脑微出血对急性脑梗死患者认知功能的影响:前瞻性病例系列研究

目的 探讨急性脑梗死患者认知功能与脑微出血(cerebral microbleed,CMB)的相关性.方法 前瞻性分析急性脑梗死患者的临床和影像学资料,根据MRI结果对CMB进行计数,详细记录患者的一般情况、CMB部位和脑白质疏松严重程度,在入院次日应用蒙特利尔评估量表(Montreal Assessment Scale,MoCA)对患者进行认知功能评估,在3、6和9个月时进行MoCA评估随访.分析急性脑梗死患者的认知功能变化及其与CMB的关系.结果 共纳入82例缺血性卒中患者,其中33例伴有CBM,49例无CBM.CMB组收缩压[(155.03±19.68)mm Hg对(142.20±21.22)mm Hg(1 mm Hg=0.133 kPa);t=2.762,P=0.007]和美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分[(6.21±4.57)分对(4.00±3.98)分;t=2.322,P=0.023]均显著性高于非CMB组.多变量logistic回归分析显示,收缩压水平[优势比(odds ratio,OR)1.032,95％可信区间(confidence interval,CI)1.008～1.057;P=0.009]和NIHSS评分(OR 1.163,95％ CI l.013～1.311;P=0.014)是急性脑梗死患者存在CMB的独立预测因素.CMB与MoCA量表评分密切相关,且随访时间越长,相关性越强.在CMB患者中,执行功能(rs=-0.318,P=0.004)、视空间功能(rs=-0.403,P=0.000)和计算功能(rs=-0.362,P=0.001)均显著受损,CMB越严重,这3个认知域评分越低,损害也越严重.结论 CMB与急性脑梗死患者认知功能损害密切相关,CMB越严重,认知功能损害越明显,且CMB患者的认知功能损害随着时间的推移而加重.     

