亚低温治疗对实验性脑出血大鼠死亡率及脑组织钙含量的影响

目的本研究观察３２℃亚低温对实验性脑出血大鼠２４ｈ内死亡率和脑组织钙含量的影响。方法１３４只大鼠分成两部分：（１）６８只大鼠用于死亡率观察;（２）６６只大鼠用于脑组织钙含量测定。每一部分分成假手术对照组、常温脑出血组及亚低温脑出血组。结果常温组２４ｈ内死亡率为３６．６７％,亚低温组为４．５５％;脑组织钙含量常温组较对照组和亚低温组为高。结论亚低温治疗能显著减少实验性脑出血大鼠２４ｈ内死亡率,减少脑出血后脑组织钙含量。     

头部局部亚低温对实验性脑出血大鼠脑组织TNF-α、NF-κB影响的研究

目的 建立大鼠实验性脑出血(1CH)模型,研究头部局部亚低温对大鼠脑组织炎性细胞因子和核转录因子-κB(NF-κB)表达的影响,从而探讨头部局部亚低温的脑保护作用.方法 选用Wistar大鼠,采用大鼠脑内缓慢注入非肝素化自体血的方法,建立实验性ICH动物模型.随机分为亚低温组、常温组、假手术组.亚低温组在建立模型后立即应用头部局部亚低温治疗48h.48h后用HE染色法观察实验组与对照组脑组织的病理变化,用免疫组化法研究肿瘤坏死因子-α (TNF-α)、NF-κB在各组表达的差异.结果 成功地建立了大鼠实验性ICH模型.ICH后48h,亚低温组血肿周围炎细胞较常温组显著减少,脑组织水肿明显轻于常温组,胶质细胞反应较轻,周围小血管出血现象轻于常温组.常温组血肿周围及注血侧皮质、胼胝体、脉络丛内TNF-α、NF-κB表达较假手术组明显增多(P＜0.01),亚低温组的表达较常温组有显著减少(P＜0.05).结论 (1)大鼠脑内缓慢注入非肝素化自体血,可建立可靠、重复性好的实验性ICH动物模型.(2)大鼠ICH急性期脑组织内NF-κB和前炎性细胞因子TNF-α显著增加.(3)头部局部亚低温治疗可以抑制大鼠ICH后脑组织TNF-α和NF-κB的表达.(4)头部局部亚低温治疗在抑制实验性ICH炎症反应方面的脑保护作用与它抑制NF-κB的表达有关.     

亚低温治疗对实验性大鼠脑出血的保护作用研究

目的　本文观察了３２ ℃亚低温对脑出血大鼠脑 Ｎａ＋ 、 Ｋ＋ 、水含量及超微结构的影响。方法　６６ 只大鼠随机分成三组： （１） 假手术对照组; （２） 常温脑出血组; （３） 亚低温脑出血组。结果常温出血组水、 Ｎａ＋ 含量随时间而增加, 而 Ｋ＋ 含量减少; 亚低温组水、 Ｎａ＋ 含量比常温组低, 而 Ｋ＋含量增加。超微结构显示亚低温组脑超微结构损害较常温组轻。结论　亚低温治疗对脑出血后脑水肿, 脑细胞结构有保护作用。     

局部亚低温对脑出血后水肿影响的实验研究

目的探讨局部亚低温对大鼠脑出血后水肿形成的影响及其可能机制。方法雄性Wistar大鼠230只随机分为:对照组;脑出血组;脑出血加局部亚低温组;凝血酶加局部亚低温组。应用Evans-Blue测定血脑屏障(BBB)通透性,应用干湿重法测定脑水含量。结果与对照组相比,大鼠注血后6h开始出现脑组织水含量和BBB通透性的增加,在72h达到高峰,然后逐渐消退。不同时程局部亚低温均可以显著降低脑出血后72h时脑组织水含量及BBB通透性(P<0.01),其中给以4h局部亚低温时,降低最明显。注射凝血酶6h后,脑组织水含量及BBB通透性显著增高(P<0.01),于24~48h达高峰,然后逐渐下降。凝血酶 局部亚低温组在各个时间点与凝血酶组相比,脑组织水含量及BBB通透性明显降低(P<0.01)。结论局部亚低温可能是通过抑制凝血酶的毒性作用来减轻脑出血后水肿的形成及血脑屏障的破坏。     

