构建腭中缝牵张实验大鼠动物模型

背景：以往曾采用猴、犬、猪、兔等大动物作为腭中缝牵张动物模型,但存在费用高,样本量小,检测抗体难获得等缺点。Wistar大鼠头部较宽阔,便于腔方面的操作,且成本低,繁殖率高,作为腭中缝牵张模型,有可能克服以上缺陷。 目的：建立大鼠腭中缝牵张实验动物模型,为进一步进行腭中缝牵张的实验动物研究提供基础。 方法：5周龄Wistar雄性大鼠20只,平均体质量65 g,随机分成实验组与对照组,每组10只。实验组采用0.014澳丝弯制双眼圈簧样扩弓装置,插入第一、二磨牙牙间隙,用光固化树脂粘结在大鼠磨牙舌侧进行固位;对照组安装未加力的同型扩弓装置。主动加力1周。在扩弓结束后分别对大鼠腭中缝进行X射线片,组织学观察。 结果与结论：上颌骨X射线片发现实验组腭中缝明显扩宽,磨牙明显颊向倾斜。经光镜观察发现,实验组腭中缝偏口腔侧明显增宽,间充质细胞呈梭性,与牵张力方向一致。在其下方出现创伤性炎症反应,有明显的出血区。结果证实,实验大鼠腭中缝牵张动物模型满足实验研究的需要,具有操作简单、设计科学、可重复性强的特点。     

外周肿瘤中枢神经系统转移的实验动物模型构建

资料显示国内中枢神经系统(CNS)转移瘤占CNS肿瘤的7%～17%,CT和MRI的广泛应用使CNS转移瘤发现率有所增高.建立外周肿瘤CNS转移的实验动物模型可深入理解原发瘤和CNS转移瘤的病理学、生物学及瘤细胞侵袭特征,有助于提高诊治水平.目前研究外周肿瘤CNS转移实验动物模型的评价标准、瘤细胞接种部位、瘤细胞和实验动物的选择和预处理差异很大,本文就这些模型的构建机制作一综述.     

植入异物法构建自发性脑出血实验动物模型

目前对于自发性脑出血的病理生理机制及治疗方法的研究大多基于动物试验。国内外不同实验室已经针对多种动物制作了实验性脑出血模型。根据其脑内移植的组织不同，分为缺血诱发脑出血、外伤导致脑出血、自发性脑出血和颅内植入异物导致脑出血4类。颅内植入异物导致脑出血根据植入异物的不同，又分为植入惰性物质导致的脑出血、植入生物制剂诱导脑出血、植入自体动脉血模拟脑出血3种。文章归纳总结实验性脑出血动物模型总类、制作方法和特点。     

慢性肺动脉栓塞实验动物模型构建的技术进展

目的：综述国内外关于慢性血栓栓塞性肺动脉高压(chronic thromboembolism pulmonary hypertension, CTEPH )实验动物模型构建技术的研究概况。 方法：应用计算机检索PubMed数据库2006/2009相关文章,检索词为“model of pulmonary thromboembolism”。同时计算机检索中国期刊全文数据库2003/2009相关文章,检索词为“肺动脉栓塞,实验”。此外还手工查阅相关专著数部。纳入标准：①文章所述内容应与CTEPH实验研究相关,包括慢性血栓栓塞性肺动脉高压流行病学,不同实验动物及不同制备方式。②同一领域选择近期发表或在权威杂志上发表的文章。排除标准：①重复研究。②Meta分析。 结果与结论：目前用于CTEPH模型制备的实验动物主要有犬、猪和鼠等。很多研究者都尝试模仿深静脉血栓形成后,多次急性肺栓塞事件所导致的CTEPH形成机制,建立CTEPH验动物模型。建立犬CTEPH模型主要有反复自体血凝块注入法及陶瓷念珠输入法,可用于CTEPH病理生理特点、数字剪影检查、解剖研究以及肺动脉内膜剥脱手术和介入治疗等干预治疗血栓栓塞性肺动脉高压的研究与影像学诊断技术的研究。建立猪CTEPH模型主要采用体外注入栓子法,可用于影像技术诊断CTEPH研究。建立鼠CTEPH模型主要采用反复自体血凝块注入法与肺动脉结扎法,可用于CTEPH病理生理及诊断方面研究。目前对CTEPH的研究主要是使用犬、猪和鼠实验动物模型,各有优缺点,在具体的实验研究中需根据实验目的和设计选择适当的实验动物及制作方法,以便取得最佳的实验结果。     

