CR16在特发性无精子症患者睾丸组织中的表达

目的:研究糖皮质激素区域表达基因16(corticosteroids and regional expression 16,CR16)在特发性无精子症患者睾丸组织中的表达,探讨CR16在精子发生中的作用。方法:采用免疫组化法和逆转录-聚合酶链反应(RT-PCR)检测CR16蛋白和CR16 mRNA在48例特发性无精子症患者(病例组)和10例正常生育男性(正常组)睾丸组织中的表达情况。结果:CR16蛋白表达于睾丸生精小管上皮,主要分布在支持细胞与生精细胞连接区,在特发性无精子症患者睾丸组织中的表达显著弱于正常生育男性睾丸组织中的表达。CR16 mRNA在病例组睾丸组织中的表达水平显著低于正常组。结论:特发性无精子症患者睾丸组织中CR16表达水平显著降低,这可能与无精子症相关。     

温下肠腑方对Lewis肺癌PCNA、p16、CyclinD1蛋白表达的影响

目的 观察温下肠腑方对Lewis肺癌移植瘤的抑制作用及对PCNA、p16、cyclinD1表达的影响.方法 :C57BL/6小鼠皮下接种Lewis肺癌,随机分为4组,即模型组,化疗组,温下方组和综合治疗组,化疗组和综合治疗组DDP 0.1 mg腹腔注射3 d,温下方组和综合治疗组中药灌胃10 d.计算抑瘤率,免疫荧光组织化学方法,激光共聚焦显微镜观察PCNA、p16、cyclinD1的表达.结果 温下方组抑瘤率为34.5%,平均瘤重低于模型组(P＜0.05);温下方组、综合治疗组和化疗组PCNA、cyclinD1表达明显低于模型组(P＜0.05),其余各组无显著差异.结论 温阳除滞法为主的温下肠腑方有一定的抑制肺癌生长的作用,且与顺铂有协同作用,温下肠腑方可能通过对PCNA、cyclinD1的抑制,从而抑制肿瘤生长.     

16排螺旋CT多期增强扫描对早期肝癌的诊断

目的：分析早期肝癌的各期增强图像的特点,提高早期肝癌的检出率.方法：经手术病理或临床随访证实的直径3cm以下的肝占位74例,应用16排螺旋CT多期增强扫描,进行各期图像重建.结果：原发性肝细胞癌在动脉期表现为高密度强化,在静脉期表现为低密度无强化,在平衡期表现为低密度无强化.结论：16排螺旋CT多期增强扫描是诊断早期肝癌行之有效的方法.     

中医之“痰”与黏蛋白

中医之"痰"有狭义之痰和广义之痰,与现代医学之痰大有不同,但现代医学的发展,可尝试揭示中医之痰的科学性。黏蛋白不仅参与中医狭义之痰的形成,而且在分布、致病方面与中医广义之痰极其相似。提示黏蛋白是中医之"痰"的物质基础之一。     

人参皂苷Rg1延缓造血干细胞衰老与 p16INK4a表达关系的研究

目的:探讨人参皂苷单体Rg1延缓造血干细胞(HSC)衰老与p16INK4a的表达调控关系,为寻找延缓HSC衰老途径提供理论和实验依据.方法:免疫磁性分选法分离纯化Sca-1+HSC后分组.对照组常规培养;衰老组运用三丁基过氧化氢(t-BHP)复制衰老模型;Rg1组在对照组基础上加入10μmol·L-1Rg1共培养;Rg1延缓衰老组给予10μmol·L-1Rg1预处理后,复制衰老模型;Rg1治疗衰老组,衰老模型复制后,给予10μmol·L-1Rg1抗衰老处理.衰老相关β半乳糖苷酶(SA-β-gal)细胞化学染色、流式细胞术分析细胞周期和造血祖细胞混合集落(CFU-Mix)培养确定Rg1延缓或治疗Sca-1+HSC衰老生物学作用.RT-PCR及Western blotting检测衰老相关基因pl6INK4amRNA及蛋白的表达.结果:Rg1延缓衰老组,Rg1治疗衰老组与衰老组相比,SA-β-gal染色阳性细胞百分比降低,G1期细胞比例下降,生成造血祖细胞混合集落数增加,p16INK4amRNA及蛋白的表达下降;Rg1延缓衰老组的SA-β-gal染色阳性细胞百分比、G1期比例、pl6INK4amRNA及蛋白的表达均低于Rg1治疗衰老组,形成造血祖细胞混合集落数高于Rg1治疗衰老组.结论:Rg1具有延缓和治疗Sca-1+HSC衰老的作用,Rg1延缓衰老比治疗衰老效果更好.Rg1可能通过调控p16INK4a的表达发挥其对抗t-BHP诱导的Sca-1+HSC衰老的作用.     

