活化转录因子4基因敲除小鼠完全缺失晶状体致小眼症

旨在研究活化转录因子4(ATF4)基因敲除对小鼠眼睛发育的影响。将小鼠分为野生型(WT)组和ATF4敲除(KO)组,采用器官大体观察和组织病理学分析,明确ATF4基因敲除后对小鼠眼睛发育的影响。结果发现,WT小鼠眼球大小及组织结构正常。而ATF4^-/-小鼠眼球体积缩小;脉络膜和视网膜层层次结构基本存在,各个层次结构紊乱;神经节细胞层细胞数基本正常,约2层细胞,但细胞排列不整齐;内丛状层结构疏松,厚度增加;外核层细胞层次增加,超过10层,同时结构松散、形成裂隙和囊样结构;内核层细胞层次减少、约6层~8层细胞,细胞排列轻度紊乱。整个视网膜在局部形成乳头状突起;脉络膜基本正常,但没有乳头状的睫状突形成。眼球内玻璃体缺失,由水肿的纤维结缔组织构成,中央可见多个小血管。总之,ATF4^-/-小鼠展示了小眼表型,同时ATF4^-/-小鼠眼睛结构异常。     

硼元素对大鼠淋巴结和视网膜组织结构的影响

为了研究硼元素对大鼠淋巴结和视网膜组织结构的影响,试验选用断乳(21 d±2 d)清洁级SD大鼠60只,适应性饲养1周后,随机分为对照组和试验Ⅰ、Ⅱ、Ⅲ、Ⅳ、Ⅴ组,各组分别通过饮水添加0、40、80、160、320和640 mg/L硼,试验期60 d。结果显示,与对照组相比,试验Ⅰ和Ⅱ组大鼠淋巴结皮质内淋巴小结数量增多,体积增大,淋巴细胞密集,副皮质区增厚,髓质内髓索明显增粗;视网膜组织结构发育良好,节细胞层、内核层和外核层细胞数量有所增多。试验Ⅲ组大鼠淋巴结皮质内淋巴小结减少,体积变小,副皮质区变薄,淋巴细胞排列较为疏松;视网膜组织结构出现轻微损伤,内核层变薄,节细胞层细胞数量排列疏松,数量减少。试验Ⅳ和Ⅴ组大鼠淋巴结皮质内淋巴小结体积显著减小,生发中心不明显甚至消失,淋巴细胞明显减少,副皮质区变薄,髓索变细;视网膜节细胞层变薄,数量减少,部分细胞出现空泡,内核层和外核层细胞排列疏松。说明饮水添加40~80 mg/L硼对大鼠淋巴结和视网膜组织结构发育具有一定的促进作用,而添加320~640 mg/L硼则对大鼠淋巴结和视网膜组织结构产生明显的损伤作用。     

兔生后舌和食管发育的组织学研究

对18只法比兔生后舌和食管进行组织学观察的结果表明,免出生时舌背侧粘膜上皮未角化,并含有大量丝状乳头（平均高为135.7μm）和少量菌状乳头。固有膜不发达。舌肌为纵向、横向及垂直方向排列的横纹肌。舌腹侧粘膜表面平滑。15日龄以后,舌背侧菌状乳头高为200～521μm,其顶部直径为93～221μm。1日龄时,兔食管粘膜上皮只有4～5层细胞（平均厚28.5μm）。60日龄时,已达30层左右（平均厚164.3μm)。固有膜与粘膜下层分界不清。肌层由内纵、中环、外纵3层组成。肌层随年龄增长而逐渐增厚,1日龄时平均厚度121.4μm,60日龄时平均厚度达750μm。     

饲料中添加厨余发酵产物对"中科3号"异育银鲫肝脏、肠道及肾脏显微结构的影响

试验旨在评估厨余发酵产物(fermentation products of kitchen waste,FPKW)对鲫鱼肝脏、肠和肾脏显微结构的影响。在饲料中分别添加0%、3%、6%、9%、12%、15%和30%FPKW饲喂初始体重为(7.4±0.21) g"中科3号"异育银鲫60 d。结果表明:①0%、3%～12%FPKW组鲫鱼整个肝细胞轮廓清晰、结构完整;而15%和30%FPKW组鲫鱼肝细胞肿胀、透明空泡化,细胞核出现偏离、萎缩,胞浆中充满脂肪滴;②与对照组相比,3%～15%FPKW组鲫鱼肠绒毛数量及高度呈现递增趋势,肌层厚度则呈现降低;当FPKW添加30%时,肠绒毛肌层厚度[(71.05±4.91)μm]显著高于对照组(P<0.05),肠绒毛高度[(229.98±44.03)μm]及数量(16.75±0.5)虽与对照组无显著差异(P>0.05),但中肠上皮组织中的细胞核增多且排列混乱,肠绒毛中的杯状细胞显著增多;③对照组及3%～12%FPKW组鲫鱼肾小管结构完整,无明显病理病灶,而在15%和30%FPKW组鲫鱼肾脏出现明显的炎性细胞浸润,组织纤维化等病理特征。综上各器官显微结构表明,当饲料中FPKW添加量不高于12%时,对异育鲫鱼肝脏、肠和肾脏的显微结构均无不良影响。     