面肌痉挛动物模型的实验研究

目的建立面肌痉挛的动物模型,以探讨其发病机理。方法28只新西兰大白兔随机分为4组：面神经脱髓鞘并血管压迫组（模型组）13只;单一面神经血管压迫组5只;单一面神经脱髓鞘组5只;假手术对照组5只。术后第3、6周,分别用电生理技术检测面肌痉挛所特有的异常肌反应（AMR）。结果术后第3周,4组动物均未诱发出AMR：模型组有10只动物于术后第6周诱发出明显的AMR,而其他各组动物仍未诱发出AMR。结论面神经脱髓鞘和血管压迫是引起面肌痉挛的两个必要条件;建立合适的面肌痉挛动物模型为进一步研究其发病机理提供厂良好的实验基础。     

混合性中风的实验动物模型研究

目的探讨混合性中风的实验动物模型的制作方法，从而了解其发病机理。方法利用１８０只肾血管性高血压鼠（ＲＨＲｓ）通过升高或降低血压来改变血流动力学，及加用纤维蛋白原后再升高或降低血压，注意控制药物剂量及持续时间来引发脑卒中。筛选出梗塞出血并存的动物模型。结果发现加用纤维蛋白原（２００±５０）ｍｇ后，利血平０３ｍｇ，间隔２ｈ注射３次组引发混合性中风的发生率最高，达９５％。受损部位以小脑、内囊、皮质、海马、丘脑为多，以大梗塞－小出血型中风为多，梗塞以小脑、海马为著。这些梗塞灶和出血灶都在２４ｈ内发生。结论长期高血压脑动脉硬化是混合性中风的病理基础，血压剧烈的波动和血液粘滞度的变化是引起混合性中风的重要因素。     

病毒性肝炎住院病人的心理卫生状况研究

目的 探讨社会心理因素在病毒性肝炎的发展、治疗和预防中所起的作用，为本病的防治及心理治疗提供某些依据。方法 根据诊断标准，将１８６例住院病人分为急性肝炎、慢性肝炎、肝炎肝硬化三个观察组与７１位健康人作对照，采用有较高信度和效度的问卷（ＥＰＱＬＥＳ、ＳＡＳ－ＣＲ、ＳＯＳ－ＣＲＭ，ＭＣＭＱ、ＰＳＳＳ），用ＳＰＳＳ套装软件作统计分析，结果慢性肝炎与肝硬化患者有较高的神经质倾向；生活事件发生频率；肝炎肝硬     

脑胶质瘤实验动物模型研究的进展

绝大多数人脑胶质瘤的实验研究必须在动物体内进行,许多学者往往把建立一个或数个摸拟性好的动物模型作为他们从事胶质瘤研究的开端和奠基石。随着研究的深入,对实验动物模型的要求也越来越高,已有从动物诱发的脑胶质瘤模型向人脑原发胶质瘤异种移植模型过渡的趋势。本文报告有关这方面的进展情况。     

Alzheimer病的实验动物模型

总结阿尔茨海默病(Ａｌｚｈｅｉｍｅｒ Ｄｉｓｅａｓｅ,ＡＤ)的动物模型近几年的研究成果,从神经纤维缠结、β淀粉样蛋白、脑组织损伤模型和转基因动物等几个方面讨论并比较这些动物模型在复制ＡＤ病理和行为改变方面的优点和不足,探讨如何制作出更理想的动物模型。     

面神经损伤实验动物模型的自愈性研究

目的探讨卡压时间对面神经损伤实验兔模型自愈的影响。方法将日本大耳白兔20只分为空白组、卡压组、模型组(模型组分为术后3周和5周两时间点),对卡压组和模型组制作兔面神经压榨损伤模型。对受损面神经标本行醋酸铀及枸橼酸铅双色染色、HE染色,观察受损面神经的形态学改变。结果与空白组相比,卡压组、模型组3周和5周时神经束包膜不完整,神经纤维可见不同程度变性、水肿、脱髓鞘,轴突萎缩变细。模型组3周时和模型5周组髓鞘厚度分别为(1.099±0.245)mm、(1.294±0.220)mm,与空白组〔(1.597±0.212)mm〕比较均有统计学差异(P<0.05),卡压组髓鞘厚度〔(1.350±0.147)mm〕与模型3周组比较有统计学差异(P<0.05),与空白组及模型5周组相比无统计学意义(P>0.05)。结论延长面神经卡压时间可以使模型动物在较长时间(5周内)不可自愈,为下一步客观评估针灸疗效奠定基础。     

