血小板膜糖蛋白Ⅱb HPA-3多态性与天津地区汉族人群缺血性卒中风险和转归的相关性

目的 探讨血小板膜糖蛋白(glycoprotein,GP)ⅡbHPA-3基因多态性与天津地区汉族人群缺血性卒中发病风险和转归的相关性.方法 连续纳入急性缺血性卒中患者和性别、年龄相匹配的健康体检者.采用聚合酶链反应-限制性片段长度多态性方法检测GPⅡbHPA-3基因多态性.转归不良定义为6个月时改良Rankin量表评分＞2分.结果 共纳入224例急性缺血性卒中患者和98例性别、年龄相匹配的健康体检者.急性缺血性卒中组bb基因型(45.09％对15.06％;x2=40.618,P＜0.001)和b等位基因(63.84％对33.67％;x2 =50.064,P＜0.001)频率显著高于对照组;多变量logistic回归分析显示,bb基因型是缺血性卒中的独立危险因素(优势比5.838,95％可信区间2.653～ 12.843;P＜0.001).在各TOAST亚型中,大动脉粥样硬化型组bb基因型(x2=10.912,P=0.028)和b等位基因(x2 =11.801,P=0.019)频率显著高于其他各组.转归不良组大动脉粥样硬化性卒中的患者构成比(64.52％对29.63％;x2=29.456,P＜0.001)以及bb基因型(66.13％对37.04％;x2=17.422,P＜0.001)和b等位基因(75.00％对59.57％;x2=9.252,P=0.002)频率显著高于转归良好组;多变量logistic回归分析显示,bb基因型是缺血性卒中患者转归不良的独立危险因素(优势比3.842,95％可信区间1.782～8.283;P =0.001).结论 bb基因型可能是天津地区汉族人群缺血性卒中发病和转归不良的独立危险因素.     

缺血性卒中患者的认知功能与脑微出血:回顾性病例系列研究

目的 探讨血管性认知损害的危险因素以及脑微出血(cerebral microbleed,CMB)对缺血性卒中患者认知功能的影响.方法 收集50岁以上缺血性卒中患者的资料.采用MRI评价CMB、白质损害和梗死体积.采用蒙特利尔认知评估量表(Montreal Cognitive Assessment,MoCA)、阿尔茨海默病评定量表认知分表评价认知功能、汉密尔顿抑郁量表(Hamilton Depression Scale,HAMD)评价抑郁状况以排除抑郁患者.根据量表评价结果将缺血性卒中患者分为认知损害组和无认知损害组,比较两组人口统计学和临床特征,并采用多变量logistic回归分析寻找缺血性卒中患者认知损害的独立危险因素.采用Spearman等级相关法分析CMB程度与MoCA总分和MoCA各认知领域评分的相关性.结果 共纳入169例缺血性卒中患者.认知损害组80例,无认知损害组89例;34例存在CMB,135例无CMB.认知损害组年龄较大[(71.99±6.01)岁对(64.47 ±6.15)岁;t=8.014,P=0.000],受教育年限较少[(4.51±1.534)年对(6.94±2.357)年;t=8.023,p=0.000],收缩压较高[(156.19±17.53)mm Hg对(142.04±16.03) mmHg(1 mmHg=0.133 kPa);t=5.479,P=0.000],脑白质损害评分较高[(7.33±2.04)分对(4.39±2.17)分;t=8.951,P=0.000],脑梗死体积较大[(7 123.8±1 587.11)mm3对(5 628.4±1 017.76)mm3;=7.201,P=0.000],既往卒中或短暂性脑缺血发作史比例较高(46.2％对28.1％;x2 =5.982,P=0.014),CMB数量较多(x2=17.565,P=0.000).多变量logistic回归分析显示,年龄[优势比(odds ratio,OR)1.115,95％可信区间(confidence interval,CI)1.013 ～1.227;P=0.026]、受教育年限少(OR0.490,95％ CI0.325 ～0.739;P=0.001)、收缩压(OR1.048,95％ CI1.014～1.083;P=0.005)、脑白质损害(OR 2.044,95％ CI 1.466～2.851;P=0.000)和脑梗死体积(OR2.204,95％ CI1.386 ～3.503;P=0.001)均为缺血性卒中患者认知损害的独立危险因素.与无CMB组比较,CMB组患者年龄较大[(72.06±5.59)岁对(67.01 ±7.15)岁;t=4.427,P=0.000],受教育年限较少[(3.97±1.381)年对(6.25 ±2.317)年;=7.367,P=0.000],收缩压较高[(155.03 ±20.16) mm Hg对(147.16±17.32)mm Hg;t =2.290,P=0.023],脑白质损害评分较高[(7.03±2.139)分对(5.47±2.591)分;t=3.247,P=0.001],脑梗死体积较大[(6 968.5±1 507.37) mm3对(6 177.0±1 477.08) mm3;t =2.735,P=0.007],高血压(82.4％对41.5％;x2=18.149,P=0.000)、高脂血症(88.2％对39.3％;x2 =26.067,P=0.000)、既往卒中或短暂性脑缺血发作史(70.6％对28.1％;x2 =21.061,P=0.000)及冠心病(94.1％对45.2％;x2 =26.278,P=0.000)比例较高.CMB组MoCA总分[M(Q1～Q3)][24 (24 ～ 25)分对28(27 ～28)分;Z=-7.092,P=0.000]及注意力[6(5 ～6)分对6(6 ～6)分;Z=-2.502,P=0.012]、抽象思维[2(1 ～2)分对2(2 ～2)分;Z=-2.382,P=0.017]、视空间执行功能[2(1 ～2)分对4(4 ～5)分;Z=-7.321,P=0.000]评分均显著性低于无CMB组(P均＜0.05).Spearman等级相关分析显示,CMB分级与MoCA总分(rs=-0.879,P=0.000)、视空间执行功能(rs=-0.895,P=0.000)、注意力(rs=-0.337,P=0.005)和抽象思维(rs=-0.333,P=0.006)评分呈负相关.结论 年龄、受教育年限、收缩压、脑白质损害程度和脑梗死体积是血管性认知损害的危险因素.伴有CMB的缺血性卒中患者视空间执行功能障碍、注意力和抽象思维减退明显.CMB及其数量与认知功能损害密切相关,CMB数目越多,认知功能损害越显著.     

