瑞舒伐他汀与阿托伐他汀对急性脑梗死患者血脂、血清超敏C反应蛋白及颈动脉粥样硬化斑块作用的比较

目的比较瑞舒伐他汀与阿托伐他汀对急性脑梗死患者血脂、超敏C反应蛋白(hs-CRP)及颈动脉粥样硬化斑块的影响。方法在标准缺血性脑卒中治疗的基础上,瑞舒伐他汀组加用瑞舒伐他汀10mg/d,阿托伐他汀组加用阿托伐他汀片20 mg/d,治疗6个月。于治疗前及治疗后6个月,检测患者血脂、hsCRP水平,颈动脉超声检查颈动脉粥样硬化斑块情况。结果与治疗前比较,瑞舒伐他汀组与阿托伐他汀组6个月时总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)和hs-CRP水平均显著降低(均P0.05)。6个月时,瑞舒伐他汀组TC、TG、LDL-C及hs-CRP水平显著低于阿托伐他汀组及对照组(均P0.05)。3组间治疗前内-中膜厚度(IMT)差异无统计学意义;与治疗前及对照组比较,瑞舒伐他汀组与阿托伐他汀组6个月时IMT及低回声斑块比率显著降低,高回声斑块率显著增高(均P0.05)。瑞舒伐他汀组、阿托伐他汀组及对照组患者第6个月的NIHSS评分及mRS评分均显著低于治疗前(均P0.05)。治疗前及治疗后6个月时,3组间NIHSS评分及mRS评分差异无统计学意义。结论瑞舒伐他汀与阿托伐他汀能显著降低急性脑梗死患者血脂及血清hs-CRP水平,抑制动脉粥样硬化斑块的形成。瑞舒伐他汀的降脂及抗炎作用比阿托伐他汀更强。     

分析阿托伐他汀和瑞舒伐他汀对短暂性脑缺血发作患者颈动脉斑块的影响

目的探讨阿托伐他汀和瑞舒伐他汀对短暂性脑缺血患者颈动脉斑块的影响。方法选取2014-05—2015-05在我院接受治疗的短暂性脑缺血发作患者82例,按照随机数字表分为A组(阿托伐他汀组,n=41)和B组(瑞舒伐他汀组,n=41)。A组给予阿托伐他汀(10mg/d)联合阿司匹林(100mg/d),B组给予瑞舒伐他汀(10mg/d)联合阿司匹林(100mg/d),连续治疗6个月;比较2组治疗前后颈动脉中层厚度(IMT)和粥样硬化斑块面积,甘油三酯(TG)、胆固醇(TC)、高密度脂蛋白(HDL-C)和低密度脂蛋白(LDL-C)水平,比较2组6个月内的脑血管事件发生率。结果治疗前,2组IMT和粥样硬化斑块面积差异无统计学意义(P0.05),治疗后,B组IMT和斑块面积显著小于A组(P0.05);治疗前2组TG、TC、LDL-C和HDL-C水平差异无统计学意义(P0.05),治疗后2组TG、TC、LDL-C和HDL-C水平与治疗前差异具有统计学意义(P0.05);2组患者6个月内的脑血管事件发生率差异无统计学意义(P0.05)。结论阿托伐他汀和瑞舒伐他汀均能够很好地降低短暂脑缺血发作患者的血脂水平、降低脑血管事件的发生率,治疗剂量为10mg/d瑞舒伐他汀稳定及改善颈动脉粥样硬化斑块的疗效优于10mg/d阿托伐他汀。     

瑞舒伐他汀与阿托伐他汀对急性脑梗死患者血脂CRP及颈动脉粥样硬化斑块的影响比较

目的比较瑞舒伐他汀与阿托伐他汀对急性脑梗死患者血脂、CPR及颈动脉粥样硬化斑块的影响。方法将480例急性脑梗死患者随机分为瑞舒伐他汀组和阿托伐他汀组各240例,2组采用相同的基础治疗,瑞舒伐他汀组在此基础上加载瑞舒伐他汀,10mg/(次·d),阿托伐他汀组则加载阿托伐他汀,10mg/(次·d),均连续治疗24周。所有患者均于治疗前及治疗后12、24周采血,测定血脂四项,并于治疗前及治疗后12、24周行颈动脉超声检查,测量颈动脉粥样斑块内膜-中膜厚度(IMT)并采血测量C反应蛋白(CRP)。结果治疗后12周、24周,2组TC、TG、LDL-C和CRP较疗前有不同程度的下降,其治疗后瑞舒伐他汀组中者TC、TG、LDL-C水平均显著低于阿托伐他汀组;瑞舒伐他汀组颈动脉粥样硬化斑块厚度较疗前显著下降且低于同时期阿托伐他汀组(P0.05)。结论急性脑梗死患者长期应用瑞舒伐他汀,可降低血脂水平并减少颈动脉斑块IMT及斑块内炎症反应,疗效优于阿托伐他汀。     

