热休克蛋白90对氧化应激激活的大鼠血管平滑肌细胞细胞外信号调节激酶的作用

目的探讨热休克蛋白90对氧化应激激活的细胞外信号调节激酶的作用。方法取SD雄性大鼠胸主动脉做原代平滑肌细胞培养。用1μmol/L可溶性鸟苷酰环化酶抑制剂6-Anilinoquinoline-5,8-quinolinedione(LY83583)处理4~12代大鼠血管平滑肌细胞不同时间,蛋白免疫印迹检测细胞内热休克蛋白90、磷酸化和未磷酸化细胞外信号调节激酶1/2。用格尔德霉素(热休克蛋白90的特异性阻断剂)预处理细胞30 min,再用LY83583处理120 min,免疫共沉淀和蛋白免疫印迹检测热休克蛋白90与细胞外信号调节激酶及磷酸化的细胞外信号调节激酶的结合,免疫荧光检测细胞核内磷酸化的细胞外信号调节激酶。结果LY83583处理120 min时细胞内热休克蛋白90表达达高峰,较0 min时增加9倍,与细胞外信号调节激酶1/2的第二个活化高峰一致。LY83583处理血管平滑肌细胞120 min后,热休克蛋白90与磷酸化的细胞外信号调节激酶1/2结合较对照组升高了5.5倍(P<0.01),磷酸化的细胞外信号调节激酶1/2的量增加了6.1倍(P<0.01),而细胞核内的磷酸化的细胞外信号调节激酶1/2也明显增加;5μmol/L格尔德霉素预处理后,LY83583的这些效应则被阻断。结论氧化应激增加大鼠血管平滑肌细胞内热休克蛋白90,并增加其与细胞外信号调节激酶1/2及磷酸化的细胞外信号调节激酶1/2的结合,促进磷酸化的细胞外信号调节激酶1/2核转位。这可能是氧化应激激活大鼠中膜血管平滑肌细胞内细胞外信号调节激酶1/2信号通路活性的重要机制之一,为抗氧化应激引起的血管中膜平滑肌细胞增殖提供新的分子靶点。     

主动免疫AT1受体对自发性高血压大鼠血管重构的影响

目的观察血管紧张素Ⅱ的Ⅰ型(AT1)受体细胞外不同肽段主动免疫自发性高血压大鼠(SHR)对血压及血管重构的影响.方法2月龄SHR在血压升高后,以合成的AT1受体细胞外的多肽片段ATR12185、ATR10014和ATR12181作为抗原,分别主动免疫,用药组给予氯沙坦(10 mg/(kg·d))灌胃.同龄Wistar大鼠免疫干预组同SHR,对照组只用免疫佐剂.ELISA法检测抗体滴度,大鼠尾动脉血压计测量血压.试验结束前,测定肠系膜三级动脉中层及内径,观察肠系膜动脉病理改变,以及胸主动脉超微病理结构改变.结果SHR于2月龄血压开始升高;所有免疫组动物均产生了针对特定短肽的抗体.ATR12181免疫组SHR收缩压于免疫后1月降低,并持续至实验结束[(145.4±8.5)mm Hg,n=7],与SHR对照组[(197.0±7.7)mm Hg,n=7,P＜0.05]相比,收缩压降低,与氯沙坦治疗组[(139.3±17.2)mm Hg,n=7,P＞0.05]相比,无显著性差异,而ATR12185和ATR10014免疫组SHR收缩压无明显变化.Wistar大鼠免疫前后收缩压无明显变化.ATR12181免疫组SHR肠系膜三级动脉中膜厚度/管腔半径(1.10±0.18)及中膜面积/管腔面积(3.21±0.98),分别较SHR对照组(1.39±0.21)及(4.62±1.21)降低.结论用ATR12181主动免疫SHR,可降低SHR血压,降低肠系膜三级动脉中膜厚度/管腔半径及中膜面积/管腔面积,逆转主动脉超微结构的损害.     

