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Dual-phase contrast-enhancement multislice computed tomography imaging for the assessment of elderly patients with acute myocardial infarction after primary percutaneous coronary intervention

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Journal of Geriatric Cardiology 2009年第1期6卷 20-25页

作者： Shaofeng Guan weiyi fang Xinkai Qu Jianding Ye Yan Shen Jing Jiao Department of Cardiology Shanghai Chest Hospital affiliated to Shanghai JiaoTong UniversityShanghai 200030China

Background Evaluation of acute myocardial infarction after reperfusion by dual phase contrast-enhancement multislice computed tomography(MSCT)was implicated in porcine *** have been few attempts to use this diagnostic modality for the early assessment of coronary reperfusion in patients with ST-elevation myocardial infarction(STEMI),especially after primary percutaneous coronary intervention(PCI).In elderly patients with STEMI,the safety issues remain *** Dual phase contrast-enhancement MSCT examinations were performed in 11 elderly patients(≥60 years old)with STEMI within one week after primary *** presence,location and enhancement pattern on MSCT were *** findings were compared with the catheter angiographic results and area under the curve of creatine kinase(CK)*** creatinine level was recorded before and after MSCT *** MSCT scans were successfully performed in all the *** myocardial perfusion defect(early defect,ED)was detected in all of the 11 patients(100%)in the early phase of the contrast bolus(subendocardial ED in 10 patients and transmural in 1 patient).Mean CT attenuation value of ED was significantly different from CT attenuation value of remote myocardium(46±17 HU vs 104±17 HU;P<0.01).Location of ED area correlated well with infarction related artery territory on catheter angiography in all of the 11 patients(100%).On delayed phase of MSCT scan,different enhancement patterns were observed:isolated subendocardial late enhancement(LE)in 6 patients,subendocardial residual perfusion defect(RD)and subepicardial LE in 1 patient,subendocardial RD in 4 *** volume assessed by MSCT correlated well with area under the curve CK release(R=0.72,P<0.01).Serum creatinine level after MSCT scan showed no difference with that before MSCT *** Dual phase MSCT could be safely implicated in elderly patients with *** abnormal myocardial enhancement patterns were seen on dual ph

关键词： Computed tomography myocardial infarction percutaneous coronary intervention

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VPS33B suppresses lung adenocarcinoma metastasis and chemoresistance to cisplatin

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Genes & Diseases 2021年第3期8卷 307-319页

作者： Zhen Liu Jiahao Liu Yang Li Hao Wang Zixi Liang Xiaojie Deng Qiaofen Fu weiyi fang Ping Xu Affiliated Cancer Hospital&Institute of Guangzhou Medical University Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and DegradationState Key Laboratory of Respiratory DiseaseSchool of Basic Medical SciencesGuangzhou Medical UniversityGuangzhouGuangdong Province510095PR China Cancer Center Integrated Hospital of Traditional Chinese MedicineSouthern Medical UniversityGuangzhouGuangdong Province510310PR China Cancer Institute School of Basic Medical SciencesSouthern Medical UniversityGuangzhouGuangdong Province510515PR China Respiratory Department Peking University Shenzhen HospitalShenzhenGuangdong Province518034PR China

The presence of VPS33B in tumors has rarely been *** VPS33B protein expression is an unfavorable factor that promotes the pathogenesis of lung adenocar-cinoma(LUAD).Overexpressed VPS33B was shown to reduce the migration,invasion,metas-tasis,and chemoresistance of LUAD cells to cisplatin(DDP)in vivo and in *** analyses have indicated that VPS33B first suppresses epidermal growth factor receptor(EGFR)Ras/ERK signaling,which further reduces the expression of the oncogenic factor ***-regulated c-Myc expression reduces the rate at which it binds the p53 promoter and weakens its transcription inhibition;therefore,decreased C-Myc stimulates p53 expression,leading to decreased epithelial-to-mesenchymal transition(EMT)***1 has been shown to be an unfavorable indicator of non-small-cell lung cancer(NSCLC).Here,NESG1 Was identified as an interactive protein of *** addition,NESG1 was found to exhibit mutual stimulation with VPS33B via reduced RAS/ERK/c-Jun-mediated transcription *** of NESG1 activated EGFR/Ras/ERK/c-Myc signaling and further downregulated p53 expression,which thus activated EMT signaling and promoted LUAD migration and ***,we observed that nicotine suppressed VPS33B expression by inducing PI3K/AKT/c-Jun-mediated transcription *** study demonstrates that VPS33B as a tumor suppressor is signif-icantly involved in the pathogenesis of LUAD.