斑马鱼中脑微细结构及相关免疫组化反应

为深入了解斑马鱼中脑的微细结构,采用光镜技术对斑马鱼中脑结构进行观察研究,并利用免疫组化反应显示脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)和CD34的分布特征。选用成年AB型斑马鱼,对其中脑连续切片后进行HE染色。观察辨认中脑神经核团结构,包括有视顶盖、半环枕、被盖、中央层、边缘层、纵枕等十多个核团,并与其他鱼类进行比较,根据试验结果绘制出斑马鱼中脑结构概念图。免疫组化试验观察BDNF和CD34都分布在斑马鱼中脑视顶盖边缘层和中央层交界处。本次结果可为斑马鱼神经生物学模型的建立与应用提供有效的理论基础。     

羊驼视网膜组织学结构

用光镜观察了羊驼视网膜的组织学结构,以及3级神经元的细胞胞核层数及胞核特点。结果表明:羊驼视网膜结构与昼行性的哺乳动物的视网膜结构相似,但米勒细胞较明显、水平细胞为一层、内网层细胞很厚等形成了羊驼视网膜结构的特性,显示了羊驼视网膜结构和机能与其行为学特性的一致性。     

羊驼视网膜组织学结构

用光镜观察了羊驼视网膜的组织学结构,以及3级神经元的细胞胞核层数及胞核特点。结果表明：羊驼视网膜结构与昼行性的哺乳动物的视网膜结构相似,但米勒细胞较明显、水平细胞为一层、内网层细胞很厚等形成了羊驼视网膜结构的特性,显示了羊驼视网膜结构和机能与其行为学特性的一致性。     

禽流感病毒感染血管内皮细胞研究进展

内皮细胞(endothelialcells,ECs)是内衬于血管和淋巴管内侧的单层扁平细胞,有可能是动物体内最大、最广泛的组织细胞。血管内皮细胞(Vascularendothelialcells,VEC)是指连续被覆在血管内膜的一层细胞群,厚度不一,在大血管中厚度约为1μm,在微静脉和毛细血管中厚度约为0.1μm。VEC大小相差不大,形态扁平,呈多边形。VEC是组织和血液间的第一道屏障,具有合成代谢和分泌的功能,并参与凝血、免疫和炎症反应和组织修复过程,对维持内环境的稳态具有重要作用。     

羊驼视网膜组织学结构

用光镜观察了羊驼视网膜的组织学结构,以及3级神经元的细胞胞核层数及胞核特点。结果表明:羊驼视网膜结构与昼行性的哺乳动物的视网膜结构相似,但米勒细胞较明显、水平细胞为一层、内网层细胞很厚等形成了羊驼视网膜结构的特性,显示了羊驼视网膜结构和机能与其行为学特性的一致性。     

6月龄苏尼特羊小肠黏膜结构及上皮内淋巴细胞和杯状细胞的分布

应用组织学和组织化学方法研究了6月龄苏尼特羊小肠黏膜结构、肌层厚度及黏膜上皮内淋巴细胞和杯状细胞分布数量的变化规律。结果显示,肠绒毛长度以十二指肠最长,为(353.25±60.48)μm,其次为空肠(317.27±72.02)μm和回肠(275.36±47.62)μm,且空肠和回肠之间差异显著(P<0.05);黏膜厚度以十二指肠最厚,为(669.15±139.04)μm,空肠和回肠分别为(586.72±134.50)和(551.85±91.32)μm,十二指肠与后两者间差异极显著(P<0.01);肌层厚度以回肠最厚,为(280.45±58.33)μm,与空肠(167.16±42.63)μm和十二指肠(148.78±38.36)μm相比,差异极显著(P<0.01);隐窝深度以十二指肠最深,为(309.36±74.21)μm,其次为空肠(286.23±57.23)μm,回肠最浅,为(237.83±48.86)μm,相互之间差异极显著(P<0.01);十二指肠和空肠的V/C比值分别为(1.80±0.45)和(2.00±0.48),空肠和回肠(1.39±0.34)相比,差异显著(P<0.05);小肠各段黏膜上皮内淋巴...     

