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| 1 | Characterization of microRNAs in serum: a novel class of biomarkers for diagnosis of cancer and other diseases显示文摘在各种各样的纸巾的 microRNAs (miRNAs ) 的 Dysregulated 表示与许多疾病被联系了,包括癌症。这里,我们证明 miRNAs 在象老鼠,老鼠,牛的胎儿,小牛,和马那样的人和另外的动物的浆液和血浆是在场的。在浆液的 miRNAs 的层次在一样的种类的个人之中稳定、可再现、一致。采用 Solexa,我们定序健康中国题目的所有浆液 miRNAs 并且分别地在男、女的题目发现超过 100 和 91 浆液 miRNAs。我们也为肺癌症, colorectal 癌症,和糖尿病识别了浆液 miRNAs 的特定的表示模式,提供证据那浆液 miRNAs 为各种各样的疾病包含指纹。癌症特定的浆液 miRNAs 由 Solexa 获得了的二个非小的房间肺进一步在 75 个健康施主和 152 个癌症病人的独立审判被验证,用量的反向的抄写聚合酶链反应试金。通过这些分析,我们断定浆液 miRNAs 能为各种各样的癌症和另外的疾病的察觉用作潜在的 biomarkers。 | Xi Chen Yi Ba Lijia Ma Xing Cai Yuan Yin Kehui Wang Jig ang Guo Yujing Zhang Jiangning Chen Xing Guo Qibin Li Xiaoying Li Wenjing Wang Yan Zhang Jin Wang Xueyuan Jiang Yang Xiang Chen Xu Pingping Zheng Juanbin Zhang Ruiqiang Li Hongjie Zhang Xiaobin Shang Ting Gong Guang Ning Jun Wang Ke Zen Junfeng Zhang Chen-Yu Zhang | 2008 | Cell Research2008，18，10： | 975 |
| 2 | Tissue clearing of both hard and soft tissue organs with the PEGASOS method显示文摘织物空地技术由转织物在 3 尺寸(3-D ) 启用不透明的机关和纸巾的可视化透明。当前的组织空地方法被能与每个单个协议被清除的纸巾的有限类型限制,它不可避免地导致了存在在整个身体或身体部分成像以内盲点。包括骨头和牙齿的难纸巾仍然是要清除的最困难的机关。另外,内长的荧光的损失为基于溶剂的空地方法仍然是一颗主要担心。这里,我们发展了聚乙烯乙二醇(木钉) 联系了溶剂系统(PEGASOS ) ,它将近显示了纸巾的所有类型透明、保存的内长的荧光。骨头和牙齿能被转在变清以后将近不可见。PEGASOS 方法转了透明的整个成年老鼠身体,我们对一个成年老鼠头骨头,牙齿,大脑,肌肉,和其它填写了的图象有能力没有盲目区域的纸巾。难织物透明性使我们能重建在 3-D 的未经触动的上颚,牙齿,腿节,或膝关节。另外,我们在长距离上在亚 cellular 分辨率并且到踪迹个人神经原和轴突管理了未经触动的鼠标大脑到图象。我们也通过 vertebrae 直接设想了背面的根中心。最后,我们在长骨头的髓空间以内在 3-D 揭示了神经网络的分发模式。这些结果建议 PEGASOS 方法是为一般生物医学的研究的一个有用工具。 | Dian Jing Shiwen Zhang Wenjing Luo Xiaofei Gao Yi Men Chi Ma Xiaohua Liu Yating Yi Abhijit Bugde Bo O. Zhou Zhihe Zhao Quan Yuan Jian Q. Feng Liang Gao Woo-Ping Ge Hu Zhao | 2018 | Cell Research2018，28，8： | 18 |
| 3 | A novel partner of Scalloped regulates Hippo signaling via antagonizing Scalloped-Yorkie activity显示文摘由调整 transcriptional 激活剂 Yorkie (Yki ) 的活动的河马(Hpo ) 小径控制织物生长和机关尺寸,它在原子核与抄写因素 Scalloped (Sd ) 联系下游地支持指向基因表示。这里,我们识别新奇蛋白质 Sd-Binding-Protein (SdBP )/Tgi,它直接通过它的 TDU 域为绑定与 Yki 竞争到 Sd 并且禁止 Sd-Yki transcriptional 活动。我们也发现 SdBP 经由它的 PPXY 主题与 Yki WW 领域通过协会在原子核保留 Yki。一起,我们作为 Hpo 小径的一个新奇部件识别 SdBP,否定地调整 Sd-Yki 的 transcriptional 活动限制织物生长。 | Tong Guo Yi Lu Peixue Li Meng-Xin Yin Dekang Lv Wenjing Zhang Huizhen Wang Zhaocai Zhou Hongbin Ji Yun Zhao Lei Zhang | 2013 | Cell Research2013，23，10： | 13 |
| 4 | Investigation on natural resources and species conservation of Ophiocordyceps sinensis, the famous medicinal fungus endemic to the Tibetan Plateau显示文摘 | Wenjing Wang Ke Wang Xiaoliang Wang Ruiheng Yang Yi Li Yijian Yao | 2018 | Protein & Cell2018，9，8： | 5 |
| 5 | Nano-hydroxyapatite accelerates vascular calcification via lysosome impairment and autophagy dysfunction in smooth muscle cells显示文摘Vascular calcification(VC)is a common characteristic of aging,diabetes,chronic renal failure,and atherosclerosis.The basic component of VC is hydroxyapatite(HAp).Nano-sized HAp(nHAp)has been identified to play an essential role in the development of pathological calcification of vasculature.However,whether nHAp can induce calcification in vivo and the mechanism of nHAp in the progression of VC remains unclear.We discovered that nHAp existed both in vascular smooth muscle cells(VSMCs)and their extracellular matrix(ECM)in the calcified arteries from patients.Synthetic nHAp had similar morphological and chemical properties as natural nHAp recovered from calcified artery.nHAp stimulated osteogenic differentiation and accelerated mineralization of VSMCs in vitro.Synthetic nHAp could also directly induce VC in vivo.Mechanistically,nHAp was internalized into lysosome,which impaired lysosome vacuolar H+-ATPase for its acidification,therefore blocked autophagic flux in VSMCs.Lysosomal re-acidification by cyclic-3′,5′-adenosine monophosphate(cAMP)significantly enhanced autophagic degradation and attenuated nHAp-induced calcification.The accumulated autophagosomes and autolysosomes were converted into calcium-containing exosomes which were secreted into