简介:以便揭示在二CCDD染色体种,Oryzaalta和Oryzalatifolia之间的起源和进化关系,在situ杂交(鱼)的荧光被采用从O与C0t-1DNA分析二种的染色体。alta作为一根探针。Karyotype比较地也在O之间被分析。alta和O。latifolia基于他们杂交的类似的乐队模式发信号。在O之间有高相同和靠近的关系。alta和O。然而,在杂交之间的区别表明的latifolia也是清楚的。C0t-1DNA被证明是种类--并且染色体类型特定。C0t-1DNA鱼能是更有效的分析在不同种类之间的genomic关系,这被建议。根据在二allotetraploidy种之间的高度并且中等重复的DNA序列的比较分析,O。alta和O。latifolia,可能的起源和Oryza的allotetraploidy的进化机制被讨论。
简介:AbstractBackground:Long non-coding RNA (lncRNA) actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) functions as a competing endogenous RNA to regulate target genes expression by sponging microRNAs (miRs) to play cancer-promoting roles in cancer stem cells. However, the regulatory mechanism of AFAP1-AS1 in cervical cancer (CC) stem cells is unknown. The present study aimed to provide a new therapeutic target for the clinical treatment of CC.Methods:Hyaluronic acid receptor cluster of differentiation 44 variant exon 6 (CD44v6)(+) CC cells were isolated by flow cytometry (FCM). Small interfering RNAs of AFAP1-AS1 (siAFAP1-AS1) were transfected into the (CD44v6)(+) cells. The levels of AFAP1-AS1 were measured by quantitative real-time PCR (qRT-PCR). Sphere formation assay, cell cycle analysis, and Western blotting were used to detect the effect of siAFAP1-AS1. RNA pull-down and luciferase reporter assay were used to verify the relationship between miR-27b-3p and AFAP1-AS1 or vascular endothelial growth factor (VEGF)-C.Results:CD44v6(+) CC cells had remarkable stemness and a high level of AFAP1-AS1. However, AFAP1-AS1 knockdown with siAFAP1-AS1 suppressed the cell cycle transition of G(1)/S phase and inhibited self-renewal of CD44v6(+) CC cells, the levels of the stemness markers octamer-binding transcription factor 4 (OCT4), osteopontin (OPN), and cluster of differentiation 133 (CD133), and the epithelial-mesenchymal transition (EMT)-related proteins Twist1, matrix metalloprotease (MMP)-9, and VEGF-C. In the mechanism study, miR-27b-3p/VEGF-C signaling was demonstrated to be a key downstream of AFAP1-AS1 in the CD44v6(+) CC cells.Conclusions:LncRNA AFAP1-AS1 knockdown inhibits the CC cell stemness by upregulating miR-27b-3p to suppress VEGF-C.
简介:本研究探讨供受者HLA-A/B/C/DRB1/DQB1等位基因不合的数目和位点对非血缘造血干细胞移植的影响。选取北京市道培医院101例非血缘造血干细胞移植病例,分别根据供受者HLA-A/B/C/DRB1/DQB1位点0-3个等位基因不合和HLA-C位点的不同,分组统计移植后1年以上总生存率、急性GVHD发生率和复发率。结果表明:①按供受者HLA等位基因水平10/10全相合组(30例)与9/10相合组(32例),8/10相合组(31例)以及7/10相合组(8例)分组比较,10/10和9/10组的1年以上总活存率(OS)较8/10组(78%and82%vs50%,p=0.39)增多;10/10组、9/10组和8/10组复发率为16%和18%vs20%;10/10组没有Ⅱ度以上GVHD发生,9/10和8/10组10%左右。7/10组虽然病例数少,缺乏统计学意义,但结果证实安全有效。②)对比HLA-C位点等位基因不合组与HLA-10/10全合组,HLA-C不合组有延长1年以上总生存率(77%vs85%,p=0.30),降低复发率的趋势(8%vs17%,p=0.47),其Ⅱ度以上GVHD发生率明显增高,统计学有明显差异(0%vs25%,p=0.006)。③按抑制性KIR的配体HLA-C1/C2将HLA-10/10组与HLA-C一个等位基因不合组按供受者HLA-C1/C2match和mismatch分为两组(37例和5例),发现1年以上总生存率、复发率,GVHD发生率无明显差异(78%vs80%,14%vs20%,和5%vs20%)。结论:供受者HLA-A/B/C/DRB1/DQB1等位基因不相合数目0-2个情况下,数目越少,1年以上生存率越高,复发率和急性GVHD无明显差异。7/10组是安全的。HLA-C不相合组GVHD发生率明显增高,有减少复发和延长生存率的趋势,但其原因是否与抑制性KIR与其配体HLA-C1/C2有关,尚待研究。
