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1.
目的 :探讨血脂异常对血清细胞间黏附分子 1(ICAM 1)、血管细胞黏附分子 1(VCAM 1)和E 选择素水平的影响。方法 :入选 12 0例研究对象 ,其中高胆固醇血症 (Ⅰ组 ) 31例 ;高三酰甘油血症 (Ⅱ组 ) 30例 ;混合性高脂血症 (Ⅲ组 ) 2 9例 ;血脂正常 (Ⅳ组 ) 30例。用酶联免疫吸附法检测血清ICAM 1、VCAM 1和E 选择素水平 ,比较上述 3个指标在各组间的差异。结果 :总胆固醇水平 ,Ⅰ组 [(6 .5 5± 0 .6 7)mmol/L]和Ⅲ组 [(6 .2 7±0 .6 7)mmol/L]显著高于Ⅳ组 [(4.38± 0 .4 9)mmol/L],P <0 .0 1;三酰甘油水平 ,Ⅱ组 [(3.39± 0 .6 0 )mmol/L]和Ⅲ组 [(3.4 4± 0 .6 2 )mmol/L]显著高于Ⅳ组 [(1.39± 0 .4 0 )mmol/L],P <0 .0 1。同时 ,血清ICAM 1水平在Ⅰ组 [(76 4± 71) μg/L]、Ⅱ组 [(74 9± 71) μg/L]和Ⅲ组 [(82 3± 80 ) μg/L]明显高于Ⅳ组 [(6 0 4± 6 7) μg/L],P <0 .0 1;血清VCAM 1水平在Ⅰ组 [(1837± 16 4 ) μg/L]、Ⅱ组 [(1836± 16 0 ) μg/L]和Ⅲ组 [(196 3± 181) μg/L]明显高于Ⅳ组 [(130 7± 14 9) μg/L],P <0 .0 1;血清E 选择素水平在Ⅰ组 [(6 6± 12 ) μg/L]、Ⅱ组 [(70± 14 ) μg/L]和Ⅲ组 [(81± 17) μg/L]明显高于Ⅳ组 [(39± 11) μg/L],P <0 .0 1。结论 :血脂异常可使血清I  相似文献   

2.
目的 探讨急性缺血性卒中患者循环CD133+/KDR+内皮祖细胞(endothelial progenitor cells,EPCs)水平与转归的关系.方法 纳入发病24 h内的首次急性缺血性卒中住院患者以及年龄和性别相匹配的健康体检者.收集患者人口统计学和临床资料.采用流式细胞术检测CD133+/KDR+EPCs水平.在发病后90 d时对所有患者进行随访,采用改良Rankin量表评价临床转归,0~2分定义为转归良好,>2分定义为转归不良.结果 共纳入连续126例缺血性卒中患者以及60例年龄和性别相匹配的健康体检者.在缺血性卒中患者中,大动脉粥样硬化(large artery atherosclerosis,LAA) 33例(26.19%),小动脉闭塞(small artery occlusion,SAO)74例(58.73%),心源性栓塞(cardioembolism,CE)19例(15.08%);82例(65.08%)转归良好,44例(34.92%)转归不良.LAA型(0.071%±0.018%)、CE型(0.068%±0.016%)和SAO型(0.118%±0.012%)患者基线循环EPCs数量均显著低于对照组(0.246%±0.052%;P均<0.05);CE型(P=0.028)和LAA型(P=0.037)均显著低于SAO型;CE型低于LAA型,但差异无统计学意义(P=0.762).转归不良组LAA型(40.91%对18.29%;χ2=7.577,P=0.006)和CE型(29.55%对7.32%;χ2=11.049,P=0.001)和心房颤动(29.55%对10.98%;χ2=6.582,P=0.009)患者的构成比以及年龄[(69.64±9.62)岁对 (61.12±7.31)岁;t=5.570,P<0.001]、基线NIHSS评分[(14.16±4.22)分对 (6.96±2.04)分;t=12.919,P<0.001]、基线收缩压[(176.06±13.42)mmHg对 (164.12±11.69)mmHg,1 mmHg=0.133 kPa;t=5.187,P<0.001]、低密度脂蛋白胆固醇[(2.92±0.52)mmol/L对 (2.49±0.36)mmol/L;t=5.447,P<0.001]、空腹血糖[(8.76±2.88)mmol/L对 (6.82±2.24)mmol/L;t=4.185,P<0.001]、C反应蛋白[(7.62±1.82)mg/L对 (4.57±1.58)mg/L;t=9.790,P<0.001]和D-二聚体[(1.14±0.08)mg/L对 (0.97±0.22)mg/L;t=4.946,P<0.001]水平均显著高于转归良好组,而SAO型患者构成比(29.55%对74.39%;χ2=23.759,P<0.001)以及高密度脂蛋白胆固醇[(0.94±0.68)mmol/L对 (1.16±0.14)mmol/L;t=2.829,P=0.005]和基线EPCs(0.069%±0.018%对0.098%±0.021%;t=7.755,P<0.001)水平显著低于转归良好组.多变量logistic回归分析显示,基线NIHSS评分较高(优势比1.242,95%可信区间1.126~1.372;P<0.001)、CE型(优势比3.460,95%可信区间1.312~5.146;P=0.016)和基线EPCs数量较低(优势比1.632,95%可信区间1.006~3.024;P<0.001)是急性缺血性卒中患者转归不良的独立危险因素.结论 急性缺血性卒中患者循环EPCs水平显著降低,基线EPCs水平较低是缺血性卒中患者90 d时转归不良的独立预测因素.  相似文献   

