Preliminary investigation of tumor angiogenesis and blood flow pattern in solitary bronchogenic
关于抗衰老研究进展的英文原文文献
Aging by Telomere Loss Can Be ReversedBruno Bernardes de Jesus 1and Maria A.Blasco 1,*1Telomeresand Telomerase Group,Molecular Oncology Program,Spanish National Cancer Centre (CNIO),Melchor Ferna´ndez Almagro 3,Madrid E-28029,Spain*Correspondence:mblasco@cnio.es DOI 10.1016/j.stem.2010.12.013Recently in Nature ,Jaskelioff et al.(2010)demonstrated that multiple aging phenotypes in a mouse model of accelerated telomere loss can be reversed within 4weeks of reactivating telomerase.This raises the major question of whether physiological aging,likely caused by a combination of molecular defects,may also be reversible.Accumulation of short/damaged telo-meres with increasing age is considered one of the main sources of aging-associ-ated DNA damage responsible for the loss of regenerative potential in tissues and during systemic organismal aging (Harley et al.,1990;Flores et al.,2005).Mounting evidence suggests that telome-rase is a longevity gene that functions by counteracting telomere attrition.Thus,telomerase-deficient mice age prema-turely,and telomerase overexpression results in extended longevity in mice (Tomas-Loba et al.,2008).Moreover,human mutations in telomerase compo-nents produce premature adult stem cell dysfunction and decreased longevity (Mitchell et al.,1999).Previous work had shown that restora-tion of telomerase activity in mouse zygotes with critically short telomeres,owing to a deficiency in the telomerase RNA component (Terc),rescues critically short telomeres and chromosomal instability in the resulting mice (Samper et al.,2001).Restoration of telomerase activity in zygotes also pre-vented the wide range of degenerative pathologies that would otherwise appear in telomerase-deficient mice with critically short telomeres,including bone marrow apla-sia,intestinal atrophy,male germ line depletion,and adult stem cell dysfunction (Samper et al.,2001;Siegl-Cachedenier et al.,2007),and resulted in a normal organismal life-span (Siegl-Cachedenier et al.,2007).Together,all the above find-ings indicate that aging provoked by crit-ical telomere shortening can be prevented or delayed by telomerase reactivation.From these grounds,reversion of aging caused by telomere loss was the next frontier.A recent study in Nature takes an important step forward from these previous findings by using a new mouse model for telomerase deficiency,de-signed to permit telomerase reactivation in adult mice after telomere-induced aging phenotypes have been established (Jas-kelioff et al.,2010).Specifically,DePinho and colleagues generated a knockin allele encoding a 4-OH tamoxifen (4-OHT)-inducible mouse telomerase (TERT-ER)under the control of the TERT endogenous promoter.In the absence of tamoxifen,these mice exhibit premature appearance of aging pathologies and reduction in survival (Figure 1).These mice phenocopy previously described Terc -deficient mice,which highlights that elongation of short telomeres by telomerase is the main mechanism by which telomerase protects from aging pathologies.Importantly,4weeks of tamoxifen treatment to induce TERT re-expression in adult TERT-ER mice with clear signs of premature aging was sufficient to extend their telomeres and rescue telomeric DNA damage signaling and associated check-point responses.Dramatically,tamox-ifen-induced TERT re-expression also led to resumption of proliferation in quies-cent cultured cells and eliminated the degenerative phenotypes across multiple organs,including testis,spleen,and intes-tines (Figure 1).Reactivation of telome-rase also ameliorated the decreased survival of TERT-ER mice.These findings represent an important advance in the aging field,as they show that aging induced by telomere loss can be reversed in a broad range of tissues and cell types,including neuronal function.Looking to the future,the next key question is to whatextent natural,physiological aging is caused by the pres-ence of critically short telo-meres and,consequently,to what extent telomere restora-tion will be able to reverse physiological aging.In this re-gard,other recent findings support the idea that telomere shortening does impactnatural mouse aging.On onehand,despite the long-standing belief that mouseaging was not linked to telo-mere shortening giventhat Figure 1.Antiaging Effects of Telomerase Schematic showing the major findings of Jaskelioff et al.(2010).Telomerasereactivation in late generation telomerase-deficient mice (G4TERT-ER )couldrevert some of the aging phenotypes observed,demonstrating the regenera-tive potential capacity of different tissues.Cell Stem Cell 8,January 7,2011ª2011Elsevier Inc.3Cell Stem CellPreviewsmice are born with very long telomeres—much longer than human telomeres—mouse telomeres do suffer extensive shortening associated with aging(Flores et al.,2008).In particular,while mouse cells maintain relatively long telomeres during theirfirst year of life,there is a dramatic loss of telomeric sequences at2years of age,even in various stem cell populations, and this change is concomitant with the loss of regenerative capacity associated with mouse aging.In addition,telome-rase-deficient mice from thefirst genera-tion(G1TercÀ/À)exhibit a significant decrease in median and maximum longevity and a higher incidence of age-related pathologies and stem cell