Development of the Retina in the Porcine Fetus A Light Microscopic Study

Morphogenesis of the porcine retina was studied using light microscopy from 4 weeks of gestation until birth (18 to 310 mm crown-rump length), and compared with the adult stage (6 months). Tissue samples were examined from the posterior and peripheral parts of the retina. At 18 mm the retina consists of an inner marginal layer and an outer layer of neuroblastic cells. At 18-40 mm the latter layer is divided into an inner and an outer neuroblastic layer by the transient layer of Chievitz. Subsequently, the development of the different retinal layers begins at the inner retinal border and moves progressively outwards; it also spreads from the posterior to the peripheral part of the neural retina. Many cells of the inner neuroblastic layer are prospective ganglionic cells which migrate inwards, thus forming the ganglion cell layer and the inner plexiform layer at 90 mm. At 120 mm, primitive horizontal cells appear within the outer neuroblastic layer. Separation of this layer into the inner nuclear, outer plexiform and outer nuclear layers is first evident at 180 mm. At this stage all retinal layers are present, except the layer of the photoreceptor cells which is not widespread until at 220 mm. The inner and outer segments of the photoreceptor cells lengthen considerably during the last month of gestation. During the late fetal stage the nerve fiber layer, the inner and outer plexiform layers and the layer of rods and cones all continue to increase in thickness. Concurrently, the ganglion cell layer and the inner and outer nuclear layers have reached their maximal thickness and become thinner. After the total thickness of the neural retina amounts to approximately 180 microns at two to three weeks before birth, it then thins to approximately 160 microns in the adult stage.     

Outer retinal degeneration in two closely related Goeldi's monkeys (Callimico goeldii)

This case report comprises studies of four Goeldi's monkeys (Callimico goeldii) from the same enclosure. Globe samples from two related C goeldii (the female C goeldii and her male offspring) were available for a histopathological evaluation. Both cases presented histopathologically evident outer retinal degeneration with differences in severity. There was marked outer retinal atrophy characterized by loss of the outer and inner photoreceptor segments, and depletion of the outer retinal nuclear layer. Furthermore, we report a reduction in the thickness of the outer retinal plexiform, inner retinal nuclear layer, and inner retinal plexiform layer in these C goeldii monkeys. To the authors’ knowledge, these findings have not yet been reported in wild‐ or captive‐bred population of C goeldii.     

Spectral domain optical coherence tomography (SD-OCT) assessment of the healthy female canine retina and optic nerve

Objective To provide normative data for canine whole retinal thickness (WRT), nerve fiber layer thickness (NFL), photoreceptor layer thickness (PR), and outer nuclear layer thickness (ONL) using spectral domain optical coherence tomography. Animal studied: Twelve healthy adult intact female beagles. Procedure Horizontal volume scans through the area dorso‐temporal from the optic nerve (superior retina), and the area ventro‐temporal from the optic nerve (inferior retina) were used to evaluate the thickness of retinal NFL, PR, ONL, and WRT. Peripapillary circular scans were used to evaluate NFL thickness. Statistical analyses were performed to compare the thickness of the individual layers between the superior and inferior retina (paired t‐test). One‐way analysis of variance (ANOVA) was used to compare the thickness of peripapillary NFL between the superior, inferior, temporal and nasal quadrants of the circle scan. Results The WRT, PR, and NFL thickness were greater in the superior than in the inferior retina (198.7 ± 9.6 μm vs. 164.4 ± 6.4 μm, P < 0.0001; 95.5 ± 6.5 μm vs. 78.8 ± 7.4 μm, P < 0.0001; and 26.4 ± 1.6 μm vs. 25.0 ± 1.9 μm, P = 0.0236, respectively). No statistical difference was found between the ONL thickness of the superior and inferior retina (50.1 ± 6.4 μm vs. 44.3 ± 3.6, P = 0.0578). Peripapillary NFL thickness showed a similar tendency as the linear scans, with the superior quadrant having the greatest thickness (91.26 ± 7.0 μm) and the inferior quadrant being the thinnest (76.42 ± 9.2 μm) (P < 0.001). Conclusions Results of our in vivo studies showed significant differences between thickness values for the superior (tapetal) and inferior (nontapetal) retinal regions.     