缺血性脑小血管病患者轻度认知障碍的危险因素和临床特征:回顾性病例系列研究

目的 探讨缺血性脑小血管病(small vessel disease,SVD)患者轻度认知障碍(mild cognitive impairment,MCI)的危险因素和临床特征,为早期诊断和早期干预提供依据.方法 应用蒙特利尔认知评估量表(Montreal Cognitive Assessment,MoCA)筛查MCI,收集相关危险因素和其他临床资料,并进行其他神经心理学测试.根据MRI表现将SVD分为脑白质疏松(leukoaraiosis,LA)、腔隙性梗死(lacunar infarction,LI)和LA与LI并存(LA-LI)3种类型.结果 共纳入143例SVD患者,其中MCI组68例,非MCI组75例.单变量分析显示,MCI组年龄、性别构成比与非MCI组无显著差异,但MCI组受教育年限显著短于非MCI组,而高血压(69.11％对45.33％;x2=8.215,P=0.004)、糖尿病(57.35％对40.00％;x2=4.301,P=0.038)、高脂血症(48.53％对24.00％;x2 =9.352,P=0.002)、颈动脉粥样硬化(41.18％对21.33％;x2=6.592,P=0.010)和吸烟(32.35％对14.67％;x2=6.285,P=0.012)的构成比以及尿酸[(351.81±83.21)mmol/L对(323.03±80.43)mmol/L;t=2.102,P=0.037]和总胆固醇[(5.26±1.26) mmol/L对(4.56±1.23) mmol/L;=3.326,P=0.001]水平显著高于非MCI组.多变量logistic回归分析显示,高血压[优势比(odds ratio,OR)2.227,95％可信区间(confidence interval,CI)1.001 ～4.954;P =0.026]、糖尿病(OR 2.056,95％ CI 1.862～4.937;P=0.046)、高脂血症(OR 2.528,95％ CI 1.361 ～5.770;P=0.028)、颈动脉粥样硬化(OR 2.658,95％ CI 1.110 ～6.367; P=0.029)、吸烟(OR2.566,95％ CI1.017 ～6.474;P=0.046)和受教育年限(OR0.825,95％ CI 0.745～0.914;P=0.000)是SVD患者出现MCI的独立危险因素.MCI组MoCA总分[(18.44±5.60)分对(27.09±1.37)分;t=-12.422,P=0.000]以及视空间/执行能力[(2.65±1.39)分对(4.49±0.74)分;t=-9.762,P=0.000]、注意力[(4.48±1.70)分对(5.89±0.31)分;t=6.706,P=0.000]、语言[(1.69±0.80)分对(2.41 ±0.95)分;t=4.893,P=0.018]、抽象能力[(0.85±0.69)分对(1.71 ±0.53)分;t=-7.081,P=0.000]、延迟回忆[(1.29±1.01)分对(4.04±0.99)分;t=13.824,P=0.000]等亚项得分均显著低于非MCI组,而命名和定向力得分无显著差异.