简介:客观:在主要胃的癌症的开始和发展调查染色体错误和他们的角色。方法:从稳固的肿瘤的改进、直接染色体准备为分析在decolored乐队G染色体上由鱼跟随了的乐队G被采用以便染色体错误能在DNA水平被证实。结果:28个主要胃的癌症标本的一个总数是研究。大小写1和大小写2有的简单染色体数字变化:49,XY,+2,+8,+9并且48,+8,+20分别地。几乎,大小写1和2有复杂染色体畸形。经常的出现结构的染色体深奥del(7q)(21/26),del(3p)(14/26),del(lp)(U/26)和del(17p)(10/26)。染色体畸形能简单、复杂。在前者,包含1~3个染色体的数字变化能被观察。8和9可能代表的三染色体性主要胃的癌症的细胞发生的亚群。在里面以后,del(7q)是最一致的错误。7q32-qter是通常失去的片断结论:染色体的数字、结构的改变在主要胃的癌症是在场的。Del(7q)是主要胃的癌症的结构的变化特征之一。在7q32-qter碎片,肿瘤suppressor基因可能存在并且它可以有靠近的关系到胃的癌症的开始和前进。
简介:男不孕可能清楚地在人的精子与异常DNAmethylation模式被联系。在氧化应力和精子染色体的全球methylation地位之间的一个协会也被建议了。现在的学习的目的是决定全球精子DNAmethylation地位是否在染色体的搬运人的精子被影响结构的错误。在5-methylcytosine之间的关系(m5C)在精子和染色质正直地位的层次被评估。学习病人包括了染色体的男搬运人有繁殖失败的结构的错误(n=24),并且控制包括了normozoospermic精子志愿者(n=23)。全球m5C水平用薄层的层析(TLC)和immunofluorescence被测量(如果)技术。精子染色质正直用染色的苯胺蓝色(AB)和TUNEL试金被估计。吝啬的m5C层次在调查染色体之间是类似的结构的错误搬运人(P)和控制(K)。然而,精子染色质完整测试比在控制在chromosomal重新整理搬运人揭示了显著地更高的值(P<;0.05)。尽管在精子染色质正直地位和精子DNA破碎和m5在两个都分析的组(P对K)并列的C水平以一种清楚地相反的方式被代表,低染色质正直可能与在染色体的搬运人观察的精子DNA的高hypomethylation地位被联系结构的错误。
简介:Thereareabout17chromosomesinyeastSaccharomycescerevisiae.Amiddlesizedchromosome,chromosomeV,waschoseninthisworkforstudyingandconstructingthephysi-calmaps.ChromosomeVfromstrainA364awasisolatedbypulsed-fieldgradientgelelectrophoresis(PFGE).GelslicescontainingchromosomeVDNAweredigestedwithtworarecuttingenzymes,NotⅠandSfiⅠ,andthree6-Ntrecognizingenzymes,SmaⅠ,SstⅡandApaⅠ.Severalstrategies-partialorcompletedigestions,digestionwithdifferentsetsoftwoenzymes,andhybrid-izationwithclonedgeneticallymappedprobes(CAN1,URA3,CEN5,PRO3,CHO1,SUP19,RAD51,RAD3)——wereusedtoaligntherestrictionfragments.Thereare9,9,15,17,and20sitesforNotⅠ,SfiⅠ,SmaⅠ,SstⅡandApaⅠrespectivelyinthemapoftheA364achromosomeV.Itstotallengthwascalculatedtobe620Kb(Kilo-bases).Thedistributionsofthecuttingsitesforthesefiveenzymesthroughthewholechromosomearenotuniform.Acomp-arisonbetweenthephysicalmapandthegeneticmapwasalsomade.