骨质疏松动物模型的研究现状☆

背景：骨质疏松的发病机制十分复杂,但又不能直接在人体上进行实验,需要复制类似人类骨质疏松的动物模型进行研究。 目的：全面分析各种骨质疏松动物模型的造模方法及优缺点,为今后研究骨质疏松症,在模型选择上提供参考。 方法：电子检索中国知识资源总库(CNKI)系列数据库和ESBCO Medline数据库1990-01/2010-07收录的骨质疏松模型的相关综述和论文报告。中文检索词为“骨质疏松,动物模型”;英文检索词为“osteoporosis,animal models”。共检索到469篇相关文献,对文章进行初审,纳入文献主题内容与此文联系紧密;原创、论点论据可靠的试验文章;观点明确,分析全面的文章。排除内容陈旧或重复文献及试验设计中不是采用随机对照试验的文章。 结果与结论：共纳入符合标准的38篇文献。目前用于骨质疏松症研究的动物模型主要有诱发性动物模型和转基因动物模型。各种骨质疏松动物模型可能只侧重于表现该疾病的某种病因、某一阶段、某些主要症状及某些病理生理变化,必须根据研究目的,选择合适的造模方法和实验动物。     

精神分裂症动物模型研究进展

精神分裂症是一种常见而严重的精神疾病,给家庭和社会带来沉重的负担。虽然目前对精神分裂症的病因及发病机制尚不完全清楚,但随着对疾病认识的逐步深入,已经可以利用动物模型模拟精神分裂症的不同临床症状。制备可靠的、可预测的动物模型,对理解复杂精神疾病的神经生物学基础和开发新型抗精神病药物都是非常必要的。现针对目前研究较多的精神分裂症动物模型的研究进展进行综述,包括药物诱导动物模型、基因相关动物模型、神经发育动物模型、脑损伤动物模型、基因环境交互作用动物模型,可为今后精神分裂症的相关研究提供一定的参考。     

多发性硬化与乙肝病毒感染

应用ELISA法,配对检测46例(确诊和拟诊各23例)多发性硬化(MS),43例其它神经科疾病(其它组)和34例非神经科病对照组的血清和CSF的HBsAg,抗—HBs,HBeAg,抗—HBe和抗—ABc。结果为:(1)血清中有HBV感染者:确诊MS组18例(78％),可疑MS组13例(56％),其它组13例(30％),对照组16例(47％)。(2)各组血清中仅含有抗—HBs和/或抗—HBe阳性者在确诊MS组的阳性率与其它组及对照组有极显著性差异(P<0.01)。本研究提示:MS血清中HBV感染显著增高。     

铁离子诱发癫痫动物模型的特征和应用

外伤性癫痫（posttraumatic epilepsy，PTE）是颅脑损伤后一种常见的并发症，目前研究认为，外伤性脑损害后红细胞外渗、溶解和含铁血黄素沉积于神经组织内，引起一系列的病理变化，导致癫痫发作，是PTE的显著特征。与其类似的还有海绵状血管瘤，常常出现反复出血，其中多数患者合并癫痫发作，MRI和手术中往往发现在海绵状血管瘤周围显示含铁血黄素沉积带。同样在出血性脑中风患者，如脑出血、脑梗塞后出血和蛛网膜下腔出血，也有相当的患者早期或者晚期并发癫痫。     

Demyelinating neuropathy associated with hepatitis B virus infection. Detection of immune complexes composed of hepatitis B virus surface antigen

We observed 4 patients with the Guillain-Barré syndrome (GBS) type of polyneuropathy and one patient with chronic relapsing polyneuropathy associated with hepatitis B virus infection, and examined the sera, cerebrospinal fluid (CSF) and sural nerve specimens from the patients in search of the pathogenetic factors involved. It was demonstrated that hepatitis B surface antigen(HBsAg)-immune complexes were significantly increased in both the sera and the CSF of the 4 patients with GBS. The serum levels of immune complexes were also closely related to the clinical status of these patients. In all patients, HBsAg-positive labelling of immunofluorescence was found around the endoneural small blood vessels and in the endoneurium. Electron-dense deposits, suggestive of immune complexes composed of hepatitis B virus, were demonstrated in the endoneurium of the patient with chronic relapsing polyneuropathy. These results suggest that HBsAg immune complexes may be of importance in the etiology of GBS or chronic relapsing polyneuropathy associated with hepatitis B virus infection.     

