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<正>根据有关读者举报并经本刊初步查证,近一段时间来有人冒充本刊名义和盗用本刊的合法刊号(ISSN1674-3806/CN45-1365/R)进行非法出版活动(该非法出版物的编辑部地址为:北京市100036信箱27分箱;邮政编号:100036;联系电话:010-87013678;网址:http://www.zglcxyx010.com;E-mail:zglcxyx010@126.com、ZGLCXYX@163.com),严重地侵犯本     

中华心血管病杂志2005年度继续教育园地思考多选题答案

第1期急性冠状动脉综合征的概念演化与治疗策略更新:1.A、B、C、D;2.A、D;3.A、B。第2期低分子肝素与血栓栓塞性疾病:1.A、B、C;2.B、C;3.D;4·A、C、D。第3期神经内分泌拮抗剂在慢性心力衰竭治疗中的常见问题:1.B;2.D;3.A;4.D。第4期心率与心血管病危险性:1.B;2.A;3.C;4.D。第5期神经内分泌拮抗治疗慢性心力衰竭的几个热点问题:1.A;2.C;3.E。第6期肾上腺髓质素与心血管病研究现状:1.B;2.C;3.D;4.D。第7期对中国2004年、欧洲2003年高血压防治指南和JNC7血压分类的比较及评价:1.B;2.C;3.B。第8期心肾综合征研究进展:1.B;2.A…     

2012年第二届亚太地区幽门螺杆菌会议

会议主题:科学向临床医学的转化:亚太地区新千年幽门螺杆菌感染特别工作组:早期胃癌的内镜诊断和治疗;H.pylori的微生物学、免疫学和分子遗传学会议热点:H.pylori与胃癌;H.pylori的分子流行病学;H.pylori的最佳治疗方法;H.pylori感染中具有争议的问题:胃食管反流病,消化不良,NSAID肠病以及胃外疾病。时间:2012年1月13～15日     

慢性肾衰血液透析患者血浆儿茶酚胺水平及其心率变异性分析

目的 :观察心透患者血浆儿茶酚胺水平与心率变异性 ,并探讨两者的相关性。方法 :测定慢性肾衰血透患者血浆儿茶酚胺水平及记录 2 4h动态心电图 ,分析其心率变异性。结果 :慢性肾衰血液透析患者血浆多巴胺和去甲肾上腺素水平较对照组明显升高 （分别为 P <0 .0 1和 P≤ 0 .0 5 ） ;心率变异性时域指标 SDNN,SDANN ,SDNNindex及 r MSSD均较对照组明显降低 （P<0 .0 1） ;血浆多巴胺水平与 HRV呈明显的负相关 （SDNN:r=- 0 .45 ,P≤ 0 .0 1;SDANN:r=- 0 .43,P≤ 0 .0 1;SDNN index:r=- 0 .5 1,P<0 .0 1;r MSSD:r=- 0 .49,P<0 .0 1） ,血浆去甲肾上腺素水平亦呈类似的相关性。结论 :尿毒症心脏交感神经病变以血浆儿茶酚胺水平升高和心率变异性降低为特点 ,提示交感神经作用代偿性增强     

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<正>根据有关读者举报并经本刊初步查证,近一段时间来有人冒充本刊名义和盗用本刊的合法刊号(ISSN1674-3806/CN45-1365/R)进行非法出版活动(该非法出版物的编辑部地址为:北京市100036信箱27分箱;邮政编号:100036;联系电话:010-87013678;网址:http://www.zglcxyx010.com;E-mail:zglcxyx010@126.com、ZGLCXYX@163.com),严重地侵犯本刊的合法权益,损害了本刊的名义,在社会上造成     

本刊严正声明

根据有关读者举报并经本刊初步查证,近一段时间来有人冒充本刊名义和盗用本刊的合法刊号(ISSN1674-3806/CN45-1365/R)进行非法出版活动(该非法出版物的编辑部地址为:北京市100036信箱27分箱;邮政编号:100036;联系电话:010-87013678;网址:http://www.zglcxyx010.com;E-mail:zglcxyx010@126.com、ZGLCXYX@163.com),严重地侵犯本     

中华心血管病杂志2004年度继续教育园地思考多选题答案

第 1期心血管超声医学的研究进展: 1.D; 2.C; 3.B; 4 A。β-受体阻滞剂在心肌梗死中的应用: 1.D; 2.D; 3.A、B、C。第 2期贯彻循证医学的原则作好动脉粥样硬化的预: 1.D; 2.B、D; 3.C; 4.B、C。高血压病肾脏损害的诊断与防治: 1.A、B、C、D; 2.A、B、D; 3.D。第 3期易损斑块及易损患者的新定义及危险分层: 1.A、B、C、D; 2.A、B、C; 3.D; 4.A、B、C、D。β受体阻滞剂治疗慢性心力衰竭临床试验的启示: 1 C;2 B; 3 D; 4 A。第 4期冠心病整体防治中他汀类药物的重要地位: 1.A、B、C、D; 2.A; 3.C。高血压与心力衰…     