缺血性卒中患者踝肱指数与颅内动脉粥样硬化关系的研究

目的:探讨缺血性卒中患者踝肱指数(ABI)与颅内动脉粥样硬化的关系.方法:73例缺血性卒中患者,使用血管多普勒超声测量仪测定ABI,使用1.5 T磁共振成像系统进行头颅磁共振血管造影(MRA)对颅内动脉狭窄程度进行分级,分析缺血性卒中患者ABI与颅内动脉狭窄分级的相关性.结果:无颅内动脉狭窄者(n=38)ABI显著高于有颅内动脉狭窄者(n=35)(0.975±0.114对0.837±0.096,P<0.001),ABI与颅内动脉狭窄程度呈显著负相关性(r=-0.736,P=0.001).结论:ABI与颅内动脉粥样硬化狭窄程度呈负相关,可作为颅内动脉粥样硬化的初步筛查手段.     

血清脂蛋白(a)水平与中青年缺血性卒中患者颈动脉粥样硬化的相关性:回顾性病例系列研究

目的 探讨中青年缺血性卒中患者颈动脉粥样硬化的危险因素以及血清脂蛋白(a)[lipoprotein (a),Lp(a)]水平对中青年缺血性卒中患者颈动脉粥样硬化的影响.方法 收集18 ～55岁的缺血性卒中患者.采用颈动脉超声评价颈动脉粥样硬化程度,并检测血清总胆固醇、三酰甘油、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、极低密度脂蛋白胆固醇、载脂蛋白A1、载旨蛋白B和Lp(a)浓度.根据颈动脉超声结果分为无动脉粥样硬化组、有斑块无狭窄组和颈动脉狭窄组,比较三组的人口统计学和临床特征,并采用多变量logistic回归分析确定中青年缺血性卒中患者颈动脉粥样硬化的独立危险因素.结果 共纳入106例缺血性卒中患者,无动脉粥样硬化组50例,有斑块无狭窄组44例,颈动脉狭窄组12例,三组间年龄[分别为(45.98±7.12)、(50.07±4.79)和(50.92± 1.83)岁;F =7.169,P=0.001]、高血压(分别为26.0％、47.7％和58.3％;x2=6.862,P=0.032)、糖尿病(分别为22.0％、45.5％和66.7％;x2=10.729,P=0.005)、高脂血症(分别为24.0％、40.1％和75.0％;x2=11.372,P=0.003)和吸烟(分别为34.0％、61.4％和75.0％;x2=10.393,P=0.006)患者的构成比以及血清高密度脂蛋白胆固醇[分别为(1.03±0.26)、(0.95 ±0.26)和(0.76±0.08) mmol/L;F=5.882,P=0.004]和Lp(a)[分别为(0.108±0.044)、(0.155±0.028)和(0.200±0.011)g/L;F=41.556,P=0.000]水平存在显著性差异.