3.
目的 :探讨微粒化非诺贝特对高三酰甘油血症患者血管内皮功能的作用。方法 :对 30例高三酰甘油血症患者 (口服微粒化非诺贝特 2 0 0mg/d治疗 4周前后 )和 30例正常人采用高分辨超声技术检测血流介导的和硝酸甘油介导的肱动脉舒张功能 ,并测定血浆内皮素 (ET)和血脂。结果 :①高三酰甘油血症组血流介导的肱动脉舒张反应较正常组明显减弱 [(2 .7± 2 .0 ) %∶(15 .0± 8.0 ) % ,P <0 .0 1],而两组对硝酸甘油的血管舒张反应差异无显著性意义 [(15 .0± 5 .0 ) %∶(16 .8± 9.0 ) % ,P >0 .0 5 ]。②高三酰甘油血症患者微粒化非诺贝特治疗后血流介导的肱动脉舒张显著改善 [(11.0± 9.0 ) % ,P <0 .0 1],而硝酸甘油介导的血管舒张较治疗前无明显改变[(16 .2± 6 .0 ) % ,P >0 .0 5 ]。③高三酰甘油血症患者血浆ET水平显著高于正常人 [(10 6 .2± 19.2 ) μg/L∶(72 .4± 14 .1) μg/L ,P <0 .0 1],微粒化非诺贝特治疗后血浆ET水平显著降低 [(82 .7± 15 .5 ) μg/L ,P <0 .0 1],血清三酰甘油明显降低 (P <0 .0 5 )。结论 :微粒化非诺贝特对高三酰甘油血症患者受损的血管内皮依赖性舒张功能有改善作用。改善血管内皮功能亦是微粒化非诺贝特防治冠心病的作用机制之一  相似文献   

4.
用ELISA法检测188例癌症患者血浆TM和24例癌组织及其邻近正常组织浸液的TM浓度。结果:癌症患者血浆TM水平[(33.47±14.25)μg/L]明显高于对照组[(20.40±7.22)μg/L,P<0.01,癌症转移组(41.68±16.96)μg/L明显高于对照组(P<0.01),术后组患者TM(18.45±9.96)μg/L]比术前组TM[(28.29±11.74)μg/L]明显回落(P<0.01),  相似文献   

