化学诱变剂EMS对知母种子萌发的影响

以知母（Anemarrhena asphodeloides）种子为材料,分别采用1%、2%、4%、6%浓度的EMS处理6、8、12和24 h,在恒温培养箱内进行种子萌发实验,研究不同浓度的化学诱变剂甲基磺酸乙酯（ethyl methane sulfonate,EMS）处理对知母种子萌发的影响,筛选适宜的诱变浓度和诱变时间。结果表明：随EMS浓度的增加和处理时间的延长,知母种子发芽率呈现逐渐降低的趋势,以相对发芽率达到半致死浓度为标准,6%EMS浸种12和24 h可作为EMS诱导知母建立突变体库的适宜条件。     

64排螺旋CT对粗隆间骨折Evans分型的影响研究

目的:探讨64排螺旋CT对粗隆间骨折Evans分型的影响,为临床使用提供参考依据。方法:2015年3月至2017年3月,三甲医院高年资创伤骨科主任医师2名,医师1、医师2分别按照术前X线、术前64排螺旋CT平扫和三位重建结果对128例新鲜闭合单侧粗隆间骨折患者进行Evans分型,分别记为X线分型、CT分型。本院术者依据围术期X线、CT及术中所见骨折情况进行Evans分型(逆粗隆间骨折定义为Ⅴ型)作为最终分型。记录分型结果,计算并对比准确率、误诊率。结果:(1)剔除5例,90.09%(123/128)的患者完成研究。(2)分型结果:X线分型中,3例(最终分型Ⅲ型2例,Ⅳ型1例)无法定型;Ⅰ型正确1例,改为Ⅱ型1例;Ⅱ型正确18例,改为Ⅰ型2例,改为Ⅲ型3例,Ⅳ型2例;Ⅲ型正确45例,改为Ⅱ型7例,改为Ⅳ型1例;Ⅳ型正确19例,改为Ⅱ型3例,改为Ⅲ型15例。CT分型中,Ⅰ型正确3例,Ⅱ型正确29例,Ⅲ型正确64例,改为Ⅳ型1例,Ⅳ型正确22例,Ⅴ型正确3例。(3)CT分型的总准确率、总误诊率优于X线分型(99.19%vs67.48%、0.81%vs30.08%,P0.05)。(4)Ⅰ型、Ⅱ型、Ⅲ型、Ⅳ型骨折进行CT分型,准确率高于X线分型(P0.05),误诊率低于X线分型(P0.05);Ⅴ型骨折,两种分型准确率、误诊率相等。结论:64排螺旋CT平扫及三维重建是粗隆间骨折Evans分型较为可靠的辅助检查,可考虑推广运用。     

丁香油酚在牙槽骨组织中的骨保护作用评价

绝经后雌激素缺乏会引起牙槽骨质流失、重塑和炎症。丁香油酚是一种酚类化合物,在牙科应用广泛并具有抗炎特性。在本研究中,以卵巢切除的大鼠为模型,服用不同剂量丁香油酚(2mg·kg-1·d-1和4mg·kg-1·d-1)12周(卵巢切除组),研究丁香油酚在牙槽骨组织中的骨保护作用。使用ELISA法检测血清中骨代谢标记物和促炎细胞因子,使用高分辨率微型计算机断层摄影术(CT)扫描牙槽骨形态,并进行骨组织学分析(H&E染色)。研究结果表明,丁香油酚不会增加卵巢切除大鼠体重和延缓子宫萎缩。由丁香油酚处理的卵巢切除大鼠的骨代谢标志物和炎性细胞因子含量显著提高,特别是高剂量组。丁香油酚的处理显著减弱了牙槽骨的形态测量变化,改善了牙槽吸收功能和牙龈渗透。卵巢切除大鼠的牙槽骨由于丁香油酚处理得到改善,炎性细胞因子表达降低。本研究初步结论表明,丁香油酚可以防止卵巢切除动物实验性诱导的牙槽骨损失,具有抗炎作用,对牙槽骨组织具有保护作用。     

慢性酒精中毒大鼠在学习记忆方面差异基因的生物信息学分析

借助基因芯片获取慢性酒精中毒大鼠海马相关基因的表达数据集,通过生物信息学的分析方法对差异表达基因进行筛选与分析。从分子水平揭示慢性酒精中毒对大鼠大脑海马体的影响,为慢性酒精中毒的损伤机制以及相关疾病发病机制的基础研究与临床治疗提供新的方向。同时,还通过Y迷宫实验对实验大鼠的学习记忆功能进行了检测,借助电镜拍摄其线粒体。结果显示,我们一共筛选出208个差异表达基因,其中51个表达上调,157个表达下调。其中涉及的主要信号通路有氧化磷酸化通路、D-谷氨酰胺和谷氨酸代谢通路、阿尔茨海默病信号通路、帕金森病信号通路、膀胱癌信号通路、B细胞受体信号通路和亨廷顿病信号通路等。由此我们得出结论,慢性酒精中毒可能影响了海马多个基因的表达,其中包括Rpsa、Wdr31、Rps11、Rps9、Ndufa2、Mrto4、Rpl6、Dap3、Ndufb8、Ndufb6、Ephb2、Cox6c、Prkcd、Rela、Raf1、Ubd、Mrps28、Mrpl35等关键基因,进而损伤了电子传递链复合体Ⅰ,最终损伤线粒体,导致大鼠学习记忆能力的损伤。     

Regulation of mitochondrial NAD pool via NAD+ transporter 2 is essential for matrix NADH homeostasis and ROS production in Arabidopsis

