阿托伐他汀对急性脑梗死患者血清基质金属蛋白酶9及预后的影响

目的 研究短期应用阿托伐他汀后急性脑梗死患者血清基质金属蛋白酶9（matrix metalloproteinase-9,MMP-9）及血脂水平的变化,探讨其对急性脑梗死患者预后的影响。方法 采用随机、双盲、安慰剂对照的研究方法,将发病48 h内入院的大面积脑梗死患者40例随机分为对照组和阿托伐他汀组（阿托伐他汀20 mg/d,连续用药14 d）。治疗前后检测血清MMP-9、血脂、血清谷草转氨酶（AST）及血清肌酸激酶（CK）水平,应用美国国立卫生研究院卒中量表（NIHSS）及Barthel指数（BI）记分法对入院后当天及3个月时神经功能缺损程度进行评分。结果 共39例进入结果分析（对照组20例,阿托伐他汀组19例）。全部患者治疗前MMP-9水平与入院时及3个月时病情显著相关（P＜0.01）,血脂水平则无此相关性。治疗后阿托伐他汀组MMP-9水平下降,且与对照组相比,差异有统计学意义（P＜0.05）。各组3个月后神经功能缺失程度评分与入院时相比,差异有统计学意义（P＜0.01）,但两组之间相比无统计学差异。治疗后各组AST及CK水平无明显变化。结论 急性脑梗死患者血清MMP-9水平与病情的严重程度及预后相关。短期应用阿托伐他汀可以降低急性脑梗死患者血清MMP-9水平,且安全性好,但对梗死后3个月的预后无明显改善作用。     

阿托伐他汀对急性脑梗死患者血清超敏C反应蛋白及一氧化氮水平的影响

目的研究阿托伐他汀对急性脑梗死(ACI)患者血清超敏C反应蛋白(hs-CRP)及一氧化氮(NO)水平的影响。方法将60例ACI患者随机分为阿托伐他汀组(30例)和常规治疗组(30例)。阿托伐他汀组在常规治疗基础上加用阿托伐他汀20mg,每日1次,连续服用14d。在治疗前后检测血清hs-CRP和NO含量,并进行神经功能缺损程度评分(NDS)评定。结果治疗14d时两组血清hs-CRP水平均较治疗前明显下降(均P<0.01),且阿托伐他汀组较常规治疗组下降明显(P<0.01);两组血清NO水平较治疗前明显升高(均P<0.01),且阿托伐他汀组较常规治疗组升高明显(P<0.05);两组NDS评分较治疗前明显下降(均P<0.01),且阿托伐他汀组较常规治疗组下降明显(P<0.05)。结论阿托伐他汀能明显降低ACI患者血清hs-CRP水平,升高NO水平;有助于ACI患者的神经功能恢复。     

进展性与非进展性脑卒中患者阿托伐他汀治疗前后血清超敏C反应蛋白和基质金属蛋白酶-9的变化

目的观察进展性和非进展性急性期脑卒中患者阿托伐他汀治疗前后血清超敏C反应蛋白(hs-CRP)和基质金属蛋白酶-9(MMP-9)的变化,探讨阿托伐他汀治疗进展性脑卒中患者的可能机制。方法选择137例急性脑卒中患者,分为进展组45例和非进展组92例,应用免疫比浊法和酶联免疫吸附试验方法检测两组患者阿托伐他汀治疗前后hs-CRP和MMP-9的表达水平,评价患者阿托伐他汀治疗前后神经功能缺损程度并评估治疗效果。结果进展组卒中患者阿托伐他汀治疗前后比较hs-CRP和MMP-9的表达水平显著降低;非进展组治疗前后比较hs-CRP的表达水平显著降低,而MMP-9变化不明显;进展组和非进展组脑卒中患者阿托伐他汀治疗有效率分别为85.34%和84.37%,两组间相比差异无统计学意义。结论阿托伐他汀治疗进展性和非进展性卒中均有效,两组比较差异无统计学意义,但是阿托伐他汀治疗前后两种类型卒中患者hs-CRP和MMP-9发生了不同程度好转的改变。     