5.
目的通过观察慢性情绪应激对高脂饮食大鼠脂代谢、炎症反应和主动脉内皮细胞TLR4表达的影响,探讨慢性情绪应激在动脉粥样硬化病变形成中的作用、机制。方法雄性Wistar大鼠40只,随机分为正常对照组(NC)、无应激组(NS)、生理应激组(PS)和情绪应激组(ES),每组各10只,并制作慢性情绪应激模型。于末次应激结束后采集血标本,全自动生化分析仪检测血清TC、TG、HDL-C、LDL-C和hs-CRP,ELISA法测定血清ox-LDL、放免法检测TNF-α水平;HE染色观察大鼠主动脉形态学变化;免疫组化法(S-P)测定主动脉内皮细胞TLR4表达。结果 (1)ES组大鼠较其他3组出现了明显的脂代谢紊乱和炎症反应。与PS组、NS组、NC组比较,ES组TC、LDL-C、ox-LDL水平明显升高[TC:(5.30±0.69)mmol/L比(3.94±0.42)mmol/L、(3.82±0.48)mmol/L、(2.07±0.26)mmol/L;LDL-C:(1.57±0.22)mmol/L比(1.18±0.13)mmol/L、(1.11±0.11)mmol/L、(0.75±0.11)mmol/L;ox-LDL:(65.18±6.51)μg/dl比(45.65±2.70)μg/dl、(38.35±2.27)μg/dl、(14.99±1.46)μg/dl,均为P<0.01];ES组HDL-C[(0.94±0.14)mmol/L]低于NS组[(1.09±0.14)mmol/L,P<0.05],低于NC组[(1.16±0.18)mmol/L,P<0.01];与PS组、NS组、NC组比较,ES组hs-CRP、TNF-α水平升高[hs-CRP:(1.748±0.082)mg/L比(1.485±0.067)mg/L、(1.381±0.067)mg/L、(0.757±0.069)mg/L;TNF-α:(2.447±0.083)μg/L比(2.189±0.099)μg/L、(2.181±0.085)μg/L、(1.772±0.075)μg/L,均为P<0.01];(2)ES组大鼠主动脉出现早期动脉粥样硬化性改变;(3)ES组大鼠主动脉内皮细胞TLR4表达明显上调,其阳性细胞单位面积平均吸光度值(A)高于PS组、NS组和NC组[(0.334±0.010)比(0.250±0.012)、(0.238±0.015)、(0.082±0.008),均为P<0.01]。结论慢性情绪应激可能在动脉粥样硬化形成的早期,部分通过激活TLR4释放炎性细胞因子引起机体的炎症反应,进而导致动脉粥样硬化病变形成。  相似文献   

6.
目的研究重组人促红细胞生长素(recombinant human erythropoietin,rhEPO)治疗老年急性缺血性脑卒中患者的有效性及安全性。方法入选74例年龄≥75岁的老年急性缺血性脑卒中患者,经磁共振弥散加权成像检查证实在大脑中动脉的范围内,将患者随机分为治疗组36例和对照组38例,患者入院后前3 d每日分别给予rhEPO或生理盐水静脉注射治疗。观察第1、3、7、20和30天美国国立卫生研究院卒中量表(NIHSS)评分和脑梗死体积变化,ELISA法检测损伤标记物S100B水平。结果与对照组比较,治疗组第20、30天NIHSS评分明显下降(P<0.05);第20天脑梗死体积明显降低[(46.5±32.3)cm~3 vs(89.6±68.9)cm~3,P<0.01];第3、7和20天血清S100B水平明显下降[(1.45±0.25)μg/L vs(1.58±0.13)μg/L,(1.41±0.20)μg/L vs(1.69±0.15)μg/L,(0.38±0.14)μg/L vs(0.78±0.26)μg/L,P<0.01]。结论老年急性缺血性脑卒中患者对静脉注射高剂量rhEPO治疗耐受性良好,并且可改善患者30 d后的临床预后。  相似文献   