在MCI组中,LA-LI组MoCA总分[(17.04±6.15)分对(21.04±3.98)分;P＜0.05]以及视空间/执行功能[(1.68± 1.16)分对(3.24±1.13)分;P＜0.05]、注意力[(3.92±2.03)分对(5.19±0.87)分;P＜0.05]、延迟回忆[(1.35±1.01)分对(1.86±1.58)分;P＜0.05]等亚项得分显著低于U组;LA组MoCA总分[(18.18±5.31)分对(21.04±3.98)分;P＜0.05]以及视空间/执行功能[(2.56±1.78)分对(3.24±1.13)分;P＜0.05]、语言[(0.64±0.23)分对(1.24±0.83)分;P＜ 0.05]、延迟回忆[(0.69±0.58)分对(1.86±1.58)分;P＜0.01]等亚项得分显著低于LI组;LA-LI组视空间/执行功能评分显著低于LA组[(1.68±1.16)分对(2.56±1.78)分;P＜0.05]和LI组[(1.68±1.16)分对(3.24±1.13)分;P＜0.05].结论 高血压、糖尿病、高脂血症、颈动脉粥样硬化、吸烟和受教育水平较低是SVD患者MCI的独立危险因素.SVD后MCI的认知损害表现为包括视空间/执行功能、延迟回忆在内的多个认知域损害,不同类型脑小血管病之间的认知损害有所不同.     

缺血性卒中后认知损害的危险因素:回顾性病例系列研究

目的 探讨缺血性卒中后认知损害的危险因素.方法 应用简易智能状态检查量表(mini-mental state examination,MMSE)筛查在缺血性卒中发病后3d内出现认知损害的患者.根据MMSE评分将患者分为认知损害组与非认知损害组,比较两组人口统计学、血管危险因素、临床资料.采用多变量logistic回归分析缺血性卒中后认知损害的独立危险因素.结果 共纳入缺血性卒中患者202例,其中认知损害组48例(23.8％).认知损害组年龄[(66 ±6)岁对(57±5)岁;t=2.231,P=0.038]、糖尿病(39.6％对18,2％;χ2=9.388,P=0.003)、卒中或短暂性脑缺血发作史(39.6％对20.8％;x2=6.856,P=0.007)的比例、基线美国国立卫生研究院卒中量表评分[(11.8±2.4)分对(8.1±1.9)分;t=2.046,P=0.043]以及血清同型半胱氨酸[(29.2±7.8)μmol/L对(19.9±6.5) μmol/L;t =2.781,P=0.008]、尿酸[(401.5±51.1) μmol/L对(312.4± 60.7) μmol/L;t=3.042,P=0.003]和C反应蛋白[(18.4±5.2)μmol/L对(11.3±4.2)μmol/L; =2.903,P=0.004]水平均显著高于非认知损害组.多变量logistic回归分析显示,年龄[优势比(odds ratio,OR)1.812,95％可信区间(confidence interval,CI)1.138～3.205;P=0.039]、糖尿病史(OR2 520,95％ CI 1.854 ～4.111;P=0.025)、卒中或短暂性脑缺血发作史(OR4.232,95％ CI 1.905 ～8.582;P=0.014)以及血清同型半胱氨酸(OR3.618,95％ CI 2.061 ～6.312;P =0.018)、尿酸(OR 2.179,95％ CI 1.654 ～3.836;P =0.031)和C反应蛋白(OR 2.716,95％ CI 1.507 ～5.552;P=0.022)水平增高为缺血性卒中后认知损害的独立危险因素.结论 缺血性卒中发病后的认知损害发生率较高,年龄、卒中或短暂性脑缺血发作病史、糖尿病史以及血清C-反应蛋白、尿酸和同型半胱氨酸水平增高为缺血性卒中后发生认知损害的独立危险因素.     

