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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 | Iron-doped Mn-Ce/TiO_2 catalyst for low temperature selective catalytic reduction of NO with NH_3显示文摘The catalysts of iron-doped Mn-Ce/TiO 2(Fe-Mn-Ce/TiO 2) prepared by sol-gel method were investigated for low temperature selective catalytic reduction(SCR) of NO with NH 3.It was found that the NO conversion over Fe-Mn-Ce/TiO 2 was obviously improved after iron doping compared with that over Mn-Ce/TiO 2.Fe-Mn-Ce/TiO 2 with the molar ratio of Fe/Ti = 0.1 exhibited the highest activity.The results showed that 96.8% NO conversion was obtained over Fe(0.1)-Mn-Ce/TiO 2 at 180°C at a space velocity of 50,000 hr 1.Fe-Mn-Ce/TiO 2 exhibited much higher resistance to H 2 O and SO 2 than that of Mn-Ce/TiO 2.The properties of the catalysts were characterized using X-ray diffraction(XRD),N 2 adsorption,temperature programmed desorption(NH 3-TPD and NOx-TPD),and Xray photoelectron spectroscopy(XPS) techniques.BET,NH3-TPD and NOx-TPD results showed that the specific surface area and NH3 and NOx adsorption capacity of the catalysts increased with iron doping.It was known from XPS analysis that iron valence state on the surface of the catalysts were in Fe3+ state.The doping of iron enhanced the dispersion and oxidation state of Mn and Ce on the surface of the catalysts.The oxygen concentrations on the surface of the catalysts were found to increase after iron doping.Fe-Mn-Ce/TiO2 represented a promising catalyst for low temperature SCR of NO with NH3 in the presence of H2 O and SO2. | Boxiong Shen ,Ting Liu,Ning Zhao,Xiaoyan Yang,Lidan Deng College of Environmental Science and Engineering,Nankai University,Tianjin 300071,China. | 2010 | Journal of Environmental Sciences2010，22，9： | 63 |
| 3 | Relocation of the mainshock and aftershock sequences of M_S7.0 Sichuan Lushan earthquake显示文摘The mainshock of April 20,2013 Sichuan Lushan MS7.0 earthquake was relocated using a 3-D velocity model.Double difference algorithm was applied to relocate aftershock sequences of Lushan earthquake.The locations of 2405 aftershocks were determined.The location errors in E-W,N-S and U-D direction were 0.30,0.29 and 0.59 km on average,respectively.The location of the mainshock is 102.983°E,30.291°N and the focal depth is 17.6 km.The relocation results show that the aftershocks spread approximately 35 km in length and 16 km in width.The dominant distribution of the focal depth ranges from 10 to 20 km.A few earthquakes occurred in the shallow crust.Focal depth profiles show fault planes dip to the northwest,manifested itself as a listric thrust fault.The dip angle is steep in the shallow crust and gentle in the deep crust.Although the epicenters of aftershocks distributed mainly along both sides of the Shuangshi-Dachuan fault,the seismogenic fault may be a blind thrust fault on the eastern side of the Shuangshi-Dachuan fault.Earthquake relocation results reveal that there is a southeastward tilt aftershock belt intersecting with the seismogenic fault with y-shape.We speculate it is a back thrust fault that often appears in a thrust fault system.Lushan earthquake triggered the seismic activity of the back thrust fault. | FANG LiHua WU JianPing WANG WeiLai Lü ZuoYong WANG ChangZai YANG Ting CAI Yan | 2013 | Chinese Science Bulletin2013，58，28： | 74 |
