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创伤性膈疝在胸腹部创伤中发生率不高 ,但伤情及症状复杂 ,易被延误诊治。 1 987年 3月至 1 998年 5月我院共收治 1 2例 ,现报告如下。1 临床资料1 .1 一般资料 :1 2例中男 1 0例 ,女 2例 ,年龄 1 8~ 50岁 ,30岁以下 9例。闭合性挤压伤 1 0例 ,开放性锐器伤 2例。左侧膈疝 1 1例 ,右侧膈疝 1例。1 1例伤后即有不同程度胸腹痛及进行呼吸困难、心悸、紫绀 ,于 2 4小时内来诊 ,1例伤后 5月始出现食欲不振、恶心、腹胀、胸腹痛方来诊。伴患侧肩背部放射痛 6例 ,患侧胸部隆起 5例 ,叩诊鼓音 3例 ,浊音 3例 ,听诊有肠鸣音 3例 ,胸穿出出胃内容… 相似文献
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高热惊厥合并抗利尿激素异常分泌综合征的研究 总被引:3,自引:0,他引:3
【目的】 探讨高热惊厥 (FC)是否会合并抗利尿激素异常分泌综合征 (SIADH) ,FC在 1次病程中再发惊厥是否与合并SIADH有关。 【方法】 测定 74例FC患儿 (其中在病程中无再发惊厥者 46例 ,有再发惊厥者 2 8例 )及 60例有发热但无惊厥的单纯上呼吸道感染者的血钠、尿钠、血和尿渗透压。 【结果】 在 74例FC患儿中检出合并SIADH者 18例 ,单纯上感组中未检出合并SIADH者。合并SIADH的FC患儿 66.67%发生再次惊厥 (12 /18) ,未合并SIADH的FC患儿发生再次惊厥者仅为 2 8.5 7% (16/5 6)。差异有非常显著性 (χ2 =8.40 46,P <0 .0 1)。 【结论】 高热惊厥可以合并SIADH ,合并SIADH的高热惊厥患儿在病程中发生再次惊厥的危险性高于未合并SIADH者。 相似文献
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Objective To investigate the mechanism of inducing apoptosis of Omi/HtrA2 in renal tubular cells with postasphyxial serum of neonate. Methods Human renal proximal tubular cell line HK-2 cell was used as target cell. They were divided into three groups: control group, asphyxia group and Ucf-101 (Omi/HtrA2 special inhibitor) treated group. The challenge concentration of serum obtained from neonates 24 hours after asphyxia was 20%,and the treatment concentration of Ucf-101 was 10 μmol/L.The Omi/HtrA2 translocation in renal tubular cells was observed with confocal microscopy, and the rate of apoptosis was detected with flow cytometer. Results It was found that Omi/HtrA2 was translocated into cytoplasm in asphyxia group, and the rate of Omi/HtrA2 translocation in HK-2 cells of asphyxia group was significantly increased [(28. 1 % vs. (9.4±2.1)%, P<0. 01]. Compared with the control group, after being treated with postasphyxial serum, the rate of apoptosis of HK-2 cells in asphyxia group wa ssignificantly increased [(36. 3±4. 4)% vs. (12. 4±2. 9) %, P<0. 01]. Compared with asphyxia group, the rate of apoptosis in HK-2 cells in Ucf-101 treated group was significantly decreased [(27. 0± 3. 9)% vs. (36.3±4.4) %, P<0. 01]. Conclusion These experimental data demonstrates that postasphyxial serum of neonate can induce apoptosis of HK-2 cells, and translocation of Omi/HtrA2 from mitochondria into cyto-plasm may play an important role in its intracellular signal transduetion mechanism in induction of apoptosis. 相似文献
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Objective To investigate the mechanism of inducing apoptosis of Omi/HtrA2 in renal tubular cells with postasphyxial serum of neonate. Methods Human renal proximal tubular cell line HK-2 cell was used as target cell. They were divided into three groups: control group, asphyxia group and Ucf-101 (Omi/HtrA2 special inhibitor) treated group. The challenge concentration of serum obtained from neonates 24 hours after asphyxia was 20%,and the treatment concentration of Ucf-101 was 10 μmol/L.The Omi/HtrA2 translocation in renal tubular cells was observed with confocal microscopy, and the rate of apoptosis was detected with flow cytometer. Results It was found that Omi/HtrA2 was translocated into cytoplasm in asphyxia group, and the rate of Omi/HtrA2 translocation in HK-2 cells of asphyxia group was significantly increased [(28. 1 % vs. (9.4±2.1)%, P<0. 01]. Compared with the control group, after being treated with postasphyxial serum, the rate of apoptosis of HK-2 cells in asphyxia group wa ssignificantly increased [(36. 3±4. 4)% vs. (12. 4±2. 9) %, P<0. 01]. Compared with asphyxia group, the rate of apoptosis in HK-2 cells in Ucf-101 treated group was significantly decreased [(27. 0± 3. 9)% vs. (36.3±4.4) %, P<0. 01]. Conclusion These experimental data demonstrates that postasphyxial serum of neonate can induce apoptosis of HK-2 cells, and translocation of Omi/HtrA2 from mitochondria into cyto-plasm may play an important role in its intracellular signal transduetion mechanism in induction of apoptosis. 相似文献
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目的:观察凯时治疗急性脑梗死的疗效。方法:选取急性期脑梗死患者,随机分为两组各30例。治疗组在常规治疗的基础上加用凯时,对照组只用常规治疗。采用全国第四届脑血管病学术会议通过“脑卒中患者临床神经功能缺损程度评分标准”进行疗效评定。结果:两周后评定临床神经功能缺损程度,结果凯时治疗急性脑梗死疗效优于对照组。结论:凯时治疗急性脑梗死疗效明显,副作用小,可作为治疗急性脑梗死的主要药物之一。 相似文献
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丙泊酚、咪唑安定和硫喷妥钠是全麻常用的诱导药,近年来常将其相互复合使用,以期降低气管插管应激反应,防止循环系的过度扰乱。我院采用的三种全麻诱导药复合使用方法,下文将三法对循环系影响的观察比较结果加以报道,以供临床选择参考。 相似文献
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