脑血肿周围细胞间黏附分子-1 mRNA表达及白细胞浸润的实验研究

目的　探讨大鼠脑血肿周围细胞间黏附分子 1(ICAM 1)mRNA表达及白细胞浸润情况 ,明确脑血肿周围是否存在急性炎性反应。方法　胶原酶Ⅶ型脑立体定向注射制作脑出血模型 ,应用逆转录聚合酶链(RT PCR)技术检测ICAM 1mRNA表达 ;通过测定髓过氧化物酶 (MPO)活性来检测中性粒细胞的浸润情况。结果　脑出血后 6hICAM 1mRNA表达开始增加 (P <0 0 5 ) ,2 4h达高峰 (P <0 0 1) ,然后逐渐减退。脑出血后 2 4hMPO活性明显增加 (P <0 0 5 ) ,4 8h达高峰 (P <0 0 1) ,然后逐渐减退。结论　脑血肿周围存在明显的炎性反应 ,它可能参与了脑出血后周围组织的继发性损伤     

地塞米松对新生大鼠缺氧缺血性脑病脑组织细胞间黏附分子-1表达与白细胞浸润的影响

目的　研究地塞米松预处理对新生大鼠缺氧缺血性脑损伤时脑组织细胞间黏附分子 1(ICAM 1)的表达与白细胞浸润的影响。方法　将 4 8只新生大鼠制作成缺氧缺血性脑病 (HIE)模型 ,于制作模型前 2 4小时即分别予地塞米松预处理组和对照组大鼠腹腔内注射地塞米松 0 1mg/kg、生理盐水 10ml/kg。模型后2 4小时处死大鼠 ,分别进行脑组织ICAM 1免疫组织化学检测、白细胞计数及组织HE染色。结果　ICAM 1平均吸光度 :预处理组 (3 6 2± 1 2 1) ,对照组 (9 4 2± 2 6 5 ) (P <0 0 5 ) ;神经细胞损伤评分 :预处理组 (0 38±0 13) ,对照组 (1 6 3± 0 74 ) (P <0 0 0 1) ;白细胞浸润 :预处理组 (8 4± 1 7) ,对照组 (16 3± 4 6 ) (P <0 0 0 1)。结论　地塞米松预处理能减少HIE时脑组织的ICAM 1蛋白表达及白细胞浸润 ,能减轻脑组织损害程度     

实验性脑出血后脑组织核因子-κB表达和含水量的变化及其相关性

目的 研究实验性脑出血(ICH)后血肿周围脑组织核因子-κB(NF-κB)表达和脑组织含水量的改变及其相关性.方法 采用自体不凝血注人大鼠尾状核制备ICH模型;用免疫组化法检测血肿周围脑组织NF-κB表达;用干湿重法测脑组织含水量.结果 与对照组相比,ICH 6h组血肿周围脑组织NF-κB表达开始明显增加,ICH 48h组达高峰,并持续到ICH 1周(P＜0.01～0.05);脑组织含水量ICH 12h组开始增多,24h组显著增高,72h组达高峰;NF-κB表达和脑组织含水量ICH 24h～1周组与假手术组之间差异有统计学意义(均P＜0.01);ICH后NF-κB阳性细胞数与脑组织含水量呈正相关(r=0.644,P＜0.01),NF-κB表达从开始到高峰均早于脑组织含水量的变化.结论 ICH后脑组织NF-κB表达增加,NF-κB可能通过炎性机制参与了ICH后继发脑水肿的形成.     