急性缺血性卒中患者认知损害与脑动脉粥样硬化的相关性

目的 探讨急性缺血性卒中患者认知损害与脑动脉粥样硬化的相关性.方法 选择发病前无认知损害的急性缺血性卒中患者.采用蒙特利尔认知评估量表(Montreal Cognitive Assessment,MoCA)评价认知功能,MRI确定梗死部位和侧别,磁共振血管造影、CT血管造影或数字减影血管造影确定粥样硬化动脉.结果 共纳入101例急性缺血性卒中患者,其中75例(74.3％)存在认知损害,认知损害组年龄[(54.54±12.59)岁对(64.43±10.37)岁;t=-3.960,P＜0.001]以及受教育年限≤6年(50.7％对11.5％;x2=12.257,P＜0.001)和脑动脉粥样硬化(89.3％对50.0％;x2=18.137,P＜0.001)患者构成比显著高于认知功能正常组.多变量logistic回归分析显示,脑动脉粥样硬化是急性缺血性卒中患者认知损害的独立危险因素(优势比1.720,95％可信区间1.005～2.942;P=0.048).MoCA评分与责任血管(r=-0.365,P＜0.001)和粥样硬化程度最重血管(r=-0.243,P=0.014)均呈显著负相关.结论 多数急性缺血性卒中患者在发病后早期即存在认知损害,且MoCA评分与脑动脉粥样硬化程度呈负相关,脑动脉粥样硬化是急性缺血性卒中患者认知损害的独立危险因素.     

后循环缺血性卒中的危险因素和影像学特征:回顾性病例系列研究

目的 探讨后循环缺血性卒中的主要危险因素以及合并糖尿病的后循环缺血性卒中患者的临床和影像学特征.方法 收集急性缺血性卒中患者的临床资料,并对后循环缺血性卒中组与前循环缺血性卒中组进行比较;后循环卒中患者进一步分为糖尿病组和非糖尿病组,比较两组血管危险因素和影像学特征;将后循环缺血性卒中患者按病变血管分布分为近段组、中段组、远段组和混合组,分析糖尿病与各组之间的相关性和影像学特征.结果 共纳入328例后循环缺血性卒中病例,其中男性194例,糖尿病组108例;前循环缺血性卒中336例,其中男性214例,糖尿病组59例.后循环缺血性卒中组糖尿病(32.9％ 对21.7％;x2=10.501,P=0.001)、高脂血症(60.1％对47.9％;x2=9.852,P=0.002)、既往卒中或短暂性脑缺血发作史(29.0％对22.0％;x2 =4.213,P=0.040)患者构成比均显著性高于前循环缺血性卒中组(P均＜0.05),而吸烟患者构成比显著性低于前循环缺血性卒中组(18.3％对26.2％;x2 =5.977,P=0.014);总胆固醇[(4.72±1.07) mmol/L对(4.56 ±0.98) mmol/L;t =2.079,P=0.038]、三酰甘油[(1.54±1.07) mmot/L对(1.33±0.71)mmol/L;t3.085,P=0.002]和低密度脂蛋白胆固醇[(2.91±0.90) mmol/L对(2.75±0.80)mmol/L;t 2.373,P=0.018]均显著性高于前循环缺血性卒中组,而高密度脂蛋白胆固醇显著性低于前循环缺血性卒中组[(1.13 ±0.31) mmol/L对(1.18±0.32)mmol/L;t2.045,P=0.041].多变量logistic回归分析显示,糖尿病[优势比(odds ratio,OR)1.560,95％可信区间(confidence interval,CI)1.086～2.239;P=0.016]和既往卒中或短暂性脑缺血发作史(OR 1.455,95％ CI 1.013～2.090;P=0.042)是后循环缺血性卒中的独立危险因素.在后循环缺血性卒中患者中,糖尿病组(n=108)高脂血症(66.7％对55.5％;x2=5.069,P=0.024)和饮酒(13.0％对4.5％;x2=7.568,P =0.006)患者构成比显著性高于非糖尿病组(n =220),心房颤动患者的构成比显著性低于非糖尿病组(3.7％对11.4％;x2=5.274,P=0.022);三酰甘油[(1.70±0.93) mmol/L对(1.45±1.11)mmol/L; t=1.989,P=0.048]、空腹血糖[(8.46±2.96) mmol/L对(5.30±0.96) mmol/L;t 10.706,P=0.000]和糖基化血红蛋白[(8.36±1.94)％对(6.07±0.55)％;t=10.576,P=0.000]显著性高于非糖尿病组;大动脉粥样硬化性卒中患者构成比显著性高于非糖尿病组(73.1％对60.0％;x2=5.457,P=0.019),而心源性脑栓塞显著性低于非糖尿病组(2.8％对9.1％;x2=4.428,P=0.035);后循环中段梗死患者构成比显著性高于非糖尿组(49.1％对31.4％;x2 =9.726,P=0.002);脑干梗死(60.2％对48.2％;x2 =4.182,P=0.041)和单发性脑干梗死(55.6％对30.5％;x2=19.235,P=0.000)患者构成比均显著性高于非糖尿病组.在单发性脑干梗死患者中,糖尿病组脑桥梗死(43.5％对25.9％;x2=10.374,P=0.001)和延髓梗死(7.4％对1.8％;P =0.023)患者构成比均显著性高于非糖尿病组.结论 糖尿病和既往卒中或短暂性脑缺血发作史是后循环缺血性卒中的独立危险因素.糖尿病与脑干梗死关系密切,更易导致脑桥梗死.     