PAS三联疗法对急性脑梗死患者血清相关蛋白及颈动脉易损斑块的影响

目的 探讨普罗布考+阿司匹林+阿托伐他汀(PAS)三联疗法对急性脑梗死患者血清氧化型低密度脂蛋白(ox-LDL)、血清妊娠相关蛋白A(PAPP-A)及基质金属蛋白酶-3(MMP-3)水平的影响,观察其对颈动脉易损斑块的消退作用. 方法 选择武汉市第五人民医院神经内科自2007年9月至2010年7月收治的135例急性脑梗死患者为研究对象,根据颈动脉超声检查结果分为颈动脉稳定斑块组(n=45)和颈动脉易损斑块组(n=90).易损斑块组抽血检查后按随机数字表法分为阿托伐他汀+阿司匹林(AS)组45例(阿司匹林100 mg/d、阿托伐他汀20mg/d,口服)和PAS组45例(阿司匹林1 00 mg/d、阿托伐他汀20 mg/d、普罗布考0.25/次,2次/d,口服).比较治疗前和治疗4周后各组患者血清ox-LDL、PAPP-A和MMP-3水平,观察治疗前及治疗12月后颈动脉内中膜厚度(IMT)、斑块面积及斑块回声变化. 结果 治疗前,易损斑块组中两亚组(AS组和PAS组)血清ox-LDL、PAPP-A和MMP-3水平均明显高于稳定斑块组,差异有统计学意义(P＜0.05),但两亚组间该3项指标比较差异无统计学意义(P＞0.05).治疗4周后,PAS组患者血清ox-LDL、PAPP-A和MMP-3水平均明显低于AS组和稳定斑块组,距治疗前下降幅度均大于AS组和对照组,差异有统计学意义(P＜0.05).治疗12月后,易损斑块组中两亚组(AS组和PAS组)IMT值和斑块面积均较治疗前减少,且PAS组该2项指标低于AS组,差异均有统计学意义(P＜0.05);PAS组低回声斑块数量较AS组明显减少,斑块消失数量增加,差异有统计学意义(P＜0.05). 结论 PAS三联疗法具有更强的抗氧化降脂作用,可逆转和稳定斑块.     

不同剂量阿托伐他汀钙治疗急性脑梗死临床观察

目的比较急性脑梗死患者应用不同剂量阿托伐他汀钙对血脂、超敏C反应蛋白(hs-CRP)及颈动脉粥样斑块的影响。方法选取商丘市中心医院2015-03—2016-09符合入选条件的急性脑梗死患者84例,采用随机数字表法分为对照组和观察组各42例,在标准脑梗死治疗基础上,对照组给予阿托伐他汀钙片20mg,观察组给予阿托伐他汀钙片40 mg,1次/d。入院时及治疗3个月后检测血脂、hs-CRP水平,彩色多普勒超声检查颈动脉粥样硬化斑块情况,采用NIHSS评定神经功能缺损程度,并统计不良反应情况。结果与治疗前比较,2组总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)和hs-CRP水平均显著降低(P0.05),且观察组低于对照组(P0.05);治疗3个月时,2组颈动脉内中膜厚度(IMT)、斑块积分及NIHSS评分均较前减少,观察组减少程度更大,差异有统计学意义(P0.05)。2组不良反应差异无统计学意义(P0.05)。结论阿托伐他汀可以降血脂、hs-CRP水平,具有稳定及缩小颈动脉粥样斑块、改善神经功能缺损程度的作用,40mg阿托伐他汀效果更佳,不良反应无明显增加,有较好的安全性。     