Levels of plasma des-γ-carboxy protein C and prothrombin in patients with liver diseases

AIM: To study the plasma des-γ-carboxy protein C activity, antigen and prothrombin levels in patients with liver diseases and their clinical significance. METHODS: Plasma protein C activity (PC:C) was detected by chromogenic assay and antigen (PC:Ag) and des-γ-carboxy protein C (DCPC) were detected by ELISA. Total prothrombin and unabsorbed prothrombin in plasma were detected by ecarin chromogenic assay. RESULTS: Compared with the control, the levels of PC:C and PC:Ag in patients with hepatocellular carcinoma (HCC) and liver cirrhosis (LC) were lower (PCC: 104.65&#177;23.0%,62.50&#177;24.89%, 56.75&#177;20.14%, PC:Ag: 5.31&#177;1.63 μg/mL, 2.28&#177;1.15 μg/mL, 2.43&#177;0.79 μg/mL, P&lt;0.05). The levels of PC:Ag in patients with acute viral hepatitis (AVH) also was lower (2.98&#177;0.91 μg/mL, P&lt;0.01), but PC:C was close to the control (93.76&#177;30.49%, P&gt;0.05). The levels of DCPC in patients with HCC were remarkably higher (0.69&#177;0.29 μg/mL,1.18&#177;0.63 μg/mL, 0.45&#177;0.21 μg/mL, P&lt;0.05) and its averagewas up to 50% of total PC:Ag. But those of DCPC in patients with AVH were not significantly different from the control. The levels of total prothrombin were lower in patients with LC, but higher in patients with HCC. The levels of unabsorbed prothrombin were predominantly higher than those of other groups. CONCLUSION: PC:C and PC:Ag in patients with liverdiseases (except PC:C in AVH) were lower. The total prothrombin was lower in patients with LC. The higher level of unabsorbed prothrombin may be used as a scanning marker for HCC. DCPC may be used as a complementary marker in the diagnosis of HCC.     

书籍及统计学符号的著录方法

<正>[书籍]著者(列名格式与期刊作者相同).书名.卷次:版次(如是第1版可不标出).出版者.年份:引文页码(如专著整体做为文献引用可不著录页码.或:析出文献作者.析出文献题名//专著责任者.书名.卷次:版次(如是第1版可不标出).出版地:出版者.年份:析出     

慢性乙型肝炎患者外周血淋巴细胞亚群与病程相关性的研究

目的对慢性乙型肝炎轻中度、重度和肝硬化患者外周血淋巴细胞亚群的百分比和绝对细胞数进行观察,探讨慢性乙型肝炎患者外周血淋巴细胞亚群的变化与病程的关系.方法采集88例慢性乙型肝炎患者柠檬酸钠新鲜抗凝血,经流式细胞仪进行免疫分型检测.结果慢性乙型肝炎重度患者的CD3+CD4+细胞百分比显著低于轻中度患者(P＜0.05),肝硬化患者的CD3+和CD3+CD8+细胞百分比显著低于轻中度患者(P＜0.01).肝硬化患者CD3CD19+细胞百分比显著高于重度和轻中度患者(P＜0.01).CD4/CD8比例在慢性乙型肝炎轻中度、重度和肝硬化患者间无显著差异.肝硬化和重度患者淋巴细胞、CD3+、CD3+CD4+、CD3+CD8+细胞的绝对细胞数均显著低于轻中度患者(P＜0.01),且肝硬化患者CD3-CD16+56+细胞的绝对细胞数显著低于轻中度患者(P＜0.05).肝硬化患者与轻中度患者的DNA载量分布差异有显著性(P＜0.01),其高水平病毒载量的患者比例高于轻中度患者.结论慢性乙型肝炎轻中度发展为重度和肝硬化的过程中,外周血淋巴细胞亚群绝对细胞数随病情的进展显著减少,主要表现为CD3+CD4+和CD3+CD8+的T淋巴细胞亚群的百分比进行性降低.     

