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1.
目的探讨脊髓小脑共济失调2型(SCA2)致病基因ATXN2异常等位基因中间重复个体的表型和分子遗传学特点。方法针对2005—2018年中日友好医院神经科运动障碍与神经遗传病研究中心收集的1383个常染色体显性遗传共济失调家系的先证者和部分家系成员,采用荧光标记毛细管电泳片段分析方法进行动态突变检测,对携带ATXN2基因中间重复的个体进行临床表型和遗传特征分析。结果共检出163个家系(包含先证者和家系成员共203人)携带异常扩展的ATXN2基因CAG重复序列,其中93个家系中有107例的异常扩展等位基因重复次数在29~34次之间。在其中的20个亲子对中,父系遗传16个,异常等位基因的代间扩展增加0~28次,母系遗传4个,异常等位基因的代间扩展增加0~4次。结论对于临床拟诊SCA2家系患者,需对其亲代或成年子代个体进行ATXN2基因检测,以免漏诊。动态突变基因检测有助于识别中间重复的个体,对明确家系致病基因和遗传咨询至关重要。 相似文献
2.
Weina Cheng Yazhi Wang Jingxian Liu Xiaofei Li Ming Yu Cancan Duan Liu Liu Jianyong Zhang 《Journal of applied toxicology : JAT》2022,42(6):970-980
Cantharidin (CTD) is an effective antitumor agent. However, it exhibits significant hepatotoxicity, the mechanism of which remains unclear. In this study, biochemical and histopathological analyses complemented with ultra-high-performance liquid chromatography–tandem mass spectrometry (UHPLC-MS/MS)-based targeted metabolomic analysis of bile acids (BAs) were employed to investigate CTD-induced hepatotoxicity in rats. Sixteen male and female Sprague–Dawley rats were randomly divided into two groups: control and CTD (1.0 mg/kg) groups. Serum and liver samples were collected after 28 days of intervention. Biochemical, histopathological, and BA metabolomic analyses were performed for all samples. Further, the key biomarkers of CTD-induced hepatotoxicity were identified via multivariate and metabolic pathway analyses. In addition, metabolite–gene–enzyme network and Kyoto Encyclopedia of Genes and Genomes pathway analyses were used to identify the signaling pathways related to CTD-induced hepatotoxicity. The results revealed significantly increased levels of biochemical indices (alanine aminotransferase, aspartate aminotransferase, and total bile acid). Histopathological analysis revealed that the hepatocytes were damaged. Further, 20 endogenous BAs were quantitated via UHPLC-MS/MS, and multivariate and metabolic pathway analyses of BAs revealed that hyocholic acid, cholic acid, and chenodeoxycholic acid were the key biomarkers of CTD-induced hepatotoxicity. Meanwhile, primary and secondary BA biosynthesis and taurine and hypotaurine metabolism were found to be associated with the mechanism by which CTD induced hepatotoxicity in rats. This study provides useful insights for research on the mechanism of CTD-induced hepatotoxicity. 相似文献
3.