| 4 | Transmission Dynamics of an Outbreak of the COVID-19 Delta Variant B.1.617.2——Guangdong Province,China,May-June 2021显示文摘On May 21,2021,a local case of coronavirus disease 2019(COVID-19)was confirmed in a 75-year-old woman(experienced onset of symptoms on May 18)in Liwan District,Guangzhou City,Guangdong Province,China.The number of infections has increased in the following 10 days and led to 5 generations of transmission. | Meng Zhang Jianpeng Xiao Aiping Deng Yingtao Zhang Yali Zhuang Ting Hu Jiansen Li Hongwei Tu Bosheng Li Yan Zhou Jun Yuan Lei Luo Zimian Liang Youzhi Huang Guoqiang Ye Mingwei Cai Gongli Li Bo Yang Bin Xu Ximing Huang Yazun Cui Dongsheng Ren Yanping Zhang Min Kang Yan Li | 2021 | China CDC weekly2021，3，27： | 51 |
| 5 | Paeoniflorin suppresses TGF-β mediated epithelial- mesenchymal transition in pulmonary fibrosis through a Smad-dependent pathway显示文摘 | Yu JI Yan-nong DOU Qian-wen ZHAO Ji-zhou ZHANG Yan YANG Ting WANG Yu-feng XIA Yue DAI Zhi-feng WEI | 2016 | Acta Pharmacologica Sinica2016，37，6： | 48 |
| 6 | Erianin,a novel dibenzyl compound in Dendrobium extract,inhibits lung cancer cell growth and migration via calcium/calmodulin-dependent ferroptosis显示文摘Ferroptosis,a novel form of programmed cell death,is characterized by iron-dependent lipid peroxidation and has been shown to be involved in multiple diseases,including cancer.Stimulating ferroptosis in cancer cells may be a potential strategy for cancer therapy.Therefore,ferroptosis-inducing drugs are attracting more attention for cancer treatment.Here,we showed that erianin,a natural product isolated from Dendrobium chrysotoxum Lindl,exerted its anticancer activity by inducing cell death and inhibiting cell migration in lung cancer cells.Subsequently,we demonstrated for the first time that erianin induced ferroptotic cell death in lung cancer cells,which was accompanied by ROS accumulation,lipid peroxidation,and GSH depletion.The ferroptosis inhibitors Fer-1 and Lip-1 but not Z-VAD-FMK,CQ,or necrostatin-1 rescued erianin-induced cell death,indicating that ferroptosis contributed to erianin-induced cell death.Furthermore,we demonstrated that Ca^(2+)/CaM signaling was a critical mediator of erianin-induced ferroptosis and that blockade of this signaling significantly rescued cell death induced by erianin treatment by suppressing ferroptosis.Taken together,our data suggest that the natural product erianin exerts its anticancer effects by inducing Ca^(2+)/CaMdependent ferroptosis and inhibiting cell migration,and erianin will hopefully serve as a prospective compound for lung cancer treatment. | Peng Chen Qibiao Wu Jiao Feng Lili Yan Yitian Sun Shuiping Liu Yu Xiang Mingming Zhang Ting Pan Xiaying Chen Ting Duan Lijuan Zhai Bingtao Zhai Wengang Wang Ruonan Zhang Bi Chen Xuemeng Han Yicong Li Liuxi Chen Ying Liu Xingxing Huang Ting Jin Wenzheng Zhang Hong Luo Xiaohui Chen Yongqiang Li Qiujie Li Guohua Li Qin Zhang Lvjia Zhuo Zuyi Yang Huifen Tang Tian Xie Xiaoping Ouyang Xinbing Sui | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 42 |
| 7 | The Serum Exosome Derived MicroRNA-135a,-193b, and-384 Were Potential Alzheimer's Disease Biomarkers显示文摘Objective MicroR NAs(mi Rs) are attractive molecules to be considered as one of the blood-based biomarkers for neurodegenerative disorders such as Alzheimer's disease(AD). The goal of this study was to explore their potential value as biomarkers for the diagnosis of AD. Methods The expression levels of exosomal miR-135 a,-193 b, and-384 in the serum from mild cognitive impairment(MCI), dementia of Alzheimer-type(DAT), Parkinson's disease with dementia(PDD), and vascular dementia(VaD) patients were measured with a real-time quantitative reverse transcriptase PCR(qR T-PCR) method. Results Both serum exosome mi R-135 a and miR-384 were up-regulated while miR-193 b was down-regulated in serum of AD patients compared with that of normal controls. Exosome