CT引导下胶原酶注射颈椎间盘溶解术的临床研究

目的:研究CT引导下胶原酶注射颈椎间盘溶解术治疗颈椎间盘突出症的价值。方法:对15例颈椎间盘突出症患者在CT引导下行胶原酶注射颈椎间盘溶解术。结果:15例均成功,随访1~16个月,优良率93.3%,未见并发症发生。结论:CT引导下行胶原酶注射颈椎间盘溶解术治疗颈椎间盘突出症安全有效,值得进一步研究。     

Dexamethasone treatment attenuates early seawater instillation-induced acute lung injury in rabbits.

There is very little evidence on the value of giving corticoids in cases of seawater drowning induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Therefore, this study aimed to investigate whether dexamethasone treatment can attenuate seawater instillation-induced acute lung injury in rabbits. Seawater (4 ml/kg body weight) was instilled into the lower trachea of ventilated, anesthetized rabbits. Then these rabbits were assigned randomly 20 min later to receive intravenous injection of 1mg/kg body weight of dexamethasone (dissolving in 2 ml of normal saline) or 2 ml of normal saline. All animals demonstrated immediate drops in arterial oxygen tension (PaO2) and the total thoracic compliance, which were significantly improved after 2 h of dexamethasone treatment. Histopathological study also indicated that dexamethasone treatment markedly attenuated lung histopathological changes, alveolar hemorrhage and inflammatory cells infiltration with evidence of decreasing of myeloperoxidase (MPO) activity and tumor necrosis factor-alpha (TNF-alpha) concentration in lung tissue. In addition, dexamethasone treatment reduced extravascular lung water and lung epithelial-endothelial barrier permeability, up-regulated the expression of surfactant protein-A (SP-A) and alpha-epithelial Na+ channel, and increased Na+/K+-adenosine triphosphatase (Na+/K+-ATPase) activity and Na+/K+-ATPase-alpha1 protein abundance. Thus, these data indicate that dexamethasone treatment might be of benefit in patients with seawater aspiration-induced ALI.     

Effect of Induction Therapy Protocols on Transplant Outcomes in Crossmatch Positive Renal Allograft Recipients Desensitized with IVIG

Here we retrospectively examine the efficacy of two antibody induction regimens using Zenapax or Thymoglobulin in patients with positive complement-dependent cytotoxicity crossmatches (CDC-CMXs) desensitized with IVIG (intravenous immunoglobulin). Between January 1999 and March 2005, 97 patients with (+) CDC-CMXs received kidney transplants (43 deceased donors/54 living donors). All patients received at least 2 g/kg IVIG (maximum four doses) until an acceptable CMX was obtained. Patients were divided into two groups: 1. IVIG + Zenapax (n = 58), 2. IVIG + Thymoglobulin (n = 39). A total of 94% of patients in Group 1 and 84% in G2 have at least 2 years of follow up. Patient and graft survival was 96%/84% in Group 1 and 100%/90% in Group 2, p = NS. The number and severity of AR episodes were similar (36% Group 1 vs. 31% Group 2, p = NS) as was the incidence of C4d (+) antibody-mediated rejection (AMR) (Banff Grade II/III) (22% Group 1 vs. 21% Group 2). Mean serum creatinines (SCrs) at 24 months were similar (Group 1: 1.4 +/- 0.7 vs. G2: 1.5 +/- 0.7 mg/dL). Induction therapy with Zenapax or Thymoglobulin results in excellent patient, graft survival and graft function at 2 years. There was no increased risk of viral infections or malignancies with either agent. Neither agent was effective in reducing the incidence of AMR.     

