基于视觉感知机制的织物疵点轮廓检测

针对传统人工织物疵点检测存在的误检及低效等问题,提出了一种基于视觉感知机制的自适应织物疵点轮廓检测方法.首先,模拟视觉系统中视网膜感受野对视觉信息的处理机制对织物疵点图像进行滤波及疵点增强;其次,依据初级视皮层(V1)区对视觉信息响应的方向选择性机制构建织物疵点图像边缘检测模型,实现对织物疵点图像的边缘检测.最后,采用自适应阈值选择的方法对检测到的边缘进行二次处理,获得织物图像疵点的轮廓.为验证本文方法的有效性和准确性,对4类织物疵点图像进行测试,并定性和定量两方面进行比较分析,结果表明文中提出的方法能够较好地检测出织物疵点轮廓信息,不仅可以得到质量较高的织物疵点轮廓图像,而且在整个检测过程中能够自适应的选择参数,避免受人的主观因素影响,具有实际的应用价值.     

基于自适应阈值和区域生长的SD-OCT糖网图像亮斑分割

硬性渗出是糖尿病性视网膜病变的一个比较显著的症状,频域光学相干断层视网膜图像中的高信号亮斑与渗出有着密切的联系。为了研究渗出与病变的关系,有必要找到一种提取亮斑的方法。但是,目前关于糖网图像亮斑提取的研究还非常少。首先运用层分割算法限制亮斑所在区域,然后采用自适应阈值法确定种子集合,最后使用基于人类视觉特性的区域生长方法提取出亮斑。实验结果表明,本方法可以较准确地分割出糖网图像中的亮斑。     

Development of an image-based model for capillary vasculature of retina

The paper presents a method of development of a detailed network model to represent retinal capillary vasculature. The capillary model is a circular mesh consisting of concentric rings with an increasing diameter. Each of the rings has uniformly distributed bifurcation nodes to represent capillary vessels. The model is customized using the data that has been measured from confocal microscopic images of a mouse retina. The capillary model developed can be connected to networks of larger vessels of the vasculature such as arterial and venous networks to form a complete model of the retinal network. A method to automate such interface connections between capillary and other vascular networks using connecting vessels (i.e., pre-capillary and post-capillary) is also presented in the paper. Such a detailed image-based capillary model together with the arterial and venular networks can be used for various circulation simulations to obtain accurate information on hemodynamic quantities such as the spatial distribution of pressure and flow in the vasculature for both physiological and pathological conditions. The method presented for the development of the capillary model can also be adopted for vasculatures of other organs.     

Artificial retina chips for image processing

Artificial retina chips which can simultaneously sense and process real world images are described. The comparison between artificial retinal systems and conventional image processing systems is described. Variable sensitivity photodetection, which is an essential technology for the artificial retina chips, is introduced in detail. The concept, structure, fundamental performance, operating principle, and processing functions for the fabricated artificial retinal chips are described. Applications including interactive games by gesture-input are also introduced. This work was presented, in part, at the International Symposium on Artificial Life and Robotics, Oita, Japan, February 18–20, 1996.     

Photoreceptor Cells Constitutively Express IL-35 and Promote Ocular Immune Privilege

Interleukin-27 is constitutively secreted by microglia in the retina or brain, and upregulation of IL-27 during neuroinflammation suppresses encephalomyelitis and autoimmune uveitis. However, while IL-35 is structurally and functionally similar to IL-27, the intrinsic roles of IL-35 in CNS tissues are unknown. Thus, we generated IL-35/YFP-knock-in reporter mice (p35-KI) and demonstrated that photoreceptor neurons constitutively secrete IL-35, which might protect the retina from persistent low-grade inflammation that can impair photoreceptor functions. Furthermore, the p35-KI mouse, which is hemizygous at the il12a locus, develops more severe uveitis because of reduced IL-35 expression. Interestingly, onset and exacerbation of uveitis in p35-KI mice caused by extravasation of proinflammatory Th1/Th17 lymphocytes into the retina were preceded by a dramatic decrease of IL-35, attributable to massive death of photoreceptor cells. Thus, while inflammation-induced death of photoreceptors and loss of protective effects of IL-35 exacerbated uveitis, our data also suggest that constitutive production of IL-35 in the retina might have housekeeping functions that promote sterilization immunity in the neuroretina and maintain ocular immune privilege.     