dysfunc-tion compared with wild-type mice(Flores et al.,2005;Garcia-Cao et al.,2006),indi-cating that,as in humans,telomerase activity is rate limiting for natural mouse longevity and aging.These results suggest that strategies aimed to increase telome-rase activity may delay natural mouse aging.Further supporting this notion,it was recently shown that overexpression of TERT in the context of mice engineered to be cancer resistant owe to increase expression of tumor suppressor genes(Sp53/Sp16/SARF/TgTERT mice)wassufficient to decrease telomere damagewith age,delay aging,and increase medianlongevity by40%(Tomas-Loba et al.,2008).However,it remains to be seenwhether telomerase reactivation late in lifewould be sufficient to delay natural mouseaging and extend mouse longevity withoutincreasing cancer incidence.In summary,these proof-of-principlestudies using genetically modified miceare likely to encourage the developmentof targeted therapeutic strategies basedon reactivation of telomerase function.Indeed,small molecule telomerase acti-vators have been reported recently andhave demonstrated some preliminaryhealth-span beneficial effects in humans(Harley et al.,2010).Identifying drugabletargets and candidate activators clearlyopens a new window for the treatment ofage-associated degenerative diseases.REFERENCESFlores,I.,Cayuela,M.L.,and Blasco,M.A.(2005).Science309,1253–1256.Flores,I.,Canela,A.,Vera,E.,Tejera,A.,Cotsare-lis,G.,and Blasco,M.A.(2008).Genes Dev.22,654–667.Garcia-Cao,I.,Garcia-Cao,M.,Tomas-Loba,A.,Martin-Caballero,J.,Flores,J.M.,Klatt,P.,Blasco,M.A.,and Serrano,M.(2006).EMBO Rep.7,546–552.Harley, C.B.,Futcher, A.B.,and Greider, C.W.(1990).Nature345,458–460.Harley, C.B.,Liu,W.,Blasco,M.,Vera, E.,Andrews,W.H.,Briggs,L.A.,and Raffaele,J.M.(2010).Rejuvenation Res.14,in press.Publishedonline September7,2010.10.1089/rej.2010.1085.Jaskelioff,M.,Muller,F.L.,Paik,J.H.,Thomas,E.,Jiang,S.,Adams,A.C.,Sahin,E.,Kost-Alimova,M.,Protopopov,A.,Cadinanos,J.,et al.(2010).Nature.10.1038/nature09603.Mitchell,J.R.,Wood,E.,and Collins,K.(1999).Nature402,551–555.Samper,E.,Flores,J.M.,and Blasco,M.A.(2001).EMBO Rep.2,800–807.Siegl-Cachedenier,I.,Flores,I.,Klatt,P.,andBlasco,M.A.(2007).J.Cell Biol.179,277–290.Tomas-Loba, A.,Flores,I.,Fernandez-Marcos,P.J.,Cayuela,M.L.,Maraver,A.,Tejera,A.,Borras,C.,Matheu,A.,Klatt,P.,Flores,J.M.,et al.(2008).Cell135,609–622.HGPS-Derived iPSCs For The AgesTom Misteli1,*1National Cancer Institute,NIH,Bethesda,MD20892,USA*Correspondence:mistelit@DOI10.1016/j.stem.2010.12.014In this issue of Cell Stem Cell,Zhang et al.(2011)generate patient-derived iPSCs for one of the major prema-ture aging diseases,Hutchinson-Gilford Progeria Syndrome(HGPS).These cells are a much-needed new tool to study HGPS,and their use may lead to novel insights into mechanisms of aging.Some problems in biology are more difficult to study than others.Human aging is certainly one of them.Most conclusions regarding molecular mecha-nism of human aging rely on mere correla-tion,and direct experimental testing is generally not feasible.One approach to dissect the molecular basis of human aging is to study naturally occurring premature aging disorders.One of the most dramatic and prominent of such diseases is Hutchinson-Gilford ProgeriaSyndrome(HGPS).Zhang et al.(2011)now report the generation of inducedpluripotent stem cells(iPSCs)fromHGPS cells,providing a powerful newtool to unravel the molecular and physio-logical mechanisms of premature andnormal aging.HGPS is a truly remarkable disease inmany ways.To start with,it affects anunusually wide spectrum of tissues andleads to the development of highly diversesymptoms ranging from depletion ofsubcutaneous fat to loss of hair andtendon contractures.The diversity ofaffected tissues pointed early on to stemcell defects as a likely disease mecha-nism.Most relevant in patients arevascular defects and recurring strokes,which invariably are fatal in patients intheir mid-to late teens(Hennekam,2006).The disease is exceedingly rare4Cell Stem Cell8,January7,2011ª2011Elsevier Inc.Cell Stem Cell Previews。
眼科常用英文缩略语名词解释
中华实验眼科杂志2021年2月第39卷第2期Chin J Exp Ophthalmol, February2021,Vol.39,No.2-171-stripping endothelial keratoplasty+J].J Cataract Refract S ui/,2007, 33(1':152-155.DOI：10.1016/j.jcrs.2006.07.044.+40]Cheng YY,HendriCsc F,Pels E,et at.Preliminary results of oemtosecond aasea-a s isted Descemetstaippingendotheaiaakeaatopaasty +J].Arch Ophthalmol,2008,126(10':1351-1356.DOI：10.1001/ aachopht.126.10.1351.+41]Hosny MH,Marric A,Ka/m Sidky M,et at.Results of femtosecand aasea-a s isted Descemetstaipping automated endotheaiaakeaatopaasty +J/OL].J Ophthalmol,2017,2017:8984367+2020-06-06].h t ps：jjwww.ncbi.n jpmc ja atic aes jPMC5485480j.DOI：10.1155/2017/8984367.+42]Rosa AM,Silva MF,Quadrado MJ,et at.Femtosecand laser and micaokeaatome-a s isted Descemetstaippingendotheaiaakeaatopaasty：oiast clinical results+J].Br J Ophthalmol,2013,97(9':1104-1107.DOI:10.1136jb.ophtha amo a-2012-302378.+43]Hjorthal J,Nielsen E,Vesteryaard A,et at.Inverse cutting of posterior lamellar carneal grafts by a femtosecand laser+J].Open Ophthalmol J, 2012,6:19-22.DOI：10.2174/1874364101206010019.+44]Pilger D,van Sonnleithnes C,Bertelmann E,et at.Femtosecand1^-assisted descemetoahexis：a noveatechnique in Descemetmembaane endothelial keratoplasty+J].Cornea,2016,35(10':1274-1278.DOI:10.1097jICO.0000000000000987.