7.
目的 探讨缺血性卒中患者并发急性肾损伤(acute kidney injury, AKI)的危险因素.方法 回顾性纳入缺血性卒中患者,收集一般临床资料、血管危险因素、药物使用情况、卒中病因学分型、卒中严重程度和基线生化指标等.根据是否发生AKI分为并发AKI组和对照组.采用多变量logistic回归分析缺血性卒中患者发生AKI的独立危险因素.结果 共纳入214例缺血性卒中患者,其中32例(14.95%)发生AKI,182例(85.05%)未发生AKI.AKI组心力衰竭(62.50%对41.21%;χ2=4.998,P=0.025)、应用甘露醇(87.50%对43.96%;χ2=20.643,P<0.001)和呋塞米(87.50%对43.96%;χ2=20.643,P<0.001)、应用对比剂(37.50%对19.23%;χ2=5.300,P=0.021)和对比剂用量>200 ml(28.13%对9.89%;χ2=6.637,P=0.010)患者构成比以及NIHSS评分[(18.0±4.5)分对(8.0±3.2)分;t=15.249,P<0.001]、舒张压[(89.98±9.12)mmHg对(80.56±8.19)mmHg,1 mmHg=0.133 kPa;t=5.898,P<0.001]、空腹血糖[(10.54±4.31)mmol/L对(6.32±1.32)mmol/L;t=5.898,P<0.001]、血尿素氮水平[(11.21±2.13)mmol/L对(7.98±2.34)mmol/L;t=7.293,P<0.001]、动脉血乳酸浓度[(3.98±0.12)mmol/L对(0.91±0.25)mmol/L;t=68.003,P<0.001]均显著高于非AKI组.多变量logistic回归分析示,在校正各种混杂因素后,NIHSS评分较高[优势比(odds ratio, OR) 1.910,95%可信区间(confidence interval, CI) 1.517~6.012;P=0.024]、舒张压较高(OR 1.816,95% CI 1.652~3.876;P=0.018)、动脉血乳酸浓度(OR 1.553,95% CI 1.256~1.763;P=0.019)、应用脱水剂(甘露醇:OR 3.765,95% CI 2.081~9.658,P=0.017;呋塞米:OR 5.329,95% CI 3.085~8.763,P=0.010)、应用对比剂(OR 2.097,95% CI 1.364~2.456;P=0.031)以及对比剂>200 ml(OR 3.294,95% CI 1.464~2.786;P=0.021)是缺血性卒中患者AKI的独立危险因素.结论 NIHSS评分、舒张压、动脉血乳酸浓度、应用甘露醇和呋塞米以及应用对比剂和对比剂剂量>200 ml与缺血性卒中患者AKI独立相关.  相似文献   

8.
广州市省公医系统部分干部血脂改变近况   总被引:1,自引:0,他引:1  
目的 了解广州市省公医系统 40岁以上部分干部近三年血脂水平的改变。方法  1995~ 1998年 2次对2 6 10例和 2 970例干部采用常规酶法检查血清总胆固醇(TC)、甘油三酯 (TG)、高密度脂蛋白 -胆固醇 (HDL -C)水平。结果  1998年组TC水平 [(5 5 1± 1 0 0 )mmol/L]与 1995年组 [(5 5 3± 1 0 6 )mmol/L]无明显差异 ;1998年组TG水平[(1 5 9± 1 0 4)mmol/L]明显高于 1995年组 [(1 2 7± 0 84)mmol/L];1998年组HDL -C水平 [(1 0 1± 0 33)mmol/L]明显低于 1995年组 [(1 35± 0 37)mmol/L]。 1995年组和 1998年组女性TC水平明显高于男性 ;1998年组男性TG水平明显高于女性。结论 近三年来TG明显升高 ,HDL -C明显降低 ,应继续加强对血脂的调控。  相似文献   

