萎缩小肠粘膜上皮细胞凋亡及增殖细胞核抗原表达变化的研究

目的：探讨小肠粘膜萎缩的发生机制。材料和方法;采用原位末端标记和免疫组化的方法,对正常和萎缩肠粘膜上皮细胞凋亡的发生,分布及增殖细胞核抗原（ＰＣＮＡ０的表达进行对比研究。结果：调亡细胞主要位于肠绒毛的顶部,萎缩小肠粘膜上皮细胞凋亡的发生率明显高于正常小肠（Ｐ〈０．０５）;而ＰＣＮＡ阳性表达细胞主要位于腺隐窝区,萎缩小肠粘膜上皮细胞ＰＣＮＡ的阳性计数较正常小肠显著降低。     

高胆固醇血症大鼠LDL受体与apoA—1mRNA的水平变化及苯甲…

本文研究了实验性高胆固醇血症大鼠肝及小肠中低密度脂蛋白（ＬＤＬ）受体ｍＲＮＡ和载脂蛋白（ａｐｏ）Ａ－１ｍＲＮＡ的水平变化以及苯甲酸雌二醇（ＥＢ）对二者的影响。发现高脂（ＨＣ）组肝及小肠ＬＤＬ受体ｍＲＮＡ水平分别低于正常组５０％和６０％（Ｐ〈０．０５），小肠ａｐｏＡ－１ｍＲＮＡ水平低于正常组５８％（Ｐ〈０．０５），此时血清总胆固醇（ＴＣ）及ＬＤＬ胆固醇（ＬＤＬ－ｃ）均明显于正常组（Ｐ〈０．０１），血     

高胆固醇血症大鼠LDL受体与apoA－1mRNA的水平变化及苯甲酸雌二醇对其影响

本文研究了实验性高胆固醇血症大鼠肝及小肠中低密度脂蛋白（ＬＤＬ）受体ｍＲＮＡ和载脂蛋白（ａｐｏ）Ａ－１ｍＲＮＡ的水平变化以及苯甲酸雌二醇（ＥＢ）对二者的影响。发现高脂（ＨＣ）组肝及小肠ＬＤＬ受体ｍＲＮＡ水平分别低于正常组５０％和６０％（Ｐ＜０．０５），小肠ａｐｏＡ－１ｍＲＮＡ水平低于正常组５８％（Ｐ＜０．０５），此时血清总胆固醇（ＴＣ）及ＬＤＬ胆固醇（ＬＤＬ－ｃ）均明显高于正常组（Ｐ＜０．０１），血清ａｐｏＡ－１低于正常组（Ｐ＜０．０５）。ＨＣ＋ＥＢ组血清ＴＣ及ＬＤＬ－ｃ明显低于ＨＣ组，而肝ＬＤＬ受体ｍＲＮＡ水平则显著高于ＨＣ组，为ＨＣ组的３．５倍（Ｐ＜０．００２）。结果提示：（１）高胆固醇负荷时细胞可通过转录水平下行调节ＬＤＬ受体；（２）小肠可能在ａｐｏＡ－１的代谢中起重要作用；（３）ＥＢ可能通过诱导肝ＬＤＬ受体基因表达而降血脂。     

SLE病人外周血Bcl—2／JH基因重排检测的意义

应用聚合酶链反应（ＰＣＲ）方法检测３１例ＳＬＥ病人外周血单个核细胞（ＰＢＭＣ）Ｂｃｌ－２／ＪＨ基因重排现象和流式细胞仪间接双标记法分析其Ｔ（ＣＤ３）、Ｂ（ＣＤ１９）细胞Ｂｃｌ－２蛋白的表达。结果显示，ＳＬＥ病人Ｔ细胞Ｂｃｌ－２蛋白表达明显高于正常人（４２．９５％±２８．４７％对比９．９４％±４．９６％，Ｐ＝０．０００４），尤其以活动期ＳＬＥ病人为明显，而Ｂ细胞Ｂｃｌ－２蛋白表达与正常人之间并无统计学差异（７９．２１％±１０．６９％对比８１．９６％±６．９７％；Ｐ＝０．４６０２）。７例ＳＬＥ病人具有典型的Ｂｃｌ－２／ＪＨ基因重排（占２２．５８％），且均为ＳＬＥ活动期病人，其Ｔ细胞Ｂｃｌ－２蛋白表达明显高于无基因重排的ＳＬＥ病人，其Ｂ细胞Ｂｃｌ－２表达并无差异（Ｐ＞０．３９０５）。说明Ｂｃｌ－２／ＪＨ基因重排现象可见于ＳＬＥ，并与Ｔ细胞Ｂｃｌ－２蛋白高表达有关，表明细胞凋亡抑制基因Ｂｃｌ－２在ＳＬＥ发病机制中具有重要作用。     