+45]McKee HD,Jhanji V.Femtosecand laser-assisted graft preparation for Desccmet membrane endothelial keratoplasty+J].Cornea,2018,37(10):1342-1344.DOI：10.1097/ILO.0000000000001633.+46]Jones YJ,Goins KM,Sutphin JE,et parison of the femtosecand laser(IntraLase)versus manual microkeratome(Moria ALTK)in di s ection oothedonoain endotheaiaakeaatopaasty：initiaastudyin eye bank eyes+J].Cornea,2008,27(1):88-93.DOI：10.1097/ILO.0b013e31815771o5.+47]Cheng YY,van den Bera TJ,Schouten JS,et at.Quality of vision after oemtosecond aasea-assisted Descemetstaippingendotheaiaakeaatopaasty and penetrating keratoplasty：a randomized,multicentes clinical trial +J].Am J Ophthalmol,2011,152(4):556-566.DOI：10.1016/j.a.o.2011.03.012.+48]Soong HK,Mian S,Abbasi O,et at.Femtosecand laser-assisted posterior aame a akeaatopaasty：initiaastudiesoosuagicaatechniquein eyebank eyes[J].Ophthalmolooy,2005,112(1):44-49.DOI：10.1016/j.ophtha.2004.06.037.+49]Hindman HB,McCally RL,Myrowitz E,et at.Evaluation of deep aame a a a endotheaiaa keaatopaasty suageay using sca t eaometay and wavefront analyses+J].Ophthalmolooy,2007,114(11):2006-2012.DOI：10.1016j..ophtha.2007.01.009.(收稿日期：2020-11-20修回日期：2020-12-10)(本文编辑:刘艳施晓萌)读者•作者•编者眼科常用英文缩略语名词解释AMD:年龄相关性黄斑变性(aac-related maculaf degenerLion) ANOVA:单因素方差分析(ong-poy analysiz of variance)BUT:泪膜破裂时间(breakup time o-tear file)DR:糖尿病视网膜病变(diabetic retinopathy)EAU:实验性自身免疫性葡萄膜炎(expe/mentat auwimmune uveitif) EGF：表皮生长因子(epidermal growth factor)ELISA：酶联免疫吸附测定(enzyme-linked imimunosorbent assay) ERG：视网膜电图(xcctroretinovram)FFA:荧光素眼底血管造影(fundus tuoresccin angiovraphy)F'F:成纤维细胞生长因子(fibroblait growth factor)GFP：绿色荧光蛋白(green iuorescent protein)IPN--:$干扰素()00X0--$)IL：白细胞介素(interleukin)IOL：人工晶状体(intraoculaf lent)IRBP：光间受体视黄类物质结合蛋白(inteaphotoaeceptoaaetinoid binding protein)LASIK：准分子激光角膜原位磨镶术(laser in situ keratomileusif) ICGA：吲哚菁绿血管造影(indacyonine green angiovraphy) LECs:晶状体上皮细胞(lent epithelial calls)miRNA：微小RNA(micaoRNA)MMP:基质金属蛋白酶(matrin metaLoproteinase)mTOR:哺乳动物类雷帕霉素靶蛋白(mammalian target of aapamycin)MTT:四甲基偶氮唑盐(methyl thiazolyS tetrazoLum)NF:核转录因子(nuclear factor)OCT：光相干断层扫描(optica acohe ence tomog aphy)OR：优势比(odds4atio)PACG：原发性闭角型青光眼(primary anglc-closurc glauccma) PCR:聚合酶链式反应(polymerase chain reaction)RGCs：视网膜节细胞(retinal ganglion ceHs)POAG：原发性开角型青光眼(primary open angle glauccma) RB：视网膜母细胞瘤(retinoblastoma)RPE:视网膜色素上皮(retinal pigment epitheLum)RNV:视网膜新生血管(retinal necvvscularization)RP:视网膜色素变性(retinitiz pigmentosa)S I t：基础泪液分泌试验(Schirmcr I test)shRNA:小发夹RNA(short hairpin RNA)siRNA:小干扰RNA(small interfering RNA)a-SMA:a-平滑肌肌动蛋白(acmooth musclc actin)TAO：甲状腺相关眼病(thy aoid-associated ophthamopathy)T'F:转化生长因子(transforming growth factor)TNF:肿瘤坏死因子(tumor nccrosiz factor)UBM:超声生物显微镜(ultrasound biomicrosccpc)VEGF：血管内皮生长因子(vascular endothelial growth factor) VEP:视觉诱发电位(visual cveked potential)(本刊编辑部)。
医学英语写作与翻译
第三部分医学英语的写作任务一标题的写作（Title）标题的结构1. 名词+介词Blindness（视觉缺失）after Treatment for Malignant Hypertension 2. 名词+分词Unilateral Neurogenic Pruritus Following Stroke中风后单侧神经性瘙痒3. 名词+不定式Suggestion to Abolish Icterus Index Determination（黄疸指数测定）where Quantitative Bilirubin Assay（胆红素定量）is Available建议能做胆红素定量的化验室不再做黄疸指数测定4. 名词+同位语Gentamicine, a Selelctive Agent for the isolation of Betahemolytic Streptocc ociβ-溶血性链球菌庆大霉素是分离β-溶血性链球菌的选择性药物5. 名词+从句Evidence that the V-sis Gene Product Transforms by Interaction with the Receptor for Platelet-derived Growth Factor血小板源性生长因子.V-sis 基因产物由血小板生成因子受体相互作用而转化的依据6. 动名词短语Preventing Stroke in patients with Atrial Fibrillation心房纤维性颤动心旁纤颤患者中风预防Detecting Acute Myocardial Infarction（急性心肌梗死）byRadio-immunoassay for Creative Kinase（酐激酶）用放射免疫法测定酐激酶诊断急性心肌梗死7. 介词短语On Controlling Rectal Cancer8. 陈述句Dietary Cholesterol is Co-carcinogenic协同致癌因素for Human Colon Cancer9. 疑问句Home or Hospital BirthsIs Treatment of Borderline Hypertension Good or Bad?注意副标题的作用1．数目：Endoluminal Stent-graft 带支架腔内搭桥for Aortic Aneurysms动脉瘤: A report of 6 cases带支架腔内搭桥治疗动脉瘤的六例报告2．重点：Aorto-arteritis 大动脉炎Chest X-ray Appearance and Its Clinical Significance大动脉炎胸部X线表现及临床意义3．方法：Gallstone Ileus（胆结石梗阻）: A Retrospective Study 4．作用：Carcinoembryonic Antigen in Breast-cancer Tissue: A useful prognostic indictor乳腺癌组织中癌胚抗原——一种有用的预后指示5．疑问：Unresolved—Do drinkers have less coronary heart disease? 6．连载顺序：Physical and Chemical Studies of Human Blood Serum: II. A study of miscellaneous Disease conditions人类血清的理论研究：II. 多种病例的研究7．时间：A Collaborative 综合Study of Burn Nursing in China: 1995-1999常见标题句式举例1. 讨论型：Discussion of/ on; An approach to; A probe into; Investigation of; Evaluation of / on汉语中的“初步体会”、“试论”、“浅析”之类的谦辞可以不译。
硕士研究生学位论文
北京大学硕士学位论文硕士研究生学位论文题目：放疗后非小细胞肺癌原发灶退缩规律初步探讨姓 名： 郑东勇学 号： 10601050院 系： 数学科学学院专 业： 概率论与数理统计研究方向： 数理统计理论及应用导师姓名： 刘力平教授 姜明教授二00九 年 六 月版权声明任何收存和保管本论文各种版本的单位和个人，未经本论文作者同意，不得将本论文转借他人，亦不得随意复制、抄录、拍照或以任何方式传播。
否则，引起有碍作者著作权之问题，将可能承担法律责任。
北京大学硕士学位论文摘要现阶段我国肺癌的发病率持续增高，其中非小细胞肺癌占大多数。
对于这类患者目前标准治疗为同时放化疗，然而放疗后大部分患者有部分肿瘤残存，这成为日后肿瘤复发和远地转移的根源。
目前多数方法采取对肺内肿块的整体加大治疗剂量，然而整体加量方法可能会引起各类放疗并发症。
如果能够结合放疗前后的临床数据建立肿瘤的退缩规律，在实际治疗的过程中对原始肿块整体适当加量的同时利用调强放疗技术给予预测的部位施加更高剂量，从而达到减少乃至消除肿瘤残存的目的。
本文利用回归分析方法处理得到的临床样本数据，得到非小细胞肺癌退缩规律的初步结果，主要工作有：1.简单介绍几种常用的回归方法，重点介绍支持向量机方法。
2.结合已有的样本数据，比较各种方法的优劣，得到非小细胞肺癌退缩规律的初步结果。