miR-384 was the best among the three miR s to discriminate AD, VaD, and PDD. Using the cut-off value could better interpret these laboratory test results than reference intervals in the AD diagnosis. ROC curve showed that the combination of mi R-135 a,-193 b, and-384 was proved to be better than a particular one for early AD diagnosis. Conclusion Our results indicated that the exosomal miR s in the serum were not only potential biomarker of AD early diagnosis, but might also provide novel insights into the screen and prevention of the disease. | YANG Ting Ting LIU Chen Geng GAO Shi Chao ZHANG Yi WANG Pei Chang | 2018 | Biomedical and Environmental Sciences2018，31，2： | 35 |
| 8 | A novel m6A reader Prrc2a controls oligodendroglial specification and myelination显示文摘While N6-methyladenosine (m6A), the most abundant internal modification in eukaryotic mRNA, is linked to cell differentiation and tissue development, the biological significance of m6A modification in mammalian glial development remains unknown. Here, we identify a novel m6A reader, Prrc2a (Proline rich coiled-coil 2A), which controls oligodendrocyte specification and myelination. Nestin-Cre-mediated knockout of Prrc2a induces significant hypomyelination, decreased lifespan, as well as locomotive and cognitive defects in a mouse model. Further analyses reveal that Prrc2a is involved in oligodendrocyte progenitor cells (OPCs) proliferation and oligodendrocyte fate determination. Accordingly, oligodendroglial-lineage specific deletion of Prrc2a causes a similar phenotype of Nestin-Cre-mediated deletion. Combining transcriptome-wide RNA-seq, m6A-RIP-seq and Prrc2a RIP-seq analysis, we find that Olig2 is a critical downstream target gene of Prrc2a in oligodendrocyte development. Furthermore, Prrc2a stabilizes Olig2 mRNA through binding to a consensus GGACU motif in the Olig2 CDS (coding sequence) in an m6A-dependent manner. Interestingly, we also find that the m6A demethylase, Fto, erases the m6A modification of Olig2 mRNA and promotes its degradation. Together, our results indicate that Prrc2a plays an important role in oligodendrocyte specification through functioning as a novel m6A reader. These findings suggest a new avenue for the development of therapeutic strategies for hypomyelination-related neurological diseases. | Rong Wu Ang Li Baofa Sun Jian-Guang Sun Jinhua Zhang Ting Zhang Yusheng Chen Yujie Xiao Yuhao Gao Qingyang Zhang Jun Ma Xin Yang Yajin Liao Wei-Yi Lai Xiaolong Qi Shukun Wang Yousheng Shu Hai-Lin Wang Fengchao Wang Yun-Gui Yang Zengqiang Yuan | 2019 | Cell Research2019，29，1： | 32 |
| 9 | Efficacy and safety of a novel anti-HER2 therapeutic antibody RC48 in patients with HER2-overexpressing,locally advanced or metastatic gastric or gastroesophageal junction cancer:a single-arm phase II study显示文摘Background:Current treatment options for human epidermal growth factor receptor 2(HER2)-overexpressing gastric cancer at third-line have shown limited clinical benefit.Further,there is no specific treatment for HER2 immunohistochemistry(IHC)2+and fluorescence in-situ hybridization-negative patients.Here,we report the efficacy and safety of a novel anti-HER2 antibody RC48 for patients with HER2-overexpressing,advanced gastric or gastroesophageal junction cancer.Methods:Patients with HER2-overexpressing(IHC 2+or 3+),locally advanced or metastatic gastric or gastroesophageal junction cancer who were under at least second-line therapy were eligible and received RC482.5 mg/kg alone every 2 weeks.The primary endpoint was the objective response rate(ORR)assessed by an independent review committee.Secondary endpoints included progressionfree