Different experimental approaches in modelling cataractogenesis: An overview of selenite-induced nuclear cataract in rats

Cataract, the opacification of eye lens, is the leading cause of blindness worldwide. At present, the only remedy is surgical removal of the cataractous lens and substitution with a lens made of synthetic polymers. However, besides significant costs of operation and possible complications, an artificial lens just does not have the overall optical qualities of a normal one. Hence it remains a significant public health problem, and biochemical solutions or pharmacological interventions that will maintain the transparency of the lens are highly required. Naturally, there is a persistent demand for suitable biological models. The ocular lens would appear to be an ideal organ for maintaining culture conditions because of lacking blood vessels and nerves. The lens in vivo obtains its nutrients and eliminates waste products via diffusion with the surrounding fluids. Lens opacification observed in vivo can be mimicked in vitro by addition of the cataractogenic agent sodium selenite (Na2SeO3) to the culture medium. Moreover, since an overdose of sodium selenite induces also cataract in young rats, it became an extremely rapid and convenient model of nuclear cataract in vivo. The main focus of this review will be on selenium (Se) and its salt sodium selenite, their toxicological characteristics and safety data in relevance of modelling cataractogenesis, either under in vivo or in vitro conditions. The studies revealing the mechanisms of lens opacification induced by selenite are highlighted, the representatives from screening for potential anti-cataract agents are listed

University of West Georgia Institutional STEM Excellence (UWise)

UWise, funded by the Georgia BOR STEM II initiative, provides support to STEM majors through a summer bridge program. UWise also supports faculty members with mini-grants that focus on improving student success in STEM courses and involving them in faculty-directed undergraduate research. Students in the summer bridge program outperformed non-bridge students in English and STEM courses, as well as the overall GPA. A total of 30 STEM majors participated in UWise-funded research projects, which resulted in 14 student presentations and seven peer-reviewed publications. In conjunction with a Complete College Georgia (CCG) Grant, we have expanded the STEM to STEAM based ENGL 1101/1102 sections from 10 to 12 each term in 2015-2016. A total of 25 faculty members took part in the mini-grant projects, which focused on reducing DFW rates, and resulted in positive gains for students. Ten conference presentations and two peer-reviewed SoTL publications resulted from activities supported by mini-grants

STEM Initiative

UWise, funded by the GA BOR STEM II initiative, provides support to STEM majors through a summer bridge program, freshman learning community and freshman seminar courses. UWise also supports faculty with mini-grants for projects that focus on improving instruction and enhancing the success of students in STEM courses and involving them in faculty-directed undergraduate research. Participation in UWise summer bridge program decreased DFW rates in English and STEM courses, as well as improved the GPA. UWise funded research projects results in 30 student publications and 5 peer-reviewed publications. In conjunction with a CCG Replication Grant, we have expanded the STEM to STEAM based ENGL 1101/1102 sections from two to twelve during this funding period

University of West Georgia Institutional STEM Excellence (UWISE)

UWise, funded by the GA BOR STEM II initiative, provides support to STEM majors through a summer bridge program, freshman learning community and freshman seminar courses. UWise also supports faculty with mini-grants for projects that focus on improving instruction and enhancing the success of students in STEM courses and involving them in faculty-directed undergraduate research. Within three years of funding, UWise has made significant progress in students’ enthusiasm for STEM courses, retention and grades. We continue to modify and improve our program. An example is STEM to STEAM model, a product of interdisciplinary collaboration between English and the STEM disciplines

RAGE-dependent signaling in microglia contributes to neuroinflammation, Aβ accumulation, and impaired learning/memory in a mouse model of Alzheimer’s disease

Microglia are critical for amyloid-β peptide (Aβ)-mediated neuronal perturbation relevant to Alzheimer’s disease (AD) pathogenesis. We demonstrate that overexpression of receptor for advanced glycation end products (RAGE) in imbroglio exaggerates neuroinflammation, as evidenced by increased proinflammatory mediator production, Aβ accumulation, impaired learning/memory, and neurotoxicity in an Aβ-rich environment. Transgenic (Tg) mice expressing human mutant APP (mAPP) in neurons and RAGE in microglia displayed enhanced IL-1β and TNF-α production, increased infiltration of microglia and astrocytes, accumulation of Aβ, reduced acetylcholine esterase (AChE) activity, and accelerated deterioration of spatial learning/memory. Notably, introduction of a signal transduction-defective mutant RAGE (DN-RAGE) to microglia attenuates deterioration induced by Aβ. These findings indicate that RAGE signaling in microglia contributes to the pathogenesis of an inflammatory response that ultimately impairs neuronal function and directly affects amyloid accumulation. We conclude that blockade of microglial RAGE may have a beneficial effect on Aβ-mediated neuronal perturbation relevant to AD pathogenesis.—Fang, F., Lue, L.-F., Yan, S., Xu, H., Luddy, J. S., Chen, D., Walker, D. G., Stern, D. M., Yan, S., Schmidt, A. M., Chen, J. X., Yan, S. S. RAGE-dependent signaling in microglia contributes to neuroinflammation, Aβ accumulation, and impaired learning/memory in a mouse model of Alzheimer’s disease