查詢結果分析
相關文獻
- No Association of Urokinase Gene 3'-UTR Polymorphism with Bronchopulmonary Dysplasia for Ventilated Preterm Infants
- 早產兒肺動脈高壓(3)--從病生理學角度回顧肺高壓與肺支氣管發育不全
- 一位經產婦努力成為早產兒母親的經驗
- The Use of Prophylactic Intravenous Immunoglobulin Therapy in Very Low Birthweight Infants
- 極低出生體重早產兒造成腦性麻痺的危險因子之探討
- Home Oxygen Therapy for Chronic Lung Disease in Very Low-Birth-Weight Infants
- Optimal Timing of Retina Examinations for Premature Infants
- 早產兒父母的調適過程及其護理
- 早產兒父母支持團體推展方案--Stetler研究應用模式
- 極度早產兒的體內含鐵量過高會增加早產兒視網膜病變的危險性
頁籤選單縮合
題 名 | No Association of Urokinase Gene 3'-UTR Polymorphism with Bronchopulmonary Dysplasia for Ventilated Preterm Infants=早產兒肺支氣管發育不全和尿溶素多型性基因間無相關性 |
---|---|
作 者 | 林鴻志; 蘇百弘; 林宗文; 許欽木; 萬磊; 蔡長海; 蔡輔仁; | 書刊名 | 臺灣兒科醫學會雜誌 |
卷 期 | 45:6 民93.11-12 |
頁 次 | 頁315-319 |
分類號 | 417.534 |
關鍵詞 | 早產兒; 肺支氣管發育不全; 尿溶素多型性基因; Urokinase polymorphism; Polymerase chain reaction bronchopulmonary dysplasia; |
語 文 | 英文(English) |
中文摘要 | 肺支氣管發育不全的病理發現和延長的肺發炎反應及癒合不全是一致的。纖維蛋白分解和凝固化之間競爭性的平衡可說明早産兒肺部對急性傷害的反應。本研究的目的是探討懷孕週數小於30週且使用呼吸器的早産兒其尿溶素的多型性基因和肺支氣管發育不全的相關性。肺支氣管發育不全的定義是早産兒在出生後28天或矯正週數36週時仍需依靠呼吸器支持且(或)氧氣的供給,同時有胸部X光上特殊的變化。共有204個早產兒進入此研究。我們取其血液中白血球之DNA,使用polymerase chain reaction (PCR),限制酶,及電泳之方法以分析其位於第十對染色體之Urokinase 3'-UTR C/R之基因多形體,並進一步比較兩組基因多形體之分佈與差異。研究結果顯示不論出生後28天或矯正週數36週,兩組間Urokinase基因多形體之分布並無明顯之差異。Urokinase 3'-UTR基因多形體分佈與呼吸器使用天數無關聯性。我們的結論是Urokinase 3'-UTR C/T基因多形體並不是預測BPD發生率和嚴重性之合適工具。 |
英文摘要 | Pathological findings pertaining to bronchopulmonary dysplasia (BPD) are consistent with a process of prolonged lung inflammation and impaired healing. The balance of the competing activities of coagulation and fibrinolysis may contribute to the premature lung's response to acute injury. We investigated the association of the urokinase gene polymorphism with BPD in ventilated preterm infants whose gestational age was below 30 weeks. BPD is defined as infants remaining dependent upon active respiratory support and/or oxygen supplementation and featuring characteristic radiographic changes in the lung fields on the 28(superscript th) postnatal day (BPD-28d) and at a corrected age of 36 weeks of gestation (BPD-36w). Two hundred and four ventilated preterm infants were enrolled in the study. The typing of each specific genotype polymorphism was performed by polymerase chain reaction (PCR) and restriction analysis. Perinatal risk factors for BPD, genotype distribution, and allelic frequencies were compared between infants suffering from BPD (28-d), BPD (36-w) and their respective ventilated preterm infants who did not develop BPD infants. The genotype proportions of the urokinase 3'-UTR polymorphism for BPD (28-d), BPD (36-w) and their respective ventilated preterm infants who did not develop BPD did not differ significantly. There was no difference in allelic frequency for the urokinase 3'-UTR polymorphism between BPD (28-d), BPD (36-w) and their respective ventilated preterm infants who did not develop BPD infants. We concluded that urokinase gene 3'-UTR CIT polymorphism is not a suitable marker for predicting susceptibility and severity to BPD for preterm infants of Taiwanese. |
本系統中英文摘要資訊取自各篇刊載內容。