Experimental eye research最新文献

{"title":"Corrigendum to “Anti-inflammatory and neuroprotective properties of the corticosteroid fludrocortisone in retinal degeneration” [Exp. Eye Res. 212 (2021) 108765]","authors":"Tanja Racic , Andrew Chang , Nilisha Fernando , Alice Brandli , Riccardo Natoli , Philip Penfold , Jan M. Provis , Matt Rutar","doi":"10.1016/j.exer.2024.110092","DOIUrl":"10.1016/j.exer.2024.110092","url":null,"abstract":"","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"249 ","pages":"Article 110092"},"PeriodicalIF":3.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142344368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of rose bengal-green light scleral crosslinking in rabbit eyes using different infiltration protocols - An Ex Vivo study","authors":"Rongrong Gao ,&nbsp;Yuyan Huang ,&nbsp;Aodong Chen ,&nbsp;Qingqing Jiang ,&nbsp;Shengnan Ding ,&nbsp;Keith M. Meek ,&nbsp;Qinmei Wang ,&nbsp;A-Yong Yu ,&nbsp;Jinhai Huang","doi":"10.1016/j.exer.2024.110183","DOIUrl":"10.1016/j.exer.2024.110183","url":null,"abstract":"<div><div>Different concentrations and infiltration times of rose bengal (Rb) were assessed for their impact on penetration depth and crosslinking efficacy in rabbit sclera. Fresh rabbit eyes were used. Rb solution with concentrations of 0.1%–0.9% were applied for 5–30 min to infiltrate the sclera. The penetration depth of Rb was observed with confocal microscopy. After infiltration, the sclera was irradiated by green light for crosslinking. The sclera's biomechanical stiffness and the resistance to enzyme digestion post-treatment were evaluated. Histopathological analysis and transmission electron microscopy were performed to observe the morphology. As the infiltration time increased, the penetration depth and the fluorescence intensity of the Rb in sclera increased. After 32 h, 48.6% of the scleral tissue was undissolved in the 0.5% Rb-10min group, followed by the 0.1% Rb-20min group (13.8%) and 0.05% Rb-30min group (7.7%). At 8% strain, the Young's modulus of the 0.05%Rb-30min, the 0.1% Rb-20min and the 0.5% Rb-10min group were respectively 1.77, 2.45 and 3.19 times greater than that of the untreated group. There were no morphological differences between the experimental group and the untreated group. RG-SXL significantly increased the diameter of large collagen fibers in the middle and inner layers of the sclera. Ultimately, 0.5% Rb infiltration for 10 min achieves an appropriate infiltration depth and crosslinking effect, and may thus be a feasible schedule for scleral crosslinking.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"250 ","pages":"Article 110183"},"PeriodicalIF":3.0,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-23a-3p targets PTEN as a novel anti-ferroptosis regulator in Fuchs endothelial corneal dystrophy","authors":"Miaomiao Chi ,&nbsp;Yaning Zhao ,&nbsp;Bowei Yuan ,&nbsp;Zifeng Qiu ,&nbsp;Rongmei Peng ,&nbsp;Jing Hong","doi":"10.1016/j.exer.2024.110180","DOIUrl":"10.1016/j.exer.2024.110180","url":null,"abstract":"<div><div>Fuchs endothelial corneal dystrophy (FECD) is the leading cause of keratoplasty without drug treatment. Research indicated that oxidative stress and lipid peroxidation play significant roles in FECD. However, the underlying pathogenesis and potential treatment remain poorly understood. We analyzed the mRNA expression of FECD using the GEO database (GSE171830). Utilizing the STRING database and Cytoscape's MCODE plugin, we identified hub genes that intersect with ferroptosis-related genes listed in FerrDb. FECD cell and animal models were developed, induced by Ultraviolet A exposure. We assessed ferroptosis by measuring GPX4 expression and ROS fluorescence intensity. MiR-23a-3p was compared between FECD model and normal control, and the target gene PTEN was confirmed through Western blot and dual-luciferase reporter assays. Treatment with PTEN, PI3K, Akt, and mTOR inhibitors provided insights into the role of the PTEN/PI3K/Akt/mTOR pathway in FECD model. Corneal endothelium and cellular structure were evaluated before and after delivery of miR-23a-3p. Bioinformatics analysis of the GSE171830 revealed the top five hub genes: TP53, PTEN, EGFR, EPAS1, and IL-1β. Ferroptosis is the predominant mechanism in FECD pathogenesis, distinct from apoptosis and necrosis. We uncovered a protective role for miR-23a-3p in corneal endothelial cells (CEnCs), mitigating ferroptosis by downregulating PTEN. Corroborating this, bpV (a PTEN inhibitor) was found to attenuate ferroptosis in CEnCs. Mechanistically, PTEN inhibition coupled with sustained PI3K/Akt/mTOR pathway activation emerged as a protective strategy against ferroptosis in CEnCs. Ferroptosis contributes to FECD pathogenesis, and targeted delivery of miR-23a-3p as a ferroptosis inhibitor may offer therapeutic potential by regulating PTEN/PI3K/Akt/mTOR signaling.