[Studies on normal developing process of the retinal vessels and effect of oxygen on the developing retinal vessels of the young rabbit (author's transl)].
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This study examines the risk of developing cytomegalovirus (CMV) retinitis as a function of the duration and degree of CD4+ lymphocyte depletion. A retrospective analysis of 135 persons infected with the human immunodeficiency virus (HIV) was performed. Kaplan-Meier estimates for the percentage of patients developing CMV retinitis during the 27-month study period were calculated. Twenty-six patients were diagnosed as having CMV retinitis. In 14 of these patients, T cell phenotyping was done within the 3 months preceding diagnosis. The mean CD4+ lymphocyte count for these patients was 15.6 cells/mm3 (range, 2-33/mm3). At 27 months, the percentage of patients developing CMV retinitis with baseline CD4+ lymphocyte counts of 0-50, 51-100, and 101-250 cells/mm3 was 41.9%, 26.3%, and 14.7%, respectively (log-rank test, p = 0.003). The odds ratio for developing CMV retinitis for those with baseline CD4+ lymphocyte counts of 0-50 cells/mm3 compared with those with CD4+ lymphocyte counts of 101-250 cells/mm3 was 4.62 (p = 0.002). Twenty-four patients had CD4+ lymphocyte counts of < or = 50 cells/mm3 for an average of 13.1 months prior to diagnosis. Twenty-two patients had an acquired immune deficiency syndrome (AIDS)-defining illness diagnosed for an average of 18.0 months prior to the onset of retinitis. CMV retinitis is most likely to develop in patients with AIDS when the CD4+ lymphocyte count is < or = 50 cells/mm3.
Pou domain transcription factor Pou4f2 is essential for the development of retinal ganglion cells (RGCs) in the vertebrate retina. A distant orthologue of Pou4f2 exists in the genome of the sea urchin (class Echinoidea) Strongylocentrotus purpuratus (SpPou4f1/2), yet the photosensory structure of sea urchins is strikingly different from that of the mammalian retina. Sea urchins have no obvious eyes, but have photoreceptors clustered around their tube feet disc. The mechanisms that are associated with the development and function of photoreception in sea urchins are largely unexplored. As an initial approach to better understand the sea urchin photosensory structure and relate it to the mammalian retina, we asked whether SpPou4f1/2 could support RGC development in the absence of Pou4f2. To answer this question, we replaced genomic Pou4f2 with an SpPou4f1/2 cDNA. In Pou4f2-null mice, retinas expressing SpPou4f1/2 were outwardly identical to those of wild-type mice. SpPou4f1/2 retinas exhibited dark-adapted electroretinogram scotopic threshold responses, indicating functionally active RGCs. During retinal development, SpPou4f1/2 activated RGC-specific genes and in S. purpuratus, SpPou4f2 was expressed in photoreceptor cells of tube feet in a pattern distinct from Opsin4 and Pax6. Our results suggest that SpPou4f1/2 and Pou4f2 share conserved components of a gene network for photosensory development and they maintain their conserved intrinsic functions despite vast morphological differences in mouse and sea urchin photosensory structures.
One hundred patients had bilateral aphakia, primary rhegmatogenous retinal detachment, and adequate visualization of the retinal and vitreous in the fellow eye. Of 43 patients with posterior vitreous separation and no retinal tear in the fellow eye, only one (2%) subsequently developed retinal detachment. Of 40 patients without posterior vitreous separation in the fellow eye, eight (20%) later developed retinal detachment following posterior vitreous separation. The remaining 17 patients had posterior vitreous separation and retinal tear or detachment at the time of initial examination. Thus, if posterior vitreous separation occurs without forming retinal tear, the risk of developing retinal detachment is significantly lowered.
A direct causal relationship between a human DNA virus, adeno serotype 12, and malignant transformation in target cells (sensory retinal neuronal precursors) was suggested by the development of a remarkably uniform retinoblastoma-like neoplasm in rats. In order to focus upon incipient photoreceptor differentiation, 27 3-day-old CD rats were selected for intraocular virus inoculation. A single injection of 0.03 ml of the virus fluid, 104.5 TCID50 HeLa cells/0.1 ml was given in the left eye. Within 73 to 167 days after the virus inoculation, 12 rats (44.4%) developed retinal tumors in the left eye. Although retinal tumors mimicking human retinoblastoma with true rosettes were anticipated, the highly uniform histopathologic appearance of all 12 eyes was virtually indistinguishable from that of 0-day-old rats. However, multiple foci of malignant cells fusing with the inner segment of relatively well-differentiated retinal layers were found haphazardly throughout the cases; such retinal remnants were not detectable in tumors of 0-day-old rats. Electron microscopy revealed poorly differentiated tumor cells that possessed a single cilium consisting of a typical ring of nine doublets with no axial pair (a 9 plus 0 pattern). Advenovirus-specific T-antigens detected in vivo by the immunofluorescein microscopic procedure in abortively infected or transformed cells clearly indicated that some neuronal precursors destined for part of the ganglioneuronic layer are selectively susceptible to viral oncogenesis. No preferential involvement of the photoreceptor cells was observed. No control animals developed retinal neoplasms.
