2024 Poster Presentation Competition Info Coming Soon. Follow Us onLinkedIn to Get Notifications from Us!
See 2023 CBB Conference Poster Presentation Competition Info Below!
Posters can be posted on Friday October 13th from 4-5pm or early morning before conference begins (Pharmacy Building Atrium). Please remove posters immediately following conference.
Session 1 (12:00-12:45pm)- odd numbered posters will be presented
Session 2 (12:45-1:30pm)-even numbered posters will be presented
CBB will keep award winning poster (or get a copy) to be displayed for the year at the CBB
(1) The poster board has a 44" H x 68" W area for mounting the posters.
(2) Lettering and illustrations on the poster pages must be large enough to be read by attendees from a distance of 3 feet or more.
(3) Each poster must have a title, authors and affiliation section at the beginning. Material should be displayed in logical sequence (e.g., introduction, objectives, results, conclusion).
(4) Authors are responsible for mounting their own poster material on poster boards which will be provided at the conference. The Center will provide magnets for the poster boards.
Example of a previous poster-other examples can also be seen in past archived programs
1) CATIONIC CaMKIIN-LOADED LIPOSOMES AIMED TO REDUCE CHLORINE-INDUCED AIRWAY OXIDATIVE STRESS
Esraa Mohamed1, Andrea Adamcakova-Dodd2, Isabella Grumbach3, Peter S. Thorne2,4, Aliasger K. Salem1,5*.
1Department of Pharmaceutical Sciences and Experimental Therapeutics, College of Pharmacy, University of Iowa, Iowa City, IA 52242
2Department of Occupational and Environmental Health, College of Public Health, University of Iowa, Iowa City, IA 52242
3Abboud Cardiovascular Research Center, Division of Cardiovascular Medicine, Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA 52242
4Human Toxicology Program, Graduate College, University of Iowa
5Holden Comprehensive Cancer Center, University of Iowa Hospitals & Clinics, Iowa City, IA 52242
Background: Glutamate (Glu) is the major excitatory neurotransmitter in the central nervous system (CNS) involved in synaptic plasticity, neuronal outgrowth and survival, and memory. Although intracellular Glu concentration is often quantified in the millimolar range, extracellular Glu concentration must remain in the micromolar range. When extracellular levels of Glu rise, aberrant synaptic signaling leads to excitotoxicity which is thought to contribute to many neurodegenerative diseases, including epilepsy and Alzheimer’s disease. In previous reports, limonoids isolated from Dictamnus dasycarpus showed significant neuroprotective activity against Glu excitotoxicity. Of the previously studied limonoid natural products, fraxinellone was one of four compounds that proved to be effective in protecting against Glu excitotoxicity in vitro. With this information, a library of analogues was synthesized from the natural product fraxinellone that proved to be more effective at protecting against Glu toxicity than natural fraxinellone.
Methods: In vitro methods were used to measure the protective properties of the new fraxinellone analogues and to determine their mechanism of protection, which has not been achieved before. PC12 cells were first pre-treated with each compound at a range of 0.05 to 1.0 μM. The compounds were then washed from the cells and 100 μM Glu was added for 24 hours. MTT analysis was then performed to measure cell viability to determine if the compounds were effective at protecting the cells against Glu toxicity. Of the fifteen analogues that were synthesized, six proved to be protective against Glu toxicity, even more than natural fraxinellone. With this information, we then investigated their mechanism of protection by considering potential targets of these compounds, specifically the Nrf2 pathway, through qPCR analysis. We also determined the time course for Glu-mediated ROS production.
Results. Six of the fifteen compounds protected against Glu excitotoxicity. When cells were pre-treated with the compounds that afforded protection before adding the Glu insult, we saw enhancement of gene expression of antioxidant response elements (AREs), a key mechanism of Nrf2 activation. Antioxidant gene expression was not seen for compounds that did not provide protection.
Conclusions: Our findings suggest high levels of Glu are toxic to PC12 cells and induce ROS production in a time-dependent manner. Current findings suggest the compounds protect through Nrf2 activation and induction of an antioxidant response.