急性出血坏死性胰腺炎肝损伤中TLR2/4mRNA的表达及氯喹的干预效应

目的： 研究急性出血坏死性胰腺炎（AHNP）肝损伤中Toll-样受体(TLR)2/4mRNA表达的变化及氯喹的干预效应。 方法：采用逆行胰胆管牛磺胆酸钠（TAC）注射造成大鼠AHNP肝损伤动物模型。动物分为假手术组（S组）、胰腺炎组和氯喹（CQ）治疗组。后2组于术后3，6，12 h分批剖杀，S组于术后6 h剖杀。观察血清淀粉酶、ALT和AST及肝组织NO和TNF-α的变化，RT-PCR方法检测各组不同时点肝组织TLR2和TLR4mRNA的表达。 结果：相对于S组，胰腺炎组大鼠3 h肝组织TLR2和TLR4mRNA表达开始增高，术后6～12 h肝组织TLR2和TLR4mRNA表达迅速达到峰值（P<0.05），肝损伤加重，血清淀粉酶升高，肝组织TNF-α浓度升高，NO浓度逐渐降低（P<0.05）；相对胰腺炎组，CQ治疗组TLR2/4mRNA表达降低（P<0.05），肝损伤程度减轻，血清淀粉酶降低，肝组织TNF-α浓度降低，NO浓度显著升高（P<0.05）。 结论：AHNP大鼠肝组织内TLR2和TLR4的基因表达上调；其表达增高可能在AHNP肝损伤的发生、发展中起重要作用。氯喹对大鼠AHNP过程中肝损伤可能有保护作用。     

Implant wear induces inflammation, but not osteoclastic bone resorption, in RANK(-/-) mice.

Signaling of RANK (receptor activator of nuclear factor kappa B) through its ligand RANKL appears critical in osteolysis associated with aseptic loosening (AL). The purpose of this study was to investigate the role of RANK in a murine osteolysis model developed in RANK knockout (RANK(-/-)) mice. Ultra high molecular weight polyethylene (UHMWPE) debris was introduced into established air pouches on RANK(-/-) mice, followed by implantation of calvaria bone from syngeneic littermates. Wild type C57BL/6 (RANK(+/+)) mice injected with either UHMWPE or saline alone were included in this study. Pouch tissues were collected 14 days after UHMWPE inoculation for molecular and histology analysis. Results showed that UHMWPE stimulation induced strong pouch tissue inflammation in RANK(-/-) mice, as manifested by inflammatory cellular infiltration, pouch tissue proliferation, and increased gene expression of IL-1beta, TNFalpha, and RANKL. However, the UHMWPE-induced inflammation in RANK(-/-) mice was not associated with the osteoclastic bone resorption observed in RANK(+/+) mice. In RANK(+/+) mice subjected to UHMWPE stimulation, a large number of TRAP(+) cells were found on the implanted bone surface, where active osteoclastic bone resorption was observed. No TRAP(+) cells were found in UHMWPE-containing pouch tissues of RANK(-/-) mice. Consistent with the lack of osteoclastic activity shown by TRAP staining, no significant UHMWPE particle-induced bone resorption was found in RANK(-/-) mice. A well preserved bone collagen content (Van Gieson staining) and normal plateau surface contour [microcomputed tomography (microCT)] of implanted bone was observed in RANK(-/-) mice subjected to UHMWPE stimulation. In conclusion, this study provides the evidence that UHMWPE particles induce strong inflammatory responses, but not associated with osteoclastic bone resorption in RANK(-/-) mice. This indicates that RANK signaling is essential for UHMWPE particle-induced osteoclastic bone resorption, but does not participate in UHMWPE particle-induced inflammatory response.     

LKB1表达下调对培养海马神经元突触mEPSC的影响

目的研究离体培养的海马神经元LKB1表达下调对于神经元微小兴奋性突触后电流(mEP-SC)的影响。方法选用17d的胚胎大鼠培养海马神经元,分别用电穿孔的方法转染CAG-RE质粒和LKB1RNAi质粒,培养10~12d后进行电生理记录,选用全细胞膜片钳方式及自由记录模式,细胞外液加TTX阻断动作电位,加Bicucullin抑制GABA电流,记录神经元的mEPSC,比较2组神经元的mEPSC频率和幅度的差别。结果转染CAG-RE的神经元mEPSC幅度平均为25.6pA,频率平均为(5.21±0.25)Hz,是基线的99.8%;转染LKB1RNAi的神经元mEPSC幅度平均为35.1pA,频率平均为(5.79±0.27)Hz,是基线的127.1%;比较2组间频率、幅度变化,差别有显著性意义(P<0.05)。结论LKB1基因表达下调增强了培养海马神经元突触传递的效率。     