Cataracts and optic nerve hypoplasia in turkey poults

Newly hatched commercial turkey poults culled because of grossly visible cataracts were studied. A total of 43 affected and 23 unaffected control poults at various ages were necropsied, and the ocular changes in affected poults were compared with those of aged-matched controls. Affected poults had consistent cataracts coupled with a marked depletion in retinal inner plexiform, ganglion cell, and optic nerve fiber layers, with a resultant reduction in the size of the optic nerves. Lesions were seen in 1-day-old poults. Lens changes included microphakia and lens fiber degeneration throughout the lens, with nuclear liquefaction. The depletion in the numbers of retinal ganglion cells did not appear to progress over several weeks time. The ganglion cell depletion was not uniform within the retina. The cause for these ocular changes is unknown.     

Angiostatin and integrin alphavbeta3 in the feline, bovine, canine, equine, porcine and murine retina and cornea

PURPOSE: Angiogenesis is tightly controlled in the ocular tissues of domestic animals but its mechanisms are not fully understood. This is largely because of insufficient data on the expression of molecules that impact angiogenesis. Because angiostatin and one of its receptors integrin alphavbeta3 inhibit and promote angiogenesis, respectively, we hypothesized that the normal retina and cornea of domestic animals would express angiostatin but not integrin alphavbeta3. PROCEDURE: Normal eyes of the cat, cow, dog, horse, pig and rat were evaluated for angiostatin and integrin alphavbeta3 by light and electron immunocytochemistry and estern blots. RESULTS: Angiostatin was detected in the corneal epithelium of the cat, dog, horse, pig and rat, but was not found in cow corneal epithelium. Angiostatin was localized in the nerve fiber layer, ganglion cell layer, inner and outer plexiform layers, and the photoreceptor layer of the cat, cow, dog and rat. Horse and pig retinas showed additional staining in the matrix of the inner nuclear layer. Immunogold electron microscopy further confirmed angiostatin in cat retina. Western blots showed angiostatin in corneal and retinal homogenates. Integrin alphavbeta3 was absent in cornea and retina of all the species studied. CONCLUSION: These data show that angiostatin, an inhibitor of angiogenesis, is present while integrin alphavbeta3, which promotes angiogenesis, is absent in normal cornea and retina of the domestic animals in this study with the exception being angiostatin absence in cow corneal epithelium. Therefore, angiostatin may contribute to the anti-angiogenic environment in the normal domestic animal eye while its absence in the cow may contribute to greater propensity for corneal vascularization. Because integrin alphavbeta3 is one of the receptors for angiostatin, its absence may prevent angiostatin from killing normal retinal and corneal cells.     

Assessment of the pigeon (Columba livia) retina with spectral domain optical coherence tomography

BackgroundTo assess the normal retina of the pigeon eye using spectral domain optical coherence tomography (SD-OCT) and establish a normative reference.MethodsTwelve eyes of six ophthalmologically normal pigeons (Columba livia) were included. SD-OCT images were taken with dilated pupils under sedation. Four meridians, including the fovea, optic disc, red field, and yellow field, were obtained in each eye. The layers, including full thickness (FT), ganglion cell complex (GCC), thickness from the retinal pigmented epithelium to the outer nuclear layer (RPE-ONL), and from the retinal pigmented epithelium to the inner nuclear layer (RPE-INL), were manually measured.ResultsThe average FT values were significantly different among the four meridians (p < 0.05), with the optic disc meridian being the thickest (294.0 ± 13.9 µm). The average GCC was thickest in the optic disc (105.3 ± 27.1 µm) and thinnest in the fovea meridian (42.8 ± 15.3 µm). The average RPE-INL of the fovea meridian (165.5 ± 18.3 µm) was significantly thicker than that of the other meridians (p < 0.05). The average RPE-ONL of the fovea, optic disc, yellow field, and red field were 91.2 ± 5.2 µm, 87.7 ± 5.3 µm, 87.6 ± 6.5 µm, and 91.4 ± 3.9 µm, respectively. RPE-INL and RPE-ONL thickness of the red field meridian did not change significantly with measurement location (p > 0.05).ConclusionsMeasured data could be used as normative references for diagnosing pigeon retinopathies and further research on avian fundus structure.     