Why MUC16 mutations lead to a better prognosis: A study based on The Cancer Genome Atlas gastric cancer cohort

BACKGROUND MUC16, encoding cancer antigen 125, is a frequently mutated gene in gastric cancer. In addition, MUC16 mutations seem to result in a better prognosis in gastric cancer. However, the mechanisms that lead to a better prognosis by MUC16 mutations have not yet been clarified.AIMTo delve deeper into the underlying mechanisms that explain why MUC16 mutations signal a better prognosis in gastric cancer.METHODSWe used multi-omics data, including mRNA, simple nucleotide variation, copy number variation and methylation data from The Cancer Genome Atlas, to explore the relationship between MUC16 mutations and prognosis. Cox regression and random survival forest algorithms were applied to search for hub genes. Gene set enrichment analysis was used to elucidate the molecular mechanisms. Single-sample gene set enrichment analysis and “EpiDISH” were used to assess immune cells infiltration, and “ESTIMATE” for analysis of the tumor microenvironment.RESULTSOur study found that compared to the wild-type group, the mutation group had a better prognosis. Additional analysis indicated that the MUC16 mutations appear to activate the DNA repair and p53 pathways to act as an anti-tumor agent. We also identified a key gene, NPY1R (neuropeptide Y receptor Y1), which was significantly more highly expressed in the MUC16 mutations group than in the MUC16 wild-type group. The high expression of NPY1R predicted a poorer prognosis, which was also confirmed in a separate Gene Expression Omnibus cohort. Further susceptibility analysis revealed that NPY1R might be a potential drug target for gastric cancer. Furthermore, in the analysis of the tumor microenvironment, we found that immune cells in the mutation group exhibited higher anti-tumor effects. In addition, the tumor mutation burden and cancer stem cells index were also higher in the mutation group than in the wild-type group.CONCLUSIONWe speculated that the MUC16 mutations might activate the p53 pathway and DNA repair pathway: alternatively, the tumor microenvironment may be involved.     

胃癌前病变大鼠中抑癌基因APC、P16表达与浊毒的相关性研究

目的：观察化浊解毒中药对胃癌前病变模型大鼠胃黏膜APC、P16蛋白表达的影响,探讨胃癌前病变大鼠中抑癌基因APC、P16的表达与浊毒之间所存在的相关性。方法：采用结合致癌物的综合造模方法复制胃癌前病变大鼠模型,将造模大鼠随机分为化浊解毒中药组（以下简称＂中药组＂）、模型对照组、空白对照组3组。造模成功后中药组给予化浊解毒中药灌服,模型对照组和空白对照组均给予生理盐水灌胃。连续给药4周后将大鼠断头处死,解剖取胃,石蜡包埋连续切片,用免疫组化方法检测胃黏膜APC和P16蛋白的表达。结果：与空白对照组相比,模型组大鼠胃黏膜APC和P16蛋白的表达明显降低（P〈0.05）。与模型对照组比较,中药组大鼠胃黏膜APC和P16蛋白的表达明显升高（P〈0.05）。结论：化浊解毒中药能上调胃癌前病变大鼠抑癌基因APC、P16的水平,增加APC、P16蛋白的表达,从而抑制细胞增殖和诱导细胞凋亡,说明胃癌前病变大鼠中抑癌基因APC、P16表达与浊毒之间存在相关性。     

泻肺化痰汤对肺炎咳嗽痰热闭肺证患儿NK细胞及其活性的影响

目的:探讨痰热闲肺证惠几经泻肺化痰汤治疗前后NK细胞亚群CD16+、CD16+CD56+及NK细胞活性的变化.方法:肺炎喘嗽痰热壅肺证患儿80例,随机分为2组,两组均采用西药常规治疗,治疗组40例采用泻肺化痰汤治疗.采用流式细胞术动态测定肺炎喘嗽第1天、第7天空腹外周血液NK细胞(CD16+,CD16+CD56+)亚群...