The role of intrahepatic immune effector cells in inflammatory liver injury and viral control during chronic hepatitis B infection

Summary. Cytotoxic T lymphocytes (CTL) and Kupffer cells play an important role in the immune control of hepatitis B virus (HBV), but may also induce liver injury during infection. We investigated the intrahepatic immune response in liver biopsies of chronic HBV patients in relation to inflammatory liver injury and viral control. Forty-seven liver biopsies from patients with chronic HBV with varying degrees of inflammation (ALT values) were selected. Acute hepatitis and normal liver specimens served as controls. Immune effector cells, cytotoxic effector molecules and cytokine producing cells were quantified after immunohistochemical staining in lobular and portal areas of the biopsies. The intralobular number of CD8+ T-lymphocytes was significantly decreased in biopsies of patients with high ALT ( r  = −0.54; P  < 0.001). Higher ALT-values were correlated with increased numbers of granzyme+ cells in portal areas ( r  = 0.65; P  < 0.001) and higher numbers of intralobular Fas-L+ cells ( r  = 0.32; P  = 0.05). Fas-L was expressed on Kupffer and lymphoid cells. More intralobular CD8+ T-lymphocytes were found in HBeAg− than in HBeAg+ patients ( P  = 0.002). But IFN- γ and TNF- α producing cells were observed sporadically in chronic HBV patients. Hence, in chronic HBV infection, low viral replication and HBeAg negativity is related to increased presence of intralobular CD8+ T-lymphocytes. Persistence of the virus may be caused by the absence of cells producing anti-viral cytokines in the liver. Inflammatory liver injury during chronic HBV infection is probably not the result of increased numbers of infiltrating CD8+ T-lymphocytes, but of Fas-L expression by Kupffer cells and increased cytolytic activity of cells in portal areas.     

免疫耐受期和非活动复制期乙型肝炎病毒感染者的肝脏病理与临床特征

目的了解免疫耐受期和非活动复制期HBV感染者的肝脏病理与临床特征,以及它们的区别。方法分析和比较54例免疫耐受期和47例非活动复制期HBV感染者年龄、性别、血清HBV DNA水平、肝脏炎症活动度及纤维化程度、肝脏HBsAg和HBcAg表达情况。并对不同血清ALT水平的肝脏炎症活动度及纤维化程度进行比较。结果两组患者性别构成比无明显差异,但非活动复制期HBV感染者年龄明显高于免疫耐受期[分别为（28．11±8．60）和（24．93±7．21）岁, P〈0．05]。免疫耐受期患者血清HBV DNA水平较高,106拷贝／ml以上者占94％,而89％的非活动复制期患者血清HBV DNA为阴性,其余患者表现为低水平复制。两组患者肝脏炎症活动度、HBsAg和HBcAg的表达无明显差异,但非活动复制期患者纤维化程度明显高于免疫耐受期（u=2．004, P〈0．05）。血清ALT在正常范围内较高水平患者的肝脏纤维化程度明显高于低水平患者（u=3.274, P〈0．01）。结论非活动复制期HBV感染者可能经历多次隐匿的免疫清除过程,因此年龄较大、纤维化程度较高。ALT持续处于正常范围内的较高水平患者可能纤维化程度较重,建议行肝脏病理学检查。     

外周血淋巴细胞亚群在慢性HBV感染过程中表达的变化分析

目的探讨HBV感染患者外周血淋巴细胞亚群在疾病进展过程中的表达变化。方法选取2018年1月-2019年4月在天津市第二人民医院住院的慢性HBV感染患者共132例,其中慢性乙型肝炎患者47例,乙型肝炎肝硬化患者44例,乙型肝炎肝硬化相关原发性肝癌患者41例。另选取同期健康体检者42例作为对照组。采用流式细胞术检测4组外周血淋巴细胞亚群精准计数,比较4组外周血淋巴细胞亚群的表达水平。正态分布的计量资料,组间方差不齐采用Welch方差分析,两两比较采用GamesHowell检验。非正态分布的计量资料多组间及进一步两两比较采用Kruskal-Wallis H检验。计数资料组间比较采用χ2检验。相关性分析采用Spearman检验。结果与对照组和慢性乙型肝炎组相比,肝硬化组和肝癌组CD3^+、CD4^+T淋巴细胞数量明显减少,差异均有统计学意义(P值均<0.05)。与对照组相比,肝癌组CD8^+T淋巴细胞数量明显减少,差异有统计学意义(P<0.05);与慢性乙型肝炎组相比,肝硬化组和肝癌组CD8^+T淋巴细胞数量明显减少,差异均有统计学意义(P值均<0.05)。与对照组和慢性乙型肝炎组相比,肝硬化组和肝癌组CD19^+B淋巴细胞数量明显减少,差异均有统计学意义(P值均<0.05)。与对照组相比,肝硬化组和肝癌组CD16^+CD56^+NK细胞数量明显减少,差异均有统计学意义(P值均<0.05);与慢性乙型肝炎组比较,肝癌组CD16^+CD56^+NK细胞数量明显减少,差异有统计学意义(P<0.05)。4组疾病进展与外周血CD3^+T淋巴细胞、CD4^+T淋巴细胞、CD8^+T淋巴细胞、CD19^+B淋巴细胞、CD16^+CD56^+NK细胞呈明显负相关(r值分别为-0.414、-0.503、-0.269、-0.435、-0.402,P值均<0.01)。结论随着疾病的进展,慢性HBV感染患者免疫状态发生变化。外周血淋巴细胞亚群精准计数能够反应机体的免疫状态,可作为慢性HBV感染临床病情演变、治疗效果及疾病预后的参考依据。     

