冠心病患者血清对氧磷酶活性的测定

目的探讨冠心病患者血清对氧磷酶1活性及其与冠心病之间的关系。方法选择冠状动脉造影确诊的冠心病患者106例和非冠心病组62例,用乙酸苯酯法和比色法分别测定两组血脂、血清对氧磷酶1活性、超氧化物歧化酶及丙二醛含量,并进行对比分析。结果冠心病组血清中对氧磷酶1活性和超氧化物歧化酶水平分别为113±64μkat/L和43.8±8.2 kU/L,均较对照组降低(134±72μkat/L和63.4±5.7 kU/L)(P<0.05);而丙二醛含量较对照组升高(9.4±1.8μmol/L比4.1±0.5μmol/L,P<0.01)。对氧磷酶1活性与高密度脂蛋白和超氧化物歧化酶水平呈正相关,与丙二醛水平呈负相关。冠状动脉狭窄者对氧磷酶1活性较无狭窄者明显减低(P<0.001),2、3支血管病变者较1支血管病变者对氧磷酶1活性降低(P<0.05)。结论冠心病患者血清对氧磷酶1活性降低,低对氧磷酶1活性与冠心病严重程度有关。     

苯扎贝特对牛主动脉内皮细胞一氧化氮合酶基因表达的影响及其机制的研究

目的研究过氧化物酶体增生物激活受体α(peroxisomeproliferator-activatedreceptoralpha,PPARα)的配体苯扎贝特对原代牛主动脉内皮细胞(bovineaortaendothelialcells,BAEC)一氧化氮合酶(endothelialnitricoxidesynthase,eNOS)基因表达的影响并探讨其机制。方法分离和培养牛主动脉内皮细胞,采用Northern印迹法、Western印迹法检测苯扎贝特对BAECeNOSmRNA和蛋白质表达的影响,采用定量PCR的方法及NO试剂盒检测苯扎贝特对eNOSmRNA半衰期及NO产生的影响;继而采用Western印迹法,给予不同的信号转导通路抑制剂研究苯扎贝特影响eNOS表达所通过的信号转导途径,此外,构建了由人eNOS启动子驱动的荧光报告基因,研究苯扎贝特对eNOS启动子活性的影响。结果苯扎贝特以浓度(50~200μmol/L)依赖的方式明显上调BAEC细胞eNOS的mRNA和蛋白质表达(P<0.05),并促进一氧化氮(nitricoxide,NO)的生成[对照组(14.97±1.29)μmol/L,苯扎贝特不同浓度组(25.12±1.25)μmol/L,(30.12±1.85)μmol/L,(33.47±1.22)μmol/L],增强eNOS-ser-1179位点的磷酸化表达(P<0.05),但是对eNOS-thr-497位点的磷酸化表达几乎没有抑制作用,定量PCR证实苯扎贝特增加eNOSmRNA的半衰期(从3.1~6.1h),进一步的研究显示苯扎贝特以浓度依赖的方式增加人eNOS启动子驱动的荧光报告基因的荧光活性(相对的荧光活性在100μmol/L和200μmol/L组分别为4429.43±391.41,6187.5±307.53,对照组为3361.81±316.85),增加磷酸化丝裂原激活的蛋白激酶(mitogen-activatedproteinkinase,MAPK)的蛋白质表达(P<0.05及P<0.01),而PPARα、磷脂酰肌醇3-激酶(phosphatidylinositol3-kinase,PI3K)和MAPK抑制剂可明显逆转苯扎贝特对eNOS表达的上调作用(P<0.01)。结论苯扎贝特通过上调eNOS的蛋白质表达、促进eNOS的磷酸化、增强eNOS的转录及eNOSmRNA的稳定性,从而促进NO的生成,其效应的发挥既通过依赖于PPARα的方式,也可以经MAPK和PI3K信号通路介导的不依赖于PPARα的“非基因效应”,揭示了PPARα的配基苯扎贝特的降脂外作用包括抗动脉粥样硬化和抗高血压的可能作用机制。     

