埋线美容致高流量头皮动静脉瘘经血管内介入治疗1例

头皮动静脉瘘是面部埋线美容治疗的少见并发症, 该文报道了1例23岁女性患者, 面部埋线美容术后出现左耳杂音, 后杂音逐渐加重并伴心悸症状。全脑血管造影显示左侧颞部高流量头皮动静脉瘘, 使用弹簧圈及医用胶经血管内介入栓塞, 完全封闭瘘口后取得了满意的疗效, 随访1年瘘口无复发。     

特瑞普利单抗联合同步放化疗治疗中晚期鼻咽癌的疗效观察

目的观察特瑞普利单抗联合同步放化疗治疗中晚期鼻咽癌的临床疗效。 方法将48例中晚期鼻咽癌患者随机均分为对照组和联合组。对照组给予同步放化疗治疗,联合组在对照组基础上加用特瑞普利单抗。比较两组患者临床疗效、免疫指标和不良反应。 结果治疗后,对照组的治疗总有效率低于联合组(P＜0.05);联合组患者外周血CD4＋和CD4＋/CD8＋水平高于对照组(P＜0.05);两组不良反应发生率比较差异无统计学意义(P＞0.05)。 结论特瑞普利单抗联合同步放化疗能改善鼻咽癌患者免疫功能,提高疗效,有较高临床应用价值。     

健康教育在冠心病患者中的应用及效果评价

2005年2月～2006年4月,我们对148例冠心病患者实施系统的健康教育,效果满意.现报告如下.……     

Effect of intercellular adhesion molecule-1 and hyaluronic acid on monocyte-renal tubular epithelial cell adhesion induced by tumor necrosis factor α

Objective To investigate the effect of tumor necrosis factor ot (TNF-α) on monocyte-renal tubular epithelial cell adhesion and to explore its associated mechanism. Methods Human renal proximal tubular epithelial cell line (HK2 cells)and monocyte cell line (U937)were used to perform cell co-culture. TNF-α (10 μg/L)was used to stimulate HK2 cells and then U937 was put into the HK2 monolayers. Three locational parts of hyaluronan around HK2 cells were extracted by different ways and the HA expression was detected by enzyme-linked binding protein assay. Monocyte adhesion was detected by florescence recording assay. Flow cytometry was applied to assess intercellular adhesion molecule-1 (ICAM-1) expression in HK2 cells. Results Stimulation of HK2 cells with TNF-α significantly increased U937 binding to HK2 cell monolayer [(2.25±0.05) folds vs control, P<0.01]. Incubation of TNF-α (10 μg/L) with HK2 cells for 24 hours did not induce the change of total HA expression surrounding the HK2 cells, whereas HA redistribution happened with conditioned medium fraction (CM-HA) increased [(1.17±0.16) fold vs control, P<0.05], the pericellular fraction (trypsin extract fraction, TE-HA) decreased (83%±11% vs control, P<0.05) and the remaining cells-associated HA (cell associated fraction, CA) did not change significantly. In addition, pre-treatment of HK2 cells with TNF-α significantly increased the ICAM-1 expression [(1.85±0.22) folds vs control, P<0.01] and ICAM-1-dependent monocytes binding. Removal of HA from the surface of confluent monolayers of HK2 cells by hyaluronidase before addition of U937 cells increased monocyte binding[ (1.35±0.06) folds vs control, P<0.05]. In contrast, the presence of either sICAM-1 (400 μg/L) or anti-CDI8 antibody (10 mg/L) led to a significant decrease in ICAM-1-dependent monocyte binding (78%±7%, P<0.05; 75%±8%, P<0.01 vs those before adding sICAM-1 or anti-CD18 antibody, respectively). Conclusion HA redistribution induced by TNF-α may facilitate ICAM-1-dependent monocyte-epithelium binding, and pericellular HA plays a protective role in monocyte-driven tissue inflammation.     

