TRAIL联合紫杉醇对卵巢癌细胞凋亡影响的研究

目的:探讨TRAIL联合紫杉醇对卵巢癌3AO细胞株凋亡的影响,以进一步研究其诱导细胞凋亡的原理。方法:应用MTT法检测TRAIL和紫杉醇作用组的抑制率,并以流式细胞仪检测各组凋亡率。结果:亚毒剂量的TRAIL、紫杉醇及联合作用组致卵巢癌3AO细胞凋亡率分别为17.6%、16.1%、64.3%。单独应用组与联合应用组之间存在显著性差异(P<0.01)。结论:TRAIL在诱导卵巢癌细胞凋亡的同时,也显著提高了其对紫杉醇(taxol)的化疗敏感性。     

玻璃体腔注药有必要散瞳吗?

玻璃体腔注药是目前眼科最常用的治疗手段之一,操作简单,手术时间较短。但是对于注药前是否有必要进行散瞳国内尚未达成共识,为此我们进行了一项网络问卷调查,在参阅国外相关研究的基础上,就上述问题进行了讨论并提出我们的主张,玻璃体腔注药术前常规散瞳没有必要。     

Mometasone furoate inhibits growth of acute leukemia cells in childhood by regulating PI3K signaling pathway

Objectives: Acute lymphoblastic leukemia (ALL) is the most common cancer before the age of 15 years, seriously endangering the health of children. The main treatment for Childhood ALL was pharmacotherapy. But these drugs have many side effects and some of them could develop drug resistance quickly. Mometasone furoate (MF) is an efficient glucocorticoid for topical treatment of inflammation on the skin, lung and nose.

Methods: In this study, we investigated whether the MF had effects on ALL cells proliferation and migration.

Results: The CCK-8 proliferation test showed that the cell viability was the lowest at 25?nM MF treatment and the increased OD value was time-dependent. In transwell assay, the number of CCRF-CEM cells was reduced in MF treated group. We found the expression of anti-apoptotic protein bcl-2 decreased the expression of pro-apoptotic protein caspase3 and bax increased in CCRF-CEM cell line treated with MF. The expression of p-AKT, p-mTOR, p70S6?K, vascular endothelial growth factor and CyclinD1 were decreased in MF treated group.

Conclusion: This study reveals that MF can inhibit proliferation and invasion/migration and induce apoptosis in Childhood ALL cells, which may be regulated by Phosphatidylinositol 3-kinase signaling pathway. These results suggest MF may be a potential new drug target for clinical ALL treatment.     

Retrospective analysis of molecular biology mechanism of ABO blood group typing discrepancy among blood donors in Jinan blood station

BackgroundTo accurately identify ABO blood typing in pre-transfusion testing is very important to ensure blood transfusion safely, which is a major responsibility of blood station.MethodsEighty-one blood donors samples with ABO blood group typing discrepancy was collected among 61952 donor samples in our blood station from January 2019 to July 2020. Blood group serological method was used to detect ABO blood group. DNA Sequencing was used to determine the genotype. The antibody screening test detects antibodies other than ABO.ResultsIn total, 61,952 donor samples were analysed for ABO typing discrepancies. The incidence among blood donors was 0.13% (81/61952). The most common reason of ABO typing discrepancies was due to specific antibody or non-specific agglutination (54.32%, 44/81), mainly anti-M antibody, cold autoantibody, anti-D antibody, anti-N antibody and anti-Lea antibody. The major cause of forward typing discrepancies among blood donors was ABO subgroups (25.93%, 21/81), including 10 cases of A subtype (1 case of A2, 2 cases of A3, 2 cases of Ax, 3 cases of AxB, 1 case of Ael, 1 case of Ahm), 6 cases of B subtype (2 cases of B3, 1 case of Bel, 3 cases of AB3), 2 cases of B subtype (A), 1 case of cisAB, and 2 cases of acquired B. The serum antibody was weakened in 16 cases (19.75%).ConclusionsThe blood types should be correctly identified by combining serology with gene sequencing to ensure the safety of clinical blood transfusion, when the forward and reverse typing discrepancies among the blood donors.     