血浆可溶性CD40配体、甲胎球蛋白和妊娠相关血浆蛋白-A与缺血性卒中患者颈动脉斑块的关系

目的 探讨急性缺血性卒中患者血浆可溶性CD40配体(soluble CD40ligand、sCD40L)、甲胎球蛋白和妊娠相关血浆蛋白-A(pregnancy associated plasma protein-A,PAPP-A)水平与颈动脉斑块的关系.方法 纳入急性缺血性卒中患者.采用颈动脉超声对颈动脉进行评估,根据评估结果分为颈动脉斑块组和非颈动脉斑块组,前者根据斑块性质进一步分为稳定斑块亚组和不稳定斑块亚组.采用酶联免疫吸附法检测血浆sCD40L、甲胎球蛋白和PAPP-A水平.对颈动脉斑块组与非颈动脉斑块组以及稳定斑块亚组与不稳定斑块亚组之间的人口统计学、既往史、合并症、实验室检查和血浆炎性标记物进行比较.采用多变量logistic回归分析探讨血浆炎性标记物与颈动脉斑块的关系.结果 共纳入200例急性缺血性卒中患者.其中,男性122例,女性78例,年龄33 ～ 87岁,平均(60.1±10.3)岁;颈动脉斑块组139例,非斑块组61例;稳定斑块亚组43例,不稳定斑块亚组96例.颈动脉斑块组平均年龄显著性大干非斑块组[(63.2±8.7)岁对(50.3±9.5)岁;t=10.179,P=0.000],男性(68.3％对44.3％;x2=10.336,P=0.001)、高血压(71.2％对54.1％;x2 =5.540,P＝0.019)、糖尿病(46.8％对29.5％;x2=5.199,P=0.023)和高脂血症(78.4％对37.7％;x2=31.31,P=0.000)患者的构成比显著性高于菲斑块组,总胆固醇[(5.7±1.1)mmol/L对(5.3±1.0)mmol/L;t＝2.433,P=0.016]、低密度脂蛋白胆固醇[(4.5±1.0) mmol/L对(4.1±0.9)mmol/L;t =2.683,P=0.008]和空腹血糖[(7.5±2.5)mmol/L对(6.4±2.1)mmol/L; t=3.002,P=0.003]以及sCD40L[(151.4±55.8)pg/ml对(102.8±65.9)pg/ml;t＝ 5.360,P=0.000]、甲胎球蛋白[(390.1±80.6)μg/ml对(352.9±98.6)μg/ml;t=2.591,P=0.011]和PAPP-A[(11.49±4.67) mIU/L对(8.46±3.99) mIU/L;t =4.409,P=0.000]水平显著性高于非斑块组.多变量logistie回归分析显示,高脂血症[优势比(odds ratio,OR)6.582,95％可信区间(confidence interval,CI)2.321～18.662;P =0.000]、sCD40L(OR6.372,95％ CI2.174 ～ 18.670;P=0.010)和甲胎球蛋白(OR4.101,95％ CI 1.012～ 16.619;P=0.048)为急性缺血性卒中患者存在颈动脉斑块的独立预测因素.稳定颈动脉斑块亚组平均年龄显著性小于不稳定斑块亚组[(59.6±9.3)岁对(64.1±7.2)岁;t=3.231,P=0.002],高血压患者构成比显著性低于不稳定斑块亚组(55.8％对78.1％;x2=7.213,P=0.007),总胆固醇[(5.4±0.9) mmol/L对(6.0±1.1)mmol/L;t =3.136,P=0.002]、低密度脂蛋白胆固醇[(4.0±1.2) mmol/L对(5.7±1.0)mmol/L;t=8.696,P=0.000],空腹血糖[(7.1±2.3)mmol/L对(7.9± 1.9) mmol/L; t=2.147,P=0.034]以及sCD40L[(135.3±74.3)pg/ml对(176.5±64.5)pg/ml;t=3.319,P=0.001]和PAPP-A[(10.96 ±5.02) mIU/L对(13.98 ±4.63)mIU/L;t ＝3.463、P ＝0.001]水平显著性低于不稳定斑块亚组,而高密度脂蛋白胆固醇水平则显著性高于不稳定斑块亚组[(1.2±0.2)mmol/L对(1.1±0.3)mmol/L;t =2.314,P=0.022].多变量logistic回归分析显示,高密度脂蛋白胆固醇(OR0.234,95％ CI0.060 ～0.906;P =0.022)是斑块不稳定的独立保护性因素,而sCD40L(OR 5.290,95％ CI1.613 ～ 17.351;P=0.029)和PAPP-A(OR4.125,95％ CI1.281～13.283;P=0.021)是斑块不稳定的独立预测因素.结论 sCD40L、PAPP-A和甲胎球蛋白水平与颈动脉斑块的存在和稳定性相关.血浆sCD40L和甲胎球蛋白增高是急性缺血性卒中患者存在颈动脉斑块的独立预测因素,而血浆sCD40L和PAPP-A水平增高是急性缺血性卒中患者颈动脉斑块不稳定的独立预测因素.     

脑微出血的危险因素及其对认知功能影响的临床研究

目的探讨腔隙性脑梗死患者脑微出血(CMB)的危险因素及其对认知功能影响。方法选择腔隙性脑梗死患者113例,根据头颅MRI磁敏感加权成像(SWI)检查结果分为CMB组33例和无CMB组80例。比较2组患者的一般临床资料及生化指标,并进一步回归分析CMB发生的相关危险因素。于入院后第2天应用蒙特利尔认知评估量表(MoCA)对患者的认知功能进行评估。结果 CMB组收缩压和同型半胱氨酸(Hcy)高于无CMB组[(158.3±13.7)mm Hg vs(138.2±15.2)mm Hg(1mm Hg=0.133kPa)和(13.7±4.5)μmol/L vs(9.4±2.4)μmol/L],差异有统计学意义(P=0.000);CMB组总胆固醇低于无CMB组[(4.2±0.9)mmol/L vs(4.9±0.8)mmol/L],差异有统计学意义(P=0.000);与无CMB组比较,CMB组的MoCA总分、视空间与执行功能和注意得分明显降低[(22.98±2.30)分vs(27.49±1.15)分、(2.73±0.94)分vs(3.78±0.66)分及(3.70±1.35)分vs(4.23±1.08)分],差异有统计学意义(P=0.000,P=0.030)。logistic回归分析显示,Hcy是CMB的独立危险因素(OR=0.735,95%CI:0.532⁰.921,P=0.001)。结论 Hcy是CMB的独立危险因素;CMB会引起认知功能障碍,表现为视空间与执行功能和注意障碍。     