多变量logistic回归分析显示,年龄＞48岁[有斑块无狭窄:优势比(odds ratio,OR)2.89,95％可信区间(confidence interval,CI)1.20 ～ 6.96,P=0.018;颈动脉狭窄:OR4.43,95％ CI 1.19 ～ 16.57,P=0.027]、高血压(有斑块无狭窄:OR 2.60,95％ CI 1.09～6.18,P=0.031;颈动脉狭窄:OR3.99,95％ CI l.08～14.77,P=0.039)、糖尿病(有斑块无狭窄:OR2.96,95％ CI 1.21～7.23,P=0.018;颈动脉狭窄:OR 7.09,95％ CI 1.79 ～ 28.02,P=0.005)、高脂血症(有斑块无狭窄:OR2.19,95％ CI 0.91 ～5.31,P=0.082;颈动脉狭窄:OR9.50,95％ CI 2.21 ～40.86,P=0.002)、吸烟(有斑块无狭窄:OR 3.08,95％ CI 1.33～7.16,P=0.009;颈动脉狭窄:OR 5.82,95％ CI1.39 ～24.38,P=0.016)和Lp(a)(有斑块无狭窄:OR 4.38,95％ CI l.76 ～ 10.90,P=0.001;颈动脉狭窄:OR 12.80,95％ CI2.73 ～ 52.67,P=0.001)为中青年缺血性卒中患者颈动脉粥样硬化的独立危险因素.结论 年龄、吸烟、高血压、糖尿病和Lp(a)为中青年缺血性卒中患者颈动脉粥样硬化的独立危险因素.     

CD40-1C/T基因多态性与大动脉粥样硬化性卒中的相关性

目的 探讨CD40基因启动子区- 1C/T基因多态性与颈动脉粥样硬化斑块和大动脉粥样硬化性卒中的相关性.方法 研究对象为急性大动脉粥样硬化性卒中患者(病例组)和无卒中史的体检者(对照组).病例组进一步分为不稳定斑块亚组、稳定斑块亚组和无斑块亚组.采用聚合酶链反应-限制性片段长度多态性技术检测CD40 - 1C/T基因多态性.结果 共纳入大动脉粥样硬化性卒中患者170例(病例组)和61名无卒中史的体检者(对照组).在病例组中,不稳定斑块亚组51例,稳定斑块亚组60例,无斑块亚组59例.病例组C等位基因频率显著高于对照组(52.9％对38.5％;x2=7.466,P=0.006).在病例组中,不稳定斑块亚组C等位基因频率(75.5％)显著性高于稳定斑块亚组(53.3％),且两者均显著高于无斑块亚组(33.1％)(稳定斑块亚组与无斑块亚组比较:x2 =9.970,P=0.002;不稳定斑块亚组与稳定斑块亚组比较:x2=11.680,P=0.001;不稳定斑块亚组与无斑块亚组比较:x2 =39.532,P=0.000).多变量logistic回归分析显示,高血压(OR9.513,95％ CI1.291 ～20.779;P =0.028)、TC水平增高(OR 4.235,95％ Cl 1.069 ～ 19.034;P=0.032)、LDL水平增高(OR 4.201,95％ CI 1.803 ～9.672;P=0.001)以及携带C等位基因(OR 1.759,95％ CI 1.177～2.738;P =0.006)是大动脉粥样硬化性卒中的独立危险因素.结论 CD40 - 1C/T基因多态性与颈动脉粥样硬化斑块形成、不稳定性以及缺血性卒中风险相关,C等位基因可能为大动脉粥样硬化性卒中的易感因素.     

