体外循环中血浆内皮素、血管紧张素Ⅱ和前列环素的变化及临床意义

目的:分析体外循环心内直视手术中血浆内皮素、血管紧张 和前列环素的变化及临床意义。 方法 :应用放免法分别于 7个时点测定 30例心内直视手术病人血浆内皮素、血管紧张素 和前列环素 (终产物 6 - keto-PGF1α)水平。结果 :血浆内皮素水平在转机时高于术前 (P <0 .0 5 ) ,转流中逐渐升高 ,停转流时达高峰 (P <0 .0 1) ,术后 2 h及 2 4 h逐渐降低 ,但仍高于术前 (P <0 .0 5 )。血管紧张素 水平在转机时高于术前 (P <0 .0 5 ) ,转流 30 min降低 ,主动脉开放时升高 ,停转流时达高峰 (P <0 .0 1) ,术后 2 4 h呈下降趋势 ,但仍高于术前 (P <0 .0 5 )。 6 - keto- PGF1α在转流即刻显著升高 ,以后各时点降低。结论:体外循环期间血浆内皮素、血管紧张素 水平显著增高 ,6 - keto- PGF1α水平逐渐降低。体外循环期间加入内皮素、血管紧张素 拮抗剂或前列环素合成剂有利于心功能恢复     

Skeletal unloading induces resistance to insulin-like growth factor-I (IGF-I) by inhibiting activation of the IGF-I signaling pathways.

We showed that unloading markedly diminished the effects of IGF-I to activate its signaling pathways, and the disintegrin echistatin showed a similar block in osteoprogenitor cells. Furthermore, unloading decreased alphaVbeta3 integrin expression. These results show that skeletal unloading induces resistance to IGF-I by inhibiting activation of the IGF-I signaling pathways at least in part through downregulation of integrin signaling. INTRODUCTION: We have previously reported that skeletal unloading induces resistance to insulin-like growth factor-I (IGF-I) with respect to bone formation. However, the underlying mechanism remains unclear. The aim of this study was to clarify how skeletal unloading induces resistance to the effects of IGF-I administration in vivo and in vitro with respect to bone formation. MATERIALS AND METHODS: We first determined the response of bone to IGF-I administration in vivo during skeletal unloading. We then evaluated the response of osteoprogenitor cells isolated from unloaded bones to IGF-I treatment in vitro with respect to activation of the IGF-I signaling pathways. Finally we examined the potential role of integrins in mediating the responsiveness of osteoprogenitor cells to IGF-I. RESULTS: IGF-I administration in vivo significantly increased proliferation of osteoblasts. Unloading markedly decreased proliferation and blocked the ability of IGF-I to increase proliferation. On a cellular level, IGF-I treatment in vitro stimulated the activation of its receptor, Ras, ERK1/2 (p44/42 MAPK), and Akt in cultured osteoprogenitor cells from normally loaded bones, but these effects were markedly diminished in cells from unloaded bones. These results were not caused by altered phosphatase activity or changes in receptor binding to IGF-I. Inhibition of the Ras/MAPK pathway was more impacted by unloading than that of Akt. The disintegrin echistatin (an antagonist of the alphaVbeta3 integrin) blocked the ability of IGF-I to stimulate its receptor phosphorylation and osteoblast proliferation, similar to that seen in cells from unloaded bone. Furthermore, unloading significantly decreased the mRNA levels both of alphaV and beta3 integrin subunits in osteoprogenitor cells. CONCLUSION: These results indicate that skeletal unloading induces resistance to IGF-I by inhibiting the activation of IGF-I signaling pathways, at least in part, through downregulation of integrin signaling, resulting in decreased proliferation of osteoblasts and their precursors.     

Hyperfractionated radiation therapy combined with concomitant chemotherapy for inoperable stage III non-small cell lung cancer: clinical analysis of 70 cases]

OBJECTIVE: To evaluate the effect of hyperfractionated radiation therapy and concomitant chemotherapy for inoperable stage III non-small cell lung cancer (NSCLC). METHODS: Seventy patients were randomized equally into two group. The therapy group received radiotherapy with hyperfractionated radiation therapy combined with concomitant chemotherapy, and the control group was treated with chemotherapy only. RESULT: The overall response rate, including the rate of both complete (CR) and partial responses (PR), in the therapy group was 60.0% with a CR rate of 8.6%. The overall response rate in the control group was 40.0% with a CR rate of 5.7%. The difference in overall response rate was statistically significant between the two groups (P<0.05). The median survival time, 1- and 2-years survival rate were 12.8 months, 48.6%, and 25.7%, respectively, in the hyperfractionated radiotherapy group, and 9.4 months, 34.3%, and 17.1%, respectively, in the chemotherapeutic group (P 0.031). The major toxic effects of the chemotherapy were myelosuppression and radiation esophagitis. CONCLUSION: Hyperfractionated radiation therapy plus concomitant chemotherapy with paclitaxel for inoperable stage III NSCLC improves the short-term response of the patients, but fail to raise the survival rate.     