简介:Amurinemacrophage-likecelllineJ774,acquired,inresponsetoLPS,anabilitytokilltumornecrosisfactor(TNF)-insensitivetargetP815mastocytomacellswhereasanothercellline,P388D1didnot,LPStriggeredsignalingmechanismsbetweenthetwocelllineswerecomparedwithanaimtoinquireaboutthepossiblenatureoftheabove-mentioneddifference,TheresultswhowedthattwocelllinesrespondtoLPS-treatmentbyparallelactivationofbothphospholipasesCandA2(PLCandPLA2)toapproximatelythesameextent.ThemaximumresponseoftothenzymesofJ774cellswasnotedwithin10minthetreatmentwhereasthatofP388D1cellsrequiredmorethan20min,TheotherpropertiesofLPS-responsiveenzymesstudiedweresimilarbetweentwocelllines,includingActivationofPLCandPLA2andPKCinmacrophagesbyLPS.Ca2+augmentationofenzymeactivation,participationofguaninenucleotidebinding(G)proteinsintheinitialactivationpreocesses,andinhibitionofenzymeactivationbythepriortreatmentofcellswithcholeraorpertussistoxinsetc.Moreover,LPS-triggeredactivationofPLCandPLA2wasfoundtobefollowedbytheincreaseofPKCactivitiesinbothcelllines.Inspiteofthesesimilarities.J774cellspossessedbothbasicandacidicformsofPKCactivities,whileP388D1cellsownedonlyPKCofbasicform,Nevertheless,thequestionwhyJ774cellsbutnotP388D1cells,canacquirethetumoricidalactivity,aganistP815,cellsfollowingLPStreatmentrematinstobeanswered.
简介:摘要目的初探BCAR1、PDE1C、OPRD1以及NRXN1基因启动子区甲基化水平的改变与原发性痛风及高尿酸血症的相关性。方法在中国科学院大学宁波华美医院门诊及体检中心同期随机选取原发性痛风患者50例、高尿酸血症患者30例和健康对照体检者50名,提取脱氧核糖核酸(DNA),经甲基化转化后对3组受试者BCAR1、PDE1C、NRXN1以及OPRD1 4个基因启动子区的目标序列进行焦磷酸测序,得到其甲基化率。采用方差分析和非参数检验对3组病例的4种基因启动子区甲基化率进行统计学分析。结果受试者工作特征曲线(ROC曲线)分析提示PDE1C(pos4、pos5、pos6)的甲基化水平对诊断痛风有较高的准确性,ROC曲线下面积(AUC)为0.712、0.772、0.775,P均<0.05;OPRD1 pos4的甲基化水平对诊断高尿酸血症有较高的准确性(AUC=0.733,P<0.05)。结论DNA甲基化可能与痛风及高尿酸血症的发病和炎症反应具有一定的相关性,但仍需进一步研究。
简介:以柠檬酸铁、乙酸锰、乙酸钴和磷酸二氢锂为原料,采用喷雾干燥法制备LiFe1/3Mn1/3Co1/3PO4/C正极材料。采用X射线衍射(XRD),扫面电镜(SEM)以及电化学测试对合成材料进行表征。结果表明,在700℃下焙烧16h合成的LiFe1/3Mn1/3Co1/3PO4/C为结晶良好的橄榄石型结构,颗粒呈球形,球径在0.5-5μm之间。该样品在0.1C倍率下的首次放电比容量为128.3mAh/g,同时具有良好的倍率性能。
简介:AbstractIntroduction:Muir-Torre syndrome is a phenotypic variant of Lynch syndrome characterized by a predisposition for the development of visceral malignant disease and sebaceous gland neoplasms, and it is caused by germline mutations in the mismatch repair genes MSH2 and MLH1.Here, we reported a patient with sebaceous neoplasm containing MLH1 c.199G>A mutation.Case presentation:The proband was a 42-year-old man who had undergone surgical resection of colorectal adenocarcinoma at 28 years. He presented with macular rashes and red papule. Histological examination of the lesion on his head revealed a sebaceoma at 37 years. Follow-up of the family history revealed that the proband’s 65-year-old mother had been highly suspected to have Lynch syndrome with colorectal cancer at 40 years of age. The proband’s daughter underwent colonoscopy because of blood in the stool at the age of 13 years, but no abnormalities were found.Discussion:We have herein reported a pathogenic missense mutation c.199G>A (p.Gly67Arg) in exon 2 of MLH1 in patients with MTS. This mutation has been reported in patients with Lynch syndrome who have no skin tumors. However, we also found that some patients with MTS had no history of any internal malignancy or skin tumor. Our data support the idea that a hiatus of many years may pass before both elements-a sebaceous neoplasm and an internal cancer-are present in a patient, thus finally allowing the diagnosis of MTS.Conclusion:A pathogenic Lynch syndrome mutation c.199G>A in exon 2 of the MLH1 gene was found in a patient with MTS who presented with a sebaceous neoplasm.