细胞因子在免疫复合物型肾小球肾炎发病机制中的作用

按Ｄｉｘｏｎ方法制造血清病型肾小球肾炎动物模型，进而研究其发病机制，模型ＡＥＳＳＲ血清ＣＩＣ水平明显高于正常值（Ｐ〈０．０１）；ＣＭＳＣ水平明显低于正常值（Ｐ〈０．０１），ｓＩｌ－２Ｒ，ＩＬ－８，ＩＦＮ，ＴＮＦ和ＩＬ－２水平均明显高于正常值（Ｐ〈０．０１），ＣＩＣ与ＣＭＳＣ呈高度负相关，ｒ＝－０．９４３（Ｐ〈０．０５），ＣＩＣ与ＩＬ－８呈高度正相关，相关系数ｒ＝０．８２９（Ｐ〈０．０５）。进一步证     

丙型肝炎病毒感染者血清细胞因子的检测

目的 探讨丙型肝炎病毒（ＨＣＶ）感染慢性化的宿主免疫机制。方法 用酶联免疫吸附实验测定了１８例慢性ＨＣＶ感染者、１１例正常对照和１０例慢性ＨＢＶ感染者的Ｔ辅助淋巴细胞（Ｔｈ０细胞因子ＩＦＮ－γ,ＩＬ－２,ＩＬ－４和ＩＬ－１０的血清浓度。结果 ＨＣＶ感染者的ＩＬ－２（Ｔｈ１细胞因子）、ＩＬ－４的ＩＬ－１０（Ｔｈ２细胞因子）较正常对照均明显增高（Ｐ〈０．０５,Ｐ〈０．０２５,Ｐ〈０．００１）,但以Ｔｈ     

系统性红斑狼疮患者B淋巴细胞EBV-LMP1和ZEBRA的表达研究

目的：探讨ＥＢＶ－ＬＭＰ１和ＺＥＢＲＡ在系统性红斑狼疮患者（ＳＬＥ）的表达情况。方法：间接荧光免疫标记，流式细胞仪检测。结果：ＳＬＥ患者Ｂ淋巴细胞中ＥＢＶ－ＬＭＰ１和ＺＥＢＲＡ的表达显著高于正常对照组（Ｐ＜０．０１）。活动期患者ＣＤ２３＋细胞ＥＢＶ－ＬＭＰ１和ＺＥＢＲＡ的表达率均高于ＣＤ１９＋细胞（Ｐ＜０．０１）。非活动期患者ＣＤ２３＋细胞ＥＢＶ－ＬＭＰ１表达也高于ＣＤ１９＋细胞（Ｐ＜０．０１）。但ＥＢＶ－ＺＥＢＲＡ表达在两亚群间差异没有统计学意义（Ｐ＞０．０５）。结论：朋病毒参与了ＳＬＥ的发病机制，病毒主要以潜伏期状态存在于患者中，病毒复制促进病情发展，检测Ｂ淋巴细胞ＥＢＶ－ＬＭＰ１和ＺＥＢＲＡ的表达率，有助于病情活动指标的判断。     

急性早幼粒细胞白血病患者诱导分化治疗前后血清IL—2受体的…

ＥＬＩＳＡ法检测２７例急性早幼粒细胞白血病患者（ＡＰＬ）血清白细胞介素２受体（ｓＩＬ－２Ｒ）水平。结果表明ＡＰＬ患者血清ｓＩＬ－２Ｒ高于正常对照（Ｐ〈０．０１），经维甲酸治疗后逐渐降低，但治疗中期患者血清ｓＩＬ－２Ｒ仍高于正常和治疗后（缓解期）患者血清ｓＩＬ－２Ｒ（Ｐ〈０．０５）。治疗后血清ｓＩＬ－２Ｒ虽略高于正常对照。却已恢复正常范围（Ｐ〈０．０５）。同时发现治疗中ＷＢＣ却明显升高，治疗后又下降     