简介:Asimplemethodtocreateachromosome-specificDNAlibrqaryofrice,includingmicrodissection,amplification,charterizationandcloning,isdescribed.Ricechromosome4fromametaphasecellhasbeenisolatedandamplifiedbytheLinkerAdapterPCR(LA-PCR).ThePCRproductswerelabeledasprobeswithDIG-11-dUTPusingtherandomprimingmethod.SouthernblotanalysiswithricegenomicDNAandspecificRFLPmarkersdemonstratedthatthePCRproductswerederivedfromricechromosome4.Alargelibrarycomprisingover100,000recombinantplasmidmicroclonesfromricechromosome4wasconstructed.Colonyhybridizationshowedthat58%oftheclonescontainedsingleorlow-copysequencesand42%containedrepetitivesequences.ThesizeofinsertsgeneratedbyPCRrangedfrom140bpto500bp.ThismethodwillfacilitatecloningofthespecificchromosomeDNAmarkersandimportantgenesofrice.
简介:为在米饭的壳硅内容的QTLqHUS6以前位于米饭染色体6的短手臂。由使用在在一个isogenic背景怀有qHUS6的RM587RM19784区域分离的一张F2:3人口,为壳硅内容的二QTL被检测,哪个qHUS6-1在对着丝点近似的区域位于远侧的区域和qHUS6-2。在目标区域带小异质接合的片断的三米饭植物被选择,哪个二盖住qHUS6-1区域,其它盖住qHUS6-2区域。三张F2:3人口分别地从三植物的selfed种子被导出。印射的QTL用在qHUS6-1区域分离的二张人口被执行,并且qHUS6-1被标记RM510和RM19417限定到147.0-kb区域flanked。有在qHUS6-2区域的不同genotypic作文的五组F3线从另外的F2:3人口被选择。二QTL用双向ANOVA,qHUS6-2a位于RM19706RM19795和qHUS6-2b在间隔RM314RM19665定义的间隔被分开。
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简介:为合适的染色体分离,所有kinetochores必须完成双极的微导管(MT)附件并且以前随后在锭子赤道排列后期发作。减指导结束的马达dynein/dynactin的TheMT在职业人员中期绑kinetochores并且长在染色体大会离子被含有。不幸地,在达因在的激活通常扰乱锭子组织,因此妨碍它的kinetochore角色的评估。这里我们明确地由ZW10的调停RNAi的弄空的eliminatedkinetochoredynein/dynactin,为马达的kinetochorelocalization的蛋白质必需品。微速摄影的显微镜学显示了显著地减少的大会离子效率,尽管congressing染色体作为在控制房间显示了类似的速度。而且,房间经常没能完成完整的染色体排列,尽管有他们的正常锭子。Confocalmicrocopy表明没有对齐的kinetochores是单音的面向或独立、主要躺的外面锭子,建议一个困难从相反的杆捕获MT。Kinetochoresonmonoastral锭子远被驱散离开杆并且展出了仅仅温和的摆动。而且,使达因失去活性在由另外的工具产生类似的显型。因此,kinetochoredynein在单音的面向的kinetochores上生产拉力量的一个杆病房,它可以由象完整的染色体排列一样便于他们的合适的微导管俘获到promotecongression贡献有效双极的附件。
简介:TheTK-selectedchromosome-mediategenetransferlineswereanalysedusingDNAdotblotmethod,G-11bandingandinsituhybridization.TheresultsshowedthatCMGTcanprovideawidevarietyofintermediatesizeofthetransgenomefromgreaterthan80,000kbtolessthan2,000kb.SomeoftransfectantsareintergratedintomousechromosomewhichcanbedetectedbyG-11bandingandinsituhybridization
简介:AbstractPurpose:The pathogenesis of gastrinomas is largely unknown, and there is a lack of reliable genetic determinants that are useful to distinguish malignant and benign forms of this tumor or predict the prognosis of patients with this disease. Loss of heterozygosity (LOH) on chromosome 3p is reported to occur in pancreatic neuroendocrine tumors (PNETs) as well as in non-PNETs and its presence is reported to correlate with tumor prognosis in non-endocrine tumors. However, little data are available from prospective studies on gastrinomas.Experimental design:We assessed occurrence of 3p LOH in 24 gastrinomas and correlated its presence with tumor biological behavior and other clinicopathological features of gastrinomas.Results:Either 3p LOH or microsatellite instability involving 3p occurred in 11 of 24 tumors (46%). Seven (29%) gastrinomas had 3p LOH. Of the 7 gastrinomas with 3p LOH, 5 (71%) had 3p12 LOH with the marker D3S2406, which was the shortest region of highest overlap (SRO). Chromosome 3p LOH was not associated with aggressive biological behavior of gastrinomas or with poor prognosis of patients with gastrinoma. Similarly, 3p12 LOH (SRO) was not correlated with aggressive growth of tumors and/or liver metastases.Conclusion:Gastrinomas have a relative high frequency of 3p12 LOH suggesting this area may harbor putative tumor suppressor gene(s), which may play a role in the tumorigenesis, but not aggressiveness, of a subset of these tumors.