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"250 ","pages":"Article 110180"},"PeriodicalIF":3.0,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of vitamin A on the ocular surface","authors":"Huanhuan Ge ,&nbsp;Guohu Di ,&nbsp;Peirong Song ,&nbsp;Wenshuo Han ,&nbsp;Peng Chen ,&nbsp;Ye Wang","doi":"10.1016/j.exer.2024.110179","DOIUrl":"10.1016/j.exer.2024.110179","url":null,"abstract":"<div><div>Vitamin A is an essential fat-soluble vitamin that cannot be endogenously synthesized by the human body. Retinoic acid (RA) is the biologically active form of vitamin A. Utilizing both nuclear and non-nuclear receptor-mediated pathways, RA plays a crucial role in regulating various biological processes, including apoptosis, differentiation, and anti-inflammatory properties within the cornea and conjunctiva. In addition, RA has been demonstrated to exert a significant influence on anti-tumor mechanisms. Disruption of RA signaling can result in corneal defects, anophthalmia, and microphthalmia. However, the beneficial effects of RA are only observed when it is administered at appropriate dosages, and higher doses have an adverse impact. Ocular abnormalities are often early indicators of a vitamin A deficiency. The lacrimal gland secretes vitamin A onto the ocular surface, where it is metabolized into RA via two sequential steps. This article provides a comprehensive overview of how vitamin A is transformed and transported from the intestine to the ocular surface, ultimately contributing to the maintenance of the normal physiological function of the ocular surface.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"250 ","pages":"Article 110179"},"PeriodicalIF":3.0,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142705792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture improves V1 cortex synaptic plasticity via the CREB/BDNF/TrkB pathway in juvenile rats with monocular deprivation","authors":"Lin Wang ,&nbsp;Yangbin Ji ,&nbsp;Haibo Mei ,&nbsp;Xin Gong ,&nbsp;Huachun Miao ,&nbsp;Zaiman Zhu ,&nbsp;Jian Ding","doi":"10.1016/j.exer.2024.110169","DOIUrl":"10.1016/j.exer.2024.110169","url":null,"abstract":"<div><div>The present study aims to investigate the impact of the CREB/BDNF/TrkB signaling pathway on synaptic plasticity in the visual cortex of juvenile amblyopic rats that have undergone monocular deprivation (MD). This study involved sixty 2-week-old Sprague-Dawley (SD) juvenile rats, which were not specified by gender. In the first part of the study, 24 rats were randomized into control and MD groups; In the second part, 36 rats were randomized into MD, electroacupuncture (EA) and EA + CREB antagonist (666–15) groups. The MD model was established using the monocular suture method. 14 d after monocular suture, EA treatment was started for 30 min daily, at a frequency of 2–10 Hz and an intensity of 1 mA, for 2 weeks. According to the results from part 1, the P100 wave latency in the MD group was prolonged, and its amplitude was lower compared to the control group. Additionally, the neuron number in the V1 cortex of the MD group decreased, along with reduced expression levels of CREB, BDNF, p-TrkB, and the key plasticity proteins PSD95 and SYN. In part 2, EA treatment significantly increased the electrophysiological activity of neurons in V1 cortex, shortened the latency of P100 peaks to varying degrees, increased the amplitude significantly, and restored the morphology and structure of neurons to normal levels; The expression of synaptic proteins PSD95 and SYN, as well as the expression of signaling molecules CREB, BDNF, and p-TrkB proteins were increased. However, the effects of EA were reversed when the specific CREB inhibitor 666–16 was administered. These data indicate that EA enhances the expression of V1 cortical synaptic plasticity-related proteins by regulating the expression of CREB/BDNF/TrkB signaling pathway, thereby enhancing V1 neural synaptic plasticity and reversing the effects of MD on visual acuity.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"250 ","pages":"Article 110169"},"PeriodicalIF":3.0,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel three-dimensional method for detailed analysis of RGC central projections under acute ocular hypertension","authors":"Wenhan Lu ,&nbsp;Yu Wang ,&nbsp;Wei Hu ,&nbsp;Xinyi Lin ,&nbsp;Xiaoyu Tong ,&nbsp;Yi Tian ,&nbsp;Yuning Chen ,&nbsp;Yicong Wang ,&nbsp;Yan Xiao ,&nbsp;Hongfang Yang ,&nbsp;Yi Feng ,&nbsp;Xinghuai Sun","doi":"10.1016/j.exer.2024.110157","DOIUrl":"10.1016/j.exer.2024.110157","url":null,"abstract":"<div><div>Normal perception of visual information relies not only on the quantity and quality of retinal ganglion cells (RGCs), but also on the integrity of the visual pathway, within which RGC central projection predominates. However, the exact changes of RGC central projection under particular pathological conditions remain to be elucidated. Here, we report a whole-brain clearing method modified from iDISCO for 3D visualization of RGC central projection. The CTB-labeled RGC central projection was visualized three-dimensionally