The University of Utah Department of Ophthalmology and Visual Sciences invites applications for a full-time position at the level of Assistant/Associate Professor (commensurate w/experience) in the field of visual system function and or/disease. Successful candidates are expected to establish a strong research program funded by federal sources (NIH, NSF), to strengthen the current research carried out at the Moran Eye Institute as well as bring new areas of research into focus.
There is a new Explorer special based on an article in the latest issue of National Geographic with Michael Stevens (@tweetsauce), Unlocking The Eyes that is well worth checking out. In the video above, Michael interviews Marty Banks and William Sprague about why many prey animals like goats have the eye anatomy they do. i.e., why are their eyes have horizontal pupils and why their eyes are positioned on the sides of their heads?
This short video features the art of Steven Erra, a photographer who is losing his vision due to a retinal degenerative disease, yet is generating beautiful work by light painting. Steven is a member of The Seeing With Photography Collective, a group of sight impaired artists who are making waves in the art world through their imagery and inspiring the work of both sighted and non-sighted photographers alike.
There is a short video from National Geographic that is a companion to an article by Ed Yong (@edyong209) in National Geographic here. The photography is wonderful as is typical of National Geographic and is well worth your time.
George RedHawk is a legally blind artist who’s medium is animated gifs and his work is truly stunning. There is a really interesting portfolio of his work on Graphic Art News as well as some background on how he manages to create these amazing works here. In short, he uses photo morphing software to morph one image into another, then he makes animated gifs. Check out his website for more work from his portfolio of on-going works titled “The World Through My Eyes” here.
The extinct Neanderthals had orbital eye sockets that are much larger than ours. Recently, there has been an discussion covered in a fascinating article linked the other day on the BBC discussing the large orbital eye sockets of the Neanderthals and whether these eye represented a reason for the Neanderthals’ demise or not.
Shizuya Saika, Professor and Chairman of Wakayama Medical University will be delivering a seminar on EMT and myofibroblast generation in an injured lens: modulation of TGFb/Smad signal by extracellular matrix on Tuesday, October 6th at Noon in the the Moran Eye Center auditorium.
Abstract: EMT and myofibroblast appears in the fibrotic tissues that are undergoing wound healing process. In the eye it is observed in the crystalline lens or other ocular tissues. Transforming growth factor beta (TGFβ)/Smad signal plays a central role in the process of EMT and myofibroblast generation in an injured mouse lens. However, EMT is further modulated by signals derived from binding of extracellular matrix (ECM) to cell surface receptors. In the current talk the mechanisms of modulation of EMT by matricellular proteins, i. e., osteopontin, tenscin-C and lumican through modulation of TGFβ signal. Lacking one of these component suppressed activation of TGFβ signal as revealed by mutant mouse lines. Although overall signals derived from these ECM components support Smad signal and positively modulate EMT, the detailed mechanisms of actions seem differ among each other.
There is an interesting paper out demonstrating that CST3 exerts a recessive effect on susceptibility to AMD. Cystatin C is a potent inhibitor of cysteine proteinases expressed by many tissues and in the eye, it is highly expressed by the retinal pigment epithelium (RPE). The team led by Luminita Paraoan recently reported data identifying a polymorphism in the cystatin C gene (CST3) that increases the risk of two major degenerative diseases, age-related macular degeneration (AMD) and Alzheimer’s disease. Both these multifactorial diseases involve the age-related accumulation of extracellular deposits, linked to dysregulation of protein homeostasis. Since the advent of the genome-wide association study (GWAS) many SNPs have been found to be associated with these two diseases. However the SNP in CST3, which translates into an amino acid change in the leader sequence of the precursor protein, is the first identified to increase the risk of developing both diseases. Moreover the authors demonstrate that the risk associated with the mutant allele follows the same recessive model for both diseases. Thus only those individuals with two copies of the mutant cystatin allele are at elevated risk of developing both diseases.
Bruch’s membrane is a highly specialized and multi-laminar structure in our retinas that forms the basis for mediating interactions between the retinal pigment epithelium and blood flow from the choroid. I’ve not seen many good images online, so figured this image from mouse would be a good addition showing the relationship of the basal surface of the RPE with Bruch’s membrane.
One of my favorite movie lines is in Blade Runner when Hannibal Chew tells Roy Batty that he designed his eyes. Until reality catches up with science fiction, eye design is still in the hands of designing prosthetic and attractive, but non-functional eyes.
This intriguing video features David Carpenter of the Ocular prosthetics division of Moorfields Eye Hospital discussing how to make a prosthetic eye to replace one lost due to trauma or disease. Every year, David and his team craft 1,400 customized prosthetic eyes for patients, filling a fundamental cosmetic need.
These retinal images are from an 84 year old white male who presented to the Moran Eye Center in 2008. He was diagnosed and followed for dry age-related macular degeneration (AMD) with serial autofluorescent photographs showing progression of geographic atrophy of the RPE from 2008 to 2014.
These images were prepared by James Gilman of the Moran Eye Center.
This is a 58 year old white female with a retinal astrocytic hamartoma on her right optic nerve. Retinal astrocytic hamartomas are glial tumors of the retinal nerve fiber layer arising from retinal astrocytes.
This animated GIF file illustrates the height of the hamartoma and is another example of where animated gifs can be a fantastic teaching tool.
The left and right stereo images shown were taken with a Zeiss FF-4 Fundus camera by James Gilman of the Moran Eye Center.
Purpose: Müller cells (MCs) play a critical role in glutamate (E) metabolism and carbon skeleton cycling in retina. MCs demonstrate changes in metabolism and morphology during retinal degeneration. The timing, extent, regulation, and impacts of these changes are not yet known. We evaluated metabolic phenotypes of MCs and evaluated their capacity to transport glutamate during degeneration.
Methods: Retinas were harvested from wild-type (WT) and rhodopsin Tg P347L rabbits, divided into chips mounted on filters, and incubated in Ames medium with 5 mM D-aspartate (D-Asp), D-glutamate (D-Glu), or D-glutamine (D-Gln) for 10 min at 35 deg to explore transport and metabolism. Chips were fixed in mixed aldehydes and resin embedded for computational molecular phenotyping (CMP) of a range of L- and D-amino acid markers and selected proteins including glutamine synthetase (GS) (J Comp Neurol. 464:1, 2003).
Results: CMP revealed wide variations in metabolite levels across individual MCs from Tg P347L retinas, generating chaotic patterns. GS decreased significantly while glutamine levels (Q) increased, although to varying degrees. Remarkably, E levels were variable and much higher in some MCs than normal, but did not correlate (inversely) with GS levels. Transport experiments using D-Glu, D-Asp, and D-Gln showed that alterations in MC metabolites are not the product of defective transporters, in contrast to previous reports. These results are also inconsistent with conventional models of GS-based E-Q metabolism and microenvironmental regulation of MC phenotypes.
Conclusions: These observations suggest three conclusions. (1) Although degeneration of the retina is certainly the trigger, MC phenotype changes are not a coherent response to the surrounding microenvironment but are, rather, uncoordinated individual MC responses. (2) Although GS is accepted as the primary enzyme responsible for the conversion of E to Q in the normal retina, alternative pathways appear unmasked in the degenerate state. (3) It has been previously hypothesized that MCs in retinal degenerations exhibit deficient E transport. Our experiments show no transport deficiency. This indicates that chaotic metabolite levels emerge from changes in individual MC metabolic processing.