PURPOSE: PCSK9 inhibitors (PCSK9i) are a newer class of lipid-lowering drug that may be effective at lowering risk for retinal artery occlusion (RAO) and retinal vein occlusion (RVO). This study aims to investigate the relationship between PCSK9i use and retinal vascular occlusion among patients with hyperlipidemia. DESIGN: Retrospective, comparative clinical cohort study SUBJECTS, PARTICIPANTS, AND/OR CONTROLS: Patients with hyperlipidemia, defined as serum low-density lipoprotein level of ≥130 mg/dL and total cholesterol level of ≥220 mg/dL, prescribed a lipid-lowering medication were identified. Patients prescribed a PCSK9i were included in the study group and compared with control patients prescribed any other type of lipid-lowering drug. METHODS: This study was conducted using electronic health record data from health organizations in the United States through the TrinetX platform. Propensity score matching was completed based on relevant patient demographics, comorbidities, and laboratory values. Comparison of main outcomes between the PCSK9i and non-PCSK9i groups was performed using measures of association analysis to determine risk ratio (RR) with 95% CI. MAIN OUTCOME MEASURES: The outcomes measured consisted of occurrence of retinal vascular occlusion, RAO, RVO, central RAO, and central RVO at 3-year, 5-year, and 7-year time points. RESULTS: After propensity score matching, a total of 12,960 patients were included in each cohort. The analysis revealed that the PCSK9i cohort had a significantly lower risk for development of retinal vascular occlusions at multiple points, including 3-year (RR = 0.56, CI = 0.39-0.79), 5-year (RR = 0.50, CI = 0.37-0.67), and 7-year (RR = 0.46, CI 0.35-0.61) time points. This lower risk was also found in the PCSK9i group for an outcome of RVO at 5 years (RR = 0.50, CI = 0.34-0.73) and 7 years (RR = 0.47, CI = 0.33-0.67). For occurrence of RAOs (RR = 0.47, CI = 0.30-0.76) and central RVO (RR = 0.46, CI = 0.29-0.74) separately, the PCSK9i cohort had a lower risk at 7 years. CONCLUSION: These findings suggest that PCSK9i may reduce the risk of retinal vascular occlusion compared with other classes of lipid-lowering medications.
Retrolental fibroplasia is a continuing problem in ophthalmology and may lead to retinal detachment. In this study, two groups of patients with retrolental fibroplasia and retinal detachment are described. The first group consists of youngsters who develop retinal detachment during their teenage years and frequently have not been diagnosed as having the disease until the retina detaches. Usually definite retinal breaks can be found near the equator and these are round or oval in appearance and without opercula. A second group of patients was noted to develop retinal detachment at an earlier age. The configuration of these detachments suggested a rhegmatogenous etiology, but retinal breaks were hard to detect because the peripheral retina was frequently obscured by a membrane or cataract. Additional evidence to support this opinion was provided when a small retinal hole was identified in one youngster whose ora could be easily seen. Because of the progressive nature of vitreoretinal adhesion in retrolental fibroplasia, it is advocated that youngsters with any evidence of retrolental fibroplasia at the time of discharge from the premature nursery be followed at one month, three months, and six months of age and at four-month intervals thereafter until the age of four years. If no difficulty develops by the time, yearly examinations suffice. Follow-up examinations are important because when prompt diagnosis of retinal detachment is made, the involved eye can often be salvaged with surgery.
Five hundred and sixty-four consecutive eyes after cataract surgery with intraocular lens implantation were studied in relationship to the incidence of retinal detachment and cystoid macular edema in the intra vs the extracapsular extraction technique. In 124 eyes undergoing intracapsular cataract extraction, three (2.4%) developed retinal detachment. In 440 eyes undergoing extracapsular cataract extraction two (0.45%) developed retinal detachment. In 87 eyes undergoing intracapsular cataract extraction 7 (8%) developed cystoid macular edema. In 327 eyes undergoing extracapsular cataract extraction 4 (1.2%) developed cystoid macular edema. This study cannot be compared with other series in the literature because high risk cases and those with vitreous loss were excluded.
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Experiments were designed to test whether nonrandom segregation of sister chromatids at mitosis has a role in the production of cell diversity during embryogenesis, Segregation was examined in vivo in retinal cells from embryonic chicks. Chromatids were labelled with bromouracil and stained by the fluorescence plus Giemsa technique. No evidence of nonrandom segregation was observed in a frequency distribution of pairs of bifilarly labelled sister chromatids at the third metaphase after the start of labeling. Nor was there evidence that chromatids from homologous chromosomes segregated nonrandomly. Nonrandom segregation is probab;y not a mechanism for cell diversification.
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In the central area of the retina of mouse the rate of synaptogenesis in the inner plexiform layer (IPL) drops precipitously at about the time the eyes open. To determine if the visual input at eye opening provides a signal for the neurons to stop adding synapses, mice were raised in darkness during the period of maximal synaptogenesis and through eye opening. Retinal synaptic arrays of dark-reared and normally reared animals were compared quantitatively. The rate of synaptogenesis after eye opening in dark-reared mice indicated that the onset of visual stimulation was not the cue to stop synaptogenesis. However, the synaptic arrays of the IPL of dark-reared mice consistently had more conventional synapses than those of normally reared mice. It is concluded that the number of conventional synapses in the central retina was increased by dark-rearing.
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