血脂康胶囊临床应用中国专家共识（节选）

背景 近年来,血脂异常成为导致心血管疾病的重要原因。2002年中国居民营养与健康状况调查显示,中国血脂异常者达1．6亿。我国一项队列研究表明,总胆固醇（TC）和低密度脂蛋白胆固醇（LDL—C）升高是我国冠心病的独立危险因素。因此,干预血脂异常是防治心血管疾病的重要措施。     

血脂异常症的治疗

心血管疾病是当今社会患病率和病死率最高的疾病。其中血脂异常是心血管疾病发生发展的重要危险因素之一,因此,干预血脂异常是预防和治疗心血管疾病的重要措施。     

血脂水平评价与疾病相关性分析

动脉粥样硬化性心血管疾病是全球范围内对人类健康危害最为严重的疾病之一。血脂异常是心血管病的重要危险因素”。对血脂异常及时进行合理干预．从而达到一级预防或二级预防的目的，是降低心血管疾病发病率和死亡率的重要手段。     

糖尿病患者的血脂管理

血脂异常特别是高胆固醇血症是动脉粥样硬化性心血管疾病的重要危险因素,当2型糖尿病患者并存血脂异常时其发生心血管事件的危险性进一步增高。因此,对于2型糖尿病患者应常规检测血脂水平。对于存在血脂异常的患者应予以及时有效的干预。改善生活方式应成为伴有血脂异常的2型糖尿病患者的基础治疗,其主要措施包括：控制饮食总热量摄入;减少饱和脂肪酸、反式脂肪酸和胆固醇摄人;     

官兵体检中血脂异常的诊断治疗问题及对策

<正>作为动脉粥样硬化性疾病和心血管事件的主要危险因素,血脂异常越来越受到关注。因此,血脂异常高危人群的早期发现、定期监测、规范治疗和强化预防,应成为控制心血管疾病发病的重要措施之一。近两年我区部队官兵体检中血脂偏高、脂肪肝均有上升趋势。在平时除积极做好官兵认识血脂异常对     

稳心颗粒改善心律失常的临床观察

心血管疾病已经成为全球主要的疾病负担之一，我国人口众多，老龄化也迅速，同时随着经济的高速增长，生活方式亦发生了巨大的改变，如超重肥胖人数增加，血脂异常增高，生活节奏加快，体育运动减少等这些均导致了我国心血管疾病的发生率急速增长，而心律失常是最常见的心血管疾病，重要的可控制的危险因素。患病人数极为庞大，发病人可在各个年龄段，不论男女性别，可由多种因素而发生，通过临床控制心律失常可显著减少心脏病的发病率或死亡率，因此努力提高心血管疾病的控制率，从而减轻心血管疾病负担是我们亟待研究解决的重要课题。     

中老年人血脂状况与分析

心脑血管疾病近年来呈逐步上升趋势,已成为当前严重危害人类健康和生命的一组疾病。在我国,心血管疾病的死亡率仅次于恶性肿瘤,居第二位[1]。作为冠心病、动脉硬化、脑梗死等疾病的重要因素之一的血脂异常[2],越来越受到人们的重视,特别是中老年人的重视。     

中医“治未病”思想在血脂异常社区管理中的应用探讨

正近年来,随着冠心病发病率和死亡率的逐步上升,心血管疾病已经成为我国城市和乡村人群的第一位死亡原因。大量研究表明,血清总胆固醇和低密度脂蛋白胆固醇的升高是冠心病和缺血性脑卒中等心脑血管疾病的独立危险因素之一[1]。血脂异常的预防与治疗显得迫切而重要。作为一名社区中医师,我们有责任发挥中医药特长特色,运用中医"治未病"理论,探索中医特色预防保健服务体系,提高血脂异常的控制率。     

澄清认识误区防治高脂血症

近年来,我国人群血脂异常检出率明显增高。椐一项流行病学调查显示,我国35岁以上人群约有23．5％血液中的胆固醇超过正常水平。血脂异常是引发心肌梗死和中风的重要危险因素之一,我国每年死于心血管疾病的人数为300万左右,应引起足够重视。但公众对血脂异常造成的健康损害,特别是对心血管的影响普遍认识不足,     