文题释义:
细胞膜片技术:是在体外接种培养高密度的细胞,使其相互融合生长至100%而形成的透明致密膜状物。该技术不需要胰酶消化即可收集细胞,因此保留了大量的胞外基质、细胞间连接以及细胞-基质连接等结构。目前细胞膜片技术已成为组织工程领域的研究热点,已被推广应用于牙周膜、角膜、心脏、软骨、食管等多种组织器官修复。
成骨细胞:主要由内外骨膜和间充质始祖细胞分化而来,在复杂的骨形成过程中发挥着主要的功能,承担着骨基质的合成、分泌和矿化。骨髓间充质干细胞具有多向分化潜能,能定向分化为成骨细胞,其成骨分化过程可受多种因素的影响,如细胞因子的调控、遗传因素和激素水平等。背景:现阶段骨形态发生蛋白2和碱性成纤维生长因子2对骨髓间充质干细胞膜片增殖、成骨分化的影响和作用机制还尚未可知,如何将生长因子与组织工程细胞膜片技术相整合,最终将其用于骨缺损修复具有重要意义。
目的:探讨单独及联合应用骨形态发生蛋白2和碱性成纤维生长因子2对骨髓间充质干细胞膜片增殖和成骨分化的影响。
方法:体外分离培养鉴定SD大鼠骨髓间充质干细胞并构建细胞膜片,选用不同质量浓度的骨形态发生蛋白2和碱性成纤维生长因子2单独及联合诱导骨髓间充质干细胞膜片,CCK-8法结合碱性磷酸酶活性检测确定2种因子促进膜片增殖和成骨分化的最佳有效质量浓度;然后对骨髓间充质干细胞膜片进行成骨诱导,通过大体及显微镜观察、Vonkossa染色、茜素红染色、RT-PCR检测相关成骨标志物来评估诱导效果。
结果与结论:单独应用骨形态发生蛋白2可增强骨髓间充质干细胞膜片的碱性磷酸酶活性,最佳质量浓度为100 μg/L(P < 0.001),单独应用碱性成纤维生长因子2能加速骨髓间充质干细胞膜片的增殖,最佳质量浓度为20 μg/L(P < 0.001),而联合应用既可以促进膜片增殖又能提高其碱性磷酸酶活性(P < 0.001);经成骨诱导后,4组膜片在形态学上无明显差异,均能诱导骨髓间充质干细胞膜片的成骨分化,其中联合组钙结节最明显(P < 0.001),可显著促进膜片晚期成骨分化并抑制其早期成骨分化,具有明显的协同促进作用(P < 0.001)。结果表明,骨形态发生蛋白2和碱性成纤维生长因子2联合应用时具有协同作用,既可以促进骨髓间充质干细胞膜片增殖,又能显著增强其成骨诱导能力。ORCID: 0000-0003-1918-579X(何惠宇)
中国组织工程研究杂志出版内容重点:干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程 相似文献
4.
Assessment of Myocardial Infarct Size by Three‐Dimensional and Two‐Dimensional Speckle Tracking Echocardiography: A Comparative Study to Single Photon Emission Computed Tomography
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5.
目的 基于基因组Survey分析对刺果甘草Glycyrrhiza pallidiflora Maxim.基因组大小和杂合率进行估计,并通过叶绿体基因组序列特征对其在甘草属Glycyrrhiza L.中的系统发育位置进行研究。方法 使用二代测序技术对刺果甘草进行测序,采用K-mer方法对测序reads进行分析,估算刺果甘草基因组大小和杂合率,使用生物信息学方法进行叶绿体基因组组装、注释和系统发育分析。结果 Survey分析结果显示其基因组大小约为577.82 Mb,杂合度约为0.31%,重复序列比例约为53.72%。叶绿体基因组长度为127,267 bp,不具有典型的四分体结构,总GC含量为34.32%,包含110个基因,其中76个蛋白质编码基因,30个tRNA基因和4个rRNA基因。系统发育分析表明,刺果甘草与圆果甘草G. squamulosa Franch.亲缘较接近。结论 刺果甘草存在低杂合和重复序列较多的特点,为了更好地对全基因组进行序列拼接和组装,可尝试采用三代测序结合二代测序的分析策略进行基因组组装;刺果甘草叶绿体全基因组比对和系统发育分析,为后续开展甘草属遗传多样性研究和分子鉴定标记筛选提供了重要依据。 相似文献
6.
7.