局部亚低温对大鼠脑出血后血肿周围脑组织白介素-1β表达的影响

目的 观察局部亚低温对脑出血大鼠血肿周围脑组织的形态学变化和对白介素(IL)-1β表达的影响.方法 72只Wistar大鼠随机分为假手术组和脑出血后6 h、24 h、48 h、72 h、7 d组,每组再分为常温亚组和亚低温亚组,每个亚组6只大鼠.采用自体不凝血注人大鼠尾状核制备脑出血模型.各亚低温亚组注血后实施亚低温治疗4 h,维持脑温在(33±0.5)℃.观察血肿周围组织的形态学改变和IL-1β表达的变化.结果 亚低温亚组各时间点脑组织水肿明显轻于常温亚组;神经元变性坏死、炎症反应及胶质细胞增生程度明显轻于常温亚组.脑出血后6 h血肿周围脑组织IL-1β开始表达,48 h达高峰,7 d时仍明显高于对照亚组(均P＜0.01).脑出血24 h～7 d亚低温亚组IL-1β表达水平较相应时点常温亚组显著降低(均P＜0.01).结论 亚低温治疗能明显抑制血肿周围IL-1β的过度表达,减轻血肿周围脑组织的炎症反应.     

亚低温治疗大鼠缺血性脑水肿研究

目的研究亚低温对延迟时间窗再灌注的局灶脑缺血大鼠缺血性脑水肿的治疗作用。方法 SD雄性大鼠96只,线栓法制作大脑中动脉闭塞模型后随机分为缺血3 h组、缺血6 h组、缺血9 h组(每组各30只),分别在造模3 h、6 h和9 h后拔出线栓,使大脑中动脉再灌注。各缺血组按照再灌注后是否给予亚低温治疗及亚低温持续时间分为常温、亚低温3 h和亚低温5 h三个亚组,每个亚组有10只大鼠。另设假手术组6只。缺血组大鼠在再灌注24 h后处死取脑,假手术组在术后24 h处死取脑,干-湿重法测定各组缺血侧脑组织含水量并进行比较。结果与假手术组比较,缺血组缺血侧脑组织含水量明显增高。缺血3 h组中3 h亚低温和5 h亚低温亚组的缺血侧脑组织含水量与缺血3 h常温组比较,差异有统计学意义(79.39%±2.44%vs82.16%±1.50%,P0.05;79.20%±1.55%vs 82.16%±1.50%,P0.05)。其余各缺血组中经过亚低温治疗的大鼠与常温亚组的脑组织含水量无统计学差异。结论亚低温可减轻缺血早期(3 h)再灌注的脑组织水肿,保护缺血脑组织,而对晚期(6 h和9 h)再灌注的缺血性脑水肿无论亚低温时间长短均无明显保护作用。     

亚低温对大鼠脑缺血再灌注后炎性反应的影响

目的：观察亚低温的不同时程对大鼠脑缺血再灌注后炎性反应的影响。方法：24只SD大鼠随机分为4组：常温组，亚低温1／2h组，亚低温1h组和亚低温3h组。每组各6只大鼠。参照Zea Longa的方法建立脑缺血再灌注动物模型，于再灌注24h断头取脑，行HE染色，观察脑组织中自细胞浸润及神经细胞的变化情况。结果：常温组在缺血梗死灶周围区可见白细胞浸润明显及深染受损的神经元；随亚低温时间的延长，白细胞浸润逐渐减少，神经元亦表现为淡染的轻度损伤。结论：亚低温可抑制脑缺血再灌注后的白细胞浸润，具有神经保护作用。     