大鼠脑缺血再灌注模型ICAM-1表达与白细胞浸润关系及亚低温干预治疗的研究

目的　研究大鼠局灶性脑缺血再灌注后不同时程脑组织中的细胞间粘附分子 1 (ICAM 1 )表达规律 ,及其与白细胞浸润的关系 ,并探讨亚低温的治疗作用。方法　采用大鼠大脑中动脉 (MCA)线拴闭塞 /再通法建立大鼠局灶性脑缺血 再灌注模型 ,常温组分别于脑缺血 3小时再灌注 2小时、8小时、2 4小时、48小时、72小时后断头取脑 ;假手术组及亚低温组于脑缺血 3小时再灌注 2 4小时断头取脑 ,行ICAM 1免疫组化及组织HE染色 ,测定ICAM 1表达阳性微血管数及白细胞计数。结果　⑴脑缺血再灌注后 2小时 ,脑缺血的坏死周边区的微血管内皮细胞表达ICAM 1出现增高趋势 ,并于 2 4小时达到高峰 ,各组之间及各组与假手术组间均有显著差异 (均P <0 0 5) ;⑵脑缺血再灌注 8小时出现白细胞浸润 ,且浸润高峰也在 2 4小时 (P <0 0 1 ) ;⑶ICAM 1的表达与白细胞浸润呈正相关 (r =0 .82 7,P <0 0 1 ) ;⑷缺血早期进行亚低温治疗能明显减轻缺血再灌注后ICAM 1的表达及减少白细胞浸润 (P <0 0 1 )。结论　脑缺血再灌注后ICAM 1可介导白细胞和内皮细胞的粘附 ,加速白细胞的浸润 ,提示ICAM 1是造成脑缺血损伤的重要因素之一 ;亚低温的干预治疗能明显减轻缺血再灌注后脑组织病理形态学的损害程度。     

实验性脑出血后脑组织核因子-κB表达和含水量的变化及其相关性

目的研究实验性脑出血（ICH）后血肿周围脑组织核因子-кB（NF-кB）表达和脑组织含水量的改变及其相关性。方法采用自体不凝血注入大鼠尾状核制备ICH模型;用免疫组化法检测血肿周围脑组织NF-кB表达;用干湿重法测脑组织含水量。结果与对照组相比,ICH6h组血肿周围脑组织NF-кB表达开始明显增加,ICH48h组达高峰,并持续到ICH1周（P〈0.01~0.05）;脑组织含水量ICH12h组开始增多,24h组显著增高,72h组达高峰;NF-кB表达和脑组织含水量ICH24h~1周组与假手术组之间差异有统计学意义（均P〈0.01）;ICH后NF-кB阳性细胞数与脑组织含水量呈正相关（r=0.644,P〈0.01）,NF-кB表达从开始到高峰均早于脑组织含水量的变化。结论ICH后脑组织NF-кB表达增加,NF-кB可能通过炎性机制参与了ICH后继发脑水肿的形成。     

缺血性脑卒中血脑屏障内皮细胞ICAM-1的实验研究

目的　探讨高血压大鼠脑卒中过程中血脑屏障 (BBB)内皮细胞细胞间粘附分子 - 1 (ICAM - 1 )的表达。　　方法　采用尼龙线栓堵自发性高血压大鼠和正常血压SD大鼠大脑中动脉建立局灶性永久性脑缺血模型 ,在缺血至梗塞不同时期 ,用免疫组化ABC法观察脑组织BBB内皮细胞ICAM - 1表达。　　结果　自发性高血压大鼠脑缺血 1h ,BBB之内皮细胞开始出现ICAM - 1的表达 ,至 6h达高峰 ,并持续至 1 68h;正常血压大鼠则在脑缺血至 3h开始出现ICAM - 1的表达 ,至 1 2h达高峰 ,并持续至 1 2 0h。两种大鼠在缺血早期对侧非缺血区脑组织BBB之内皮细胞亦有少量ICAM - 1的表达。　　结论　自发性高血压大鼠在未缺血时BBB内皮细胞未见ICAM - 1的表达 ;缺血性脑卒中时ICAM - 1开始表达及达高峰时间均早于正常血压大鼠 ,持续时间亦较正常血压大鼠为长。     

N-乙酰半胱氨酸对大鼠脑出血后核因子-κB表达的影响

目的 探讨N-乙酰半胱氨（N-acetylcysteine,NAC）在大鼠脑出血（ICH）继发脑损伤中的作用机制。方法 采用立体定向技术注入自体不凝血制作实验性ICH模型,造模后即刻和6h后用NAC干预,行免疫组化染色观察血肿周围惦组织核因子κB（NF—κB）和细胞间黏附分子-l（ICAM-1）的表达变化。结果 ICH后6h血肿周围脑组织NF—κB开始表达,48h迭高峰,ICAM—l12h开始表迭,72h迭高峰。各组与假手术组之间有显著差异（均P〈0．05）;脑出血后NF—KB与ICAM—l呈正相关（r=0．868,P〈0．05）,NF—κB表达从开始到高峰均早于ICAM—l。NAC可明显降低ICH24h、72h亚组NF—κB、ICAM—l的表达（P〈0．05）。结论 ICH时,NAC可通过抑制NF—κB的活性,下调ICAM—l的表达,从而发挥脑保护作用。     