血浆同型半胱氨酸水平与急性卒中患者脑微出血和脑白质疏松的相关性:回顾性病例系列研究

目的 探讨急性卒中患者血浆同型半胱氨酸(homocysteine,Hey)水平与脑微出血(cerebral microbleed,CMB)和脑白质疏松(leukoaraiosis,LA)的关系.方法 回顾性分析急性卒中患者的临床和影像学资料,根据MRI结果对CMB进行计数和对LA严重程度进行分级,在入院后次日抽取空腹静脉血测定血浆Hey浓度.结果 共纳入139例急性卒中患者,其中男性72例,女性67例,平均(70.1±10.2)岁;出血性卒中24例,缺血性卒中115例.严重LA组(n=46)的年龄[(76.23±8.74)岁对(64.58±7.42)岁;t=4.621,P=0.012]、高血压比例(89.13％对67.74％;x2=8.324,P=0.0370)和血浆Hey水平[(14.53±4.31)mmol/L对(11.31 ±3.16) mmol/L;t =6.538,P=0.008]显著高于非严重LA组(n=93).Spearman相关分析显示,血浆Hcy水平与LA严重程度显著相关(rs=0.365,P=0.002).多变量logitic回归分析显示,血浆Hcy水平升高[优势比(odds ratio,OR)1.336,95％可信区间(confidence interval,CI)1.141 ～1.526;P=0.001]和年龄(OR1.093,95％ CI 1.031～1.162;P=0.016)均是严重LA的独立危险因素.CMB组(n=57)的年龄[(74.37±6.35)岁对(67.56±8.52)岁;t=6.628,P=0.038]和高血压比例(94.74％对62.20％;x2 =8.773,P=0.002)显著高于非CMB组(n=82).Spearman相关分析显示,血浆Hcy水平与CMB数量无显著相关性(rs=0.038,P=0.813).多变量logistic回归分析显示,高血压(OR5.762,95％ CI 1.633～22.718;P=0.010)为CMB的独立危险因素.结论 血浆Hcy水平增高与LA相关而与CMB无关.     

卒中高危人群的睡眠质量:基于社区的调查

目的 调查卒中高危人群的睡眠质量并探讨睡眠障碍的危险因素.方法 2016年3月对天津市南开区水上公园及王顶堤社区的卒中高危人群进行横断面调查,根据匹兹堡睡眠质量指数量表(Pittsburgh Sleep Quality Index,PSQI)将研究对象分为睡眠良好组和睡眠障碍组,采用多变量logistic回归分析确定影响睡眠质量的危险因素;根据高危人群既往有无卒中史分为有卒中史组和无卒中史组,比较2组睡眠质量,并分析睡眠障碍与卒中转归的相关性.结果 共纳入565例卒中高危人群,睡眠障碍者178例(31.5％).睡眠障碍组年龄显著大于睡眠良好组[(66.70±8.97)岁对(62.87±9.46)岁;t=-4.540,P＜0.001],女性(68.0％对49.1％;x2=16.190,P＜ 0.001)、高血压(69.7％对57.9％;x2=7.154,P=0.005)、缺血性心脏病(48.9对35.4％;x2=9.253,P=0.002)、既往卒中或短暂性脑缺血发作(transient ischemic attack,TIA)史(30.9％对18.9％;x2=10.080,P=0.001)、颈动脉斑块(71.9％对53.7％;x2=16.688,P＜0.001)构成比显著高于睡眠良好组.多变量logistic分析表明,在校正年龄和性别后,既往卒中或TIA史[优势比(odds ratio,OR)1.712,95％可信区间(confidence interval,CI)1.105～2.653;P=0.016]、颈动脉斑块(OR1.583,95％ CI 1.003～2.498;P =0.048)是睡眠障碍的独立危险因素.既往有卒中史者PSQI总分显著高于无卒中史者[(7.25±4.71)分对(6.13±4.20)分;t=-2.578,P=0.010];既往有卒中史者入睡时间评分[(1.24±1.06)分对(0.95±1.02)分;t=-2.868,P=0.004]和睡眠障碍评分[(1.23±0.63)分对(1.07±0.61)分;t=-2.622,P=0.009]显著高于无卒中史者.根据改良Rankin量表评分将有卒中史者分为转归良好组(0～2分)和转归不良组(＞2分),分别包括105例(82.0％)和23例(18.0％).转归不良组睡眠障碍患者比例(78.3％对35.2％;x2=14.251,P＜0.001)和PSQi评分[中位数和四分位数间距:6(3 ～8)分对12(8～18)分;Z=-4.392,P＜0.001]均显著高于转归良好组.结论 卒中高危人群睡眠障碍发生率高,既往卒中或TIA史、颈动脉斑块是卒中高危人群睡眠障碍的独立危险因素,而且睡眠障碍与卒中转归不良相关.因此,应积极关注卒中高危人群的睡眠质量,控制导致其睡眠障碍的危险因素,特别是对于既往有卒中史者,将有助于降低卒中的发病风险.     