局部亚低温对大鼠脑出血后血红素氧合酶1表达的影响

目的观察局部亚低温对大鼠自体血注入法脑出血模型血红素氧合酶(HO-1)表达的影响,探讨局部亚低温减轻脑出血后脑水肿的可能机制。方法雄性Wistar大鼠120只,随机分为脑出血(control)组和脑出血加局部亚低温(LMH)组。每组分为对照和脑出血后6h、24h、72h,5d、7d共6个亚组,亚低温组于注血后给予4h的局部亚低温治疗,应用Evans-blue测定血脑屏障(BBB)通透性,应用干湿重法测定脑水含量以及应用免疫组化对血肿周围脑组织HO-1的表达进行测定。结果对照组大鼠脑组织含水量、BBB通透性以及HO-1表达的增加始于脑出血后6h均至72h达高峰。HO-1表达的变化与脑血肿周围组织水含量的变化成呈正相关(r=0.79)。LMH组的脑组织水含量、BBB通透性和HO-1各时间点与对照组相比明显下降。结论脑出血后红细胞的破坏可以导致HO-1表达上升。局部亚低温可抑制脑出血后HO-1表达,减轻血脑屏障完整性的破坏,减轻脑出血后脑水肿形成。     

亚低温对脑出血大鼠神经细胞凋亡及神经功能缺损的影响

目的 研究延迟性亚低温对大鼠脑出血后神经细胞凋亡及神经功能缺损的动态影响.方法 将大鼠随机分为正常组(N),假手术组(S),脑出血组(M),延迟12h亚低温组(HT12)和延迟24h亚低温组(HT24).应用立体定向技术将Ⅳ型胶原酶注人大鼠尾壳核制作脑出血模型,模型制备后于12h及24h点将大鼠放入冷室降温,维持肛温在(33±1)℃,均持续12h,各组在模型制作后12h、24h、36h、3d、7d记录大鼠神经功能缺损评分及死亡率.大鼠脑组织做HE染色及TUNEL染色,流式细胞技术观察神经细胞凋亡数目的变化.结果 亚低温(HT12,HT24)可减少脑出血后大鼠各时间点的TUNEL染色的阳性细胞数(P＜0.05);与模型组相比,3d时亚低温组( HT12,HT24)神经细胞凋亡率及大鼠7d的死亡率明显降低(P＜0.05),差别有统计学意义;延迟24h的亚低温可降低大鼠7d的NDS评分(P＜0.05),而12h的延迟治疗无此作用(P＞0.05).结论 延迟的亚低温治疗可减少大鼠脑出血后神经细胞的凋亡,降低死亡率,发挥脑保护作用.     

亚低温对局灶性脑缺血大鼠模型C3表达的影响

目的观察亚低温（32～35℃）对局灶性脑缺血后大鼠脑组织C3表达的影响。方法 100只大鼠随机分成假手术组、常温组和亚低温组,各组根据观察时间点分为术后6h、1d、2d、3d、7d五个亚组。建立大鼠左侧大脑中动脉闭塞（MCAO）模型,应用冰袋降温的方法使亚低温组大鼠肛温10min内降至（33℃±1℃）,维持低温6h后复温。假手术组和常温组大鼠保持肛温（37℃±0.5℃）。在各时间点采用神经缺陷评分对各大鼠进行神经功能评分后断头取脑,行苏木素伊红染色观察脑缺血病理学改变,免疫组织化学染色观察不同时间点C3表达情况。结果假手术组大鼠清醒后无神经功能障碍,常温组及亚低温组大鼠清醒后均出现左侧Horner征及不同程度右侧前肢为重的偏瘫,两组大鼠神经功能缺损3d时最明显,7d时均有所减轻。除6h外各时间点亚低温组大鼠神经功能缺损评分均较常温组低（P〈0.05）,各时间点亚低温组大鼠脑组织病理学损伤较常温组轻。在各时间点假手术组大鼠脑组织中C3可见少许表达,各组间比较差异无统计学意义（P〉0.05）。常温组和亚低温组大鼠缺血侧脑组织于缺血后6h补体C3阳性细胞数均开始增加,至3d均达到高峰,到7d时C3阳性细胞数明显减少,与常温组相比,亚低温组各时间点缺血侧脑组织C3表达明显减少（P〈0.05）。结论脑缺血时,缺血侧脑组织C3有表达,亚低温可使C3表达减少。亚低温可能通过降低C3的表达减轻补体级联反应起脑保护作用。     

