非临床专业解剖学线上教学的效果分析与思考*

为有效应对疫情,确保疫情防控期间"停课不停学"[1-4],重庆医科大学积极开展疫情期间线上教学工作.非临床专业的解剖学学时少,本教研室结合其教学目标制定了全新的线上教学模式,并积累了一些经验.在后疫情时代,对于这些专业,仍延续线上教学为主的教学模式.现将本教研室在疫情期间线上课程建设的过程及存在的问题进行浅析,供同行参考.     

C086, a novel analog of curcumin, induces growth inhibition and down-regulation of NFκB in colon cancer cells and xenograft tumors

New analogues of curcumin with improved properties are needed to meet therapeutic requirements. In this study, the effects of C086 on growth inhibition and NFκB pathway regulation were investigated in colon cancer cells and xenograft tumors. C086 exhibited potent antiproliferative activity in all 6 colon cancer cell lines. In a xenograft model of SW480 cells in nude mice, the oral administration of C086 showed significant growth suppression of SW480 tumors, and both Western blot and immunohistochemistry analyses showed decreased NFκB (p65) expression in tumor tissues. Using TNF-α to induce NFκB activation in SW480 cells, it was revealed that C086 inhibited IκBα phosphorylation and its subsequent degradation, and suppressed the nuclear translocation and DNA binding activity of NFκB. C-Myc, cyclin D1, and Bcl-2, NFκB-regulated gene products involving in cellular proliferation and antiapoptosis, were decreased in the C086 treated groups. This effect was accompanied by pro-apoptosis of C086 in colon cancer cells and lower expression of PCNA in C086 treated colon cancer xenografts. Immunostaining for CD31 showed that there were fewer microvessels in C086 treated SW480 tumors, and NFκB-targeted gene products involved in angiogenesis (i.e., vascular endothelial growth factor, matrix metalloproteinase-9) were also downregulated. C086 also inhibited bovine aortic endothelial cell (BAEC) proliferation and tube formation in Matrigel. Overall, our results suggest that C086 is a potent antitumor agent and has promising future in colon cancer. C086 suppressed NFκB activation through inhibition of IκBα phosphorylation. Downregulation of NFκB-regulated gene products contributed to the antiproliferation, pro-apoptosis, and antiangiogenesis effect of C086.     

Androgen suppresses proliferation of castration-resistant LNCaP 104-R2 prostate cancer cells through androgen receptor, Skp2, and c-Myc

Androgen ablation therapy is the primary treatment for metastatic prostate cancer. However, this therapy is associated with several undesired side-effects, including increased risk of cardiovascular diseases. To study if termination of long-term androgen ablation and restoration of testosterone levels could suppress the growth of relapsed hormone-refractory prostate tumors, we implanted testosterone pellets in castrated nude mice carrying androgen receptor (AR)-positive LNCaP 104-R2 cells, which relapsed from androgen-dependent LNCaP 104-S cells after long-term androgen deprivation. 104-R2 tumor xenografts regressed after testosterone pellets were implanted. Of 33 tumors, 24 adapted to elevation of testosterone level and relapsed as androgen-insensitive tumors. Relapsed tumors (R2Ad) expressed less AR and prostate-specific antigen. We then studied the molecular mechanism underlying the androgenic regulation of prostate cancer cell proliferation. Androgen suppresses proliferation of 104-R2 by inducing G(1) cell cycle arrest through reduction of S-phase kinase-associated protein 2 (Skp2) and c-Myc, and induction of p27(Kip1). 104-R2 cells adapted to androgen treatment and the adapted cells, R2Ad, were androgen-insensitive cells with a slower growth rate and low protein level of AR, high levels of c-Myc and Skp2, and low levels of p27(Kip1). Nuclear AR and prostate-specific antigen expression is present in 104-R2 cells but not R2Ad cells when androgen is absent. Overexpression of AR in R2Ad cells regenerated an androgen-repressed phenotype; knockdown of AR in 104-R2 cells generated an androgen-insensitive phenotype. Overexpression of Skp2 and c-Myc in 104-R2 cells blocked the growth inhibition caused by androgens. We concluded that androgens cause growth inhibition in LNCaP 104-R2 prostate cancer cells through AR, Skp2, and c-Myc.     

基于酵母双杂交技术筛选肉苁蓉降血脂活性成分

目的 利用酵母双杂交系统对肉苁蓉中的单体成分进行降血脂活性的筛选.方法 将肉苁蓉中的5种化学成分加入到含有AH109菌株(携带大鼠apo-AI及其受体SR-BI全基因)的培养基中,通过报告基因β-半乳糖苷酶的活力,比较它们对大鼠apo-AI和SR-BI蛋白间相互作用的影响.结果 尿囊素可提高β-半乳糖苷酶的活力,8-表马钱子苷酸、松果菊苷、管花肉苁蓉苷B可降低β-半乳糖苷酶的活力,8-羟基-香叶醇-1-β-D-葡萄糖苷对β-半乳糖苷酶的活力无明显影响.结论 尿囊素可明显增强apo-AI和SR-BI蛋白的相互作用,具有一定的降血脂活性.     

食管癌根治术的手术配合体会

食管癌是我国常见的恶性肿瘤之一,占男女性恶性肿瘤发病率的前4位,男女之比为3∶1.食管癌严重危害着我国人民身体健康,它也是老年人群中的常见的恶性肿瘤之一.通过对80例食管癌手术患者的临床观察护理,认为食管癌患者术前呼吸道准备及术后仔细观察患者的生命体征变化为手术的成功率奠定了基础.如患者血氧饱和度低表示呼吸道不畅,心率增快、血压下降、尿量减少表示血容量不足等,需要及时处理.从而减轻患者的痛苦,减少并发症的发生.     

