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Characteristics and sources of peroxyacetyl nitrate(PAN)in the rural North China Plain:Results from1-year continuous observations

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Journal of Environmental Sciences 2024年第4期138卷 719-731页

作者： Xin Liu Xiaowei He Chenglong Zhang Yifei Song shuyang xie Chengtang Liu Pengfei Liu Yuanyuan Zhang Yujing Mu Junfeng Liu Research Center for Eco-Environmental Sciences Chinese Academy of SciencesBeijing 100085China University of Chinese Academy of Sciences Beijing 100049China

Peroxyacetyl nitrate(PAN)is an important photochemical pollutant in the troposphere,whereas long-term measurements are scarce in rural areas in North China Plain(NCP),resulting in unclear seasonal variations and sources of PAN in rural *** this study,we conducted a 1-year observation of PAN during 2021-2022 at the rural NCP *** average concentrations of PAN were 1.10,0.75,0.65,and 0.88 ppbv in spring,summer,autumn,and winter,respectively,with a 1-year average of 0.81±0.60 *** indicate that the loss of PAN through thermal decomposition in summer accounts for 43.2% of the total formed PAN,which is an important reason for the low concentration of PAN in *** speculate that since the correlation between PAN and O_(3) in winter is significantly lower than that in other seasons,the observed regional transport of PAN cannot be ignored in *** budget analysis,regional transport accounted for 12.8% and 55.9% of the observed PAN on the spring and winter pollution days,respectively,which showed that regional transport played key roles during the photochemical pollution of the rural NCP in *** potential source contribution function revealed that the transported PAN mainly comes from southern Hebei in *** winter,the transported PAN was mainly from Langfang,Hengshui,and southern *** findings may aid in understanding PAN variations in different seasons in rural areas and highlight the impact of regional transport on the PAN budget.

关键词： Photochemical pollution Peroxyacetyl nitrate(PAN) Seasonal variations Regional transport Rural area

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MicroRNA-181a is elevated by 10-hydroxycamptothecin and represses lung carcinoma progression by downregulating FOXP1

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BIOCELL 2022年第2期46卷 417-431页

作者： LI PAN WENTING YI DONGMIN LIANG YULONG ZHAO RANRAN WANG PINGYU WANG YOUJIE LI JIAXUAN XIN YUNFEI YAN shuyang xie Department of Biochemistry and Molecular Biology Binzhou Medical UniversityYantai264003China Department of Medical Laboratory Yantai Affiliated Hospital of Binzhou Medical UniversityYantai264100China

Tumor progression is usually characterized by proliferation,migration,and angiogenesis,which is essential for supplying both nutrients and oxygen to the tumor ***,targeting angiogenesis has been considered a promising therapeutic strategy for cancer prevention and *** the present study,we demonstrated that in addition to suppressing lung cancer cell proliferation and migration in vitro,10-hydroxycamptothecin(10-HCPT)is also capable of inhibiting angiogenesis in vivo with a miR-181a-dependent ***,by upregulating miR-181a,which in turn downregulating FOXP1,10-HCPT can inhibit the PI3K/Akt/ERK signaling pathwaymediated ***,reduced levels of miR-181a have been found in both lung cancer cell lines and xenograft with concurrently elevated levels of FOXP1,VEGF,bFGF,and *** with the findings from the in vitro experiments,miR-181a impairs neovascularization in our xenograft *** summary,our findings have not only established the anti-oncogenic role of miR-181a in lung cancer angiogenesis but also suggest that 10-HCPT could be a potential therapeutic reagent for lung cancer treatment.

关键词： microRNA-181a 10-hydroxycamptothecin Angiogenesis Lung carcinoma

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Production of transgenic mice carrying green fluorescence protein gene by a lentiviral vector-mediated approach

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Progress in Natural Science:Materials International 2006年第8期16卷 827-832页

作者： ZHANG Jingzhi, GUO Xinbing, xie shuyang, ZHU Yiwen, HUANG Ying, WANG Shu and REN Zhaorui (Shanghai Institute of Medical Genetics, Shanghai JiaoTong University, Shanghai 200040, China) [a]Shanghai Institute of Medical Genetics Shanghai JiaoTong University Shanghai China

A pseudo-lentivirus, which carries green fluorescence protein (GFP) expressing cassette, was injected into the periv itelline space of murine fertilized oocytes before transplanting into the oviducts of the foster mothers. The GFP transgenic pups were then obtained. By PCR amplification, fluorescent microscopy and flow assisted cytometry sorting analysis, we found that the integration rate of the transgene was estimated at above 40% . Real-time PCR analysis indicated that the copy number of the integrated GFP cassette was around 40. Fluorescent in situ hybridization analysis demonstrated that the integration pattern was random but inheritable. The transgenic mice with multi-integration sites and various expression levels possessed a great value in practice as well as research. The approach reported herein provides an efficient way to generate and screen the transgenic mouse strains.

