大鼠心肌缺血再灌注时心肌细胞凋亡caspase-3活性变化规律及药物对其影响

目的　探讨大鼠心肌缺血再灌注 (Ischemiareperfusion ,IR)不同时相的心肌细胞凋亡、caspase 3活性变化规律及caspase 3抑制剂Ac DEVD CHO的影响。方法　Wistar大鼠 12 2只 ,设立IR组 ,IR +Ac DEVD CHO组和假手术对照组并分设缺血 3 0min后再灌注 1、3、6、12、2 4h 5个时相点 ;以缺口末端标记法 (TUNEL)标记凋亡细胞 ,用荧光分析法检测caspase 3活性 ,行TTC染色测定心肌梗死范围。结果　心肌细胞凋亡与caspase 3活性随心肌再灌注不同时相而变化 ,心肌细胞凋亡指数 (Apoptosisindex ,AI)与caspase 3活性于再灌注 12h最高 [AI :( 3 4 83± 9 3 5 ) % ;caspase 3活性 :( 1 3 4±0 2 ) ] ,其后基本维持在平台状态 ;心肌梗死范围随IR时间逐渐增加 ,至 2 4h仍未见下降趋势 ,三者间呈显著正相关 (P <0 0 5 )。IR +Ac DEVD CHO组上述指标虽也明显增高 ,但比IR组明显减小 (P <0 0 5 )。结论　Caspase 3激活及心肌细胞凋亡参与了心肌缺血再灌注损伤过程 ,Ac DEVD CHO减轻心肌缺血再灌注损伤可能部分与其抑制心肌细胞凋亡有关。     

超声心动图测定未闭动脉导管内径及临床意义

目的　探讨超声心动图测定未闭动脉导管内径的可靠性及其在导管法封堵动脉导管未闭症 (PDA)中的临床意义。　方法　 4 4例 PDA患者 ,男 18例 ,女 2 6例 ,平均 10 .8± 10 .5岁。应用二维超声心动图 (2 DE)及彩色多普勒血流显像 (CDFI)测定 PDA近端及最小内径 ,并与 X线造影测值及最终所选择的封堵器直径比较。　结果　 2 DE及 CDFI显示 PDA解剖全程及测量 PDA内径的成功率分别为 5 7%和 10 0 % ;2 DE对 PDA直径测量的均值显著低于 X线测值及封堵器实际尺寸 ,其回归方程斜率更偏离 1,截距较大 ,估计标准误高 ;CDFI对 PDA直径测量的平均值与 X线测值差异无显著性 ,但平均小于封堵器尺寸 2 .9mm,其回归方程斜率更接近 1,截距小及估计标准误小。　结论　与 2 DE相比 ,CDFI能更准确地测量 PDA直径 ;在导管封堵术中选择封堵器时 ,CDFI的 PDA直径测值可与 X线测量互相补充甚至可替代 X线造影 ,避免穿刺股动脉的技术困难及大量注射造影剂的副作用     

视盘血管主干位置在青光眼视神经损害诊断中的作用

目的观察视盘血管主干位置对上、下方盘沿宽度的影响，探讨视盘血管主干位置在青光眼视神经损害诊断中的作用。方法评价眼底照片清晰、视盘血管主干位置明确的视盘459例，其中大视盘131例，中视盘145例，横椭圆形视盘75例，小视盘108例。应用两组独立样本t检验，比较各类视盘的血管偏上组、血管偏下组的上、下方盘沿宽度的差异；比较上方盘沿窄组和下方盘沿窄组的血管位置的差异。结果总体及大视盘、小视盘的血管偏上组的盘沿比（0.467±0.051，0.445±0.040，0.508±0.056）较血管偏下组的盘沿比（0.500±0.066，0.474±0.062，0.546±0.048）小，差异有统计学意义（P=0.000，P=0.045，P=0.018，P值均<0.05）；总体及大视盘、小视盘的上方盘沿窄组的血管比（0.510±0.051，0.508±0.055，0.512±0.036）较下方盘沿窄组的血管比（0.528±0.045，0.533±0.048，0.534±0.045）小，差异有统计学意义（P=0.000，P=0.046，P=0.022，P值均<0.05）。结论视盘血管主干位置偏向侧的盘沿较窄，视盘血管主干位置远离侧的盘沿较宽。大视盘、中视盘、横视盘出现盘沿下方窄、上方宽，血管主干位置偏上，小视盘盘沿上方窄、下方宽，血管主干位置偏下，提示青光眼视神经改变。（中华眼底病杂志，2007，23：118-121）     

院内急性脑卒中52例临床分析

目的探讨院内脑卒中临床特点。方法对52例院内脑卒中患者的临床资料进行综合分析。脑梗死46例，脑出血4例，蛛网膜下腔出血2例，死亡2例，临床治愈18例，32例有较轻的神经系统后遗症。院内卒中的发病原因众多，预后较好，各级医护人员要重视院内脑卒中并防止医疗纠纷的产生。结果结论     

山东省医学影像研究所所长——连世海

山东省医学影像研究所所长连世海副研究员是解放后我国自己培养的一代科学家之一,1945年参加革命,1953年毕业于山东医学院,1958年任山东省立医院放射科主任,副主任医师。     

Synergistic effects of Nell-1 and BMP-2 on the osteogenic differentiation of myoblasts.

