Severity of the presence of pyknotic nuclei in cells in ganglion cell layer (GCL) after transient inner retinal ischemia.

<p>Severity of the presence of pyknotic nuclei in cells in ganglion cell layer (GCL) after transient inner retinal ischemia.</p

Semi-quantitative rt-PCR analysis showing total ET-1 mRNA expression in the retinae of non-transgenic (NTg), heterozygous (He) and homozygous (Hm) TET-1 mice.

<p>A: Ethidium bromide-stained agarose gels of rt-PCR products of ET-1, showing increased ET-1 mRNA expression in transgenic mouse retina. The molecular size marker (M) was 1 kb plus marker. B: Histograms showing the levels of ET-1 mRNA expression normalized to that of GAPDH. n = 4 for each experimental group. *: <i>p</i><0.05 (Kruskal-Wallis Test).</p

Thicknesses of inner nuclear layer (INL), inner plexiform layer (IPL) to inner limiting membrane (ILM) and the whole inner retina (µm).

<p>Thicknesses of inner nuclear layer (INL), inner plexiform layer (IPL) to inner limiting membrane (ILM) and the whole inner retina (µm).</p

Validation of the diabetes screening tools proposed by the American Diabetes Association in an aging Chinese population

<div><p>Aim</p><p>Diabetes is a serious global health problem. A simple and effective screening tool should have substantial public health benefit. We investigated the performance of the latest American Diabetes Association diabetes screening methods in our aging Chinese population.</p><p>Methods</p><p>Subjects without diabetes who returned for the 4th Hong Kong Cardiovascular Risk Factors Prevalence Study in 2010–2012 were evaluated for the probability of having diabetes with reference to the age- and body mass index-based screening criteria (screening criteria) and the diabetes risk test (risk test), and the conclusion drawn was compared to their measured glycaemic status. Diabetes was defined by fasting glucose ≥ 7 mmol/L or 2-hour post oral glucose tolerance test glucose ≥ 11.1 mmol/L.</p><p>Results</p><p>1415 subjects, aged 58.1±10.2, were evaluated. 95 (6.7%) had diabetes. The risk test showed good accuracy (area under the receiver operating curve 0.725) in screening for diabetes with an optimal cut-off score of five. Compared to the screening criteria, the risk test had significantly better specificity (0.57 vs. 0.41, p<0.001), positive predictive value (0.12 vs. 0.09, p<0.001) and positive diagnostic likelihood ratio (1.85 vs. 1.37, p<0.001). To diagnose one case of diabetes, fewer subjects (11 vs. 18) needed to be tested for blood glucose if the risk test was adopted.</p><p>Conclusion</p><p>The risk test appears to be a more effective screening tool in our population. It is simple to use and can be adopted as a public health strategy for identifying people with undiagnosed diabetes for early intervention.</p></div

Immunohistochemical staining of glial fibrillary acidic protein (GFAP).

<p>Compared with the contralateral retinae of NTg and Hm TET-1 mice, GFAP signal was up-regulated in the ipsilateral retinae in the astrocytes around capillaries in the inner limiting membrane (arrowheads) and the Müller cell processes in IPL (arrows). n = 5 for each experimental group. Scale bar = 50 µm.</p

Immunohistochemical staining of aquaporin-4 (AQP4).

<p>Up-regulation of AQP4 signal was found in the Müller cell processes in IPL (arrows) and Müller cell bodies in INL (arrowheads) in the ipsilateral retina of Hm TET-1 mice compared with the corresponding contralateral retina, while similar intensity of AQP4 signal was present in the contralateral and ipsilateral retinae of NTg mice. n = 5 for each experimental group. Scale bar = 50 µm.</p

Different cut-off points for the ADA diabetes risk test when applied in the CRISPS population (n = 1415).

<p>Different cut-off points for the ADA diabetes risk test when applied in the CRISPS population (n = 1415).</p

Baseline characteristics of 1415 subjects at CRISPS4.

<p>Baseline characteristics of 1415 subjects at CRISPS4.</p

Statistics measures of the performance of the two ADA screening strategies.

<p>Statistics measures of the performance of the two ADA screening strategies.</p

A schematic diagram summarizing the interplay between adiponectin and ADM.

<p>Adiponectin and ADM could regulate each other in 3 ways: 1. Gene-gene interactions from the respective SNPs; 2. ADM could increase adiponectin gene expression and secretion [13. Liao et al., 2012]; 3. In type 2 diabetes, plasma adiponectin level tends to be lower [36. Tso et al., 2006], while plasma ADM level tends to be higher [6. Cheung and Leung, 1997).</p