关键词：非小细胞肺癌、退缩规律、回归分析、支持向量机、核函数The Preliminary Study of Tumor Regression forNon-small Cell Lung Cancer after RadiotherapyDong Yong Zheng (Statistics)Directed by Professor Li Ping Liu & Professor Ming JiangLung cancer is one of the most common causes of cancer-related death. For a large number of patients surgery is inappropriate either because of locally advanced disease or because of comorbidity. For these patients the only potentially curative treatment modality is radical radiotherapy or concurrent radiochemotherapy.However, most patients after radiotherapy have tumor nidus, which has become the source of future recurrence and metastasis.The current popular method is increasing treating dose overall the tumor, but it may cause some complications.If we can develop the shrinkage principle of the tumor with clinical data before and after treatment, then we can increase the treating dose overall tumor in treatment process, at the same time use Intensity Modulated Radiation Technology to give the forecast position a higher dose, this may results in the reduction or elimination of tumor nidus.This thesis deals with clinical samples with regression analysis methods, and gets the preliminary results of shrinkage principle for non-small cell lung cancer.Keywords: non-small cell lung cancer shrinkage principle regression analysis support vector machine kernel function.北京大学硕士学位论文目录第一章 序言 (6)1.1 国内外研究热点 (6)1.2 “瘤根靶向放疗”理论 (7)1.3 技术路线和实验目的 (8)第二章 传统回归分析方法 (10)2.1 线性回归 (10)2.1.1 最小二乘估计及性质 (11)2.1.2 拟合和预测 (12)2.1.3 异常值检验 (13)2.1.4 最小一乘估计 (13)2.2 非参数回归 (15)2.2.1 核函数估计 (15)2.2.2 非参数估计的优缺点 (17)第三章 支持向量机 (19)3.1 支持向量分类 (19)3.1.1 线性可分情况 (20)3.1.2 近似线性可分情况 (23)3.1.3 一般情况 (26)3.2 核函数 (30)3.2.1 多项式空间和多项式核 (30)3.2.2 Mercer核和正定核 (31)3.2.3 核函数的构造原则及常用的核函数 (33)3.3 VC维和结构风险最小化原则 (35)3.3.1 损失函数和期望风险 (35)3.3.2 经验风险和函数集的VC维 (35)3.3.3 结构风险最小化原则 (37)3.4 支持向量回归 (41)3.4.1 常用的损失函数 (42)3.4.2 支持向量回归 (42)第四章 实验结果 (52)4.1 线性回归 (52)4.1.1 样本所含变量相关性分析 (52)4.1.2 线性回归分析 (54)4.2 最小一乘回归 (61)4.3 非参数回归 (61)4.4 支持向量回归 (63)4.5 各种方法的比较 (68)第五章 结论 (69)5.1结论 (69)5.2效果不理想可能存在的原因 (69)第一章 序言本文的工作来自于国家自然科学基金委员会《放疗后非小细胞肺癌原发灶退缩规律数学模型建立》课题组，课题编号：30870738，该课题是北京大学临床肿瘤学院和北京大学数学科学学院的合作项目，项目负责人为北京大学临床肿瘤医院的朱广迎教授。
脑部肿瘤图像分割技术的研究
医学图像分割方法 ...............................................................................6 不含噪声的 MRI 脑部肿瘤图像分割结果........................................14 含噪声的 MRI 脑肿瘤图像分割结果................................................15 粒子群优化算法流程图 .....................................................................21 不含噪声的 MRI 脑部肿瘤图像分割结果........................................22 含噪声的 MRI 脑部肿瘤图像分割结果............................................23 平面曲线演化 .....................................................................................27 曲线的曲率演化 .................................................................................27 闭合曲线的常量演化(V=1) ...............................................................28 “曲线变短流” 和“面积减小流”的对比 ............................................28 演化的水平集及嵌入的曲面 .............................................................30 具有不同初始轮廓的 MRI 脑部肿瘤图像分割结果........................39 初始轮廓不完全包含脑肿瘤的分割结果 .........................................39 含噪声的 MRI 脑部肿瘤图像分割结果............................................39 不含噪声的 MRI 脑部肿瘤图像分割结果........................................45 初始轮廓不完全包含脑肿瘤的分割结果 .......................................46 分析法工作流程 .................................................................................49 实验法工作流程 .................................................................................50 本文研究算法的分割结果 .................................................................52
灵芝三萜化合物的抗肿瘤靶点预测与活性验证
灵芝三萜化合物的抗肿瘤靶点预测与活性验证作者：杜国华王宏旭闫征刘莉莹陈若芸来源：《中国中药杂志》2017年第03期[摘要]研究发现灵芝三萜类化合物具有抗肿瘤活性，但其作用靶点尚不清楚，该试验主要研究灵芝三萜类化合物的抗肿瘤活性并对其可能的作用靶点进行预测。
采用Discovery Studio 软件的LibDock模块，以灵芝子实体中的26种三萜类化合物作为配体，分别与抗肿瘤作用明确的11个靶点蛋白进行分子对接，获得对接的打分结果，评判配体与靶点蛋白受体结合的亲和力，从而进行灵芝三萜类化合物抗肿瘤的虚拟筛选，探讨可能的作用靶点。
同时，MTT实验检测26种灵芝三萜类化合物对5种肿瘤细胞的抑制能力，计算IC50，以此反映化合物的抗肿瘤活性。
对接结果表明，对接位置数目大于5，且对接得分高于100，可以作为判断化合物是否具有活性的阈值，据此筛选出8种灵芝三萜类化合物可能具有抗肿瘤活性，其中5个具有多靶点作用的三萜成分。
MTT细胞实验显示，灵芝酸Y对肺癌细胞H460显示了一定的抑制活性，IC50为22.4 μmol·L-1，其次是7-oxo-ganoderic acid Z2，IC50为43.1 μmol·L-1。
其他三萜类化合物对被测肿瘤细胞株未显示活性或活性很弱。
该研究建立的分子对接虚拟筛选方法可用于灵芝抗肿瘤活性成分的初步筛选，通过该方法的筛选，结合MTT细胞毒活性实验结果，发现灵芝酸Y具有抗肿瘤，尤其抗肺癌开发的潜在可能性，7-oxo-ganoderic acid Z2和ganoderon B具有一定的抑制活性，其抗肿瘤作用有待于进一步深入研究，该研究结果可为抗肿瘤药物的研制提供参考。
[关键词]灵芝子实体；三萜类化合物；抗肿瘤；分子对接；虚拟筛选[Abstract]It has reported that Ganoderma lucidum triterpenoids had anti-tumor activity. However， the anti-tumor target is still unclear. The present study was designed to investigate the anti-tumor activity of G. lucidum triterpenoids on different tumor cells， and predict their potential targets by virtual screening. In this experiment， molecular docking was used to simulate the interactions of 26 triterpenoids isolated from G. lucidum and 11 target proteins by LibDock module of Discovery Studio2016 software， then the anti-tumor targets of triterpenoids were predicted. In addition， the in vitro anti-tumor effects of triterpenoids were evaluated by MTT assay by determining the inhibition of proliferation in 5 tumor cell lines. The docking results showed that the poses were greater than five， and Libdock Scores higher than 100， which can be used to determine whether compounds were activity. Eight triterpenoids might have anti-tumor activity as a result of good docking， five of which had multiple targets. MTT experiments demonstrated that the ganoderic acid Y had a certain inhibitory activity on lung cancer cell H460， with IC50of 22.4 μmol·L-1，followed by 7-oxo-ganoderic acid Z2， with IC50of 43.1 μmol·L-1. However， the other triterpenoids had no anti-tumor activity in the detected tumor cell lines. Taking together， molecular docking approach established here can be used for preliminary screening of anti-tumor activity of G.lucidumingredients. Through this screening method， combined with the MTT assay， we can conclude that ganoderic acid Y had antitumor activity， especially anti-lung cancer， and 7-oxo-ganoderic acid Z2 as well as ganoderon B， to a certain extent， had anti-tumor activity. These findings can provide basis for the development of anti-tumor drugs. However， the anti-tumor mechanisms need to be further studied.[Key words]fruiting bodies of Ganoderma lucidum； triterpenoids； anti-tumor； molecular docking； virtual screening灵芝Ganoderma lucidum（Leyss. Ex Fr）Karst.又称瑞草、灵芝草，是灵芝属药食两用真菌，世界各地均有分布，以热带和亚热带地区为多。