冠状动脉再次血运重建患者血清对氧磷酶-1的活性研究

目的了解血清对氧磷酶-1活性水平对再次冠状动脉血运重建的预测价值。方法以比色法测定200例行经皮冠状动脉介入治疗获得完全血运重建患者的血清对氧磷酶-1活性水平。术后随访1年,在首次介入手术后第6个月进行造影随访。将随访期内需要再次血运重建的患者归入再次血运重建组,无需再次血运重建的患者归入单次血运重建组,同期冠状动脉造影排除冠状动脉粥样硬化性心脏病(冠心病)患者100例作为非冠心病对照组。分析各组血清对氧磷酶-1活性水平的差异。结果再次血运重建组62例,单次血运重建组138例。所有患者均完成1年随访,6个月冠状动脉造影复查率88.5%(177/200),12个月造影复查率69%(138/200)。再次血运重建组、单次血运重建组、非冠心病组的血清对氧磷酶-1活性水平值分别为(109.2±98.6)μkat/L、(132.8±79.4)μkat/L、(156.4±82.8)μkat/L,方差分析示3组血清对氧磷酶-1活性水平差异有统计学意义(P0.05)。结论冠心病再次血运重建组血清对氧磷酶-1活性水平低于单次血运重建组和非冠心病对照组,故血清对氧磷酶-1活性水平对预测RCR有重要的价值。     

重组人松弛素对舒张性心力衰竭模型兔心肌组织蛋白激酶G活性的调控

目的探讨重组人松弛素(RLX)对舒张性心力衰竭(DHF)模型兔心肌组织蛋白激酶G(PKG)活性的调控作用。方法采用腹主动脉缩窄术建立DHF模型兔,新西兰家兔28只随机分为假手术组6只、DHF组6只、RLX小剂量组8只[30μg/(kg·d)]、RLX大剂量组8只[98μg/(kg·d)],给药2周。术后第10周,取血清标本,分别采用ELISA法检测钠尿肽、RLX,制备10%心肌匀浆液样本ELISA法测3-硝基酪氨酸(3-NT)、NO、环磷酸鸟苷(cGMP)、PKG。结果与假手术组比较,DHF组、RLX小剂量组、RLX大剂量组血清钠尿肽、心肌匀浆3-NT水平明显升高,NO、cGMP、PKG活性明显降低,差异有统计学意义(P0.05)。与DHF组比较,RLX大剂量组心肌匀浆中NO、cGMP、PKG活性明显升高[(18.70±0.27)μmol/L vs(16.38±0.16)μmol/L,(10.63±0.34)nmol/L vs(9.15±0.27)nmol/L,(528.58±3.66)U/L vs(493.26±5.68)U/L,P0.05],3-NT水平明显降低[(239.98±2.75)μmol/L vs(261.79±4.48)μmol/L,P0.05]。结论大剂量RLX减轻家兔左心室舒张功能可能是通过NO-cGMP-PKG通路减轻DHF模型兔氧化应激反应,提升NO生物学利用度、PKG活性,从而拮抗心肌纤维化,进而减轻左心室的舒张功能障碍。     

经胃肠道给予氯化血红素对压力负荷性心衰大鼠氧化应激状态的影响

目的探讨经胃肠道给予氯化血红素后体内血红素氧合酶-1(HO-1)-CO-胆红素的反应和对大鼠慢性压力负荷性心力衰竭进程中氧化应激的影响。方法成年雄性SD大鼠63只,随机分为血红素组、心衰组和对照组,每组21只,各组再分为4、8、12周三个小组,每小组7只。心衰组、氯化血红素组行腹主动脉缩窄术,对照组行假手术。从术后3周开始血红素组以60mg/(kg·d)氯化血红素灌胃,对照组和心衰组同时间灌以同体积生理盐水。各小组在相应的时间点检测血清HO-1、碳氧血红蛋白(COHb)、丙二醛(MDA)、氧化低密度脂蛋白(ox-LDL)的含量,检测血清超氧化物歧化酶(SOD)的活性。结果 (1)氯化血红素组在给药后4、8、12周血清HO-1含量明显高于心衰组,分别是(6.80±0.92)μg/Lvs(2.5±0.22)μg/L;(10.70±0.69)μg/Lvs(4.50±0.28)μg/L;(13.30±0.99)μg/Lvs(6.07±0.71)μg/L(P0.01);COHb含量均明显高于心衰组,分别为(4.34±0.31)%vs(1.68±0.11)%;(6.32±0.44)%vs(2.46±0.20)%;(7.80±0.39)%vs(3.01±0.42)%(P0.01)。(2)氯化血红素组在给药4、8、12周血清MDA含量均低于心衰组,分别为(8.3±1.3)μmol/Lvs(14.2±2.3)μmol/L(P0.05);(9.6±0.5)μmol/Lvs(20.2±3.2)μmol/L(P0.01);(11.8±1.1)μmol/Lvs(26.1±3.7)μmol/L(P0.01);(3)氯化血红素组SOD活性在4、8、12周均高于心衰组,分别是(125±6)kU/Lvs(95±10)kU/L(P0.01);(109±9)kU/Lvs(67±5)kU/L(P0.01);(72±10)kU/Lvs(40±6)kU/L(P0.01)。(4)氯化血红素组ox-LDL含量在4、8、12周均低于心衰组,分别为(1.14±0.16)μmol/Lvs(1.80±0.22)μmol/L;(1.38±0.14)μmol/Lvs(2.34±0.25)μmol/L;(1.83±0.16)μmol/Lvs(3.17±0.31)μmol/L(均P0.01)。结论经胃肠道给予氯化血红素可以对体内的HO-1产生诱导作用;HO/CO-胆红素系统的诱导可改善压力负荷心衰大鼠的体内氧化/抗氧化失衡状态。     