过敏性哮喘豚鼠血小板激活因子的变化及川芎嗪的影响

本研究采用生物定量测定方法观察了豚鼠实验性哮喘时血浆ｌｙｓｏ－ＰＡＦ和肺泡灌洗（ＢＡＬＦ）中ＰＡＦ的变化。结果显示：致敏级豚鼠哮喘发作时血浆ｌｙｓｏ－ＰＡＦ水平显著高于对照组（Ｐ〈０．０１），ＢＡＬＦ中ＰＡＦ水平也明显高于对照组（Ｐ〈０．０５），同时伴有血浆及ＢＡＬＦ中ＴＸＢ２、ＴＸＢ２／６－酮－ＰＧＦ１α水平的升高（Ｐ〈０．０１）。致敏＋川芎嗪组豚鼠血浆ｌｙｓｏ－ＰＡＦ明显低于致敏组豚鼠（Ｐ〈０     

胆囊结石患者的血清脂质研究

本文对５１例胆石病患者和１９例非胆石病者，测定了２０项与脂质代谢有关的指标。ｔ检验提示：胆石组血ａｐｏＢ－１００和血清胰岛素高于非胆石组（Ｐ〈０．０５），红细胞超氧化物歧化酶低于非胆石组（Ｐ〈０．０５）。对２０项指标作逐步判别分析发现，ａｐｏＡ－１、ＨＤＬ－Ｃｈ和ＬＤＬ－Ｃｈ三项指标所构成的函数式对两类判别起重要作用（Ｐ〈０．０５），其中胆石组ａｐｏＡ－１和ＨＤＬ－Ｃｈ高于非胆石组、ＬＤＬ－Ｃｈ低     

miR-222通过调控BCL2L13基因促进HBx-HepG2细胞生长

目的:探讨HBx-Hep G2细胞中微小RNA-222(mi R-222)对BCL2L13基因表达的调控作用以及对细胞生长和凋亡的影响,并研究其潜在的分子作用机制。方法:利用实时荧光定量PCR检测mi R-222的表达水平;MTT和集落形成实验检测细胞的生长;流式细胞术检测细胞周期和凋亡;构建BCL2L13 3’UTR双萤光素酶报告载体,通过采用双萤光素酶报告实验验证mi R-222的靶基因。结果:与正常的肝细胞L02相比,mi R-222在HBx-Hep G2细胞过量表达(P0.05)。mi R-222过表达可促进HBx-Hep G2细胞的生长,改变细胞周期,降低细胞的凋亡率;mi R-222表达下调可抑制HBx-Hep G2细胞的生长,改变细胞周期,增加细胞的凋亡率,和对照组相比差异有统计学显著性(P0.05)。与正常肝细胞L02相比,BCL2L13在HBx-Hep G2细胞表达下调(P0.05);mi R-222表达下调可促进BCL2L13的表达(P0.05)。双萤光素酶报告实验和pc DNA3.1-BCL2L13转染实验结果提示mi R-222可以通过作用于BCL2L13的3’UTR区,负向调控其表达,从而促进细胞的生长。结论:mi R-222可以通过靶向调控BCL2L13基因进而促进HBx-HepG2细胞的生长。     

Ischemic postconditioning provides protection against ischemia-reperfusion injury in intestines of rats

In the present study, we investigated the protective role of ischemic postconditioning (IPOST) against intestine ischemia-reperfusion (I/R) injury in rats. Male Sprague-Dawley rats were divided into sham-operation group (S), I/R group (I/R), ischemic preconditioning group (IPC), ischemic postconditioning group (IPOST). After reperfusion, small intestines were resected for histopathologic evaluations. To evaluate DNA fragmentation, resolving agarose gel electrophoresis was performed. To measure cellular apoptotic rates in intestine tissues, we performed TUNEL staining. To examine lipid peroxidation, production of superoxide radicals and tissue neutrophil infiltration, we tested the content of malondialdehyde and activities of superoxidase dismutase and myeloperoxidase in intestine tissues, respectively. Under light microscope, intestinal mucosal impairment in IPOST and IPC groups was found milder than that in I/R group (P < 0.05). The number of apoptosis cells in I/R group was significantly higher than that in IPOST and IPC groups (P < 0.05). The content of malondialdehyde and activity of myeloperoxidase were significantly reduced in IPOST group and IPC group compared with I/R group, but the activity of superoxidase dismutase in IPOST group and IPC group was enhanced compared with I/R group (P < 0.05). These results suggest that IPOST results in protection against intestine I/R injury, which may be related to reduced production of reactive oxygen species, enhanced activities of antioxidant systems and inhibited apoptosis of intestinal mucosal cells.     