Osteogenesis is synergistically enhanced by the combined effect of complimentary factors. This study showed that Nell-1 and BMP-2 synergistically enhanced osteogenic differentiation of myoblasts and phosphorylated the JNK MAPK pathway. The findings are important because of the osteochondral specificity of Nell-1 signaling and the potential therapeutic effects of coordinated BMP-2 and Nell-1 delivery. INTRODUCTION: BMPs play an important role in the migration and proliferation of mesenchymal cells and have a unique ability to alter the differentiation of mesenchymal cells toward chondrogenic and osteogenic lineages. Signaling upstream of Cbfa1/Runx2, BMPs effects are not limited to cells of the osteoblast lineage. Thus, additional osteoblast-specific factors that could synergize with BMP-2 would be advantageous for bone regeneration procedures. NELL-1 (NEL-like molecule-1; NEL [a protein strongly expressed in neural tissue encoding epidermal growth factor like domain]) is a novel growth factor believed to preferentially target cells committed to the osteochondral lineage. MATERIALS AND METHODS: C2C12 myoblasts were transduced with AdLacZ, AdNell-1, AdBMP-2, or AdNell-1+AdBMP-2 overexpression viruses. Effects were studied by cell morphology, alkaline phosphatase activity, osteopontin production, and MAPK signaling. Additionally, in a nude mouse model, viruses were injected into leg muscles, and new bone formation was examined after 2 and 8 wk. RESULTS: C2C12 myoblasts co-transduced with AdNell-1+AdBMP-2 showed a synergistic effect on osteogenic differentiation as detected by alkaline phosphatase activity and osteopontin production. Nell-1 stimulation on AdNell-1 + AdBMP-2 preconditioned C2C12 cells revealed significant activation of the non-BMP-2 associated c-Jun N-terminal kinase (JNK) MAPK signaling pathway, but not the p38 or extracellular signal-regulated kinase (ERK1/2) MAPK pathways. Importantly Nell-1 alone did not induce osteogenic differentiation of myoblasts. In a nude mouse model, injection of AdNell-1 alone stimulated no bone formation within muscle; however, injection of AdNell-1+AdBMP-2 stimulated a synergistic increase in bone formation compared with AdBMP-2 alone. CONCLUSIONS: These findings are important because of the confirmed osteochondral specificity of Nell-1 signaling and the potential therapeutic effects of enhanced BMP-2 action with coordinated Nell-1 delivery.     

BKV in Simultaneous Pancreas-Kidney Transplant Recipients: A Leading Cause of Renal Graft Loss in First 2 Years Post-Transplant

With the introduction of more potent immunosuppressive agents, rejection has decreased in simultaneous pancreas/kidney transplant (SPK) recipients. However, as a consequence, opportunistic infections have increased. The purpose of this report is to outline the course of SPK patients who developed polyomavirus-associated nephropathy (PVAN). A retrospective review of 146 consecutive SPK recipients from January 1, 1996 to December 31, 2002 was performed. Immunosuppression, rejection and development of PVAN were reviewed. Nine patients were identified. All received induction with either OKT3 or thymoglobulin. Immunosuppression included tacrolimus/cyclosporine, MMF/azathioprine and sirolimus/prednisone. Two patients were treated for kidney rejection prior to the diagnosis of PVAN. Time to diagnosis was an average of 359.3 days post-transplantation. Immunosuppression was decreased but five ultimately lost function. However, none developed pancreatic abnormalities as demonstrated by normal glucose and amylase. Two underwent renal retransplantation after PVAN diagnosis and both have normal kidney function. PVAN was the leading cause of renal loss in SPK patients in the first 2 years after transplantation and is a serious concern for SPK recipients. The pancreas, however, is spared from evidence of infection, and no pancreatic rejection occurred when immunosuppression was decreased.     

癌症病人症状与生活质量的相关性研究

[目的]探讨恶性肿瘤病人的症状对生活质量(QOL)的影响,以寻找提高其生活质量的护理对策。[方法]采用癌症病人生存质量表,对600例住院恶性肿瘤病人进行调查,并分析其症状与生活质量的相关性。[结果]癌症病人生活质量总分83.00分±22.00分,且症状与生活质量呈负相关(r=0.289,P<0.05)。[结论]在护理过程中,应根据病人的具体情况,实施护理干预,积极控制病人症状,以提高癌症病人生活质量。