颅底中线区大型和巨大型脑膜瘤的显微手术切除

目的探讨颅底中线区不同部位大型和巨大型脑膜瘤手术入路和切除方式,并分析特殊类型脑膜瘤手术治疗方法。方法本组93例,男性26例,女性67例;平均年龄48.4岁。术前行神经影像学检查,根据肿瘤部位,选择相应手术入路,采用显微手术切除肿瘤。结果肿瘤全切除80例(86.02%),大部分切除13例(13.98%),死亡1例(10.75%)。除单条颅神经功能术前完全丧失外,术后神经功能改善者75例(81.52%),不变者10例(10.86%),加重者7例(7.6%)。经6月￣7年随访,13例(14.13%)肿瘤复发。结论颅底中线区大型和巨大型脑膜瘤手术切除难度大。要取得良好的手术效果,必须选择正确手术入路,采用分块切除方式,精心保护重要血管和神经。     

Fas/FasL在各阶段婴幼儿血管瘤中的表达及意义

目的 检测Fas／FasL在各阶段婴幼儿血管瘤组织中的表达，探讨Fas／FasL在婴幼儿血管瘤细胞凋亡中的作用。方法 应用EnVision法免疫组化染色和RT-PCR检测Fas／FasL蛋白及mRNA在各阶段血管瘤组织中的表达。结果 ①增生早期和增生中期，部分血管瘤细胞表达Fas；增生晚期，阳性细胞明显增多，Fas mRNA表达最强；消退早期，仍有少量微血管内皮细胞表达Fas，之后Fas表达迅速减弱。②最早期细胞团中没有FasL（＋）细胞；增生中期，血管瘤组织中出现少量FasL（＋）细胞；增生晚期FasL（＋）细胞显著增多，FasL mRNA表达最强；消退早期之后，FasL（＋）细胞迅速减少以至消失。结论 Fas／FasL与婴幼儿血管瘤演变过程有密切联系，Fas／FasL介导的血管瘤细胞凋亡可能是婴幼儿血管瘤自行消退的重要原因。     

人精子体外氧化损伤对线粒体tRNA~(LeuUUR)基因的影响

目的:探讨活性氧(ROS)对人类精子线粒体tRNALeuUUR基因的氧化损伤。方法:采用Percoll梯度离心法筛选具有正常生理功能的精子,作为正常精子模型,并分为损伤组20例和对照组20例,分别加入次黄嘌呤-黄嘌呤氧化酶体系或不予处理,37℃有氧环境中孵育60min。分别提取精子DNA,以Fpg酶切损伤碱基并采用接头介导PCR(LM-PCR)检测线粒体tRNALeuUUR基因的氧化损伤。采用Rhodamine(Rh123)荧光探针标记精子,通过流式细胞仪检测线粒体膜电位,观察精子的功能。结果:与对照组相比,损伤组精子孵育后线粒体膜电位明显降低[(116.27±11.72)%vs(64.00±4.88)%,P<0.05]。Fpg酶切和LM-PCR显示精子线粒体tRNALeuUUR基因损伤。结论:ROS可能通过对精子线粒体tRNALeuUUR基因氧化损伤而影响精子功能(线粒体膜电位明显降低),从而引起不育。     

中医健脾祛瘀法治疗胃癌40例

目的探讨健脾、祛瘀、通络散结类中药配伍对胃癌的治疗效果。方法采用枳朴六君汤加味(枳壳、厚朴、白术、茯苓、陈皮、半夏、党参、乌蛇、蜈蚣、土鳖、甘草等)内服,配合中成药平消片,治疗胃癌40例。结果中医证候有效率为82.50%;生存质量提高13例,稳定23例,降低4例;体重增加12例,稳定24例,下降4例。提示本方法有健脾祛瘀、通络散结,改善临床症状,提高生存质量的功效。