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     

帕金森病运动症状进展分析

目的分析帕金森病(PD)患者运动症状进展特点。方法采用PD统一评分量表(UPDRS)Ⅲ对912例PD患者进行评估。结果与病程1年的患者比较,除病程1~2年的患者外,其他病程患者的UPDRSⅢ评分、强直分、姿势或步态异常分、轴性症状总分、言语分、步态分显著升高(均P0.05),病程5~6年及14年患者的震颤分,病程5~6年、7~8年、9~13年、14年患者的运动迟缓分、姿势分显著升高(P0.05~0.01)。轴性症状进展速度高于UPDRSⅢ评分。结论 PD患者病程早期UPDRSⅢ评分进展快,震颤症状进展独立于其他症状,轴性症状评分较UPDRSⅢ更敏感地反映疾病加重趋势。     

Frequency of accumulation of filaments in adaxonal cytoplasm of Schwann cells of myelinated fibers of rat spinal roots

Summary The frequency of accumulation of 6-nm filaments in the adaxonal cytoplasm of Schwann cells in the 6th lumbar dorsal and ventral roots was evaluated in 4-, 8-, 26- and 45-week-old Sprague-Dawley rats. The frequency was higher in 4- and 8-week-old (growing) rats than in 26- and 45-week old (mature) rats, and also higher in ventral than in dorsal roots in 4-, 8- and 26-week old rats. There were no clusters on certain groups of myelinated fibers according to the size of transverse axonal area, in both the ventral and dorsal roots. Therefore, this accumulation may reflect certain functions of the adaxonal cytoplasm of Schwann cell during natural growth and maturation of the axon and myelin sheath.     

Function of circle of Willis

Nearly 400 years ago, Thomas Willis described the arterial ring at the base of the brain (the circle of Willis, CW) and recognized it as a compensatory system in the case of arterial occlusion. This theory is still accepted. We present several arguments that via negativa should discard the compensatory theory. (1) Current theory is anthropocentric; it ignores other species and their analog structures. (2) Arterial pathologies are diseases of old age, appearing after gene propagation. (3) According to the current theory, evolution has foresight. (4) Its commonness among animals indicates that it is probably a convergent evolutionary structure. (5) It was observed that communicating arteries are too small for effective blood flow, and (6) missing or hypoplastic in the majority of the population. We infer that CW, under physiologic conditions, serves as a passive pressure dissipating system; without considerable blood flow, pressure is transferred from the high to low pressure end, the latter being another arterial component of CW. Pressure gradient exists because pulse wave and blood flow arrive into the skull through different cerebral arteries asynchronously, due to arterial tree asymmetry. Therefore, CW and its communicating arteries protect cerebral artery and blood–brain barrier from hemodynamic stress.     

他汀类药物的使用和颅内动脉瘤破裂相关性分析

目的 探讨他汀类药物对颅内动脉瘤破裂的影响。方法 2010年3月至2014年3月收治颅内囊状动脉瘤67例,其中破裂者32例,未破裂者35例。采用多变量Logistic回归评估他汀类药物的使用和颅内动脉瘤破裂的关系。结果 破裂组术前使用他汀类药物4例（12.5%,4/32）,未破裂组16例（45.7%,16/35）。破裂组服用他汀类药物的百分比显著低于未破裂组（P<0.01）。纠正潜在的混杂干扰后（or值: 0.30,95%可信空间:0.12~="" 0.64）显示,颅内动脉瘤破裂与他汀类药物的使用呈显著负相关,也与高血清总胆固醇浓度有关。结论 本结果提示他汀类药物对颅内动脉瘤破裂有一定的预防效果。     

