基于Watersnake的视神经纤维的自动识别

在视神经横切面图像中，将每个神经纤维的边界精确地分割出来，是视神经形态分析的重要环节。由于神经纤维数量巨大、形态各异，单纯采用一种分割方法无法获得满意效果。采用基于Watersnake的分割方法，整合Watershed和Snake在图像分割方面的优势，分两步进行纤维分割。首先由Watershed获取纤维的粗轮廓，在此基础上由Snake经曲线演化获得纤维的精细轮廓。实验结果表明，Watersnake能较好地识别神经纤维的内外轮廓，为后续的神经纤维形态分析奠定基础。     

基于改进的CV-RSF模型的甲状腺结节超声图像自适应分割算法

目的甲状腺结节超声图像的精确分割对甲状腺结节的良恶性诊断尤为重要。目前,对于甲状腺结节超声图像的分割,有学者提出利用主动轮廓模型分割算法,但是由于活动轮廓分割算法需要手动设置迭代次数,未实现模型的自适应性。因此,本文提出了一种基于改进的无边缘主动轮廓-局部区域可控的拟合(Chan-Vese-region scalable fitting,CV-RSF)模型的甲状腺结节超声图像自适应分割算法。方法选取南京同仁医院12例患者的甲状腺结节超声图像用于实验。首先,在无边缘主动轮廓(Chan-Vese,CV)模型中,引入一个基于梯度的边缘引导函数,根据面积变化率,自适应地获取甲状腺结节的粗分割轮廓;然后,将粗分割轮廓作为局部区域可控的拟合(region-scalable fitting,RSF)模型的初始轮廓,并根据面积变化率,自适应地获取甲状腺结节最终分割结果。将改进模型分割的结果与CV模型、RSF模型分割的结果进行比较,并分析甲状腺结节边缘清晰度对分割结果的影响。结果本文模型算法分割结果的平均迭代次数、平均面积重叠率、平均Hausdorff分别达到了134、90.34%、9.77,均优于CV模型、RSF模型的分割算法。结论该算法有效地分割出边缘清晰和不清晰的甲状腺结节超声图像,并解决手动设置迭代次数的问题,从而实现甲状腺结节的有效、准确、自动分割。     

交互式GACV模型的肿瘤图像分割

目的:提取医学图像中肿瘤区域,用以测量肿瘤体积问题。方法:提出一种基于GACV(Geodesic-Aided C-Vmethod)的交互式模型。该模型首先人工选取感兴趣区域,并在区域内设定初始水平集与肿瘤内部种子点,然后在感兴趣区域上应用将图像梯度边缘信息与图像区域灰度特性统一到同一分割中的GACV模型,得到肿瘤的粗分割结果。最后为去除目标内外孔洞,提出一种无损边缘的膨胀搜索算法,作为细分割。结果:将该模型应用于不同形状的肿瘤图像中,能成功检测肿瘤轮廓。通过实验与其它活动轮廓分割方法结果对比,结果显示该模型在准确分割肿瘤边界与分割算法耗时方面均具有良好表现。结论:本文提出的分割方法能高效率、准确识别肿瘤区域。     

基于改进区域生长算法的肝脏分割方法研究

目的：把肝脏从医学图像中提取出来,为肝脏三维定位以及放疗计划制定提供准确的数据。肝脏与其周围器官组织灰度差别小、边界不明显,而传统区域生长算法生长准则单一,不能满足分割精确度需求,并且未经处理的轮廓比较粗糙。针对这些问题,本文提出一种改进的区域生长算法。方法：本文算法主要从三个方面改进：基于先验经验和肝脏特性的种子区域选择;基于Canny算子边缘检测结果的区域生长准则动态优化;基于漫水填充法和曲线拟合的轮廓后处理。结果：本文使用多套临床实际腹部CT序列测试算法,以医生手动勾画结果为标准进行评价。在大多数CT切片上的肝脏自动分割都能取得较好的结果,并且分割用时很短,保证了效率。结论：测试结果表明,本文算法在动态控制区域生长和平滑轮廓方面有很好的作用,在保证速度的同时有效提高了肝脏自动分割精度。     

基于自适应标记分水岭算法的肝脏CT图像自动分割

目的为减少人工交互提出了基于自适应标记分水岭的CT系列图像肝脏区域自动分割算法。方法首先对图像进行形态学重构运算以平滑图像,然后计算多尺度形态学梯度,同时提出利用梯度图像非零的局部极小值点的均值进行自适应标记提取,以避免分水岭的过分割和欠分割,再结合肝脏为最大的实质性脏器和相邻图像的相似性实现CT系列图像的肝区自动分割。结果该算法能自动、快速地提取CT系列图像中的肝脏区域。结论分水岭算法能准确定位区域的边缘,通过选择合适的阈值对梯度图像进行标记以抑制分水岭的过分割,实现医学图像中感兴趣区域的自动分割。     