ECM and accelerated vascular calcium deposit.Inhibition of exosome release in VSMCs decreased calcium deposition.Altogether,our results demonstrated a repressive effect of nHAp on lysosomal acidification,which inhibited autophagic degradation and promoted a conversion of the accumulated autophagic vacuoles into exosomes that were loaded with undissolved nHAp,Ca^(2+),Pi and ALP.These exosomes bud off the plasma membrane,deposit within ECM,and form calcium nodules.Vascular calcification was thus accelerated by nHAP through blockage of autophagic flux in VSMCs. | Qi Liu Yi Luo Yun Zhao Pingping Xiang Jinyun Zhu Wangwei Jing Wenjing Jin Mingyao Chen Ruikang Tang Hong Yu | 2022 | Bioactive Materials2022，7，2： | 5 |
| 6 | The deubiquitinase OTUB1 augments NF-κB-dependent immune responses in dendritic cells in infection and inflammation by stabilizing UBC13显示文摘Dendritic cells(DCs)are indispensable for defense against pathogens but may also contribute to immunopathology.Activation of DCs upon the sensing of pathogens by Toll-like receptors(TLRs)is largely mediated by pattern recognition receptor/nuclear factor-κB(NF-κB)signaling and depends on the appropriate ubiquitination of the respective signaling molecules.However,the ubiquitinating and deubiquitinating enzymes involved and their interactions are only incompletely understood.Here,we reveal that the deubiquitinase OTU domain,ubiquitin aldehyde binding 1(OTUB1)is upregulated in DCs upon murine Toxoplasma gondii infection and lipopolysaccharide challenge.Stimulation of DCs with the TLR11/12 ligand T.gondii profilin and the TLR4 ligand lipopolysaccharide induced an increase in NF-κB activation in OTUB1-competent cells,resulting in elevated interleukin-6(IL-6),IL-12,and tumor necrosis factor(TNF)production,which was also observed upon the specific stimulation of TLR2,TLR3,TLR7,and TLR9.Mechanistically,OTUB1 promoted NF-κB activity in DCs by K48-linked deubiquitination and stabilization of the E2-conjugating enzyme UBC13,resulting in increased K63-linked ubiquitination of IRAK1(IL-1 receptor-associated kinase 1)and TRAF6(TNF receptor-associated factor 6).Consequently,DC-specific deletion of OTUB1 impaired the production of cytokines,in particular IL-12,by DCs over the first 2 days of T.gondii infection,resulting in the diminished production of protective interferon-γ(IFN-γ)by natural killer cells,impaired control of parasite replication,and,finally,death from chronic T.encephalitis,all of which could be prevented by low-dose IL-12 treatment in the first 3 days of infection.In contrast,impaired OTUB1-deficient DC activation and cytokine production by OTUB1-deficient DCs protected mice from lipopolysaccharide-induced immunopathology.Collectively,these findings identify OTUB1 as a potent novel regulator of DCs during infectious and inflammatory diseases. | Floriana Mulas Xu Wang Shanshan Song Gopala Nishanth Wenjing Yi Anna Brunn Pia-Katharina Larsen Berend Isermann Ulrich Kalinke Antonio Barragan Michael Naumann Martina Deckert Dirk Schlüter | 2021 | Cellular & Molecular Immunology2021，18，6： | 4 |
| 7 | Clinical features and predictors of remission in children under the age of 7 years with Graves’disease显示文摘Importance:Graves’disease(GD)is rare in children under the age of 7 years.Children with this disease exhibit greater thyrotoxicity at diagnosis and require a longer course of medical therapy,compared with pubertal and postpubertal children and adults.Objective:To investigate the clinical features and identify predictors of remission in children under the age of 7 years with GD.Methods:This retrospective study included 77 children who were diagnosed with GD under the age of 7 years and were treated in the Department of Endocrinology,Beijing Children’s Hospital from 2010 to 2018.Clinical manifestations,laboratory data,and follow-up records were collected for all patients.Children who achieved remission of treatment with methimazole were compared with those who had persistent disease to identify which variables were associated