2016年辽宁省肿瘤登记地区恶性肿瘤流行情况分析

目的 分析2016年辽宁省肿瘤登记地区恶性肿瘤流行状况。方法 收集2016年辽宁省肿瘤登记地区(35个县区)上报的恶性肿瘤发病与死亡资料,计算发病与死亡粗率、标化率、累积率(0~74岁)和年龄别率等,标化率使用Segi's世界标准人口年龄构成和2000年中国人口年龄构成为标准进行计算。结果 2016年辽宁省肿瘤登记地区恶性肿瘤发病率为383.54/10万,世标率为200.06/10万,中标率为204.44/10万,城市地区发病中标率(201.40/10万)高于农村地区(186.43/10万);40-岁及以上各年龄组发病率快速升高,在80-岁组达到峰值;35-岁以上各年龄组城市男性和女性恶性肿瘤发病率分别高于农村男性和女性;肺癌、结直肠癌、乳腺癌是辽宁省发病最高的恶性肿瘤。2016年恶性肿瘤死亡率为249.79/10万,世标率为123.00/10万,中标率为124.32/10万,城市地区死亡中标率(121.93/10万)低于农村地区(131.03/10万)。恶性肿瘤年龄别死亡率峰值在80-岁组。20~79岁男性各年龄组死亡率均为农村高于城市,55~79岁女性各年龄组死亡率均为农村高于城市。肺癌、肝癌、结直肠癌是辽宁省死亡率最高的肿瘤。结论 辽宁省恶性肿瘤发病和死亡均高于全国水平,总发病率和死亡率均为男性高于女性,城市发病率高于农村,农村死亡率高于城市,城乡居民恶性肿瘤负担差异明显。     

The effect of acetylation on the protein stability of BmApoLp‐III in the silkworm,Bombyx mori

Acetylation is an important, reversible posttranslational modification to a protein. In a previous study, we found that there were a large number of acetylated sites in various nutrient storage proteins of the silkworm haemolymph. In this study, we confirmed that acetylation can affect the stability of nutrient storage protein Bombyx mori apolipophorin‐III (BmApoLp‐III). First, the expression of BmApoLp‐III could be upregulated when BmN cells were treated with the deacetylase inhibitor panobinostat (LBH589); similarly, the expression was downregulated when the cells were treated with the acetylase inhibitor C646. Furthermore, the increase in acetylation by LBH589 could inhibit the degradation and improve the accumulation of BmApoLp‐III in BmN cells treated with cycloheximide and MG132 respectively. Moreover, we found that an increase in acetylation could decrease the ubiquitination of BmApoLp‐III and vice versa; therefore, we predicted that acetylation could improve the stability of BmApoLp‐III by competing for ubiquitination and inhibiting the protein degradation pathway mediated by ubiquitin. Additionally, BmApoLp‐III had an antiapoptosis function that increased after LBH589 treatment, which might have been due to the improved protein stability after acetylation. These results have laid the foundation for further study on the mechanism of acetylation in regulating the storage and utilization of silkworm nutrition.     

急性前葡萄膜炎中医体质与生存质量的相关性

目的：评估急性前葡萄膜炎患者中医体质与生存质量的相关性。方法：横断面研究。选取2014年12月 至2017年12月于温州医科大学附属眼视光医院中医眼科专科就诊并经体质评分判定为病理体质的 患者196例，应用中华生存质量量表进行生存质量评分。采用t检验及线性回归分析中医体质与生存 质量评分各领域的相关性。结果：196例患者中单纯体质者147例，复合体质者49例。经广义线性回 归分析，患者的不同体质类型及体质评分与中华生存质量量表评分有显著相关性，进一步分析发现 体质评分与中华生存质量量表评分中的形、情有显著相关性（均P<0.05），与神无显著相关。经线性 回归分析，不同类型中医体质中，气虚、痰湿、血瘀、阳虚、阴虚体质与中华生存质量量表中的形有 显著相关性（均P<0.05）；气郁体质与情有显著相关性（P=0.001）；而湿热体质与形和情均有显著相关 性（均P<0.001）。结论：急性前葡萄膜炎患者的不同中医体质与中医生存质量密切相关，且对形的影 响最大。     

