药理实验室绿色环保化建设探讨

实现药理实验室绿色化是药理实验教学和科研人员所面对的新课题。本文探讨了目前高校药理实验室存在的主要问题,并从实验教学、实验准备和实验室管理等几个方面讨论了构建绿色药理实验平台的重要性及实施的主要措施,从而进一步提高师生的绿色实验意识。     

经颅多普勒超声在儿童颅内压增高性疾病中的应用

经颅多普勒超声(transcranial doppler ultrasonography,TCD)是一种非侵入性评价颅内动脉的检测手段,自上世纪80年代问世以来,已被广泛性应用于临床工作的各个领域.由于其操作简便、重复性好,可以对患者进行床旁连续、动态观察,尤其适用于监测危重症患者.颅内压增高是儿童致病致死的再要原因之一,它可使脑血流灌注下降,造成脑功能障碍等严重后果,因此颅内压监测有重要临床意义.TCD作为一种无创性监测工具,可根据其血流速度、相关参数及血流频谱的变化对颅内压增高患者脑血流动力学进行动态监测与评估,从而达到监测颅内压改变的目的.本文着重阐述TCD在几种常见的儿童颅内高压性疾病中的应用进展.     

组蛋白去乙酰化酶抑制剂Apicidine对宫颈癌HeLa细胞的抑制作用及机制研究

目的:探讨组蛋白去乙酰化酶抑制剂Apicidine对宫颈癌细胞的杀伤作用和机制。方法:用不同浓度的Apicidine作用于体外培养的宫颈癌细胞株HeLa和正常呼吸道上皮细胞REC;用MTT法检测细胞生长存活率;用流式细胞术(FCM)定量检测细胞凋亡及细胞周期的变化;用RT-PCR法和Western blot法分析Apicidine作用后宫颈癌细胞中p21WAF1和p53表达的变化。结果:Apicidine纳摩尔级浓度即能有效地抑制宫颈癌细胞增殖,对正常细胞无明显抑制效应。FCM结果表明,Apicidine能显著诱导宫颈癌细胞发生凋亡,对正常细胞无明显促凋亡作用;加入2μmol/L Apicidine作用24h和48h后宫颈癌细胞HeLa凋亡率分别为(10.11±0.63)%和(23.28±0.34)%,差异有显著性(P<0.05),正常呼吸道上皮细胞REC凋亡率分别为(5.81±0.92)%和(6.8±0.55)%,差异无显著性(P>0.05);FCM结果亦表明,Apicidine主要引起G0/G1期细胞周期阻滞,1μmol/L Apicidine处理24h后HeLa细胞G0/G1期细胞显著增多,由(46.8±3.2)%增至(69.5±6.1)%,差异有统计学意义(P<0.05);RT-PCR和Western blot结果显示,Apici-dine能显著诱导p21WAF1RNA和蛋白水平表达,对p53表达无明显影响。上述结果都呈现明显的量-效与时-效关系。结论:Apicidine在体外能有效地抑制人宫颈癌细胞生长,对人正常细胞无明显影响,其抗肿瘤生长机制之一可能是通过上调p21WAF1蛋白水平和引起G0/G1期细胞周期阻滞实现的。     

Special manifestations and treatment of rare cases of snoring with special facial features and hearing loss in children

This current case report describes two rare cases of children with both hearing loss and snoring. Case 1, a 17-month-old male patient, and case 2, an 11-year-old male patient, both presented with nasal obstruction, snoring and hearing loss. Physical examinations showed obvious enlargement of the head circumference and special facial features. The two children underwent otolaryngology examinations, endoscopy, hearing tests, laboratory examinations for bone metabolism markers, cranial computed tomography, X-rays and genome-wide exon sequencing. The first case was diagnosed with craniometaphyseal dysplasia, which was relieved after giving a low-calcium diet. The second case was diagnosed with osteopathia striata with cranial sclerosis by gene sequencing. Snoring improved after medication and the speech and quality of life improved with a hearing aid. Paediatric otolaryngological physicians need to have a deeper understanding of congenital diseases involving the bones. Only by genetic testing to determine the pathogenesis can those children be given the correct treatment, which is of great importance for improving their prognosis.     

胆道发育不良患儿的临床病理特点回顾

目的 探讨胆道发育不良患儿的临床表现、病理特点、诊断、治疗及预后,提高对该病的认识.方法 回顾性分析天津市儿童医院外科2010年6月至2016年11月收治的5例胆道发育不良患儿的发病情况、治疗过程,并通过复习国内外文献对胆道发育不良的疾病特点进行总结.结果 5例胆道发育不良患儿均因生后不久出现皮肤、巩膜黄染,内科治疗病情无改善入外科治疗;肝功能检查见胆红素水平升高,以直接胆红素升高为主,伴肝酶不同程度增高;超声检查示胆囊干瘪未充盈或胆囊腔狭小,胆总管显示不清.5例患儿行手术探查,术中造影显示肝内、外胆道通畅,管腔纤细;病理检查见部分汇管区中小叶间胆管缺失,小叶间胆管/汇管区＜0.5,诊断为胆道发育不良,予留置胆囊引流管,术后抗炎、补液、保肝及对症治疗.经2个月～6年门诊随访,5例患儿均存活至今,其中3例黄疸清除,1例皮肤仍黄染并伴有瘙痒,1例未退黄.结论 术前检查提示梗阻性黄疸患儿,术中造影提示胆道纤细,结合病理检查证实小叶间胆管/汇管区比例＜0.5,可以明确胆道发育不良的诊断.     