关键词： Chemoresistance Lung adenocarcinoma Metastasis Nicotine VPS33B

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Glioma cell membrane camouflaged cinobufotalin delivery system for combinatorial orthotopic glioblastoma therapy

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Nano Research 2023年第8期16卷 11164-11175页

作者： Zibin Song Liqian Zhao weiyi fang Siyun Guo Anqi Xu Zhengming Zhan Yonghua Cai ShuaiShuai Xue Peng Chai Qiuhua Jiang Peng Zhao Ye Song Department of Neurosurgery Southern Medical University Nanfang HospitalGuangzhou 510515China Institute of Brain Diseases Nanfang Hospital of Southern Medical UniversityGuangzhou 510515China Cancer Center Integrated Hospital of Traditional Chinese MedicineSouthern Medical UniversityGuangzhou 510515China NMPA Key Laboratory for Research and Evaluation of Drug Metabolism Guangdong Provincial Key Laboratory of Cardiac Function and Microcirculation GuangdongProvincial Key Laboratory of New Drug ScreeningSchool of Pharmaceutical SciencesSouthern Medical UniversityGuangzhou 510515China Department of Neurosurgery Ganzhou People's HospitalGanzhou 341000China

Glioblastoma(GBM)belongs to the deadliest primary malignancies with high mortality rate and poor *** the past decades,less progress has been made to treat GBM,owing largely to the lack of effective chemotherapeutics and poor drug accumulation in the glioma *** order to address this issue,we present an efficient biomimetic nanocomposite(Cu_(2−x)Se-CB@MEM,CCM),consisting of Cu_(2−x)Se nanoparticle core modified by cinobufotalin(CB),a toad venom extract,which is camouflaged with glioma cell Ln229 *** is demonstrated that CB can decrease the protein activity of inosine monophosphate dehydrogenase 1(IMPDH1),a key target correlated with prognosis,through intermolecular hydrogen bonding with amino acid residues ARG-105 and *** glioma cell membrane-camouflage endows the CCM with blood-brain barrier penetration and homology tumor-targeted *** optimized cinobufotalin based chemotherapy combining with the near-infrared-II(NIR-II)irradiation shows outstanding inhibition effect to glioma cells,by blocking cell cycle and inducing *** vivo mice bearing orthotopic Ln229 GBM treated with CCM+NIR-II(CCM+L)have significantly suppressed tumor growth and extended survival,without side *** glioma cell membrane camouflaged nanocomposite of Cu_(2−x)Se and cinobufotalin with its significant anti-glioma property and well biosafety will provide novel alternatives for clinical treatment of GBM.

关键词： glioblastoma cinobufotalin biomimetics photothermal therapy blood-brain barrier

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2011-2020年乌鲁木齐市手足口病流行病学特征分析及SARIMA预测模型构建

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中国医药导报 2024年第16期21卷 24-28页

作者：方惟一郝文渊祖力皮卡尔·吐迪陈薇卢耀勤新疆乌鲁木齐市疾病预防控制中心新疆乌鲁木齐830026

目的分析2011-2020年乌鲁木齐市手足口病(HFMD)流行病学特征,构建SARIMA模型预测发病趋势,为完善防控举措提供依据。方法对2011-2020年乌鲁木齐市HFMD病例数据进行描述性流行病学特征分析,建立SARIMA模型。结果乌鲁木齐市2011-2020年HFM... 详细信息