关键词： lentiviral vector transgene mouse integration GFP.

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Amelioration of β^(654)-thalassemia in mouse model with the knockdown of aberrantly spliced β-globin mRNA

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Journal of Genetics and Genomics 2008年第10期35卷 595-601页

作者： shuyang xie Wei Li Zhaorui Ren Jingzhi Zhang Xinbin Guo Shu Wang Shuzhen Huang Fanyi Zeng Yi-Tao Zeng Shanghai Institute of Medical Genetics Shanghai Children＇s Hospital Shanghai Jiao Tong University School of Medicine Shanghai 200040 China.

Large amounts of aberrantly spliced mRNA from the β^654 allele was present in erythroid cells, which might impair the erythropoiesis. A therapeutic strategy for β-thalassemia was explored by knocking down the aberrantly spliced mRNA of β-globin. Lentiviral vector with siRNA fragment targets on the specific portion of β^654-globin aberrantly spliced pre-mRNA was constructed. In HeLa β^654 cells, the siRNA vector could reduce approximately 60% of aberrantly spliced mRNA, which was assessed by RT-PCR and qRT-PCR. Furthermore, a disease model of β^654 thalassemia mice with lentiviral-mediated siRNA was produced by subzonal injection （named Hβi-Hbb^th-4/Hbb^＋ transgenic mice）. Our results showed that the hemotological parameters were improved in Hβi-Hbb^th-4/Hbb^＋ transgenic mice. This study provides a potential way for β^654-thalassemia therapy by knocking down the aberrantly spliced β-globin mRNA, whilst supporting that the aberrantly spliced β-globin mRNA may aggravate the disease.

关键词： β-thalassemia small interfering RNA (siRNA) hemoglobin

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miR-98 inhibiting IL-10-related JAK2/STAT3 pathway prevent pulmonary fibrosis

miR-98 inhibiting IL-10-related JAK2/STAT3 pathway prevent p...

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中华医学会呼吸病学年会——2013（第十四次全国呼吸病学学术会议）

作者： shuyan gao youjie li weili liu shuyang xie chang jun lv Key Laboratory of Tumour Molecular Biology in Binzhou Medical University Department of Biochemistry and Molecular Biology Binzhou Medical University Department of Clinical Medicine Binzhou Medical University

Objective This study was conducted to investigate whether the over-expression of anti-inflammation factor IL-10 can induce pulmonary fibrosis(PF) by activating JAK2/STAT3 pathway phosphorylation and thereby pro mote the expression of such down-stream target as the apoptotic protein ***-10 up-stream regulated micro RNA,miR-98 was also investigated. Methods Bleomycin intratracheal instillation was perfor med in Wister rats to build PF models.A549 cells transf ected with miR-98,ASO-98 and scrambled oligos in vitr

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A study of familial congenital cyanosis caused by Hb-MYantai(α-76 G→T,Asp→Tyr)

A study of familial congenital cyanosis caused by Hb-MYantai...

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华东六省一市生物化学与分子生物学会2010年学术交流会

作者： Youjie Li Shuai Zhang Zunling Li Ying Ma Yanbo Sun shuyang xie Department of Biochemistry and Molecular Biology Bin Zhou Medical University

Methemoglobin(Hb-M)is a rare hemoglobinopathy in *** report a family living in Yantai City,East China,with congenital cyanosis due to a Hb-M *** proband,a 65-year-old female,presented with oxygen saturation of 63%.The Hb-M concentration and arterial oxygen saturation remained unchanged after intravenous treatment with methylene blue. Her blood color was chocolate-brown and did not change after adding 0.1%*** was

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TRIB2 regulates the expression of miR-33a-5p through the ERK/c-Fos pathway to affect the IM-resistance of CML cells

TRIB2 regulates the expression of miR-33a-5p through the ERK...

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2021年中国肿瘤标志物学术大会暨第十五届肿瘤标志物青年科学家论坛

作者： Hang Sun Dongmin Liang Xiao Wang Simin Rong shuyang xie Youjie Li Binzhou medical university