钳夹法构建视神经损伤兔模型:复明颗粒治疗损伤视神经的应力松弛分析

背景:有研究表明,中成药复明颗粒对治疗是神经损伤具有一定的疗效,但仍需进行大量的实验研究进行验证。目的:以应力松弛实验的方法验证中成药复明颗粒干预治疗视神经损伤的效果。方法:以钳夹法造成家兔视神经损伤,用复明颗粒稀释灌胃干预,并设模型组和正常对照组作对比,连续给药30 d后取各组动物视神经进行应力松弛实验和组织形态观察。结果与结论:正常对照组视神细胞核分别均匀,无明显水肿及增大,无炎症细胞,轴突等内容物形态清晰。模型组视神经纤维排列稀疏,结构模糊,轴突、核碎裂轴突等内容物形态发生了改变。复明颗粒治疗组视神经横断面较大面积神经纤维排列较密集,多数轴突形态正常。视神经7 200 s应力下降量和和应力松弛下降值均为正常对照组复明颗粒治疗组模型组(P0.05)。结果证实,中成药复明颗粒加快了损伤视神经轴浆恢复,使轴突形态恢复正常,有利于损伤视神经的恢复。     

基于局部调整动态轮廓模型提取超声图像乳腺肿瘤边缘

提出一种基于局部调整动态轮廓模型提取超声图像乳腺肿瘤边缘的算法.该算法在Chan-Vese (CV)模型基础上,定义了一个局部调整项,采用基于水平集的动态轮廓模型提取超声图像乳腺肿瘤边缘.将该算法应用于89例临床超声图像乳腺肿瘤的边缘提取实验,结果表明:该算法比CV模型更适用于具有区域非同质性的超声图像的分割,可有效实现超声图像乳腺肿瘤边缘的提取.     

短期丰富生存环境对老年雄性大鼠大脑白质及白质内有髓神经纤维的影响

目的 探讨短期丰富生存环境干预对老年雄性大鼠大脑白质及白质内有髓神经纤维的影响.方法 将20只24月龄雄性SD大鼠分别在丰富生存环境条件和普通标准环境下饲养4个月后,从每组随机抽取4只大鼠,用透射电子显微镜和体视学方法比较两组大鼠大脑白质及白质内有髓神经纤维的改变. 结果 丰富生存环境组大鼠的白质总体积,白质内有髓神经纤维总长度和总体积,有髓神经纤维轴突总体积分别较标准对照组显著增大,但有髓神经纤维平均内径、外径、髓鞘总体积、髓鞘平均厚度、髓鞘平均内、外周长、有髓神经纤维断面面积、髓鞘断面面积及轴突断面面积较对照组均无明显差异. 结论 短期丰富生存环境干预对24月龄雄性大鼠的大脑白质和白质内有髓神经纤维均有明显的影响.提示短期丰富生存环境可能促使老年雄性大鼠白质内已经发生脱髓鞘改变的有髓神经纤维出现髓鞘再生.     

PTPα基因敲除小鼠坐骨神经纤维的超微结构分析

目的探讨受体酪氨酸磷酸酶α(PTPα)在周围神经系统髓鞘形成中的作用。方法同窝出生60天的PTPα-/-和野生型小鼠,用透射电镜观察其坐骨神经横断面的超微结构,并对有髓神经纤维的髓鞘厚度和数量进行形态计量分析。结果与野生型小鼠相比,PTPα-/-小鼠坐骨神经的髓鞘无明显异常,有髓纤维的比例与野生型无显著差异,但髓鞘显著增厚。结论PTPα在周围神经髓鞘形成中对轴突包裹可能起反向调节作用。     

一种基于Snake模型的脑部CT图像分割新算法

针对目前传统的Snake模型图像分割算法的力场捕捉范围小、对初始轮廓的选取敏感以及对轮廓曲线难以收敛到 细小深凹边界的缺陷,提出一种基于Snake 模型的脑部CT图像分割新算法。算法首先运用Canny 边缘算子对图像进行 边缘检测,将边缘检测图像叠加到原始图像上,然后再运用Snake模型和梯度向量流（GVF）Snake模型分别对叠加图像进 行分割。实验结果表明,该算法克服了传统Snake 模型和GVF Snake 模型因边缘轮廓不清晰造成的漏分割情况,防止了 GVF Snake模型由于GVF力场的相互作用所造成的过分割现象,同时,还能促使轮廓线收敛到细小深凹边界,提高定位精 度,具有更好的分割效果。     