肿瘤突变负荷应用于肺癌免疫治疗的专家共识
肿瘤突变负荷应用于肺癌免疫治疗的专家共识Cancer Immunotherapy: Expert Consensus on the Application of Tumor Mutation Burden in Lung Cancer TreatmentIntroduction:In recent years, immunotherapy has emerged as a promising treatment option for lung cancer patients. Harnessing the power of the immune system to recognize and destroy cancer cells, this revolutionary approach has shown remarkable success in extending survival rates and improving overall outcomes. One important aspect of lung cancer immunotherapy is the utilization of tumor mutation burden (TMB) as a predictive biomarker. This article will delve into TMB's significance in guiding treatment decisions and explore the expert consensus surrounding its application in lung cancer immunotherapy.Understanding TMB:Tumor mutation burden refers to the number of mutations present within a tumor cell's genome. These mutations can broadly be categorized as either synonymous (not affecting protein function) or non-synonymous (affecting protein function). TMB serves as an indicator of genomicinstability and has been found to correlate with the likelihood of neoantigen creation, which plays a crucial role in triggering an immune response against tumors.Expert Consensus on TMB in Lung Cancer Immunotherapy:1. Predictive Value for Immune Checkpoint Inhibitors (ICI):Immune checkpoint inhibitors have revolutionized lung cancer treatment by targeting proteins that hinder immune responses against tumors. Research studies haveconsistently demonstrated that higher TMB levels are associated with improved response rates and increased efficacy of ICIs such as pembrolizumab and nivolumab. As a result, experts widely agree that TMB can serve as a reliable predictive biomarker for selecting suitable candidates for ICI therapy.2. Combination Therapies:Due to intrinsic heterogeneity within tumors, utilizing a single biomarker might not capture the complexity of tumor-immune interactions accurately. Experts propose combining TMB assessment with other biomarkers, such as programmed death-ligand 1 (PD-L1) expression, to enhance patient stratification and optimize treatment decisions. This approach allows for a more comprehensive understanding of the tumor microenvironment and helps identify patients who are most likely to benefit from immunotherapy.3. Potential Utility in Small Cell Lung Cancer (SCLC):While TMB has been extensively studied in non-small cell lung cancer (NSCLC), its role in SCLC remains under investigation. Preliminary findings show promise, suggesting that TMB may have predictive value in SCLC patients as well. Expert consensus acknowledges the need for further research in this area to establish the true potential of TMB as a biomarker for SCLC immunotherapy.4. Challenges and Future Directions:Though significant progress has been made, challenges remain in standardizing TMB assessment methods, ensuring reproducibility, and defining optimal cutoff values for clinical decision-making. Experts emphasize the importance of collaborative efforts to establish guidelines and validate TMB as a standard biomarker across different laboratories and institutions. Additionally, ongoing research aims to identify additional genomic alterations beyond single nucleotide variants that could enhance the predictive power of TMB.Conclusion:In conclusion, tumor mutation burden has emerged as an important biomarker in lung cancer immunotherapy, particularly when considering immune checkpoint inhibitor therapy. Expert consensus supports its use as a predictive tool for treatment selection and patient stratification. Collaboration among researchers, clinicians, and regulatoryauthorities is crucial in establishing standardized protocols for TMB assessment and refining its application to further improve patient outcomes. With continued advancements in genomic profiling techniques, precise targeting of therapies based on individual tumor characteristics holds great promise for the future of lung cancer treatment.。
外周血中循环肿瘤细胞检测在肺部良恶性病变诊断中的价值
外周血中循环肿瘤细胞检测在肺部良恶性病变诊断中的价值陈卫琴【摘要】目的:探究外周血中循环肿瘤细胞(CTC)检测在肺部良恶性病变诊断中的应用价值.方法:选取2014年11月～2016年11月期间于某院经X线／CT检查确诊为肺部实性占位性病变患者133例为研究对象,经手术病理证实为良性病变53例(良性病变组),恶性病变80例(恶性病变组),分别检测两组患者CTC和肿瘤标志物表达水平.结果:两组患者CYFRA21-1水平比较无显著差异(P>0.05);恶性病变组CTC和CEA水平显著高于良性病变组,差异具有统计学意义(P<0.05);ROC曲线分析结果显示,CTC和CEA诊断肺部良恶性病变的ROC曲线下面积分别为0.817(95%CI:0.743～0.891)和0.613(95%CI:0.508～0.718).结论:较之传统肿瘤标志物的检测,外周血CTC检测对肺部良恶性病变的诊断价值更高,能为肿瘤的临床诊断、疗效评估和预后恢复提供极重要依据.【期刊名称】《数理医药学杂志》【年(卷),期】2018(031)003【总页数】3页(P337-339)【关键词】肿瘤细胞;循环;肺部病变;诊断【作者】陈卫琴【作者单位】番禺区中医院检验科微生物室广州511400【正文语种】中文【中图分类】R446.1肺癌是世界范围内发病率和死亡率增长最快、最高，对人类生命健康威胁最大的恶性肿瘤之一，远处转移是造成患者死亡的主要原因[1]。
外周血中的循环肿瘤细胞(Circulating Tumor Cell，简称CTC)是指存在于外周血的肿瘤细胞，具有高度活力和高度转移潜能的CTC可以在循环系统中存活，并在合适的环境中增殖，导致肿瘤的复发和转移[2]。
为探究外周血中CTC检测在肺部良恶性病变诊断中的应用价值，本院选取133例经X线/CT检查确诊为肺部实性占位性病变患者为研究对象进行CTC检测和肿瘤标志物检测，现将结果报道如下。