miR-145调控肝癌腹水模型Th9细胞升高的机制研究

目的:探讨miR-145调控肝癌腹水模型Th9细胞升高的作用机制。方法:构建小鼠H22肝癌腹水模型。造模两周后处死小鼠并分离出脾脏组织，流式细胞术分析肝癌腹水组（MA组）与正常对照组（Control 组）小鼠脾脏Th9细胞表达水平。ELISA法检测脾脏IL-9表达水平。RT-PCR法检测脾脏miR-145表达水平。Western Blot法检测脾脏中PI3K/Akt/mTOR/P70S6K/HIF-1α相关蛋白表达水平。分选小鼠脾脏CD4+T细胞，随机分为miR-145 mimics组和NC组，分别应用miR-145-5P mimics、阴性对照寡核苷酸（negative control，NC）进行转染，RT-PCR检测各组miR-145、HIF-1α mRNA及IL-9 mRNA表达水平。结果:与Control 组相比，MA组Th9细胞及其细胞因子IL-9表达均升高（P<0.05），miR-145表达降低（P<0.05），p-PI3K、p-Akt、mTOR、p-mTOR、p-P70S6K、HIF-1α蛋白均升高（P<0.05）。与NC组相比，miR-145 mimics组miR-145显著升高，HIF-1α mRNA及IL-9 mRNA表达下降。结论:肝癌腹水中Th9细胞升高可能与miR-145下降导致的PI3K/Akt/mTOR/P70S6K/HIF-1α通路激活有关。     

Mutation status and burden can improve prognostic prediction of patients with lower‐risk myelodysplastic syndromes

Patients with lower‐risk myelodysplastic syndromes (LR‐MDS) as defined by the International Prognostic Scoring System (IPSS) have more favorable prognosis in general, but significant inter‐individual heterogeneity exists. In this study, we examined the molecular profile of 15 MDS‐relevant genes in 159 patients with LR‐MDS using next‐generation sequencing. In univariate COX regression, shorter overall survival (OS) was associated with mutation status of ASXL1 (P = .001), RUNX1 (P = .031), EZH2 (P = .049), TP53 (P = .016), SRSF2 (P = .046), JAK2 (P = .040), and IDH2 (P = .035). We also found significantly shorter OS in patients with an adjusted TET2 variant allele frequency (VAF) ≥18% versus those with either an adjusted TET2 VAF <18% or without TET2 mutations (median: 20.4 vs 47.8 months; P = .020; HR = 2.183, 95%CI: 1.129‐4.224). After adjustment for IPSS, shorter OS was associated with mutation status of ASXL1 (P < .001; HR = 4.306, 95% CI: 2.144‐8.650), TP53 (P = .004; HR = 4.863, 95% CI: 1.662‐14.230) and JAK2 (P = .002; HR = 5.466, 95%CI: 1.848‐16.169), as well as adjusted TET2 VAF ≥18% (P = .008; HR = 2.492, 95% CI: 1.273‐4.876). Also, OS was increasingly shorter as the number of mutational factors increased (P < .001). A novel prognostic scoring system incorporating the presence/absence of the four independent mutational factors into the IPSS further stratified LR‐MDS patients into three prognostically different groups (P < .001). The newly developed scoring system redefined 10.1% (16/159) of patients as a higher‐risk group, who could not be predicted by the currently prognostic models. In conclusion, integration of the IPSS with mutation status/burden of certain MDS‐relevant genes may improve the prognostication of patients with LR‐MDS and could help identify those with worse‐than‐expected prognosis for more aggressive treatment.     

Chronic exposure to ethanol in male mice may be associated with hearing loss in offspring

Although paternal ethanol (EtOH) abuse has been shown to affect the growth and behavior of offspring, the exact molecular and mechanistic basis remains largely unclear. Methylation alterations in imprinted genes may be related to well-documented teratogenic effects of ethanol. Here we show that chronic paternal ethanol exposure increases the susceptibility to abnormal behavior in offspring through male game epigenetic alteration. In our study, different doses of ethanol (0, 1.1, 3.3 g kg⁻¹) were administered intra-gastrically to male mice and decreased sperm motility was found in the highest ethanol-exposed group compared with the controls. Data also showed a dose-dependent increase in deaf mice of the paternally ethanol-exposed groups. The methylation of H19, Peg3, Ndn and Snrpn was assessed in paternal spermatozoa and in the cerebral cortices of deaf mice. EtOH affected methylation of Peg3 (CpG 3, 7 and 9) in paternal spermatozoa and in the cerebral cortices of deaf mice, but the level of mRNA expression did not change, suggesting that other gene regulation may be involved in these processes. Overall, chronic paternal ethanol exposure could alter the methylation of imprinted genes in sire spermatozoa that could also be passed on to offspring, giving rise to developmental disorders. Our results provide possible epigenetic evidence for a paternal ethanol exposure contribution to Fetal Alcohol Syndrome (FAS).     

脂氧素调控炎症信号通路的研究进展

脂氧素是花生四烯酸的代谢产物。随着对脂氧素研究的深入,已发现其多种生物学活性,如抗炎症、调节免疫反应、促进细胞损伤修复等。脂氧素被公认为是重要的内源性抗炎介质,尤其对多种炎性细胞和炎症反应起负性调节,具有广泛的抗炎及促炎症消退作用,被誉为炎症反应的"刹车信号"。脂氧素在发挥抗炎活性时通过不同方式调控多种炎症信号通路,现就此方面最新进展做一综述。