An immunohistochemical study of protein kinase C in the bovine retina

The expression of protein kinase C (PKC) was studied in the bovine retina by immunohistochemical analysis. Western blot analysis showed that PKC isoforms, including alpha, betaI, delta and theta, were detected in the bovine retina. By immunohistochemistry, both PKC alpha and betaI were expressed in all retinal layers, with an intense localization of both PKC alpha and betaI detected in bipolar cells in the inner nuclear cell layer and in some glial cells in ganglion cell layers. The immunoreactivity of both PKC delta and theta was quite weak in the retinal layers, compared with that of PKC alpha and betaI. These findings suggest that both conventional and novel PKCs are differentially expressed in the bovine retina.     

Abnormal prion accumulation associated with retinal pathology in experimentally inoculated scrapie-affected sheep

The purpose of this study was to characterize the patterns of PrP(Sc) immunoreactivity in the retinae of scrapie-affected sheep and to determine the extent of retinal pathology as indicated by glial fibrillary acidic protein immunoreactivity (GFAP-IR) of Müller glia. Sections from the retina of 13 experimentally inoculated scrapie-affected and 2 negative control sheep were examined with immunohistochemical staining for PrP(Sc), GFAP, and PrP(Sc)/GFAP double staining. GFAP-IR of Müller glia is suggestive of retinal pathology in the absence of morphologic abnormality detected by light microscopy. Sheep with the least amount of PrP(Sc) in the retina have multifocal punctate aggregates of prion staining in the outer half of the inner plexiform layer and rarely in the outer plexiform layer. In these retinae, GFAP-IR is not localized with prion accumulation, but rather is present in moderate numbers of Müller glia throughout the sections of retina examined. The majority of sheep with retinal accumulation of PrP(Sc) have intense, diffuse PrP(Sc) staining in both plexiform layers, with immunoreactivity in the cytoplasm of multiple ganglion cells and lesser amounts in the optic fiber layer and between nuclei in nuclear layers. This intense PrP(Sc) immunoreactivity is associated with diffuse, intense GFAP-IR that extends from the inner limiting membrane to the outer limiting membrane. This is the first report of a prion disease in a natural host that describes the accumulation of PrP(Sc) in retina associated with retinal pathology in the absence of overt morphologic changes indicative of retinal degeneration.     

Ocular lesions of 6-aminonicotinamide toxicosis in rabbits

6-Aminonicotinamide, an antimetabolite of nicotinamide, given by intraperitoneal injection produced diarrhea, ascending paresis/paralysis, death, and bilateral ocular alterations in both sexes of New Zealand white and Dutch belted rabbits. Ocular vascular lesions consisted of iridal congestion with iridal hemorrhage and associated acute iritis and aqueous flare in some rabbits. Cytoplasmic swelling, vacuolation, and loss of staining affinity that represented hydropic change were present in both layers of ciliary epithelium and the inner layer of iridal epithelium. Cells in the outer layer of the iridal processes and the ciliary ridge, were most severely affected. Vacuoles were also present in the retinal pigment epithelium and scattered throughout the outer plexiform layer of the retina with a few in the inner and outer nuclear layers. Ocular alterations were prevented by simultaneous administration of nicotinamide and their development appeared related to nicotinamide deficiency. No ocular alterations were caused by nicotinamide administration alone.     

Prenatal development of retina in buffalo (Bubalus bubalis)

The development of retina in Indian buffalo (Bubalus bubalis) has not been reported previously. The aim of the present study was therefore to report the major landmarks and the time course in the development of retina. Serial histological sections of Indian buffalo embryos and foetuses were used as group1 (<20.0 cm CVRL), group2 (>20.0 but <40.0 cm CVRL) and group3 (>40.0 cm CVRL). Age estimation was made on the basis of crown vertebral‐rump length (CVRL), which ranged between 36 and 286 days (1.6–94.0 cm). The retina in Indian buffalo was developed in a similar manner to that of the other mammals with the principal differences in the time of occurrence of various layers of this nervous tunic. In 36 days (1.6 cm stage), the foetal retina was composed of pigmented layer and the layer of neuroblasts. Differentiation of layers was first observed in 47 days (4.0 cm CVRL) which became prominent in 52 days (5.1 cm stage). At 120 days (20.5 cm stage), the differentiation of inner plexiform layer and inner nuclear layer was evident. At 143 days (31.0 cm) foetal age, the faint line in neuroblastic layer was the first evidence of the future outer plexiform layer. In foetuses of group III, the retina was comprised of all 10 layers (eight cell layers and two membranes) viz. pigmented epithelium, layer of rods and cones, outer limiting membrane, outer nuclear layer, outer plexiform layer, inner nuclear layer, inner plexiform layer, ganglion cell layer, layer of nerve fibres and the inner limiting membrane.