手法治疗腰椎术后骶髂关节源性下腰痛的疗效观察

目的探讨腰椎术后骶髂关节源性下腰痛的临床特点和手法治疗的要点。方法对64例腰椎术后骶髂关节源性下腰痛患者,根据骶髂关节错位的分型予不同手法调整,并予封闭术治疗,通过VAS、活动能力及改良M acnab标准来评定治疗疗效。结果随访8~42个月(平均22.7个月),患者治疗后的VAS评分、活动能力评分均较治疗前改善明显。结论根据骶髂关节错位分型予手法调整,辅以封闭术治疗腰椎术后骶髂关节源性下腰痛是一种简单、安全、目的性强的方法。     

依达拉奉对血管性痴呆大鼠脑组织β淀粉样蛋白、Tau蛋白表达的影响

目的研究依达拉奉对血管性痴呆(VD)大鼠脑组织β淀粉样蛋白(Aβ)、Tau蛋白表达的影响。方法通过Morris水迷宫筛选出雄性SD大鼠64只,随机分为正常组、假手术组、对照组、治疗组,术后7,14,28 d分别用Morris水迷宫测试大鼠空间学习记忆能力缺失情况,并取脑组织冰冻切片检测Aβ、Tau蛋白表达情况。结果对照组脑缺血再灌注后1周,神经细胞中Aβ、Tau蛋白的表达阳性细胞数均明显增多(P均<0.01),缺血再灌注4周后更明显(P均<0.001)。治疗组缺血再灌注1周后神经细胞中Aβ、Tau蛋白的表达阳性细胞数均明显少于对照组(P均<0.01),缺血再灌注2周后更明显(P均<0.001)。结论依达拉奉可抑制脑缺血再灌注后脑组织中Aβ、Tau蛋白的表达。     

穴位埋线结合免煎中草药颗粒治疗功能性消化不良临床观察

目的观察穴位埋线结合免煎中草药颗粒治疗功能性消化不良(FD)的效果。方法治疗组40例给予穴位埋线结合免煎中草药颗粒治疗;对照组40例给予奥美拉唑结合莫沙必利治疗,疗程均为8周。观察2组临床疗效及治疗前后胃电图变化。结果治疗后2组症状均较治疗前明显好转,治疗组治愈17例,显效13例,有效7例,无效3例,总有效率92%;对照组治愈7例,显效9例,有效12例,无效12例,总有效率70%,2组总有效率比较有显著性差异(P<0.05)。餐后正常慢波百分比治疗组治疗前为(42.87±21.32)%,治疗后为(54.46±19.38)%,治疗前后比较有显著性差异(P<0.05);对照组治疗前后无明显变化(P>0.05)。结论穴位埋线结合免煎中草药颗粒治疗FD患者有明显效果。     

冯建华教授临证用药经验

冯建华教授在30余年的临床工作中积累了丰富的用药经验。对单味中药的应用更是有其独特的心得体会,善从中医和西医两个角度来来指导用药,且临床效果显著。     

单眼发病的原发性开角型青光眼黄斑脉络膜厚度及影响因素初探

目的初步探讨原发性开角型青光眼(POAG)单眼发病患者黄斑中心凹下脉络膜厚度(SFCT)与其对侧眼和健康人的差异及其影响因素。方法横断面研究。收集2018年9月至2019年9月就诊于首都医科大学附属北京同仁医院青光眼门诊确诊为POAG的单眼发病、对侧眼正常的患者(POAG组)以及健康志愿者(健康对照组)。对所有参与者进行系统眼科检查,应用高分辨率频域的相干光层析成像术测量SFCT及距黄斑中心凹鼻侧和颞侧500、1000、2000μm共7个位置的脉络膜厚度。应用配对t检验比较脉络膜厚度在POAG组患眼与对侧眼的差异。应用协方差分析比较POAG组患眼与健康对照组之间脉络膜厚度的差异。应用多元线性回归分析年龄、性别、等效球镜度数、视野平均缺损值对POAG组患眼黄斑各个位置脉络膜厚度的影响。结果POAG组纳入75例患者(平均年龄46岁,男性48例,女性27例),健康对照组纳入61名(61只右眼)健康受试者(平均年龄44岁,男性34名,女性27名)。POAG组患眼SFCT为(244.41±83.18)μm,其对侧眼SFCT为(254.28±88.92)μm,二者差异无统计学意义(P>0.05)。健康对照组SFCT为(272.98±55.87)μm,校正年龄、性别和等效球镜度数后,POAG组患眼与健康对照组SFCT差异无统计学意义(P>0.05)。POAG组患眼在距离黄斑中心凹鼻侧2000μm处的脉络膜厚度为(167.84±70.44)μm,其对侧眼为(188.84±89.06)μm,二者差异有统计学意义(t=-3.55;P<0.01)。POAG组患眼与其对侧眼及健康对照组在距黄斑中心凹鼻侧和颞侧其他距离处的脉络膜厚度差异均无统计学意义(均P>0.05)。POAG患眼的SFCT变薄与视野平均缺损值下降(β=14.66,P<0.05)和近视屈光度数增高(β=14.95,P<0.01)有关,与年龄和性别无关(均P>0.05)。结论单眼发病的POAG患眼SFCT较对侧眼和健康人未见明显变薄,仅黄斑鼻侧2000μm的脉络膜薄于对侧眼。视野缺损的严重程度及近视屈光度数程度与SFCT变薄相关,提示脉络膜变薄可能参与青光眼的发生、发展过程。(中华眼科杂志,2021,57:194-200)