目的分析2011-2020年乌鲁木齐市手足口病(HFMD)流行病学特征,构建SARIMA模型预测发病趋势,为完善防控举措提供依据。方法对2011-2020年乌鲁木齐市HFMD病例数据进行描述性流行病学特征分析,建立SARIMA模型。结果乌鲁木齐市2011-2020年HFMD年均发病率为68.60/10万,重症32例,死亡4例;2011-2019年呈隔年高发趋势,2018年发病率为近10年最高(105.69/10万),季节性明显,呈双峰流行。HFMD年均发病率最高的区县为经开区(头区),达到107.35/10万。男性年均发病率为80.55/10万,女性为56.12/10万,男女比为1.50∶1.00,2011-2019年男性发病率高于女性,差异有统计学意义(P0.05)。发病最小年龄为1 d,最大为67岁,5岁以下儿童病例数占比最高(85.82%);主要为托幼和散居儿童。2011-2020年共检测HFMD标本7778份,阳性率为81.15%,以其他肠道病毒占比最高(46.28%)。SARIMA(1,0,0)(0,1,1)12模型为最优模型。结论乌鲁木齐市HFMD有周期性、季节性、性别、年龄差异,应持续做好监测,加强重点人群防控工作;SARIMA(1,0,0)(0,1,1)12模型拟合较好,与实际发病情况趋势一致,可用于预测乌鲁木齐市HFMD未来发病情况,对指导乌鲁木齐市HFMD防控存在一定理论价值;关注病原分布和变化情况,完善实验室病毒分型。

关键词：手足口病流行病学特征 SARIMA模型

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护士反思性实践与职业偏差行为的关系研究

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护理管理杂志 2024年第7期24卷 625-628页

作者：赵宏张红鸽李莎李媛媛方唯一董静陕西中医药大学第二附属医院心内科咸阳市712046 陕西中医药大学第二附属医院妇三科咸阳市712046 陕西中医药大学第二附属医院科研科咸阳市712046

目的探究护士反思性实践、职业偏差行为现状,分析二者的关系,为实施针对性干预措施提供参考。方法2023年5月至8月,采用一般资料问卷、护士反思性实践问卷、护士职业偏差行为量表对陕西省5所三级甲等医院的1532名临床护士开展调查。结果... 详细信息

目的探究护士反思性实践、职业偏差行为现状,分析二者的关系,为实施针对性干预措施提供参考。方法2023年5月至8月,采用一般资料问卷、护士反思性实践问卷、护士职业偏差行为量表对陕西省5所三级甲等医院的1532名临床护士开展调查。结果护士反思性实践总分为(146.29±9.23)分、职业偏差行为总分为(34.66±5.68)分。护士反思性实践与职业偏差行为呈负相关性(r=-0.532,P<0.01)。年龄、职称、工作年限、反思性实践是护士职业偏差行为的主要影响因素(P<0.001)。结论护士反思性实践处于较高水平,职业偏差行为处于较低水平,护理管理者可以从反思性实践层面出发,引导护士在实践过程中进行反思,提高分析问题、解决问题的能力,从而指导护理行为,进一步减少护士职业偏差行为。

关键词：护士反思性实践职业偏差行为

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CCDC65,A Gene Knockout That Leads to Early Death of Mice,Acts as A Potentially Novel Tumor Suppressor in Lung Adenocarcinoma

CCDC65,A Gene Knockout That Leads to Early Death of Mice,Act...

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2022CCTB中国肿瘤标志物学术大会暨中国整合肿瘤学大会暨第十六届肿瘤标志物青年科学家论坛暨中国肿瘤标志物产业创新大会

作者： Ziyan Zhang weiyi fang Integrated Hospital of Traditional Chinese Medicine Southern Medical University