简介:摘要目的探讨肝X受体α(LXRα)/固醇调节元件结合蛋白1c(SREBP-1c)在砷致大鼠脂代谢紊乱中的作用,为砷致脂代谢紊乱的机制研究提供依据。方法将24只健康清洁级Wistar大鼠,按体质量(80~100 g)采用随机数字表法分为4组,每组6只,雌雄各半。对照组给予去离子水灌胃;低、中、高砷剂量组分别给予2.5、5.0、10.0 mg·kg-1·d-1亚砷酸钠水溶液灌胃,每周染砷6 d,连续处理4个月,实验终期采集各组大鼠血液及肝脏样本。采用电感耦合等离子体质谱仪(ICP-MS)检测大鼠肝组织砷含量;全自动生化分析仪检测大鼠血清甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)水平;实时荧光定量PCR法检测肝组织LXRα、SREBP-1c mRNA表达水平;蛋白免疫印迹法(Western blot)检测肝组织LXRα、SREBP-1c、乙酰辅酶A羧化酶(ACC)、磷酸化ACC(pACC)蛋白表达水平。结果低、中、高砷剂量组大鼠肝砷含量分别为(61.04 ± 4.98)、(62.66 ± 6.71)、(87.86 ± 13.89)μg/g,均高于对照组[(2.43 ± 0.63)μg/g,P均< 0.05],且高砷剂量组大鼠肝砷含量高于低、中砷剂量组(P均< 0.05)。低、中、高砷剂量组大鼠血清TG水平分别为(0.90 ± 0.17)、(1.28 ± 0.24)、(1.82 ± 0.18)mmol/L,均高于对照组[(0.50 ± 0.12)mmol/L,P均< 0.05];低、中、高砷剂量组大鼠血清LDL-C水平分别为(0.54 ± 0.04)、(0.63 ± 0.07)、(0.69 ± 0.08)mmol/L,均高于对照组[(0.27 ± 0.05)mmol/L,P均< 0.05];中、高砷剂量组大鼠血清TC水平分别为(1.88 ± 0.23)、(2.10 ± 0.10)mmol/L,均高于对照组[(1.51 ± 0.14)mmol/L,P均< 0.05];中、高砷剂量组大鼠血清HDL-C水平分别为(0.84 ± 0.11)、(0.71 ± 0.14)mmol/L,均低于对照组[(1.15 ± 0.08)mmol/L,P均< 0.05];且中、高砷剂量组大鼠血清TG、LDL-C水平均高于低砷剂量组(P均< 0.05),高砷剂量组大鼠血清TG水平高于中砷剂量组(P < 0.05)。高砷剂量组大鼠肝组织LXRα mRNA表达水平高于对照组及低砷剂量组(P均< 0.05);低、中、高砷剂量组和对照组大鼠肝组织SREBP-1c mRNA表达水平比较,差异无统计学意义(P > 0.05)。中、高砷剂量组大鼠肝组织LXRα蛋白表达水平均高于对照组(P均< 0.05);高砷剂量组大鼠肝组织LXRα蛋白表达水平高于低砷剂量组(P < 0.05);高砷剂量组大鼠肝组织SREBP-1c、ACC蛋白表达水平均高于对照组(P均< 0.05)。染砷大鼠血清TG、TC、LDL-C水平,肝组织LXRα mRNA及LXRα、SREBP-1c、ACC蛋白表达水平与肝砷含量均呈正相关(r = 0.84、0.62、0.89、0.55、0.54、0.64、0.70,P均< 0.05),血清HDL-C水平与肝砷含量呈负相关(r = - 0.75,P < 0.001)。结论亚砷酸钠可引起大鼠血清TG、TC、LDL-C水平升高、HDL-C水平降低以及肝脏LXRα、SREBP-1c蛋白表达水平升高,提示砷致大鼠脂代谢紊乱可能与其上游LXRα/SREBP-1c调控机制有关。