老年脑梗死患者血清对氧磷酶1活性与氧化应激的关系及其在动脉粥样硬化中的作用

目的 探讨老年脑梗死患者血清对氧磷酶1活性与氧化应激的关系及其在动脉粥样硬化中的作用.方法 通过DSA检查确诊颈动脉狭窄的老年脑梗死患者72例作为研究对象(其中轻度狭窄33例,中度狭窄24例,重度狭窄15例),以非脑血管病健康体检者38例作为对照组,用分光光度计法、黄嘌呤氧化酶法和硫代巴比妥酸反应物质法分别测定血清对氧磷酶1活性、超氧化物歧化酶和丙二醛含量,分析对氧磷酶1活性与超氧化物歧化酶、丙二醛之间的关系.结果 脑梗死组患者血清对氧磷酶1活性(95.62±18.26 ku/L)和超氧化物歧化酶含量(69.59±10.56 ku/L)显著低于对照组(分别为168.36±27.82 ku/L和98.34±13.42 ku/L,P<0.01],而丙二醛含量(24.46±5.68nmol/L)显著高于对照组(15.64±8.26 nmol/L,P<0.01).轻度、中度和重度狭窄组患者对氧磷酶1活性(分别为112.48±19.32、98.64±10.84和81.95±13.42 ku/L)、超氧化物歧化酶(分别为80.62±13.26、70.26±14.09和58.82±10.06ku/L)和丙二醛含量(分别为19.52±8.48、23.56±9.81和27.28±9.89nmol/L)差异均有显著性(均P<0.01),并且对氧磷酶1活性和超氧化物歧化酶含量随颈动脉狭窄程度加重,呈逐渐下降的趋势,而丙二醛含量随颈动脉狭窄程度加重呈上升趋势.相关分析表明,对氧磷酶1活性与超氧化物歧化酶含量正相关(r=0.628,P<0.01),而与丙二醛含量负相关(r=－0.541,P<0.01).结论 老年脑梗死患者血清对氧磷酶1活性降低及氧化应激增强,对氧磷酶1活性和氧化应激及其复杂的相互作用参与动脉粥样硬化发生和发展.     

苯扎贝特对兔动脉粥样硬化单核细胞趋化因子的影响

目的探讨苯扎贝特对兔动脉粥样硬化（AS）时单核细胞趋化因子（MCP-1）的影响。方法 24只新西兰大白兔随机分为高脂组、苯扎贝特组和正常对照组,每组8只。对照组饲以常规颗粒饲料,高脂组饲以高胆固醇饲料（1%胆固醇＋5%猪油的颗粒饲料）,苯扎贝特组饲以高胆固醇饲料加苯扎贝特[5mg/（kg·d）],共饲养4个月。HE染色检测免胸主动脉AS程度,并用免疫组化检测AS斑块的MCP-1蛋白及RT-PCR检测MCP-1 mRNA的转录水平,同时检测血胆固醇和甘油三酯的浓度。结果与高脂组比较,苯扎贝特显著降低了甘油三酯的浓度[（0.71±0.11）vs（1.72±0.96）mmol/L,P〈0.05]。在苯扎贝特组动脉粥样硬化的程度明显减轻,动脉内膜面积减少[（2.92±0.54）vs（4.16±0.98）mm~2,P〈0.05]。苯扎贝特治疗组斑块内的MCP-1蛋白表达减少[（19.8±2.2）%vs（26.2±3.1）%,P〈0.01],RT-PCR结果显示,苯扎贝特组MCP-1 mRNA的水平亦明显减少[（0.61±0.06）vs（1.06±0.06）,P〈0.05]。结论使用苯扎贝特明显减轻了动脉粥样硬化程度,其中MCP-1基因及蛋白表达的下降具有重要的作用。     