凝胶渗透色谱-多角度激光散射联用技术研究 红芪多糖中4个组分分子特征

目的:测定红芪多糖3(HPS-3)中4个组分的绝对分子量,相对分子质量分布,均方根旋转半径(Rg),多分散系数(Mw/Mn)等分子特征参数,以均方根旋转半径(Rg)对重均分子量(Mw)作图,计算4个组分在溶液状态的构象。方法:采用凝胶渗透色谱-多角度激光散射(GPC-MALLS)联用技术,流动相为含0.02%NaN3的0.1 mol.L-1NaNO3溶液,Ultrahydro-gelTM1000,500色谱柱串联。结果:HPS-3的4个组分中,HPS-3-C的Mw最大(1.986×105g.mol-1);其次为HPS-3-B(1.113×105 g.mol-1)和HPS-3-D(8.457×104 g.mol-1);HPS-3-A的Mw最小(1.223×104 g.mol-1),而Rg最大(55.5 nm)。HPS-3-D相对分子质量分布范围最广,Mw/Mn 2.543。在流动相中,HPS-3-A为球型构象,HPS-3-C为无规则线团构象,HPS-3-B和HPS-3-D则均为高枝化度结构。结论:为进一步研究HPS-3中4个组分分子特征与其生物活性的关系提供必要依据。     

不同切口方法对超声导引下改良塞丁格技术PICC置管后减少渗液的效果观察

目的 探讨不同切口方法对超声导引下改良塞丁格技术(MST)行经外周中心静脉置管(PICC)后减少穿刺点渗液的效果观察.方法 将680例需行PICC置管患者根据切口方法的不同随机分为纵切口组(342例)和横切口组(338例).比较2组患者置管后渗液发生率及渗液量的发生情况.结果 纵切口组患者渗液发生率及渗液量低于横切口组,差异均有统计学意义(P均＜0.05).结论 超声导引下MST行PICC穿刺时采用纵向切口法,可有效降低置管后渗液发生率,减少穿刺部位的渗液量,提高患者满意度.     

刍议飞行人员健康管理

健康管理是对个体或群体的健康进行全面监测、分析、评估,提供健康咨询和指导以及对健康危险因素进行干预的全过程.构建完善的飞行人员健康管理模式,遵循全员、全程、全科、个性化、互动性、制度化等原则,树立先进的健康管理理念,这对于提高飞行人员健康管理水平,延长飞行年限,节约军费开支,增强军队战斗力具有重要的意义.     

右美托咪定辅助全身麻醉对心脏瓣膜置换术患者血流动力学和脑氧代谢及认知功能的影响

目的 探讨右美托咪定辅助全身麻醉对心脏瓣膜置换术患者血流动力学、脑氧代谢及认知功能的影响。方法 选取2018年3月至2019年5月于山东大学齐鲁医院拟行心脏瓣膜置换术的108例患者作为研究对象,采用随机数字表法分为对照组与观察组,每组54例。对照组行常规全身麻醉,观察组在对照组基础上于麻醉诱导前给予右美托咪定辅助麻醉。比较两组手术时间、麻醉时间、体外循环时间、血流动力学、血气和脑氧代谢指标及简易精神状态评价量表(MMSE)评分。结果 两组手术时间、麻醉时间及体外循环时间比较差异无统计学意义。T₂、T₄时,观察组收缩压(SBP)、舒张压(DBP)、心率(HR)均低于对照组,且T3时,观察组SBP、DBP均低于对照组(P<0.05)。T₂、T₃、T₄时,观察组动脉-颈内静脉血氧含量差(Da-jvO₂)、脑氧摄取率(CERO2)均高于对照组(P<0.05)。术后24、72 h,观察组简易精神状态评价量表(MMSE)评分均高于对照组(P<0.05...     

Rotenone,an environmental toxin,causes abnormal methylation of the mouse brain organoid's genome and ferroptosis

More and more reports have pointed out that rotenone, as an insecticide, has high neurotoxicity and reproductive toxicity to livestock and mammals. As a highly physiological correlation system of internal organs, quasi-organs have great potential in the fields of drug toxicity and efficacy test, toxicology research, developmental biology and so on. In this study, brain organs (mBOs) derived from mouse neural stem cells were used to investigate the effects of rotenone on the physiological activity and epigenetic modification of mBOs. At the same time, Rotenone could significantly stimulate the increase of the concentration of LPO, lactic acid and hydroxyl radical in mBOs, and inhibit the expression of neuronal marker Tuj1, CHAT, PAX6 and so on. Further analysis showed that Rotenonem could induce mitochondrial damage in mBOs. The results of qPCR and Western blot showed that Rotenone could up-regulate the expressions of ferroptosis promoting protein p53, Cox2 and so on, while inhibit the expressions of negative regulatory protein of ferroptosis GPX4, FTH1, SLC7A11. In addition, the results of RRBS-Seq sequencing showed that the methylation modification at DMR level in Rotenone-treated mBOs group was significantly higher than that in Ctrl group. The results of KEGG analysis showed that compared with Ctrl, the genes with hypermethylation of promoter and Genebody in Rotenone-treated mBOs were mainly located in the Neuro active ligand-receptor interaction signal transduction pathway. In summary, rotenone can significantly lead to abnormal methylation of mouse brain organs, and lead to the loss of normal physiological function of neurons by inducing ferroptosis.