CT引导下Seldinger穿刺接种法建立适合非血管介入治疗研究的兔椎体肿瘤模型

目的 CT引导下采用Seldinger穿刺技术接种VX2肿瘤细胞建立适合非血管介入治疗研究的兔椎体肿瘤模型。方法 CT导引下采用Seldinger穿刺技术,对30只新西兰大白兔以18G血管穿刺针穿刺L4或L5椎体接种VX2瘤块,建立椎体肿瘤模型。接种术后评估动物是否发生后肢瘫痪;于接种后14天、21天、28天行兔腰椎MR和CT检查;于接种后21天和28天,各选4只影像检查提示肿瘤生长但无瘫痪的动物直接行病理检查或于经皮椎体成形术(PVP)后行病理检查;余22只动物兔至后肢瘫痪或3个月后行MR、CT及病理检查。结果 影像学及病理学证实建模成功率为93.33%(28/30)。接种术后21天,19只(19/28,67.86%)动物影像学检查显示建模成功,其中17只动物无后肢瘫痪;接种术后28天,9只(9/28,32.14%)动物影像学检查显示建模成功,其中8只动物无后肢瘫痪。建模成功动物出现后肢瘫痪的中位时间为26天。4只接受PVP治疗的椎体肿瘤模型动物均成功完成治疗。结论 利用CT引导下Seldinger穿刺接种兔VX2瘤块法制作椎体肿瘤模型,操作简便、成功率高,有望用于椎体肿瘤非血管介入治疗方法的临床前研究。     

经TACE治疗及降糖药物治疗的原发性肝癌并2型糖尿病Child—Pugh分级变化危险因素分析

目的探讨接受降糖药物治疗的原发性肝癌并2型糖尿病患者经TACE治疗Child-Pugh分级变化的相关因素。方法回顾性分析TACE治疗接受降糖药物治疗的原发性肝癌并2型糖尿病患者126例;主要研究年龄、性别、Child-Pugh分级、二甲双胍治疗、服用其他口服降糖药治疗、是否接受肝癌手术后、糖化血红蛋白（HbAlc）、体质量指数（BMI）、既往有无发生酮症或高渗、超选择栓塞肿瘤供血支与否、胰岛素治疗及有无动静脉瘘等相关数据。观察术前后Child-Pugh分级变化,分析相关因素。结果单因素分析结果显示：既往有无发生酮症或高渗、超选择栓塞肿瘤供血支与否、胰岛素治疗及有无动静脉瘘手术前后Child-Pugh分级肝功能变化差异有统计学意义（P〈0．05）。Logistic回归分析显示：胰岛素治疗（P=0．006）、超选择栓塞肿瘤供血支与否（P=0．037）及有无动静脉瘘（P=0．003）与接受降糖药物治疗的原发性肝癌并2型糖尿病患者TACE术后肝功能Child．Pugh评分变化相关。结论胰岛素治疗、超选择栓塞肿瘤供血支与否及有无动静脉瘘是影响接受降糖药物治疗的原发性肝癌并2型糖尿病患者TACE术后肝功能主要因子。     

X线透视下经鼻十二指肠营养管的置入及临床应用

目的探讨X线透视下十二指肠营养管的置入及其临床应用价值。方法从2003年6月3日至2007年8月17日,59例患者在X线透视下行经鼻十二指肠营养管置入,置管成功后营养管末端位于十二指肠空肠连接部。结果59例患者中首次成功放置空肠营养管57例,成功率96.6%,2例患者因明显胃扩张首次置管失败后在充分胃肠减压后置管成功。置管时间为3.9～68.6 min,平均17.8 min。置管中及置管后未发生严重并发症。结论X线透视下经鼻十二指肠营养管置入是一种安全、经济、有效的肠内营养途径,因而具有广泛的临床应用价值。     

Effect of intercellular adhesion molecule-1 and hyaluronic acid on monocyte-renal tubular epithelial cell adhesion induced by tumor necrosis factor α