CCDC65 is a member of coiled-coil domain-containing protein family and was only reported in gastric cancer by our *** first observed that it is downregulated in lung adenocarcinoma based on TCGA database and *** CCDC65protein was shown as an unfavorable factor promoting the clinical progression in lung ***,CCDC65-/-mice were found possibly dead of *** with the CCDC65+/+ mice,the downregulation of CCDC65 in CCDC65+/-mice significantly increased the formation ability of lung cancer induced by *** subsequent investigation,we observed that CCDC65 functions as a tumor suppressor repressing cell proliferation in vitro and in *** mechanism showed that CCDC65recruits E3 ubiquitin ligase FBXW7 to induce the ubiquitination degradation of c-Myc,an oncogenic transcription factor in tumors,and reduces the binding with ENO1 promoter and thus suppresses the expression of ENO1 in mRNA *** addition,CCDC65 also recruited FBXW7 to degrade ENO1 protein by ubiquitinated *** downregulated ENO1 further reduced the phosphorylation activation of AKT1,which thus inactivated cell cycle *** data demonstrated that CCDC65 is a potential tumor suppressor by recruiting FBWX7 to suppress c-Myc/ENO1-induced cell cycle signal in lung adenocarcinoma.

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ENKUR expression induced by chemically synthesized cinobufotalin suppresses malignant activities of hepatocellular carcinoma by modulating β-catenin/c-Jun/MYH9/USP7/c-Myc axis

ENKUR expression induced by chemically synthesized cinobufot...

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2022CCTB中国肿瘤标志物学术大会暨中国整合肿瘤学大会暨第十六届肿瘤标志物青年科学家论坛暨中国肿瘤标志物产业创新大会

作者： Rentao Hou weiyi fang Cancer Center Integrated Hospital of Traditional Chinese MedicineSouthern Medical University

ENKUR plays a crucial role in lung and colorectal *** synthesized cinobufotalin(CB) showed its significant anti-cancer effect in nasopharyngeal ***,the roles of ENKUR and CB along with their correlation are still unknown in hepatocellular carcinoma(HCC).In this study,ENKUR expression in HCC tissue and cells were *** relationship between ENKUR expression and clinical pathology was also *** vivo and in vitro experiments were conducted to explore the effects and molecular basis of ENKUR and CB in *** expression was correlated with HCC progression and patient ***,ENKUR could inhibit tumor proliferation,metastasis,and sorafenib resistance in *** studies showed that ENKUR or its Enkurin domain could bind to MYH9 and decrease its expression by binding to β-catenin and inhibiting its nuclear transfer,thus decreasing c-Jun *** expression of MYH9suppressed recruitment of deubiquitination enzyme USP7,promoting degradation of the ***,cell cycle and EMT signals were *** as a safe and effective anti-cancer compound up-regulates the expression of ENKUR via inhibiting PI3K/AKT/c-Jun-mediated transcription *** findings show that ENKUR induced by CB antagonizes β-catenin/c-Jun/MYH9/USP7 pathway,thus increasing c-Myc ubiquitin degradation and finally suppressing cell cycle and EMT signals.

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Chemically synthesized cinobufagin suppresses nasopharyngeal carcinoma metastasis by inducing ENKUR to stabilize p53 expression

Chemically synthesized cinobufagin suppresses nasopharyngeal...

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2022CCTB中国肿瘤标志物学术大会暨中国整合肿瘤学大会暨第十六届肿瘤标志物青年科学家论坛暨中国肿瘤标志物产业创新大会

作者： Rentao Hou weiyi fang Cancer Center Integrated Hospital of Traditional Chinese MedicineSouthern Medical University

Clinically,the metastasis of tumor cells is the key factor of death in patients with *** this study,we used a model of metastatic nasopharyngeal carcinoma(NPC) to explore the effects of a new chemical,cinobufagin(CB),combined with cisplatin(DDP).We observed that chemically synthesized CB strongly decreased the metastasis of ***,a better therapeutic effect was shown when CB was combined with *** analysis revealed that CB induced ENKUR expression by deregulating the PI3K/AKT pathway and suppressing c-Jun,an oncogenic transcriptional factor that binds to the ENKUR promoter and negatively modulated its expression in *** as a tumor suppressor binds to MYH9and decreases its expression by recruiting β-catenin via its enkurin domain to prevent its nuclear accumulation,which therefore suppresses c-Jun-induced MYH9 ***,downregulated MYH9 reduces the enlistment of E3 ligase UBE3A and thus decreases the UBE3A-mediated ubiquitination degradation of p53,a key tumor suppressor that decreases epithelial-mesenchymal transition(EMT).Clinical sample analysis demonstrated that the ENKUR expression level was significantly reduced in NPC *** decreased expression substantially promoted clinical progression and reflected poor prognosis for patients with *** study demonstrated that CB induced ENKUR to repress the β-catenin/c-Jun/MYH9 signal and thus decreased UBE3A-mediated p53 ubiquitination *** a result,the EMT signal was inactivated to suppress NPC metastasis.

