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1.
Figure 5

Figure 5. From: Ocular expression of avian thymic hormone: changes during the recovery from induced myopia.

Distribution of ATH in the sclera and choroid of control and recovering chick eyes. Monoclonal antibodies specific for ATH were used together with AlexaFluor 488-conjugated rabbit anti-mouse immunoglobulin to localize ATH in sclera and choroid of control and recovering eyes. A: Intense ATH immunolabeling is detected in the fibrous sclera (FS) and in perivascular and extravascular regions of the choroid. ATH was absent in the cartilaginous scleral layer (CS). B: IgG control section of the sclera and choroid of a control eye, where nonimmune mouse IgG was used in the first incubation, followed by incubation in AlexaFluor 488-conjugated rabbit anti-mouse immunoglobulin. C: ATH immunolabelling in the sclera of a recovering chick eye is shown in a region artifactually separated from the choroid. ATH can be seen localized in the outer fibrous sclera (FS) as well as in the thin inner fibrous sclera on the choroidal side of the sclera. D: ATH immunolabeling in the choroid of a recovering chick eye is shown. ATH can be seen throughout the stroma of the markedly expanded choroid and on the choroidal side of Bruch’s membrane (arrow), but is absent in the RPE. Nuclei were stained with DAPI (blue). Choriocapillaris is abbreviated CC. Scale bar (A–D) represents 50 μm.

Jody A. Summers Rada, et al. Mol Vis. 2009;15:778-792.
2.
Figure 5

Figure 5. The thickness of the peripapillary sclera, and the size and shape of the scleral canal influence the magnitude and distribution of IOP-related stress within the peripapillary sclera. From: The Mechanical Environment of the Optic Nerve Head in Glaucoma.

Stress plots within 3D biomechanical models of the posterior sclera and ONH demonstrate that stress concentrates around a defect (scleral canal) in a pressure vessel (eye) and varies according to the geometry of the peripapillary sclera and scleral canal. The idealized model in (A) shows the stress concentration around a circular canal in a perfectly spherical pressure vessel with uniform wall thickness (the ONH has been removed from these images for visualization purposes). The model in (B) shows the IOP-related stress concentration around an anatomically shaped scleral canal with realistic variation in peripapillary scleral thickness. In this case, the highest stresses (red) occur where the sclera is thinnest and the lowest stresses (blue) occur where the sclera is thickest, and also tend to concentrate around areas of the scleral canal with the smallest radius of curvature. The response of the sclera to this load is determined by its structural stiffness, which is the combination of geometry (how much tissue is bearing the load) and material properties (how rigid or compliant is the tissue).

J. Crawford Downs, et al. Optom Vis Sci. ;85(6):425-435.
3.
Figure 1

Figure 1. From: Standard Enucleation with Aluminium Oxide Implant (Bioceramic) Covered with Patient's Sclera.

Phases of surgical preparation of the phthisis globe. (a) Enucleation of phthisis bulbous. A traction suture is placed on the cornea. (b) The sclera covers only the anterior surface of the porous implant; a mesh Vicryl suture maintains the sclera in a fixed position. (c) The sclera is longitudinally marked in blue color. (d) The posterior Tenon's fascia is dissected to receive the prothesis.

Gian Luigi Zigiotti, et al. ScientificWorldJournal. 2012;2012:481584.
4.
FIGURE 9.

FIGURE 9. From: Knockdown of Zebrafish Lumican Gene (zlum) Causes Scleral Thinning and Increased Size of Scleral Coats.

