低场MRI对早期股骨头缺血坏死的诊断分析

目的:探讨早期股骨头缺血坏死(ANFH)的低场MRI表现及诊断价值.方法:回顾分析41例早期股骨头缺血坏死病人的X线和MRI表现.结果:41例中,双侧病变29例,单侧病变12例.依据Ficat分期:Ⅰ期51髋,Ⅱ期19髋,X线片检查均为阴性.结论:低场强MRI对早期ANFH的诊断明显优于普通X线片,对早期ANFH的诊断具有重要价值.     

《护理专业设置标准》的研究与探索

《护理专业设置标准》的研究过程分为学习提高、转变观念和实施完善3个阶段。《护理专业设置标准》突出了“以能力为本位。以就业为导向”的新型职业教育理念,细化了有关专业设置标准的具体要求,将原来的基本能力、专业能力、岗位能力升华为方法能力、社会能力、专业能力。其研究指导以护理岗位需要为依据,梳理出专业职业能力体系,明确了培养目标,为职业教育专业建设指明了方向;该研究促进了护理专业建设,起到了引领作用,促使学校办学水平整体提高;推动了学校教育教学改革的深入和专业教学水平的全面提高。     

拉西地平对高血压患者血压晨峰的影响

资料与方法研究对象选择我院2007年7月~2009年10月原发性高血压住院患者,高血压的诊断采用《中国高血压防治指南》2005年修订版的诊断标准。除外心力衰竭,心律失常,肝功能异常,睡眠障碍,服药期间出现头痛、眩晕等不良反应未能继续服药者,共入选129例,其中男73例,女56例,年龄50～75岁。     

150例尿毒症患者腹膜透析临床分析

腹膜透析(简称腹透)已是治疗尿毒症的一种比较成熟的替代方式,与血液透析比较,具有可居家治疗、操作简单、心血管稳定性好、较少血源感染、残余肾功能丢失较慢、相对费用省等优点,但存在腹膜感染的可能性,且腹透患者的管理亦是一个新的课题。当前慢性肾脏病(CKD)发病率越来     

理论实践一体化教学在医学基础课程中的探索与思考

理论实践一体化教学是对传统教学模式的改革,在理论教学过程中加入技能训练,旨在提高学生的动手能力和综合素质,适用于医学基础课程的教学.理论实践一体化教学不仅有助于改善单调的教学方法,改善教学环境,更能培养学生的学习兴趣,提高课堂教学效率和教学质量.同时,对教师的业务能力提升也会起到积极的促进作用.     

指骨骨折伴指动脉损伤9例治疗体会

单纯的外力作用造成指骨骨折较为常见,诊断治疗并不困难.近年来,随着工业机械的发展,致伤原因的多样化、复杂化,指骨骨折伴动脉损伤的病例屡见不鲜.我科2011年诊治该类患者9 例,经及时处理效果良好,现将治疗体会总结如下: 1 临床资料 1.1 一般资料本组9 例,男6 例,女3 例,年龄18～40岁.致伤原因:钻床卷伤4 例,皮带卷伤4 例,车祸伤1 例,均为近中节指骨骨折.5 例开放性骨折,4 例闭合性骨折.7例粉碎性骨折,2 例横断性骨折.动脉损伤为双侧挫伤或断裂,有不同程度的神经损伤,受伤至手术时间在2h 以内.     

多排泵连续静脉泵入多巴胺、硝酸甘油、呋塞米治疗顽固性心衰疗效观察

目的观察多排泵连续静脉泵入多巴胺、硝酸甘油、呋塞米治疗顽固性心力衰竭的疗效及安全性。方法将68例常规治疗后心功能Ⅳ级(NYHA分级)患者,予以多巴胺、硝酸甘油、呋塞米静脉泵入治疗,保持每日尿量≥1500ml。治疗前后分别评价体重、血压、心率、心功能及血清生化指标(电解质、肌酐、NT-proBNP)。结果持续泵入多巴胺、硝酸甘油、呋塞米治疗可显著改善患者症状,使左室射血分数、心率、体重和血压以及NT-proBNP明显降低(P<0.05)。结论多排泵连续静脉泵入多巴胺、硝酸甘油、呋塞米静脉泵入治疗可以显著改善顽固性心衰患者症状,并且安全可靠。     

