孩尔来福甲型肝炎灭活疫苗免疫儿童后近期抗体动态观察

为观察孩尔来福 (Healive)甲型肝炎 (甲肝 )灭活疫苗免疫儿童后的抗体水平及下降规律 ,探讨甲肝灭活疫苗诱导的抗体所提供的持续保护时间 ,对曾接种 5 0 0U/剂 (0、3个月和 0、6个月免疫程序 )Healive甲肝灭活疫苗的113名儿童 ,用酶联免疫吸附试验 (ELISA)分别检测免疫后 12、2 4、36个月的血清抗甲肝病毒抗体。结果显示 :至第 36个月检测时 ,10 0 %的儿童甲肝抗体保持阳性 ;0、3个月程序组 74 1% ,0、6个月程序组 85 4 %的儿童甲肝抗体滴度≥ 2 0 0mIU/ml。     

Human immunodeficiency virus 1 favors the persistence of infection by activating macrophages through TNF

Macrophages play a major role in HIV-1 persistence. In the present paper, we demonstrate that the absence of apoptosis in HIV-1-infected primary human monocyte-differentiated macrophages (MDM) correlates with an increase in anti-apoptotic (Bcl-2 and Bcl-x(L)) and a decrease in pro-apoptotic (Bax and Bad) proteins. This is associated with macrophage activation as shown by tumor necrosis factor (TNF) production and NF-kappaB activation upon infection. TNF production was shown to be involved in the upregulation of Bcl-2 and Bcl-x(L) because this increase was abolished by an anti-TNF anti-serum or an inhibitor of TNF synthesis. In parallel, inhibition of TNF production induced an increase in the number of apoptotic cells. Furthermore, using an inhibitor of NF-kappaB activation, we demonstrated that TNF-induced upregulation of Bcl-x(L) and Bcl-2 occurs, respectively, through a NF-kappaB-dependent and an NF-kappaB-independent pathway.     

戊型肝炎病人IgG抗体持续时间观察

[目的 ]　了解本市戊型肝炎病人IgG抗体持续时间情况。　[方法 ]　选择 1992～ 2 0 0 2年本市经临床和血清确诊为戊型肝炎的 497例病人作为本次调查对象。采集调查对象血清用酶联免疫吸附法 (ELISA)检测抗HEV -IgG。　 [结果 ]　调查对象抗HEVIgG总阳性率为 65 .4% ,当年发病者IgG抗体阳性率保持在较高水平 (达 88.9% ) ,随着发病年限的增长 ,发病者的抗HEVIgG基本保持在一个较稳定的水平 (约 60 %上下 ) ;发病者体内 10年后仍有抗HEVIgG(阳性率 3 3 .3 % )。　 [结论 ]　戊型肝炎病人发病后IgG抗体持续时间长短不一 ,一般可以维持较长时间     

Establishment of chronic hepatitis C virus infection:Translational evasion of oxidative defence

Hepatitis C virus(HCV)causes a clinically important disease affecting 3%of the world population.HCV is a single-stranded,positive-sense RNA virus belonging to the genus Hepacivirus within the Flaviviridae family.The virus establishes a chronic infection in the face of an active host oxidative defence,thus adaptation to oxidative stress is key to virus survival.Being a small RNA virus with a limited genomic capacity,we speculate that HCV deploys a different strategy to evade host oxidative defence.Instead of counteracting oxidative stress,it utilizes oxidative stress to facilitate its own survival.Translation is the first step in the replication of a plus strand RNA virus so it would make sense if the virus can exploit the host oxidative defence in facilitating this very first step.This is particularly true when HCV utilizes an internal ribosome entry site element in translation,which is distinctive from that of cap-dependent translation of the vast majority of cellular genes,thus allowing selective translation of genes under conditions when global protein synthesis is compromised.Indeed,we were the first to show that HCV translation was stimulated by an important prooxidant-hydrogen peroxide in hepatocytes,suggesting that HCV is able to adapt to and utilize the host antiviral response to facilitate its own translation thus allowing the virus to thrive under oxidative stress condition to establish chronicity.Understanding how HCV translation is regulated under oxidative stress condition will advance our knowledge on how HCV establishes chronicity.As chronicity is the initiator step in disease progression this will eventually lead to a better understanding of pathogenicity,which is particularly relevant to the development of anti-virals and improved treatments of HCV patients using anti-oxidants.     