with minimized both fluorescence quenching and the time taken. For observation of RGC axonal degeneration pattern under pathological conditions, we took acute ocular hypertension (AOH) as an example. Mice were intracamerally irrigated, and fluorescent signal in brain subregions where RGC axons projected to were quantified. The novel methodology is well-applied for rapid clearing and observation of RGC central projection in C57BL/6J, showing damaged RGC central projection on the AOH side and the most statistically significant degeneration in the superior colliculi (SC). Detailed analysis also revealed a distinct injury pattern among lateral geniculate nuclei (LGN) subregions, with the parvocellular part of the pregeniculate nuclei (PrGPC) being more vulnerable compared with the magnocellular part (PrGMC). The intracranial retrograde labeling of RGC subgroups based on brain damage variation showed PrGPC-projecting RGCs (<em>Plgn</em> RGC) being smaller than PrGMC-projecting RGCs (<em>Mlgn</em> RGC) in size and less in number, yet more vulnerable in terms of degeneration under AOH. Our data revealed the methodology for visualizing selective neuronal vulnerability under AOH, and in the meantime provided novel approach for future mechanisms exploration regarding RGC degeneration.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"250 ","pages":"Article 110157"},"PeriodicalIF":3.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TGF-β1-induced apoptosis in retinal endothelial cells is implicated in retinal vein occlusion","authors":"Fengyu Chen ,&nbsp;Qi Wang ,&nbsp;Yujin Li ,&nbsp;Fen Li ,&nbsp;Lin Zhang ,&nbsp;Xuezhong Gu","doi":"10.1016/j.exer.2024.110168","DOIUrl":"10.1016/j.exer.2024.110168","url":null,"abstract":"<div><div>Retinal vein occlusion (RVO) is a serious vascular condition that impairs vision due to retinal endothelial cell injury and apoptosis. This study aimed to identify key molecular pathways and therapeutic targets involved in RVO pathogenesis. Transcriptomic analysis of the retinal tissues from a mouse RVO model was performed to identify differentially expressed genes and co-expression modules associated with RVO. Protein-protein interaction network analysis pinpointed putative hub genes. <em>In vitro</em> experiments using human retinal microvascular endothelial cells (HRMECs) validated the involvement of identified genes/pathways in apoptosis induced by oxygen-glucose deprivation/reperfusion (OGD/R) and UV exposure. Gene expression was assessed by RT-qPCR, while protein levels and phosphorylation were measured by ELISA and Western blotting. Apoptosis was evaluated using flow cytometry, and reactive oxygen species (ROS) were quantified using a fluorescence-based assay. A total of 392 genes were identified as putatively involved in RVO-associated apoptosis, enriched in MAPK, TGF-β and other signaling pathways. Among top hub genes, TGF-β1 emerged as a central regulator whose expression and signaling (pSmad2/3) increased after OGD/R induction or UV exposure in HRMECs. TGF-β1-induced HRMEC apoptosis was mediated by p38/JNK activation. Similar effects were observed for OGD/R and UV triggering TGF-β1-dependent p38/JNK signaling and apoptosis. Pharmacological inhibition of TGF-β signaling attenuated the apoptotic and oxidative stress responses induced by OGD/R and UV exposure. This study elucidates TGF-β1 as a crucial mediator of retinal endothelial injury through p38/JNK-induced apoptosis, suggesting TGF-β1 pathway inhibition as a potential therapeutic strategy for RVO.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"250 ","pages":"Article 110168"},"PeriodicalIF":3.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tracking astrocyte polarization in the retina in retinopathy of prematurity","authors":"Xiaoxiao Feng,&nbsp;Liwei Zhang,&nbsp;Kangwei Jiao,&nbsp;Yunqing Li,&nbsp;Min Wu,&nbsp;Yu Xie,&nbsp;Libo Xiao","doi":"10.1016/j.exer.2024.110170","DOIUrl":"10.1016/j.exer.2024.110170","url":null,"abstract":"<div><div>Astrocyte patterns affect the normal development of the retinal vascular network in retinopathy of prematurity (ROP), which is associated with VEGF secretion. However, the role of the astrocyte polarization in this process remains unknown. Therefore, this study aimed to track the status of A1/A2 reactive astrocytes in the retinas of the oxygen-induced retinopathy (OIR) model and their association with VEGF expression. The C57BL/6 mouse OIR model was constructed to characterize the pathological changes in ROP. Immunofluorescence of iB4 and GFAP staining was performed to observe changes in the vascular network and astrocyte pattern at different time points (P0, P7, P12, P17, and P21). C3-labeled A1 reactive and S100A10-labeled A2 reactive astrocytes and VEGF were also observed. The pattern of GFAP-labeled astrocyte was altered concurrently with the iB4-positive vascular network during OIR. Astrocyte activity was significantly weakened at P12 and significantly enhanced at P17. Notably, the number of C3-labeled A1 reactive astrocytes was significantly increased at P12, decreased at P17, and normalized at P21 in OIR models. S100A10-labeled A2 reactive astrocytes were significantly increased at P17 but did not change significantly at P12 or P17. VEGF levels were decreased at P7-P12 and increased at P12-P17. The expression pattern of VEGF was opposite to that of C3-labeled A1 reactive astrocytes and identical to that of S100A10-labeled A2 reactive astrocytes. In conclusion, the astrocyte pattern and vascular network exhibited similar changes during the OIR process, and the periods of vaso-obliteration and neo-vascularization display an abnormal activation in A1-and A2-reactive astrocytes.