缺血后处理通过抑制线粒体途径减轻缺血/再灌注诱导的肠黏膜细胞凋亡

目的：探讨缺血后处理减轻缺血/再灌注损伤肠黏膜细胞凋亡的机制。方法:SD大鼠随机分为4组（n=8）：假手术（sham）组、缺血/再灌注（I/R）组、缺血预处理（IPreC）组、缺血后处理（IPostC）组;应用透射电子显微镜和激光共聚焦扫描显微镜分别观测各组大鼠肠黏膜细胞线粒体形态结构改变和线粒体跨膜电位的变化。应用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法（TUNEL）、逆转录-聚合酶链反应（RT-PCR）方法和免疫组织化学方法分别检测各组大鼠肠黏膜细胞凋亡发生情况以及肠黏膜细胞bcl-2、bax mRNA及Bcl-2、Bax蛋白表达的变化。结果:与I/R组相比,IPostC组和IPreC组大鼠肠黏膜细胞线粒体形态结构改变明显减轻,线粒体跨膜电位显著升高（均P<0.05）,肠黏膜细胞凋亡率明显降低（均P<0.05）,肠黏膜细胞bcl-2 mRNA和Bcl-2蛋白表达水平显著上升,bax mRNA和Bax蛋白表达水平明显下降（均P<0.05）,IPostC组和IPreC组相比各项指标差异无显著差异（均P>0.05）。结论:缺血后处理可能通过抑制线粒体途径减轻缺血/再灌注诱导肠黏膜细胞的凋亡。     

Menstrual-like breakdown and apoptosis in human endometrial explants

BACKGROUND: Apoptosis occurs in late secretory and menstrual human endometrium and is thought to play an important role in endometrial physiology. Menstrual-like breakdown has been observed in vitro in endometrial explants. The purpose of this study was to assess the role of apoptosis in menstrual-like breakdown in human endometrial explants. METHODS: Human endometrial tissue was obtained during the mid-secretory phase and cultured with or without estrogen and progesterone. The occurrence of breakdown was assessed by histology. Apoptosis was determined by gel electrophoresis for the detection of DNA fragmentation and by immunohistochemistry using the M30 CytoDEATH and anti-cleaved caspase-3 (CASP3) antibodies for the detection of caspase activity. Expression of BCL2 and BAX was quantified using real-time PCR analysis. RESULTS: Apoptosis occurred in human endometrial explants at all time-points studied. Cleaved CASP3 and M30 antigen expression increased in all explants, suggesting the involvement of CASP3 in the apoptosis. Low BCL2:BAX ratios were observed in all samples when compared with pre-culture controls. Estradiol and progesterone supplementation of the culture media reduced or eliminated menstrual-like breakdown but did not affect the degree of apoptosis observed. CONCLUSIONS: The apoptosis observed in endometrium during the late secretory phase and menstrual phase does not appear to be mechanistically related to the tissue breakdown but rather may be involved in the impending remodelling that occurs in the endometrium in the transition from secretory to proliferative phase following the menses.     

