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| 1 | Reactivation of γ-globin expression through Cas9 or base editor to treat β-hemoglobinopathies显示文摘Dear Editor,Mutations in the β-globin gene,the essential component of adult hemoglobin(HbA;a2p2),results in either a production of aberrant sickle hemoglobin(HbS)leading to sickle cell disease(SCD)or an insufficient β-globin synthesis leading to β-thalassemia.These two major forms of β-hemoglobinopathies cause impaired erythropoiesis and life-threatening anemia.Clinical evidence has suggested that reaaivation of fetal γ-globin(HBG)gene expression which is normally silenced after birth by certain genetic mutations can ameliorate the clinical course of β-hemoglobinopathies. | Liren Wang Linxi Li Yanlin Ma Handan Hu Qi Li Yang Yang Wenbang Liu Shuming Yin Wei Li Bin Fu Ryo Kurita Yukio Nakamura Mingyao Liu Yongrong Lai Dali Li | 2020 | Cell Research2020，30，3： | 14 |
| 2 | FBW7 regulates endothelial functions by targeting KLF2 for ubiquitination and degradation显示文摘F 盒子和 WD 重复包含域 7 (FBW7 ) , E3 ubiquitin ligase SCF FBW7 (SKP1, cullin-1 和 FBW7 的建筑群) ,在各种各样的生理、病理学的过程起重要作用。尽管 FBW7 为脉管的开发被要求,它在内皮细胞层的函数尚待被调查。在这研究,我们证明 FBW7 是 endothelial 功能的一个重要管理者,包括 angiogenesis,白血球粘附和 endothelial 障碍正直。用 RNA 干扰,我们发现 FBW7 的弄空显著地在 vitro 并且在 vivo 损害 angiogenesis。我们识别了锌手指抄写因素 Krü象 ppel 一样因素 2 (KLF2 ) 作为在 endothelial 房间的 FBW7 的一个生理的目标。FBW7 击倒表示在 endothelial 房间导致了内长的 KLF2 蛋白质的累积。调停 FBW7 的 KLF2 破坏被显示在二保存 phosphodegrons 经由肝糖 synthase kinase-3 (GSK3 ) 取决于 KLF2 的 phosphorylation。变异这些 phosphodegron 主题废除了 KLF2 的调停 FBW7 的降级和 ubiquitination。调停 siRNA 显示出的 FBW7 击倒 KLF2 是在 endothelial 的规定的 FBW7 的一个必要目标,这工作。而且,调停 FBW7 的 KLF2 降级被显示为在 teratomas 并且在 zebrafish 开发的 angiogenesis 批评。一起拿,我们的学习在 endothelial 房间移植, angiogenesis,发炎和障碍完整的进程为 FBW7 建议一个角色,并且在 vivo 提供新奇卓见进 KLF2 稳定性的规定。 | Rui Wang Yah Wang Ning Liu Chunguang Ren Cong Jiang Kai Zhang Su Yu Yunfei Chen Hui Tang Qi Deng Cong Fu Yingcong Wang Rong Li Mingyao Liu Weijun Pan Ping Wang | 2013 | Cell Research2013，23，6： | 7 |
| 3 | 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 |
| 4 | Progresses in pharmaceutical and surgical management of premature ejaculation显示文摘Objective:Premature ejaculation(PE)is regarded as one of the most common male sexual dysfunctions.This review introduced several pharmaceutical and surgical methods for the management of PE.The definition,etiology,behavioral,and psychological therapy of PE were also discussed.Data sources:'Premature,''ejaculation,'or'sexual dysfuction'were used as the medical subject headings(MeSH)to obtain relevant articles before June 2019 on Pubmed,Google Scholar and CNKI.Most articles used were written in English and several Chinese articles were also cited.Study selection:Full-text articles of retrospective/prospective/randomized controlled trials were analyzed.Animal experiments and letters were excluded.Results:There are four PE sub-types:lifelong PE,acquired PE,natural variable PE,and subjective PE.Behavioral therapy,psychotherapy,medication,topical anesthetics,and surgery are currently used for the treatment of PE.However,all the above treatments have limitations.Therefore,novel ways should be investigated to more efficiently control PE.Conclusions:The pharmaceutical therapy that is currently being used in clinical practice for the management of PE is still the main choice globally due to its good efficacy.Surgery may be a choice for patients who are resistant to medication.However,it should be performed cautiously. | Qin-Bo Hu Dong Zhang Liang Ma Derry Mingyao Ng Maria Haleem Qi Ma | 2019 | Chinese Medical Journal2019，，19： | 1 |
| 5 | Using virtual forest environment on collaborative forest management显示文摘 | Mingyao Qi Tianhe Chi Xin Zhang | 2004 | Geoscience and Remote Sensing Symposium2004，7，7： | 1 |
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