血脂代谢与心血管的发生关系

目的 探讨各项血脂指标与心血管疾病发生发展的关系,及其疾病的临床预测价值,为心血管疾病的一、二级预防提供一定的依据.方法 选取某大学附属医院门诊诊治的血脂异常患者100例及进行体检的健康人40例作为研究对象,其中血脂异常组患者根据血脂异常的程度分为极高危、高危、中危及低危组,通过各组比较,探讨各项血脂指标及其相应比值与心血管疾病的相关性.结果 经过统计学分析,血脂异常组患者的总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、非高密度脂蛋白胆固醇（n-HDL-C）、载脂蛋白B（apoB）、TC/HDL-C、apoB/apoA1、LDL-C/HDL-C的值均较健康人群显著升高,且在血脂异常极高危组中apoB/apoA1比值显著高于低中高危组患者;在血脂异常患者中与心血管疾病相关的指标主要有三酰甘油（TG）、TC、LDL-C、n-HDL-C、apoB、TC/HDL-C、LDL-C/HDL-C、apoB/apoA1均呈现正相关关系.结论 血脂异常患者,其单项血脂及相关的血脂比值均明显高于健康人群,在极高危的血脂异常组apoB、TC/HDL-C、LDL-C/HDL-C、apoB/apoA1均高于低中高危组患者,结果表明通过检查血脂比值的大小对预测心血管事件有着重要的临床意义,可以作为预测心血管事件的重要指标.     

透过现象看本质：腺癌国际新分类更有利于肺癌个体化治疗吗?

国际肺癌研究协会（International Association for the Study of Lung Cancer,IASLC）／美国胸科学会（American Thoracic Society,ATS）／欧洲呼吸学会（European Respiratory Society,ERS）于今年2月份颁布了肺腺癌的国际多学科分类新标准（Travis,et al．JTO 2011）。     

Effect of ALA-PDT on the expressions ofMMP-9, MMP-13 TIMP-1 of hypertrophic scar model in rabbit ears

Objective： To investigate the effect of 5-aminolevulinic （ALA）-photodynamic therapy （PDT） on the expressions of MMP-9, MMP-13 and TIMP-1 of hypertrophic scar model in rabbit ears, and analyze the possible therapeutic mechanisms of ALA-PDT treatment to hypertrophic scars of rabbit ears. Methods： The experimental animals were randomly divided into normal control negative control, high concentration of ALA-PDT, low concentration of ALA-PDT and PDT groups. The latter three groups received ALA-PDT treatment or PDT treatment once a week for 3 weeks. The specimens of the rabbits were collected respectively 1, 2 and 3 months after treatment to be used for RT-PCR and Western-blot test. Results： 1, 2 and 3 months after PDT treatment, the expressions of MMP-9 and MMP-13 （including mRNA and protein） in hypertrophic scar tissues of three treatment groups were significantly higher than those of the negative control group （P〈0.01）, and the expression of TIMP-1 mRNA and protein of three treatment groups were significantly lower than that of the negative control group （P〈0.01）. There were also significant differences between high-concentration ALA-PDT treatment group and the low one （P〈0.05）. Conclusion： ALA-PDT is effective in treating hypertrophic scars of rabbit ears, and its possible therapeutic mechanisms are that ALA-PDT treatment generates oxidation activation effect to activate the activity of MMPs and induces the photoaging of fibroblasts of hypertrophicscar tissues of rabbit ears to inhibit the activity of TIMPs, which causes the up-regulation of MMPs and the down-regulation of TIMPs. Because of this, the degradation of collagen and ECM is accelerated and the formation of scars is suppressed     

基于SUV的PET对 4周期化疗后的弥漫大B细胞淋巴瘤患者预后的评估

在过去的十来年中,18氟脱氧葡萄糖（fluorodeoxyglucose,FDG）PET已经成为多种淋巴瘤疗效评价的有力工具,它主要通过视觉分析来评估疗效。修订后的判读标准适合评估化疗结束后的疗效。而不适用于化疗期间的疗效评价。     