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"250 ","pages":"Article 110170"},"PeriodicalIF":3.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Choroidal macrophages in homeostasis, aging and age-related macular degeneration","authors":"Adnan H. Khan ,&nbsp;Kelly Mulfaul","doi":"10.1016/j.exer.2024.110159","DOIUrl":"10.1016/j.exer.2024.110159","url":null,"abstract":"<div><div>With increasing age, the optimal functioning of the choroid is essential for efficient removal of waste products formed from photoreceptor renewal. A decline in regulatory elements of the immune system, termed immunosenescence, and the failure of para-inflammation to restore tissue homeostasis can result in the progression of healthy aging to sight-threatening inflammation of the choroid. Macrophages are uniquely situated between the innate and adaptive immune systems, with a high capacity for phagocytosis, recognition of complement components, as well as antigen presentation. In this review, we provide an overview of macrophages and their properties in the healthy choroid and cover the impact of aging, immunosenescence and inflammaging on the function of choroidal macrophages. We will discuss the impact of age on macrophage phenotype and behaviour in the pathophysiology of age-related macular degeneration.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"250 ","pages":"Article 110159"},"PeriodicalIF":3.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conditioned media from dental pulp stem cells to counteract age-related macular degeneration","authors":"Giulia Carozza ,&nbsp;Darin Zerti ,&nbsp;Fanny Pulcini ,&nbsp;Loreto Lancia ,&nbsp;Simona Delle Monache ,&nbsp;Vincenzo Mattei ,&nbsp;Rita Maccarone","doi":"10.1016/j.exer.2024.110167","DOIUrl":"10.1016/j.exer.2024.110167","url":null,"abstract":"<div><h3>Purpose</h3><div>Age-related macular degeneration (AMD) is the leading cause of blindness in the elderly. To date, there are no effective therapies to counteract AMD towards the most severe stages characterised by a progressive loss of photoreceptors triggered by retinal pigmented epithelium dysfunction. Given their easy source and their high proliferative potential, Dental Pulp Stem Cells (DPSCs) are considered promising for regenerative medicine. The main advantage of DPSCs is related to their paracrine immunosuppressive and immunoregulatory abilities, including the capability to promote regeneration of damaged tissues. Recent studies demonstrated the therapeutic potential of DPSCs-conditioned media (CM) in neurodegenerative diseases. In addition, we have already shown a differential expression of some growth factors and cytokines in CM derived from DPSCs cultured in hypoxia and normoxia conditions.</div></div><div><h3>Aim</h3><div>In this study we evaluated the capability of DPSCs-CM to counteract retinal degeneration in an animal model of AMD. DPSCs-CM were intravitreally injected the day before the exposure of albino rats to high intensity light (LD).</div></div><div><h3>Results</h3><div>We evaluated the retinal function, and we performed morphological and molecular analysis a week after the LD, in accordance with the well-established protocol of our light damage model. DPSCs-CM obtained from hypoxia (HYPO-CM) or normoxia (NORM-CM), were able to preserve the retinal function, to reduce the damaged area and to counteract the upregulation of key factors involved in retinal degeneration, like FGF-2. Furthermore, we demonstrated that neither conditioned media modified inflammatory activation, as shown by both microglia activation and GFAP upregulation, but <em>in vitro</em> studies demonstrated a significant effect of both CM to counteract oxidative stress, one of the main causes of AMD.</div></div><div><h3>Conclusion</h3><div>Taken together, our study demonstrated that NORM-CM and HYPO-CM, albeit with a different chemical composition, could represent eligible candidates to counteract retinal degeneration in an animal model of AMD. Further studies are needed to obtain conditioned media with the best performance in term of retinal protection.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"250 ","pages":"Article 110167"},"PeriodicalIF":3.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}