加强型鼻咽通气道应用于鼻腔手术后气道管理临床研究

目的研制加强型鼻咽通气道应用于五官科鼻腔手术后的气道管理。方法选取2014年1月至2015年3月行五官科鼻腔手术的患者60例,将其分为A组和B组,各30例。A组作为加强型鼻咽通气道组,术毕在膨胀止血海绵中放置加强型鼻咽通气道保留鼻腔通气;B组作为对照组,术毕采用传统单纯填塞膨胀止血海绵。通过术后24、48 h随访,对两组患者进行疼痛、睡眠质量、口干程度评分,并对其进行对比分析。结果加强型鼻咽通气道具有良好的抗压抗折性;A组患者24、48 h睡眠质量、口干程度评分均明显优于B组,差异均有统计学意义(P<0.05)。结论加强型鼻咽通气道用于五官科鼻腔手术后气道管理可增强气道管理安全性及患者舒适度。     

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。     

Comparison of the practicability of ultrasound and spiral computed tomography in the diagnosis of colon cancer: A protocol for systematic review and meta-analysis

Background:Colon cancer is a common malignant tumor of the gastrointestinal tract. Therefore, a clear diagnosis is particularly important for the treatment of colon cancer. Ultrasound and spiral computed tomography (CT) can both be used in the diagnosis, but each has its own advantages and disadvantages, which could cause confusion in clinical choice. The purpose of this study was to systematically evaluate the practicability of spiral CT and ultrasound in the diagnosis of colon cancer.Methods:A systematic search was performed by retrieving on English databases (PubMed, Embase, Web of Science, the Cochrane Library) and Chinese databases (CNKI, Wanfang, Weipu [VIP], CBM). Besides, manually search for Google and Baidu academic of diagnostic experimental study of ultrasound and spiral CT in the diagnosis of Colon Cancer. The retrieval time limit was from the establishment of the database to October 2020. Two researchers independently extracted and evaluated the quality of the data in the included study. A meta-analysis was performed using Meta Disc1.4 and RevMan5.3 software.Results:Sensitivity, specificity, positive Likelihood ratio, negative likelihood ratio, and diagnostic odds ratio were used to determine the diagnostic efficacy of ultrasonography and helical CT in colorectal cancer.Conclusions:This study will compare the practicability of CT and ultrasound in the diagnosis of colon cancer and provide reliable evidence-based basis for clinicians to choose the appropriate or best evidence-based basis.Ethics and dissemination:The private information from individuals will not be published. This systematic review also will not involve endangering participant rights. Ethical approval is not required. The results may be published in a peer-reviewed journal or disseminated in relevant conferences.OSF Registration number:DOI 10.17605/OSF.IO/WAJHQ     

放射性心脏损伤动物模型相关实验研究进展

当利用放射线对胸部恶性肿瘤进行治疗时，位于纵隔的心脏会不可幸免受到照射，从而诱发放射性心脏损伤（radiation-induced heart disease, RIHD）。随着手术以及放化疗技术的提升，肿瘤患者生存时间得到延长，使得RIHD这一放疗远期并发症被越来越多的报道。因此，学者们对于RIHD的研究逐渐升温。目前国内外学者关于该疾病尚未形成统一的认识，临床上缺乏有效阻止其发生的方法。动物模型研究可为临床该疾病治疗及预防提供可靠证据，为此本文回顾分析近年来放射性心脏损伤动物模型实验研究情况，旨在为后续实验开展及临床应用提供参考。     

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.     

microRNA-613调控CDK14来抑制老年胶质瘤患者瘤细胞的增殖和侵袭作用

目的 探讨microRNA-613调控细胞周期蛋白依赖性激酶14(CDK14)通路来抑制老年胶质瘤患者瘤细胞增殖和侵袭的机制。方法 购自上海北诺生物科技有限公司的人脑胶质瘤细胞株U251共24株,分为shNC组、shmicroRNA-613组、Vector组、microRNA-613组,每组各6株; Western Blotting法和qRT-PCR法检测敲减microRNA-613和过表达microRNA-613后的人脑胶质瘤细胞株U251中CDK14蛋白表达水平,CCK-8细胞增殖实验、Transwell小室实验验证敲除microRNA-613和过表达microRNA-613后U251细胞的增殖、侵袭能力。结果 人胶质瘤细胞株U251敲减microRNA-613后CDK14蛋白表达增加(P<0.05); 人胶质瘤细胞株U251过表达microRNA-613后CDK14蛋白表达减少(P<0.05); 转染第24、36、48 h microRNA-613组U251细胞增殖率P<0.05); microRNA-613组U251细胞侵袭能力>Vector组,shNC组>shmicroRNA-613组(P<0.05)。结论 microRNA-613可通过调控CDK14信号转导通路来抑制人脑胶质瘤细胞U251增殖、转移。