Palomo手术治疗儿童精索静脉曲张

目的:对经腹膜后集束结扎精索血管(Palomo手术)治疗儿童精索静脉曲张的可行性及疗效进行评价。方法:对采用Palomo术式治疗的36例精索静脉曲张患儿,于手术前、术后6个月、术后12个月采用彩色Doppler检查睾丸,测量患儿双侧睾丸体积。结果:全部治愈,术后随访12～36个月,所有患儿临床症状消失,所有患儿均未发生睾丸萎缩。术后患侧睾丸血供无明显减少,患侧睾丸体积术后增长明显快于对侧。结论:Palomo手术是一种治疗儿童精索静脉曲张简单易行、疗效可靠的手术方式。     

睾丸肿瘤细胞凋亡相关基因及研究现状

睾丸肿瘤细胞的凋亡是一个多基因参与的复杂过程 ,受HTERT、P53、Bc1_2、MDM_2和C_myc等多种肿瘤相关基因的调控。目前研究发现端酶粒活性与细胞凋亡存在密切关系 ,药物诱导凋亡时端粒酶活性下降 ;大部分的研究也发现P53基因是一种肿瘤抑制基因(TSG) ,对睾丸肿瘤的生长有负性调节作用 ,与细胞凋亡密切相关 ;而在多步骤致癌作用的过程中Bc1_2基因异常表达可能赋予细胞抵抗凋亡信号的能力 ;MDM_2蛋白表达与睾丸肿瘤局部浸润、淋巴结转移及远端转移呈正相关 ;C_myc基因编码的P62蛋白过量表达可能参与正常细胞向恶性肿瘤细胞的转化过程 ,降低其水平可诱导细胞发生凋亡 ;另外 ,Ras、Fas/Fas_L睾丸肿瘤凋亡过程中亦发挥重要作用。     

巨大血管瘤伴血小板综合征的临床护理体会

目的:总结对巨大血管瘤伴血小板减少综合征(KMS)患儿的护理经验。方法:收集9年来我院收住的8例KMS患儿的完整资料,分析8例患儿的临床表现、治疗经过以及护理特点。结果:4例瘤体基本消退,痊愈出院,2例好转,瘤体缩小,1例死亡,1例病情控制不佳,家属放弃治疗。结论:本病如能早期选择正确的治疗,多数病例预后较好,加强全身出血倾向的观察及基础护理是本病的护理重点。     

儿童肾上腺皮质肿瘤8例临床分析

目的:总结小儿肾上腺皮质肿瘤的临床特点,探讨诊断、鉴别诊断方法和治疗经验。方法:分析1989年10月至2004年10月年我院诊治的8例小儿肾上腺皮质肿瘤患儿的临床资料,回顾总结其临床特点及诊断治疗情况。结果:患儿8例,男3例,女5例,年龄10个月～13岁,平均5.9岁。左侧6例,右侧2例。肾上腺皮质腺瘤7例,肾上腺皮质腺癌1例。本组1例因乳房发育、月经来潮就诊,其余7例均因库欣氏症就诊,其中2例女孩伴阴蒂肥大、面部痤疮。低钾血症2例,高血压3例。围手术期6例应用了皮质激素,2例未使用,均在气管插管全麻下手术,2例采用上腹部横切口,6例采用十二肋缘下切口,本组8例患儿均行手术治疗而痊愈。结论:(1)小儿肾上腺皮质肿瘤以皮质醇症多见。(2)对于性早熟患儿要考虑到本病可能。(3)围手术期应用皮质激素可有效防止肾上腺危象的发生。(4)检测皮质醇、17-OH、17-KS类固醇、肾素、醛固酮,对诊断、鉴别诊断及判断预后有价值。     

小儿睾丸卵黄囊瘤细胞的体外培养及生物学特性研究

目的 采用组织培养技术在体外培养取自人体的睾丸卵黄囊瘤组织,探讨小儿睾丸卵黄囊瘤组织的体外培养方法及生物学特性.方法 采用组织块培养法培养1例睾丸卵黄囊瘤患儿手术的标本,从形态学、细胞生长动力学、肿瘤内分泌、染色体分析、细胞DNA分析等方面初步研究了小儿睾丸卵黄囊瘤细胞的生物学特性.结果 小儿睾丸卵黄囊瘤细胞无论形态学观察,还是功能学测定,均符合卵黄囊瘤细胞的特征,染色体众数39～97条,并具有体外分泌AFP功能.其特有表现为:细胞贴壁生长,呈短梭形或多角形,细胞密集时可多层重叠生长,肿瘤细胞表面有明显的微绒毛,细胞核形态怪异,细胞倍增时间较长.结论 小儿睾丸卵黄囊瘤细胞在体外生长稳定,增殖活跃,肿瘤细胞的纯度较高,可以用于后续的实验研究.

