基于Oncomine数据库分析PD-L1基因在头颈部癌中的表达及预后

目的:研究程序性死亡因子配体1(programmed death factor 1,PD-L1/CD274)在头颈部癌中的表达情况,并分析其与临床病理特征及预后的相关性。方法:挖掘Oncomine数据库中关于PD-L1基因在头颈部癌中的相关数据,进行PD-L1表达量与头颈部癌临床生物学特性的相关分析,并利用数据库中生存数据进行生存分析。结果:Oncom-ine数据库中有关PD-L1基因癌组织/正常组织表达量的分析共176项,其中高表达的癌种共4项,低表达2项;在头颈部癌组织中,显著高表达1项。Meta分析显示,PD-L1在头颈部癌中呈现高表达,显著高于正常组织。在人乳头瘤病毒(human papillomavirus,HPV)阳性的HNC患者中PD-L1的表达显著高于HPV阴性HNC患者(0.38 vs 0.16,P=0.018),有远处转移的患者显著高于无转移者(1.36 vs 0.55,P=0.004)。生存分析显示PD-L1表达量与生存期无显著相关。结论:PD-L1在头颈部癌中表达水平高,与人乳头瘤病毒状态及肿瘤转移相关,与生存期不相关。     

丙戊酸钠通过EGFR下调CD44表达抑制胶质瘤细胞生长

目的:探讨丙戊酸钠通过抑制A172胶质瘤细胞表皮生长因子受体（epidermal growth factor receptor，EGFR）的活化，下调CD44表达，进而调节细胞生长的机制。方法:实时荧光定量PCR和Western blot检测A172胶质瘤细胞中CD44以及siRNA下调CD44表达的情况，MTT检测CD44和丙戊酸钠对细胞生长的影响，Western blot检测丙戊酸钠对细胞中p-EGFR、EGFR和CD44表达影响。结果:丙戊酸钠抑制A172胶质瘤细胞生长，并具有浓度依赖性。A172胶质瘤细胞表达CD44，siRNA下调CD44表达后，细胞生长较正常组显著减缓。活化EGFR促进A172胶质瘤CD44蛋白表达，而EGFR的抑制剂Lapatinib可显著抑制上述效应。丙戊酸钠抑制EGFR磷酸化，下调CD44蛋白表达。结论:丙戊酸钠抑制A172胶质瘤细胞的生长。抑制A172胶质瘤细胞中EGFR的活化，下调CD44的表达，是丙戊酸钠抑制胶质瘤细胞生长的其中一个机制。     

针刀松解激痛点治疗颈源性头痛39例影响

目的分析针刀松解激痛点治疗方法用于颈源性头痛患者的效果。方法对医院接受针刀松解激痛点治疗的39例颈源性头痛患者纳入试验组,选于2017年2月—2018年9月,抽取同期接受针刺治疗的39例颈源性头痛患者纳入对照组,评比两组治疗有效总计率、治疗前和治疗3个疗程后头痛程度评分值、头痛维持时间、头痛发生频率。结果试验组治疗有效总计率明显高于对照组统计值(P<0.05)。试验组治疗3个疗程后头痛程度评分值、头痛维持时间、头痛发生频率显著低于治疗前及对照组统计值(P<0.01)。结论对颈源性头痛患者实行针刀松解激痛点治疗的效果较优。     

持续性颅内压监测在颅脑外伤治疗的效果探讨

目的对急性重型颅脑外伤患者在临床治疗中实施持续性颅内压监测的价值进行研究。方法选择本院在2017年8月—2018年8月期间收治的确诊为重型颅脑外伤的患者共计28例作为研究对象,按照硬币法将这些患者划分为两个小组,对照组14例,实验组14例。采用常规治疗方式对对照组加以治疗,采用持续性颅内压监测对实验组加以治疗,对两组患者的治疗效果进行比较。结果对照组的预后神经功能NHISS评分为(15.83±0.31)分、预后GOS评分为(3.19±0.15)分,实验组的预后神经功能NHISS评分为(11.18±0.45)分、预后GOS评分为(4.90±0.17)分。实验组预后神经功能NHISS评分、GOS评分均明显优于对照组,且差异具有统计学意义(P<0.05)。结论在急性重型颅脑外伤患者的临床治疗中应用持续性颅内压监测具有重要作用,其能够对患者的治疗予以有效指导,提升患者的治疗效果。     

剔络养血明目方对青光眼患者视功能改善的疗效分析及对视神经血流密度的影响

目的:探讨剔络养血明目方对青光眼患者最佳矫正视力(the best corrected visual acuity,BCVA),视野等改善的作用,分析该方剂对视神经血流密度(vessel density,VD)和视网膜神经纤维层厚度(retinal nerve fiber layer thickness,RNFL thickness)的影响。方法:回顾分析2017年1月至2020年7月采用剔络养血明目方治疗的117例原发性青光眼患者共计234只眼的临床数据;回顾剔络养血明目方治疗的57只眼作为治疗组,另选取性别、年龄、疗程相匹配的未行该方治疗的57只眼作为对照组。分析治疗前后BCVA,视野平均敏感度(value and mean sensitivity,MS),平均缺损(mean deviation,MD)的变化。利用光学相干断层扫描血管成像技术(optical coherence tomography angiography,OCTA)分析治疗前后视神经VD及RNFL厚度的变化。结果:治疗后较治疗前BCVA提升(P=0),MS值增加(P=0),MD值减小(P=0.001),整个视盘扫描区域(P=0),视盘内(P=0.004)及盘周各分区(P0.05)的VD增加,RNFL厚度(除视盘下方鼻侧区外)无明显变化。治疗组治疗后较治疗前,MS增加(P=0.003),MD减少(P=0.024),对照组视野各指标治疗后较治疗前变化无统计学差异。结论:对于眼压稳定在目标眼压范围内的青光眼患者,剔络养血明目方能够改善其视功能和视神经VD,但对RNFL厚度无明显影响。     