伊立替康联合雷替曲塞三线治疗晚期胃癌的临床疗效观察
不良反应 白细胞降低 血小板降低 血红蛋白下降 延迟性腹泻 恶心及呕吐 肝功能损伤 口腔黏膜炎
表 １ 主要不良反应
Ⅰ度
Ⅱ度
Ⅲ度
７（１８．９） ２（５．４） １（２．７）
２（５．４） １（２．７） ２（５．４）
９（２４．３） ０（０．０） ０（０．０）
６（１６．２） ２（５．４） ２（５．４）
５（１８．９） ３（８．１） １（２．７）
·２１５·
小剂量 ＣＶ序贯 ＣＨＯＰ方案东，刘丽英
（郑州市第一人民医院肿瘤内科，河南 郑州 ４５０００４）
［摘要］ 目的 观察小剂量 ＣＶ序贯 ＣＨＯＰ方案治疗初治原发性胃弥漫大 Ｂ细胞淋巴瘤的临床疗效及安全 性。方法 初治原发性胃弥漫大 Ｂ细胞淋巴瘤患者 １７例均给予小剂量 ＣＶ序贯 ＣＨＯＰ方案，２１ｄ为 １周 期，每化疗 ２周期评价疗效及不良反应。结果 １７例患者均可评价疗效，完全缓解 ９例（５２．９４％），部分缓 解 ７例（４１．１８％），疾病进展 １例（５．８８％），总有效率为 ９４．１２％。不良反应主要为骨髓抑制和消化道反应， 未继发消化道出血及穿孔，无化疗相关性死亡病例。结论 小剂量 ＣＶ序贯 ＣＨＯＰ方案治疗初治原发性胃 弥漫大 Ｂ细胞淋巴瘤疗效好，不良反应轻，安全性高。 ［关键词］ 环磷酰胺；长春新碱；多柔比星；醋酸泼尼松；胃淋巴瘤 ＤＯＩ：１０．３９６９／ｊ．ｉｓｓｎ．１６７３５４１２．２０１８．０３．０１０ ［中图分类号］ Ｒ７３３．１；Ｒ７３０．５３ ［文献标识码］ Ａ ［文章编号］１６７３－５４１２（２０１８）０３－０２１５－０３
·２１４·
ＪＯＵＲＮＡＬＯＦＢＡＳＩＣＡＮＤＣＬＩＮＩＣＡＬＯＮＣＯＬＯＧＹＶｏｌ３１Ｎｏ３Ｊｕｎ２０１８
影像学检查至少有 １个可测量病灶，ＥＣＯＧ评分 ＜２ 分，血常规、肝功能、肾功能及心电图等检查均达到可 化疗指标，无化疗禁忌证，预计生存时间 ＞３个月。 １．２ 治疗方法 伊立替康 １８０ｍｇ·ｍ－２加入生理盐 水 ２５０ ｍＬ 中 静 脉 滴 注 ９０ ｍｉｎ，ｄ１；雷 替 曲 塞 ３ｍｇ·ｍ－２加入 ５０ｍＬ生理盐水中静脉滴注 １５ｍｉｎ， ｄ２。每 ３周为 １周期。化疗止吐采用托烷司琼；出现 腹泻症状者则应用易蒙停及补液治疗。连续化疗 ２周 期以上进行疗效评价。 １．３ 临床 疗 效 及 不 良 反 应 评 价 标 准 近 期 疗 效 按 ＷＨＯ实体瘤 疗 效 评 定 标 准 进 行 评 估，分 为 完 全 缓 解 （ＣＲ）、部分缓解 （ＰＲ）、稳定 （ＳＤ）和进展 （ＰＤ）。以 ＣＲ＋ＰＲ计算有效率，以 ＣＲ＋ＰＲ＋ＳＤ计算疾病控制 率。疾病进展时间为化疗开始至出现疾病进展的时 间。不良反应评价标准按 ＷＨＯ抗肿瘤药物不良反应 分度标准分为 ０～Ⅳ度。
《头颈部肿瘤》
213 pts Median follow-up 105 months
TPF vs. PF
The 5- and 10-year larynx preservation rates 74.0% vs. 58.1%
70.3% vs. 46.5% The 5- and 10-year LDFFS rates
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复发和(或)转移
复发病变可治愈：应积极寻求根治性手术 或同步放化
（靶）疗
无局部治愈可能：姑息性化疗和(或)靶向治疗 支持治疗
姑息化疗的中位生存时间大约为6个月，1年生存率大约为20%
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Induction Chemotherapy
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Induction chemotherapy plus radiation compared with surgery plus radiation in patients with advanced laryngeal cancer. The Department of Veterans Affairs Laryngeal Cancer Study Group
头颈部肿 瘤
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头颈部肿瘤概述 口腔肿瘤 新辅助化疗 2015 ASCO
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流行病学
占全身恶性肿瘤的5％ 第6大常见的恶性肿瘤 肿瘤相关死亡原因的第8位 头颈部肿瘤的患者有可能罹患第2个原发性的头颈部、肺
部或食管的肿瘤
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病因
吸烟和嗜酒 口咽癌：人乳头瘤病毒(HPV) 60-70% 鼻咽癌：EBV
For selected patients with hypopharyngeal and laryngeal cancers less than T4a in extent, induction chemotherapy—used as part of a larynx preservation strategy—is category 2A
乳腺癌超声造影增强特征与免疫组化及腋窝淋巴结转移的相关性分析
关键词 乳腺癌 超声造影 免疫组化 淋巴结 中图分类号 R445. 1 文献标识码 A DOI 10. 11969 / j. issn. 1673-548X. 2021. 06. 025
Correlation Analysis of Enhanced Features of Breast Cancer Ultrasound Contrast with Prognostic Indexes and Axillary Lymph Node Metastasis. Hu Tian, Jia Chunmei, Xue Ying,et al. Department of Imaging and Nuclear Medicine, Shanxi Medical University, Shanxi 030001, China
pni预测不同部位、不同分期结直肠癌患者预后价值的初步研究
专题论著
PNI 预测不同部位、不同分期结直肠癌患者预后价值的初步研究*
柳俊刚，黄晓量，羊文康，张楚乔，李政甜，李婵，陈少梅，莫显伟，唐卫中△
广西医科大学附属肿瘤医院胃肠外科/广西结直肠癌临床研究中心 广西南宁 530021
唐卫中 主任医师，教授，博士、硕士研究生导师，广西医科大学附属肿瘤医院院长，肿瘤精准治 疗首席专家。主要从事结直肠肿瘤的临床诊治及相关基因的分子生物学研究。担任中国抗癌协会常务理 事，国家结直肠肿瘤质控专家委员会常务委员，中国医师协会结直肠肿瘤专业委员会第一届委员会委 员，广西抗癌协会理事长，广西医师协会结直肠肛门专业委员会主任委员，广西抗癌协会肿瘤精准治疗 专业委员会主任委员，广西医师协会外科医师分会结直肠肛门专业委员会主任委员等重要学术职务。 《中国癌症防治》 杂志主编，《结直肠肛门外科》 杂志副主编，在国内外期刊发表学术论文 60 余篇，其中 SCI 收录论文 17 篇，主持国家自然基金 2 项、省部科研课题 4 项、横向课题 2 项、厅级课题 5 项。
［Abstract］ Objectives To investigate whether perineural invasion(PNI) could predict prognosis of patients with colorectal cancer at different locations and of different stages. Methods This was a retrospective analysis of clinical data of 1013 patients with colorectal cancer treated in our hospital between April 2012 and June 2018. All patients were diagnosed with colorectal cancer by pathology and had complete clinical data. Patients were divided into with (n = 520, 51.3% ) or without (n = 493, 48.6% ) PNI. Patient characteristics, pathology report, and genetic report were collected. Kaplan-Meier survival curves were drawn and sur⁃ vival was compared between the two groups by Log- rank test. Results There was no significant difference between the two groups in age, sex, location of tumor, microsatellite testing, and mutation of Ras gene (P > 0.05). There was significant between-
食管肿瘤研究现状英文综述范文
食管肿瘤研究现状英文综述范文Esophageal cancer is one of the most aggressive malignancies, with a high mortality rate due to its late diagnosis and limited treatment options. This review aims to provide an overview of the current state of research into esophageal tumors, highlighting recent advances and potential future directions.Etiology and Risk FactorsEsophageal cancer is predominantly classified into two histological types: squamous cell carcinoma (SCC) and adenocarcinoma (AC). The risk factors for esophageal cancer are multifaceted, including tobacco and alcohol consumption, obesity, gastroesophageal reflux disease (GERD), andBarrett's esophagus. Recent studies have also implicated dietary factors and genetic predispositions in the development of esophageal tumors.DiagnosisEarly detection of esophageal cancer remains a challenge due to its asymptomatic nature in the initial stages. Endoscopy with biopsy is the gold standard for diagnosis. Advances in imaging techniques, such as endoscopic ultrasound (EUS) and positron emission tomography (PET), have improved the staging and management of the disease. Additionally, molecular biomarkers are being explored for their potentialin early detection and personalized treatment.Treatment ModalitiesSurgical resection remains the primary treatment for localized