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Elevated nuclear CCND1 expression confers an unfavorable prognosis for early stage lung adenocarcinoma patients

Elevated nuclear CCND1 expression confers an unfavorable pro...

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第八次全国中西医结合变态反应学术会议暨首届深圳市中西医结合变态反应学术会议暨第十届深圳呼吸论坛

作者： Ping Xu Mengyang Zhao weiyi fang Peking University Shenzhen Hospital

Purposes:To examine the expression pattern of CCND1 and analyze the correlation of its nuclear expression with clinicopathologic features and prognosis in lung ***:CCND1 mRNA and protein levels in lung adenocarcinoma tissues were *** relationship between nuclear CCND1 protein expression and clinical features including survival prognosis was

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Chemical compound cinobufotalin potently induces FOXO1-stimulated cisplatin sensitivity by antagonizing its binding partner MYH9

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Signal Transduction and Targeted Therapy 2019年第1期4卷 214-225页

作者： YongHao Li Xiong Liu Xian Lin Menyang Zhao Yanyi Xiao Chen Liu Zixi Liang Zelong Lin Renhui Yi Zibo Tang Jiahao Liu Xin Li Qingping Jiang Libo Li Yinyin Xie Zhen Liu weiyi fang Cancer Center Integrated Hospital of Traditional Chinese MedicineSouthern Medical University510315GuangzhouChina Department of Otolaryngology-Head and Neck Surgery Nanfang HospitalSouthern Medical UniversityGuangzhouChina Cancer Institute Southern Medical University510515GuangzhouChina Department of Pathology Third Affiliated HospitalGuangzhou Medical University510150GuangzhouChina Key Laboratory of Protein Modification and Degradation School of Basic Medical SciencesAffiliated Cancer Hospital and Institute of Guangzhou Medical University511436GuangzhouChina

In this study,we present novel molecular mechanisms by which FOXO1 functions as a tumor suppressor to prevent the pathogenesis of nasopharyngeal carcinoma(NPC).First,we observed that FOXO1 not only controlled tumor stemness and metastasis,but also sensitized NPC cells to cisplatin(DDP)in vitro and in *** studies demonstrated that FOXO1-induced miR-200b expression through the GSK3β/β-catenin/TCF4 network-mediated stimulation of ZEB1,which reduced tumor stemness and the epithelial–mesenchymal transition(EMT)***,we observed FOXO1 interaction with MYH9 and suppression of MYH9 expression by modulating the PI3K/AKT/c-Myc/P53/miR-133a-3p *** MYH9 expression not only reduced its interactions with GSK3β,but also attenuated TRAF6 expression,which then decreased the ubiquitin-mediated degradation of GSK3β*** GSK3βexpression stimulated theβ-catenin/TCF4/ZEB1/miR-200b network,which increased the downstream tumor stemness and EMT ***,we observed that chemically synthesized cinobufotalin(CB)strongly increased FOXO1-induced DDP chemosensitivity by reducing MYH9 expression,and the reduction in MYH9 modulated GSK3β/β-catenin and its downstream tumor stemness and EMT signal in *** clinical samples,the combination of low FOXO1 expression and high MYH9 expression indicated the worst overall survival *** studies demonstrated that CB potently induced FOXO1-mediated DDP sensitivity by antagonizing its binding partner MYH9 to modulate tumor stemness in NPC.

关键词： FOXO1 GSK3β cisplatin

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