Institution
Jules Stein Eye Institute
About: Jules Stein Eye Institute is a based out in . It is known for research contribution in the topics: Retina & Retinal. The organization has 1386 authors who have published 1822 publications receiving 79406 citations. The organization is also known as: UCLA Department of Ophthalmology & Jules Stein Eye Institute (UCLA).
Topics: Retina, Retinal, Glaucoma, Visual acuity, Retinal pigment epithelium
Papers published on a yearly basis
Papers
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TL;DR: Cell differentiation in the retina of the mouse during the postnatal period was studied by autoradiography to determine when these cells completed their final mitosis prior to differentiating.
Abstract: Cell differentiation in the retina of the mouse during the postnatal period was studied by autoradiography. Animals were injected with 3H-thymidine at ages extending from the day of birth through postnatal day 11. Six weeks later the distribution of labeled nuclei in the cells of the mature neural retina was analyzed to determine when these cells completed their final mitosis prior to differentiating. Central and peripheral zones were analyzed separately. Cell division ceases by 5–6 days in the center of the retina and by 11 days in the periphery. Among cells produced postnatally, 73% differentiate as rods, 20% as bipolar cells, 6% as Muller cells, and 1% as amacrine and ganglion cells. At all stages of embryogenesis, the differentiation of at least three and as many as six distinct types of specialized cells is initiated simultaneously within the ventricular cell population.
1,052 citations
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TL;DR: Disruption of the RPE-based metabolism of all-trans-retinyl esters to 11-cis-retinal thus appears to underlie the Rpe65-/- phenotype, although cone pigment regeneration may be dependent on a separate pathway.
Abstract: Mutation of RPE65 can cause severe blindness from birth or early childhood, and RPE65 protein is associated with retinal pigment epithelium (RPE) vitamin A metabolism. Here, we show that Rpe65-deficient mice exhibit changes in retinal physiology and biochemistry. Outer segment discs of rod photoreceptors in Rpe65-/- mice are disorganized compared with those of Rpe65+/+ and Rpe65+/- mice. Rod function, as measured by electroretinography, is abolished in Rpe65-/- mice, although cone function remains. Rpe65-/- mice lack rhodopsin, but not opsin apoprotein. Furthermore, all-trans-retinyl esters over-accumulate in the RPE of Rpe65-/- mice, whereas 11-cis-retinyl esters are absent. Disruption of the RPE-based metabolism of all-trans-retinyl esters to 11-cis-retinal thus appears to underlie the Rpe65-/- phenotype, although cone pigment regeneration may be dependent on a separate pathway.
909 citations
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TL;DR: The human cDNA and genomic characterization of a new homeobox gene, RIEG, causing Rieger syndrome is reported, providing opportunities for understanding ocular, dental and umbilical development and the pleiotropic interactions of pituitary and limb morphogenesis.
Abstract: Rieger syndrome (REG) is an autosomal–dominant human disorder that includes anomalies of the anterior chamber of the eye, dental hypoplasia and a protuberant umbilicus. We report the human cDNA and genomic characterization of a new homeobox gene, RIEG, causing this disorder. Six mutations in RIEG were found in individuals with the disorder. The cDNA sequence of Rieg, the murine homologue of RIEG, has also been isolated and shows strong homology with the human sequence. In mouse embryos Rieg mRNA localized in the periocular mesenchyme, maxillary and mandibular epithelia, and umbilicus, all consistent with RIEG abnormalities. The gene is also expressed in Rathke's pouch, vitelline vessels and the limb mesenchyme. RIEG characterization provides opportunities for understanding ocular, dental and umbilical development and the pleiotropic interactions of pituitary and limb morphogenesis.
888 citations
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TL;DR: Evidence is presented that the candidate cDNA is the murine homologue of bovine phosphodiesterase β cDNA and that the mouse rd locus encodes the rod photoreceptor cGMP-phosphodiesterases β subunit.
Abstract: MICE homozygous for the rd mutation display hereditary retinal degeneration and the classic rd lines serve as a model for human retinitis pigmentosa1,2. In affected animals the retinal rod photo-receptor cells begin degenerating at about postnatal day 8, and by four weeks no photoreceptors are left3. Degeneration is preceded by accumulation of cyclic GMP in the retina4 and is correlated with deficient activity of the rod photoreceptor cGMP-phospho-diesterase5. We have recently isolated a candidate complementary DNA for the rd gene6 from a mouse retinal library and completed the characterization of cDNAs encoding all subunits of bovine photoreceptor phosphodiesterase7. The candidate cDNA shows strong homo logy with a cDNA encoding the bovine phospho-diesterase β subunit. Here we present evidence that the candidate cDNA is the murine homologue of bovine phosphodiesterase β cDNA. We conclude that the mouse rd locus encodes the rod photoreceptor cGMP-phosphodiesterase β subunit.
849 citations
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TL;DR: The acquired immune deficiency syndrome (AIDS) is a recently described disorder of cellular immunity in homosexuals, intravenous drug abusers, and Haitians and the presence of cotton-wool spots in patients with this syndrome indicates a poor prognosis.
831 citations
Authors
Showing all 1386 results
Name | H-index | Papers | Citations |
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Harry V. Vinters | 108 | 566 | 51351 |
Michael H. Gelb | 94 | 506 | 34714 |
Wayne L. Hubbell | 93 | 276 | 26591 |
Gang Li | 93 | 486 | 68181 |
Michael F. Seldin | 91 | 347 | 33210 |
Stephen R. Marder | 87 | 406 | 33103 |
John E. Lisman | 86 | 217 | 32380 |
Gary Duckwiler | 80 | 308 | 25690 |
Srinivas R. Sadda | 77 | 712 | 25519 |
Terry J. Smith | 74 | 441 | 17869 |
Kym F. Faull | 70 | 344 | 17926 |
Narendra Tuteja | 68 | 354 | 27042 |
David S. Williams | 67 | 322 | 16933 |
Richard A. Gatti | 65 | 333 | 19693 |
Simon Law | 65 | 408 | 17829 |