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A production process of low-M.W. Hepatopoeitin (HPN, M. W.<10KD) from fetal porcine liver by heating at 95 ℃, trypsin digestion and uliraf iltration has been reported. The related treating conditions and chemical/physical properties of HPN are also studied. The experiments in vitro and in vivo indicate that the resulting HPN can specially stimulate the proliferation of hepatoayto and antagonize the function of tumor necrosis factor (TNF) . The experiments with animal prove that this product is safe and reliable... A production process of low-M.W. Hepatopoeitin (HPN, M. W.<10KD) from fetal porcine liver by heating at 95 ℃, trypsin digestion and uliraf iltration has been reported. The related treating conditions and chemical/physical properties of HPN are also studied. The experiments in vitro and in vivo indicate that the resulting HPN can specially stimulate the proliferation of hepatoayto and antagonize the function of tumor necrosis factor (TNF) . The experiments with animal prove that this product is safe and reliable without any toxic and side effect, which would be efficient to fulminant hepatitis and TNF-induced toxic shock 本文报道以乳猪肝脏为原料,采用加热、蛋白酶降解和超滤等手段,分离纯化低分子量肝细胞生长素(HPN,M.W.<10KD)的生产工艺.并对有关处理方法及其理化特性进行了初步的研究.经药效学研究证实,该制品能特异性地刺激肝细胞生长,具有保护肝脏、对抗肿瘤坏死因子的作用;另经毒理药理实验证实,该制品安全可靠,无任何毒副作用.因此,可望用于治疗重型肝炎及肿瘤坏死因子引起的中毒性休克等疾病 HGV RNA was detected by Rt- nested PCR in sera from4 9patients with fulminant hepatitis.The results showed:a) HGV RNA positive rate was16. 3% ( 8/ 4 9) in patients with fulminant hepatitis including4 subjects with HBV coinfection,1subject with HCV coinfection,2 subjects with HBV and HCV coinfection and1subject with HGV infection alone.b) mortality in patients with fulminant hepatitis with HGV infection was75% ( 6/ 8) ,suggesting that:a) both infection with HGV alone and super infections of other... HGV RNA was detected by Rt- nested PCR in sera from4 9patients with fulminant hepatitis.The results showed:a) HGV RNA positive rate was16. 3% ( 8/ 4 9) in patients with fulminant hepatitis including4 subjects with HBV coinfection,1subject with HCV coinfection,2 subjects with HBV and HCV coinfection and1subject with HGV infection alone.b) mortality in patients with fulminant hepatitis with HGV infection was75% ( 6/ 8) ,suggesting that:a) both infection with HGV alone and super infections of other types of hepatitis virus can result in fulminant hepatitis. b) clinical manifestaitions of fulminant hepatitis with HGV infection may appear to be more severe and with higher mortality. 为调查重型肝炎的庚型肝炎病毒 ( HGV)的感染状况。我们应用逆转录 -巢式聚合酶链反应 ( Rt- nested PCR)检测了 4 9例重型肝炎患者血清中的庚型肝炎病毒核酸 ( HGV RNA)。结果显示 :8例 HGV RNA阳性 ( 16.3% ) ,其中 6例死亡 ( 75% ) ;8例 HGV感染的重型肝炎患者中 7例重叠感染乙型肝炎病毒 ( HBV)或丙型肝炎病毒 ( HCV) ,1例为单纯 HGV感染。提示 :HGV与其它肝炎病毒重叠感染及单纯 HGV感染均可引起重型肝炎 ;而且其临床表现较重 ,病死率高。 Objective To determine the effect of T1762A1764 mutation in regulatory sequence of core gene of hepatitis B virus oncore promoter. Methods Patients with fulminant hepatitis were investigated for T1762A1764 mutation by direct sequencing of PCRproducts. PCR products containing HBV precore/core gene regulatory sequences were directly cloned into chloramphenicol acetyltransferase (CAT) expressing plasmid. Sequences of core promoter of T1762A1764 mutant were compared with that of wild typestrain. CAT assay... Objective To determine the effect of T1762A1764 mutation in regulatory sequence of core gene of hepatitis B virus oncore promoter. Methods Patients with fulminant hepatitis were investigated for T1762A1764 mutation by direct sequencing of PCRproducts. PCR products containing HBV precore/core gene regulatory sequences were directly cloned into chloramphenicol acetyltransferase (CAT) expressing plasmid. Sequences of core promoter of T1762A1764 mutant were compared with that of wild typestrain. CAT assay was done to compare the CAT expression level aller transfection of the sequences into HepG2 cells and transientexpression. Results It was revealed that T1762A1764 mutation was a main factor that repressed CAT expression in vitro.Conclusion T1762A1764 mutation may play a main role in repressing the activity of core promoter of hepatitis B virus. 目的了解C基因启动子区T1762A1764变异对其启动子的影响。方法PCR产物直接测序,检测重症乙型肝炎患者乙型肝炎病毒(HBV)前C和C基因调节序列的T1762A1764变异;并将该调节序列插入到氯霉素乙酰转移酶(CAT)表达质粒中,转染HepG2细胞并瞬时表达,比较T1762A1764野株及变异株的C基因启动小区序列及CAT表达水平。结果T1762A1764变异在使CAT表达下调中起主要作用。结论T1762A1764变异使C基因启动子活性下调中起重要作用。
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