主动免疫AT1受体对自发性高血压大鼠血管重构的影响

目的观察血管紧张素Ⅱ的Ⅰ型(AT1)受体细胞外不同肽段主动免疫自发性高血压大鼠(SHR)对血压及血管重构的影响。方法2月龄SHR在血压升高后,以合成的AT1受体细胞外的多肽片段ATR12185、ATR10014和ATR12181作为抗原,分别主动免疫,用药组给予氯沙坦(10mg/(kg·d))灌胃。同龄Wistar大鼠免疫干预组同SHR,对照组只用免疫佐剂。ELISA法检测抗体滴度,大鼠尾动脉血压计测量血压。试验结束前,测定肠系膜三级动脉中层及内径,观察肠系膜动脉病理改变,以及胸主动脉超微病理结构改变。结果SHR于2月龄血压开始升高;所有免疫组动物均产生了针对特定短肽的抗体。ATR12181免疫组SHR收缩压于免疫后1月降低,并持续至实验结束[(145.4±8.5)mmHg,n=7],与SHR对照组[(197.0±7.7)mmHg,n=7,P<0.05]相比,收缩压降低,与氯沙坦治疗组[(139.3±17.2)mmHg,n=7,P>0.05]相比,无显著性差异,而ATR12185和ATR10014免疫组SHR收缩压无明显变化。Wistar大鼠免疫前后收缩压无明显变化。ATR12181免疫组SHR肠系膜三级动脉中膜厚度/管腔半径(1.10±0.18)及中膜面积/管腔面积(3.21±0.98),分别较SHR对照组(1.39±0.21)及(4.62±1.21)降低。结论用ATR12181主动免疫SHR,可降低SHR血压,降低肠系膜三级动脉中膜厚度/管腔半径及中膜面积/管腔面积,逆转主动脉超微结构的损害。     

血管紧张素AT1受体短肽对自发性高血压大鼠血压、心脏及血管的影响

目的观察血管紧张素Ⅱ的Ⅰ型(AT1)受体细胞外的不同肽段对主动免疫自发性高血压大鼠(SHR)血压及靶器官的影响.方法4周龄SHR随机分成5组,每组7只.免疫组有3组,在SHR血压升高后,以合成的AT1受体细胞外的多肽片段ATR12185、ATR10014和ATR12181作为抗原,分别主动免疫,SHR用药组给予氯沙坦(10mg·kg-1·d-1)灌胃治疗,对照组饮水灌胃.同龄Wistar大鼠随机分成4组,每组7只,免疫干预组同SHR,对照组只用免疫佐剂.ELISA法检测免疫组动物的抗体滴度,用大鼠尾动脉血压计观察大鼠血压的变化.试验结束前,测定心脏及左心室重量、肠系膜三级动脉中层及内径,观察心肌及肠系膜三级动脉病理改变,以及心肌超微病理结构改变.结果SHR于6周龄血压开始升高;所有免疫组动物均产生了针对特定短肽的抗体.ATR12181免疫组SHR收缩压于免疫后一个月降低,并持续至实验结束[(145.42±8.46)mmHg,n=7],与SHR对照组[(197.0±7.7)mmHg,n=7,P＜0.05]相比,收缩压明显降低,与氯沙坦治疗组[(139.3±17.2)mmHg,n=7]相比,P＞0.05],而ATR12185免疫组[(183.42±19.26)mm Hg,n=7]和ATR10014免疫组(191.6±15.0)mm Hg,n=7]SHR收缩压无明显变化.Wistar大鼠免疫前后收缩压无明显变化,试验结束时,ATR12181收缩压[(116.6±5.5)mm Hg,n=7],ATR12185收缩压[(116.0±9.5)mm Hg,n=7],ATR10014收缩压[(121.57±4.79)mm Hg,n=7],与对照组[(113.14±9.52)mm Hg,n=7,P＞0.05]无差别.ATR12181免疫组SHR心脏/体重(4.66±0.50)mg/g以及左心室/体重(3.6±0.5)mg/g较SHR对照组心脏/体重(5.16±0.11)mg/g、左心室/体重(4.2±0.1)mg/g降低,P＜0.05,与氯沙坦心脏/体重(4.4±0.6)mg/g及左心室/体重(3.5±0.3)mg/g相比,无显著性差异,P＞0.05.同时肠系膜三级动脉中膜厚度/管腔半径及中膜面积/管腔面积降低.结论用ATR12181主动免疫SHR,可降低SHR血压,降低心脏重量,逆转心脏超微结构的损害,同时降低肠系膜三级动脉中膜厚度/管腔半径及中膜面积/管腔面积降低.     

