摘要:目的:分析本院住院城鎮(zhèn)及農(nóng)村患者的乙型肝炎病毒感染及免疫情況,推測(cè)不同區(qū)域發(fā)病及免疫狀況,為免疫預(yù)防及臨床提供參考。方法:收集我科2000年度,2004年度,2008年度住院患者的乙肝五項(xiàng)檢測(cè)報(bào)告,按患者長(zhǎng)期居住地分為農(nóng)村組及城鎮(zhèn)組,對(duì)比分析兩組患者乙型肝炎病毒感染、具有免疫力及無免疫力年度變化情況及不同組別的差異。結(jié)果:同農(nóng)村組相比,城鎮(zhèn)組乙型肝炎病毒感染率、無免疫率低于農(nóng)村組,免疫率高于農(nóng)村組。年度對(duì)比乙型肝炎病毒感染率及免疫率呈上升趨勢(shì),無免疫率呈下降趨勢(shì)。結(jié)論:近年來乙型病毒性肝炎發(fā)病有上升趨勢(shì),農(nóng)村地區(qū)免疫普及率相對(duì)較低,仍為發(fā)病及預(yù)防免疫的重點(diǎn)區(qū)域,應(yīng)給予足夠重視。Abstract: Objective: To observe the disposition of infection and immunifaction on type B hepatitis in patients from hospital, suppose the disposition of infection and immunifaction in differently region, and provide information for immunifaction and clinical treatment. Methods: Reports of type B hepatitis from patients in hospital were collected, and were divided into town group and country group according to the habitation of patients. The difference of infection, immunifaction and no immunifaction were compared between two groups. Results: In comparison with the country group, the percentage of infection and no immunifaction was lower in town, and immunifaction was higher, attack rate of type B hepatitis had a tendency to increasing and no immunifaction was decreased by contrasting with annum. Conclusion: Recent years, attack rate of type B hepatitis has a tendency to increasing, and the popular rate of immunifaction is lower in country, so country is still the focal point of immunifaction and infection, and sufficient attention must be paid.
目的 探討透明質(zhì)酸（HA）延遲創(chuàng)面愈合的作用。方法 成年日本大耳白兔8只，建立兔耳創(chuàng)傷愈合模型，隨機(jī)分成2%HA治療組（A組），1%HA治療組（B組），磷酸鹽緩沖液（PBS）對(duì)照組（C組，進(jìn)行大體形態(tài)、組織學(xué)變化、平均愈合時(shí)間、創(chuàng)面收縮情況、殘余創(chuàng)面面積、成纖維細(xì)胞α-平滑肌肌動(dòng)蛋白表達(dá)及超微結(jié)構(gòu)，觀察12天。結(jié)果 ①三組創(chuàng)面平均愈合時(shí)間為（11.7±0.6）、（11.3±0.6）和（10.8±1.0）天,三組之間有顯著差異（Plt;0.05）；A、B組與C組比較創(chuàng)面收縮速率及殘余面積也有統(tǒng)計(jì)學(xué)意義（Plt;0.05）。②組織學(xué)見A、B兩組膠原纖維較細(xì)，排列整齊；C組膠原纖維較粗大，排列紊亂。③ A、B組α平滑肌肌動(dòng)蛋白的表達(dá)少于C組，有統(tǒng)計(jì)學(xué)意義（Plt;0.01）。結(jié)論 HA通過抑制成纖維細(xì)胞向肌成纖維細(xì)胞轉(zhuǎn)化而抑制創(chuàng)面收縮，是延遲創(chuàng)面愈合的原因之一；且這一作用與其濃度有依賴關(guān)系。