阿托伐他汀对进展性脑梗死神经功能的影响

目的探讨阿托伐他汀对进展性脑梗死神经功能的影响。方法 2009-02-2011-02收治的164例符合入选标准进展性脑梗死患者,对照组80例采取常规治疗,治疗组84例在常规治疗基础上加用阿托伐他汀。结果 2组患者入院时神经功能缺损评分比较,差异无统计学意义（P〉0.05）;进展停止时、发病1周时神经功能缺损评分,差异有统计学意义（P〈0.05）。结论进展性脑梗死应用阿托伐他汀能够有效改善患者神经功能,减少致残率。     

急性脑梗死患者血清S100B蛋白的动态测定及其与神经功能缺损的相关性

目的动态观察急性脑梗死(ACI)患者血清S100B蛋白的表达,探讨其与神经功能缺损程度的相关性。方法应用酶联免疫双抗体夹心法(ELISA)动态观察52例ACI患者血清S100B蛋白水平变化,并与52名健康对照者血清S100B蛋白水平进行比较。同时应用美国国立卫生研究院卒中量表(NIHSS)进行神经功能缺损评分,探讨S100B蛋白与NIHSS评分的相关性。结果健康对照组血清S100B蛋白水平为(0.025±0.009)ng/mL。ACI组血清S100B蛋白水平于发病后第3天[(0.217±0.142)ng/mL]已升高,于发病后第7天[(0.250±0.143)ng/mL]达高峰,发病后第15天为[0.198±0.109)ng/mL],均高于健康对照组(P0.01)。ACI组发病后第7天S100B蛋白水平高于发病后第3天和第15天(分别P0.05、P0.01),而后两者比较差异无统计学意义(P0.05)。发病后第3、7、15天S100B蛋白水平与同期临床神经功能缺损程度评分成正相关[分别r=0.736,P0.01;r=0.327,P0.05;r=0.654,P0.01]。结论血清S100B蛋白水平与神经功能缺损程度具有相关性,可以作为反应缺血性脑损伤程度的一个指标。     

S-100b蛋白、神经元特异性烯醇化酶与进展性卒中的关系

目的探讨血清S-100b蛋白、神经元特异性烯醇化酶与进展性缺血性脑卒中的关系。方法应用ELISA法检测150例急性脑梗死患者入院72h内S-100b蛋白及NSE的水平变化,并根据美国国立卫生院卒中量表判断是否为进展性卒中。同时进行神经功能缺损评分(NIHSS评分)、改良神经功能评分(mRS评分)及颅脑MRI/MRA扫描。结果 150例急性脑梗死患者中有30例(20%)于入院后3d内发展为进展性脑卒中,进展组患者入院后24h、36h、48h、72h血清S-100b蛋白、NSE明显高于无进展组(P0.01)。急性脑梗死患者S-100b蛋白、NSE与NIHSS评分、mRS评分及脑梗死体积呈正相关(r=0.65～0.75,P0.01;r=0.59～0.69,P0.01),颈内动脉颅内段、大脑中动脉M1段闭塞/狭窄的患者血清S-100b蛋白、NSE的水平较无血管闭塞组明显增高(P0.05)。结论急性脑梗死患者血清S-100b蛋白及NSE水平可能是进展性脑卒中的有效预测指标,且S-100b蛋白及NSE水平与颅内动脉狭窄、神经功能评分以及脑梗死体积密切相关。     

阿托伐他汀对进展性脑梗死进展时间及神经功能的影响

目的探讨阿托伐他汀对进展性脑梗死进展时间及神经功能缺损程度的影响。方法选取2007-10~2010-05我院神经内科住院的进展性脑梗死患者120例,随机分为治疗组和对照组各60例,对照组采用阿司匹林肠溶片抗血小板治疗,应用脑保护剂,尼莫地平降颅压,以及常规内科综合治疗。治疗组在对照组治疗基础上加用阿托伐他汀片20 mg/d,睡前服用,连用4周。观察入院时、进展停止时、发病4周时神经功能缺损程度和发病至症状达高峰时间及治疗前后血脂变化。结果阿托伐他汀可以缩短发病至症状达峰时间,在发病4周时NIHSS评分方面与对照组相比差异有统计学意义。结论进展性脑梗死早期应用阿托伐他汀可降低血脂水平和改善预后。     

