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  1. Cheah CK, Vijaya Singham N, Gun SC
    Int J Rheum Dis, 2017 Dec;20(12):2253-2255.
    PMID: 26864240 DOI: 10.1111/1756-185X.12827
    Matched MeSH terms: Retina/physiopathology
  2. Sharanjeet-Kaur, Ismail SA, Mutalib HA, Ngah NF
    J Optom, 2018 05 26;12(3):174-179.
    PMID: 29843983 DOI: 10.1016/j.optom.2018.03.007
    PURPOSE: The purpose of this study was to determine the relationship between HbA1c values and retinal sensitivity at central 10° using the MP-1 microperimeter.

    METHODS: A prospective study was carried out on 32 healthy subjects (control group) and 60 diabetic patients. The diabetic patients were divided into 2 groups. Group 1 comprised of 30 patients without diabetic retinopathy (DR) and group 2 had 30 patients with mild non-proliferative DR. A full-threshold microperimetry of the central 10° of retina (the macula) was performed on all subjects, utilizing 32 points with the MP-1. The relationship between light sensitivity and HbA1c value was calculated using linear regression analysis.

    RESULTS: Total mean sensitivity at 10° for group 1 without DR, group 2 with mild NPDR and control group were 18.67±0.83, 17.98±1.42 and 19.45±0.34 (dB), respectively. There was a significant difference in total mean retinal sensitivity at 10° between the 3 groups (F(2,89)=18.14, p=0.001). A simple linear regression was calculated to predict HbA1c based on retinal sensitivity. A significant regression equation was found (F(1,90)=107.61, p=0.0001, with an R2 of 0.545). The linear regression analysis revealed that there was a 0.64dB decline in mean retinal sensitivity within the central 10° diameter with an increase of 1mmHg of HbA1c.

    CONCLUSION: Retinal sensitivity at the central 10° of the macula is affected by changes in HbA1c values.

    Matched MeSH terms: Retina/physiopathology*
  3. Sng CC, Wong WL, Cheung CY, Lee J, Tai ES, Wong TY
    J Hypertens, 2013 Oct;31(10):2036-42.
    PMID: 23787404 DOI: 10.1097/HJH.0b013e328362c201
    OBJECTIVE(S): To examine the effect of blood pressure (BP) on retinal vascular fractal dimension (Df), a measure of microvascular network complexity and density in a multiethnic cohort.
    METHODS: A population-based study of 3876 Chinese, Malay and Indian participants in Singapore. Retinal Df was measured using a computer-based program from digital retinal photographs. Associations between retinal Df and mean arterial BP (MABP) in the whole cohort and in each racial group were analysed using linear regression analysis. Logistic regression was used to examine the association between retinal Df and hypertension status.
    RESULTS: The mean retinal Df of the study population was 1.45 (standard deviation 0.03). After adjustment for age, sex, race, diabetes, BMI, cholesterol and creatinine levels, persons with smaller Df had higher MABP (mean difference MABP was 6.18 mmHg comparing lowest to highest Df quartiles, P<0.001). This was similar in Chinese, Malay and Indian persons [mean difference 6.40 (P<0.001), 4.72 (P=0.011) and 6.62 (P<0.001)mmHg, respectively]. Persons with smaller retinal Df were more likely to have uncontrolled treated or untreated hypertension [odds ratio 1.79 (P=0.003) and 2.60 (P=0.003), respectively, comparing lowest to highest Df quartiles] than those with no hypertension; this relationship was not seen comparing persons with controlled treated hypertension with no hypertension (odds ratio 1.01, P=0.972).
    CONCLUSION: Hypertension was associated with a sparser retinal vascular network, which was similar across different racial/ethnic groups and most apparent in those with uncontrolled or untreated hypertension. These data suggest that microvascular remodelling can be quantified by measuring retinal vasculature.
    Matched MeSH terms: Retina/physiopathology
  4. Kim Y, Griffin JM, Nor MNM, Zhang J, Freestone PS, Danesh-Meyer HV, et al.
    Neurotherapeutics, 2017 Oct;14(4):1148-1165.
    PMID: 28560708 DOI: 10.1007/s13311-017-0536-9
    The cis benzopyran compound tonabersat (SB-220453) has previously been reported to inhibit connexin26 expression in the brain by attenuating the p38-mitogen-activated protein kinase pathway. We show here that tonabersat directly inhibits connexin43 hemichannel opening. Connexin43 hemichannels have been called "pathological pores" based upon their role in secondary lesion spread, edema, inflammation, and neuronal loss following central nervous system injuries, as well as in chronic inflammatory disease. Both connexin43 hemichannels and pannexin channels released adenosine triphosphate (ATP) during ischemia in an in vitro ischemia model, but only connexin43 hemichannels contributed to ATP release during reperfusion. Tonabersat inhibited connexin43 hemichannel-mediated ATP release during both ischemia and reperfusion phases, with direct channel block confirmed using electrophysiology. Tonabersat also reduced connexin43 gap junction coupling in vitro, but only at higher concentrations, with junctional plaques internalized and degraded via the lysosomal pathway. Systemic delivery of tonabersat in a rat bright-light retinal damage model (a model for dry age-related macular degeneration) resulted in significantly improved functional outcomes assessed using electroretinography. Tonabersat also prevented thinning of the retina, especially the outer nuclear layer and choroid, assessed using optical coherence tomography. We conclude that tonabersat, already given orally to over 1000 humans in clinical trials (as a potential treatment for, and prophylactic treatment of, migraine because it was thought to inhibit cortical spreading depression), is a connexin hemichannel inhibitor and may have the potential to be a novel treatment of central nervous system injury and chronic neuroinflammatory disease.
    Matched MeSH terms: Retina/physiopathology
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