黄芪多糖对脑出血大鼠脑组织含铁血红素氧合酶-1蛋白表达及含水量、超微结构的影响

目的 研究黄芪多糖对脑出血大鼠脑组织含铁血红素氧合酶-1(HO-1)蛋白表达及含水量、超微结构的影响.方法 139只雄性SD大鼠随机分为假手术组、脑出血组与黄芪多糖治疗组.采用Ⅶ型胶原酶诱导法制作SD大鼠脑出血模型,假手术组以等量生理盐水代替Ⅶ型胶原酶;黄芪多糖治疗组给予黄芪多糖25 mg/kg腹腔注射,每天1次,直至处死.分别于脑出血后12 h、24 h、2 d、4 d、7 d 5个时间点对各组大鼠进行神经行为学评分,测量脑组织含水量和用免疫组化法检测HO-1蛋白表达,透射电镜观察脑出血后4 d 血肿周围神经元的超微结构.结果 脑出血组与黄芪多糖治疗组大鼠脑出血后脑组织 HO-1 表达以及脑组织含水量较假手术组显著增高(均P＜0. 01);脑出血后12 h HO-1蛋白即有表达, 2 d 达高峰, 尔后逐渐下降. 黄芪多糖治疗组与脑出血组比较, HO-1表达的变化相同,但各时间点表达均高于脑出血组(P＜0.05～0.01);脑组织含水量各时间点均显著降低(P＜0.05～0.01);4 d、7 d时大鼠神经行为学评分明显减少(均P＜0.01),神经元超微结构病理改变轻.结论 黄芪多糖可促进脑出血后脑组织HO-1的表达, 这可能是其减轻脑出血后脑水肿和脑组织损伤的机制之一.     

脑出血后脑组织内凝血酶受体1(PAR1)的表达及其病理意义

目的　探讨脑出血后脑组织内凝血酶受体 1(PAR1)的表达规律及其意义。方法　成年大鼠分为 3组 ,分别向大脑基底节区注入全血、全血加水蛭素、或生理盐水。于注射后 6 h、2 4 h、72 h和 7d,取脑组织 ,检测脑内PAR1表达 (免疫组织化学法 )。同时 ,观察神经细胞的凋亡情况 (Tunel法 )和脑组织水含量 (干燥法 )。结果　与生理盐水对照组比较 ,脑出血后血肿周围脑组织内 PAR1免疫阳性细胞数明显升高 (P<0 .0 5 )。同时 ,脑组织内凋亡细胞数和脑组织水含量也明显增加。时效学研究显示 ,PAR1表达上调开始于脑出血后 6 h,72 h达高峰 ,7d后下降。加用凝血酶抑制剂 -水蛭素者 ,出血周围组织内 PAR1表达明显抑制 ,同时脑组织水肿和神经凋亡显著减轻。结论　脑出血后脑组织 PAR1表达增加。 PAR1高表达可能介导了脑出血后神经损伤的过程。     

水通道蛋白-4在脑出血大鼠脑组织的分布

目的 观察脑出血大鼠水通道蛋白-4(AQP4)在脑组织的分布变化及其在出血性脑水肿中的作用。方法 采用定量胶原酶注人大鼠尾状核建立脑出血模型，应用免疫组化法观察脑出血后不同时间大鼠脑组织AQP4的表达。结果 AQP4阳性细胞主要分布在脑出血血肿周围区和大脑皮质的星形胶质细胞、脑室周围、视上核和室旁核。脑出血后6h起，AQP4表达增强，出血后72h达高峰，出血1周后仍高于正常水平。结论 脑出血后，AQP4在与水代谢密切相关的部位表达明显增强，提示AQP4在出血性脑水肿的形成过程中起重要作用。     