生大黄、芒硝湿敷联合集束化护理对骨折患者使用甘露醇期间发生静脉炎的预防效果观察

目的:观察生大黄、芒硝湿敷联合集束化护理对骨折患者甘露醇使用期间静脉炎的预防效果。方法:选取使用20%甘露醇静脉滴注治疗的300例骨折患者,按随机数字表法分为对照组和观察组各150例。2组均实施集束化护理,观察组在甘露醇静脉滴注后使用生大黄、芒硝湿敷。比较2组患者静脉炎发生率、留置针留置时间和针口处疼痛、红肿情况。结果:观察组静脉炎严重程度轻于对照组,差异有统计学意义(P0.05)。观察组和对照组静脉炎发生率分别为12.67%、37.33%,2组比较,差异有统计学意义(P0.05)。观察组留置针留置时间2 d的比率为24.67%,低于对照组的39.33%(P0.05);观察组留置针时间5 d的比率为30.00%,高于对照组的18.67%(P0.05)。干预后,2组针口处疼痛评分、红肿直径均较干预前改善(P0.05);观察组针口处疼痛评分、红肿直径改善情况均优于对照组(P0.05)。结论:生大黄、芒硝湿敷联合集束化护理能减少骨折患者甘露醇使用期间静脉炎发生,延长留置针留置时间,减轻针口处疼痛、肿胀。     

The PROFILE of assessment program for internal medicine internship of Sun Yat-Sen University

Objective: To reflectively look at the present methods by which the clinical competence of 5th-year medical students (i.e. interns) in Sun Yat-Sen University (SYSU) are assessed upon finishing internship rotation in internal medicine (IM).

Methods: Current procedures for the competence assessment of end-of-rotation IM interns in the First Affiliated Hospital of SYSU were reviewed, along with a point-by-point appraisal based on the PROFILE approach to structured assessment, and, whenever possible, suggestions for future improvement.

Results and discussions: On a scale of 1–10, with 10 being the best or the most ideal, our marks for current methods to assess end-of-rotation IM interns in terms of being Programmatic, Real-World, Outcome-based, Formative, Impactful, Learner-engaged, and Evaluation-guaranteed were 7, 9, 3, 4, 6, 8, and 1, respectively. The strengths, weaknesses as well as potential solutions in each of the seven aspects are also discussed separately.

Conclusions: Current assessment program for IM internship is strong in being programmatic, real-world, educationally impactful and learner engaged, and has room for further improvement in its time-based arrangements, relative shortage of feedback provision, as well as a systematic lack of quality control measures.     

1例房间隔缺损并肺动脉高压患者术后的药学监护

1例23岁女性患者,因"发现房间隔缺损7个月"收入院,诊断为先天性心脏病,房间隔缺损,肺动脉高压(中-重度),行房间隔缺损修补术。术后为维持血流动力学相对稳定,需要用到镇静止痛药、肌肉松弛药、强心利尿药以及多种肺动脉高压靶向制剂。药物种类较多,且呈现不同药代动力学特点。临床药师查阅相关资料,挖掘每个药物的监护点,警惕可能存在的药物相互作用,提出合理用药的建议,保障临床用药安全有效。经积极治疗,最终患者病情稳定出院。     

Epidermal growth factor‐induced COX‐2 regulates metastasis of head and neck squamous cell carcinoma through upregulation of angiopoietin‐like 4

Epidermal growth factor receptor (EGFR) expression and activation are the major causes of metastasis in cancers such as head and neck squamous cell carcinoma (HNSCC). However, the reciprocal effect of EGF‐induced COX‐2 and angiopoietin‐like 4 (ANGPTL4) on HNSCC metastasis remains unclear. In this study, we revealed that the expression of ANGPTL4 is essential for COX‐2‐derived prostaglandin E₂ (PGE₂)‐induced tumor cell metastasis. We showed that EGF‐induced ANGPTL4 expression was dramatically inhibited with the depletion and inactivation of COX‐2 by knockdown of COX‐2 and celecoxib treatment, respectively. Prostaglandin E₂ induced ANGPTL4 expression in a time‐ and dose‐dependent manners in various HNSCC cell lines through the ERK pathway. In addition, the depletion of ANGPTL4 and MMP1 significantly impeded the PGE₂‐induced transendothelial invasion ability of HNSCC cells and the binding of tumor cells to endothelial cells. The induction of molecules involved in the regulation of epithelial‐mesenchymal transition was also dependent on ANGPTL4 expression in PGE₂‐treated cells. The depletion of ANGPTL4 further blocked PGE₂‐primed tumor cell metastatic seeding of lungs. These results indicate that the EGF‐activated PGE₂/ANGPTL4 axis enhanced HNSCC metastasis. The concurrent expression of COX‐2 and ANGPTL4 in HNSCC tumor specimens provides insight into potential therapeutic targets for the treatment of EGFR‐associated HNSCC metastasis.