Eliminating Synaptic Ribbons from Rods and Cones Halves the Releasable Vesicle Pool and Slows Down Replenishment

Glutamate release from rod and cone photoreceptor cells involves presynaptic ribbons composed largely of the protein RIBEYE. To examine roles of ribbons in rods and cones, we studied mice in which GCamP3 replaced the B-domain of RIBEYE. We discovered that ribbons were absent from rods and cones of both knock-in mice possessing GCamP3 and conditional RIBEYE knockout mice. The mice lacking ribbons showed reduced temporal resolution and contrast sensitivity assessed with optomotor reflexes. ERG recordings showed 50% reduction in scotopic and photopic b-waves. The readily releasable pool (RRP) of vesicles in rods and cones measured using glutamate transporter anion currents (I_A(glu)) was also halved. We also studied the release from cones by stimulating them optogenetically with ChannelRhodopsin2 (ChR2) while recording postsynaptic currents in horizontal cells. Recovery of the release from paired pulse depression was twofold slower in the rods and cones lacking ribbons. The release from rods at −40 mV in darkness involves regularly spaced multivesicular fusion events. While the regular pattern of release remained in the rods lacking ribbons, the number of vesicles comprising each multivesicular event was halved. Our results support conclusions that synaptic ribbons in rods and cones expand the RRP, speed up vesicle replenishment, and augment some forms of multivesicular release. Slower replenishment and a smaller RRP in photoreceptors lacking ribbons may contribute to diminished temporal frequency responses and weaker contrast sensitivity.     

532nm激光照射后的兔视网膜损伤修复

目的:观察532nm激光照射后的兔视网膜损伤和修复。方法:采用(光斑直径约为2mm、照射时间100s、能量密度200J/cm2、532nm)激光照射家兔视网膜后极部,连续观察1d、3d、7d、14d和28d后眼底及组织学改变。结果:照后1d可见明显水肿及出血。3d后凝固斑边界清晰,出血范围扩大,可见脉络膜成纤维细胞开始增生。14d后渗出和出血大部分吸收。28d后大量纤维组织增生及新生血管形成。结论:该照射剂量可以引起家兔视网膜较为严重的损伤,其修复存在一定的规律性。     

川芎嗪预处理对大鼠视网膜缺血再灌注损伤后视网膜电流图的影响

目的:观察川芎嗪预处理对大鼠视网膜缺血再灌注损伤后视网膜电流图的影响.方法:采用前房灌注法建立大鼠视网膜缺血再灌注损伤模型,设置正常组、缺血再灌注组、5min缺血预适应组、川芎嗪预处理组,分别于缺血前,缺血30min时,再灌注1h,12h,24h,72h,168h检测双眼各时期FERGb波及OPs(O2)波波幅,分别计...     

The Stiles–Crawford Effect: spot-size ratio departure in retinitis pigmentosa

The Stiles–Crawford effect of the first kind is the retina’s compensative response to loss of luminance efficiency for oblique stimulation manifested as the spot-size ratio departure from the perfect power coupling for a normal human eye. In a retinitis pigmentosa eye (RP), the normal cone photoreceptor morphology is affected due to foveal cone loss and disrupted cone mosaic spatial arrangement with reduction in directional sensitivity. We show that the flattened Stiles–Crawford function (SCF) in a RP eye is due to a different spot-size ratio departure profile, that is, for the same loss of luminance efficiency, a RP eye has a smaller departure from perfect power coupling compared to a normal eye. Again, the difference in spot-size ratio departure increases from the centre towards the periphery, having zero value for axial entry and maximum value for maximum peripheral entry indicating dispersal of photoreceptor alignment which prevents the retina to go for a bigger compensative response as it lacks both in number and appropriate cone morphology to tackle the loss of luminance efficiency for oblique stimulation. The slope of departure profile also testifies to the flattened SCF for a RP eye. Moreover, the discrepancy in spot-size ratio departure between a normal and a RP eye is shown to have a direct bearing on the Stiles–Crawford diminution of visibility.