济南市腹泻患者沙门氏菌PFGE分子分型及耐药特征研究

目的 对2017-2020年济南市哨点医院腹泻患者中分离到的沙门氏菌进行病原学分析,了解济南市腹泻患者沙门氏菌的血清型分布特征、分子分型特征及耐药情况。方法 分别利用血清检测试剂盒和脉冲场凝胶电泳技术(PFGE)对来自济南市各医院腹泻门诊病人的的90株沙门氏菌进行血清分型和分子分型分析,酶切电泳图谱导入BioNumerics软件进行聚类分析;利用微量肉汤稀释法对40株沙门氏菌进行耐药性检测。结果 90株沙门氏菌可分为27个血清型,鼠伤寒沙门氏菌和肠炎沙门氏菌为优势血清型,分别占总数的47.78%和17.78%。PFGE电泳后产生的带型具有多态性,以鼠伤寒沙门氏菌和肠炎沙门氏菌的带型最为集中;药敏结果显示,沙门氏菌对氨苄西林耐药率最高,为72.50%,多重耐药率达67.50%。结论 济南地区沙门氏菌具有血清型多样化和遗传多样性特征,对抗生素的高耐药和多重耐药现象严重,应加强济南地区耐药检测。     

Motor unit number index (MUNIX) in children and adults with 5q-spinal muscular atrophy: Variability and clinical correlations

Spinal muscular atrophy (SMA) is a motor neuron disease associated with progressive muscle weakness and motor disability. The motor unit number index (MUNIX) is a biomarker used to assess loss of motor units in later-onset SMA patients. Twenty SMA patients (SMA types 3 and 4), aged between 7 and 41 years, were clinically evaluated through the Hammersmith Motor Functional Scale Expanded and the Spinal Muscular Atrophy-Functional Rating Scale. The patients underwent compound motor action potential (CMAP) and MUNIX studies of the right abductor pollicis brevis, abductor digiti minimi and tibialis anterior (TA) muscles. Age-matched healthy controls (n = 20) were enrolled to obtain normative CMAP and MUNIX values from the same muscles. Compared to healthy controls, SMA patients showed significant reductions in MUNIX values among all muscles studied, whereas CMAP showed reductions only in the weaker muscles (abductor digiti minimi and TA). MUNIX variability was significantly higher in the SMA group than in the control group. MUNIX variability in TA correlated with CMAP variability. Motor functional scores correlated with TA MUNIX. The MUNIX study is feasible in later-onset SMA patients, and TA MUNIX values correlate with disease severity in patients with mild motor impairment.     

血液环境下Biodentine与MTA的颜色稳定性研究

目的比较牙体牙髓治疗中常用的骨水泥材料Biodentine与三氧化矿物凝聚体(mineral trioxide aggregrate,MTA)在与血液接触条件下的颜色稳定性,并探讨其可能的变色原因。方法制备直径5 mm、高3 mm的Biodentine和MTA圆盘,将每种材料的24个圆盘随机分配到去离子水组和脱纤维羊血组中,浸泡1 d和7 d后进行后续检测。进行各类检测的3个时间点为:圆盘固化脱模后即刻、浸泡1 d和7 d后。检测指标如下:在同样光照环境下对圆盘进行拍照,直观比较两种材料的颜色变化;采用比色仪检测两种材料的色度;借助扫描电镜观察两种材料的表面形态;使用X射线能谱仪测量两种材料各元素含量。结果肉眼观察到与脱膜后即刻相比,在脱纤维羊血组浸泡1 d后仅MTA在明暗度上发生改变,脱纤维羊血组浸泡7 d后Biodentine与MTA颜色均加深变红,但MTA暗度明显增加。比色仪结果显示脱纤维羊血组MTA的7 d色差值ΔE(21.257±0.955)大于Biodentine的7 dΔE(5.833±0.501)(t=24.781,P<0.001);MTA材料自身变色随着与血液接触时间延长而加深,其7 dΔE与1 dΔE(6.233±0.888)相比,差异具有统计学意义(t=19.956,P<0.001);而Biodentine材料自身变色随时间延长则无统计学意义[7 dΔE与1 dΔE(6.790±0.831)相比,t=1.707,P=0.163]。扫描电镜结果表明:用脱纤维羊血浸泡7 d后,MTA表面孔隙率大于Biodentine,且MTA的晶体边缘相较Biodentine也更为圆钝。X射线能谱仪检测显示:在脱纤维羊血组浸泡7 d后MTA中氧元素含量下降、铋元素含量上升;与此同时Biodentine因阻射能力低未被检测出锆元素,但其他元素含量稳定。结论Biodentine在与血液接触条件下的颜色稳定性优于MTA,这主要与Biodentine表面孔隙率小、阻射剂成分稳定有关。     