Myelination and remyelination in the regenerating visual system of the goldfish

Summary The remyelination of regenerated optic axons was investigated in goldfish following either optic nerve crush or ouabain retinal intoxication. Axons grown after nerve crushing acquire thinner myelin sheaths than axons originating from reconstituted ganglion cells. If axons of reconstituted ganglion cells are crushed and allowed to regenerate, the subsequent myelination is weaker than that of control axons not interrupted by crushing, but stronger than that of axons of preexisting retinal ganglion cells.The present results suggest that a neuron is capable of inducing a normally developed myelin sheath when its axon contacts an oligodendrocyte the first time, whereas a neuron whose axon contacts an oligodendrocyte the second time is not capable of forming a normal myelin sheath in the adult animal. The present results also support the notion that the oligodendrocyte requires a neuronal signal for myelin sheath formation.Supported by the Deutsche Forschungsgemeinschaft (Wo 215/5)     

Action potentials induce uniform calcium influx in mammalian myelinated optic nerves

The myelin sheath enables saltatory conduction by demarcating the axon into a narrow nodal region for excitation and an extended, insulated internodal region for efficient spread of passive current. This anatomical demarcation produces a dramatic heterogeneity in ionic fluxes during excitation, a classical example being the restriction of Na influx at the node. Recent studies have revealed that action potentials also induce calcium influx into myelinated axons of mammalian optic nerves. Does calcium influx in myelinated axons show spatial heterogeneity during nerve excitation? To address this, we analyzed spatial profiles of axonal calcium transients during action potentials by selectively staining axons with calcium indicators and subjected the data to theoretical analysis with parameters for axial calcium diffusion empirically determined using photolysis of caged compounds. The results show surprisingly that during action potentials, calcium influx occurs uniformly along an axon of a fully myelinated mouse optic nerve.     

视神经损伤后视神经及其内毛细血管的早期超微结构的变化

目的观察视神经损伤后视神经和神经内毛细血管的超微结构变化,探讨视神经损伤的机制。方法建立家兔视神经损伤的动物模型,利用透射电子显微镜观察视神经及神经内毛细血管超微结构的变化。结果视神经损伤0.5h后,轴突部分肿胀,髓鞘疏松,微管、微丝排列出现紊乱,线粒体肿胀,毛细血管内皮细胞中的吞饮小泡和微绒毛明显减少;损伤6h后,线粒体出现髓样变和空泡样变性,血管内皮细胞肿胀,管腔变窄;损伤12h后,轴突空泡样变性,髓鞘脱失,毛细血管周围间隙增宽;损伤48h后,轴质密度增加,部分髓鞘板层完全分离,微管、微丝及线粒体发生颗粒性溶解,内皮细胞中的线粒体出现广泛变性;损伤96h时,轴索崩解呈空泡状变性,髓鞘更广泛崩解,毛细血管扩张破裂,红细胞外溢。结论视神经损伤早期轴突肿胀、空泡样变性,线粒体水肿变性,微管、微丝数量减少;视神经内毛细血管扩张,通透性增加。     

Retrograde degeneration of myelinated axons and re-organization in the optic nerves of adult frogs (Xenopus laevis) following nerve injury or tectal ablation

Summary The optic nerve proximal to the lesion (toward the retina) was examined by light and electron microscopy in adultXenopus laevis after various types of injury to optic nerve fibres. Intraorbital resection, transection or crush of the optic nerve or ablation of the contralateral optic tectum all resulted in marked alterations in the myelinated axon population and in the overall appearance of the nerve proximal to the site of injury. Examination of the nerves from 3 days to 6 months postoperatively indicated that a progressive, retrograde degeneration of myelin and loss of large-diameter axons occurred throughout the retinal nerve stump regardless of the type of injury or distance of the injury from the retina. The retinal stump of nerves receiving resection or transection showed a nearly complete loss of myelin and large-diameter axons while the degree of degeneration was subtotal in nerves receiving crush injury or after lesions farther from the retina (i.e. tectal ablation). In addition, the entire retinal nerve stump after all types of injury was characterized by the appearance of an actively growing axon population situated circumferentially under the glia limitans. The latter fibres are believed to represent regrowing axons which are being added onto the nerve, external to the original axon population and are suspected to modify actively the glial terrain and glia limitans.     

Axon diameter and myelin thickness—unusual relationships in dorsal root ganglia

Peripheral nerve fibers close to the sensory neurons of dorsal root ganglia displayed unusually thin myelin sheaths in relation to their axon diameter. Myelinated internodes along each fiber showed large differences in the numbers of myelin lamellae. These fibers are thought to represent spatial progression in degree of myelination as the axon egresses from the nonmyelinated glomerulus to the position of axonal bifurcation. This region is termed the initial complex of dorsal root ganglion cells. While the usual relationship between axon diameter and myelin sheath thickness is seen in the majority of dorsal root ganglion fibers, the fiber comprising each initial complex shows an atypical relationship in that the myelin sheath is unusually thin. Since the pattern of myelination in this small area is incongruous with previous reports attributing the control of myelin sheath thickness solely to axon diameter, the present findings indicate that other, unknown factors are operative in the control of myelination.     