简介:AbstractPreimplantation genetic testing (PGT) is a widely adopted screening method that can be performed to identify and select embryos with normal ploidy; however, PGT relies on embryo biopsy, that is, polar body, embryo cells, or trophectoderm biopsy, to obtain embryonic DNA, increase its technical limitations. Studies have indicated that biopsy may have an influence on the quality and development of embryos, and increase the chance of abnormal epigenetic modifications. Therefore, non-invasive PGT (niPGT) detection of cell-free DNA (cfDNA) has gradually become a hot research topic in the field of assisted reproduction. Studies showed cfDNA could be detected in blastocyst fluid and spent culture medium (SCM) in vitro cultured embryos. The cfDNA collection requires less skill and makes lower risk to embryos. Some studies have been conducted to evaluate the feasibility of SCM-based niPGT approaches. When comparing the ploidy consistency of cfDNA in SCM, its consistency to the conventional PGT for aneuploidies results fluctuated widely, it is critical to recognize the factors influencing accuracy. These contradictory results may be related to factors such as the difference in SCM sampling methods and sampling time, and the definition of consistency. In this review, we aimed to comprehensively summarize how researchers use embryonic cfDNA to conduct niPGT detection. It also systematically reviews the factors affecting the accuracy of the test and its underlying issues, as well as prospective applications. We hope to provide a basis for future niPGT research and a useful reference for the standardized operation of niPGT that can be widely applied in clinical practice.
简介:Objective:Previousworkindicatedthataneuploidyofchromosome8incirculatingtumorcells(CTCs)correlatedwiththerapeuticefficacyforadvancedgastriccancer(AGC)patients.Inthisfollow-upstudyperformedonthesamepopulationofAGCpatients,weinvestigatedwhetherandhowaneuploidyofchromosome8inCTCscorrelateswithpatients'clinicalprognosis.Methods:Theprospectivestudywasperformedon31patientswithnewlydiagnosedAGC.Previouslyestablishedintegratedsubtractionenrichment(SE)andimmunostaining-fluorescenceinsituhybridization(iFISH)platformwasappliedtoidentify,enumerateandcharacterizeCTCs.QuantificationofCTCsandanalysisoftheiraneuploidyofchromosome8wereperformedonpatientsbeforeandaftertherapy.Results:CTCsweremeasuredin93.5%ofAGCpatients,andtwoCTCsubtypeswithdiversethresholdvalueswereidentified,multiploidCTCswiththethresholdof≥2per7.5mLandmultiploidplustriploidCTCswiththethresholdof≥4,whichwerefoundtosignificantlycorrelatewithpoorprogression-freesurvival(PFS)andoverallsurvival(OS).Inparticular,patientswith≥10%increasedmultiploidCTCsafteraninitial6weeksoftherapyhadpoorPFSandOS,whereasimprovedPFSandOSwereobservedonthosewhohad≥10%decreasedmultiploidCTCs.Afteradjustingforclinicallysignificantfactors,≥10%increasedpost-therapymultiploidCTCswastheonlyindependentpredictorofPFSandOS.Conclusions:AneuploidyofCTCscorrelateswithprognosisofAGCpatients.QuantitativecomparisonmonitoringmultiploidCTCsbeforeandaftertherapymayhelppredictimprovedorinferiorprognosisandchemoresistance.
