莱菔硫烷促进神经胶质瘤细胞凋亡的机制探讨

目的探讨莱菔硫烷(SFN)促进神经胶质瘤细胞凋亡的作用机制。方法采用噻唑蓝(MTT)法与流式细胞法检测不同浓度的SFN对神经胶质瘤U251细胞系生长的抑制作用,测定半数抑制浓度,空白对照设为对照组;采用Western blot研究SFN对U251细胞内Cyt-c的表达情况。结果不同浓度SFN组A值均低于对照组,差异有统计学意义(P<0.05)。不同浓度SFN均对U251细胞生长有一定抑制作用,12.5μmol/l、25μmol/l、50μmol/l、100μmol/l浓度的SFN对U251细胞生长抑制率逐渐增强,各组间比较差异均有统计学意义(P<0.05)。但100μmol/l与200μmol/l浓度的SFN对U251细胞生长抑制率比较无统计学意义(P>0.05)。不同浓度SFN诱导细胞凋亡率及Cyt-c蛋白表达均显著高于对照组,且随着SFN浓度递增,U251细胞凋亡率、Cyt-c蛋白表达逐渐增加,各组间比较差异均有统计学意义(P<0.05)。结论SFN可能参与神经胶质瘤细胞的凋亡过程,表现为诱导凋亡U251细胞,可能与Cyt-c表达增高存在关系。     

磁锚定技术辅助腹腔镜阑尾切除术的实验研究

目的:验证自行设计加工的磁锚定装置在减戳孔腹腔镜阑尾切除术中应用的可行性。方法:设计加工适用于辅助减戳孔腹腔镜阑尾切除术的磁锚定装置,该装置包括内置抓钳和锚定磁体2个部分。以6只健康雄性Beagle犬为模型,用磁锚定装置代替传统腹腔镜阑尾切除术中的副操作孔抓钳,经主操作孔置入磁锚定内置抓钳并钳夹于阑尾尖部,体外放置锚定磁体,锚定磁体与内置抓钳的靶磁体相吸,移动锚定磁体即可改变内置抓钳的牵拉方向,从而有效牵拉暴露手术术野,完成减戳孔腹腔镜阑尾切除手术。记录手术操作时间、术中出血量,评价利用磁锚定装置进行阑尾切除时操作的安全性和可行性。结果:6只Beagle犬均顺利完成磁锚定技术辅助减戳孔腹腔镜阑尾切除,手术时间27~38 min,出血量均小于10 ml,术后实验犬状态良好,未出现并发症。结论:磁锚定装置用于减戳孔腹腔镜阑尾切除手术操作简单、安全可行,在相关设计进一步优化基础上,可尝试或试验性用于临床。     

持续质量改进在体检科护理质量管理中的应用效果探讨

目的探究持续质量改进在体检科护理质量管理中的应用效果。方法该次将该院在2018年7-12月的体检者200名作为研究的对象,视为对照阶段,采取常规护理管理方法;将该院2019年1-6月的体检者200名作为观察阶段对象,在护理管理工作中采取持续质量改进管理模式,进一步对比两个阶段患者对于体检科工作质量的评分。结果在体检工作质量、服务态度、体检满意度这3个模块,观察阶段评分对照阶段比较均明显更高,差异有统计学意义(P<0.05)。结论持续质量改进应用于体检科护理质量管理中,可有效提升体检服务品质,值得推广应用。     

Rabs and axonal regeneration

Membrane trafficking processes are presumably vital for axonal regeneration after injury, but mechanistic understanding in this regard has been sparse. A recent loss-of-function screen had been carried out for factors important for axonal regeneration by cultured cortical neurons and the results suggested that the activity of a number of Rab GTPases might act to restrict axonal regeneration. A loss of Rab27b, in particular, is shown to enhance axonal regeneration in vitro, as well as in C. elegans and mouse central nervous system injury models in vivo. Possible mechanisms underlying this new finding, which has important academic and translational implication, are discussed.     

多原发结直肠癌的临床特征和预后

目的探讨多原发结直肠癌的临床特征和预后。方法回顾性分析南京医科大学第一附属医院2013年1月至2018年12月收治的42例多原发结直肠癌患者的临床资料,对其临床病理特征、诊治及预后进行总结。结果符合多原发结直肠癌诊断的患者42例,占同期收治的所有结直肠癌患者的1.20%(42/3499),病理类型以腺癌为主。其中,同时性多原发癌32例,年龄38~86岁,中位年龄66岁,共发现73处结直肠癌灶,多位于近端结肠、乙状结肠及直肠;共检出淋巴结527枚,阳性10枚(1.9%),淋巴结阳性患者占同时性多原发癌的37.5%(12/32);27例为双原发癌,3例为三原发癌,2例为五原发癌;1、3年总生存率分别为83.75%和74.38%。异时性多原发癌10例,年龄33~86岁,第一癌多位于直肠和乙状结肠区域,第二癌多位于升结肠区域;共检出淋巴结276枚,阳性率12.3%(34枚),1、3年总生存率分别为100.00%和66.67%。结论多原发结直肠癌在临床上不少见,其分布有一定规律。临床中应引起重视,提高早期诊断率。应早期手术治疗以提高患者的生存率。     

Protein kinase Cδ mediates trimethyltin-induced neurotoxicity in mice in vivo via inhibition of glutathione defense mechanism

We investigated whether protein kinase C (PKC) is involved in trimethyltin (TMT)-induced neurotoxicity. TMT treatment (2.8 mg/kg, i.p.) significantly increased PKCδ expression out of PKC isozymes (i.e., α, βI, βII, δ, and ?) in the hippocampus of wild-type (WT) mice. Consistently, treatment with TMT resulted in significant increases in cleaved PKCδ expression. Genetic or pharmacological inhibition (PKCδ knockout or rottlerin) was less susceptible to TMT-induced seizures than WT mice. TMT treatment increased glutathione oxidation, lipid peroxidation, protein oxidation, and levels of reactive oxygen species. These effects were more pronounced in the WT mice than in PKCδ knockout mice. In addition, the ability of TMT to induce nuclear translocation of Nrf2, Nrf2 DNA-binding activity, and upregulation of γ-glutamylcysteine ligase was significantly increased in the PKCδ knockout mice and rottlerin (10 or 20 mg/kg, p.o. × 6)-treated WT mice. Furthermore, neuronal degeneration (as shown by nuclear chromatin clumping and TUNEL staining) in WT mice was most pronounced 2 days after TMT. At the same time, TMT-induced inhibition of phosphoinositol 3-kinase (PI3K)/Akt signaling was evident, thereby decreasing phospho-Bad, expression of Bcl-xL and Bcl-2, and the interaction between phospho-Bad and 14-3-3 protein, and increasing Bax expression and caspase-3 cleavage were observed. Rottlerin or PKCδ knockout significantly protected these changes in anti- and pro-apoptotic factors. Importantly, treatment of the PI3K inhibitor LY294002 (0.8 or 1.6 µg, i.c.v.) 4 h before TMT counteracted protective effects (i.e., Nrf-2-dependent glutathione induction and pro-survival phenomenon) of rottlerin. Therefore, our results suggest that down-regulation of PKCδ and up-regulations of Nrf2-dependent glutathione defense mechanism and PI3K/Akt signaling are critical for attenuating TMT neurotoxicity.