一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的乙型肝炎病毒X基因变异方式

目的:证实乙型肝炎病毒(hepatitis B virus,HBV)X基因一种新的变异方式.方法:从HBV慢性感染患者血清中提取HBVDNA,扩增X基因序列,克隆入pMD19 T载体,选择阳性克隆进行DNA测序,与已知HBV基因相应序列比较该患者体内HBV基因变异位点以及变异形式.结果:从21例患者中共挑选74个克隆测序,测序结果提示54个克隆X基因下游大段缺失突变,长度达234 nt,位于1601-1834 nt处,另有1个克隆发生245 nt缺失突变.发生缺失变异的病毒株同时存在G/A1515C、G1518C和A1585T替换突变,这两种突变具有联动特征.缺失突变株HBx仅编码76 aa其第44和45位编码为LL,具有特异性.结论:观察到一种X蛋白变异方式,这种大段缺失突变导致X蛋白下游编码序列丢失,其为X因子还是X蛋白以及这种变异是否为常态形式尚需进一步研究.     

腭裂术后并发症的预防

目的 探讨腭裂术后并发症的原因及其预防措施。方法 对1982—2001年494例腭裂手术治疗后发生并发症43例进行回顾性分析。结果 腭裂术后并发症的发生率为8．70％，其中以出血为最多，占32．56％；急性喉梗阻为最危险，占9．30％；其它并发症为瘘孔及黏骨膜瓣坏死27．91％，复裂13．95％，术后中耳炎16．28％。结论 腭裂术后并发症的发生有其独立和相关的危险因素。强调在术中、术后应采取适当措施防止并发症的发生。     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

中年男性骨质疏松症患者1例的全科诊疗与管理

介绍1例中年男性原发性骨质疏松症患者在基层和专病门诊双向转诊并取得良好治疗效果的全科诊疗及管理过程, 结合案例分析其诊断、评估、治疗、随访管理的关键点与难点, 并充分体现基层诊疗指南的实践指导性。     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

目的 检测HBV核心启动子区(CP)基因变异方式.方法 自HBV慢性感染患者血清中提取HBV DNA,扩增CP区域序列,克隆入pMD19 T载体,选择阳性克隆进行DNA测序,与已知HBV基因相应序列比较患者体内HBV基因变异位点以及变异形式.结果 自21例患者中共挑选74个克隆测序,54个克隆中病毒基因序列CP区发生大段缺失突变,长度达234个核苷酸,另有1个克隆发生245个核苷酸缺失突变.缺失突变区域包括CP区、HBeAg起始密码子和直接重复序列(DR)Ⅰ区,命名为CP缺失突变,发生CP缺失突变的病毒株同时存在A1585T替换突变,这两个部位的突变具有联动特征.结论 观察到一种导致HBeAg阴性慢性乙型肝炎的新方式,即CP、HBeAg起始密码子缺失突变,并提出一种简明的CP缺失检测方式.     

双歧三联活菌辅助治疗对2型糖尿病患者肠道菌群及血清网膜素-1的影响

目的：探讨双歧三联活菌辅助治疗对2型糖尿病患者肠道菌群及血清网膜素-1的影响。方法：选取本院2019年1月—2021年6月收治的120例2型糖尿病患者作为研究对象,将其分为观察组（n=60）和对照组（n=60）。观察组采用常规治疗与双歧三联活菌辅助治疗,对照组单独采用常规治疗,比较两组治疗前后肠道菌群、血清网膜素-1、脂肪酸结合蛋白、血糖相关指标、血脂相关指标。结果：观察组双歧杆菌、乳酸杆菌高于对照组,肠球菌、拟杆菌、肠杆菌低于对照组（P<0.05）;观察组血清网膜素-1高于对照组,脂肪酸结合蛋白低于对照组（P<0.05）;观察组空腹血糖、餐后2h血糖、糖化血红蛋白低于对照组（P<0.05）;观察组胆固醇、三酰甘油、低密度脂蛋白胆固醇低于对照组,高密度脂蛋白胆固醇高于对照组（P<0.05）。结论：双歧三联活菌辅助治疗可以改善2型糖尿病患者肠道菌群与血清网膜素-1,且可降低患者血糖指标,改善患者血脂指标,值得临床应用。