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简介:瞄准:开发高产量的复合、快、简单的试金扫描精子缺乏因素(AZF)区域Y染色体上的微删除并且建立Ychromosomal的流行在有精子缺乏或oligozoospermia的中国不肥沃的男性的微删除。方法:总共,有精子缺乏的178个不肥沃的病人(非妨碍),有oligozoospermia的134个不肥沃的病人以及40肥沃的人控制在现在的学习被包括。样品为AZF微删除使用被屏蔽优化multi-analyte暂停数组(MASA)技术。结果:312个病人,(11.5%)36被发现在AZF区域有删除。微删除频率是14%(25/178)在精子缺乏组织,(11/134)8.2%在oligospermia组织。在有微删除的36个病人之中,19在AZFb在AZFc区域,在AZFa的七有的删除和六有的删除有删除。另外,四个病人有AZFb和AZFc删除。在AZF区域的删除都没在40肥沃的控制被发现。结论:有Ychromosomal的高流行在有精子缺乏或oligozoospermia的中国不肥沃的男性的微删除。MASA技术,在现在的学习被建立了,为检测Y染色体的删除提供一个敏感、高产量的方法。并且结果建议基因屏蔽应该在开始帮助繁殖治疗前被劝告到不肥沃的人。
简介:干旱是到在rainfed低地的米饭生产的主要不能生活的限制并且不足地灌溉区域。干旱的改进容忍的变化是策略之一减少干旱的否定效果。为与染色体上的干旱忍耐(DT)有关的主要、第二等的特点的量的特点loci(QTL)1,3,4,8和9从线从在CT9993和IR62266之间的一个十字导出的两倍haploid决定了那是introgressed并且在Khao邮政马里105的基因背景(KDML105)把了进小片开发染色体片断替换线(CSSL)人口。CSSL在干旱应力下面为他们的农学的表演和收益部件在繁殖阶段被评估,并且结果与灌溉状况相比。CSSL线的flowering比KDML105早是6~7d。在CSSL的谷物收益的吝啬的价值比在干旱下面的KDML105高并且灌溉了条件。以灌溉状况,谷物从4和8是的染色体带DT-QTLs的基因渗入线让步比KDML105的高,而另外的特点与KDML105显示出小差别。当否定地与天相关到flowering时,分析显示谷物产量在干旱应力下面每植物每植物,和全部的谷物重量与植物高度,tiller和圆锥花序数字有积极关联。是提及在上面,在干旱应力下面显示出好改编的CSSL能被用作基因材料,并且作为材料在引起节目的泰国rainfed低地米饭改进干旱忍耐把基因位于\O下面干旱忍耐。
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简介:AbstractBackground:Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), such as erlotinib and gefitinib, are widely used to treat non-small cell lung cancer (NSCLC). However, acquired resistance is unavoidable, impairing the anti-tumor effects of EGFR-TKIs. It is reported that histone deacetylase (HDAC) inhibitors could enhance the anti-tumor effects of other antineoplastic agents and radiotherapy. However, whether the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) can overcome erlotinib-acquired resistance is not fully clear.Methods:An erlotinib-resistant PC-9/ER cell line was established through cell maintenance in a series of erlotinib-containing cultures. NSCLC cells were co-cultured with SAHA, erlotinib, or their combination, and then the viability of cells was measured by the 3-(4,5-Dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and apoptosis was determined by flow cytometry and western blotting. Finally, the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) was assessed by western blotting.Results:The half-maximal inhibitory concentration of parental PC-9 cells was significantly lower than the established erlotinib-acquired resistant PC-9/ER cell line. PC-9/ER cells demonstrated reduced expression of PTEN compared with PC-9 and H1975 cells, and the combination of SAHA and erlotinib significantly inhibited cell growth and increased apoptosis in both PC-9/ER and H1975 cells. Furthermore, treating PC-9/ER cells with SAHA or SAHA combined with erlotinib significantly upregulated the expression of PTEN mRNA and protein compared with erlotinib treatment alone.Conclusions:PTEN deletion is closely related to acquired resistance to EGFR-TKIs, and treatment with the combination of SAHA and erlotinib showed a greater inhibitory effect on NSCLC cells than single-drug therapy. SAHA enhances the suppressive effects of erlotinib in lung cancer cells, increasing cellular apoptosis and PTEN expression. SAHA can be a potential adjuvant to erlotinib treatment, and thus, can improve the efficacy of NSCLC therapy.