替米沙坦对胰岛素抵抗大鼠肾脏脂联素表达的影响

目的 探讨替米沙坦对胰岛素抵抗大鼠肾脏脂联素(APN)表达的影响.方法 采用高脂饲料喂养10周建立胰岛素抵抗大鼠模型,并用正常血糖一高血浆胰岛素钳夹技术评估.光镜及电镜行肾脏形态学检查,逆转录聚合酶链反应方法测定APNmRNA表达,免疫组化染色观察APN蛋白水平变化.结果 胰岛素抵抗大鼠肾脏APN mRNA和蛋白表达明显低于正常对照组(P均<0.05),同时大鼠肾脏出现病理变化;替米沙坦干预后,肾组织APN mRNA和蛋白表达较胰岛素抵抗组升高(P均<0.05),同时肾脏病理变化也得到明显改善.结论 替米沙坦可能通过调节肾脏APN的表达,起到保护胰岛素抵抗相关的肾脏损伤的作用.     

卡络磺钠联合雷贝拉唑治疗溃疡性上消化道出血的临床研究

目的 探讨卡络磺钠联合雷贝拉唑治疗溃疡性上消化道出血的临床疗效。方法 选取2018年1月—2021年12月在梧州市工人医院住院治疗的74例溃疡性上消化道出血患者,按照随机数字法将所有患者分为对照组和治疗组,每组各37例。对照组早晨口服雷贝拉唑钠肠溶胶囊,20 mg/次,1次/d。治疗组在对照组的基础上静滴滴注注射用卡络磺钠,60 mg加入0.9%氯化钠注射液250 mL中稀释,1次/d。两组均连续用药7 d。观察两组的临床疗效,比较两组腹胀、腹痛、头晕、烧心症状缓解时间及治疗前后血清丙二醇（MDA）、抗利尿激素（ADH）、皮质醇（COR）、白细胞介素6（IL-6）、白细胞介素17（IL-17）、肿瘤坏死因子α（TNF-α）、C反应蛋白（CRP）水平的变化情况和不良反应。结果 治疗后,治疗组总有效率是97.29%,显著高于对照组的81.08%（P＜0.05）。经治疗,治疗组腹胀、腹痛、头晕、烧心症状缓解时间均显著短于对照组（P＜0.05）。治疗后,两组MDA、ADH、COR水平均较治疗前显著降低（P＜0.05）,且治疗后治疗组MDA、ADH、COR水平低于对照组（P＜0.05）。治疗后,两组血清IL-6、IL-17、TNF-α、CRP水平均较治疗前显著降低（P＜0.05）,且治疗后,治疗组血清学指标水平低于对照组（P＜0.05）。治疗组患者不良反应发生率是8.11%,显著低于对照组患者的18.92%（P＜0.05）。结论 卡络磺钠联合雷贝拉唑治疗溃疡性上消化道出血可有效提高治疗效果,并能极大地缓解患者临床症状,改善机体氧化应激反应,降低炎性因子水平,具有一定的临床推广应用价值。     