with remission;multiple logistic regression and Cox regression analyses were used to evaluate interactions among predictive variables.Results:Sixty-three boys and 14 girls were included;the median age at diagnosis was 4.2 years(interquartile range:3.2-5.3 years).Forty-six(56.7%)patients had no family history of thyroid disease,17 patients had family history of thyroid disease and 14 patients with unknown family history.Of the 77 patients,18(23.4%)patients achieved remission of treatment with methimazole and 59 patients did not;moreover,51(66.2%)had Graves’ophthalmopathy.Univariate analyses revealed no significant differences between the remission group and non-remission group in terms of age at diagnosis,sex,initial goiter size,or initial thyroid hormone concentration.However,there were a trend of correlation between the initial level of thyroid peroxidase antibody(TPOAb)and remission status(univariate analysis OR 1.002,P=0.038;multivariate analysis OR 1.004,P=0.019).Similar results were observed in univariate analysis of the initial thyrotropin receptor antibody(TRAb)level,but this association was not significant in multivariate analysis.Cox regression analyses revealed that children with high TRAb level required longer duration of remission,compared with low TRAb level(OR 0.950,95%CI 0.904-0.997,P=0.037).Interpretation:Initial TRAb level was an independent predictor of remission outcome in young children under the age of 7 years with GD.Initial TRAb level may predict the likelihood of remission in patients with young-age-of-onset GD. | Yi Gu Xuejun Liang Ming Liu Di Wu Wenjing Li Bingyan Cao Yuchuan Li Chang Su Jiajia Chen Chunxiu Gong | 2020 | Pediatric Investigation2020，4，3： | 3 |
| 8 | ALLIANCE-ROS:A Software Framework on ROS for Fault-Tolerant and Cooperative Mobile Robots显示文摘Programming control systems for mobile robots is complicated and time-consuming, due to three aspects, i.e., the robot behavior coordination, the distributed multi-robot cooperation and the robot software reusability. Subsumption model is a robust control architecture for mobile robots. ALLIANCE model extends it to multirobot systems, which is a fully distributed, fault-tolerant model. Robot operating system(ROS) provides a lot of reusable robot modules. By combining the above three, we propose a software framework named ALLIANCE-ROS for developing fault-tolerant cooperative multi-robot systems with abundant software resources available. We encapsulate the ROS facilities to build the framework prototype.We also use some high-performance plugin-based mechanism to optimize the bottom of the framework. One may use the framework-provided API conveniently to construct single-robot and multi-robot applications with all ROS resources available. This work is demonstrated by three application cases including an autonomous roving robot, a security patrol robot and multiple patrol robots. They are constructed and tested in both the simulated and the real environment. The experimental results validate the usability and availability of ALLIANCE-ROS. | GUO Zhongyuan YANG Wenjing LI Minglong YI Xiaodong CAI Zhongxuan WANG Yanzhen | 2018 | Chinese Journal of Electronics2018，27，3： | 2 |
| 9 | Paraventricular Nucleus P2X7 Receptors Aggravate Acute Myocardial Infarction Injury via ROS-Induced Vasopressin-V1b Activation in Rats显示文摘The present study was designed to investigate the mechanisms by which P2X7 receptors(P2X7Rs)mediate the activation of vasopressinergic neurons thereby increasing sympathetic hyperactivity in the paraventricular nucleus(PVN) of the hypothalamus of rats with acute myocardial ischemia(AMI). The left anterior descending branch of the coronary artery was ligated to induce AMI in rats. The rats were pretreated with BBG(brilliant blue G, a P2X7R antagonist), nelivaptan(a vasopressin V1b receptor antagonist), or diphenyleneiodonium(DPI) [an nicotinamide adenine dinucleotide phosphate(NADPH)oxidase inhibitor]. Hemodynamic parameters of the heart were monitored. Myocardial injury and