture prevention in romosozumab therapy.</div></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"28 ","pages":"Article 101900"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073557","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}