脑动静脉畸形实验动物模型的建立

脑动静脉畸形是一种比较常见的严重威胁人们生命安全和生存质量的脑血管疾病，目前人们主要是通过尸体解剖以及CT、MRI等影像学的方法认识。近年来，学者们应用各种动物模型来研究脑动静脉畸形的血流动力学，病理生理学以及脑动静脉畸形栓塞材料的评估，栓塞后临床疗效评价，放射照射剂量对脑动静脉畸形的影响等。本文就脑动静脉畸形实验动物的常用种类，动物模型的建立方法以及动物模型的实际应用进行了综述。     

神经根慢性嵌压损伤的动物模型建立

目的：建立一种由自身骨性增生造成神经根慢性嵌压损伤的动物模型，为相关实验提供造模方法一方法：30只健康家猫，手术显露右侧C7、C8和L5、L6冲经根及其椎问孔内口，用牙髓钻破坏椎间孔周围骨皮质后，将“V”形松质骨块沿骨壁嵌于神经根通道的骨性管道内及侧隐窝后方，左侧做正常对照。在造模术前和术后第2、4、8、12、24周行磁刺激运动诱发电位(MEP)检测，每次随机选6只，4～5只行影像学检查，以确定神经根通道的狭窄程度和神经根受压状态，6只均做病理组织学检查和椎间孔截面积测量。结果：术后早期实验侧肢体出现行为异常：而后有不同程度肌萎缩；后期部分肢体远端出现溃疡。影像学检查随着嵌压时间延长．实验侧椎间孔骨痂增多，狭窄加重。神经根受压变形，椎间孔骨性截面积8周后明显减小，与对照侧比较有显著性差异。术后2周，神经根组织学检查主要表现为神经束膜、内膜的水肿。髓鞘肿胀；4周后发生节段性脱髓鞘：8周时神经轴突增粗、断裂，远端瓦勒氏变性；12周后变性冲经结构崩解、吸收，形成空洞：24周时整个神经干纤维化。术后4周时实验侧MEP开始出现潜伏期延长；8周时伴有波形分化不清；12周波幅明显下降：24周MEP的引出困难，部分电位消失。结论：采用椎问孔内自体松质骨植入，造成神经根慢性嵌压性损伤模型成功率高，操作简单，适用于脊柱各个节段，其损伤部位和形式与临床更为接近。     

Removing the effect of SVD algorithmic artifacts present in quantitative MR perfusion studies.

Quantitative cerebral blood flow (CBF) values can be obtained from dynamic susceptibility contrast (DSC) MR perfusion studies using the standard singular value decomposition (sSVD) deconvolution algorithm. Reports in the literature from simulation and in vivo studies suggest that CBF estimates obtained using sSVD deconvolution depend on the arterial-tissue delay (ATD). By contrast, Fourier transform (FT) deconvolution produces CBF estimates that are independent of ATD. The diagnostic reliability of quantitative CBF measurements to define areas of normal tissue flow and tissue at risk is brought into doubt by such gross sensitivity to the specifics of the deconvolution approach. This variation of CBF values with ATD is shown to be an artifact associated with the current implementation of the sSVD deconvolution algorithm. A reformulated version of the SVD deconvolution algorithm (rSVD) is presented and compared to the standard SVD algorithm through simulation and patient case studies.     

从ECCE到Phaco的转变--核处理技术的实验研究

目的通过化学方法制成动物核性白内障模型,探讨相对能量复合指数(RECP)与角膜内皮细胞活性的关系。方法将5种化学物质注入晶状体,以透过黑白条纹的清晰程度判断晶状体混浊程度并分级。然后将实验眼球分为6组(Ⅰ组为对照组;Ⅱ-Ⅵ为实验组),行标准超声乳化白内障摘除手术。手术后立即取下角膜,作锥蓝-茜素红联合染色标本和扫描电镜标本。结果晶状体内注入甲醛、冰醋酸、无水乙醇、丙酮和苯扎溴铵均能形成晶状体混浊,其中:冰醋酸致晶状体混浊能力最弱,无水乙醇、丙酮次之,甲醛、苯扎溴铵最强。当RECP≤90时,锥蓝-茜素红双重染色和扫描电镜均表明角膜内皮细胞活性好,其形态和细胞联接均无改变。当RECP=120时,角膜内皮细胞形态尚正常,但是细胞联结和胞膜部分破坏。当RECP=150时,角膜内皮细胞严重损伤。结论用化学方法制作核性白内障模型供过渡训练使用是可行的。当RECP超过某一数值(>90)时,即与角膜内皮细胞的活性成负相关。     