老年冠心病患者血清对氧磷酶活性分析

目的:了解老年人血清对氧磷酶(PON1)活性及其与冠心病(CHD)之间的关系。方法:冠状动脉造影确诊的CHD患者106例(老年组62例,非老年组44例),用乙酸苯酯法和比色法分别测定老年组和非老年组血脂、血清PON1活性、超氧化物歧化酶(SOD)及丙二醛(MDA)含量并进行对比分析。结果:老年CHD患者PON1活性为(103±84)μkat/L,SOD为(43.6±5.7)kU/L,MDA为(9.8±1.6)μmol/L,均显著低于非老年组的(121±75)μkat/L,(54.2±6.1)kU/L,(5.5±0.8)μmol/L(均P<0.01),PON1活性与HDL、SOD呈正相关(r=0.392、r=0.485,P<0.05),与MDA呈负相关(r=-0.426,P<0.05),与其余血脂无相关性。结论:CHD患者PON1活性均呈减少趋势,老年患者血清PON1活性更低。     

非诺贝特对脂肪组织凝血和纤溶因子表达的影响

目的:探讨动脉粥样硬化兔脂肪组织组织因子(TF)和Ⅰ型纤溶酶原激活物抑制剂(PAI-1)表达及非诺贝特对其的影响。方法:15只兔随机等分为3组,正常组予普通饲料喂养12周,动脉粥样硬化组给予高胆固醇饮食12周,非诺贝特组在高胆固醇饮食8周后加非诺贝特30mg·kg-1·d-1干预4周。实验第12周末取兔皮下脂肪组织,RT-PCR测定脂肪组织TF和PAI-1mRNA表达;同时采血10ml,分离血浆,用ELISA方法测定血浆TF活性,发色底物法测定血浆PAI-1活性。结果:高胆固醇饮食可显著升高血清总胆固醇(TC)(P<0·05),血清三酰甘油(TG)无明显升高;加用非诺贝特治疗4周,TC和TG均无明显改变。动脉粥样硬化组脂肪组织TF和PAI-1mRNA表达(分别为1.15±0.01和1.20±0.01)明显高于正常组(分别为1.03±0.01和1.10±0.01),均P<0·01;血浆TF和PAI-1活性[分别为(74.4±28.8)ng/L和(15.6±1.9)×103AU/L]较正常组[分别为(33.1±10.7)ng/L和(6.9±0.9)×103AU/L]增高(P<0·05)。非诺贝特组TF和PAI-1mRNA表达(分别为1.02±0.01和1.06±0.01)、血浆TF和PAI-1活性[分别为(40.3±12.2)ng/L和(7.5±1.5)×103AU/L]均有显著降低(P<0.01或P<0·05)。结论:动脉粥样硬化兔脂肪组织表达TF和PAI-1增加,活性增强,非诺贝特能抑制动脉粥样硬化兔脂肪组织TF和PAI-1的表达及活性,提示非诺贝特可能具有独立于降脂作用之外的抗血栓作用。     