Temperament and one-year outcome of gastric bypass for severe obesity

BackgroundThe role of temperament traits in shaping the outcome of gastric bypass for severe obesity has not been established yet. This study evaluated whether temperament traits influence weight loss 1 year after gastric bypass, controlling for the potential confounding effect of Axis I and II disorders.MethodsForty-nine patients with severe obesity (body mass index = 46.4±6.7) undergoing gastric bypass completed a thorough psychiatric evaluation before surgery, including structured interviews, rating scales, and questionnaire assessing the presence and severity of co-morbid Axis I and II disorders. Temperament was evaluated with the Temperament and Character Inventory (TCI). Weight loss 1 year after surgery was calculated as percent total weight loss (%TWL). Predictors of weight loss were investigated with multivariate linear hierarchical regression.ResultsAfter accounting for psychiatric covariates, higher TCI persistence scores independently predicted 1-year outcome of gastric bypass and explained 40% of the variance in %TWL. Patients with low persistence scores showed a significantly lesser weight loss than patients with high scores.ConclusionTemperament traits denoting the ability to persevere in one’s goals in spite of immediate frustration (persistence) are associated with greater weight loss 1 year after gastric bypass. These data suggest the utility of preoperatively assessing and reinforcing such capacity to optimize surgical outcome. Future research will clarify the behavioral mechanisms mediating this relationship as well as the influence of temperament on weight maintenance.     

Adherence to evidence-based statin guidelines reduces the risk of hospitalizations for acute myocardial infarction by 40%: a cohort study.

AIMS: To investigate the 'real world' effectiveness of robust statin therapy, focusing on the effect of dose and early treatment discontinuation on the risk of hospitalization for acute myocardial infarction (AMI). METHODS AND RESULTS: In the PHARMO database, including among others drug-dispensing and hospital discharge records for more than two million subjects in the Netherlands, 59,094 new users of statins in the period 1 January 1991 until 31 December 2004, >or=18 years of age were identified. In these patients, exposure to statins, both in terms of persistence and dose, was determined over the first two treatment years. To determine the risk for AMI, patients were followed from this 2-year time point until the first hospital admission for AMI, death, or end of the study period. A total of 31,557 patients (53%) discontinued statin use within 2 years; 20 883 patients (35%) were persistent users with an average equipotent dose>or=4. A 30% reduction in risk of hospitalization for AMI with persistent statin use was observed. The protective effect increased with a higher dose (20 and 40% risk reduction with an equipotent doseor=4, respectively). CONCLUSION: These results show that statins are suboptimally used in real life for having the maximum benefit in terms of preventing AMI.     

Adherence, Internalization, and Persistence of Helicobacter pylori in Hepatocytes

Although Helicobacter pylori have been identified in the liver, the role of Helicobacter sp. in human liver diseases remains unclear. This study explored whether H. pylori were internalized and could persist in hepatocytes. The majority of an inoculum of H. pylori (1 x 10(7) colony forming units) adhered to hepatocytes. Using the gentamicin invasion assay we found that approximately 2% were internalized and persisted following passage for more than 2 months. Electron microscopy confirmed the presence of intracellular Helicobacter. The number of adherent or internalized H. pylori was significantly greater with hepatocytes than with gastric epithelial cells (P < 0.05) and was also dependent on cag pathogenicity island (PAI), VacA, OipA, or BabA status. Transmission electron microscopy was used to confirm adherence and invasion of H. pylori into hepatocytes. Internalization of H. pylori was inhibited by antibodies to beta1-integrin receptors, genistein, and cytochalasin D (P < 0.05) consistent with beta1-integrin acting as a surface receptor with additional requirements for tyrosine kinase phosphorylation and actin polymerization. In summary, H. pylori both adhered to and invaded into hepatocytes in vitro, depending on the virulent factors, and persisted within hepatocytes during subcultures. beta1-integrin is likely a receptor involved in internalization of H. pylori into hepatocytes.