缺血性卒中患者氯吡格雷抵抗的危险因素:前瞻性病例系列研究

目的 探讨缺血性卒中患者中氯吡格雷抵抗(clopidogrel resistance,CR)的危险因素.方法 急性缺血性卒中患者服用氯吡格雷(75 mg/d)10～ 14 d后采用光比浊法测定血小板聚集率变化.根据血小板聚集率变化将病例分为CR组和氯吡格雷敏感(clopidogrel sensitivity,CS)组,比较两组的人口统计学和临床资料,并采用多变量 logistic回归分析确定CR的独立危险因素.结果 共纳入147例急性缺血性卒中患者,其中CR 组42例(28.57％),CS组105例(71.43％).CR组糖尿病(54.76％对11.43％;x2=31.054,P=0.000)、既往短暂性脑缺血发作(transient ischemic attack,TIA)史(80.95％对 26.67％; x2=36.251,P=0.000)或经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI)史(26.19％对3.81％;x2=16.400.P=0000)、服用钙通道阻滞药(calcium channel blocker,CCB)(83.33％对54.29％;x2=10.810,P=0.001)、血管紧张素转换酶抑制药(angiotensin converting enzyme inhibitor,ACEI)/血管紧张素受体阻滞药(angiotensin receptor blocker,ARB)(66.67％对42.86％;x2=6.803.P=0.009)和质子泵抑制药(47.62％对14.29％;x2=18.375,P=0.000)的患者比例以及血浆总胆固醇[(5.23±1.07) mmol/L对(4.60±1.11) mmol/L;t=3.121.P=0.002]、血糖浓度[(6.65±2.19)mmol/L对(5.43±1.15)mmol/L;t=3.442.P=0.001]和糖化血红蛋白水平[ (6.40±1.42)％对(5.48±1.09)％;t=3.780,P=0.000]均显著高于CS组.多变量logistic 回归分析显示,糖尿病[优势比(odds ratio,OR) 13.711,95％可信区间(confidence interval,CI)1.667～112.784;P =0.015]、总胆固醇增高(OR2.828,95％ CI1.574～5.080;P =0.001)、既往TIA史(OR16.627,95％ CI4.691～58.934;P =0.000)以及长期服用CCB( OR 4.147,95％ CI1.053～16.332;P=0.042)、ACEI/ARB( OR 4.841,95％ CI 1.539～15.231;P=0.007)为CR的独立危险因素.结论 缺血性卒中患者的CR与多种因素有关,其中糖尿病、总胆固醇增高以及长期服用 CCB和ACEI/ARB是CR的独立危险因素.     

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.     

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.     

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.     

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.