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。     

进展性与非进展性脑梗死患者阿托伐他汀治疗前后T淋巴细胞亚群的变化

目的通过研究进展性和非进展性脑梗死在阿托伐他汀治疗前后T淋巴细胞亚群的变化,探讨他汀类药物治疗脑梗死的免疫学机制。方法选择53例急性脑梗死患者,分为进展和非进展组,应用流式细胞分析仪检测两组患者阿托伐他汀治疗前后T淋巴细胞亚群相对计数,并且根据患者治疗前后神经功能缺损程度进行效果评价。结果进展组治疗前后比较:CD4+T细胞和CD4/CD8值显著升高,CD8+T细胞显著降低;非进展组治疗前后比较:CD4/CD8值显著升高;两组治疗前后神经功能缺损评分自身比较,均明显降低。结论阿托伐他汀治疗前后,进展性和非进展性脑梗死患者体内T淋巴细胞亚群分布发生了不同程度的变化。阿托伐他汀可能通过提高CD4+T细胞水平,促进急性脑梗死的恢复。     

阿托伐他汀对急性脑梗死患者血清内脂素水平的影响

目的 观察急性脑梗死患者血清内脂素水平的变化,并进一步探讨阿托伐他汀治疗对其有无影响.方法 随机选取86例急性脑梗死患者和52名正常对照者,检测其血清内脂素水平有无差异,并分析其与临床各指标的联系.86例急性脑梗死患者再进一步随机分为常规治疗组和阿托伐他汀治疗组.每组43例.常规治疗组给予常规治疗,阿托伐他汀治疗组在常规治疗的基础上,给予阿托伐他汀20 mg/d,治疗2周,检测2组治疗前后血清内脂索水平的变化.结果 与对照组相比,急性脑梗死患者血清内脂素水平明显增高(78.52±16.41 ng/mL、42.83±13.45 ng/mL).差异有统计学意义(P<0.01).非条件Logistic回归分析显示,血清高内脂素水平是急性脑梗死患者发病的独立危险因子(OR 1.652,95%CI 1.032～2.256;P=0.014).相关性分析表明.急性脑梗死患者血清内脂素与梗死面积、空腹血糖、收缩压和三脂酰甘油呈正相关,与高密度脂蛋白呈负相关.治疗2周后,阿托伐他汀治疗组的血清内脂素水平较治疗前明显下降(62.14±14.37 ng/mL、78.52±16.41ng/mL).差异有统计学意义(P<0.01);而常规治疗组的血清内脂素水平与治疗前相比,差异无统计学意义(P>0.05).结论 阿托伐他汀具有降低急性脑梗死患者血清内脂素的作用.     

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.     

Summary of legislation of 1935 of interest to the department of Mental Hygiene

Psychiatric Quarterly -     

Summary of legislation of 1941 of interest to the Department of Mental Hygiene

Psychiatric Quarterly -     

Asymmetry of on- and off-pathways of blue-sensitive cones of the retina of macaques

Macaque retinal ganglion cells whose receptive-field center recieves input from blue-sensitive cones show an overt asymmetry of the frequency of ON-center and OFF-center varieties, an asymmetry not present in ganglion cells whose center receives input from the other two cone types. A similar asymmetry of ON/OFF responses is found in the local electrotetinogram (d-wave) mediated by signals from blue-sensitive cones. ‘Blue-ON-center’ ganglion cells have larger receptive-field centers and shorter conduction latencies than other opponent-color varieties, suggesting an appreciable degree of receptor convergence and presumably large cell bodies. Intracellular stainings of these neurons with Procion Yellow show that they correspond to diffuse stratified (Parasol) ganglion cells whose flat-topped dendritic arborization stratifies in the sclerad half of the inner plexiform layer. In view of the known characteristics of macaque bipolar cells and of the ON/OFF asymmetry, it is proposed that these ganglion cells are postsynaptic to cone-specific flat bipolars possibly mediating sign-inverting synaptic contacts. The results also indicate a reversal, for the blue-cone pathway, of the ON/OFF lamination of the inner plexiform layer that has recently been described in other species.     

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.