survival(PFS),overall survival(OS),duration of response,time to progression,disease control rate,and safety.Results:Of 179 patients screened,125 were eligible and received RC48 treatment.The ORR was 24.8%(95%confidence interval[CI]:17.5%-33.3%).The median PFS and OS were 4.1 months(95%CI:3.7-4.9 months)and 7.9 months(95%CI:6.7-9.9 months),respectively.The most frequently reported adverse events were decreased white blood cell count(53.6%),asthenia(53.6%),hair loss(53.6%),decreased neutrophil count(52.0%),anemia(49.6%),and increased aspartate aminotransferase level(43.2%).Serious adverse events(SAEs)occurred in 45(36.0%)patients,and RC48-related SAEs were mainly decreased neutrophil count(3.2%).Seven patients had adverse events that led to death were not RC48-related.Conclusions:RC48 showed promising activity with manageable safety,suggesting potential application in patients with HER2-overexpressing,advanced gastric or gastroesophageal junction cancer who have previously received at least two lines of chemotherapy. | Zhi Peng Tianshu Liu Jia Wei Airong Wang Yifu He Liuzhong Yang Xizhi Zhang Nanfeng Fan Suxia Luo Zhen Li Kangsheng Gu Jianwei Lu Jianming Xu Qingxia Fan Ruihua Xu Liangming Zhang Enxiao Li Yuping Sun Guohua Yu Chunmei Bai Yong Liu Jiangzheng Zeng Jieer Ying Xinjun Liang Nong Xu Chao Gao Yongqian Shu Dong Ma Guanghai Dai Shengmian Li Ting Deng Yuehong Cui Jianmin Fang Yi Ba Lin Shen | 2021 | Cancer Communications2021，41，11： | 29 |
| 10 | A reappraisal of CTLA-4 checkpoint blockade in cancer immunotherapy显示文摘anti-CTLA-4 抗体由阻止 B7-CTLA-4 相互作用接近否定发信号引起肿瘤拒绝,这被假定。在比临床上有效的 dosing 完成的血浆层次更加高的集中,令人惊讶地, anti-CTLA-4 抗体 Ipilimumab 不由 CTLA-4 也不 CTLA-4 绑定堵住任何一 B7 trans-endocytosis 到使不能调动或联系房间的 B7。因而, Ipilimumab 不从人性化的任何一个 CTLA4 基因在树枝状的房间(DC ) 上增加 B7 (Ctla4 h/h ) 或人的 CD34 + 茎重新组成房间的 NSG 老鼠。在 Ctla4 高效地表示人和老鼠 CTLA4 基因,绑在人的 anti-CTLA-4 抗体然而并非老鼠 CTLA-4 的 h/m 老鼠导致 Treg 弄空和 Fc 受体依赖者肿瘤拒绝。堵住的抗体 L3D10 比得上在引起肿瘤拒绝的非阻塞的 Ipilimumab。显著地,输在人类化期间堵住活动的 L3D10 子孙在导致 Treg 弄空和肿瘤拒绝仍然保持充分能干。有效地在淋巴的器官堵住 CD4 T 细胞激活和 de novo CD8 T 细胞 priming 的 Anti-B7 抗体否定地不影响 Ipilimumab 的 immunotherapeutic 效果。因此,临床上有效的 anti-CTLA-4 mAb 由独立于检查点封锁的机制引起肿瘤拒绝但是依赖于主人 Fc 受体。我们为 CTLA-4 检查点的一个重评价的数据电话封锁假设并且为安全、有效的 anti-CTLA-4 mAbs 的下一代提供新卓见。 | Xuexiang Du Fei Tang Mingyue Liu Juanjuan Su Yan Zhang Wei Wu Martin Devenport Christopher A Lazarski Peng Zhang Xu Wang Peiying Ye Changyu Wang Eugene Hwang Tinghui Zhu Ting Xu Pan Zheng Yang Liu | 2018 | Cell Research2018，28，4： | 25 |
| 11 | Photoactivated CRY1 and phyB Interact Directly with AUX/IAA Proteins to Inhibit Auxin Signaling in Arabidopsis显示文摘光是在 Arabidopsis 通过蓝色和调停 cryptochrome 的 red/far-red 光光敏电阻器和调停 phytochrome 的小径禁止胚轴房间延伸的关键环境暗示。相反,作为枢轴的内长的植物激素,植物生长素通过 AUX/IAA 蛋白质(AUX/IAAs ) 的植物生长素受体 TIR1/AFBs-mediated 降级支持胚轴延伸。然而,位于发信号的光和植物生长素的对抗相互作用下面的分子的机制仍然保持不清楚。这里,我们报导光禁止由 cryptochrome 的蓝、红的轻依赖者的相互作用通过 AUX/IAAs 的稳定发信号的植物生长素 1 (CRY1 ) 并且有 AUX/IAAs 的 phytochrome B 分别地。有 AUX/IAAs 的 CRY1 的蓝被触发光的相互作用与 AUX/IAAs 禁止 TIR1 的协会,导致这些蛋白质的导致植物生长素的降级的压抑。我们的结果显示光敏电阻器下游地直接作为一样与植物生长素受体分享 AUX/IAAs 表明部件。我们建议由光敏电阻器和植物生长素受体的 AUX/IAA 蛋白质稳定性的那条对抗规定允许植物平衡光和植物生长素信号优化他们的生长。 | Feng Xu Shengbo He Jingyi Zhang Zhilei Mao Wenxiu Wang Ting Li Jie Hua Shasha Du Pengbo Xu Ling Li Hongli Lian Hong-Quan Yang | 2018 | Molecular Plant2018，11，4： | 24 |
