Abstract
Purpose: To examine the effects of various cardiovascular, ocular, and lifestyle factors on retinal vessel diameters over short periods of time.
Methods: Subjects were invited to have ...photographs of their retina taken at each of three study visits. The same eye was photographed each time. The photographs were digitized and retinal vessel diameters were measured. Measurements from the retinal photographs taken consecutively (at visit 2 and visit 3), and 1, 3, and 4 weeks apart (between visits 1 and 2, 2 and 3, and 1 and 3, respectively) were compared.
Results: There were 63 persons who participated in all study visits and had gradable vessel measurements from all five images used in the analysis. Correlations for pairs of study visits were high, and decreased slightly with increasing length of the time interval. For consecutive photographs taken, and 1 week, 3 weeks, and 4 weeks apart, correlations were 0.95, 0.90, 0.91, and 0.86, respectively, for central retinal arteriolar equivalent (CRAE) and 0.95, 0.90, 0.91, and 0.87, respectively, for central retinal venular equivalent (CRVE). We examined the associations of blood pressure levels, smoking habits, time since last eating, exercising, consuming caffeine, and taking anti-hypertensive medication, and image focus with CRAE and CRVE. We found no consistent pattern of association of any of these characteristics with short-term changes in CRAE and CRVE.
Conclusion: Retinal vessel diameters are stable over short intervals of time and none of the factors studied were consistently associated with change in the diameters of either vessel type.
Age-related macular degeneration (AMD) is a common cause of blindness in older individuals. To accelerate the understanding of AMD biology and help design new therapies, we executed a collaborative ...genome-wide association study, including >17,100 advanced AMD cases and >60,000 controls of European and Asian ancestry. We identified 19 loci associated at P < 5 × 10(-8). These loci show enrichment for genes involved in the regulation of complement activity, lipid metabolism, extracellular matrix remodeling and angiogenesis. Our results include seven loci with associations reaching P < 5 × 10(-8) for the first time, near the genes COL8A1-FILIP1L, IER3-DDR1, SLC16A8, TGFBR1, RAD51B, ADAMTS9 and B3GALTL. A genetic risk score combining SNP genotypes from all loci showed similar ability to distinguish cases and controls in all samples examined. Our findings provide new directions for biological, genetic and therapeutic studies of AMD.
SUMMARY Dinoflagellates have a rich history of characterization of their membrane‐reinforcing sterols because of a structural diversity and chemotaxonomic utility uncommon to other classes of algae. ...The Kareniaceae are no exception in that they produce sterols, often containing a Δ 8(14) nuclear unsaturation, which are rare in most other dinoflagellate groups. A continuing goal of our laboratory is to examine the sterols of previously uncharacterized dinoflagellates to assess their sterol‐based chemotaxonomy compared to other members of the Dinophyceae. Asterodinium gracile , a member of the Kareniaceae, has not been commercially available for study until recently. To this end, our objective was to characterize the sterols of A. gracile to determine whether they match the 4α‐methyl‐substituted, Δ 8(14) ‐nuclear‐unsaturated sterols, such as (24 R )‐4α‐methyl‐5α‐ergosta‐8(14),22‐dien‐3β‐ol (gymnodinosterol; C 29:2 ) and 27‐ nor ‐(24 R )‐4α‐methyl‐5α‐ergosta‐8(14),22‐dien‐3β‐ol (brevesterol; C 28:2 ), of most species within the canonical genera Karenia , Karlodinium and Takayama, or instead the 4‐desmethyl sterols, such as 27‐ nor ‐(24 R )‐23‐methyl‐ergosta‐8(14),22‐dien‐3β‐ol (C 28:2 ), of its chemotaxonomically atypical, yet closest phylogenetic relative, Karenia papilionacea . We have observed A. gracile to produce two 4α‐methyl‐substituted sterols with the suggested structures of 4α‐methyl‐5α‐ergosta‐8(14)‐en‐3β‐ol (C 29:1 ) and 4α‐methyl‐5α‐ergosta‐8(14),24(28)‐dien‐3β‐ol (amphisterol, C 29:2 ), as major sterols amongst five other minor sterols, which included the common dinoflagellate sterol cholest‐5‐en‐3β‐ol (cholesterol, C 27:1 ), but did not include gymnodinosterol or brevesterol (as in most canonical Kareniaceae) or 27‐ nor ‐(24 R )‐23‐methyl‐ergosta‐8(14),22‐dien‐3β‐ol (as found in K. papilionacea ). Detection of amphisterol and 4α‐methyl‐5α‐ergosta‐8(14)‐en‐3β‐ol is notable because they are sterols associated with some species of Amphidinium , such as Amphidinium carterae , and, to our knowledge, have not been observed in a member of the Kareniaceae before. Discovery of these major sterols in A. gracile expands our knowledge of the range of sterols produced by the Kareniaceae and indicates a shared chemotaxonomy with some species of Amphidinium .
Advanced age-related macular degeneration (AMD) is a leading cause of blindness in Western countries. Causal, modifiable risk factors need to be identified to develop preventive measures for advanced ...AMD.
To assess whether smoking, alcohol consumption, blood pressure, body mass index, and glycemic traits are associated with increased risk of advanced AMD.
This study used 2-sample mendelian randomization. Genetic instruments composed of variants associated with risk factors at genome-wide significance (P < 5 × 10-8) were obtained from published genome-wide association studies. Summary-level statistics for these instruments were obtained for advanced AMD from the International AMD Genomics Consortium 2016 data set, which consisted of 16 144 individuals with AMD and 17 832 control individuals. Data were analyzed from July 2020 to September 2021.