zlum-MO knockdown induces ultrastructural changes in the CS, AS, and PS. A, WT fish at 12 dpf stage in toluidine blue staining. The figure indicates CS, AS, and PS. B, diameters of collagen fibril were analyzed in the corneal stroma, anterior and posterior sclera of 12 dpf-old-wild type, and zlum-MO-injected group. Significant increases in collagen fibril diameter of corneal stroma and anterior sclera are noted in the zlum-MO group, and the diameter of collagen fibril in the posterior sclera is not significantly different in both groups. C–H, morphological comparison of collagen fibril architecture in the corneal stroma (C and D), anterior scleral tissue (E and F), and posterior scleral tissue (G and H) between the control group (C, E, and G) and zlum-MO-injected group (D, F, and H) at the 12 dpf stage. C, TEM micrograph showing regular and smaller fibril architecture of collagen localized in the corneal stroma of the wild type group. D, irregular arrangement and increasing collagen fibril diameter was found in the corneal stroma of the zlum-MO-injected group. E, TEM micrograph showing relatively regular fibril architecture of collagen localized in the anterior sclera of the wild type group. F, irregular collagen fibrils with increasing fibril diameter were noted in the anterior sclera of the zlum-MO-injected group. G, top is adjacent to the retina. TEM micrograph showing fibril architecture of collagen localized in the posterior sclera of the wild type group. H, top is adjacent to the retina. TEM micrograph showing irregular and little collagen fibril architecture was noted in the posterior sclera of the zlum-MO-injected group. (scale bar, C–H, 100 nm.)

Lung-Kun Yeh, et al. J Biol Chem. 2010 September 3;285(36):28141-28155.
5.
 Figure 4. 

Figure 4.  . From: Bidirectional, Optical Sign-Dependent Regulation of BMP2 Gene Expression in Chick Retinal Pigment Epithelium.

Labeled section from the wall of the posterior eyecup, either double-labeled for BMP2 (red) and DAPI (blue, A), with BMP2 alone (B), with DAPI alone (C), with light microscopy image overlaid (D), or isotype control (E). CHO, choroid; SCL-C, sclera cartilaginous layer; SCL-F, sclera fibrous layer. *Basal side of RPE. ▾Inner boundary between choroid and sclera. Border between cartilaginous and fibrous layers of sclera. Scale bar = 200 μm.

Yan Zhang, et al. Invest Ophthalmol Vis Sci. 2012 September;53(10):6072-6080.
6.
Figure 3

Figure 3. From: Effects of imposed defocus of opposite sign on temporal gene expression patterns of BMP4 and BMP7 in chick RPE.

Sections from the posterior wall of the eyecup labeled for BMP4 and BMP7 (in red); nuclei were labeled with DAPI (in blue). BMP4 labeled sections (A-D), were either double-labeled for BMP4 and nuclei (A), labeled for BMP4 alone (B), or labeled for nuclei alone (C); double-labeling overlaid on unstained light microscopy image shown in D. BMP7 labeled sections (E-F) were either double-labeled for BMP7 and nuclei (E), labeled for BMP4 alone (F), or labeled for nuclei alone (G). Negative controls for BMP4 (H) and BMP7 (I) were imaged in blue and red channels. CHO, choroid; SCL-C, sclera cartilaginous layer; SCL-F, sclera fibrous layer. * Basal side of RPE, ▼ Inner boundary between choroid and sclera, ↓Border between cartilaginous and fibrous layers of sclera. Scale bar, 50 µM.

Yan Zhang, et al. Exp Eye Res. 2013 April;109:98-106.
7.
Figure 7.

Figure 7. From: IOP-Induced Lamina Cribrosa Deformation and Scleral Canal Expansion: Independent or Related?.

Scatterplot of LCD versus SCE for all cases, and for groups and subgroups split by sclera thickness and modulus. With the parametric analysis none of the subgroups shows a significant negative association between LCD and SCE, that is, consistent with the concept that “the sclera pulls the lamina taut” as IOP increases. Moreover, three of the quarter-set subgroups (E, H, and I) show a relationship in the direction opposite to that expected and seen on the whole (A). In the fourth subgroup (F) the relationship was not significant. This is an example of an effect called “reversal” and is an example of Simpson's paradox. The largest SCEs occurred with thin and soft sclera, whereas the smallest ones occurred with thick and stiff sclera. Interestingly, the SCEs were similar for thin and stiff sclera and thick and soft sclera, consistent with our previous application of the concept of structural stiffness.20 Each panel is labeled with the Pearson's product moment correlation coefficient (ρ) and Kendall's rank correlation (τ), colored blue if statistically significant (P < 0.01) or gray if not.