缺血性卒中的分型:ASCO、CISS和TOAST的比较研究

目的 探讨TOAST、ASCO和CISS分型在缺血性卒中病因学分型临床应用中的差异.方法 连续收集167例首次发病的缺血性卒中患者,分别进行TOAST、ASCO以及CISS分型,比较其对各病因学亚型诊断的差异性和一致性.结果 与TOAST比较,ASCO-1会显著性增高大动脉粥样硬化组(23.4％对19.8％;x2=4.167,P=0.031)和降低小血管疾病组(32.9％对38.3％;x2=4.923,P=0.022)的患者比例;同样,CISS也会显著性增高大动脉粥样硬化组(37.1％对19.8％;x2=27.034,P＜0.001)和降低小血管疾病组(19.2％对38.3％;x2=25.289,P＜0.001)的患者比例.不过,ASCO-1(34.1％对28.1％x2=3.682,P=0.052)和CISS(32.9％对28.1％;x2=0.880,P=0.268)均不会降低病因不明组的患者比例.3种分型方法的一致性介于中等(TOAST/ASCO-1的其他病因组,κ=0.434)和极好(TOAST/ASCO-1的心源性栓塞组,κ=0.967)之间.结论 ASCO-1和CISS分型均不能降低病因不明性卒中亚型患者的比例,但各亚型之间一致性较好.在临床应用中,应关注3种分型方法中各亚型诊断标准的设计和特点.     

急性缺血性卒中患者的脑动脉狭窄分布和危险因素

目的 探讨急性缺血性卒中患者的脑动脉狭窄分布特点及其危险因素.方法 经MRI和磁共振血管造影(magnetic resonance angiography,MRA)检查的急性缺血性卒中患者,按是否存在脑动脉狭窄分为狭窄组与非狭窄组;狭窄组患者再根据狭窄部位分为单纯颅内狭窄组、单纯颅外狭窄组和颅内合并颅外狭窄组,根据年龄分为中青年组(＜ 60岁)和老年组(≥60岁),根据血管狭窄数量分为单支病变组和多支病变组,分析脑动脉狭窄的分布特点和影响因素.结果 共纳入232例急性缺血性卒中患者,其中单纯颅内动脉狭窄者114例(62.0％),单纯颅外动脉狭窄者30例(16.3％),合并颅内外动脉狭窄者40例(21.7％).前循环狭窄(76.6％)比后循环狭窄(33.7％)更多见,分别主要见于大脑中动脉(64.4％)和大脑后动脉(53.8％).多变量logistic回归分析显示,年龄[优势比(odds ratio,OR)1.049,95％可信区间(confidence interval,CI) 1.015 ～1.084;P=0.005]、高血压(OR 10.063,95％ CI4.402 ～23.004;P＜0.001)、糖尿病(OR 3.873,95％ CI1.141～13.147;P=0.030)、吸烟(OR 3.311,95％ CI 1.112 ～9.855;P=0.031)和纤维蛋白原(OR 6.085,95％ CI1.396 ～26.533;P=0.016)为急性缺血性卒中患者存在脑动脉狭窄的独立危险因素;高血压(OR10.779,95％CI4.468 ～ 26.007;P＜0.001)、糖尿病(OR3.593,95％ CI1.018 ～ 12.685;P =0.047)、吸烟(OR 4.408,95％ CI 1.403～ 13.826;P=0.011)为单纯颅内动脉狭窄的独立危险因素;高血压(OR6.143,95％ CI1.838 ～ 20.537;P=0.003)、糖尿病(OR 8.179,95％ CI1.844～ 36.287; P=0.006)、纤维蛋白原(OR 2.410,95％ CI1.046～5.551;P=0.039)为单纯颅外动脉狭窄的独立危险因素.合并颅内外动脉狭窄组C-反应蛋白(C-reactive protein,CRP)水平显著性高于单纯颅外狭窄组(P =0.001)和单纯颅内狭窄组(P=0.018),单纯颅外动脉狭窄与单纯颅内狭窄组间无显著性差异,但3组平均水平均高于正常值.中青年组以单纯颅内、单纯颅外狭窄多见,老年组中以单纯颅内狭窄及合并颅内外狭窄较为常见.多支血管狭窄组年龄(P =0.036)和尿酸水平(P =0.006)显著性高于单支病变组,但仅年龄(OR 1.030,95％ CI 1.003 ～ 1.057;P=0.028)与多支脑动脉狭窄显著独立相关.结论 急性缺血性卒中患者的脑动脉狭窄以颅内动脉狭窄多见,合并颅内外动脉狭窄的比例随年龄增长有所升高.年龄、高血压、糖尿病、吸烟和纤维蛋白原为急性缺血性卒中患者存在脑动脉狭窄的独立危险因素,高血压和糖尿病为急性缺血性卒中患者单纯颅内、颅外动脉狭窄共同的独立危险因素,吸烟为急性缺血性卒中患者单纯颅内动脉狭窄的独立危险因素,纤维蛋白原为急性缺血性卒中患者单纯颅外动脉狭窄的独立危险因素.CRP和尿酸可能为急性缺血性卒中患者与脑动脉狭窄有关的炎性预测因素.     