Neuronal injury in simian immunodeficiency virus and other animal models of neuroAIDS

The success of antiretroviral therapy has reduced the incidence of severe neurological complication resulting from human immunodeficiency virus (HIV) infection. However, increased patient survival has been associated with an increased prevalence of protracted forms of HIV encephalitis leading to moderate cognitive impairment. NeuroAIDS remains a great challenge to patients, their families, and our society. Thus development of preclinical models that will be suitable for testing promising new compounds with neurotrophic and neuroprotective capabilities is of critical importance. The simian immunodeficiency virus (SIV)-infected macaque is the premiere model to study HIV neuropathogenesis. This model was central to the seminal work of Dr. Opendra “Bill” Narayan. Similar to patients with HIV encephalitis, in the SIV model there is injury to the synaptodendritic structure of excitatory pyramidal neurons and inhibitory calbindin-immunoreactive interneurons. This article, which is part of a special issue of the Journal of NeuroVirology in honor of Dr. Bill Narayan, discusses the most important neurodegenerative features in preclinical models of neuroAIDS and their potential for treatment development.     

Neuromuscular disorders associated with hepatitis B virus infection

Approximately 400 million worldwide are chronically infected with the hepatitis B virus (HBV). During the course of illness, approximately 20% of patients develop disease manifestations outside the liver. Neuropathy develops in approximately 5% of patients with chronic HBV infection and rarely during acute HBV infection. The pathogenesis of the various HBV-associated neuropathy syndromes possibly involves deposition of immune complexes in nerves or blood vessel walls. Direct viral infection of nerves has not been demonstrated. Management entailed supportive care with antiviral and immunomodulatory treatment as clinically indicated. Rare cases of muscle disease, mostly inflammatory myopathy, have been associated with HBV infection. Presumably, HBV-associated antigens trigger immune mechanisms directed against components of muscle tissue. There is no evidence of replicative virus infection of muscle fibers. Management entailed immunomodulatory treatment, occasionally with anti-HBV therapy. Physicians should be aware that HBV infection has the potential to trigger presumed immune-mediated neuromuscular syndromes.     

Chronic relapsing polyneuropathy associated with hepatitis B virus infection

We report the case of a 50‐year‐old woman affected by a chronic latent Hepatitis B (H.B.V.) virus infection since the age of 35, who complained of several relapses of sub‐acute sensorimotor inflammatory polyneuropathy with albumino‐cytological dissociation, successfully treated with IVIg pulse therapy during acute phase and with chronic prednisone therapy. An exacerbation of H.B.V. infection, likely induced by corticosteroid administration, associated with marked increase in serum of hepatic enzymes and high H.B.V. DNA levels in blood, coincided with a severe worsening of the neuropathy. Laboratory investigations revealed, among others, elements of renal involvement (hypoalbuminemia, proteinuria). Immunofixation electrophoresis revealed an IgM (k) monoclonal gammopathy, antibody testing high level of IgM to GD1a (1/81920). Lamivudina, rituximab and IVIg were administered: renal and liver indexes re‐entered within the ranges, sensorimotor deficits had slow and incomplete remission. In this case, polyneuropathy could be an expression of systemic H.B.V. illness mediated by a specific immunogenic attack in the phase of chronic latent infection, mediated by immune‐complexes precipitation in the reactivation phase, as the renal involvement seems to suggest. The pathological mechanism is under discussion.     

拷贝数变异及单核苷酸变异基因型自闭症动物模型研究进展

自闭症的发病率逐年升高,因其致病原因的复杂性,使得自闭症的研究成为难点.研究发现遗传因素约占自闭症发病率的50％,然而能有效反映病因的动物模型却少之又少,现综述基于拷贝数变异(CNV)和单核苷酸变异(SNVs)建立的基因型自闭症动物模型,作为以后了解自闭症机制的新高级模型工具.     

Chronic neuropathy associated with immune complexes of hepatitis B virus

In 7 patients, including one autopsied case, with neuropathy associated with hepatitis B virus infection, histologic examination of sural nerve biopsies revealed small vessel vasculitis in the vasa nervorum. In all cases, immunofluorescent deposits of hepatitis B surface antigen, immunoglobulin and C3 complement were detected in the vasa nervorum. That these deposits could represent immune complexes composed of hepatitis B virus was supported by the serologic demonstration of high serum-level of immune complexes and by the ultrastructural demonstration of electron-dense deposits around the endoneural capillary and in the endoneurium. The densities of large myelinated fibers were significantly lower than controls (P less than 0.01) in 6 of 7 cases. These results suggest that immune complexes composed of hepatitis B virus might play a significant role in the pathogenesis of endoneural and epineural vascular lesions, through which neuropathy may be induced in patients with hepatitis B virus infection.