| 12 | Baicalin induces ferroptosis in bladder cancer cells by downregulating FTH1显示文摘Ferroptosis is a non-apoptotic regulated cell death caused by iron accumulation and subsequent lipid peroxidation.Currently,the therapeutic role of ferroptosis on cancer is gaining increasing interest.Baicalin an active component in Scutellaria baicalensis Georgi with anticancer potential various cancer types;however,the effects of baicalein on bladder cancer and the underlying molecular mechanisms remain largely unknown.In the study,we investigated the effect of baicalin on bladder cancer cells5637 and KU-19-19.As a result,we show baicalin exerted its anticancer activity by inducing apoptosis and cell death in bladder cancer cells.Subsequently,we for the first time demonstrate baicalin-induced ferroptotic cell death in vitro and in vivo,accompanied by reactive oxygen species(ROS) accumulation and intracellular chelate iron enrichment.The ferroptosis inhibitor deferoxamine but not necrostatin-1,chloroquine(CQ),N-acetyl-L-cysteine,L-glutathione reduced,or carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone(Z-VAD-FMK) rescued baicalin-induced cell death,indicating ferroptosis contributed to baicalin-induced cell death.Mechanistically,we show that ferritin heavy chain1(FTH1) was a key determinant for baicalin-induced ferroptosis.Overexpression of FTH1 abrogated the anticancer effects of baicalin in both 5637 and KU19-19 cells.Taken together,our data for the first time suggest that the natural product baicalin exerts its anticancer activity by inducing FTH1-dependent ferroptosis,which will hopefully provide a prospective compound for bladder cancer treatment. | Na Kong Xiaying Chen Jiao Feng Ting Duan Shuiping Liu Xueni Sun Peng Chen Ting Pan Lili Yan Ting Jin Yu Xiang Quan Gao Chengyong Wen Weirui Ma Wencheng Liu Mingming Zhang Zuyi Yang Wengang Wang Ruonan Zhang Bi Chen Tian Xie Xinbing Sui Wei Tao | 2021 | Acta Pharmaceutica Sinica B2021，11，12： | 23 |
| 13 | Strain-induced direct-indirect bandgap transition and phonon modulation in monolayer WS2显示文摘 | Yanlong Wang Chunxiao Cong Weihuang Yang Jingzhi Shang Namphung Peimyoo Yu Chen Junyong Kang Jianpu Wang Wei Huang Ting Yu | 2015 | Nano Research2015，8，8： | 20 |
| 14 | Role of the Lung Microbiome in the Pathogenesis of Chronic Obstructive Pulmonary Disease显示文摘 | Lei Wang Ke Hao Ting Yang Chen Wang | 2017 | Chinese Medical Journal2017，，17： | 20 |
| 15 | Synthesis and Anticancer Effect of gem-Difluoromethylenated Chrysin Derivatives显示文摘Ten gem-difluoromethylenated chrysin derivatives were prepared and their anticancer activities in vitro were evaluated by the standard MTT method. The results of biological test showed that some of gem-difluoromethylenated chrysin derivatives had higher anticancer activity than chrysin. | Xing ZHENG Jian Guo CAO Duan Fang LIAO Bing Yang ZHU Hui Ting LIU | 2006 | Chinese Chemical Letters2006，17，11： | 20 |
| 16 | Precise nanomedicine for intelligent therapy of cancer显示文摘Precise nanomedicine has been extensively explored for efficient cancer imaging and targeted cancer therapy, as evidenced by a few breakthroughs in their preclinical and clinical explorations. Here, we demonstrate the recent advances of intelligent cancer nanomedicine, and discuss the comprehensive understanding of their structure-function relationship for smart and efficient cancer nanomedicine including various imaging and therapeutic applications, as well as nanotoxicity. In particular, a few emerging strategies that have advanced cancer nanomedicine are also highlighted as the emerging focus such as tumor imprisonment, supramolecular chemotherapy, and DNA nanorobot. The challenge and outlook of some scientific and engineering issues are also discussed in future development. We wish to highlight these new progress of precise nanomedicine with the ultimate goal to inspire more successful explorations of intelligent nanoparticles for future clinical translations. | Huabing Chen Zhanjun Gu Hongwei An Chunying Chen Jie Chen Ran Cui Siqin Chen Weihai Chen Xuesi Chen Xiaoyuan Chen Zhuo Chen Baoquan Ding Qian Dong Qin Fan Ting Fu Dayong Hou Qiao Jiang Hengte Ke Xiqun Jiang Gang Liu Suping Li Tianyu Li Zhuang Liu Guangjun Nie Muhammad Ovais Daiwen Pang Nasha Qiu Youqing Shen Huayu Tian Chao Wang Hao Wang Ziqi Wang Huaping Xu Jiang-Fei Xu Xiangliang Yang Shuang Zhu Xianchuang Zheng Xianzheng Zhang Yanbing Zhao Weihong Tan Xi Zhang Yuliang Zhao | 2018 | Science China Chemistry2018，61，12： | 19 |