藏羚羊和藏绵羊小肠黏膜结构和黏膜免疫相关细胞的比较

目的:比较藏羚羊和藏绵羊小肠黏膜结构和黏膜免疫相关细胞的特征。方法:采用组织学、组织化学方法和图像分析法在光镜和电镜水平对5只藏羚羊和5只藏绵羊小肠不同肠段的黏膜结构进行观测,并对上皮内淋巴细胞、杯状细胞和肥大细胞的数量进行统计分析。结果:藏羚羊小肠各段绒毛长度和绒毛长度与隐窝深度比值(villus length/crypt depth,V/C)均显著高于藏绵羊(P<0.05),其中藏羚羊十二指肠、空肠和回肠的绒毛长度分别比藏绵羊高77.25%(P<0.05)、63.61%(P<0.05)和35.38%(P<0.05),而V/C值分别比藏绵羊高65.63%(P<0.05)、20.08%(P<0.05)和35.68%(P<0.05),藏羚羊小肠黏膜的厚度显著大于藏绵羊(P<0.05),而藏羚羊和藏绵羊小肠肌层厚度差异不显著(P>0.05);藏羚羊小肠各段上皮内杯状细胞和肥大细胞数量显著多于藏绵羊(P<0.05),其中藏羚羊十二指肠、空肠和回肠中的上皮内杯状细胞数量分别比藏绵羊的多12.84%(P<0.05)、49.88%(P<0.05)和5.58%(P>0.05),藏羚羊十二指肠、空肠和回肠中的肥大细胞的数量比藏绵羊的分别多0.22%(P>0.05)、6.04%(P>0.05)和160.80%(P<0.05),而藏羚羊小肠各段上皮内淋巴细胞数量显著低于藏绵羊(P＜0.05),其中藏羚羊十二指肠、空肠和回肠的上皮内淋巴细胞数量分别比藏绵羊的少35.04%(P<0.05)、52.85%(P<0.05)和52.82%(P<0.05)。结论:藏羚羊小肠消化吸收功能强于藏绵羊,藏羚羊的小肠黏膜免疫屏障功能也强于藏绵羊,且在藏羚羊小肠杯状细胞和肥大细胞起重要的黏膜防御功能,而在藏绵羊小肠中上皮内淋巴细胞起重要的黏膜免疫屏障功能。     

Gastric mucosal inflammation and epithelial cell turnover are associated with gastric cancer in patients with Helicobacter pylori infection

BACKGROUND: Infection with a virulent Helicobacter pylori strain is associated with gastric mucosal damage and the increased risk of gastric cancer. AIMS: To examine the characteristics of host gastric mucosal responses in patients with gastric cancer, histological grade of gastritis, gastric epithelial apoptosis, and proliferation were studied. METHODS: Thirty two patients with early gastric cancer and 32 sex and age matched controls were studied. All subjects were infected with a virulent H pylori strain (vacA s1/m1, cagA positive genotype). Biopsy specimens were taken from the antrum and the corpus of the stomach. The grade of gastritis was assessed according to the updated Sydney system. Apoptotic cells were detected using terminal uridine deoxynucleotidyl nick end labelling, and epithelial cell proliferation was determined by means of the Ki-67 labelling index. RESULTS: In patients with gastric cancer, significantly higher grades were observed when glandular atrophy (p < 0.05) and intestinal metaplasia (p < 0.01) were present in the antrum, and when mononuclear cell infiltration was present in the corpus (p < 0.05). The numbers of apoptotic cells were increased in patients with cancer (p < 0.05) and the apoptotic index correlated significantly with the grade of glandular atrophy. Epithelial cell proliferation was more likely to be increased in mucosa where intestinal metaplasia was present. CONCLUSIONS: Infection with H pylori causes increased gastric epithelial apoptosis, resulting in more severe glandular atrophy in patients with gastric cancer. Increased damage of gastric epithelial DNA and the presence of more severe atrophic gastritis might contribute to the development of gastric cancer.     

解除狭窄联合Rho激酶抑制剂对颈动脉狭窄大鼠认知功能的影响

目的 观察解除狭窄联合Rho激酶抑制剂对重度颈动脉狭窄大鼠认知功能(VCI)、海马区细胞凋亡及相关基因表达.方法 用48只SD大鼠,复制重度颈动脉狭窄模型,分成假手术组、狭窄解除组、药物组和联合组,另12只为对照组.联合组给予狭窄解除和法舒地尔(8.35 mg/kg),药物组注射等量的法舒地尔,狭窄解除组给予解除狭窄,对照组注射等容积的0.9％氯化钠注射液.分别在干预2和4周后,Morris水迷宫实验检测大鼠的空间学习记忆能力;免疫组化方法检测海马区凋亡相关蛋白BCL-2及BAX免疫阳性细胞数;TUNEL染色法检测海马区凋亡神经细胞.结果 与单纯药物组和狭窄解除组比较,联合治疗组大鼠的逃避潜伏期和游泳距离百分比均有显著改善(P＜0.05),海马区凋亡相关蛋白BCL-2免疫阳性细胞数显著增加(P＜0.05),而BAX的免疫阳性细胞数显著降低(P＜0.05),且治疗4周比2周更明显(P＜0.05);联合治疗组大鼠海马区的神经细胞凋亡率为56.24％±2.25％,明显低于药物治疗组和狭窄解除组的63.86％ ±2.23％和61.89％±2.67％(P ＜0.05),且随着治疗时间延长,细胞凋亡率呈下降趋势.结论 解除颈动脉狭窄联合Rho激酶抑制剂可通过调节凋亡相关蛋白的表达而明显改善颈动脉狭窄引起的认知功能障碍.     

