Photographer Suren Manvelyan has produced an amazing collection of photographs of eyes over the last couple of years. He started with a phenomenal set of images from human eyes and has now expanded his collections to include 3 sets of animal eyes. Part 1, Part 2 and now Part 3.
Spending some time looking through them is a good investment, particularly if you consider the evolution that has shaped the biology as looking at the different structures of the outer eyes gives you clues as to the environments these organisms live in.
The NIH/NEI Audacious Goals Initiative (AGI) brochure is being distributed to researchers as well as public and private funding agencies and advocacy groups for an effort to fund vision research and vision rescues to regenerate portions of the retina that are lost in disease.
From the brochure: “The AGI began with the Audacious Goals Challenge, a prize competition that challenged participants to imagine the greatest achievement for vision research during the next 10-15 years. The challenge attracted more than 450 innovative proposals from around the world. The NEI consolidated the proposals into six themes, which were further explored by leading experts at the Audacious Goals Development Meeting.
In consultation with the National Advisory Eye Council (NAEC), the NEI chose to pursue the goal of restoring vision through the regeneration of neurons and neural connections in the eye and visual system, specifically targeting the photoreceptors and retinal ganglion cells.”
Many disorders are characterized by circadian rhythm abnormalities, including disturbed sleep/wake cycles, changes in locomotor activity, and abnormal endocrine function. Animal models with mutations in circadian “clock genes” commonly show disturbances in reward processing, locomotor activity and novelty seeking behaviors. However, circadian clock dysfunction impacts diabetic complications including diabetic retinopathy. In this presentation, the impact of mutations in clock genes on retinal vascular function will be discussed. Circadian dysregulation of stem cells release from the bone marrow in diabetes will be described.
A Lo-Fi video, but largely correct and a pretty well done explanation of why we have blind spots in our eyes and the general physiological reason for why we don’t typically “see” or notice our blind spots.
The Arnold and Mabel Beckman Foundation is pleased to announce the 2015 Beckman-Argyros Award in Vision Research.
The BECKMAN-ARGYROS AWARD IN VISION RESEARCH is an annual award established in 2013 to honor and celebrate a decades-long friendship of two remarkable men, Dr. Arnold O. Beckman and Ambassador George L. Argyros, and to continue their commitment, dedication and shared vision to make the world a better place. The Beckman-Argyros Award honors Ambassador Argyros for his 22 years of service as Chairman of the Board of the Arnold and Mabel Beckman Foundation and recognizes the special and unique friendship he shared with Arnold O. Beckman for over forty years.
The Beckman – Argyros Award in Vision Research is intended to reward one individual who has made significant transformative breakthroughs in vision research.
In an unprecedented recognition of extraordinary achievement in scientific research and to further support this research, one award will be made annually. The recipient will receive a total of $500,000 along with a commemorative medallion.
In contemplating potential nominees, please keep in mind that while the Arnold and Mabel Beckman Foundation currently supports one Initiative which focuses solely on macular degeneration (MD); the Beckman-Argyros Award is separate and apart from said Initiative and is not intended to focus solely on MD, but the broader spectrum of vision research.
Binxing Li, post-doc in Paul Bernstein’s lab will present a seminar at noon on Wednesday, September 10th in the Moran Eye Center auditorium on Inactivity of human β, β-carotene-9ʹ′, 10ʹ′-dioxygenase (BCO2) underlies retinal accumulation of the human macular carotenoid pigment.
Abstract: The macula of the primate retina uniquely concentrates high amounts of the xanthophyll carotenoids lutein, zeaxanthin, and meso-zeaxanthin, but the underlying biochemical mechanisms for this spatial- and species-specific localization have not been fully elucidated. For example, despite abundant retinal levels in mice and primates of a binding protein for zeaxanthin and meso-zeaxanthin, the pi isoform of glutathione S-transferase (GSTP1), only human and monkey retinas naturally contain detectable levels of these carotenoids. We therefore investigated whether or not differences in expression, localization, and activity between mouse and primate carotenoid metabolic enzymes could account for this species-specific difference in re0nal accumulation. We focused on β,β-carotene-9ʹ′,10ʹ′-dioxygenase (BCO2, also known as BCDO2), the only known mammalian xanthophyll cleavage enzyme. RT-PCR, Western blot analysis, and immunohistochemistry (IHC) confirmed that BCO2 is expressed in both mouse and primate retinas. Cotransfection of expression plasmids of human or mouse BCO2 into Escherichia coli strains engineered to produce zeaxanthin demonstrated that only mouse BCO2 is an ac0ve zeaxanthin cleavage enzyme. Surface plasmon resonance (SPR) binding studies showed that the binding affinities between human BCO2 and lutein, zeaxanthin, and meso-zeaxanthin are 10- to 40-fold weaker than those for mouse BCO2, implying that ineffective capture of carotenoids by human BCO2 prevents cleavage of xanthophyll carotenoids. Moreover, BCO2 knockout mice, unlike WT mice, accumulate zeaxanthin in their retinas. Our results provide a novel explanation for how primates uniquely concentrate xanthophyll carotenoids at high levels in retinal tissue.
Abstract: Excessive light exposure is known to harm the retina and exacerbates disease progression in many retinal disorders. In addition, certain genetic mutations affec6ng components in the phototransduction cascade serve as a source of “equivalent light” and cause retinal degenera6on. How light exerts its harmful effect on the retina is not well understood. Mouse models can be used to isolate distinct light damage pathways. Dr. Chen will discuss recent findings on mechanisms of retinal damage caused by environmental and genetic sources of “equivalent light”.