Ian A. Sigal, et al. Invest Ophthalmol Vis Sci. 2011 November;52(12):9023-9032.
8.
Figure 1

Figure 1. From: Osteogenesis imperfecta type I: A case report.

Left image, blue sclera in the patient. Right image, normal sclera in the patient’s father.

JIANMIN REN, et al. Exp Ther Med. 2014 June;7(6):1535-1538.
9.
Figure 1.

Figure 1. From: Mapping the Differential Distribution of Glycosaminoglycans in the Adult Human Retina, Choroid, and Sclera.

Localization of HS in retina, choroid, and sclera. Human tissue sections were stained using the pan HS antibody 10E4 (green) either without enzymatic pretreatment (left side) or after treatment with heparinases (right side). Top: the neurosensory retina; bottom: RPE, Bruch's membrane, choroid, and sclera. Here, and in all other figures, the images shown are representative of three individual donors (summarized in Table 2). Blue: DAPI staining of cell nuclei. Scale bar, 100 μm.

Simon J. Clark, et al. Invest Ophthalmol Vis Sci. 2011 August;52(9):6511-6521.
10.
Figure 2.

Figure 2. From: Alterations in Protein Expression in Tree Shrew Sclera during Development of Lens-Induced Myopia and Recovery.

Example DIGE gel image (Cy2 channel) showing the different patterns of protein expression in the sclera during myopia development (LIM) and recovery (REC). Ellipses indicate changes found during LIM, rectangles indicate changes found during REC, and hexagons indicate changes between 28N and 39N. Red: downregulation; blue: upregulation. Spot numbers are also shown in Tables 1 and 2 and Supplementary Table S1 (http://www.iovs.org/lookup/suppl/doi:10.1167/iovs.11-8354/-/DCSupplemental).

Michael R. Frost, et al. Invest Ophthalmol Vis Sci. 2012 January;53(1):322-336.
11.
Figure 2

Figure 2. α-Gal gene expression in the different developing phase of BALB/c mice ocular tissue (A1-D6) (A1-A6: centre cornea, B1-B6: limbus, C1-C6: conjunctiva, D1-D6: sclera; GSIB4: red, DAPI: blue; magnification:×200). From: The expression and distribution of ?-Gal gene in various species ocular surface tissue.

As early as mouse embryonic day 12 (A1-D1) and newborn day 1 (A2-D2), there was no GSIB4 expression in the BALB/c mice. α-Gal gene expression in the supine surface cornea/limbus, conjunctiva epithelium and sclera tissue in the 2 weeks (A3-D3) and 12 months (A6-D6). On 6 weeks, α-Gal epitopes was present on the full-thickness cornea/limbus,conjunctiva epithelium and sclera tissue (A4-D4). Cells that displayed α-Gal at 6 month often tended to be located at the supine surface cornea/limbus and conjunctiva epithelium (A5-D5).

Yi Shao, et al. Int J Ophthalmol. 2012;5(5):543-548.
12.
Figure 5.

Figure 5. From: IOP-Induced Lamina Cribrosa Deformation and Scleral Canal Expansion: Independent or Related?.

SCE versus LCD for all cases colored by each of the parameters. All panels are identical, except for the parameter used to color the symbols. The label above each plot indicates the parameter used to color the points: red for high level and blue for low level, except for Eye where each eye has a different color. The 12 cases with large LCD and SCE (top right of the scatterplots) combined compliant lamina and sclera, thin lamina and sclera, shallow lamina, and large canal size. Anteriorly LCDs were possible, as long as there was some SCE, which occurred most often, but not only, with compliant and thin sclera. The largest anteriorly LCDs occurred for cases with stiff laminas and did not have the largest SCEs. The largest SCEs had compliant and thin sclera, large canal size, and deep and compliant lamina. A thin and more elliptical lamina also increased slightly the maximum SCE, but this effect is probably too small to be important. The differences between the distribution of the points in blue and the points in red indicate the strength of the parameter or, conversely, the sensitivity of the measure on the parameter. For example, LCD was most sensitive to LC modulus (E), position (B) thickness (H), and canal size (C). SCE was most sensitive to sclera modulus (D) and thickness (G). Both responses were essentially insensitive to canal eccentricity (F) and the eye used as baseline (A). Since within a panel points with the same color share a particular level of a factor, the spread of points with a given color represents the influence of all other factors. We see, for example, that when the lamina was stiff (red points, E) the points spread over a smaller range of LCD, than when the lamina was compliant (blue points, E), and therefore that a stiff lamina reduced the sensitivity of LCD to the other factors. Similarly, the cases with stiff (D) or thick sclera (G) cover a smaller range on SCE than cases with compliant or thin sclera, again illustrating how these two parameters control, to some extent, the influence of other factors on SCE. A change in the effect of one factor, depending on the level of another factor is an interaction between the two factors.