非诺贝特对高胆固醇喂养兔主动脉斑块面积和肿瘤坏死因子α的影响

目的利用高脂饮食诱发动脉粥样硬化模型,观察非诺贝特的抗动脉粥样硬化作用,并探讨其机制。方法10只新西兰大白兔给予高胆固醇饮食饲养8周后,随机分为两组:高胆固醇组继续饲以高胆固醇饲料4周;非诺贝特组在饲以高胆固醇饲料的基础上给予非诺贝特[30 mg/(kg.d)],共4周。另选择普通饮食12周兔(n=5)作为对照组。测定饲养前后血清肿瘤坏死因子α水平和饲养后的主动脉斑块面积。半定量逆转录聚合酶链反应测定脂肪组织肿瘤坏死因子αmRNA的表达。结果非诺贝特组和高胆固醇组血清总胆固醇、低密度脂蛋白胆固醇水平均明显高于对照组(P<0.001),但两组间差异无显著性。非诺贝特组与高胆固醇组相比主动脉斑块面积(52.81%±6.92%比76.30%±8.61%,P<0.01)、血管内膜厚度(28.45±5.68μm比76.18±11.25μm,P<0.05)、血清肿瘤坏死因子α水平(2.11±0.26 ng/L比3.86±0.33 ng/L,P<0.05)以及脂肪组织肿瘤坏死因子αmRNA表达量(0.31±0.05比0.56±0.07,P<0.05)均显著降低。结论非诺贝特具有一定的抗动脉粥样硬化作用,其降低高胆固醇喂养兔血清肿瘤坏死因子α水平可能是其作用机制之一。     

Three layer functional model and energy exchange concept of aging process

Relying on a certain degree of abstraction, we can propose that no particular distinction exists between animate or living matter and inanimate matter. While focusing attention on some specifics, the dividing line between the two can be drawn. The most apparent distinction is in the level of structural and functional organization with the dissimilar streams of ‘energy flow’ between the observed entity and the surrounding environment. In essence, living matter is created from inanimate matter which is organized to contain internal intense energy processes and maintain lower intensity energy exchange processes with the environment. Taking internal and external energy processes into account, we contend in this paper that living matter can be referred to as matter of dissipative structure, with this structure assumed to be a common quality of all living creatures and living matter in general. Interruption of internal energy conversion processes and terminating the controlled energy exchange with the environment leads to degeneration of dissipative structure and reduction of the same to inanimate matter, (gas, liquid and/or solid inanimate substances), and ultimately what can be called ‘death.’ This concept of what we call dissipative nature can be extended from living organisms to social groups of animals, to mankind. An analogy based on the organization of matter provides a basis for a functional model of living entities. The models relies on the parallels among the three central structures of any cell (nucleus, cytoplasm and outer membrane) and the human body (central organs, body fluids along with the connective tissues, and external skin integument). This three-part structural organization may be observed almost universally in nature. It can be observed from the atomic structure to the planetary and intergalactic organizations. This similarity is corroborated by the membrane theory applied to living organisms. According to the energy nature of living matter and the proposed functional model, the decreased integrity of a human body's external envelope membrane is a first cause of the structural degradation and aging of the entire organism. The aging process than progresses externally to internally, as in single cell organisms, suggesting that much of the efforts towards the restoration and maintenance of the mechanisms responsible for structural development should be focused accordingly, on the membrane, i.e., the skin. Numerous reports indicate that all parts of the human body, like: bones, blood with blood vessels, muscles, skin, and so on, have some ability for restoration. Therefore, actual revival of not only aging tissue of the human body's membrane, but the entire human body enclosed within, with all internal organs, might be expected. We assess several aging theories within the context of our model and provide suggestions on how to activate the body's own anti-aging mechanisms and increase longevity. This paper presents some analogies and some distinctions that exist between the living dissipative structure matter and inanimate matter, discusses the aging process and proposes certain aging reversal solutions.     

Unusual responses of nocturnal pineal melatonin synthesis and secretion to swimming: Attempts to define mechanisms

Abstract: The effect of swimming at night on rat pineal melatonin synthesis was compared with that of light exposure at night. Rats were forced to swim at 0030 hr (lights out at 2000 hr) and sacrificed by decapitation 15 and 30 min later, immediately after swimming. Other groups of animals were exposed to white light (650μW/cm²) for 15 and 30 min at same time. Swimming caused a rapid and highly significant drop in the melatonin content in the pineal gland; however, the activity of N-acetyltransferase (NAT), the supposed rate limiting enzyme in the melatonin production, was not changed. Despite the drop in pineal melatonin levels, serum concentrations of the indole remained elevated in the rats that swam. In contrast, melatonin levels in the pineal and serum of light exposed rats fell precipitously, accompanied by a significant suppression of NAT activity. Since we anticipated that the strenuous exercise associated with swimming may induce release of artrial natriuretic peptide (ANP) from the heart, which in turn could cause the release of pineal melatonin, in a second study we injected physiological saline intravenously to stretch the cardiac muscle and release ANP. Three milliliters of normal saline was injected during the day into the jugular vein of anesthetized rats that were pretreated with isoproterenol to stimulate pineal melatonin production. Animals were killed 15 min after the saline injection, and pineal NAT activity and pineal melatonin levels were measured. The saline injections caused no alteration in the elevated levels of either NAT or melatonin. These data suggest that the disparity in pineal NAT activity (which was high) and pineal melatonin (which was low), in animals swum at night, may not be caused by ANP which is released during strenuous exercise such as swimming.     