血清促甲状腺素水平与急性缺血性卒中患者转归的相关性

目的 探讨血清促甲状腺素(thyroid-stimulating hormone,TSH)水平与急性缺血性卒中转归的相关性.方法 前瞻性纳入急性缺血性卒中患者,收集一般临床资料、血管危险因素和甲状腺.激素等生化指标.应用美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评估基线神经功能缺损程度.在发病后90 d时采用改良Rankin量表(modified Rankin Scale,mRS)评估神经功能转归,0～2分定义为转归良好.采用多变量logistic回归分析确定急性缺血性卒中患者转归不良的独立影响因素.结果 共纳入140例急性缺血性卒中患者,其中男性95例(67.86％),女性45例(32.14％),年龄35 ～94岁.亚临床甲状腺功能减退13例(9.29％),亚临床甲状腺功能亢进17例(12.14％).98例(70.00％)转归良好,42例(30.00％)转归不良.转归良好组男性(x2=4.717,P=0.047)和小动脉闭塞性卒中(r=5.564,P=0.018)患者构成比以及尿酸(t=2.602,P=0.010)、FT3(归2.406,P=0.017)和TSH(t=2.302,P=0.023)水平显著高于转归不良组,年龄(泞-3.489,P=0.001)、空腹血糖(Z=-2.178,P=0.031)和基线NIHSS评分(归-8.009,P＜0.001)显著低于转归不良组.转归良好组TSH位于第1四分位数(＜0.805 mU/L)的患者构成比显著低于转归不良组(17.35％对42.86％;x2=10.204,P=0.003),而位于第4四分位数(＞2.476 mU/L)的患者构成比显著高于转归不良组(30.61％对11.90％;x2=5.488,P=0.020).多变量logistic回归分析显示,在校正各种混杂因素后,基线NIHSS评分较高是发病后90 d时转归不良的独立危险因素(优势比1.690,95％可信区间1.317 ～2.168;P＜0.001),而基线TSH水平较高与转归良好独立相关(优势比0.520,95％可信区间0.408 ～0.867;P =0.007).结论 血清TSH水平较高与急性缺血性卒中患者发病后90 d时神经功能转归良好独立相关.     