高血压病人小动脉中磷酸化细胞外信号调节激酶1/2及ets样基因1的蛋白表达

目的 研究细胞外信号调节激酶系统(ERK)及其下游底物ets样基因1(Elk-1)在原发性高血压中的作用.方法 采用免疫组织化学方法,对比观察高血压和非高血压病人胃肠小动脉血管平滑肌细胞及内皮细胞中细胞外信号调节激酶(ERK1/2)和ets样基因1(Elk-1)的磷酸化情况.结果 高血压组胃肠小动脉血管平滑肌细胞中磷酸化ERK1/2染色阳性率(8.31%)明显高于非高血压组(0.53%),P＜0.05;高血压组内皮细胞中磷酸化ERK1/2的阳性率(4.97%)明显高于非高血压组(P＜0.05).高血压组胃肠小动脉血管平滑肌细胞中磷酸化Elk-1染色阳性率(3.53%)明显高于非高血压组(0.27%),P＜0.05.在血管平滑肌细胞、血管内皮细胞中磷酸化ERK1/2与磷酸化Elk-1的表达均有正相关关系.结论 原发性高血压患者的胃肠细小动脉血管平滑肌细胞以及内皮细胞中细胞外信号调节激酶及其下游底物Elk-1的磷酸化增加.     

高血压病人小动脉中磷酸化细胞外信号调节激酶1/2及ets样基因1的蛋白表达

目的研究细胞外信号调节激酶系统（ERK）及其下游底物ets样基因1（E1k-1）在原发性高血压中的作用。方法采用免疫组织化学方法，对比观察高血压和非高血压病人胃肠小动脉血管平滑肌细胞及内皮细胞中细胞外信号调节激酶（ERK1／2）和ets样基因1（E1k-1）的磷酸化情况。结果高血压组胃肠小动脉血管平滑肌细胞中磷酸化ERK1／2染色阳性率（8．31％）明显高于非高血压组（0．53％），P〈0．05；高血压组内皮细胞中磷酸化ERK1／2的阳性率（4．97％）明显高于非高血压组（P〈0．05）。高血压组胃肠小动脉血管平滑肌细胞中磷酸化Elk-1染色阳性率（3．53％）明显高于非高血压组（0．27％），P〈0．05。在血管平滑肌细胞、血管内皮细胞中磷酸化ERK1／2与磷酸化E1k-1的表达均有正相关关系。结论原发性高血压患者的胃肠细小动脉血管平滑肌细胞以及内皮细胞中细胞外信号调节激酶及其下游底物Elk-1的磷酸化增加。     