Nuclear Factor κB and Anesthetic Preconditioning during Myocardial Ischemia-Reperfusion

Background: Volatile anesthetic preconditioning (APC) protects against myocardial ischemia-reperfusion (IR) injury, but the precise mechanisms underlying this phenomenon remain undefined. To investigate the molecular mechanism of APC in myocardial protection, the activation of nuclear factor (NF) [kappa]B and its regulated inflammatory mediators expression were examined in the current study.

Methods: Hearts from male rats were isolated, Langendorff perfused, and randomly assigned to one of three groups: (1) the control group: hearts were continuously perfused for 130 min; (2) the IR group: 30 min of equilibration, 15 min of baseline, 25 min of ischemia, 60 min of reperfusion; and (3) the APC + IR group: 30 min of equilibration, 10 min of sevoflurane exposure and a 5-min washout, 25 min of global ischemia, 60 min of reperfusion. Tissue samples were acquired at the end of reperfusion. NF-[kappa]B activity was determined by electrophoretic mobility shift assay. The NF-[kappa]B inhibitor, I[kappa]B-[alpha], was determined by Western blot analysis. Myocardial inflammatory mediators, including tumor necrosis factor [alpha], interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase, were also assessed by Western blot analysis.

Results: Nuclear factor [kappa]B-DNA binding activity was significantly increased at the end of reperfusion in rat myocardium, and cytosolic I[kappa]B-[alpha] was decreased. Supershift assay revealed the involvement of NF-[kappa]B p65 and p50 subunits. APC with sevoflurane attenuated NF-[kappa]B activation and reduced the expression of tumor necrosis factor [alpha], interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase. APC also reduced infarct size and creatine kinase release and improved myocardial left ventricular developed pressure during IR.     

颈前部皮神经构筑研究

目的　为研究皮肤疾病和损伤提供皮神经构筑资料。方法　用S 10 0蛋白免疫组化染色法研究正常成人颈前部胸锁乳突肌前、后缘皮肤各层内皮神经的数量、分布及构筑特点。结果　 ( 1)皮肤乳头层内皮神经的小分支多分布在皮突下和乳头内血管丛附近。 ( 2 )真皮网状层内神经多位于小血管附近和汗腺、皮脂腺以及毛囊周围 ,神经分支呈串珠状或波纹形。 ( 3 )皮下组织内神经干和神经网同时存在。结论　皮肤内感觉神经树的分布及构筑特点与血管树相似。     

关木通引起慢性间质性肾炎7例报告

目的　观察关木通所致慢性肾损伤的临床和病理改变特点。方法　本组 7例中 ,男 5例 ,女 2例。 3例服关木通汤药 ,4例服含关木通成药。分析服用时间、累积总量与肾损害首发症状及症状出现时间、肾功能和肾病理改变的关系。结果　汤药组 :服药时间平均 3 3 3个月 ,累积总量平均 82 9 3 g ,首发症状为乏力 3例 ,夜尿增多 2例 ,平均时间为 8 3个月 ,Cr平均 40 2 μmol/L。肾病理 :3例均为重度寡细胞性肾间质纤维化 ,肾小管广泛萎缩。成药组 :服药时间平均 7 5个月 ,累积总量平均 13 6g ,乏力 3例 ,夜尿增多 1例 ,恶心呕吐、头痛头晕 1例 ,平均18 8个月 ,Cr 3 62 8μmol/L。肾病理为重度寡细胞性间质纤维化和灶状纤维化各 2例 ,肾小管灶状萎缩 3例 ,广泛萎缩 1例。结论　汤药组关木通积累大 ,发病时间早 ,肾病理改变重。提示关木通所致肾损其临床表现、病理改变与服用关木通时间、剂量相关。     

后腹腔镜手术切除肾上腺节细胞神经瘤疗效观察

目的 :探讨后腹腔镜微创手术治疗肾上腺节细胞神经瘤的适应证和可行性。方法 :采用后腹腔镜手术治疗肾上腺节细胞神经瘤患者 5例 ,其中左侧肾上腺节细胞神经瘤 2例 ,右侧 3例。结果 :5例后腹腔镜手术全部获得成功 ,4例肾上腺肿瘤为单发 ,1例为多发 (4个肿瘤 ) ;肿瘤最大直径 2 .5～ 8.0 (4 .2± 1.8)cm ;手术时间35～ 10 5 (5 9± 2 7)min ,估计出血量 10～ 30 (19± 7)ml,术后镇痛剂吗啡用量 0～ 2 0 (8± 8)mg ,2例未用镇痛剂 ;排气、恢复进食时间 1～ 3(1.4± 0 .5 )d ;术后住院时间 4～ 7(5 .4± 1.5 )d。无围手术期并发症发生。结论 :后腹腔镜手术切除肾上腺节细胞神经瘤是安全可行的 ,能充分体现腹腔镜手术创伤小、恢复快的优点。肾上腺节细胞神经瘤是腹腔镜手术很好的适应证。