| 17 | TRANSFORMING GROWTH FACTOR-β1 AND SMAD4 SIGNALING PATHWAY DOWN-REGULATES RENAL EXTRACELLULAR MATRIX DEGRADATION IN DIABETIC RATS显示文摘Objective To investigate the role of transforming growth factor-β1(TGF-β1)/Smad4 pathway in development of renal fibrosis in streptozotocin(STZ)-induced diabetic nephropathy(DN) rats and explore its possible mechanism.Methods Male Wistar rats weighing 180-220 g were divided into 5 groups:group A(normal control),group B [diabetes mellitus(DM) 2 weeks],group C(DM 4 weeks),group D(DM 8 weeks),and group E(DM 16 weeks).Except for the normal control group,other groups were induced DM by single injection of STZ(55 mg/kg) respectively.Blood glucose level,serum creatinine,and 24-hour urine protein were examined.Expressions of TGF-β1 and Smad4 protein and mRNA in kidney were detected using immunohistochemical technique,Western blot,and real-time PCR.mRNA expressions of stromelysin-1(MMP-3),tissue inhibitor of metalloproteinase-1(TIMP-1),and collagen Ⅲ in kidney were also detected by real-time PCR..Results The levels of blood glucose,serum creatinine,and 24-hour urine protein in rats of group B,C,D,and E were higher than those of the control group.With the progression of renal fibrosis,the expressions of TGF-β1 and Smad4 protein and mRNA in kidney of diabetic rats elevated.In addition,the renal MMP-3 mRNA expression diminished in diabetic rats,while TIMP-1 and collagen Ⅲ mRNA increased.Conclusions In STZ-induced diabetic rats,the TGF-β1/Smad4 appears to play an important role in renal fibrosis of DN.The increased expression of TGF-β1 and Smad4 might result in the transcriptional regulation of downstream target genes of TGF-β1/Smad4 pathway,which contributes to the progression of renal fibrosis in diabetic rats. | Qin Yang Ru-jia Xie Ting Yang Li Fang Bing Han Guo-zhong Zhang Ming-liang Cheng | 2007 | Chinese Medical Sciences Journal2007，22，4： | 19 |
| 18 | Whole-genome sequencing of 508 patients identifies key molecular features associated with poor prognosis in esophageal squamous cell carcinoma显示文摘Esophageal squamous cell carcinoma(ESCC)is a poor-prognosis cancer type with limited understanding of its molecular etiology.Using 508 ESCC genomes,we identified five novel significantly mutated genes and uncovered mutational signature clusters associated with metastasis and patients’outcomes.Several functional assays implicated that NFE2L2 may act as a tumor suppressor in ESCC and that mutations in NFE2L2 probably impaired its tumor-suppressive function,or even conferred oncogenic activities.Additionally,we found that the NFE2L2 mutations were significantly associated with worse prognosis of ESCC.We also identified potential noncoding driver mutations including hotspot mutations in the promoter region of SLC35E2 that were correlated with worse survival.Approximately 5.9%and 15.2%of patients had high tumor mutation burden or actionable mutations,respectively,and may benefit from immunotherapy or targeted therapies.We found clinically relevant coding and noncoding genomic alterations and revealed three major subtypes that robustly predicted patients’outcomes.Collectively,we report the largest dataset of genomic profiling of ESCC useful for developing ESCC-specific biomarkers for diagnosis and treatment. | Yongping Cui Hongyan Chen Ruibin Xi Heyang Cui Yahui Zhao Enwei Xu Ting Yan Xiaomei Lu Furong Huang Pengzhou Kong Yang Li Xiaolin Zhu Jiawei Wang Wenjie Zhu Jie Wang Yanchun Ma Yong Zhou Shiping Guo Ling Zhang Yiqian Liu Bin Wang Yanfeng Xi Ruifang Sun Xiao Yu Yuanfang Zhai Fang Wang Jian Yang Bin Yang Caixia Cheng Jing Liu Bin Song Hongyi Li Yi Wang Yingchun Zhang Xiaolong Cheng Qimin Zhan Yanhong Li Zhihua Liu-Show | 2020 | Cell Research2020，30，10： | 19 |
