教学课程资源库 更多>>

关键词： 生物物理学   学术期刊   系统生物学   神经科学   细胞生物学   栏目设置   学科范围   基因组学  

摘要： (2020年12月修订)1征稿范围与栏目设置1.1征稿范围本刊为国内外公开发行的全国性学术期刊,月刊,每月20日发行.征稿的学科范围是生物化学、分子生物学、生物物理学、细胞生物学、神经科学、免疫学,以及基因组学、蛋白质组学、系统生物学等相关学科领域.

关键词： 海绵胶煤炱菌   竹燕窝   生活史   细胞生物学  

摘要： 海绵胶煤炱菌(Scorias spongiosa),俗名竹燕窝,是一种高档的可食用真菌。竹燕窝的形成与竹子、居竹伪角蚜有关,形成复杂的竹-蚜-菌共生关系,因而具有较高的理论研究意义和应用研究前景。文章通过对乐山地区的野生竹燕窝进行采集和菌种分离,获得了竹燕窝的分生孢子纯培养菌种。在PDA培养基上对竹燕窝进行培养观察,明确了其整个生活史阶段,即分生孢子-菌丝体-胶状子实体-分生孢子器-分生孢子。在PDA培养基上,分生孢子体积膨大数倍,之后分裂形成菌丝体;菌丝体生长到一定阶段后,菌丝体中央的细胞会以螺旋盘绕的方式进行生长并分化产生子实体原基,最终形成胶质的子实体;子实体的部分菌丝进一步分化形成束状菌丝,并最终分化产生分生孢子器。分生孢子器底部呈半椭球形,负责产生分生孢子;分生孢子器中部为分生孢子梗,其作用为运输分生孢子;顶端具开孔,用于释放分生孢子,形成分生孢子球。

关键词： PBL教学法   细胞生物学实验   教学改革  

摘要： 随着高等院校进行课程改革,在课程教学的授课方式上也有了越来越多的尝试与研究。《细胞生物学实验》作为理论课程的重要补充,对于学生形成完整的知识体系有着非常重要的影响。为进一步提升课程质量,本研究将PBL教学法应用在《细胞生物学实验》课程中,包括结合授课内容制定预习清单、展开课前讨论、制定实验方案、总结实验事项。这样的设计对于学生联系理论,提升科研能力,促进思维提升等都具有积极影响。

关键词： T-cells   Cardiovascular disease   Myocardial infarction   Estradiol   Estrogen receptors   Autoimmune diseases  

摘要： Gender bias in cardiovascular disease has been extensively documented in epidemiological and clinical studies. Despite this, the precise molecular mechanisms underlying these disparities between men and women are poorly understood. It is clear that physiological concentrations of estradiol, such as those present in pre-menopausal women, exert cardioprotective effects that are absent in men or in post-menopausal women. These cardioprotective effects, in part, are due to the estrogen receptor-mediated modulation of the immune system including T-cells. Estrogen receptors (ERs) are widely expressed in different T-cell subsets which are known to play an indispensable role in the progression of cardiovascular disease. Because T-cells can be polarized into several distinct subsets depending on the activation milieu, they can have many different, potentially opposing functions, and it is unclear what roles estrogen receptor signaling may play in mediating these functions. This is further complicated by the discrete and often antagonistic actions of different ERs on T-cell biology which dictate the balance between numerous ER-dependent signaling pathways. While myriad effects of estrogen in T-cells are relevant for many cardiovascular diseases, their widespread effects on several other (patho)physiological systems introduce several obstacles to understanding ER signaling and its precise effects on the immune system. This review aims to provide a more comprehensive summary of the mechanisms of estrogen receptor-mediated modulation of T-cell function, polarization, and cytokine production in the context of cardiovascular disease.

关键词： coaggregation   haemagglutination   P   gulae   protease   protein degradation  

摘要： Porphyromonas gulae, an animal-derived periodontal pathogen, expresses several virulence factors, including fimbria, lipopolysaccharide (LPS) and proteases. We previously reported that its invasive efficiency was dependent on fimbriae types. In addition, P. gulae LPS increased inflammatory responses via toll-like receptors. The present study was conducted to investigate the involvement of P. gulae proteases in bacterial and host cell biology. Porphyromonas gulae strains showed an ability to agglutinate mouse erythrocytes and also demonstrated co-aggregation with Actinomyces viscosus, while the protease inhibitors antipain, PMSF, TLCK and leupeptin diminished P. gulae proteolytic activity, resulting in inhibition of haemagglutination and co-aggregation with A. viscosus. In addition, specific proteinase inhibitors were found to reduce bacterial cell growth. Porphyromonas gulae inhibited Ca9-22 cell proliferation in a multiplicity of infection- and time-dependent manner. Additionally, P. gulae-induced decreases in cell contact and adhesion-related proteins were accompanied by a marked change in cell morphology from well spread to rounded. In contrast, inhibition of protease activity prevented degradation of proteins, such as E-cadherin, beta-catenin and focal adhesion kinase, and also blocked inhibition of cell proliferation. Together, these results indicate suppression of the amount of human proteins, such as gamma-globulin, fibrinogen and fibronectin, by P. gulae proteases, suggesting that a novel protease complex contributes to bacterial virulence.

