Effect on Psychological Care to Patients with Pancreatogenic Portal Hypertension Complicated with Gastrointestinal Bleeding 心理护理对胰源性门脉高压并发消化道出血病人的作用
Objective To study the spiral CT features of pancreatogenic segmental occlusion of portal system ( PSOPS). 目的探讨胰源性门静脉系节段性阻塞(PSOPS)的CT征象。
Spiral CT Features of Pancreatogenic Segmental Occlusion of Portal System 胰源性门静脉系节段性阻塞的螺旋CT表现
Conclusion: In patients with pancreatogenic regional, MSCT and image post-processing techniques are very effective for displaying the collateral circulation of Portal Hypertension various location, which is very significant in clinical practice. 结论:MSCT及图像后处理技术能很好地从不同方位显示胰源性区域性门静脉高压侧支循环血管,具有重要的临床指导价值。
Spiral CT manifestation and clinical significance of venous collaterals in pancreatogenic segmental portal hypertension 胰源性区域性门静脉高压的螺旋CT表现及临床意义
Diagnostic Value of Multi-slice CT in Pancreatogenic Regional Portal Hypertension 多层螺旋CT对胰源性区域性门静脉高压的诊断价值
Objective: To observe the pathologic changes and blood gas changes of pancreatogenic lung injury in rat and the effects of herbal decoction Methods: Dynamic change of PaO 2 and PaCO 2 and the pathologic changes of the lung in pancreatogenic lung injury in rat models were observed. 目的:在制备大鼠胰源性肺损伤动物模型基础上给予中药治疗,动态观察血氧分压及二氧化碳分压变化,并对肺脏进行病理学分析。
Conclusion: The model of chronic pancreatitis induced by oleic acid demonstrated extensive acinar degeneration and overt damage of islet. So, it is suitable for research work of pancreatogenic diabetes. 结论:油酸诱导的慢性胰腺炎大鼠模型表现为外分泌腺体广泛退化,内分泌腺体继发损伤,适合进行胰源性糖尿病的研究。
Objective: To establish model of chronic pancreatitis and to observe its pathological and ultrastructural changes, so as to discuss mechanism of overt pancreatogenic diabetes developed by chronic pancreatitis, as well as to provide foundation for the medical research of pancreatogenic diabetes. 目的:建立油酸诱导的慢性胰腺炎大鼠模型,观察其病理及超微结构改变规律,为探讨慢性胰腺炎继发胰源性糖尿病的可能机制,药物防治胰源性糖尿病的研究奠定基础。
Protein and mRNA of IKK-β on liver and fatty tissue increased in model, which may be an important mechanism from chronic pancreatitis, insulin resistance on leading to pancreatogenic diabetes. 慢性胰腺炎大鼠肝脏和脂肪组织IKK-β的表达增加,可能是慢性胰腺炎胰岛素抵抗继发胰源性糖尿病发生的一个重要机制。