9.
目的探讨女性高血压患者绝经前后及绝经年限与血脂变化的关系。方法女性高血压患者131例,分绝经前组(34例)及绝经后组(97例),测晨起空腹静脉血中甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C),进行组间比较,并分析绝经年限与血脂水平的相关性。并与73例健康对照组比较。结果绝经前高血压组TC、LDL-C〔(5.27±0.47)mmol/L和(3.50±0.45)mmol/L〕显著高于对照组〔(4.33±0.70)mmol/L和(2.67±0.50)mmol/L,均为P<0.01〕。绝经后高血压组TG、TC、LDL-C〔(1.87±1.06)mmol/L、(6.41±0.78)mmol/L和(4.61±0.87)〕均显著高于对照组〔(1.26±0.79)mmol/L、(4.63±0.54)mmol/L和(2.79±0.47)mmol/L,均为P<0.01〕,HDL-C则低于对照组〔(1.36±0.32)和(1.57±0.33)mmol/L,P<0.01〕。高血压绝经后组TG、TC、LDL-C〔(1.87±1.06)mmol/L、(6.41±0.78)mmol/L和(4.61±0.87)mmol/L〕显著高于绝经前组〔(1.35±0.99)mmol/L,P<0.05;(5.27±0.47)mmol/L,P<0.01;(3.50±0.45)mmol/L,P<0.01〕,HDL-C低于绝经前组〔(1.36±0.32)和(1.51±0.26)mmol/L,P<0.05〕。TC、LDL-C与绝经年限呈显著正相关(r分别为0.88和0.81,P<0.01)。结论女性高血压患者绝经后血TG、TC、LDL-C增高,TC、LDL-C与绝经年限呈正相关,而HDL-C降低。  相似文献   

10.
目的探讨男性冠状动脉粥样硬化性心脏病(冠心病)患者体内雄激素水平与反映内皮功能异常的指标颈动脉内膜、中膜厚度(IMT)、血管细胞黏附因子-1(VCAM-1)的关系,观察雄激素减轻动脉粥样硬化的程度。方法比较51例男性冠心病患者与55例对照者的年龄、体质量、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、三酰甘油(TG)、吸烟、空腹血糖、血压、血清游离睾酮水平(FT)、VCAM-1及IMT,分析冠心病危险因素如年龄、体质量、TC、LDL-C、HDL-C、TG、吸烟、空腹血糖、血压及FT与VCAM-1、IMT的相关性。结果冠心病组的年龄、血压、吸烟史、空腹血糖、HDL-C与对照组比较,差异无统计学意义(P>0.05);体质量为(78.1±5.7)kg,大于对照组的(73.6±4.8)kg,P<0.01;TC高于对照组[(4.99±0.88)mmol/L和(4.52±0.65)mmol/L,P<0.01];LDL-C高于对照组[(3.35±0.63)mmol/L和(2.94±0.55)mmol/L,P<0.01];TG高于对照组[(2.35±0.92)mmol/L和(1.87±0.61)mmol/L,P<0.01];FT低于对照组[(13.2±3.6)×10-9g/L和(16.6±5.1)×10-9g/L,P<0.01];IMT高于对照组[(1.11±0.24) mm和(0.96±0.22)mm,P<0.01];VCAM-1含量高于对照组[(372.7±111.8)×10-6g/L和(208.2±72.5)×10-6g/L,P<0.01]。多元逐步回归分析显示FT与IMT、VCAM-1分别呈负相关(r=-0.358,r=-0.547,均为P<0.01)。结论男性冠心病患者FT水平与反映内皮功能异常的指标IMT、VCAM-1呈负相关。  相似文献   

11.
Two ligament systems of the larynx are demonstrated by dissection. The suspensory ligament of the esophagus is attached to the posterior aspect of the cricoid cartilage and is also a part of the fascial sheath which is common to the hyoid, thyroid, and cricoid. The ligaments at the inner margins of the vocal, ventricular, and aryepiglottic folds are distinctive in site and, inferentially, in function. The aryepiglottic ligaments join at the incisura between the arytenoid cartilages and are continued as the corniculopharyngeal ligament which splays into the flexible tissues in the anterior wall of the hypopharynx, posterior to the suspensory ligament of the esophagus. These ligament systems are involved in two different actions in swallow. The gross superior and anterior motions of the larynx are transmitted to the esophagus by the suspensory ligament, so that the esophagus is elevated in relation to the bolus and is also opened. These esophageal displacements resemble, in effect, the swallow displacements of the pharyngoesophageal segment and of the constrictor wall of the hypopharynx. The marginal ligaments of the laryngeal folds help to implement the constriction and closure of the larynx during swallow. By anatomical inference, the corniculopharyngeal ligament effects vertical traction within the flexible tissues of the anterior wall of the hypopharynx.  相似文献   