肺炎衣原体和巨细胞病毒感染与颈动脉粥样硬化斑块及其稳定性的相关性

目的 探讨颈动脉粥样硬化的发生与肺炎衣原体(Chlamydia pneumonia,Cpn)和巨细胞病毒(cytomegalovirus,CMV)两种微生物感染的相关性.方法 纳入颈动脉彩超显示内膜-中膜厚度(intima-media thickness,IMT)＞1.5 mm的患者作为颈动脉粥样硬化组,而IMT＜ 1.0 mm的健康体检者作为对照组.采用酶联免疫吸附法检测血清抗Cpn和抗CMV IgG抗体水平和阳性率.比较颈动脉粥样硬化组与对照组的人口统计学、血管危险因素以及抗Cpn和抗CMV IgG抗体阳性率.结果 颈动脉粥样硬化组共纳入患者92例,其中稳定斑块患者30例,不稳定斑块患者62例;对照组共纳入49例健康体检者.颈动脉粥样硬化组年龄以及男性、高血压、糖尿病、高脂血症和吸烟患者的构成比与对照组均无显著性差异(P均＞0.05).颈动脉粥样硬化组抗Cpn IgG(69.5％对26.5％彩=23.887,P＜0.001)、抗CMV IgG(75.0％对30.6％;x2 =26.156,P＜0.001)阳性率以及抗Cpn IgG+抗CMV IgG阳性率(51.2％对10.2％;x2 =24.006,P＜0.001)均显著性高于对照组.在颈动脉粥样硬化组中,不稳定斑块亚组年龄以及男性、高血压、糖尿病、高脂血症和吸烟患者的构成比与稳定斑块亚组均无显著性差异(P均＞0.05).不稳定斑块亚组抗Cpn IgG(80.6％对46.7％;x2=11.025,P=0.001)和抗CMV IgG(83.9％对56.7％;x2=7.980,P=0.005)阳性率以及抗Cpn IgG+抗CMV IgG阳性率(44.6％对7.6％;x2=10.210,P=0.006)显著性高于稳定斑块亚组.结论 颈动脉粥样硬化的发生和斑块稳定性均与Cpn和CMV感染相关,Cpn和CMV感染可能是颈动脉粥样硬化发生和斑块不稳定的重要因素.     

腔隙性卒中后疲劳与认知障碍和抑郁的相关性:回顾性病例系列研究

目的 探讨腔隙性卒中后疲劳与认知障碍和抑郁的相关性.方法 纳入2009年9月至2010年11月期间住院的103例腔隙性卒中患者,采用疲劳量表-14(Fatigue Scale,FS-14)、疲劳严重程度量表(Fatigue Severity Scale,FSS-9)评价卒中后疲劳,简易精神状态检查量表(Mini-Mental State Examinat ion,MMSE)和蒙特利尔认知评估量表(Montreal Cognitive Assessment,MoCA)评价认知功能,抑郁自评量表(Self-Rating Depression Scale,SDS)和汉密尔顿抑郁量表(Hamilton Depression Scale,HAMD)评价抑郁情况.结果 通过不同量表评定,分别有34例(33.01％) (FSS-9)和45例(43.69％)(FS-14)存在疲劳.在根据FSS-9评分确定的34例疲劳患者中,有20例存在认知损害,26例存在抑郁,16例同时存在认知损害和抑郁.Pearson相关分析显示,FS-14评分与MMSE评分(r=-0.307,P =0.002)和MoCA评分(r=-0.457,P=0.000)呈显著负相关,而与SDS评分(r=0.368,P=0.000)和HAMD评分(r=0.526,P=0.000)呈显著正相关;FSS-9评分亦与MMSE评分(r=-0.292,P=0.003)和MoCA评分(r=-0.340,P=0.000)呈显著负相关,而与SDS评分(r=0.403,P=0.000)和HAMD评分(r=0.564,P=0.000)呈显著正相关.结论 腔隙性卒中患者的疲劳、认知损害和抑郁发生率均较高,疲劳与认知损害和抑郁之间存在一定的相关性.     

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.     

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.     

Variabilité des concentrations plasmatiques de l’angiotensinogène et risque d’hypertension artérielle chez le rat transgénique

Aim

Genetic polymorphisms of the human angiotensinogen gene are frequent and may induce up to 30% increase of plasma angiotensinogen concentrations with a blood pressure increase of up to 5 mmHg. Their role for the pathogenesis of human arterial hypertension remains unclear. High plasma angiotensinogen levels could increase the sensitivity to other blood pressure stressors.

Methods

Male transgenic rats with a 9-fold increase of plasma angiotensinogen concentrations and male non-transgenic rats aged 10 weeks were treated or not with NG-Nitro-L-arginine-methyl ester for 3 weeks in their drinking water (n = 3/group). Systolic blood pressure and body weight were measured at baseline and at the end of the study when left ventricular weight and ventricular expression of angiotensin I-converting enzyme and procollagen Iα1 were determined (polymerase chain reaction).