cardiomyocyte apoptosis were assessed. In the PVN of AMI rats, P2X7R mediated microglial activation, while reactive oxygen species(ROS) and NADPH oxidase 2(NOX2) were higher than in the sham group. Intraperitoneal injection of BBG effectively reduced ROS production and vasopressin expression in the PVN of AMI rats. Moreover, both BBG and DPI pretreatment effectively reduced sympathetic hyperactivity and ameliorated AMI injury, as represented by reduced inflammation and apoptosis of cardiomyocytes.Furthermore, microinjection of nelivaptan into the PVN improved cardiac function and reduced the norepinephrine(AE) levels in AMI rats. Collectively, the results suggest that, within the PVN of AMI rats, P2X7R upregulation mediates microglial activation and the overproduction of ROS, which in turn activates vasopressinergic neuron V1b receptors and sympathetic hyperactivity, hence aggravating myocardial injury in the AMI setting. | Wenjing Cheng Yinggang Sun Qin Wu Kokwin Ooi Yi Feng Chunmei Xia Danian Zhu | 2021 | Neuroscience Bulletin2021，37，5： | 2 |
| 10 | Proteomics-based analysis of functional proteins from fermented of compound wheat embryo Chinese medicine显示文摘Compound probiotics were used to ferment compound wheat embryo Chinesemedicine(CWECM)at 37°C for a given period,and the fermentation end pointwas determined based on pHvalue.The full spectrumof the proteinswithin the fermentation supernatant was determined by ion mass spectrometry,and then the fermentation was analyzed by proteomics.The difference of functional protein ofCWECMwas analyzed before and after fermentation.Additionally,the changes in flavor of peptides were examined.Our results indicated that when the fermentationwas performed for 96 h,the pH value became stable over time,which it shifted froman initial 3.98±0.04 to a stable 2.78±0.04.Proteomicbased analysis of the fermentation supernatant indicated that the fermentation of the probiotics increased.The amount of functional proteome and protein within the supernatant increased from 60 proteomes and 136 proteins before fermentation to 70 proteomes and 149 proteins post fermentation.These proteins were primarily members of the Ubiquitin and Histone families.These families contain more specific peptides after fermentation,and the coverage was reduced.Analysis of the unique P0C512 protein after fermentation indicated that this protein is an unstable,3Deffect columnar protein.We also found that probiotic fermentation can reduce the proportion of bitter peptideswithin fermentation broth from 47.49%to 36.98%,and the proportion of sweet peptides increased after fermentation from 35.29%to 51.01%.Based on testing,we concluded that fermentation of CWECM by compound probiotics can reduce the pH of the CWECM solution,increase the number of functional proteomes and proteins,improve the taste of CWECM solutions,and improve the therapeutic efficacy of CWECM. | Jihong Huang Xing Lyu Aimei Liao Yi Zhao Yinchen Hou Wenjing Chen Canrui Yang | 2019 | Grain & Oil Science and Technology2019，2，3： | 2 |
| 11 | How can China reach its CO2 intensity reduction targets by 2020? A regional allocation based on equity and development 显示文摘 | YI Wenjing ZOU Lele GUO Jie | 2011 | Energy Policy2011，，39： | 1 |
| 12 | The role of the TLR4 signaling pathway in cognitive deficits followingsurgery in aged rats显示文摘 | Yi Wang Huijuan He Dan Li Wenjing Zhu Kaiming Duan Yuan Le Yan Liao Yangwen Ou | 2013 | Molecular Medicine Reports2013，，： | 1 |