| 19 | Thermal conductivity determination of suspended mono- and bilayer WS2 by Raman spectroscopy显示文摘我们报导单层 1L 和 bilayer 2L WS 的热传导性<潜水艇class=“ a-plus-plus ”>化学蒸汽免职 CVD 种的 2 ,它被温度的使用和 E 的刺激依赖决定<潜水艇class=“ a-plus-plus ”> 2g <啜class=“ a-plus-plus ”> 1 和 A <潜水艇class=“ a-plus-plus ”> 1g 拉曼模式。E 的一阶的温度系数 < 潜水艇 class= “ a-plus-plus ” > 2g < 啜 class= “ a-plus-plus ” > 1 和 A < 潜水艇 class= “ a-plus-plus ” > 1g 模式在支持了并且推迟 WS < 潜水艇 class= “ a-plus-plus ” > 2 层被提取。 A 的频率移动<潜水艇class=“ a-plus-plus ”>有温度的 1g 模式比 E 的大<潜水艇class=“ a-plus-plus ”> 2g <啜class=“ a-plus-plus ”>为 1L-WS 的 1 个模式<潜水艇class=“ a-plus-plus ”> 2 ,它被归因于为 A 联合的更强壮的电子声子<潜水艇class=“ a-plus-plus ”> 1g 模式比那为 E <潜水艇class=“ a-plus-plus ”> 2g <啜class=“ a-plus-plus ”> 1 模式。而且由激光加热导致的声子模式的移动的使用,在房间温度的热传导性被估计是 32 和 53 W/mmine ICL 的全面功能。给 ICL 还没完成了一个自治学科的地位的事实,询问必须以 criminalisation 的国家理论的讨论开始。文章集中于 criminalisation 的二个很重要的理论,也就是理论 o 吗? | Namphung Peimyoo Jingzhi Shang Weihuang Yang Yanlong wang Chunxiao Cong Ting Yu | 2015 | Nano Research2015，8，4： | 18 |
| 20 | p53 upregulated by HIF-la promotes hypoxiainduced G2/M arrest and renal fibrosis in vitro and in vivo显示文摘Hypoxia plays an important role in the genesis and progression of renal fibrosis.The underlying mechanisms, however, have not been sufficiently elucidated. We examined the role of p53 in hypoxia-induced renal fibrosis in cell culture (human and rat renal tubular epithelial cells) and a mouse unilateral ureteral obstruction (UUO) model. Cell cycle of tubular cells was determined by flow cytometry, and the expression of profibrogenic factors was determined by RT-PCR, immunohistochemistry, and western blotting. Chromatin immunoprecipitation and luciferase reporter experiments were performed to explore the effect of HIF-lα on p53 expression. We showed that, in hypoxic tubular cells, p53 upregulation suppressed the expression of CDK1 and cyclins Bl and DI, leading to cell cycle (G2/M) arrest (or delay) and higher expression of TGF-β, CTGF, collagens, and fibronectin. p53 suppression by siRNA or by a specific p53 inhibitor (PIF-α) triggered opposite effects preventing the G2/M arrest and profibrotic changes. In vivo experiments in the UUO model revealed similar antifibrotic results following intraperitoneal administration of PIF-α(2.2 mg/kg). Using gain-of-function, loss-of-function, and luciferase assays, we further identified an HRE3 region on the p53 promoter as the HIF-lα-binding site. The HIF-la-HRE3 binding resulted in a sharp transcriptional activation of p53. Collectively, we show the presence of a hypoxia-activated, p53-responsive profibrogenic pathway in the kidney. During hypoxia, p53 upregulation induced by HIF-la suppresses cell cycle progression, leading to the accumulation of G2/M cells, and activates profibrotic TGF-β and CTGF-mediated signaling pathways, causing extracellular matrix production and renal fibrosis. | Limin Liu Peng Zhang Ming Bai Lijie He Lei Zhang Ting Liu Zhen Yang Menglu Duan Minna Liu Baojian Liu Rui Du Qi Qian Shiren Sun | 2019 | Journal of Molecular Cell Biology2019，11，5： | 18 |
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