Results

At baseline, transgenic rats had +18 mmHg higher bood pressure and –8% lower body weight compared to non-transgenic rats (P < 0.05) without significant changes for the vehicle groups throughout the study (P > 0.05). NG-Nitro-L-arginine-methyl ester increased blood pressure, left ventricular weight and left ventricular weight indexed for body weight by +41%, +17.6% and +18.6% (P < 0.05) in transgenic and +25%, +5.3% and +6.7% (P > 0.05) in non-transgenic rats compared to untreated animals, respectively. Cardiac gene expression showed no differences between groups (P > 0.05).

Conclusion

Increased plasma angiotensinogen levels may sensitize to additional blood pressure stressors. Our preliminary results point towards an independent role of angiotensinogen in the pathogenesis of human hypertension and associated end-organ damage.     

Morphological and immunocytochemical heterogeneity of cultured pinealocytes from one-week-and two-month-old rats: Planimetric and densitometric investigations

Abstract: In vitro preparations of rat pinealocytes are widely used for biochemical analyses of signal transduction processes. This paper deals with morphological and immunocytochemical features of such preparations. Special attention was paid to the problems of whether pinealocytes represent a heterogeneous cell population and how such heterogeneity may develop during ontogeny. The investigations were performed with cells which were obtained from the pineal organ of one-week-and two-month-old rats, attached to synthetic peptide-coated coverslips or tissue culture chamber slides, and maintained under in vitro conditions overnight. The attached cells were then fixed with paraformaldehyde. These preparations yielded monolayers of spherical cells of different sizes; most cells were isolated, but some of them were aggregated and formed small clusters. On the average, the cells from the one-week-old animals were smaller than the cells from the two-month-old animals. Immunocytochemical demonstration of S-antigen, a pinealocyte-specific marker, showed that the majority of the cells from two-month-old animals were intensely or moderately labelled. Pinealocytes from one-week-old animals were less S-antigen immunoreactive. Only very few cells (less than 1% displayed glial fibrillary acidic protein (GFAP)-immunoreactivity. Planimetric investigations of the cell size and semiquantitative densitometric investigations of the intensity of the S-antigen immunoreaction revealed that (i) pinealocytes kept in vitro form a heterogeneous cell population, and that (ii) this heterogeneity increases during postnatal development from one-week-old to two-month-old animals. Two groups of pinealocytes can be distinguished based on their developmental fate: pinealocytes of one group grow dramatically, but show only a moderate increase in S-antigen immunoreactivity, and pinealocytes of the other group retain their size, but display a distinct increment in S-antigen immunoreacti vitv.     

Effects of pinealectomy and melatonin administration on certain indices of ovarian hyperplasia and/or hypertrophy in rats with both ovaries intact or after unilateral ovariectomy

Abstract: In earlier studies from other laboratories it was shown that melatonin decreased ovarian weight in rats and inhibited compensatory hypertrophy of the remaining ovary after unilateral ovariectomy. This study was designed to examine the influence of melatonin on certain indices of ovarian hyperplasia and/or hypertrophy in adult female rats with both ovaries preserved and with either an intact pineal gland or with the pineal gland removed (pinealectomy, PX) or, finally, in sham-PX animals. Similar studies were conducted on rats after unilateral ovariectomy, referring the examined parameters to the remaining intact ovary. The studies included mitotic activity of granulosa layer cells and corpus luteum cells, ovarian weight, ovarian cross-sectional area, cross-sectional area of the granulosa layer of all the Graafian follicles and the cross-sectional areas of the corpora lutea, visible on the ovarian cross-section. On the basis of results, we conclude that: 1) the effect of PX on the processes of ovarian hyperplasia and hypertrophy may vary; analogously, exogenous melatonin administration may influence ovarian hyperplasia and hypertrophy in different ways; 2) PX and exogenous melatonin may, under certain conditions, exert similar biological effects, even synergistic effects; 3) melatonin inhibits ovarian growth processes, while the effects of PX are variable; 4) the results indicate that in experiments performed on rats, with the use of two control groups, i.e., intact and sham-PX, melatonin effects on these two groups may differ.