野木瓜皂甙对大鼠神经髓鞘和轴突膜的作用

本文作者等曾发现将镇痛中草药野木瓜注射液 (IS)涂布于大鼠隐神经可导致 C类纤维轴突膜膨胀、边界模糊 ;Aδ类纤维髓鞘出现较多的空洞和髓鞘崩解。本实验从 IS中提取了野木瓜皂甙 (SS)并将 0 .3 % SS涂布于大鼠隐神经 ,经电生理研究和电镜观察发现 :60 min后隐神经复合动作电位 A成分的传导被阻滞 ,并发现 A纤维髓鞘和 C纤维的轴突膜以及神经干的胶原纤维出现类似涂布 IS后出现的黑色斑块 ,并出现了局部的髓鞘崩解和轴突膜增厚并变模糊的现象。表明 SS对髓鞘和轴突膜有亲和力 ,可引起髓鞘和轴突膜结构的变化 ,从而导致神经传导阻滞     

颈内动脉压迫视神经颅内段的组织学改变及其机制

目的:观察视神经受压后的组织学改变,探讨因压迫所致视野缺损发生的机制。方法:60-80岁的老年人脑,组织切片观察颈内动脉内膜钙化压迫视神经颅内段引起的神经组织学改变。结果:粥样硬化的颈内动脉可压迫视神经并在其表面形成明显压迹。神经受压后,中隔变窄,神经束呈条索状,束内营养小动脉硬化,管腔阻塞,节细胞轴突萎缩,重者可全部消失,少突胶质细胞增多,肿胀。结论:视神经纤维萎缩是由于阻塞了神经束内营养小动脉缺血所致,以乳头黄斑束受累为甚,是视野缺损发生的原因之一。     

Schwann cells in the regenerating fish optic nerve: evidence that CNS axons, not the glia, determine when myelin formation begins

Fish optic nerve fibres quickly regenerate after injury, but the onset of remyelination is delayed until they reach the brain. This recapitulates the timetable of CNS myelinogenesis during development in vertebrate animals generally, and we have used the regenerating fish optic nerve to obtain evidence that it is the axons, not the myelinating glial cells, that determine when myelin formation begins. In fish, the site of an optic nerve injury becomes remyelinated by ectopic Schwann cells of unknown origin. We allowed these cells to become established and then used them as reporters to indicate the time course of pro-myelin signalling during a further round of axonal outgrowth following a second upstream lesion. Unlike in the mammalian PNS, the ectopic Schwann cells failed to respond to axotomy and to the initial outgrowth of new optic axons. They only began to divide after the axons had reached the brain. Shortly afterwards, small numbers of Schwann cells began to leave the dividing pool and form myelin sheaths. More followed gradually, so that by 3 months remyelination was almost completed and few dividing cells were left. Moreover, remyelination occurred synchronously throughout the optic nerve, with the same time course in the pre-existing Schwann cells, the new ones that colonised the second injury, and the CNS oligodendrocytes elsewhere. The optic axons are the only common structures that could synchronise myelin formation in these disparate glial populations. The responses of the ectopic Schwann cells suggest that they are controlled by the regenerating optic axons in two consecutive steps. First, they begin to proliferate when the growing axons reach the brain. Second, they leave the cell cycle to differentiate individually at widely different times during the ensuing 2 months, during the critical period when the initial rough pattern of axon terminals in the optic tectum becomes refined into an accurate map. We suggest that each axon signals individually for myelin ensheathment once it completes this process.     

Formation of central and peripheral myelin sheaths in the rat: An electron microscopic study

Formation of the myelin sheath in peripheral nerve of the newborn rat is compared with its formation in postnatal cerebral white matter. The unmyelinated central axon is bare and myelination begins by the spiral wrapping of an oligodendrocytic process around the axon. The paired membranes of this process fuse on their inside surfaces, lengthen, and spiral around the axon to make a loose sheath of major dense lines. Compact myelin results after fusion of the outside surfaces to form the intraperiod line. Cytoplasm is sparse in developing central myelin, usually being restricted to inner and outer tongues. Unmyelinated peripheral axons are enclosed within a mesaxon formed by the invagination and fusion of the outside surfaces of the Schwann cell plasma membranes. Loose myelin is produced by lengthening and spiralling of the mesaxon (intraperiod line) around the axon. As Schwann cell cytoplasm is extruded from between the spirals, the major dense line forms and compact myelin results. Trapped cytoplasm, a characteristic of developing peripheral myelin, is found in the internodal compact myelin sheath as the inner and outer collars and the Schmidt-Lanterman clefts.