肝癌患者血清P-选择素测定及临床意义

目的：研究肝癌患血清P-selection(P-sel)在肝癌复发和转移中的作用。方法：采用ELISA法分别测定原发性肝癌患和对照组血清P-选择素的含量，同时测定AFP含量。结果：肝癌患P-sel含量显高于正常人，且与AFP含量呈线性正相关，术后2周浓度降低；P-sel含量以Ⅰ、Ⅲ和Ⅳ期肝癌患显高于Ⅰ期患；且大肝癌患显高于小肝癌患，有癌栓组、有肝内转移组明显高于无癌栓组和无转移组。结论：P-选择素测定在原发性肝癌的诊断和检测术后复发方面有重要价值，联合检测AFP和sP-sel可提高诊断敏感性。     

~(60)Co-γ射线照射后HeLa细胞存活曲线和数学模式

本文研究了~(60)Co-γ射线照射后HeLa细胞的存活曲线,比较了两种数学模式拟合的结果.拟合优度以对误差加权的残差平方和(Q)作为统计指标进行评价.结果表明模式的拟合度较模式为优.     

Fiber Matrix Descriptors from Permeability Data Without Requiring Membrane Thickness: Theory,Results, and Optimization

Objective: Permeability of basement membrane and all other barriers contains a term for membrane thickness (Δx). This naturally leads to development of methods for measuring Δx that are imprecise, inaccurate, expensive, subject to preparation artifact, and inattentive to variability. Although height and shape of permeability (P) vs. probe radius (α) curves are sensitive to Δx, ln(P) or ln(P/free diffusivity or D_o) curves have shapes independent of Δx. It should, thus, be possible using such characteristics to determine fiber radius (r_f) and void volume ratio (ε) without Δx. We developed such a method to derive membrane structure by the standard model of Ogston and present its experimental evaluation. Methods: Basement membranes were self-assembled using 1: 1 Matrigel: 0.01 M Tris/150 mM NaCl/1.0 mM CaCl₂ buffer on 0.4-μ polycarbonate supports with transport measured in diffusion chambers using FITC-labeled hydroxyethyl starch probes from 25 to 102 Å in radius. Sampling was at 0.5 hr and then for each hour up to 5. Other membranes were measured 7 days after formation. Results: The best fit of the new technique occurred at 3 hr with R² = 0.949 ± 0.003 SEM, r_f = 36.8 ± 2.4 Å, and ε = 0.87 ± 0.02. Membranes studied for 7 days showed more variability but essentially the same characteristics. Conclusions: Membrane thickness is not necessary to reduce permeability of basement membrane to structure, and optimum sampling time is 3 hr.     

Rising mortality from motor neurone disease in Sweden 1961–1990: the relative role of increased population life expectancy and environmental factors

Recent studies of mortality from motor neurone disease (MND) in Sweden have demonstrated rising levels of mortality from the disease, especially amongst older age groups. Case-control investigations have suggested that certain environmental factors are significantly related to variations in mortality from the disease, and are associated with a probable individual susceptibility to MND. This study applies an innovative epidemiological technique to longitudinal and cohort analysis of Swedish mortality from MND during the period 1961 to 1990. Survival modelling shows that a subpopulation susceptible to MND exists in Sweden, as has been demonstrated in other countries. The increased life expectancy of the Swedish population since 1961 has resulted in more of that susceptible population living to the ages at which MND is expressed, explaining the majority of the increase in mortality from the disease. However, environmental factors may play a role in accelerating the course of MND and may affect the timing of death within the susceptible sub-population.     

A hole in the T cell repertoire specific for a pigeon cytochrome c related peptide associated with amino acid substitutions on I-Ab molecules.

When C57BL/10(B10) mice were immunized with a pigeon cytochrome c related peptide, 50V (AEGFSYTVANKNKGIT), two helper T cell populations with different specificity were activated. A major T cell population reacted with a 50V analog, 50V54A (AEGFSYTVANKAKGIT), more potently than with the immunogen, 50V, in a heteroclitic fashion, whereas the other minor T cell population responded only to 50V. By contrast, when bm12 mice were immunized with 50V, the minor T cell population responding only to 50V could hardly be demonstrated. The apparent deletion of the minor T cell population in bm12 mice seems to be attributable to negative selection under the influence of I-Abm12 molecules, since the minor T cell population was undetectable in both I-Ab and I-Abm12 restricted T cells from (B10 x bm12)F1 mice. Thus, three mutant points on the I-A molecule in bm12 mice appear to be involved in the seemingly negative selection of the certain T cell repertoire. The present finding demonstrates that a T cell repertoire generated under the influence of a MHC product (Ab) on one parental strain is eliminated by a different MHC product (Abm12) on the other parental strain of F1 cross. The mechanism underlying the apparent negative selection is discussed.