The percentage of HITs correctly classified by the majority (>50%) of KW’s, with range of percentage of correct “votes” for each image category in brackets.

<p>The percentage of HITs correctly classified by the majority (>50%) of KW’s, with range of percentage of correct “votes” for each image category in brackets.</p

Comparative graphical illustration of the AUC for all classifications by study design (normal-abnormal) - Trial 1 (A) and Trial 2 (D); Comparative graphical illustration of the AUC for easy classifications (normal versus severely abnormal) by study design- Trial 1 (B) and Trial 2 (E); Comparative graphical illustration of the AUC for difficult classifications (normal versus mildly abnormal) by study design- Trial 1 (C) and Trial 2 (F).

<p>Comparative graphical illustration of the AUC for all classifications by study design (normal-abnormal) - Trial 1 (A) and Trial 2 (D); Comparative graphical illustration of the AUC for easy classifications (normal versus severely abnormal) by study design- Trial 1 (B) and Trial 2 (E); Comparative graphical illustration of the AUC for difficult classifications (normal versus mildly abnormal) by study design- Trial 1 (C) and Trial 2 (F).</p

The proportion correctly identified by severity of abnormality as well as the sensitivity, specificity and area under the ROC curve (AUC) for each study design in trials 1 and 2 by classification difficulty.

<p>(0.03c = study design 1; 0.05c = study design 2; 0.03c_500_90% = study design 3; 0.03c_5000_99% = study design 4).</p

The AUC and associated 95%CI for trial 1 (0.03c) as a function of the number of KW gradings per image.

<p>The AUC increases as the number of KW gradings increases with a peak at 16 individual gradings per image. A similar curve was obtained for all study designs in both trials, although a variation was seen in the optimal number of KWs needed to achieve a peak ROC.</p

Baseline characteristics of KW participation by study design for trials 1 and 2.

<p>(0.03c = study design 1; 0.05c = study design 2; 0.03c_500_90% = study design 3; 0.03c_5000_99% = study design 4).</p

Retinal ganglion cell dendritic architecture is unchanged in DBA/2J.<i>Thy1</i>(YFP) mice independent of retinal eccentricity.

<p>Sectorial damage in the retina during glaucoma has been previously reported <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0072282#pone.0072282-Howell1" target="_blank">[8]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0072282#pone.0072282-Schlamp1" target="_blank">[29]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0072282#pone.0072282-Feng1" target="_blank">[30]</a>. RGCs from superior, inferior, nasal and temporal quadrants were analysed separately. There was no significant difference in any of the parameters measured. <i>Top</i>; locations of labeled cells in DBA2J.<i>Thy1</i>(YFP) mice. RE: Right eye. LE: left eye. Scale bar 2 mm. (s,i,n,t: superior, inferior, nasal, temporal retinal segments centered on the optic nerve). Sholl plot (A) for RGC from superior retinas (shaded in panel) from eyes in which the optic nerve showed no apparent damage (NOE) filled circles (<i>n</i> = 27) or severe damage (SEV) open circles (<i>n</i> = 7). (B) For RGCs from inferior, nasal and temporal retinal segments in eyes in which the optic nerve showed no apparent damage (NOE) filled circles (n = 19), and severe damage (SEV) open circles (<i>n</i> = 6). Samples pooled from right and left eyes.</p

There is a significant shift in the Sholl analysis of DiOlistically labelled NOE DBA/2J mice but not MOD or SEV.

<p>There is a significant down and left-wards shift in the Sholl analysis of NOE compared to age and sex matched control D2-<i>Gpnmb⁺</i> mouse retinal ganglion cells representing a decrease in dendritic length as well as the number of branching points. (A) NOE v D2-<i>Gpnmb⁺</i>, (B) MOD v D2-<i>Gpnmb⁺</i>, (C) SEV v D2-<i>Gpnmb⁺</i>. Comparisons in Sholl analysis comparing the differences observed between strains (DiOlistically labelled DBA/2J and DBA/2J.Thy1(YFP)) for both mice with NOE (D) or SEV (E) optic nerve damage are shown. Error bars represent SEM.</p

Representative retinal ganglion cells from DBA/2J.<i>Thy1</i>(YFP) mice.

<p>Panel of representative retinal ganglion cells from 1–3 month NOE (<i>upper left</i>), 9.5–11 month NOE (<i>upper right</i>), 9.5–11 month MOD (<i>lower left</i>), and 9.5–11 month SEV DBA/2J.<i>Thy1</i>(YFP) mice (<i>lower right</i>). There are no observable differences in retinal ganglion cell morphologies between groups. Scale bars  = 100 µm.</p

There are no significant changes to retinal ganglion cell dendritic morphology in DBA/2J.<i>Thy1</i>(YFP) mice.

<p>To explore potential changes to retinal ganglion cell dendritic morphology caused by increasing IOP and axonal damage the retinal ganglion cells of DBA/2J.<i>Thy1</i>(YFP) mice were analysed. Mice were categorised into cohorts depending on their level of optic nerve damage; no or early damage (NOE), moderate damage (MOD) or severe damage (SEV). In 9.5–11 month old DBA/2J.<i>Thy1</i>(YFP) mice there were no significant changes to retinal ganglion cells total dendritic length, total dendritic field area (A) or Sholl analysis area under the curve (AUC) (B) (<i>P</i>>0.05 across all groups). Error bars represent SEM; numbers in bars represent the <i>n</i> of cells.</p

Representative panel of mouse retinal ganglion cells.

<p>Representative panel of mouse retinal ganglion cells from 4 month B6, D2-<i>Gpnmb⁺</i> and DBA/2J mice (<i>top row</i>) and 12 month D2-<i>Gpnmb⁺</i>, NOE and SEV DBA/2J mice (<i>bottom row</i>). Changes can be seen in the in dendritic morphology of NOE DBA/2J mice compared to age and sex matched D2-<i>Gpnmb⁺</i> mice. Scale bars  = 100 µm.</p