Objective To investigate the effect of tumor necrosis factor ot (TNF-α) on monocyte-renal tubular epithelial cell adhesion and to explore its associated mechanism. Methods Human renal proximal tubular epithelial cell line (HK2 cells)and monocyte cell line (U937)were used to perform cell co-culture. TNF-α (10 μg/L)was used to stimulate HK2 cells and then U937 was put into the HK2 monolayers. Three locational parts of hyaluronan around HK2 cells were extracted by different ways and the HA expression was detected by enzyme-linked binding protein assay. Monocyte adhesion was detected by florescence recording assay. Flow cytometry was applied to assess intercellular adhesion molecule-1 (ICAM-1) expression in HK2 cells. Results Stimulation of HK2 cells with TNF-α significantly increased U937 binding to HK2 cell monolayer [(2.25±0.05) folds vs control, P<0.01]. Incubation of TNF-α (10 μg/L) with HK2 cells for 24 hours did not induce the change of total HA expression surrounding the HK2 cells, whereas HA redistribution happened with conditioned medium fraction (CM-HA) increased [(1.17±0.16) fold vs control, P<0.05], the pericellular fraction (trypsin extract fraction, TE-HA) decreased (83%±11% vs control, P<0.05) and the remaining cells-associated HA (cell associated fraction, CA) did not change significantly. In addition, pre-treatment of HK2 cells with TNF-α significantly increased the ICAM-1 expression [(1.85±0.22) folds vs control, P<0.01] and ICAM-1-dependent monocytes binding. Removal of HA from the surface of confluent monolayers of HK2 cells by hyaluronidase before addition of U937 cells increased monocyte binding[ (1.35±0.06) folds vs control, P<0.05]. In contrast, the presence of either sICAM-1 (400 μg/L) or anti-CDI8 antibody (10 mg/L) led to a significant decrease in ICAM-1-dependent monocyte binding (78%±7%, P<0.05; 75%±8%, P<0.01 vs those before adding sICAM-1 or anti-CD18 antibody, respectively). Conclusion HA redistribution induced by TNF-α may facilitate ICAM-1-dependent monocyte-epithelium binding, and pericellular HA plays a protective role in monocyte-driven tissue inflammation.     

Effect of intercellular adhesion molecule-1 and hyaluronic acid on monocyte-renal tubular epithelial cell adhesion induced by tumor necrosis factor α

Objective To investigate the effect of tumor necrosis factor ot (TNF-α) on monocyte-renal tubular epithelial cell adhesion and to explore its associated mechanism. Methods Human renal proximal tubular epithelial cell line (HK2 cells)and monocyte cell line (U937)were used to perform cell co-culture. TNF-α (10 μg/L)was used to stimulate HK2 cells and then U937 was put into the HK2 monolayers. Three locational parts of hyaluronan around HK2 cells were extracted by different ways and the HA expression was detected by enzyme-linked binding protein assay. Monocyte adhesion was detected by florescence recording assay. Flow cytometry was applied to assess intercellular adhesion molecule-1 (ICAM-1) expression in HK2 cells. Results Stimulation of HK2 cells with TNF-α significantly increased U937 binding to HK2 cell monolayer [(2.25±0.05) folds vs control, P<0.01]. Incubation of TNF-α (10 μg/L) with HK2 cells for 24 hours did not induce the change of total HA expression surrounding the HK2 cells, whereas HA redistribution happened with conditioned medium fraction (CM-HA) increased [(1.17±0.16) fold vs control, P<0.05], the pericellular fraction (trypsin extract fraction, TE-HA) decreased (83%±11% vs control, P<0.05) and the remaining cells-associated HA (cell associated fraction, CA) did not change significantly. In addition, pre-treatment of HK2 cells with TNF-α significantly increased the ICAM-1 expression [(1.85±0.22) folds vs control, P<0.01] and ICAM-1-dependent monocytes binding. Removal of HA from the surface of confluent monolayers of HK2 cells by hyaluronidase before addition of U937 cells increased monocyte binding[ (1.35±0.06) folds vs control, P<0.05]. In contrast, the presence of either sICAM-1 (400 μg/L) or anti-CDI8 antibody (10 mg/L) led to a significant decrease in ICAM-1-dependent monocyte binding (78%±7%, P<0.05; 75%±8%, P<0.01 vs those before adding sICAM-1 or anti-CD18 antibody, respectively). Conclusion HA redistribution induced by TNF-α may facilitate ICAM-1-dependent monocyte-epithelium binding, and pericellular HA plays a protective role in monocyte-driven tissue inflammation.