HIV-Specific IL-2^＋ and/or IFN-γ^＋ CD8^＋ T Cell Reponses during Chronic HIV-1 Infection in Former Blood Donors

Objective Conflicting data have been generated from previous studies to determine which kind of relationship exists between HIV-1 specific CD8 Tcell responses and HIV-1 viral load or CD4 count over the course of infection.In this study,153 HIV-1 infected LTNPs were enrolled to investigate the role of HIV-1 specific CD8 T-cell responses in chronic HIV-1 infection among HIV-1 infected former blood donors.Methods The patients were stratified into three groups according to CD4 count：CD4≥500 cells/μL;350 cells/μL≤CD4〈500 cells/μL;CD4〈350 cells/μL.PBMCs were isolated from the patients＇ anticoagulated blood samples.IL-2 and IFN-γ secretions of CD 8 T cells against 17 HIV-1 consensus B full peptide pools were analyzed by using ICS assay.Results An overall inverse correlation were observed between CD4 count and plasma viral load.Although no significant difference was observed during the comparisons of frequency/breadth of HIV-1 specific CD8 T cell responses,CD4 count stratification analysis showed that different correlation pattern existed in three strata：as for patients whose CD4 counts were less than 350 cells/μL,no significant correlations were identified between frequency/breadth of HIV-1 specific CD8 T cell responses and CD4 count/viral load;as for patients whose CD4 counts ranged from 350 cells /μL to 500 cells/μL,significant correlation was only observed between the response breadth of IL-2＋IFN-γ＋ CD8 T cells and CD4 count;however,as for patients whose CD4 counts were more than 500 cells/μL,direct correlations were identified between IL-2＋IFN-γ＋/IL-2＋/IFN-γ＋ CD8 T cells and viral load or CD4 count.Conclusions Universal consistent inverse correlation was only indentified between CD4 count and viral load.The relationship between HIV-1 specific CD8 T cell responses and CD4 count/viral load varied in different CD4 strata,which showed that better preserved CD4 T cells were correlated with better CD8 T cell functions.     

吉非替尼或紫杉醇-卡铂治疗肺腺癌

1文献来源 Mok TS, Wu YL, Thongprasert S, et at.Gefitinib or Carboplatin-Paclitaxel in pulmonaryadenocarcinoma [J]. N Engl J Med, 2009,361（10）：947-957.     

脑胶质瘤放化疗后复发和假性进展的鉴别

1病历摘要 患者男性,66岁,因“右颞间变型少突星形细胞瘤Ⅲ级术后10个月”入院。患者曾于2012—03．23因“左下肢乏力3天,伴全身抽搐1次”收住我院神经外科。2012—04—16在全麻下行右颞开颅肿瘤切除术,     

Competition between TRAF2 and TRAF6 Regulates NF-κB Activation in Human B Lymphocytes

Objective To investigate the role of TNF receptor-associated factor 2 （TRAF-2） and TRAF6 in CD40-induced nuclear factor-κB （NF-κB） signaling pathway and whether CD40 signaling requires TRAF2. Methods Human B cell lines were transfected with plasmids expressing wild type TRAF2 or dominant negative TRAF2,TRAF2-shRNA,or TRAF6-shRNA. The activation of NF-κB was detected by Western blot,kinase assay,transfactor enzyme-linked immunosorbent assay （ELISA）,and fluorescence resonance energy transfer （FRET）. Analysis of the role of TRAF-2 and TRAF-6 in CD40-mediated NF-κB activity was examined following stimulation with recombinant CD154. Results TRAF2 induced activity of IκB-kinases （IKKα,IKKi/ε）,phosphorylation of IκBα,as well as nuclear translocation and phosphorylation of p65/RelA. In contrast,TRAF6 strongly induced NF-κB activation and nuclear translocation of p65 as well as p50 and c-Rel. Engagement of CD154-induced nuclear translocation of p65 was inhibited by a TRAF6-shRNA,but conversely was enhanced by a TRAF2-shRNA. Examination of direct interactions between CD40 and TRAFs by FRET documented that both TRAF2 and TRAF6 directly interacted with CD40. However,the two TRAFs competed for CD40 binding. Conclusions These results indicate that TRAF2 can signal in human B cells,but it is not essential for CD40-mediated NF-κB activation. Moreover,TRAF2 can compete with TRAF6 for CD40 binding,and thereby limit the capacity of CD40 engagement to induce NF-κB activation.     