氯沙坦、依那普利及其合用对腹主动脉缩窄型高血压大鼠的影响

目的　探讨依那普利、氯沙坦及其合用对腹主动脉缩窄型高血压大鼠血压、心肌肥厚程度和心肌组织丝裂原活化蛋白激酶 (MAPK)的活性及表达的影响。方法　采用腹主动脉缩窄型高血压大鼠模型 ,然后将动物随机分为 7组 (n均 =6 )。分别为氯沙坦 (10 mg· kg- 1 · d- 1 )组 ,氯沙坦 (30 mg· kg- 1 · d- 1 )组 ,依那普利 (4mg· kg- 1 · d- 1 )组 ,依那普利 (12 mg· kg- 1· d- 1 )组 ,依那普利合用氯沙坦 (4m g· kg- 1· d- 1和 10 m g· kg- 1· d- 1 )组和安慰剂组。以假手术组作对照。给药 5周后测定左心室重量与体重比值、平滑肌肌动蛋白表达和 MAPK蛋白表达变化。结果　与假手术组比较 ,大鼠腹主动脉缩窄术后 6周血压明显升高 ,心肌组织发生明显肥厚 ,平滑肌肌动蛋白和 MAPK蛋白表达增高 (P<0 .0 1)。与安慰剂组比较 ,氯沙坦、依那普利及其合用可降低平均动脉血压 ,减轻心肌肥厚 ,同时降低平滑肌肌动蛋白和 MAPK蛋白表达 (P<0 .0 1) ,且氯沙坦、依那普利的作用呈剂量依赖性。与单用氯沙坦或依那普利比较 ,氯沙坦和依那普利合用可进一步降低平均动脉血压、减轻心肌肥厚和 MAPK蛋白表达 (P <0 .0 5 )。结论　 MAPK是介导高血压心肌肥厚的重要信号分子。氯沙坦、依那普利均能减轻心肌肥厚和 MAPK蛋白?     

氯沙坦抑制自发性高血压大鼠血管合成醛固酮及CYP11B_2mRNA表达

目的　探讨氯沙坦 (losartan)在减缓高血压血管损害中的潜在作用及氯沙坦长期治疗是否发生组织及分子水平的“醛固酮逃逸”。方法　将自发性高血压大鼠 (SHR)随机分为氯沙坦治疗组 (8只 )和对照组 (8只 )。治疗组 (氯沙坦 10mg·kg- 1 ·d- 1 )连续给药至 18周时处死。用肠系膜动脉离体灌注 ,反向高效液相 (HPLC)纯化和放免检测氯沙坦对血管局部合成醛固酮的影响 ,用RT PCR证实氯沙坦对SHR血管表达醛固酮合成酶基因CYP11B2 mRNA的作用。结果　对照组SHR血管合成血管紧张素Ⅱ为 (189 1± 15 4)pg h ,氯沙坦治疗组为 (2 19 1± 2 6 4)pg h (P <0 0 5 ) ;对照组SHR血管合成醛固酮为 (10 82 6± 133 1)pg h ,氯沙坦治疗组为 (795 7± 12 5 4)pg h(P <0 0 5 ) ;氯沙坦治疗组主动脉CYP11B2 Beta actinmRNA(0 49± 0 15 )较高血压组 (0 80± 0 0 7)明显下调 ,抑制量约达 38%(P <0 0 5 ) ;对照组SHR血管合成内皮素为 (33 3± 6 2 )pg h ,氯沙坦治疗组 (2 3 9± 3 7)pg h(P <0 0 5 )。结论　氯沙坦治疗高血压的机理包括较持久地抑制血管合成醛固酮及内皮素 ,逆转血管重塑 ;虽然氯沙坦可诱导血浆及血管合成血管紧张素Ⅱ增高 ,但是长时间治疗尚未出现明显的“醛固酮逃逸”现象。     

ERK信号传导调节脑缺血再灌注中脑源性神经营养因子介导的神经保护作用

目的研究大脑缺血再灌注中脑源性神经营养因子(BPNF)神经保护效应的机制以及细胞外调节激酶信号通路在其中的作用。方法 SD大鼠被随机分为A、B、C三组,每组6只,所有的大鼠均经历大脑中动脉阻断诱发的脑局灶性缺血再灌注过程,此过程持续45 min。B组给予BDNF以产生神经保护,C组采用选择性Raf-1信号分子抑制剂Bay 43-9006抑制细胞外调节激酶信号通路。脑损伤用甲酚紫染色加图像分析评估,细胞外调节激酶1和2的磷酸化水平采用免疫印迹杂交测定。结果经过缺血再灌注过程,额叶脑组织的损伤比例为(16.48±5.72)%;在使用BD-NF预处理的情况下,脑组织损伤比例显著降低至(6.32±3.08)%(P=0.039)。使用Raf-1抑制剂之后,细胞外调节激酶的磷酸化水平显著降低,包括细胞外调节激酶1(P=0.0084)和细胞外调节激酶2(P=0.029)。与此同时,BDNF的神经保护效应明显减弱,与对照相比没有显著差异。结论在大鼠脑缺血再灌注中,BDNF可以抵抗损伤,细胞外调节激酶信号通路是BDNF这种抗损伤效应的关键信号调节通路。     