关键词： 疫情时期   医学细胞生物学   线上教学  

摘要： 基于疫情背景,从课前准备、教学实施、教学评价和教学反思等角度介绍医学细胞生物学课程在线教学的实践,并对疫情时期的在线教学进行总结和思考。

关键词： 阿魏酸   内皮祖细胞   高糖环境   超氧化物歧化酶   生物学功能  

摘要： 目的探讨阿魏酸(FA)对高糖诱导损伤的内皮祖细胞(EPCs)生物学功能和超氧化物歧化酶(SOD)的影响。方法体外分离和培养人脐带血EPCs,通过观察细胞形态、双荧光染色法及免疫荧光细胞化学染色法等技术对培养的EPCs进行鉴定。将鉴定成功的EPCs用30 mmo1/L的葡萄糖预处理120 h后,分别在不同浓度梯度FA(0、1、2、4、8、16 mg/L)条件下干预培养,确定FA促高糖受损EPCs增殖的最佳浓度。另将高糖诱导损伤的EPCs随机分为实验组(最佳浓度FA干预)和模型对照组(PBS干预),同时设置正常EPCs对照组(PBS干预)。采用细胞计数试剂盒(CCK-8)、黏附能力测定试验、Matrigel体外成管试验、划痕实验及ELISA法检测FA对细胞增殖、黏附、成血管、迁移能力及对EPCs分泌SOD的影响。结果FA促高糖受损EPCs增殖的最佳浓度为8 mg/L;与正常组比较,高糖受损EPCs增殖、迁移、黏附及成管能力显著降低(P<0.05);当用FA干预后,高糖受损EPCs增殖、黏附、迁移及成血管能力显著增强(P<0.05)。ELISA检测发现,与正常组比较,高糖受损EPCs分泌SOD能力显著下降(P<0.05),而用FA干预后,能部分逆转EPCs分泌SOD能力,但差异无统计学意义(P>0.05)。结论FA处理能改善高糖受损EPCs生物学功能,但对高糖受损EPCs分泌SOD作用不明显。

关键词： 卵巢癌   N-myc下游调节基因2   增殖   过表达   凋亡  

摘要： 目的构建N-myc下游调节基因2(NDRG2)过表达质粒,研究NDRG2基因影响卵巢癌细胞增殖、凋亡及侵袭等生物学行为的作用.方法NDRG2过表达质粒载体感染卵巢癌细胞,从而实现NDRG2基因的在卵巢癌细胞中的过表达.之后通过CCK8试验观察卵巢癌细胞的生存能力及平板克隆形成试验观察卵巢癌细胞的增殖能力.流式细胞术检测细胞凋亡和细胞周期.结果质粒转染后,Q-PCR检测NDRG2基因特异过表达.Q-PCR试验观察NDRG2过表达质粒瞬时转染后NDRG2基因表达情况,与空载体组相比,NDRG2过表达转染组卵巢癌细胞NDRG2基因表达水平明显升高(OVCAR-3、SKOV3、CAOV3卵巢癌细胞t值分别为48.000、28.667、29.784,均P<0.05).CCK8检测、平板克隆试验结果显示过表达NDRG2基因显著抑制OVCAR-3、SKOV3及CAOV3细胞生长(t=22.928、13.797、10.332;χ^(2)=5.530、4.060、4.230,P<0.05),并促使上述3种卵巢癌细胞周期停滞于G1期.结论通过真核表达载体使细胞NDRG2基因的过表达,可以明显抑制OVCAR-3、SKOV3及CAOV3细胞的生长和增殖.

关键词： 胶质瘤细胞   CYP17A1   甲基化   增殖   侵袭   转移  

摘要： 目的探讨细胞色素P450c17a酶(CYP17A1)通过介导DNA去甲基化对胶质瘤细胞生物学特性的影响,并分析其相关机制。方法人胶质瘤细胞U251分为干预组(先用DHEA处理48 h,再用TMZ预处理48 h)和阴性对照组(正常培养,不进行任何干预),各6个复孔;以正常脑组织坏死细胞(非胶质细胞)为正常组,正常培养,不进行任何干预。通过聚合酶链式反应(PCR)实验,蛋白质印迹实验对细胞中CYP17A1 mRNA及蛋白表达量进行测定;利用甲基化特异性PCR法检测CYP17A1基因在的甲基化状态;通过MTT及流式细胞仪对细胞增殖情况进行测定;通过细胞侵袭实验对细胞侵袭及转移情况进行测定。通过细胞集落形成试验检测CYP17A1的增殖能力。结果提取总RNA的完整性,28S条带比18S处条带亮2倍左右,后面未见有拖带痕迹。干预组与阴性对照组CYP17A1 mRNA的相对表达量(0.811±0.047、0.507±0.025)均显著高于正常组(0.020±0.001),而干预组显著低于阴性对照组,差异均有统计学意义(P<0.05)。干预组CYP17A1蛋白(0.405±0.031)显著低于阴性对照组(0.783±0.032),差异有统计学意义(P<0.05),该蛋白在正常组中不表达。CYP17A1基因在正常细胞中未发生甲基化,干预组中CYP17A1基因甲基化发病率[(43.93±8.93)%]显著低于阴性对照组[(89.03±10.02)%],差异有统计学意义(P<0.05)。干预组CYP17A1的细胞增殖速率以及细胞侵袭、迁移率分别为(38.97±11.32)%、(245.19±18.71)个、(69.09±6.53)%,均显著低于阴性对照组[(78.09±10.21)%、(587.36±43.25)个、(80.49±8.76)%],差异均有统计学意义(P<0.05)。干预96 h后,阴性对照组和干预组细胞集落形成能力[(62.71±15.25)%、(54.16±14.82)%]均显著高于正常组[(18.17±6.35)%],干预组显著低于阴性对照组,差异均有统计学意义(P<0.05)。结论CYP17A1可通过介导DNA去甲基化从而对胶质瘤细胞的增殖、侵袭和转移能力产生抑制作用,并进一步抑制细胞细胞集落形成能力。