Xue Yao Yan Zhang Jian Hao Hui-Quan Duan Chen-Xi Zhao Chao Sun Bo Li Bao-You Fan Xu Wang Wen-Xiang Li Xuan-Hao Fu Yong Hu Chang Liu Xiao-Hong Kong Shi-Qing Feng 《中国神经再生研究》2019,(3)
Ferroptosis is an iron-dependent novel cell death pathway. Deferoxamine, a ferroptosis inhibitor, has been reported to promote spinal cord injury repair. It has yet to be clarified whether ferroptosis inhibition represents the mechanism of action of Deferoxamine on spinal cord injury recovery. A rat model of Deferoxamine at thoracic 10 segment was established using a modified Allen's method. Ninety 8-week-old female Wistar rats were used. Rats in the Deferoxamine group were intraperitoneally injected with 100 mg/kg Deferoxamine 30 minutes before injury. Simultaneously, the Sham and Deferoxamine groups served as controls. Drug administration was conducted for 7 consecutive days. The results were as follows:(1) Electron microscopy revealed shrunken mitochondria in the spinal cord injury group.(2) The Basso, Beattie and Bresnahan locomotor rating score showed that recovery of the hindlimb was remarkably better in the Deferoxamine group than in the spinal cord injury group.(3) The iron concentration was lower in the Deferoxamine group than in the spinal cord injury group after injury.(4) Western blot assay revealed that, compared with the spinal cord injury group, GPX4, xCT, and glutathione expression was markedly increased in the Deferoxamine group.(5) Real-time polymerase chain reaction revealed that, compared with the Deferoxamine group, mRNA levels of ferroptosis-related genes Acyl-CoA synthetase family member 2(ACSF2) and iron-responsive element-binding protein 2(IREB2) were up-regulated in the Deferoxamine group.(6) Deferoxamine increased survival of neurons and inhibited gliosis. These findings confirm that Deferoxamine can repair spinal cord injury by inhibiting ferroptosis. Targeting ferroptosis is therefore a promising therapeutic approach for spinal cord injury. 相似文献
8.
Shisong Zhang Juan Li Yurui Wu Yuanjun Hu Chunhong Duan Meiyun Wang Zhongtao Gai 《Medicine》2015,94(39)
The purpose of this meta-analysis is to compare the relative merits among laparoscopic-assisted operations and laparotomy operations for patients with Hirschsprung disease.PubMed, Web of Science, and Wanfang databases were searched for the related articles. We analyzed dichotomous variables by estimating odds ratios (ORs) with their 95% confidence intervals (CIs) and continuous variables using the weighted mean difference (WMD) with the 95% CI. The random-effects model (REM) was used to combine the results. The outcome measures included operating time (OT), estimated blood loss (EBL), length of hospital stay (LOHS), mean first bowel movement (MFBM), and number of complications.Sixteen articles were included in the meta-analysis. These studies involved a total of 774 patients, 396 of whom underwent laparoscopic-assisted operations and 378 of whom underwent laparotomy operations. The EBL (WMD = −1.48, 95% CI = −1.82, −1.13), LOHS (WMD = −0.67, 95% CI = −0.86, −0.49), MFBM (WMD = −0.83, 95% CI = −1.05, −0.61), and number of complications (OR = 0.60, 95% CI = 0.40, 0.89) were significantly lower in laparoscopic-assisted operations than in laparotomy operations. The OT (WMD = 0.12, 95% CI = −0.05, 0.28) showed no significant differences between laparoscopic-assisted operations and laparotomy operations.Compared with laparotomy operations, laparoscopic-assisted operations are generally safer and more reliable for patients with Hirschsprung disease. 相似文献
9.
段前深 《实用医学影像杂志》2020,(2):127-129
目的探讨CT扫描在胸膜外孤立性纤维瘤(E-SFT)中的诊断价值。方法回顾性分析2015年4月至2018年4月于我院接受手术治疗的90例E-SFT患者术前CT检查影像资料和术后病理、免疫组织化学资料,评估CT检查在E-SFT诊断中的应用价值。结果 90例E-SFT患者均为单发肿瘤,免疫组织化学及病理学检查示良性80例,恶性10例;CT检查结果为良性72例,平扫表现为圆形或类圆形软组织密度影,密度不均匀,大部分边缘清晰,增强扫描表现为均匀强化;恶性18例,平扫示肿瘤体积较大,边界不清,密度不均,可见大片不规则低密度区,增强扫描瘤体强化不均匀,低密度区无明显强化;CT诊断的敏感度、准确度、特异性阳性率、阴性率分别为60%(6/10)、82%(74/90)、85%(68/80)、33%(6/18)、94%(68/72)。结论 E-SFT的CT检查影像图像具有一定的特征性,尤其是增强扫描有助于评估纤维瘤的良恶性,可将其作为术前诊断及术后复查评估的有效依据用于临床诊疗工作中。 相似文献
10.