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Yuanqing Yao Jun Qian Shunkang Rong Yuwen Huang Bo Xiong Gang Yang Dengqing Zhang Shimin Deng Jie Tan Que Zhu Changming Deng Dichuan Liu Haitao Ran Zhigang Wang Jing Huang 《Ultrasound in medicine & biology》2019,45(2):490-499
Stellate ganglion (SG) modification has been investigated for arrhythmia treatment. In this study, transesophageal SG imaging and intervention were explored using a homemade 30F integrated focused ultrasonic catheter in healthy mongrel canines in vivo. Anatomic details of SGs were ultrasonically imaged and evaluated. SG had a heterogeneous echoic structure and characteristic profiles sketched by hyper-echoic outlines in an ultrasonogram. Left SGs in the experimental group were successfully ablated through the esophagus under ultrasonic guidance provided by the catheter itself. Two weeks after the ablation, the QT and QTc of the experimental group decreased compared with those of the sham group and at baseline (both p values < 0.001). Histologic examination revealed that left SGs were destroyed. No major complications were observed. This approach may be further explored as a method for ganglia remodeling evaluation and as a strategy of ganglia modification for arrhythmia and for other diseases. 相似文献
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目的 探讨新生儿肺部超声在早产儿肺部感染评价中的价值。
方法 选取肺部感染早产儿80例为观察组,无肺部感染的早产儿80例为对照组,均给予新生儿肺部超声检查,比较2组肺部超声评分、氧合指数、呼吸指数,比较观察组不同病情、预后患儿肺部超声评分、氧合指数、呼吸指数,分析肺部超声评分和氧合指数、呼吸指数的相关性。
结果 观察组肺部超声评分、氧合指数低于对照组,呼吸指数高于对照组,差异有统计学意义(P<0.05)。观察组极危重患儿肺部超声评分、氧合指数低于危重和非危重患儿,呼吸指数高于危重和非危重患儿,危重患儿肺部超声评分、氧合指数低于非危重患儿,呼吸指数高于非危重患儿,差异有统计学意义(P<0.05)。肺部超声评分与呼吸指数呈负相关(r=-0.455,P<0.05),与氧合指数呈正相关(r=0.470,P<0.05)。观察组死亡患儿肺部超声评分、氧合指数低于存活患儿,呼吸指数高于存活患儿,差异有统计学意义(P<0.05)。肺部超声评分预测患儿预后的ROC曲线下面积为0.874,高于呼吸指数和氧合指数(P<0.05),其截断值为20分时,敏感度和特异度为88.50%和75.00%。
结论 新生儿肺部超声在早产儿肺部感染评价中有较好的效果,值得临床使用。 相似文献
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2013年5月至2014年2月对解放军107医院收治的80例腺样体肥大患者采用吸痰管牵拉软腭暴露鼻咽部,并在70°鼻内镜辅助下行肥大腺样体切除术,效果良好,现报告如下。1资料与方法1.1临床资料本组80例中,男43例,女37例,5~13岁,平均7岁,病程9个月~4年。临床症状均有不同程度夜寐打鼾、张口呼吸,伴有鼻塞。其中 相似文献
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Yaobin Ouyang Gongmeizi Liu Wenting Xu Zhen Yang Nianshuang Li Chuan Xie Chun Zhou Jiang Chen Yin Zhu Junbo Hong Nonghua Lu 《Oncology Letters》2021,21(2)
Helicobacter pylori (H. pylori) is a main risk factor for gastric cancer (GC). Epithelial-mesenchymal transition (EMT) is involved in the development and progression of H. pylori-associated GC. However, the exact molecular mechanism of this process remains unclear. The AKT/GSK3β signaling pathway has been demonstrated to promote EMT in several types of cancer. The present study investigated whether H. pylori infection induced EMT, and promoted the development and metastasis of cancer in the normal gastric mucosa, and whether this process was dependent on AKT activation. The expression levels of the EMT-associated proteins, including E-cadherin and N-cadherin, were determined in 165 gastric mucosal samples of different disease stages by immunohistochemical analysis. The expression levels of E-cadherin, N-cadherin, AKT, phosphorylated (p-)AKT (Ser473), GSK3β and p-GSK3β (Ser9) were further determined in H. pylori-infected Mongolian gerbil gastric tissues and cells co-cultured with H. pylori by immunohistochemical analysis and western blotting. The results indicated that the expression levels of the epithelial marker E-cadherin were decreased, whereas the expression levels of the mesenchymal marker N-cadherin were increased during gastric carcinogenesis. Their expression levels were associated with H. pylori infection. Furthermore, H. pylori infection resulted in downregulation of E-cadherin expression and upregulation of N-cadherin expression in Mongolian gerbils and GES-1 cells. In addition, an investigation of the associated mechanism of action revealed that p-AKT (Ser473) and p-GSK3β (Ser9) were activated in GES-1 cells following co-culture with H. pylori. Furthermore, following pretreatment of the cells with the AKT inhibitor VIII, the expression levels of E-cadherin, N-cadherin, p-AKT and p-GSK3β did not show significant differences between GES-1 cells that were co-cultured with or without H. pylori. The levels of p-AKT and p-GSK3β were increased in H. pylori-infected Mongolian gerbils. In conclusion, the present study demonstrated that H. pylori infection activated AKT and resulted in the phosphorylation and inactivation of GSK3β, which in turn promoted early stage EMT. These effects were AKT-dependent. This mechanism may serve as a prerequisite for GC development. 相似文献