PurposeTo evaluate the impact of segmentation error on vessel density measurements in healthy eyes and eyes with diabetic macular oedema (DMO).MethodsIn this prospective, comparative, non-interventional study, enface optical coherence tomography angiography (OCTA) images of the macula from healthy eyes and eyes with DMO were acquired. Two expert graders assessed and corrected the segmentation error. The rate of segmentation error and the changes in vessel density and inner retinal thickness after correction of the segmentation error were recorded and compared between the two groups.Results20 eyes with DMO and 24 healthy eyes were evaluated. Intergrader agreement was excellent (intraclass correlation coefficient ≥0.9) for all parameters in both groups. The rate of segmentation error was 33% and 100% in healthy and diabetic eyes, respectively (p<0.001). Nine healthy eyes (37.5%) and all eyes with DMO (100%) were noted to exhibit a change in at least one of the foveal or parafoveal vessel density measurements. The rate of any change in foveal and parafoveal vessel densities in both the superficial and deep capillary plexus was statistically significantly higher in the diabetic group (all p<0.001). No statistically significant change was observed in mean vessel density (superficial and deep capillary plexuses) after correction of the segmentation error in healthy and DMO eyes (All p>0.05). However, the mean absolute change in the vessel density measurements was statistically significantly higher in the diabetic group (all p<0.05). The mean absolute change in superficial and deep inner retinal thickness was statistically significantly higher in DMO (p=0.02 and p=0.002, respectively).ConclusionsIn this study, misidentification of retinal layers and consequent vessel density measurement error occurred in all eyes with DMO and in one-third of healthy eyes. The segmentation error should be checked and manually corrected in the OCTA vessel density measurements, especially in the presence of macular oedema.
In this study, statistically significant regression in the NVD size and flow area was observed as early as 24 hours after a single intravitreal bevacizumab injection, with a continued decreasing trend for at least a 1-month period.
The data obtained in our study confirm the involvement of miR-141 in PCa progression and metastasis. These effects could be mediated by AR via down-regulation of its co-repressor protein, i.e., SHP.
Diabetic retinopathy (DR) remained a leading cause of visual loss in working-age populations. 1 Several biochemical mechanisms including the changes in metabolic pathways, growth factors, hemodynamics, oxidative stress, and subclinical inflammation have been proposed in the pathogenesis of DR. 1 These alterations lead to retinal ischemia that is clinically evident as capillary closure and non-perfusion (CNP).Capillary non-perfusion (CNP) is a hallmark of DR. Fluorescein angiography (FA) has been the standard method for the detection of CNP for several years. However, it does not provide depth-resolved data from the retinal layers, and the leakage of dye leads to obscuration of retinal pathologies. In addition, it is an invasive procedure and needs skilled technicians. Optical coherence tomography angiography (OCTA) is a recent advancement in retinal imaging that enables non-invasive 3-dimensional visualization of the posterior segment
Purpose: To report the clinical spectrum, viral etiologies, therapeutic interventions, timing of rhegmatogenous retinal detachments (RRD), and visual outcomes in acute retinal necrosis (ARN) syndrome in a series of polymerase chain reaction (PCR)-positive eyes. Methods: From January 2010 to January 2017, consecutive patients with the clinical diagnosis of ARN and a positive aqueous viral PCR were included in this observational, retrospective study. Results: Nineteen eyes found to have a clinical diagnosis of ARN, of which 18 (94.7%) had a positive viral PCR. ARN was unilateral, except in one patient. None of the fellow eyes manifested ARN during follow-up. Varicella-zoster virus (VZV) was detected in 78.0% of ARN eyes. 61.1% of eyes experienced RRD. The median time for the occurrence of RRD was 12 weeks (range: 6–25 weeks) after disease onset. No correlation was found between the etiologic viral agent (VZV vs non-VZV; p = 1.000), extent of retinitis (1–2 quadrant vs 3–4 quadrants; p = 0.326), administration of intravitreal ganciclovir (injected vs not injected; p = 0.332), application of prophylactic laser retinopexy (applied vs not applied; p = 0.326), and subsequent occurrence of RRD. At a 2-year follow-up, visual impairment (VA ⩽ 20/200) and severe visual loss (VA ⩽ light perception) were significantly higher in those complicated by RRD compared to non-RRD eyes (81.8% vs 28.6%; p = 0.047, and 45.4% vs 0.0%; p = 0.004, respectively). Conclusion: Aqueous PCR results are highly consistent with the clinical diagnosis of ARN. Regardless of the method of management, the rate of RRD is high and is associated with a poor visual outcome.
Our results demonstrated increased expression of both K-Ras mRNA splicing variants in leiomyoma tissue. However, the ultimate result of KRAS expression on leiomyoma development depends on the overall KRAS isoform balance and, consequently, on activated signaling pathways.
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