新型FGG基因突变导致遗传性纤维蛋白原缺陷症的研究

目的:对临床发现的1例遗传性纤维蛋白原缺陷症患者及其家属进行凝血相关指标检测和基因型分析,并探讨可能的分子发病机制。方法:采集先证者及其家属共4人的外周血,检测凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、凝血酶时间(TT)、纤维蛋白原(Fg)、D-二聚体及8项凝血因子指标。对编码纤维蛋白原3条肽链的FGA、FGB和FGG基因的所有外显子和侧翼序列进行测序并进行生物信息学分析。结果:先证者及其长姐的8项凝血因子中FⅤ、FⅧ稍高,TT明显延长,Fg明显降低;测序结果显示FGG基因存在c.901C>T杂合突变。生物信息学分析显示,突变改变了原有的蛋白结构,减少了氢键数目。结论:纤维蛋白原γ链c.901C>T杂合突变是引起该家系遗传性纤维蛋白原缺陷的主要原因,该突变是首次在国内外报道。     

Shikonin protects chondrocytes from interleukin-1beta-induced apoptosis by regulating PI3K/Akt signaling pathway

Chondrocyte apoptosis is mostly responsible for the development and progression of osteoarthritis. IL-1β is generally served as an agent that induces chondrocyte apoptosis. Shikonin exerts its anti-inflammatory effect on cartilage protection in vivo. We aimed to explore the protective effect of shikonin on interleukin-1beta (IL-1β)-induced chondrocyte apoptosis and the potential molecular mechanisms. Chondrocytes were isolated from the joints of newborn Sprague-Dawley rats. The MTT assay and LDH cell death assay were used to determine the cell viability and chondrocyte apoptosis was detected by Annexin-V/PI staining and nucleosomal degradation. The contents of phosphorylated-PI3K (p-PI3k), phosphorylated-Akt (p-Akt), Bcl-2, Bax, and cytochrome c were detected by Western blotting. A quantitative colorimetric assay was used to detect the caspase-3 activity. Our results showed that pretreatment with shikonin (4 μM) inhibited cytotoxicity and apoptosis induced by IL-1β (10 ng/ml) in chondrocytes. Shikonin pretreatment also decreased the activity of IL-1β that decreased Bcl-2 expression and levels of p-PI3K and p-Akt, and increased Bax expression, cytochrome c release, and caspase-3 activation. It also reversed the activity of IL-1β that promoted the synthesis of matrix metalloproteinase-13 and inhibited the expression of tissue inhibitor of metalloproteinase-1 expression, with the net effect of suppressing extracellular matrix degradation. These data suggested that shikonin may protect chondrocytes from apoptosis induced by IL-1β through the PI3K/Akt signaling pathway, by deactivating caspase-3.     

手足口病并发脑炎患儿水通道蛋白4水平变化及其与炎症因子、神经损伤指标相关性

目的探讨手足口病并发脑炎患儿水通道蛋白4水平变化及其与炎症因子、神经损伤指标相关性。方法选取40例手足口病神经系统受累期患儿作为观察组,选取同期收治的40例手足口病出疹期患儿作为单纯手足口病组,36例排除手足口病及脑炎等其他疾病的热性惊厥患儿作为对照组。检测脑脊液中水通道蛋白4水平及外周血中炎症因子[白细胞介素-1β（IL-1β）、IL-6、IL-18、C反应蛋白（CRP）、降钙素原（PCT）、肿瘤坏死因子-α（TNF-α）]、神经损伤指标[髓鞘碱性蛋白（MBP）、神经特异性烯醇化酶（NSE）、S-100B蛋白]水平,分析脑脊液中水通道蛋白4水平与外周血中炎症因子及神经损伤指标相关性。结果入院第2天患儿脑脊液水平观察组高于单纯手足口病组和对照组（P < 0.01）;入院第7天（恢复期）,观察组脑脊液水通道蛋白4水平较入院第2天降低,仍高于单纯手足口病组（P < 0.01）。3组患儿外周血炎症因子、神经损伤指标水平差异有统计学意义（P < 0.01）。相关性分析显示,观察组第2天脑脊液水通道蛋白4与外周血中炎症因子及神经损伤指标均呈正相关关系（P < 0.05~P < 0.01）。结论手足口病并发脑炎患儿脑脊液中水通道蛋白4水平在急性期升高,在恢复期降低,且与外周血炎症因子、神经损伤指标呈正相关。