老年大鼠缺血/再灌注肾损伤修复时丝裂原活化蛋白激酶亚类活性的变化

目的　观察老年大鼠缺血 /再灌注肾损伤修复时细胞外信号调节激酶 (ERK )、c- Jun氨基末端激酶 (JNK)的变化 ,探讨其与老年大鼠肾脏早期损伤修复的关系。　方法　夹闭大鼠双肾蒂造成急性缺血 /再灌注肾损伤模型 ,电镜观察形态学改变 ,免疫组化检测增殖细胞核抗原 (PCNA)表达 ,免疫沉淀结合特异底物磷酸化法测定 ERK、JNK活性 ,Western blot法测定二者表达量。　结果　缺血 /再灌注 2 h老年鼠仅少数肾小管细胞微绒毛修复 ,PCNA阳性细胞增加不明显。老年鼠肾基础ERK活性与青年鼠无差异 ,缺血 45 m in其活性降低 (0 .5 8± 0 .0 6 ) ,与青年鼠 (0 .6 2± 0 .0 4)差异无显著性 (P>0 .0 5 ) ,再灌注 5 min青年鼠 ERK活性恢复 (1.10± 0 .14) ,而老年鼠 ERK活性再灌注 2 0m in恢复 (0 .87± 0 .14) ;青、老年鼠肾基础 JNK活性相同 ,缺血对二者 JNK活性无影响 ,再灌注 5 m inJN K活性开始增加 ,持续到 2 h,两组峰值分别是各基础值的 13.2倍和 12 .5倍 (P>0 .0 5 ) ;青、老年鼠 ERK、JNK表达量无显著差异。　结论　老年大鼠缺血 /再灌注时 ERK活性的变化 ,可能是老年大鼠肾脏损伤修复能力差的细胞内机制之一。     

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.     

The immunoneuroendocrine role of melatonin

Abstract: A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MHO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as -γ-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.     

Response of rat pineal melatonin to calcium, magnesium, and lithium is circadian stage dependent

Abstract: Herein we documented the response of pineal melatonin production to electrolytes known to be effective on pineal function in view of a possible circadian stage dependence. We studied the release of melatonin by perifused rat pineal glands at 2 different circadian stages corresponding to the middle of the light and dark periods, i.e., respectively, 7 and 19 HALO (Hours After Light Onset, L:D = 12:12). The initial efflux rates were, as expected, much higher in the perifusates of glands removed from rats sacrificed during the dark phase than of those removed during the light phase. After 3 hr of perifusion, melatonin release reached similar levels which were found constant up to the 8th hr of perifusion, whatever the circadian stage. Perifusion of the glands with physiological concentrations for the rat of calcium (5.2 mmol/1) and magnesium (1.34 mmol/1) resulted in a stimulatory effect on the pineal glands removed from rats sacrificed in the middle of the dark period (19 HALO), whereas no effects were observed on the pineal glands removed from rats sacrificed during the light (7 HALO). Lithium (0.28 and 0.55 mmol/1) was ineffective on melatonin release in pineal glands removed 7 and 19 HALO. Our results show differences in the initial efflux rates of melatonin and in the response of perifused pineal glands to calcium and magnesium according to the circadian stage.     

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.     

Conservative management of perforated duodenal diverticulum： A case report and review of the literature

Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.