No abstract

Pomoxis nigromaculatus, more commonly referred to as black crappie is indigenous to fresh water streams and lakes in the eastern United States and supports an important recreational fishery. We examined the genetic population structure of black crappie inhabiting three Georgian Lakes, Lake Sidney Lanier, Lake Seminole and Hartwell Lake. DNA sequencing of 229 fish samples, utilizing the DNA barcode marker cytochrome oxidase subunit I (COI) revealed 27 polymorphic sites which defined nine haplotypes. Only haplotype 2 was shared between all sample sites with six other haplotypes being unique for individual lakes, for an overall haplotype diversity of 0.734. Tajima's D and Fu's tests were implemented to assess departures from neutral expectations. Fst pairwise comparisons were statistically significant among all populations of black crappie evaluated in this study.

Forested aquatic streams depend heavily on forest canopy input. This input is a primary resource for the macroinvertebrate fauna. As a result, changes in the canopy impact the aquatic ecosystem. The focus of this study was to identify leaf degradation rates to determine resource availability for invertebrate communities. Specifically, leaf degradation rates were determined for oak, poplar, maple and kudzu. Oak, poplar, and maple are established stream canopy vegetation while kudzu is an invasive species. By comparing leaf degradation rates of native vs. exotic leaves, it provides an insight to changes in community structure. Furthermore, these changes in the plant canopy biodiversity have long-term implications for stream health.

It has been widely established that, in addition to its role in reproduction, progesterone (P4) also has potent anti-inflammatory effects. While the precise mechanisms have never been clearly elucidated in RAW 246.7 cells, it seems logical to assume that this response is -at least in part -a consequence of activation of and signaling through the progesterone receptor (P4-R). However, it has recently been shown that in a rat model, this anti-inflammatory effect is -in fact -independent of the progesterone receptor. In this project, the aim was to characterize this response by assaying nitric oxide production from lipopolysaccharide-challenged RAW 264.7 cells and ascertain the involvement of the P4-R. To determine the contribution of the receptor, RAW cells were incubated in the presence and absence of RU-486 -a potent P4-R antagonist. Our results indicate that the anti-inflammatory response of progesterone was in fact through the activation of the P4-R as cells incubated in RU-486 show an approximate 60% reversal of the inhibitory effect of P4 as compared to cells incubated in the absence of the antagonist. However, because we did not observe a complete reversal, suggests that perhaps other receptors come into play which will be addressed in future studies. Creative Commons LicenseThis work is licensed under a Creative Commons Attribution 4.0 License.This article is available in Proceedings of the Interdisciplinary STEM Teaching and Learning Conference:https://digitalcommons.georgiasouthern.edu/stem_proceedings/vol1/iss1/8 The Progesterone Receptor -To Be or Not to Be: The Anti-inflammatory Effects of Progesterone in RAW 264.7 CellsChristopher I Brandon Jr., Georgia Gwinnett College Bagie M. George, Georgia Gwinnett College Abstract: It has been widely established that, in addition to its role in reproduction, progesterone (P4) also has potent anti-inflammatory effects. While the precise mechanisms have never been clearly elucidated in RAW 246.7 cells, it seems logical to assume that this response is -at least in part -a consequence of activation of and signaling through the progesterone receptor (P4-R). However, it has recently been shown that in a rat model, this anti-inflammatory effect is -in fact -independent of the progesterone receptor. In this project, the aim was to characterize this response by assaying nitric oxide production from lipopolysaccharide-challenged RAW 264.7 cells and ascertain the involvement of the P4-R. To determine the contribution of the receptor, RAW cells were incubated in the presence and absence of RU-486 -a potent P4-R antagonist.Our results indicate that the anti-inflammatory response of progesterone was in fact through the activation of the P4-R as cells incubated in RU-486 show an approximate 60% reversal of the inhibitory effect of P4 as compared to cells incubated in the absence of the antagonist. However, because we did not observe a complete reversal, suggests that perhaps other receptors come into play which will be addressed in future studies.