esophageal cancer. However, the prognosis is often poor due to the advanced stage at diagnosis. Neoadjuvant therapies, including chemotherapy and radiation, are commonly used to downstage tumors before surgery. Targeted therapies and immunotherapies are emerging as promising treatment options, with several agents showing efficacy in clinical trials.Genomic and Molecular ResearchThe genomic landscape of esophageal cancer is complex and heterogeneous. Next-generation sequencing (NGS) hasfacilitated the identification of key molecular alterations and potential therapeutic targets. Studies have highlighted the role of TP53, CDKN2A, and other genes in tumorigenesis. Moreover, the tumor microenvironment and its interaction with immune cells are being intensively studied to understand resistance mechanisms and develop combinatorial therapies.Prevention and Public HealthPreventive strategies are crucial due to the aggressive nature of esophageal cancer. Public health initiatives focusing on smoking cessation, alcohol consumption reduction, and weight management are vital. Screening programs for high-risk populations, such as those with GERD or Barrett'sesophagus, are being explored to facilitate early detection.Challenges and Future PerspectivesDespite significant advances, challenges remain in improving survival rates and quality of life for patients with esophageal cancer. There is a pressing need for more effective screening methods, personalized treatment strategies, and better understanding of tumor biology. Ongoing research into the molecular underpinnings of the disease, coupled with the development of novel therapies, holds promise for the future management of esophageal cancer.In conclusion, the landscape of esophageal cancer research is rapidly evolving, with a focus on understanding the molecular mechanisms driving the disease, improving diagnostic techniques, and developing innovative treatment strategies. Collaborative efforts across disciplines will be key to overcoming the challenges faced in the field and improving outcomes for patients with esophageal tumors.。
MRI联合罗马指数在卵巢肿瘤中的应用价值
卵巢肿瘤为女多发性的生殖系统肿瘤，以卵巢癌的危害最大[1]。
卵巢癌为死亡率较高的妇科癌症，有强隐匿性，且良恶性肿瘤间症状无明显差异，易混淆，易延误恶性肿瘤的最佳治疗时机[2]，因此早诊断、早治疗对于改善卵巢癌患者预后具有积极意义。
病理学检查由于存在创伤性，对于患者耐受性要求较高，故临床应用存在局限性[3]。
磁共振成像(magnetic resonance imaging，MRI)具有扫描范围多、层面外干扰小以及空间结构显示好等多个优势，能利用多方位扫描定量定性分析卵巢肿瘤，增加诊断准确性[4-5]。
研究指出，罗马指数在卵巢癌的诊断中具有良好敏感度与特异度[6]。
鉴于此，本文将探讨MRI联合罗马指数对卵巢肿瘤的诊断价值，以期为临床完善治疗方案提供依据。
1资料与方法1.1一般资料经我院医学伦理委员会审核同意，选取2020年3月至2023年2月平煤神马集团总医院收治的107例卵巢肿瘤患者作为研究对象。
纳入标准：(1)初筛有性质不明卵巢肿块；(2)接受影像学检查和手术治疗；(3)可耐受病理检查；(4)知情本研究且签署同意协议书。
排除标准：(1)既往有卵巢手术治疗史；(2)伴有失控性出血；(3)原发性卵巢急性与慢性感染；(4)严重内分泌系统病变；(5)伴血液系统病变；(6)伴严重脏器功能损伤。
107例患者年龄45~68岁，平均(56.95±5.49)岁；体质量指数17.1~23.7kg/m2，平均(20.35±1.56)kg/m2；临床表现为下腹不适56例，月经不调46例，腹部包块33例。
1.2方法1.2.1MRI检查方法采用仰卧体位，腹部联合相控阵线圈，通过Philips公司的1.5T MRI扫描仪(Prodiva型号)对卵巢行多方位扫描，首先行MRI横断面、冠状面、矢状面序列扫描，参数为：T1WI的TR为700ms、TE为11ms，T2WI的TR为4800ms、TE为90ms、层间距为1mm、层厚为4mm、矩阵为312×256、视野为40cm×40cm，平扫后行动态增强磁共振成像(dynamic enhanced magnetic resonance imaging，DCE-MRI)，高压注射器经肘静脉快速注射0.1mmol/kg的钆喷酸葡甲胺，速度3.0mL/s；经三维容积式内插法屏气序列行多期扫描，参数为：层间距为0.8mm、层厚为4mm、矩阵为256×192，视野为34cm×34cm、翻转角15°；动态扫描获20期图像，后获延迟期冠状面、矢状面、横断面图像；原始数据导到Philips公司8.1版的QLAB对比增强定量分析软件，选肿瘤实性成分最显著区域作感兴趣区(region of interest，ROI)，注意避开囊变、出血区、大血管与坏死区，取3次平均值制作时间-信号强度曲线(time-signal ietensity curve，TIC)，计算容积转移常数(K trans)、速率常数(K ep)。
MRI对于肿块强化和非肿块强化乳腺癌病灶新辅助化疗后肿瘤回缩方式的初步探讨
MRI退 缩 方 式 分 为 向 心 型 （3 1 例 ）、树 枝 型 （1 7 例 ）和 混 合 型 （2 2 例 ）。两 种 M RI强 化 方 式 与 M RI退 缩 方 式 之 间 的 差 异 有 统 计 学
意 义 ，X2=47.043，P=0.000,肿 块 强 化 以 向 心 型 回 缩 为 主 ，占 向 心 型 回 缩 的 93.5%(29/31)，明 显 高 于 非 肿 块 强 化 组 。非肿块强化以
中 国 临 床 医 学 影 像 杂 志 2 0 2 1 年 第 3 2 卷 第 6 期 J Chin Clin Med Imaging，2021，Vol.32, N o .6
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MRI对于肿块强化和非肿块强化乳腺癌病灶 新辅助化疗后肿瘤回缩方式的初步探讨
陈 园 园 ，王 霞 ，张 嫣 ( 广 东 省 妇 幼 保 健 院 放 射 科 ，广 东 广 州 510010)
切除及增加行保乳手术机会。那么如何在术前对 NAC癌 灶 进 行 精 确 的 判 断 是 评 估 的 难 点 ，MRI是目 前公认的与病理结果吻合度最高的影像检查手段， 可通过对比NAC前后肿瘤的大小、位 置 、分 布 、累及 范 围 、瘤体内部及边缘浸润的细节，进一步准确评估
[收 稿 日 期 ] 2 0 2 0 - 1 1 - 0 5 ; [修 回 日 期 ] 2 0 2 0 - 1 1 - 1 7 [作 者 简 介 】陈 园 园 （1 9 8 3 - ) ，女 ，河 南 宜 阳 人 ，副 主 任 医 师 。E - m a i l :g u o z i y u a n 5 2 1 @ 1 6 3 . c o m [通 讯 作 者 】张 嫣 ，广 东 省 妇 幼 保 健 院 放 射 科 ，5 1 0 0 1 0 E - m a i l : doctorzhangyan@ [基 金 项 目 】广 东 省 科 技 厅 ( 2 0 1 6 Z C 0 1 8 5 )。
紫杉醇在卵巢癌医治中的应用
紫杉醇在卵巢癌医治中的应用紫杉醇（taxol）是天然植物的产物。
1963年，第一从太平洋西岸原始丛林的紫杉树树皮中分离和提取，由于其来源缺乏及难溶于水的特点，临床应用进展缓慢。
1979年，发觉紫杉醇具有增进细胞微管蛋白聚合、凝固成束并避免其解聚的独特作用机理，而引发人们的重视［1］。
1983年，美国国立癌症中心（NIC）开始了临床实验研究；1992年，美国食物药品治理局批准紫杉醇用于医治转移性卵巢癌。
1994年，美国Bristol公司被获准将紫杉醇用于中国。
紫杉醇的研究成为90年代抗肿瘤药物的热点课题。
一、紫杉醇的作用机理及代谢紫杉醇是二萜类化合物，相对分子质量为，熔点为213～216℃，具有高度亲脂性，不溶于水［2］。
紫杉醇特异作用于细胞周期的G2期和M期，使微管在有丝割裂时不能形成纺锤体和纺锤体丝，阻止肿瘤细胞的割裂和繁衍。
紫杉醇也作用于巨噬细胞上的肿瘤坏死因子（TNF）受体，促使释放白细胞介素（IL）-一、TNF-二、IL-六、干扰素（IFN）-一、IFN-2，对肿瘤细胞起杀伤或抑制作用［3］。
紫杉醇的代谢符合非线性饱和散布及排除的二室模型［4，5］。
有学者发觉，紫杉醇助溶剂-聚氧乙烯蓖麻油可能是致非线性药代动力学的物质［6］。
进入血中的紫杉醇，90%与血浆蛋白或组织蛋白结合，特异性的在肝脏微粒体酶P-450中转化成无毒产物6 β-羟基紫杉醇，这是一条重要的解毒途径。
紫杉醇投药量的25%经胆管排泄和羟化代谢，48小时内，%～%的紫杉醇以原形从尿中排出［5，6］。
因此，肾脏不是紫杉醇要紧的排泄途径。
二、紫杉醇的毒副作用1.高敏反映（hypersensitivity reac- tion）：是初期阻碍紫杉醇应用的最大问题，多发生在用药的第1天，以为紫杉醇是致敏原［7］。
还有报导，高敏反映并非紫杉醇本身所致，因有研究证明，其媒介为组织胺，并证明聚氧乙烯蓖麻油可引发组织胺释放。
曾发生严峻高敏反映者，不宜再用本药［8］。
皂角刺抗肿瘤的初步研究
型评价皂角刺的体内抗肿瘤作用，以期为皂角刺用于 日开始给药，连续灌胃３周。
肿 瘤 治 疗 提 供 有 价 值 的 资 料 ，为 药 用 植 物 应 用 于 抗 肿
治疗期间，２ｄ 监 测 小 鼠 体 质 量 １ 次，待 肿 瘤 长
瘤理论加以补充，更为了指导临床正确使用皂角刺对 出后用游标卡尺每隔２ｄ测肿瘤长和宽 １ 次，肿瘤体
途径、多个靶点、多种方式在肿瘤的治疗中发挥作用， 可消，脓已成者可使之速溃 。 ［２］ 中药皂角刺中含 有 多
因此，更引人注目。皂角刺，又称皂角针，是豆科皂荚 种皂苷、黄酮、三萜等黄酮类 生 ［３］ 物活性成分，作 用 广
