A friend of mine (and amazing landscape/nature photographer) Jim Goldstein sent me a Tweet and pointed out simmering new conjecture in the art community that Vincent Van Gogh might have been color blind, specifically a protanope. I seem to remember some discussion of this years ago, particularly given that one can rather nicely simulate both protanopia and deuteranopia in Adobe Photoshop with built in filters (View>Proof Setup>Protanopia/Deuteranopia). However, the current speculation comes about from Kazunori Asada who wrote up a Tumbler blog entry here describing how he came about his idea and a subsequent app he wrote to simulate color vision and color blindness. The image above shows Kazunori Asada’s approximation of Van Gogh’s Starry Night and Flowering Garden with Path with the original on the left and the Asada transform approximation on the right.
How photoreceptor cells go through the process of cell death has been an outstanding question. The authors of this paper by Yusuke Murakami, Hidetaka Matsumoto, Miin Roh, Jun Suzuki, Toshio Hisatomi, Yasuhiro Ikeda, Joan W. Miller, and Demetrios G. Vavvas have further defined the process and identified the receptor interacting protein kinase (RIP) pathway as a possible target for intervention in patients with retinitis pigmentosa (RP). The authors used the rd10 mouse model, a mouse model of retinitis pigmentosa to examine the cell death process. They defined RIP kinase as a mediator of necrotic cell death in cones. RIP3, has been defined as they key regulator of programmed necrosis and its expression was elevated in rd10 retinas during cone photoreceptor death and not rod photoreceptor death. Furthermore, the cone photoreceptor cell death was rescued by RIP3 deficiency and by pharmacological treatment with RIPkinase inhibitors. Continue reading “Notable Paper: Receptor interacting protein kinase mediates necrotic cone but not rod cell death in a mouse model of inherited degeneration”
Congratulations to our colleagues mentioned in the following press release. We are always enthused to hear about funding and commitments to research, particularly when federal funding of research through traditional means has been getting harder to obtain. This is where funding from private foundations like Foundation Fighting Blindness come through. It enables work to progress that otherwise would not happen and for those of us who are working so very hard to find cures for blindness or treatments to mitigate vision loss, this is invaluable.
This study by Paul S. Bernstein, Faisal Ahmed, Aihua Liu, Susan Allman, Xiaoming Sheng, Mohsen Sharifzadeh, Igor Ermakov, and Werner Gellermann in IOVS examined the macular pigment in AREDS2 patients. AREDS2 is a randomized, placebo-controlled study designed to determine whether supplementation with 10 mg of lutein and 2 mg of zeaxanthin per day can slow the rate of progression of age-related macular degeneration (AMD). Continue reading “Macular pigment imaging in AREDS2 participants: An ancillary study of AREDS2 subjects enrolled at the Moran Eye Center”
Congratulations to Scott Lauritzen and James Tucker who successfully defended their dissertations earlier this year at the Moran Eye Center. Scott will be staying with the Marclab for a postdoc while James will be returning to his medical school class to finish out his clinical years. More pics from the dissertation defenses and after party over on Jonesblog.
This is an important issue for anyone involved in using murine models of retinal degeneration. It turns out that contamination of Rd8 mutation in the B6 mice is more wide spread than the C57BL/6N mice. Labs worldwide are going to have to reassess their data due to this mutation and all reviewers will ask about this in the immediate future. The genotyping analysis of a variety of vendor lines is described in this paper by Mary J. Mattapallil, Eric F. Wawrousek, Chi-Chao Chan, Hui Zhao, Jayeeta Roychoudhury, Thomas A. Ferguson, and Rachel R. Caspi. The take home message is that the rd8 mutation is in the C57BL/6N strain which is used worldwide to produce transgenic and knockout models. The implications for non-vision labs are not as clear, but for vision labs, substantial disease can be present unrelated to another specific disease gene and will need to be accounted for.
This paper by Devid Damiani, Elena Novelli, Francesca Mazzoni and Enrica Strettoi documents continued negative plasticity in retina by examining ganglion cells in the rd1 mouse. The rd1 mouse is one of many models of retinal degenerative disease, in this case as an autosomal recessive retinal degenerative disease. This work gets at the remodeling issue in retinal degenerative diseaseby examining the last cells in the chain of retinal cells that process information before sending it out to the brain and other CNS centers for further processing. Continue reading “Undersized Dendritic Arborizations in Retinal Ganglion Cells of the rd1 Mutant Mouse: A Paradigm of Early Onset Photoreceptor Degeneration”
This study by Mark E. Pennesi, Keith V. Michaels, Sienna S. Magee, Anastasiya Maricle, Sean P. Davin, Anupam K. Garg, Michael J. Gale, Daniel C. Tu, Yuquan Wen, Laura R. Erker, and Peter J. Francis documents the use of SD-OCT as a robust, non-invasive method for monitoring retinal changes in vivo in rodent models of retinal degeneration. The approach is so good that it can discriminate retinal detachment differences in different models of retinal degeneration (rd1 and rd10) that share defects on the same gene.
While histology is still the gold standard, this paper documents the further push of new technologies into in vivo approaches of monitoring. Perhaps we’ll get another boost with 2-photon/OCT approaches coming onto the scene…
Congratulations to Dr. Crystal Sigulinsky on a successful defense to her dissertation, “Defining the relationship between the homeobox gene Vsx2 and extrinsic signaling in the regulation of retinal progenitor cell properties”.
Michalis Agathocleous, Nicola K. Love, Owen Randlett, Julia J. Harris, Jinyue Liu, Andrew J. Murray and William A. Harris have published a very interesting story on proliferating cells of the Xenopus laevis retina that documents aerobic glycolysis rather than oxidative phosphorylation. Historically, this shift in metabolism was termed the Warburg effect where it was originally described in tumorigenesis. Could it be that this shift in metabolism is more widely used than previously anticipated? Certainly in the proliferating developing Xenopus laevis retina, it appears so, even in the presence of oxygen. The only other instance of aerobic glycolosis I am aware of is in T-cells, but that too is associated with oncogenicity.
This really opens up possibilities for metabolic control of a variety of processes in not only development, but also pathology with respect to alternative methods for defining metabolic states and deriving energy.