Protective effect of autophagy inhibition on ischemia-reperfusioninduced injury of N2a cells

Autophagy is a conserved and programmed catabolic process that degrades damaged pro- teins and organelles. But the underlying mechanism and functions of autophagy in the ische- mia-reperfusion （IR）-induced injury are unknown. In this study, we employed simulated IR of N2a cells as an in vitro model of IR injury to the neurons and monitored autophagic processes. It was found that the levels of Beclin-1 （a key molecule of autophay complex, Beclin-1/elass III PI3K） and LC-3 II （an autophagy marker） were remarkably increased with time during the process of ischemia and the process of reperfusion after 90 min of ischemia, while the protein kinases pTOS6K and roTOR which are involved in autophagy regulation showed delayed inactivation after reperfusion. Admini- stration of 3-methyladenine （3MA）, an inhibitor of class III PI3K, abolished autophagy during reper- fusion, while employment of rapamycin, an inhibitor of mTORC1 （normally inducing autophagy）, surprisingly weakened the induction of autophagy during reperfusion. Analyses of mitochondria function by relative cell viability demonstrated that autophagy inhibition by 3-MA attenuated the de- cline of mitochondria function during reperfusion. Our data demonstrated that there were two distinct dynamic patterns of autophagy during IR-induced N2a injury, Beclin-1/class III PI3K com- plex-dependent and mTORCl-dependent. Inhibition of over-autophagy improved cell survival. These suggest that targeting autophagy therapy will be a novel strategy to control IR-induced neuronal damage.     

学术自述

1978年,我调往中国社会科学院哲学研究所。到了哲学所,我面临着科研方向的重要抉择。我决定选择科学哲学和生命伦理学作为我今后科研的主要方向。由于闭关多年,我们对世界科学哲学的长足发展一无所知,对波普尔、库恩等科学哲学家一无所知。实际上,自然辩证法是中国马克思主义派的科学哲学,但不参加科学哲学的国际对话,是无法进一步发展自己的。对新出现的生命伦理学这一新领域也一无所知。     

Protective Effects of Sphingosine 1-phosphate and FTY720 on Rat Pulmonary Microvascular Endothelial Cells Stimulated by TNFα

Objective In this study, the effects of sphingosine 1-phosphate （S1P） and its analogue FTY720 on lactate dehydrogenase （LDH）, prostacyclin and PGE2 release, monolayer paracellular permeability, and F-actin structural changes of cultured rat pulmonary microvascular endothelial cells stimulated by TNFα were examined. Methods Rat pulmonary microvascular endothelial cells（rPMECs） were isolated, cultured and identified by immunofluorescent stain of yon Willebrand-associatedan-antigen （vWF）. Incubation with TNFα at a dose of 150 ng/ml for 12 hours induced a significant increase in paracellular permeability determined by measurement of a paracellular solute flux, 3-kDa FD-3. Results PGE2, PGF2α and LDH productions by cell cultures exposed to TNFα for 12 hours increased significantly compared with control cells. Also, the 12-hour exposure to TNFα resulted in reorganization and retraction of the rat pulmonary microvascular endothelial cells that was visible both by phase contrast microscopy and cytoskeletal F-actin stain. Paracellular permeability of the monolayers, PGE2, PGFα and LDH productions were significantly reduced following pretreatment with S 1P or FTY-720. Moreover, S 1P or FTY-720 pretreatment prevented the changes of morphologic and cytoskeletal F-actin induced by TNFa. Conclusion S 1P and FTY-720 can inhibited the LDH, PGF2α and PGE2 release by strengthening the cytoskeleton and protecting the barrier function, and may represent a novel therapeutic method for pulmonary vascular barrier damage.