Ian A. Sigal, et al. Invest Ophthalmol Vis Sci. 2011 November;52(12):9023-9032.
13.
FIGURE 1

FIGURE 1. From: Modulation of Glycosaminoglycan Levels in Tree Shrew Sclera during Lens-Induced Myopia Development and Recovery.

Electron micrograph of normal tree shrew sclera stained with cuprolinic blue, which stains sulfated glycosaminoglycans, and showing two dark fibroblast processes (F) and several lamellae composed primarily of bundles of type 1 collagen with associated decorin and its sulfated glycosaminoglycan chain. Scale bar, 1 μm. Photograph by Edward Clarke.

Anisha G. Moring, et al. Invest Ophthalmol Vis Sci. ;48(7):2947-2956.
14.
Figure 7.

Figure 7. From: Biomechanical Changes in the Sclera of Monkey Eyes Exposed to Chronic IOP Elevations.

Structural stiffness (thickness × tangent modulus) in the peripapillary sclera in both eyes (blue: normal; red: glaucomatous) of each monkey as a function of IOP. Error bars show the 25th, 50th, and 75th percentiles. Green circle: a significant difference between the normal and glaucomatous eye (when the t-statistic is greater than the intereye differences in the eight normal monkeys).

Michaël J. A. Girard, et al. Invest Ophthalmol Vis Sci. 2011 July;52(8):5656-5669.
15.
Fig. 16

Fig. 16. From: Development of diagnostic and treatment strategies for glaucoma through understanding and modification of scleral and lamina cribrosa connective tissue.

Sclera whole mounts at the peripapillary region were stained with DAPI (blue), and labeled for alpha smooth muscle actin (green) and Ki67 (red) to identify cell division. A) untreated sclera B) 3 day treated experimental glaucoma sclera. Ki67 label is greater in B, as is alpha smooth muscle actin label, indicating transition to myofibroblasts (Scale bar= 30μm)

Harry A. Quigley, et al. Cell Tissue Res. ;353(2):231-244.
16.
Figure 1

Figure 1. From: Osteogenesis Imperfecta, Pseudoachalasia, and Gastric Cancer.

Blue sclera.

Dilsa Mizrak, et al. Case Rep Gastrointest Med. 2015;2015:685459.
17.
Figure 1

Figure 1. From: An unusual presentation of osteogenesis imperfecta type I.

Blue sclera.

Marta Rebelo, et al. Int Med Case Rep J. 2011;4:25-29.
18.
Figure 1.

Figure 1. From: A Case of Spontaneous Intestinal Perforation in Osteogenesis Imperfecta.

Blue sclera of patient.

Katherine Wheatley, et al. J Clin Med Res. 2010 August;2(4):198-200.
19.
[Table/Fig-3]:

[Table/Fig-3]:. From: Kabuki Make-up Syndrome – A Case Report with Electromyographic study.

Shows blue sclera with characteristic long eye lashes

Atul Sattur, et al. J Clin Diagn Res. 2014 November;8(11):ZD03-ZD06.
20.
Figure 1

Figure 1. From: A rare occurrence of pyloric stenosis in an infant with osteogenesis imperfecta: Anesthetic implications.

Characteristic blue sclera in osteogenesis imperfecta

Sheetal R Jagtap, et al. J Anaesthesiol Clin Pharmacol. 2014 Apr-Jun;30(2):270-272.

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