Objective: To explore the molecular mechanism of TRIB2 mediating drug resistance in chronic myeloid leukemia(CML) cells through regulation of miR-33 a-5 ***: The expressions of TRIB2 and miR-33 a-5 p in leukemia K562 cells and IM-resistant cells were detected by RT-PCR. The growth of leukemia cells and IM-resistant cells and drug half inhibition rate(IC50) were evaluated by Cell Counting Kit-8(CCK8) assay. Western blot, RT-PCR and luciferase assay were performed to determine how TRIB2 regulates miR-33 a-5 p. Immunoprecipitation(IP) and chromatin-immunoprecipitation(ChIP) were used to investigate the molecular mechanisms of *** miR-33 a-5 p promoter was truncated to explore the specific fragment of TRIB2. The point mutation method was used to mutate the active site, and the role of the site was verified by luciferase assay. Blood cell count and blood smear were used to determine the success of model ***: We found that the expression of TRIB2 in the leukemia IM-resistant cells was increased, and the high expression of TRIB2 indicated that the leukemia cells were low in drug sensitivity. Functionally,depletion of TRIB2 inhibits the proliferation of cancer cells and reduces the IC50 value, while the overexpression of TRIB2 accelerates cell growth and promotes cell resistance. At the same time, in vivo experiments with tumor-bearing mice and mouse modeling also verified this result. Through the truncation experiment of miR-33 a-5 p promoter, it was found that c-Fos could play a role in the promoter-534～-1124 fragment. Through IP and ChIP, it was found that the transcription factor c-Fos could inhibit the transcriptional activity of miR-33 a-5 p promoter. Further studies have shown that TRIB2 can regulate c-Fos through the ERK pathway and inhibit the expression of miR-33 a-5 p by enhancing the transcriptional activity of c-Fos. Overexpression of miR-33 a-5 p can inhibit cell growth and reduce the drug resistance of drug-resistant cells, knockdown of m

关键词： TRIB2 CML IM-resistance c-Fos miR-33a-5p

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RFWD2 Knockdown as a Blocker to Reverse the Oncogenic Role of TRIB2 in Lung Adenocarcinoma

RFWD2 Knockdown as a Blocker to Reverse the Oncogenic Role o...

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2021年中国肿瘤标志物学术大会暨第十五届肿瘤标志物青年科学家论坛

作者： Dongmin Liang Hang Sun Jiefei Peng Yulong Zhao Meiling Zhang Youjie Li shuyang xie Binzhou Medical University

RFWD2, an E3 ubiquitin ligase, is overexpressed in numerous human cancers. The roles of RFWD2 in cancer are related to the targeting of its substrates for ubiquitination and degradation. This study aimed to investigate the role of TRIB2 in relation to the regulation of protein degradation through *** Discover results demonstrated that TRIB2 can perform its functions by interacting with RFWD2 or other factors. TRIB2 can interact with and regulate RFWD2, which further attends the proteasome-mediated degradation of the RFWD2 substrate p-IkB-a. TRIB2 colocalizes with RFWD2-related IkB-a to form a ternary complex and further affects the IkB-a degradation by regulating its phosphorylation. TRIB2 acts as an oncogene and promotes cancer cell proliferation and migration,whereas RFWD2 knockdown reversed the role of TRIB2 in promoting cancer cell growth and colony formation in vitro and in vivo. In summary, this study reveals that TRIB2 promotes the progression of cancer by affecting the proteasome-mediated degradation of proteins through the interaction with RFWD2.

关键词： RFWD2 proteasome-mediated degradation TRIB2 cancer therapy target gene

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γ干扰素在特发性肺纤维化中的相关研究进展

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国际呼吸杂志 2014年第24期34卷 1882-1885页

作者：周雪谢书阳吕长俊滨州医学院生化教研室烟台264003 滨州医学院附属医院呼吸内科 256600

特发性肺纤维化是一种病因不明、发病机制不清、缺乏有效治疗手段的弥漫性肺间质疾病,以肺泡上皮损伤、成纤维细胞灶形成、细胞外基质积聚,最终导致肺泡结构异常重塑为病理特征.研究发现,γ干扰素（IFN-γ）能够通过调控信号通路、调控m... 详细信息

特发性肺纤维化是一种病因不明、发病机制不清、缺乏有效治疗手段的弥漫性肺间质疾病,以肺泡上皮损伤、成纤维细胞灶形成、细胞外基质积聚,最终导致肺泡结构异常重塑为病理特征.研究发现,γ干扰素（IFN-γ）能够通过调控信号通路、调控miRNA表达、调节血管再生等发挥抗肺纤维化作用.另有文献报道,IFN-γ可能具有致炎致纤维化的作用.本文针对内源性IFN-γ在特发性肺纤维化发病过程中的作用进行综述,为特发性肺纤维化的发病和治疗提供理论依据.

关键词： γ干扰素特发性肺纤维化信号通路血管再生

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Regulating cells growth by ASO inhibiting miRNA expression

Regulating cells growth by ASO inhibiting miRNA expression

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华东六省一市生物化学与分子生物学会2009年学术交流会

作者： shuyang xie Youjie Li Shuai Zhang Zunling Li Zhen Yue (Institute of Medical Molecular Genetics,Department of Biochemistry and Molecular Biology,Bin Zhou Medical University,264003,P.R.China)

＜正＞To explore the role of miRNAs to induce proliferation or apoptosis of cancer cells,antisense oligonucleotide（ASO） was chosen to inhibit the expression of *** A549/293T cells were treated with antisense oligonu...

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