调脂治疗对急性脑梗死患者血清hs-CRP、IL-18及MMP-7水平的影响及颈动脉斑块的干预作用

目的 探讨不同剂量阿托伐他汀调脂治疗对急性脑梗死患者血清高敏C反应蛋白(hs-CRP)、白细胞介素-18(IL-18)及基质金属蛋白酶-7(MMP-7)的影响,观察其对颈动脉斑块的干预作用.方法 144例急性脑梗死患者根据颈动脉超声检查结果分为颈动脉稳定斑块组(n=72)和颈动脉易损斑块组(n=72),抽血检查后分别随机分为小剂量组36例(阿托伐他汀10mg/d,口服)和大剂量组36例(阿托伐他汀40mg/d,口服).比较治疗前和治疗后4周血清hs-CRP、IL-18和MMP-7水平;观察治疗前及治疗后6个月颈动脉内-中膜厚度(IMT值)、斑块面积及斑块回声变化.结果 治疗前,在同一种性质斑块中,两治疗组(小剂量和大剂量组)间血清hs-CRP、IL-18和MMP-7水平比较,差异均无显著性(P均＞0.05).对两种性质斑块间血清hs-CRP、IL-18和MMP-7水平进行比较,无论是小剂量组还是大剂量组,三项指标均以易损斑块组高于稳定斑块组(均P＜0.05或P＜0.01);在同性质斑块组中,无论是接受小剂量还是大剂量阿托伐他汀治疗,治疗后血清hs-CRP、IL-18和MMP-7水平均明显下降,但大剂量组三项指标下降幅度均大于小剂量组(P均＜0.01).治疗6个月后,小剂量组IMT值及斑块面积稍下降,差异无显著性(P均＞0.05),而大剂量组IMT值及斑块面积均明显下降,两项指标均低于小剂量组,差异具有显著性(P均＜0.01).治疗后,小剂量组斑块回声信号无明显改善,而大剂量组低回声斑块回声增强例数高于小剂量组,差异具有显著性(P＜0.01).结论 血清hs-CRP、IL-18和MMP-7的水平可作为检测AS易损性的血清学生物指标;大剂量阿托伐他汀调脂治疗能迅速降低脑梗死患者的血清炎性因子水平,具有更强的抗炎作用,在一定程度上可逆转和稳定斑块.     

阿托伐他汀钙治疗脑梗死患者颈动脉粥样硬化的机制探讨

目的研究阿托伐他汀对脑梗死患者血清中APN、Visfatin、TNF-α和IL-6水平及颈动脉内-中膜厚度(IMT)的影响,探讨阿托伐他汀钙对脑梗死患者颈动脉粥样硬化的治疗机制。方法 118例合并颈动脉粥样硬化的脑梗死患者随机分为对照组和治疗组(阿托伐他汀组)。除脑梗死常规治疗外,治疗组加用阿托伐他汀,每晚20mg,连用6个月。在治疗前及治疗后28d、6个月时,抽取静脉血采用酶联免疫吸附试验法(ELASA)检测患者血清中APN、Visfatin、TNF-α和IL-6水平,颈动脉超声检测颈动脉内-中膜厚度(IMT)。结果与治疗前及对照组同期相比较,治疗组28d、6个月APN水平均升高,TNF-α、IL-6和Visfatin水平均下降,差异均有统计学意义。治疗28d后2组颈动脉IMT均无明显变化;治疗6个月治疗组颈动脉IMT与治疗前及对照组6个月相比均有显著性差异(P0.05)。结论阿托伐他汀长期应用可降低脑梗死患者颈动脉IMT,其作用机制除调脂外还可能通过降低血清中Visfatin、TNF-α和IL-6水平从而上调APN表达抑制血管炎症。     

阿托伐他汀联合血塞通胶囊对脑梗死颈动脉斑块稳定性及血脂水平影响的临床效果探讨

目的探讨血塞通胶囊联合阿托伐他汀治疗脑梗死对颈动脉斑块稳定性及血脂水平的影响。方法选择2014-06—2015-08我院收治的脑梗死患者128例,随机分为治疗组与对照组,每组64例,对照组单纯采用阿托伐他汀治疗,治疗组采用血塞通胶囊联合阿托伐他汀治疗,观察对比2组治疗前和治疗12个月后彩超检测颈动脉内膜-中层厚度(IMT)、斑块类型及血脂相关指标的变化。结果 2组患者治疗前彩超检测IMT组间比较,差异无统计学意义(t=0.018,P0.05),治疗12个月后组间比较,差异有统计学意义(t=-3.432,P0.05)。治疗组治疗12个月后纤维型、脂质型组内比较,差异有统计学意义(P0.05);脂质型组间比较,差异有统计学意义(P0.05);对照组治疗12个月后所有类型与治疗前相比,差异无统计学意义(P0.05)。2组患者治疗前血脂相关指标比较,差异无统计学意义(P0.05),治疗12个月后组间比较,差异有统计学意义(P0.05)。2组总急性脑血管事件发生率比较差异有统计学意义(P0.05)。结论血塞通胶囊联合阿托伐他汀治疗脑梗死有利于促进颈动脉斑块的稳定,降低心脑血管事件发生,具有重要的临床意义。     

