lncRNA-miR210HG在非小细胞肺癌发生中的作用机制

目的:探讨lncRNA-miR210HG在非小细胞肺癌（NSCLC）发生中的作用机制。方法:收集2017年01月至2020年01月我院收治确诊的54例NSCLC患者的癌组织与癌旁组织,采用生物信息学在线程序预测lncRNA-miR210HG的潜在靶标miRNA,双荧光素酶实验检测NCI-H1650 NSCLC细胞中lncRNA-miR210HG和miRNA210的相互作用,qRT-PCR检测肺癌组织中lncRNA-miR210HG、miRNA210、HIF-1α、VEGF的mRNA表达水平,NCI-H1650 NSCLC细胞分别转染miRNA210类似物及抑制物后,采用qRT-PCR检测细胞水平lncRNA-miR210HG、HIF-1α与VEGF的mRNA表达。结果:lncRNA-miR210HG与miRNA210间存在互补结合序列,野生型lncRNA-miR210HG和miRNA210的荧光素酶活性低于对照组（P＜0.01）,且lncRNA-miR210HG与miRNA210的靶向结合是通过其3'-UTR区。NSCLC组织中lncRNA-miR210HG、miRNA210、HIF-1α（P＜0.001）及VEGF（P＜0.01）的mRNA表达水平均较癌旁组织中高,差异有统计学意义。NSCLC组织中lncRNA-miR210HG表达与miRNA210表达呈负相关。细胞实验发现,miRNA210过表达后,HIF-1α、VEGF、lncRNA-miR210HG的mRNA表达水平均下降,其中lncRNA-miR210HG、HIF-1α与对照组相比差异有统计学意义（lncRNA-miR210HG:P＜0.05;HIF-1α:P＜0.01）,miRNA210被抑制后,HIF-1α、VEGF、lncRNA-miR210HG的mRNA表达水平均较对照组升高,且差异均有统计学意义（lncRNA-miR210HG:P＜0.01;HIF-1α:P＜0.05;VEGF:P＜0.01）。结论:lncRNA-miR210HG 3'-UTR区通过与miRNA210的靶向结合,从而调控下游HIF-1α、VEGF的mRNA表达,可能参与了NSCLC的发生、发展。     

Epigenetic silencing of MIR203 in multiple myeloma

Epigenetic inactivation of tumour suppressor microRNAs has been implicated in carcinogenesis. We studied the promoter methylation of MIR203 in eight normal marrow controls, eight multiple myeloma (MM) cell lines, 20 monoclonal gammopathy of undetermined significance (MGUS), 123 diagnostic MM and 19 relapsed MM samples by methylation-specific polymerase chain reaction. Promoter of MIR203 was unmethylated in normal controls but homozygously methylated in 25% MM cell lines. Treatment with 5-Aza-2'-deoxycytidine led to promoter demethylation and MIR203 re-expression. Cyclic AMP responsive element binding protein 1 (CREB1) mRNA was predicted as a MIR203 direct target. Luciferase activity was reduced in constructs carrying wild-type CREB1 3'UTR upon MIR203 expression but not in those carrying mutant CREB1 3'UTR. Moreover, restoration of MIR203 led to downregulation of CREB1 protein and inhibition of myeloma cell proliferation. In primary samples, MIR203 methylation occurred in 25·0% MGUS, 23·6% diagnostic MM, and 21·1% relapsed MM samples. In conclusion, MIR203 methylation is disease-specific with reversible gene silencing in MM. MIR203 is a tumour suppressor microRNA inhibiting cellular proliferation by targeting CREB1 mRNA in MM. Comparable occurrence of MIR203 methylation in MGUS and MM at diagnosis or relapse suggested that MIR203 methylation may be an early event in myelomagenesis instead of being acquired during disease progression.     

Targets,Treatments, and Outcomes Updates in Diabetic Stroke

Goal: Due to multiple failures to translate basic research, the need for novel therapeutic targets and strategies is still urgent to save a larger number of the stroke patients' population and to reduce the toxicity of the current stroke therapy. Method: We summarize the most recent, within past 5 years, basic and clinical diabetic stroke research findings. Findings: We aim to examine the most current understanding of stroke and neurovascular unit integrity, especially in presence of hyperglycemia and/or diabetes mellitus. From there, we are comparing the meaningful findings that aim at treating diabetic stroke to see where they differ, where they succeed, and where they open questions for new therapeutic strategies. Conclusion: The need for more clinically effective neuroprotective strategies is still mismatched with the bench side findings.     

丙,丁和庚型RNA病毒所致肝炎的免疫病理和组织病理特点及临床意义

目的探讨由ＲＮＡ病毒引起的丙型肝炎（ＨＣ）、丁型肝炎（ＨＤ）和庚型肝炎（ＨＧ）的免疫病理和组织病理不同特点及临床意义。方法　采用双重ＰＡＰ方法检测ＨＣ肝组织ＨＣＶ－ＮＳ５;采用直接酶标法检测ＨＤ肝组织ＨＤＡｇ;采用链霉菌抗生物素蛋白－过氧化酶法（ＳＰ）检测ＨＧ肝组织ＨＧＶ－ＮＳ５。同时常规苏木素伊红染色。结果在免疫病理表达中,阳性信号的位置、形态和阳性肝细胞在肝小叶的分布及周围淋巴细胞的浸润等在ＨＣ、ＨＤ和ＨＧ三者中有较明显的差异。在组织病理变化中,汇管区淋巴细胞聚集或淋巴滤泡形成、胆管损伤、脂肪性变、Ｍａｌｌｏｒｙ小体、多核巨肝细胞和玫瑰花结等在 ＨＣ、ＨＤ和 ＨＧ三者中也有较明显的差异。结论ＲＮＡ病毒所引起的ＨＣ、ＨＤ和ＨＧ在免疫病理表达和组织病理变化有可鉴别诊断的不同特点,为临床防治和预后判断提供了依据。