Protective effect of Curcumin on chemotherapy-induced intestinal dysfunction

Objective: Chemotherapy is one of most important treatments for human cancers. However, side effects such as intestine dysfunction significantly impaired its clinical efficacy. This study aimed to investigate the protective effect of Curcumin on chemotherapy-induced intestinal dysfunction in rats. Methods: Sixty healthy Wistar rats were randomly divided into control group (normal saline), 5-FU group and 5-FU+Curcumin group. The weight, serum level of endotoxin, DAO and D-lactate were determined. The pathological change of intestinal mucosa structure was studied under light microscopy and electron microscopy. The expression of Bax, Bcl-2 and Caspase-3 were assessed by immunohistochemical staining. Results: The Curcumin intragastrically administrated obviously reduced 5-FU-induced weight-loss. 5-FU induced dramatic increase of serum endotoxin, D-lactate and D-Amino-Acid Oxidase (DAO) that were significantly reversed by Curcumin treatment. Meanwhile, 5-FU-induced-damage to intestinal mucosa structure was markedly recovered by Curcumin. The expression of Bax and Caspase-3 were dramatically increased after 5-FU treatment (p<0.01) and Curcumin treatment significantly reduced Bax expression (p<0.05) but had only a moderate effect on reducing caspase-3 expression (p>0.05). Interestingly, Bcl-2 expression was low in control group but increased after 5-FU treatment (p>0.05) and Curcumin treatment further stimulated Bcl-2 expression (p<0.05). Conclusions: Curcumin can significantly reverse chemotherapy-induced weight-loss, increase of serum endotoxin, D-lactate and DAO and damage to intestinal mucosa structure. Curcumin also reduced the expression of pro-apoptotic Bax but stimulated anti-apoptotic Bcl-2 to attenuate 5-FU-induced apoptosis of intestinal epithelial cells. The clinical administration of Curcumin may improve chemotherapy-induced intestinal dysfunction, thus increasing the clinical efficacy of chemotherapy.     

Epigenetic Role of Histone 3 Lysine Methyltransferase and Demethylase in Regulating Apoptosis Predicting the Recurrence of Atypical Meningioma

Alteration of apoptosis is related with progression and recurrence of atypical meningiomas (AMs). However, no comprehensive study has been conducted regarding histone modification regulating apoptosis in AMs. This study aimed to determine the prognostic values of certain apoptosis-associated factors, and examine the role of histone modification on apoptosis in AMs. The medical records of 67 patients with AMs, as diagnosed during recent 13 yr, were reviewed retrospectively. Immunohistochemical staining was performed on archived paraffin-embedded tissues for pro-apoptotic factors (CASP3, IGFBP, TRAIL-R1, BAX, and XAF1), anti-apoptotic factors (survivin, ERK, RAF1, MDM2, and BCL2), and the histone modifying enzymes (MLL2, RIZ, EZH1, NSD2, KDM5c, JMJD2a, UTX, and JMJD5). Twenty-six (38.8%) patients recurred during the follow-up period (mean duration 47.7 months). In terms of time-to-recurrence (TTR), overexpression of CASP3, TRAIL-R1, and BAX had a longer TTR than low expression, and overexpression of survivin, MDM2, and BCL2 had a shorter TTR than low expression (P<0.05). Additionally, overexpression of MLL2, UTX, and JMJ5 had shorter TTRs than low expression, and overexpression of KDM5c had a longer TTR than low expression. However, in the multi-variate analysis of predicting factors for recurrence, low expression of CASP3 (P<0.001), and BAX (P<0.001), and overexpression of survivin (P=0.007), and MDM2 (P=0.037) were associated with recurrence independently, but any enzymes modifying histone were not associated with recurrence. Conclusively, this study suggests certain apoptosis-associated factors should be associated with recurrence of AMs, which may be regulated epigenetically by histone modifying enzymes.

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