属植 物 皂 荚 （Ｇｌｅｄｉｔｓｉａ ｓｉｎｅｎｓｉｓ Ｌａｍ）的 干 燥 棘 刺， 泛。
体内实验结果显示，与模 型 组 小 鼠 相 比 较，Ｐ ≥
的小鼠后肢右背 部 皮 下 接 种 ０．２ ｍＬ／只。 将 接 种 后 ０．０５，给药组的体质量未见显著性差异，见图１；给药
的小鼠按 体 质 量 平 均 分 为 模 型 组 和 皂 角 刺 组，每 组 组的肿瘤生长速度较慢，见图 ２；小 鼠 生 长 状 态 较 好，
全程 治 疗 结 束 后 次 日 处 死 小 鼠，眼 球 取 血，剥 离
１ 材料
背 部 肿 瘤 、肝 脏 、脾 脏 和 胸 腺 ，并 称 重 。 计 算 肿 瘤 抑 制 率 及 肝 脏 、胸 腺 、脾 脏 指 数 。 同 时 ，观 察 小 鼠 肺 部 等 其
１．１ 药 品
他脏器是否正常。
中 药 皂 角 刺 ：皂 角 刺 １５０ｇ 与 适 量 水 煎 煮 ３０ ｍｉｎ
１０只。其中模型组：灌 胃 清 水 ０．３ ｍＬ／１０ｇ；皂 角 刺 且给药组小鼠的存活率亦未见显 著 差 异，见 图 ３。 肿
中药湿敷治疗1例放射性皮炎患者的护理
2023 年第 9 卷第 11 期Vol.9， No.11， 2023中西医结合护理Chinese Journal of Integrative NursingOPEN ACCESS http ：/ / 中药湿敷治疗1例放射性皮炎患者的护理蒋玲， 黄金兰（北京中医药大学深圳医院（龙岗） 肿瘤科， 广东 深圳， 518116）摘要： 放射性皮炎是放射治疗最常见的并发症。
本文回顾1例放疗所致放射性皮炎患者的治疗和护理经验，通过综合运用中医适宜技术中药湿敷，达到抑制渗出、消肿止痛、控制感染、促进皮肤愈合等作用，减轻患者痛苦。
关键词： 放射性皮炎； 中药湿敷； 疼痛； 中医护理中图分类号： R 275 文献标志码： A 文章编号： 2709-1961（2023）11-0063-03Nursing of a patient with radiotherapy -induced radiation dermatitis treated byTraditional Chinese Medicine wet compressesJIANG Ling ，HUANG Jinlan（Department of Oncology ， Shenzhen Hospital Beijing University of Chinese Medicine ， Shenzhen ，Guangdong ， 518116）ABSTRACT ： Radiation dermatitis is the most common complication of radiation therapy. Thispaper reviewed the clinical data of a patient with radiation dermatitis caused by radiotherapy. The Traditional Chinese Medicine wet compress and related nursing interventions were carried out to inhibit exudation ， reduce swelling and pain ， control infection and promote skin healing of the pa⁃tient.KEY WORDS ： radiation dermatitis ； Traditional Chinese Medicine wet compress ； pain ； Traditional Chinese Medicine nursing 放射治疗是癌症患者最主要的治疗方法之一，放射性皮炎是放射治疗最常见的并发症，超过70%的放疗患者会出现皮肤潮红甚至溃疡等不同程度的放射性皮肤损伤［1］。
关于射频消融诱导兔肺内VX2鳞状细胞癌模型细胞凋亡
关于射频消融诱导兔肺内VX2鳞状细胞癌模型细胞凋亡作者：马连君程庆书张卫强刘锟王云杰王道喜赵正源齐海妮杜铭祥【关键词】肺肿瘤关键词: 导管消融术;VX2肿瘤;兔;肺肿瘤;脱噬作用摘要:目的探讨射频消融兔肺内VX2肿瘤诱导肿瘤细胞凋亡情况. 方法采用VX2肿瘤组织块悬液肺内注入法在20只新西兰白兔体内建立兔VX2肿瘤肺内移植模型;实验组12只新西兰白兔给予射频治疗，计数毁损中心区肿瘤组织和边缘区肿瘤组织凋亡细胞指数;对照组8只新西兰白兔，予假性治疗，计数肿瘤组织凋亡细胞指数. 结果治疗组肿瘤经射频治疗后发生凝固性坏死及细胞凋亡，毁损边缘区肿瘤组织凋亡细胞指数为（345±38），而毁损中心区肿瘤组织凋亡细胞指数为（84±12），两者差异非常显著（P<0.01）;对照组肿瘤组织凋亡细胞指数为（2.0±0.4），与治疗组毁损区中心组织凋亡细胞指数及毁损区边缘组织凋亡细胞指数相比均相差非常显著（P<0.01）. 结论射频消融诱导肿瘤细胞凋亡是射频治疗恶性肿瘤的一项重要机制.Keywords:catheter ablation;VX2tumor;rabbits;lung neo-plasms;apoptosisAbstract:AIM To observe status of cell apoptosis of VX2tumor in rabbit lung after radiofrequency ablation.METH┐ODS By injectingVX2tumor tissue suspension in the lung，the transplanted lung cancer model was established in20New Zealand white rabbits.12rabbits were treated with radiofre-quency ablatoin，while another8rabbits were not treated and served as control.Apoptotic index was calculated in the cen-ter tissue of the ablation，fringe tissue of the ablation and tis-sue of the shield ablation respectively.RESULTS Coagula-tive necrosis and cell apoptosis appeared in the tumor after the ablation.Apoptotic index of the fringe tissue of the abla-tion was（345±38），that of the center tissue of the ablation was（84±12）（P<0.01）and that of the tissue of the shield ablation was（2.0±0.4）（P<0.01）.CONCLUSION In-ducing cell apoptosis is an important mechanism of radiofre-quency ablation of malignant tumor.0 引言经皮穿刺射频消融是一种发展迅速的热损毁技术，在CT、超声、磁共振引导下经皮穿刺置入电极，确定电极位于目标区，启动射频机，射频波经电极尖导入周围组织，产生热量，使组织发生凝固性坏死.该项技术已经应用于灭活骨肿瘤［1］，颅内肿瘤［2］，肝癌［3］，肝内转移癌［4，5］，近期程庆书等［6］报道应用射频消融技术治疗肺内肿瘤，赵正源等［7］报道射频消融治疗肺内转移瘤，取得良好效果.本实验探讨射频消融兔肺内VX2肿瘤诱导细胞凋亡情况.现介绍如下.1 材料和方法1.1 材料 VX2肿瘤细胞是一种可移植的兔鳞状细胞癌株，该细胞株由第四军医大学病理学教研室提供.射频机及电极:RF2000型射频机及10尖锚状电极，美国Radiotherapeutic公司生产.CT机:EXEL2400elect型CT机，以色列Elscint Ltd.公司生产.光学显微镜:日本Olympus公司生产.透射电镜:JEM-2000EX型透射电镜，日本JEOL公司生产.荧光显微镜:日本Olympus公司生产.1.2 方法1.2.1 兔肺肿瘤模型的制作将冰冻VX2细胞悬液常规细胞培养法复苏后，取1mL（107 ・mL-1 ）接种于1兔后腿外侧肌肉内，制成荷瘤种兔，2wk后可扪及一实质性包块.无菌条件下切取肿瘤，取肿瘤边缘生长旺盛的鱼肉样组织，剪切成泥，先过20目筛，取筛下部分，再过30目筛，并用1640培养液冲洗，以除去单个细胞和过小的组织块，取30目筛上部分，以1640培养液制成组织块悬液，在X 线引导下注入兔右肺下叶内，3d后CT扫描观察肿瘤生长情况，待发现肿瘤生长至直径大于10mm后即可用于射频治疗.本实验采用上述方法在20只新西兰白兔体内建立肺内VX2肿瘤移植模型，随机将这20只新西兰白兔分为治疗组12只用于射频消融，8只用作对照进行假性治疗，只置入电极，不予射频治疗.1.2.2 射频治疗过程 RF2000型射频机采用双负极输入，可伸缩的10针锚状电极输出，电极展开最大直径为35mm，输出频率为450MHz，最大输出功率100W，可调节输出功率，可控治疗时间，可测定阻抗，并将阻抗和治疗时间输入计算机绘制成图.治疗前将兔右胸壁、腹部及背部脱毛，以速眠新（846）0.8mL・kg-1 im麻醉，仰卧固定于托板上，放置负极板于腹部和背部脱毛区，右胸壁常规消毒，铺无菌手术巾.CT扫描确定肿瘤部位及穿刺部位、方向、深度，置入电极，再CT扫描，确定电极位于肿瘤区，展开电极直径达18～20mm，开启射频机，起始输出功率为30W开始治疗，每分钟升高10W，最高输出功率达60W，当阻抗达999Ω时自动停机，退出电极，CT扫描观察肿瘤阴影变化及有无血气胸发生，术后常规饲养，并给予氨苄青霉素0.25g im，1・d-1 .1.2.3 标本采集治疗结束24h，空气栓塞法处死新西兰白兔，治疗组取消融区中心及消融区边缘组织为凋亡检测标本，对照组取肿瘤中心组织为凋亡检测标本，常规制片待检.1.2.4 凋亡细胞检测采用Clontech公司生产的ApoAlert○R DNA Fragmentation Assay Kit-TUNEL法细胞凋亡检测试剂盒对上述标本进行检测，严格按照试剂盒说明进行操作，FITC荧光标记，PI复染，荧光显微镜检查，细胞核内出现黄绿色荧光为阳性细胞，随机计数10个高倍视野中凋亡细胞数目为凋亡细胞指数.统计学方法:t检验.2 结果2.1 射频治疗后肿瘤组织和周围肺组织的病理改变射频治疗后肿瘤组织呈灰白色、干燥的凝固性坏死，中间破溃，与周围肺组织界限清楚，周围肺组织呈红褐色凝固性坏死，在坏死灶周边为出血带，在出血带外侧是大片的充血、水肿区;切面上见肿瘤坏死灶、肺组织坏死灶、出血带、水肿区呈年轮样分布.HE染色，见肿瘤组织大片凝固性坏死，细胞结构破坏，仅见组织轮廓，消融灶周围肺组织充血、出血明显，肺泡腔内充满大量渗液，肺泡间隔增宽，消融灶周围肺组织中有大量中性粒细胞、巨噬细胞、嗜酸细胞浸润.透射电镜检查发现大量细胞坏死，细胞内超微结构破坏，可见大量空泡，细胞膜、核膜破坏明显，核溶解、核碎裂明显，仅个别细胞可见残存的张力原纤维，不见桥粒结构，个别细胞内可见核内假性包涵体，于消融的肿瘤周边部分取材的标本中可见较多凋亡细胞和凋亡小体，组织内可见较多分叶核细胞浸润和巨噬细胞浸润，并可见明显的吞噬现象. 2.2 肿瘤组织凋亡细胞指数采用TUNEL法检测肿瘤组织中凋亡细胞，发现治疗组毁损区边缘部标本中由大量阳性染色细胞（Fig1），而在毁损区中心部标本中亦有较多阳性染色细胞，两者凋亡细胞指数差异非常显著（P<0.01），而对照组标本中仅发现极少数阳性细胞，其凋亡细胞指数与上述两组标本相比，差异均非常显著（P<0.01，Tab1）.图1 射频毁损区边缘部肿瘤组织中的凋亡细胞略表1 射频毁损区中央部、边缘部及对照组肿瘤组织凋亡细胞指数略4 讨论VX2肿瘤起源于Shope病毒诱导的兔乳头状瘤衍生的鳞癌［8］，是一种可移植的肿瘤细胞株.本实验采用组织块悬液肺内注入法制作兔肺VX2肿瘤模型，方法简单、成功率高、性质稳定、无自发消退现象，为研究肺癌难得的大型动物模型.细胞凋亡失衡是肿瘤发生发展的重要原因，而诱导肿瘤细胞凋亡已成为治疗恶性肿瘤的一个重要研究方向，细胞凋亡过程估计为12～24h，出现形态改变大约是最后2～3h，而DNA降解为180～200bp片段及寡核苷酸小体也是较晚时才发生［9］ 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