Smoking initiation, smoking cessation, lifetime smoking, age at smoking initiation, alcoholic drinks per week, body mass index, systolic and diastolic blood pressure, type 2 diabetes, glycated hemoglobin, fasting glucose, and fasting insulin.
Advanced AMD and its subtypes, geographic atrophy (GA), and neovascular AMD.
A 1-SD increase in logodds of genetically predicted smoking initiation was associated with higher risk of advanced AMD (odds ratio OR, 1.26; 95% CI, 1.13-1.40; P < .001), while a 1-SD increase in logodds of genetically predicted smoking cessation (former vs current smoking) was associated with lower risk of advanced AMD (OR, 0.66; 95% CI, 0.50-0.87; P = .003). Genetically predicted increased lifetime smoking was associated with increased risk of advanced AMD (OR per 1-SD increase in lifetime smoking behavior, 1.32; 95% CI, 1.09-1.59; P = .004). Genetically predicted alcohol consumption was associated with higher risk of GA (OR per 1-SD increase of log-transformed alcoholic drinks per week, 2.70; 95% CI, 1.48-4.94; P = .001). There was insufficient evidence to suggest that genetically predicted blood pressure, body mass index, and glycemic traits were associated with advanced AMD.
This study provides genetic evidence that increased alcohol intake may be a causal risk factor for GA. As there are currently no known treatments for GA, this finding has important public health implications. These results also support previous observational studies associating smoking behavior with risk of advanced AMD, thus reinforcing existing public health messages regarding the risk of blindness associated with smoking.
Reply Myers, Chelsea E; Klein, Barbara EK; Klein, Ronald
American journal of ophthalmology,
07/2015, Volume:
160, Issue:
1
Journal Article
Peer reviewed
The notion of genetic factors explaining thicker central retina as determined by OCT is supported by a heritability estimate of 0.90 in a study using monozygotic and dizygotic female twin pairs.2 A ...different study of macular thickness found thicker retinas in younger persons, which led the authors to suggest that the differences between the sexes were due, in part, to gonadal hormone levels.3 The role of genes and environmental factors that determine retinal thickness remain to be further elucidated.
To describe the relationship of change in retinal vessel diameters to the subsequent 6-year incidence and progression of diabetic retinopathy (DR) and incidence of proliferative diabetic retinopathy ...(PDR) and macular edema (ME) in persons with diabetes mellitus.
A total of 1098 persons with diabetes who had DR graded from fundus photographs and had computer-assisted measurements of the central retinal arteriolar equivalent (CRAE) and central retinal venular equivalent(CRVE) participated in examinations in 1980-1982, 1984-1986, and 1990-1992.
During the first 4-year period, the mean change in CRAE and CRVE was −0.37 and 2.54 μm, respectively.The 6-year incidence and progression of DR and the incidence of PDR and ME from 1984-1986 to 1990-1992 were 56%, 39%, 15%, and 11%, respectively. In multivariate analyses, while controlling for duration, diabetes type, and other factors, an increase of 10 μm in CRVE from 1980-1982 to 1984-1986 was associated with increases in the 6-year incidence of DR (odds ratio OR,1.26; 95% CI, 1.10-1.43), progression of DR (OR, 1.21;95% CI, 1.12-1.30), incidence of PDR (OR, 1.19; 95%CI, 1.07-1.32), and incidence of ME (OR, 1.16; 95% CI,1.03-1.31). No interactions of these associations by diabetes type were found (data not shown). Change in CRAE was unrelated to the incidence or progression of DR (data not shown).
Independent of DR severity level, glycemic control, and other factors, widening of the retinal venular but not arteriolar diameter was associated with subsequent incidence and progression of DR. The CRVE may provide additional information regarding the risk of incidence and progression of DR beyond traditional risk factors.
Previously, variation in retinal vascular caliber has been reported in association with chronic kidney disease (CKD) but findings remain inconsistent. To help clarify this we conducted individual ...participant data meta-analysis and aggregate data meta-analysis on summary estimates to evaluate cross-sectional associations between retinal vascular caliber and CKD. A systematic review was performed using Medline and EMBASE for articles published until October 2018. The aggregate analysis used a two-stage approach combining summary estimates from eleven studies (44,803 patients) while the individual participant analysis used a one-stage approach combining raw data from nine studies (33,222 patients). CKD stages 3-5 was defined as an estimated glomerular filtration rate under 60 mL/min/1.73m2. Retinal arteriolar and venular caliber (central retinal arteriolar and venular equivalent) were assessed from retinal photographs using computer-assisted methods. Logistic regression estimated relative risk of CKD stages 3-5 associated with a 20 μm decrease (approximately one standard deviation) in central retinal arteriolar and venular equivalent. Prevalence of CKD stages 3-5 was 11.2% of 33,222 and 11.3% of 44,803 patients in the individual participant and aggregate data analysis, respectively. No significant associations were detected in adjusted analyses between central retinal arteriolar and venular equivalent and CKD stages 3-5 in the aggregate analysis for central retinal arteriolar relative risk (0.98, 95% confidence interval 0.94-1.03); venular equivalent (0.99, 0.95-1.04) or individual participant central retinal arteriolar (0.99, 0.95-1.04) or venular equivalent (1.01, 0.97-1.05). Thus, meta-analysis provided little evidence to suggest that cross sectional direct measurements of retinal vascular caliber was associated with CKD stages 3-5 in the general population. Hence, meta-analyses of longitudinal studies evaluating the association between retinal parameters and CKD stages 3-5 may be warranted.
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