Mental illness in England,in Scotland and in Scots living in England

Summary Beginning from the observation that Scots living in England have much higher rates of mental hospital admission than do the English, several hypotheses are proposed to account for this. Much of the excess in rates of mental illness is accounted for by those diagnosed as having alcohol-related disorders and behaviour and personality problems. The results of an examination of offical statistics in the two countries enabled some explanations to be offered. It was found that rates of admissions to mental hospitals are higher in Scotland than in England but not as high as those found among Scots migrants who have a much higher rate of readmission to hospitals than either of the other groups. In fact, if first admissions only are considered the rates of admission in Scotland are not only higher than rates for English natives but also higher than for Scottish migrants. It seems that Scots living in England are somewhat less likely to become mental patients than Scots in Scotland but that once they do achieve this status they are very much more likely to be readmitted on subsequent occasions. It was concluded that there might be two fairly distinct groups of migrants from Scotland to England who have different backgrounds, different reasons for migrating and different psychological characteristics. On the one hand there are stable, economically motivated migrants who move south for definite employment related reasons and who show few psychological symptoms. While on the other hand there is a group of migrants who perhaps have psychological problems and who move more in hope than expectation without definite prospects and who account for the high rates of mental hospital admission found in Scottish migrants.     

Prostacyclin release in the coronary circulation during sustained stimulation in in vitro and in in vivo experimental systems

Prostacyclin release from rat isolated perfused hearts and from dog coronary circulation was studied by measuring immunoreactive 6-keto-PGF1 alpha (6-keto-PGF1a) in heart perfusate and in plasma obtained from the great cardiac vein respectively. Continuous infusion of arachidonic acid at constant concentration in isolated perfused hearts induced an increased prostacyclin release. This release showed a rapid peak within 10 min and a subsequent decrease. Low-flow ischemia induced an increased perfusate concentration of 6-keto-PGF1a but, considering the decreased flow, prostacyclin release was actually reduced. During the whole period of ischemia (60 min) prostacyclin release was constant. In open-chest anesthetized dogs 6-keto-PGF1a concentration in the great cardiac vein was increased after ligation of the left anterior descending coronary artery. A prolonged period of coronary occlusion (4.5 hours) resulted in a progressive rise of prostacyclin release. 6-keto-PGF1a determinations in the femoral vein and in the aorta did not show relevant variations during the observation period.     

癫痫与抑郁关系的研究进展

抑郁是癫痫患者中常见的精神障碍,严重地影响了患者的生活质量。传统的观点认为癫痫患者因为存在着诸多社会学问题易出现抑郁倾向,癫痫和抑郁是单向的联系,但大量的研究已经证明癫痫和抑郁之间存在双向的联系,一种异常状态的存在可能易转化为另一种异常状态的发展。癫痫和抑郁存在着共同的发病机制。本文主要就癫痫和抑郁的双向联系以及抗抑郁药物在癫痫患者中的应用进行阐述。     

神经介入：回眸2022

<正>2022年,国际上公布了多项大型神经介入领域的随机对照试验（randomized controlled trial,RCT）结果,在血管内治疗（endovascular treatment,EVT）急性大血管闭塞（large vessel occlusion,LVO）适应证的扩展、药物治疗、管理,症状性颅内动脉粥样硬化性狭窄（symptomatic intracranial atherosclerotic stenosis,sICAS）治疗,无症状性颈动脉狭窄治疗,     

Neuroimaging in epilepsy in tropics

Epilepsy is a major public health problem in many tropical countries. Also, some of the tropical diseases are major contributors to the higher prevalence of epilepsy in these countries. The etiologic factors responsible for epilepsy in these countries are quite different from those in the developed world. This article discusses the etiologic factors and neuroimaging of epilepsy in light of the conditions in these tropical countries.     

Sudanophilic lipid accumulation in astrocytes in periventricular leukomalacia in monkeys

Summary Sudanophilic lipid accumulation is a characteristic feature of periventricular leukomalacia (PVL) of infants. At least two types of lipid-containing cells have been identified, one being the macrophage, the other the pre-myelin glial cell. A third type of lipid-containing cell has been seen in two monkeys with spontaneous PVL. Electron microscopically this cell appears to be an astrocyte. This probably represents a reaction of the astrocyte to hypoxia and may be the equivalent of the hypertrophic astrocytes found in human infants.Supported in part by NIH grant HDO 8633 and the Regional Primate Research Center Grant RR-00166