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Digestion and the structure and function of the gut   总被引:1,自引:0,他引:1       下载免费PDF全文
K G Wormsley 《Gut》1986,27(12):1520-1521
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[摘要] 目的 探讨表观扩散系数(apparent diffusion coefficient, ADC)值与肝细胞癌(hepatocellular carcinoma, HCC)组织学分级的相关性以及不同直径肿瘤的ADC值与HCC的相关性。方法?回顾性分析2017年—2020年180例病理证实为HCC的病例资料,按肿瘤直径大小分为<2 cm、≥2 cm且<3 cm、≥3 cm且<5 cm、≥5 cm 4组,标为I、II、III、IV组。分析ADC值与HCC组织学分级的相关性,并分析在不同直径肿瘤ADC值与HCC的相关性。结果?高、中和低分化HCC的ADC值分别为(1.159±0.302)×10-3、(0.951±0.213)×10-3和(0.811±0.239)×10-3 mm2/s,逐级降低(P<0.05)。ADC值与总体HCC的组织学分级呈负相关(r=-0.474),与I~III组HCC的组织学分级均呈负相关(r值分别为-0.663、-0.527、-0.364),而与IV组HCC的组织学分级无相关性。结论?ADC值可以作为非侵入性预测HCC组织学分级的指标,预测结果受肿瘤大小影响,更适用于小肝细胞癌。  相似文献   

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BackgroundThe hospital is considered as one of the founding elements of modern medicine. Such an institution, originally born to be a center for housing the sick and the poor, has provided with a place to improve the medical knowledge and to educate new generations of nurses and physicians. This paper wants to remind the meaning and the development of the hospital institution in the western world.MethodsThe first part of this work analyzed the evolution of hospital, using a classical historiographical approach. In the second part, the history of the “Ospedale Maggiore” in Milan was used as a paradigm to describe the evolution of hospital from the Renaissance to nowadays through a “microhistorical approach”.ResultsThe origins of the public hospital are evidenced in early Christian age, when the Christian message led people to assist the sick and the poor and to establish centers for such interventions, initially in the house of the bishop, then in monasteries and, finally, in autonomous buildings (the hospitals). These institutions were economically supported by the donations of wealthy philanthropists. Since the nineteenth century the hospitals have changed their organization and functions, but have continued to associate the charity and the care.ConclusionChristian charity and the lay culture originated from it may be rightly credited not only as the founding element of ancient hospitals, but also as the virtue which has made possible for the development of medicine, as we know it.  相似文献   

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In studies with the isolated perfused working hearts from rats with experimentally induced diabetes, the ability of the hearts to survive during, and recovery from, 30 min of anoxia has been studied. In contrast with hearts obtained from normal rats, which gave good and sustained recoveries, the hearts from diabetic animals after an initial period of recovery (approx. 2 min), exhibited cardiac failure for periods of up to 4 min. After this period the hearts entered a second phase of recovery but did not recover to the same extent as the hearts from normal animals. Hearts of diabetic animals therefore appear to be more vulnerable to anoxic damage than do those from normal rats.Using metabolic inhibitors the biochemical basis of this transient post-anoxic failure in diabetic hearts was investigated. It was discovered that the immediate post-anoxic recovery of the hearts was supported in part by endogenous supplies of pre-formed high energy phosphates and in part from energy derived from the glycolysis of endogenous glycogen. During the initial recovery period of approx. 2 min there was little dependence upon the oxidative metabolism of either endogenous or exogenous substrates. In normal hearts the role of major energy provider was rapidly assumed by oxidative processes utilizing exogenous substrate. In the insulin deficient diabetic hearts the impaired transport of glucose into the cell and consequent energy shortage led to the transient cardiac failure and accounted for the delayed secondary recovery. This condition could be completely overcome either by the provision of exogenous insulin or by the provision of substrates such as pyruvate, acetate, citrate or hydroxybutyrate, whose efficient utilization was not impaired by an insulin deficiency.The relevance of these findings in the diabetic rat heart is discussed in relation to the known insulin deficiency occurring in the human during heart failure and the proposed importance of glucose metabolism in the support of the failing myocardium. In addition, these findings are considered in relation to the possible role of insulin both in the genesis and the treatment of heart failure with particular reference to heart failure in humans with diabetes mellitus.  相似文献   

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