舒尼替尼及联合顺铂对小儿睾丸卵黄囊瘤荷瘤鼠模型的抗肿瘤作用

目的 探讨舒尼替尼(Sunitinib)、顺铂(CDDP)及两者联合用药对小儿睾丸卵黄囊瘤(TYST)异种移植荷瘤鼠模型的抗肿瘤作用及相关作用机制.方法 肿瘤标本来自本实验室的小儿睾丸卵黄囊瘤裸鼠第17代模型,并接种在雄性裸鼠单侧腹股沟皮下区,成瘤后随机分成4组(n=5):对照组、CDDP组、Sunitinib组和Sunitinib+CDDP组.绘制肿瘤体积和裸鼠体重变化曲线图,计算肿瘤消退率;HE染色观察肿瘤组织形态学变化;免疫组织化学法检测AFP、Ki-67、Glypican-3、CD105在各组肿瘤中的表达:CD105测定微血管密度(MVD),Ki-6表示细胞增殖率(PI);TUNEL法检测肿瘤细胞凋亡率(AI);实时荧光定量PCR(RT-qPCR)验证靶向因子的mRNA表达变化.结果 各治疗组均能显著抑制肿瘤生长,并能消退肿瘤体积.在治疗后肿瘤体积上,除顺铂组与舒尼替尼组间无统计学差异外(41.61±7.61比67.15±5.39,P＞0.05),其余各组间都有统计学差异:对照组与顺铂(651.72±121.16比41.61±7.61,P＜0.05),对照组与舒尼替尼组(651.72±121.16比67.15±5.39,P＜0.05),对照组联合舒尼替尼±顺铂组(651.72±121.16比23.03±2.37,P＜0.05),舒尼替尼组与联合舒尼替尼+顺铂组(67.15±5.39比23.03±2.37,P＜0.05),顺铂组与联合舒尼替尼+顺铂组(41.61±7.61比23.03±2.37,P＜0.05);在裸鼠体重上,相比对照组,除舒尼替尼组无统计学差异外(25.90±0.75比26.66±0.65,P＞0.05),其余各组间差异均有统计学意义:对照组与顺铂组(25.90±0.75比18.90±0.63,P＜0.05),对照组与联合舒尼替尼+顺铂组(25.90±0.75比18.26±1.20,P＜0.05);AFP、Glypican-3在各治疗组阳性表达面积(Pixels)均少于对照组(AFP:对照组与顺铂组,1.26×106土1.48×105比5.54×105±8.14×104,P＜0.05;对照组与舒尼替尼组,1.26×106±1.48×105比7.09×105±6.64×104,P＜0.05;对照组与联合舒尼替尼+顺铂组,1.26×106±1.48×105比3.62×105±4.83×104,P＜0.05.Glypican-3:对照组与顺铂组,9.68×105±7.63×104比4.04×105±5.04×104,P＜0.05;对照组与舒尼替尼组,9.68×105±7.63×104比4.59×105±2.32×104,P＜0.05;对照组与联合舒尼替尼+顺铂组,9.68×105±7.63×104比1.89×105±2.55×104,P＜0.05).两者在顺铂组与舒尼替尼组的比较中差异无统计学意义(P＞0.05);PI和AI在各治疗组中相比对照组,差异都具有统计学意义(PI和AI:对照组与顺铂组,58.97土1.38比42.36±1.28和1.69±0.20比54.62±2.49,P＜0.01;对照组与舒尼替尼组,58.97±1.38比43.48±1.00和1.69±0.20比47.32±2.00,P＜0.01;对照组与联合舒尼替尼+顺铂组,58.97±1.38比33.34±1.19和1.69±0.20比63.41土2.23,P＜0.01).顺铂组相比联合舒尼替尼+顺铂组,PI:P=0.001,AI:P=0.002;舒尼替尼组相比联合舒尼替尼+顺铂组,PI和AI:P＜0.001;顺铂组相比舒尼替尼组,PI.P=0.597,AI:P=0.059;RT-qPCR证实M-CSFR、PDGFR-β、RET、VEGFR-2的mRNA表达受到抑制.结论 Sunitinib能显著抑制小儿睾丸卵黄囊瘤的生长,并消退肿瘤体积:主要通过直接抑制肿瘤细胞的生长和肿瘤血管的新生,从而诱导肿瘤细胞凋亡,同时伴有直接细胞毒作用引起坏死;Sunitinib相比CDDP具有更轻的毒副作用,且联合CDDP具有增强抗肿瘤作用.