Chronic hepatitis B: The interplay between intrahepatic lymphocyte population and viral antigens in relation to liver damage

In Chronic hepatitis B (CHB) infection, virus and immune response interplay is thought to be responsible for pathogenesis. Yet, the impact of each immune cell population and viral protein expression in liver damage is still unknown. Our aim was to study the interplay between intrahepatic immune response and viral activity in relation to CHB liver damage. Immunostaining was performed in 29 liver biopsies from untreated CHB patients to characterize liver infiltrate [Th (CD4+), CTL (CD8+), Treg (FoxP3+), Th17 (IL‐17A+) and Th1 (T‐bet+)] and viral antigen expression (HBsAg and HBcAg). Inflammatory activity and fibrosis were assessed using the HAI and METAVIR scoring system. All studied populations were identified in the portal‐periportal (P‐P) areas with a CD4+ lymphocyte predominance, while only CD8+ and FoxP3+ cells were observed in the intralobular area. Both P‐P CD4+ and intralobular CD8+ cell frequencies were increased among severe hepatitis cases. Concerning HBsAg and HBcAg expression, a mutually exclusive pattern was observed. HBcAg was mainly detected among HBeAg‐positive patients and was associated with hepatitis severity and higher frequency of P‐P FoxP3+, intralobular CD8+ and FoxP3+ cells. HBsAg was identified among HBeAg‐negative cases with less severe hepatitis grade and lower frequency of P‐P CD4+ and intralobular FoxP3+ lymphocytes. In conclusion, the HBV antigen profile expression seen during CHB infection may be reflecting different stages of viral replication which impacts the host immune response and liver damage process. While HBcAg might be an inducer of a regulatory microenvironment, the intralobular CTL population seemed to have a key role in hepatitis severity.     

乙型肝炎病毒转基因小鼠免疫耐受状态及血液生物化学指标的研究

目的 了解HBV转基因鼠HBV基因的复制表达和免疫耐受状态,为探讨乙型肝炎发病机制和抗HBV新药评价提供可靠的参考依据.方法 选取遗传背景相同的SPE级HBsAg阴性非转基因鼠和转基因鼠.化学发光法检测HBsAg、HBeAg、HBV DNA,ELISA检测前S1、HBcAg,肝组织行病理学检查,免疫组织化学染色检测不同时期转基因鼠肝HBsAg表达,流式细胞仪检测小鼠淋巴细胞增殖情况,酶联免疫斑点检测(ELISPOT)分泌IFNγ的T淋巴细胞斑点数,双色免疫荧光法检测脾细胞悬液和脾树突状细胞(DC)中Toll样受体(TLR)2和TLR9的表达.数据行t检验和F检验.结果 HBV转基因鼠可复制表达HBsAg、前S1、HBeAg、HBcAg和HBVDNA,而抗-HBs、抗-HBc、抗-HBe均阴性;肝组织无明显病理改变,肝细胞中HBsAg在胞质表达,HBcAg在胞核表达.HBsAg刺激后,HBV转基因鼠T淋巴细胞增殖能力为(697.6±67.3)cpm,显著低于非转基因鼠的(1315.5±191.6)cpm.经HBsAg刺激后,HBV转基因鼠脾细胞分泌IFNγ的T淋巴细胞斑点数为8.25±1.10,低于非转基因鼠的28.50±4.21(F=155.967,P=0.000).HBV转基因DC表达CD11c+、TLR2和TLR9与非转基因鼠比较,差异无统计学意义(均P＞0.05).在18日龄胎鼠和1日龄仔鼠肝组织观察到HBsAg表达.结论 HBV转基因鼠有HBV相关抗原表达,并对HBV相关抗原存在免疫耐受,其先天和获得性免疫功能均正常,类似于人类慢性HBV无症状携带者.HBV转基因鼠是比较理想的动物模型.     