Reactive oxygen species(ROS) play a crucial role in numerous biological processes in plants, including development, responses to environmental stimuli, and programmed cell death(PCD). Deficiency in MOSAIC DEATH 1(MOD1), a plastid-localized enoyl-ACP reductase essential for de novo fatty acid biosynthesis in Arabidopsis thaliana, leads to the increased malate export from chloroplasts to mitochondria, and the subsequent accumulation of mitochondria-generated ROS and PCD. In this study, we report the identification and characterization of a mod1 suppressor, som592. SOM592 encodes mitochondrion-localized NAD~+ transporter 2(NDT2). We show that the mitochondrial NAD pool is elevated in the mod1 mutant. The som592 mutation fully suppressed mitochondrial NADH hyper-accumulation, ROS production, and PCD in the mod1 mutant, indicating a causal relationship between mitochondrial NAD accumulation and ROS/PCD phenotypes. We also show that in wild-type plants, the mitochondrial NAD+uptake is involved in the regulation of ROS production in response to continuous photoperiod. Elevation of the alternative respiration pathway can suppress ROS accumulation and PCD in mod1, but leads to growth restriction. These findings uncover a regulatory mechanism for mitochondrial ROS production via NADH homeostasis in Arabidopsis thaliana that is likely important for growth regulation in response to altered photoperiod.     

Novel hepacivirus in Asian house shrew,China

<正>Dear Editor,Hepatitis C virus (HCV) is a leading global cause of various liver diseases, including chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. The genome of HCV is monopartite, single-stranded, positive RNA, about 10 kb in size.HCV is the prototype species of the Hepacivirus genus,which contains 14 species according to the update from the International Committee on Taxonomy of Viruses (Smith et al., 2016). Prior to 2005, humans were thought to be the only     

氰酸盐诱导氧化应激促进肾小管上皮细胞上皮–间充质转化

该研究探讨氰酸盐(cyanate)诱导肾小管上皮细胞氧化应激损伤和促进肾纤维化的作用。氰酸盐作用HK-2肾小管上皮细胞后, CCK8法检测其对细胞活力的影响;倒置显微镜观察细胞形态的改变; DCFH-DA法检测细胞ROS水平;细胞免疫荧光和Western blot分别检测E-cadherin、Fibronectin、α-SMA的表达; Western blot检测TGF-β的表达水平。结果显示, 2 mmol/L氰酸盐明显下调HK-2细胞的活力(P<0.05),细胞形态变为长梭形。氰酸盐作用24 h后, HK-2细胞内ROS水平呈浓度依赖性升高。免疫荧光和Western blot结果均显示,氰酸盐作用24 h后, HK-2的Fibronectin、α-SMA表达升高, E-cadherin表达下降; TGF-β的表达水平随氰酸盐浓度升高而上调(P<0.05)。以上结果表明,氰酸盐诱导肾小管上皮细胞产生过量ROS,上调TGF-β水平促进细胞上皮–间充质细胞转化(epithelia-mesenchymal transition, EMT)。     

Identification of a novel COL4A5 mutation in the proband initially diagnosed as IgAN from a Chinese family with X-linked Alport syndrome

Alport syndrome(AS) is a hereditary progressive nephropathy characterized by hematuria, ultrastructural lesions of the glomerular basement membrane, ocular lesions and sensorineural hearing loss. Germline mutations of COL4 A5 are associated with X-linked AS with an extreme phenotypic heterogeneity. Here, we investigated a Chinese family with Alport syndrome. The proband was a 9-year-old boy with hematuria and proteinuria. Based on the test results of renal biopsy and immunofluorescence,the proband was initially diagnosed as Ig A nephropathy and the treatment was recommended accordingly. Meanwhile, we found that the treatment outcome was poor. Therefore, for proper clinical diagnosis and appropriate treatment, targeted exome-based next-generation sequencing has been undertaken. We identified a novel hemizygous single nucleotide deletion c.1902 del A in COL4 A5 gene. Segregation analysis identified that this novel mutation is co-segregated among the affected family members but absent in unaffected family members. The clinical diagnosis of the proband was revised as AS accompanied by Ig A nephropathy,which has been rarely reported. Our findings demonstrated the significance of the application of Genetic screening, expanded the mutation spectrum of COL4 A5 associated AS patients with atypical renal phenotypes and provided a good lesson to be learned from our detour during the diagnosis.     

Up‐regulation of ZFAS1 indicates dismal prognosis for cholangiocarcinoma and promotes proliferation and metastasis by modulating USF1 via miR‐296‐5p

LncRNAs has been demonstrated to modulate neoplastic development by modulating downstream miRNAs and functional genes. In this study, we aimed to detect the interaction among lncRNA ZFAS1 miR‐296‐5p and USF1. We explored the proliferation, migration and invasion of cholangiocarcinoma. The differentially expressed ZFAS1 was discovered in both tissues and cell lines by qRT‐PCR. The targeting relationship between miR‐296‐5p and ZFAS1 or USF1 was validated by dual‐luciferase assay. The impact of ZFAS1 on CCA cell proliferation was observed by CCK‐8 assay. The protein expression of USF1 was determined by Western blot. The effects of ZFAS1, miR‐296‐5p and USF1 on tumour growth were further confirmed using xenograft model. LncRNA ZFAS1 expression was relatively up‐regulated in tumour tissues and cells while miR‐296‐5p was significantly down‐regulated. Knockdown of ZFAS1 significantly suppressed tumour proliferation, migration, invasion and USF1 expression. Overexpressed miR‐296‐5p suppressed cell proliferation and metastasis. Knockdown of USF1 inhibited cell proliferation and metastasis and xenograft tumour growth. In conclusion, ZFAS1 might promote cholangiocarcinoma proliferation and metastasis by modulating USF1 via miR‐296‐5p.