Abstract：

Objective To study the antitumor effects of Sunitinib or Sunitinib combind with cis - diamminedichloroplatinum (CDDP) on an athymic mouse human testicular yolk sac tumor xenograft model. Methods The athymic mouse human testicular yolk sac tumor xenograft model was established by subcutaneous injection of 17th passage pediatric testicular yolk sac tumor cells in the unilateral inguinal region of the male nude mice. The mice of control group didn't receive any treatment. The tumor bearing mice were treated with either CDDP, or Sunitinib group, or Sunitinib combined with CDDP. The tumor-bearing nude mice were divided into 4 groups (5 in each) according the treatment they underwent. The tumor volumes and mice weight were measured to calculate the regression rate of tumor. The tumor was collected for H&E staining and immunohistochemical staining of AFP, Ki-67,Glypican-3 and CD105. Microvessel density (MVD) was measured by analyzing the CD105 expression. The tumors' proliferation index (PI) was studied by analyzing Ki-67 expression. The apoptosis of the tumor was quantitated using TUNEL staining. The mRNA expressions of cytokines were determined by quantitative real-time PCR (RT-qPCR). Results The tumor volumes were significantly decreased after chemotherapy. No difference of tumor volume was found between CDDP group and Sunitinib group (41.61 ± 7. 61 vs. 67. 15 ± 5. 39, P＞0. 05). Significant differences of tumor volumes were found between CDDP group and CDDP+ Sunitinib group (41.61 ± 7. 61 vs. 23. 03 ± 2. 37, P＜0. 05), and between Sunitinib group and CDDP+ Sunitinib group (67. 15 ± 5. 39 vs. 23.03 ± 2. 37, P＜0. 05). Of the body weight of tumor-bearing mice, no difference was found between controls and Sunitinib group (25. 90 ± 0. 75 vs. 26. 66 ± 0. 65, P＞0. 05). And significant differences of the body weight were noted between controls and CDDP group (25.90 ± 0. 75 vs. 18. 90 ± 0. 63, P＜0. 05),controls and CDDP+ Sunitinib group (25. 90 ± 0. 75 vs. 18. 26 ± 1.20,P＜0. 05). The positive areas (pixels) of AFP in the mice with chemotherapy were less than those of control mice (Control vs. CDDP: 1.26 × 106±1.48 × 105 vs. 5. 54 × 105 ± 8. 14 × 104 , P＜0. 05. Control vs. Sunitinib: 1.26 × 106 ± 1.48 × 105 vs. 7. 09 × 105 ± 6. 64 × 104, P＜0. 05. Control vs. CDDP + Sunitinib: 1.26 × 106 ± 1.48 × 105 vs. 3. 62 × 105 ± 4. 83 × 104, P＜0. 05). The positive areas (pixels) of Glypican-3 in the mice with chemotherapy were less than those of control mice (Control vs. CDDP: 9. 68 × 105 ± 7. 63 × 104 vs. 4. 04 × 105 ± 5. 04 × 104 , P＜0. 05. Control vs. Sunitinib: 9. 68 × 105 ± 7. 63 × 104 vs. 4. 59 × 105 ± 2. 32 × 104 , P＜0. 05. Control vs. CDDP + Sunitinib: 9. 68 × 105 ± 7. 63 × 104 vs. 1.89 × 105 ± 2. 55 × 104, P＜0. 05). However, there were no statistical differences of the positive areas (pixels) of AFP and Glypican-3 between CDDP and Sunitinib groups (P＞0. 05). The PI was significantly decreased after chemotherapy (Control vs. CDDP: 58. 97 ± 1.38 vs. 42. 36 ± 1.28, P＜ 0. 01. Control vs.Sunitinib: 58. 97 ± 1.38 vs. 43. 48 ± 1.00, P＜0. 01. Control vs. CDDP+ Sunitinib: 58. 97 ± 1.38 vs.33. 34 ± 1.19, P＜0. 01 ). The apoptosis index (AI) was also significantly increased after chemotherapy (Control vs. CDDP: 1.69 ± 0. 20 vs. 54. 62 ± 2. 49, P＜0. 01. Control vs. Sunitinib: 1.69 ± 0. 20vs. 47. 32 ± 2. 00, P＜0. 01. Control vs. CDDP + Sunitinib: 1.69 ± 0. 20 vs. 63. 41 ± 2. 23, P＜0. 01). Significantly differences of PI and AI were found between CDDP and CDDP + Sunitinib groups (P＜0. 01 ), and Sunitinib and CDDP + Sunitinib (P＜0. 01 ). RT-qPCR study confirmed that the mRNA expressions of M-CSFR, PDGFR-β, RET and VEGFR-2 were decreased in the mice underwent chemotherapy. Conclusions Sunitinib is effective to suppress the pediatric testicular yolk sac tumor growth, and reduce the tumor volume. Sunitinib can inhibit the angiogenesis in tumor, induce apoptosis of tumor cells, and kill the tumor cells directly. Sunitinib is less toxic than CDDP, and synergistic with the antitumor effect of CDDP.