Activation and function of hepatic NK cells in hepatitis B infection: an underinvestigated innate immune response

Natural killer (NK) cells are abundant in the normal liver, accounting for around one-third of intrahepatic lymphocytes and are important in the defence against hepatitis B virus (HBV) infection as innate immune responses. In this review, we discuss the mechanisms of hepatic NK cell activity against HBV. Whether directly activated by HBV infection or indirectly activated by other lymphocytes such as NKT cells or antigen-presenting cells (APCs), hepatic NK cells exert their anti-viral functions by natural cytotoxicity and production of high levels of cytokines. However, activated NK cells play an important role in regulating adaptive immune responses by interaction with other lymphocytes such as T, B and APCs. In addition, NK cells may contribute to the lymphocyte-mediated liver injury during HBV infection that was previously considered to be mediated only by CD8+ T cells or/and NKT cells.     

Treating Immune‐tolerant Hepatitis B

Hepatitis B virus (HBV) infection is a major cause of cirrhosis and hepatocellular carcinoma worldwide. On the basis of virus–host interactions, the natural history of HBV carriers can be divided into four chronological phases. In the first immune tolerance phase, HBV carriers are positive for hepatitis B e antigen (HBeAg) and have high HBV replication activity, normal ALT levels as well as minimal liver disease. Ample evidence has shown that patients in the immune tolerance phase have very low viral evolution and minimal risk of fibrosis progression. However, recent immunological studies argued that HBV‐specific immune responses already exist in a proportion of immune‐tolerant patients and the immune activities are comparable to those in the immune clearance phase. Regarding antiviral therapy, whether these immune‐tolerant patients are indicated for treatment remains debated. Previous studies showed that HBeAg‐positive patients with normal or near‐normal ALT levels, who are assumed to be in the immune tolerance phase, have a lower HBeAg seroconversion rate receiving either pegylated interferon or nucleos(t)ide analogue treatment. The latest clinical trial focusing on‐treatment response of immune‐tolerant patients with tenofovir disoproxil fumarate‐based therapy also confirmed the results. The HBeAg seroconversion rates are <5% at 4 years of treatment. Considering the minimal risk of disease progression and low treatment response rates in immune‐tolerant patients, current antiviral therapy should not be recommended unless the patients have advanced liver fibrosis. In addition, novel agents targeting the HBV template known as covalently closed circular DNA and aiming to reduce or eliminate it are urgently required.     

慢性乙型肝炎病毒感染免疫耐受期患者的临床病理特征

目的:了解HBV慢性感染免疫耐受期患者的临床及病理学特征．方法:分析HBV感染不同时期380例患者的年龄、母婴垂直传播感染途径、乙肝家族史、肝细胞内HBsAg、HBcAg表达状况及肝组织病理学特征．结果:HBV慢性感染免疫耐受期患者年龄 16岁以下占61．8％,母婴垂直传播感染者占 55．0％,有乙肝家族史患者占46．6％,免疫耐受期患者89例肝组织内HBcAg阳性表达率 78．7％,均明显高于免疫活动期及感染非活动状态患者(x2=38．73,49．08,17．2,31．69, P<0．01)．免疫耐受期16岁以下的患者肝组织内HBsAg及HBcAg阳性表达率最高,分别占64．3％(45／75)和72．9％(51／79),显著高于免疫活动期和非活动HBV携带状态患者(x2= 17．51,31．17,P<0．001)．免疫耐受期16岁以上的患者肝组织内HBsAg及HBcAg阳性表达率最低,分别占35．7％(25／75)和27．1％(19／70),显著低于免疫活动期和非活动HBV携带状态患者(x2=17．51,x2=31．17,P<0．001)．结论:HBV慢性感染免疫耐受期患者中16岁以下者,母婴垂直传播感染者及乙肝家族史者所占比例明显高;HBV在肝组织复制表达以免疫耐受期患者最多,且16岁以下的患者占多数．     

Parallel decline of CD8＋CD38＋ lymphocytes and viremia in treated hepatitis B patients

AIM:To assess the peripheral T lymphocyte subsets in chronic hepatitis B virus(HBV) infection,and their dynamics in response to adefovir dipivoxil monotherapy.METHODS:Proportions and absolute counts of peripheral natural killer cells,B cells,CD8+,CD4+,CD8+ CD38+,CD8+CD28+ and CD4+CD28+ T cells were determined using three-color flow cytometry in chronic hepatitis B patients(n = 35),HBV carriers(n = 25) and healthy controls(n = 35).Adefovir dipivoxil was initiated in 17 chronic hepatitis B patients who were r...