他汀类药物联合缓释烟酸的调脂疗效及对高血压并发脑梗死患者动脉硬化的作用

目的 研究阿托伐他汀联用缓释烟酸对高血压并发脑梗死患者血脂调节和防止动脉硬化的影响.方法 96例高血压并发脑梗死患者随机分为2组:(1)对照组(48例),给予阿托伐他汀20 mg/d;(2)治疗组(48例),给予阿托伐他汀20 mg/d和烟酸缓释片1000 mg/d.分别于入院第2天空腹查血脂、肝功能,入院1～2周内查颈动脉超声,6个月后复查血脂、凝血功能、肝功能和颈动脉超声,比较治疗前后2组血清总胆固醇(TC)、血清甘油三酯(TG)、血清低密度脂蛋白(LDL-C)和高密度脂蛋白(HDL-C)水平、颈总动脉内膜中层厚度(IMT)、颈动脉斑块面积(Smax)变化.结果 (1)经过6个月治疗,2组患者LDL-C水平较治疗前比较均有明显降低(3.52±0.80 mmol/L vs 1.81±0.51 mmol/L,3.54±0.63 mmol/L vs 2.32±0.63 mmol/L,P<0.05),治疗组较对照组降低更加显著(1.81±0.51 mmol/L vs.2.32±0.63 mmol/L,P<0.05).而HDL-C水平较治疗前有所升高,具有统计学意义(0.91±0.30 mmol/L vs 1.49±0.31 mmol/L,0.96±0.28 mmol/L vs 1.25±0.55 mmol/L,P＜0.05),治疗组较对照组升高更加显著(1.49±0.31 mmol/L vs 1.25±0.55 mmol/L,P＜0.05),2组TC、TG均有明显下降(P＜0.05),但治疗组较对照组下降更显著(P<0.05).6个月随访均未发现明显肝酶升高等并发症及不良反应发生.(2)治疗6个月后,2组IMT、Smax均有不同程度下降,较治疗前比较差异有统计学意义(P＜0.05);阿托伐他汀联合烟酸缓释片治疗组较单用阿托伐他汀组IMT、Smax下降更明显,2组比较差异有统计学意义(P＜0.05).结论 两种治疗方法均有明显的调脂、降脂作用,缓释烟酸对升高HDL-C作用更明显,阿托伐他汀联用缓释烟酸更有利于全面调脂,延缓颈动脉粥样硬化并缩小斑块面积,且具有良好的安全性和耐受性.     

阿托伐他汀对脑梗死患者血脂、颈动脉内-中膜厚度及复发率的影响

目的 研究阿托伐他汀对脑梗死患者的血脂、颈动脉内-中膜厚度(IMT)及复发率的影响.方法 59例合并有高脂血症和颈动脉粥样硬化的脑梗死患者随机分为阿托伐他汀组(29例)和对照组(30例).两组患者均给予脑梗死常规治疗;阿托伐他汀组患者加用阿托伐他汀20 mg/d,连用12个月.在治疗前及治疗后3、6、12个月时,检测患者的血脂,用彩色多普勒超声仪检测颈动脉内-中膜厚度(IMT).统计治疗后12个月时脑梗死复发的例数.结果 阿托伐他汀组治疗后各时间点的血胆固醇(TC)、低密度脂蛋白(LDL)水平显著低于治疗前及对照组(均P＜0.01);治疗后12个月时高密度脂蛋白(HDL)水平显著高于治疗前及对照组(均P ＜0.05).阿托伐他汀组治疗后6个月、12个月时颈动脉IMT显著低于治疗前及对照组(P ＜0.05 ～0.01);对照组治疗后12个月时则明显高于治疗前(P＜0.05).治疗12个月后,阿托伐他汀组无脑梗死复发,对照组脑梗死复发3例(10％).结论 阿托伐他汀能显著降低脑梗死患者的血TC、LDL水平,长期治疗可降低颈动脉IMT和脑梗死的复发率.     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.