| 13 | Responses of the Sea Surface Temperature and Suspended Matter Concentration to ENSO Events in the Bohai Sea显示文摘The sea surface temperature(SST)and sea surface suspended matter concentration data in the Bohai Sea were collected by multiple NOAA satellites from 1985 to 2018.The background calibration method was used to correct the systematic errors caused by the long-term observations through multiple NOAA satellites in this paper.Then,we studied the long-term variations of the sea surface temperature(SST)and sea surface suspended matter concentration(SSC)and their response to ENSO events in the Bohai Sea.Our results show that the SST and SSC of the Bohai Sea have been increasing since 1985,with an average rate of 0.04℃per year for SST,which is higher than the global average.The average increasing rate of SSC was 0.51 mg L^(-1)yr^(-1),which may be mainly due to the enhancement of winter monsoon in the Bohai.In winter,the SST and SSC of the Bohai Sea were higher in El Niño years than in La Niña years.In El Niño years,the ocean circulations were the main factor affecting the variation in SST.The robust circulation system caused by the strong winter monsoon enhances the water exchange between the cold water of the Bohai Sea and the warm water of the Yellow Sea,resulting in a higher SST in La Niña years.In summer,the SSTs of the Bohai Sea were lower in El Niño years than those in the La Niña years because of the decrease of the SST in the Western Pacific Ocean,the weakening of the subtropical high in the western Pacific,and its eastward shift caused by the El Niño events. | LIU Xue DING Dong LI Guangxue ZHANG Yang LIU Shidong WANG Nan ZHONG Yi YANG Xue PAN Yufeng YU Di ZHANG Lei XUE Wenjing | 2023 | Journal of Ocean University of China2023，22，3： | 1 |
| 14 | How can China reach its CO2 mtensity reduction target by 2020? A regionalallocation based on equity and development 显示文摘 | Yi Wenjing Zou Lele Guo Jie | 2011 | Energy Policy2011，39，24： | 1 |
| 15 | Apoptotic vesicles ameliorate lupus and arthritis via phosphatidylserine-mediated modulation of T cell receptor signaling显示文摘Mesenchymal stem cells(MSCs)influence T cells in health,disease and therapy through messengers of intercellular communication including extracellular vesicles(EVs).Apoptosis is a mode of cell death that tends to promote immune tolerance,and a large number of apoptotic vesicles(apoVs)are generated from MSCs during apoptosis.In an effort to characterize these apoVs and explore their immunomodulatory potential,here we show that after replenishing them systemically,the apoV deficiency in Fas mutant mice and pathological lymphoproliferation were rescued,leading to the amelioration of inflammation and lupus activity.ApoVs directly interacted with CD4^(+)T cells and inhibited CD25 expression and IL-2 production in a dose-dependent manner.A broad range of Th1/2/17 subsets and cytokines including IFNγ,IL17A and IL-10 were suppressed while Foxp3^(+)cells were maintained.Mechanistically,exposed phosphatidylserine(PtdSer/PS)on apoVs mediated the interaction with T cells to disrupt proximal T cell receptor signaling transduction.Remarkably,administration of apoVs prevented Th17 differentiation and memory formation,and ameliorated inflammation and joint erosion in murine arthritis.Collectively,our findings unveil a previously unrecognized crosstalk between MSC apoVs and CD4^(+)T cells and suggest a promising therapeutic use of apoVs for autoimmune diseases. | Runci Wang Meng Hao Xiaoxing Kou Bingdong Sui Maria Laura Sanmillan Xiao Zhang Dawei Liu Jun Tian Wenjing Yu Chider Chen Ruili Yang Lingyun Sun Yi Liu Claudio Giraudo Deepak A.Rao Nan Shen Songtao Shi | 2023 | Bioactive Materials2023，，7： | 1 |
| 16 | A design of the IOT gateway for agricultural greenhouse 显示文摘 | Li Guohong Zhang Wenjing Zhang Yi | 2014 | Sensors & Transducers2014，172，6： | 1 |
| 17 | Defective EMC1 drives abnormal retinal angiogenesis via Wnt/β-catenin signaling and may be associated with the pathogenesis of familial exudative vitreoretinopathy显示文摘Endoplasmic reticulum(ER)membrane protein complex(EMC)is required for the co-translational insertion of newly synthesized multi-transmembrane proteins.Compromised EMC function in different cell types has been implicated in multiple diseases.Using inducible genetic mouse models,we revealed defects in retinal vascularization upon endothelial cell(EC)specific deletion of Emc1,the largest subunit of EMC.Loss of Emc1 in ECs led to reduced vascular progression and vascular density,diminished tip cell sprouts,and vascular leakage.We then performed