Melatonin and photoperiodic time measurement: Seasonal breeding in the sheep

Abstract: Well-established circadian physiology supports the view that photoperiodic time measurement utilizes the coincidence between the presence of light and a photosensitive phase of a 'biological clock' to alter reproductive status—the so-called external coincidence model of seasonal breeding. In this review, we examine the mechanism whereby photoperiod interacts with presumed suprachiasmatic nuclei activity to allow endogenous melatonin to normally synchronize reproductive activity to the optimal time of year. The Romney Marsh sheep is particularly explored as an experimental model. It is suggested that the on/off activity of seasonal reproduction may be a robust mechanism able to be predictably manipulated by the judicious use of the light/dark cycle and exogenous melatonin, but firmly based on circadian principles.     

MUTATION FREQUENCY IN NURSES AND PHARMACISTS WORKING WITH CYTOTOXIC DRUGS

Individuals occupationally exposed to cytotoxic drugs may be at risk owing to the effects of these agents on DNA. As an index of DNA damage, in vivo mutations were measured in lymphocytes from 24 oncology nurses or pharmacists and 24 matched controls. Mutation frequency was significantly increased in exposed individuals and appeared to be related to duration of exposure. However, the overall magnitude of the increase was small and its biological significance remains to be determined.     

A single injection of adrenergic agonists enhances pineal melatonin production in Turkish hamsters

Abstract: The purpose of this study was to determine whether the pineal gland of Turkish hamsters (Mesocricetus brandti) responds to adrenergic agonists with an increase in melatonin production, and, if it does, whether the sensitivity of the pineal gland to agonists would differ throughout the dark phase. Adult Turkish hamsters weighing 110–210 g received a subcutaneous injection of isoproterenol (ISO, 1 mg/kg B.W.) or norepinephrine (NE, 1 mg/kg B.W.) at different times of night. Animals exposed to LD 16:8 responded to ISO or NE with increased pineal melatonin content only when injected at dawn, when endogenous melatonin is at basal or near-basal levels. When the 8 hr scotophase was entirely replaced with light, the responsiveness to ISO injections at dawn disappeared. In animals exposed to light from 30 min prior to injection to the time of sacrifice, ISO injections increased pineal melatonin content (P < 0.005, three-way ANOVA), which varied, depending on the specific time of injection (effect of time of night, P < 0.05, three-way ANOVA). These results demonstrate that (1) adrenergic agonists enhance the production of pineal melatonin in Turkish hamsters, (2) this stimulatory effect takes place late, but not early in the 8 hr scotophase, and (3) the adrenergic induction of pineal melatonin production in Turkish hamsters requires priming by darkness during the appropriate circadian phase.     

Immune effector mechanisms in malaria: An update focusing on human immunity

The past decade has witnessed dramatic decreases in malaria‐associated mortality and morbidity around the world. This progress has largely been due to intensified malaria control measures, implementation of rapid diagnostics and establishing a network to anticipate and mitigate antimalarial drug resistance. However, the ultimate tool for malaria prevention is the development and implementation of an effective vaccine. To date, malaria vaccine efforts have focused on determining which of the thousands of antigens expressed by Plasmodium falciparum are instrumental targets of protective immunity. The antigenic variation and antigenic polymorphisms arising in parasite genes under immune selection present a daunting challenge for target antigen selection and prioritization, and is a given caveat when interpreting immune recall responses or results from monovalent vaccine trials. Other immune evasion strategies executed by the parasite highlight the myriad of ways in which it can become a recurrent infection. This review provides an update on immune effector mechanisms in malaria and focuses on our improved ability to interrogate the complexity of human immune system, accelerated by recent methodological advances. Appreciating how the human immune landscape influences the effectiveness and longevity of antimalarial immunity will help explain which conditions are necessary for immune effector mechanisms to prevail.     