Abstract：

Objective To establish a method for the culture of testicular yolk sac tumor in childhood and then investigate biological characteristics in vitro. Methods One specimen from testicular yolk sac tumor was cultured in vitro. Testicular yolk sac tumor cell lines were studied morphologically and subjected to karyotype analysis, DNA analysis, and tumor formation evaluation. Results Morphological observation and functional analysis show that cell lines have characteristics of testicular yolk sac tumor. The number of chromosomes varied from 39 to 97. Turours were immunostained positively for AFP in vitro and found to form multiple layers with microvilli. The nuclei were variable and bizarre in size and shape. Conclusions Testicular yolk sac tumor cell lines were cultured proliferated in a stable manner in vitro, which provides a convenient and economical object for basic researches on yolk sac tumor in future.     

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.     

婴幼儿胆道穿孔诊治体会

目的 探讨婴幼儿胆道穿孔的病因、诊断和手术方式. 方法 对我院1990~2005年间收治的10例婴幼儿胆道穿孔病例诊治情况进行回顾性分析. 结果 7例术前确诊,病因是先天性胆总管囊肿,行一期根治或引流术后二期根治术,另3例分别是胆石症、胆蛔症、医源性损伤,均治愈. 结论 婴幼儿胆道穿孔发病率低,病因主要是先天性胆总管囊肿.腹穿和腹水淀粉酶测定、B超检查有助于提高早期确诊率.初次手术提倡便捷有效的外引流术,术后需长期随访.先天性胆总管囊肿应行囊肿切除+肝总管空肠Roux-Y吻合术.     

红花对兔肠缺血再灌注损伤后肠壁ICAM-1表达的影响

目的：观察红花注射液对兔肠缺血再灌注损伤后肠组织细胞间黏附因子1表达影响。方法：制备兔肠缺血再灌注损伤模型。30只日本大耳兔,随机均分为三组：假手术组（S组）,缺血再灌注组（IR组）和缺血再灌注＋红花注射液组（SI组）。肠组织常规病理染色观察,并采用免疫组织化学法检测各组肠组织标本细胞间黏附因子1表达的改变。结果：细胞间黏附因子1蛋白在各组肠组织血管内皮细胞中均有表达,尤其在黏膜下层中表达显著。S组兔肠表达较弱,IR组肠血管上皮细胞上细胞间黏附因子1蛋白表达增强,与S组比较,差异有显著性（P〈0．01）。SI组与IR组比较明显下降（P〈0．01）。光镜观察比较SI组与IR组可见,多数肠黏膜上皮细胞变性、坏死程度明显减轻。结论：红花在兔肠缺血再灌注损伤中能有效减少炎性渗出、抑制微循环通透性的增加,阻断肠缺血再灌注损伤的病理生理过程。     

小儿肾盂输尿管连接部梗阻术中肾盂穿刺液细菌谱及药敏分析

目的通过了解小儿肾盂输尿管连接部梗阻术中肾盂穿刺液细菌谱和药物敏感特点,以指导围手术期抗菌药物选择。方法回顾性分析医院1995年1月-2010年12月收治的小儿肾盂输尿管连接部梗阻手术患儿262例,术中打开肾盂前常规用无菌注射器穿刺肾盂抽取尿液标本,进行细菌培养及药物敏感试验。结果 31例肾盂穿刺尿液培养阳性,阳性率为11.8%;病原菌中以革兰阴性杆菌为主,位于前3位的革兰阴性杆菌分别为大肠埃希菌、克雷伯菌属和奇异变形菌,分别占33.3%、19.4%、11.1%;大肠埃希菌、克雷伯菌属和奇异变形菌对氨苄西林、哌拉西林和第一、二代头孢菌素均有较高的耐药率,但对亚胺培南、呋喃妥因和阿米卡星高度敏感,对第三代头孢敏感率也较好;肠球菌属对青霉素、庆大霉素、环丙沙星高度耐药,对呋喃妥因和万古霉素高度敏感,对第三代头孢敏感率也较好。结论小儿肾盂输尿管连接部梗阻细菌感染率不高,但对临床常用抗菌药物有较明显的耐药性,术中肾盂穿刺液细菌培养及药物敏感试验对围手术期抗菌药物的选择具有指导作用。     

儿童支原体肺炎血清NO及肺功能变化

肺炎支原体肺炎(Mycop lasma Pneumoniae Pneumonia, MPP) 在小儿呼吸系统疾病中的致病地位已受到临床医生的广泛重视, 其可引起多系统器官的疾病, 作者发现于MP感染发病高峰时,支气管哮喘发病率亦明显增高.为此自2001年6月至2004年6月检测了支原体感染患儿外周血一氧化氮浓度(NO)及肺功能改变, 旨在探讨它们之间的关系及明确肺炎支原体肺炎气道损害和肺功能的改变.