an unbiased transcriptomic analysis on human retinal microvascular endothelial cells(HRECs)and revealed a pivotal role of EMC1 in theβ-catenin signaling pathway.Further in-vitro and in-vivo experiments proved that loss of EMC1 led to compromisedβ-catenin signaling activity through reduced expression of Wnt receptor FZD4,which could be restored by lithium chloride(LiCl)treatment.Driven by these findings,we screened genomic DNA samples from familial exudative vitreoretinopathy(FEVR)patients and identified one heterozygous variant in EMC1 that co-segregated with FEVR phenotype in the family.In-vitro expression experiments revealed that this variant allele failed to facilitate the expression of FZD4 on the plasma membrane and activate theβ-catenin signaling pathway,which might be a main cause of FEVR.In conclusion,our findings reveal that variants in EMC1 gene cause compromisedβ-catenin signaling activity,which may be associated with the pathogenesis of FEVR. | Shujin Li Mu Yang Rulian Zhao Li Peng Wenjing Liu Xiaoyan Jiang Yunqi He Erkuan Dai Lin Zhang Yeming Yang Yi Shi Peiquan Zhao Zhenglin Yang Xianjun Zhu | 2023 | Genes & Diseases2023，10，6： | 1 |
| 18 | How can China reach its CO2 intensity reduction targets by 2020? A regional allocation based on eq- uity and development 显示文摘 | YI Wenjing ZOU Lele GUO Jie | 2011 | Energy Policy2011，39，1： | 1 |
| 19 | Targeting HECTD3-IKKα axis inhibits inflammation-related metastasis显示文摘Metastasis is the leading cause of cancer-related death.The interactions between circulating tumor cells and endothelial adhesion molecules in distant organs is a key step during extravasation in hematogenous metastasis.Surgery is a common intervention for most primary solid tumors.However,surgical trauma-related systemic inflammation facilitates distant tumor metastasis by increasing the spread and adhesion of tumor cells to vascular endothelial cells(ECs).Currently,there are no effective interventions to prevent distant metastasis.Here,we show that HECTD3 deficiency in ECs significantly reduces tumor metastasis in multiple mouse models.HECTD3 depletion downregulates expression of adhesion molecules,such as VCAM-1,ICAM-1 and E-selectin,in mouse primary ECs and HUVECs stimulated by inflammatory factors and inhibits adhesion of tumor cells to ECs both in vitro and in vivo.We demonstrate that HECTD3 promotes stabilization,nuclear localization and kinase activity of IKKa by ubiquitinating IKKa with K27-and K63-linked polyubiquitin chains at K296,increasing phosphorylation of histone H3 to promote NF-kB target gene transcription.Knockout of HECTD3 in endothelium significantly inhibits tumor cells lung colonization,while conditional knockin promotes that.IKKa kinase inhibitors prevented LPS-induced pulmonary metastasis.These findings reveal the promotional role of the HECTD3-IKKa axis in tumor hematogenous metastasis and providea potential strategy for tumormetastasis prevention. | Fubing Li Huichun Liang Hua You Ji Xiao Houjun Xia Xi Chen Maobo Huang Zhuo Cheng Chuanyu Yang Wenjing Liu Hailin Zhang Li Zeng Yingying Wu Fei Ge Zhen Li Wenhui Zhou Yi Wen Zhongmei Zhou Rong Liu Dewei Jiang Ni Xie Bin Liang Zhenzhen Liu Yanjie Kong Ceshi Chen | 2022 | Signal Transduction and Targeted Therapy2022，7，9： | 1 |
| 20 | Variants in the Wnt co-receptor LRP6 are associated with familial exudative vitreoretinopathy显示文摘Familial exudative vitreoretinopathy(FEVR),an inherited eye disease,is characterized by abnormal retinal vascular development,such as neovascularization,vitreous hemorrhage,exudation,and retinal detachment(Criswick and Schepens,1969;Robitaille et al.,2002).FEVR is inherited as autosomal dominant,autosomal recessive,and X-linked patterns(de Crecchio et al.,1998). | Shujin Li Mu Yang Yunqi He Xiaoyan Jiang Rulian Zhao Wenjing Liu Lulin Huang Yi Shi Xiao Li Kuanxiang Sun Yeming Yang Periasamy Sundaresan Peiquan Zhao Zhenglin Yang Xianjun Zhu | 2022 | Journal of Genetics and Genomics2022，49，6： | 1 |
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