Secondary aortoduodenal fistula

Aorto-duodenal fistulae （ADF） are the most frequent aorto-enteric fistulae （80%）, presenting with upper gastrointestinal bleeding. We report the first case of a man with a secondary aorto-duodenal fistula presenting with a history of persistent occlusive syndrome. A 59-year old man who underwent an aortic-bi-femoral bypass 5 years ago, presented with dyspepsia and biliary vomiting. Computed tomography scan showed in the third duodenal segment the presence of inflammatory tissue with air bubbles between the duodenum and prosthesis, adherent to the duodenum. The patient was submitted to surgery, during which the prosthesis was detached from the duodenum, the intestine failed to close and a gastro-jejunal anastomosis was performed. The post-operative course was simple, secondary ADF was a complication （0.3%-2%） of aortic surgery. Mechanical erosion of the prosthetic material into the bowel was due to the lack of interposed retroperitoneal tissue or the excessive pulsation of redundantly placed grafts or septic procedures. The third or fourth duodenal segment was most frequently involved. Diagnosis of ADF was difficult. Surgical treatment is always recommended by explorative laparotomy. ADF must be suspected whenever a patient with aortic prosthesis has digestive bleeding or unexplained obstructive syndrome. Rarely the clinical picture of ADF is subtle presenting as an obstructive syndrome and in these cases the principal goal is to effectively relieve the mechanical bowel obstruction.     

Serological survey of HIV and syphilis in pregnant women in Madagascar

Objectives Peripartal transmission of human immunodeficiency virus (HIV) and Treponema pallidum, the causative agent of syphilis, leads to severe consequences for newborns. Preventive measures require awareness of the maternal infection. Although HIV and syphilis testing in Madagascar could be theoretically carried out within the framework of the national pregnancy follow‐up scheme, the required test kits are rarely available at peripheral health centres. In this study, we screened blood samples of pregnant Madagascan women for HIV and syphilis seroprevalence to estimate the demand for systemic screening in pregnancy. Methods Retrospective anonymous serological analysis for HIV and syphilis was performed in plasma samples from 1232 pregnant women that were taken between May and July 2010 in Ambositra, Ifanadiana, Manakara, Mananjary, Moramanga and Tsiroanomandidy (Madagascar) during pregnancy follow‐up. Screening was based on Treponema pallidum haemagglutination tests for syphilis and rapid tests for HIV, with confirmation of positive screening results on line assays. Results Out of 1232 pregnant women, none were seropositive for HIV and 37 (3%) were seropositive for Treponema pallidum. Conclusions Our findings are in line with previous studies that describe considerable syphilis prevalence in the rural Madagascan population. The results suggest a need for screening to prevent peripartal Treponema pallidum transmission, while HIV is still rare. If they are known, Treponema pallidum infections can be easily, safely and inexpensively treated even in pregnancy to reduce the risk of transmission.     

Married to M. tuberculosis: risk of infection and disease in spouses of smear-positive tuberculosis patients

Objectives To quantify the risk of infection and disease in spouses of tuberculosis patients and the extent to which intervention could reduce the risk in this highly exposed group. Methods We compared HIV prevalence, TB prevalence and incidence and tuberculin skin test (TST) results in spouses of TB patients and community controls. HIV‐positive spouses were offered isoniazid preventive therapy (IPT), and TST was repeated at 6, 12 and 24 months. Results We recruited 148 spouses of smear‐positive patients ascertained prospectively and 3% had active TB. We identified 203 spouses of previously diagnosed smear‐positive patients, 11 had already had TB, and the rate of TB was 2.4 per 100 person years(py) over 2 years (95% CI 1.15–5.09). 116 were found alive and recruited. HIV prevalence was 37% and 39% in the prospective and retrospective spouse groups and 17% in controls. TST was ≥10 mm in 80% of HIV negative and in 57% of HIV‐positive spouses ascertained retrospectively; 74% HIV negative and 62% HIV‐positive spouses ascertained prospectively, and 48% HIV negative and 26% HIV‐positive community controls. Of 54 HIV‐positive spouses, 18 completed 6‐month IPT. At 2 year follow‐up, 87% of surviving spouses had TST ≥10 mm and the rate of TB was 1.1 per 100 py (95% CI 0.34–3.29). Conclusions Spouses are a high‐risk group who should be screened for HIV and active TB. TST prevalence was already high by the time the spouses were approached but further infections were seen to occur. Uptake and adherence to IPT was disappointing, lessening the impact of short‐duration therapy.