Impact of our understanding of the genetic aetiology of epilepsy

A genetic contribution to aetiology is estimated to be present in up to 40% of patients with epilepsy. It is useful to categorise genetic epilepsies according to the mechanisms of inheritance into Mendelian disorders, non-mendelian or ‘complex’ disorders, and chromosomal disorders. Over 200 Mendelian diseases include epilepsy as part of the phenotype, and the genes for a number of these have been identified recently. These include autosomal recessive progressive myoclonic epilepsies such as Unverricht-Lundborg disease, Lafora disease and the neuronal ceroid lipofuscinoses, and three autosomal dominant idiopathic epilepsies. The last named have been shown to arise from mutations in ion channel genes. Autosomal dominant nocturnal frontal lobe epilepsy is caused by mutations in CHRNA4, benign familial neonatal convulsions by mutations in KCNQ2 and KCNQ3, and generalised epilepsy with febrile seizures plus by mutations in SCN1B. ‘Complex’, familial epilepsies are more difficult to analyse, but evidence has been obtained for loci predisposing to juvenile myoclonic epilepsy on chromosome 6p and 15q. Lastly, the genes underlying several spike-wave epilepsies in mice have been cloned, and three of these encode sub-units of voltage-gated calcium channels. Received: 29 September 1999/Accepted: 7 December 1999     

肌萎缩侧索硬化三例误诊分析

目的掌握肌萎缩侧索硬化(ALS)的诊断标准,以便早期准确诊断,避免误诊。方法分析3例ALS患者早期被误诊的临床资料。结果 3例患者均以下肢无力发病,逐渐波及上肢或对侧肢体,脊柱MR I示颈部或腰部椎间盘突出压迫硬膜囊,手术治疗后,症状无缓解,病情仍进行性加重,经肌电图检查证实为ALS。结论临床医师应熟知ALS的诊断标准,对患者详细询问病史、认真查体和电生理检查是减少ALS误诊的关键。     

Effects of prevention of afferentation of the development of the chick optic lobe

BONDY, S. C., M. E. HARRINGTON AND C. L. ANDERSON. Effects of prevention of afferentation on the developmentof the chick optic lobe. BRAIN RES. BULL. 3(5) 411–413, 1978.—The effects of unilateral extirpation of the right optic cup of the three-day incubated chick embryo upon the rate of synthesis and the stability of DNA in the non-innervated optic lobe, have been studied. This surgical procedure prevents innervation of the optic lobe contralateral to the removed eye, while the other optic lobe is normally innervated by retinal ganglion cells of the remaining eye. At the 20th day of incubation, the DNA content of the non-innervated lobe was below that of the paired lobe receiving normal innervation. This deficiency of cell number was caused by two events; death of an excess number of neurons formed early in embryogenesis and a reduced rate of glial proliferation in the later stages of incubation.     

Modelling of movement of the lamprey: Control of oscillators

This article discusses the control methods of the central pattern generator (CPG). First a control model of the CPG is presented using 2 oscillators, and we suggest that phasic modulation to the CPG by means of phasic information is effective for controlling the phase difference between oscillators. Next, two models for controlling the CPG of a lamprey are proposed. One model describes a control system from the brain stem, in which the reticulospinal neurons control the CPG by receiving feedback signals and sending control signals to the neck region of the CPG. The other is a model for learning an localized control system to generate a desired motor pattern. By means of these models, a role of the efference copy is suggested.     

利培酮对精神分裂症患者生活质量的影响

目的：比较利培酮与氟哌啶醇对精神分裂症患者生活质量的影响。方法：对门诊72例服用氟哌啶醇及74例服用利培酮的精神分裂症患者用生活质量综合评定问卷（GQOLI）、阳性与阴性症状量表（PANSS）、副反应量表（TESS）进行评定。结果：利培酮组患者治疗后生活质量有所提高,而氟哌啶醇组患者生活质量有所下降。结论：利培酮治疗有利于患者提高生活质量。