The Efficacy of Graphene Oxide Coated Sand in the Filtration of Major Heavy Metal Contaminants to Solve the Global Water Crisis

Overview

Centenary College of Louisiana Over forty percent of the world population lack access to clean water, equating to roughly seven hundred million people. 80% of illnesses in developing countries can be attributed to poor water conditions; this has resulted in a global water crisis. A chief concern is the prevalence of heavy metal contaminants in water, which can result from industrial or natural causes. Heavy metal contamination can lead to nervous system diseases, cancers, and other fatal diseases. Graphene oxide has been hailed as a revolutionary material with potential in water filtration. If this material is coated around sand, a more traditional material used in filtration, it is expected that the concentration of major heavy metals (lead and mercury) will decrease. Graphene oxide coated sand was synthesized from graphite powder using a modified Hummers method. The heavy metal solutions were filtered through regular and graphene oxide coated sand, with samples of the filtrate taken every five minutes. An elemental analysis was performed on the two sand samples, showing a greater proportion of carbon in the graphene oxide coated sand, signifying that graphene oxide was in fact synthesized. The filtration technique using the graphene oxide coated sand showed a significant decrease in the concentration of both heavy metal solutions. A one-tailed, paired t-test was performed on the last five samples of both eluents, and the resulting pvalues, which were less than 0.05, implied significance. As a result, the potential of graphene oxide coated sand in the filtration of heavy metal contaminants is evident. Acute Effects of Vaping on Human Endothelial Cells Neil Dogra Pulaski Academy Little Rock, Arkansas Supervising Scientist: Tarun Kumar Garg University of Arkansas for Medical Sciences Human Endothelial Cells (HUVECs) were exposed to concentrations of Acrolein and Propylene Oxide (PO). Both chemicals were chosen because they’re products of chemicals after vaporization. Acrolein and PO are products of glycerol and propylene glycol respectively. Because new chemicals are introduced into the body after vaporization, many effects are unknown. In this study, two experiments were conducted. Experiment 1 contained a 1-to-10 serial dilution and exposed Acrolein/PO to HUVECs in 4 trials, comparing results to media, and HUVECs exposed to media. Concentrations increased by 10 and went from 0.001 μg/ml to 100 μg/ml. Experiment 2 contained a 1-to-3 serial dilution and exposed chemicals to HUVECs in 4 trials, but Acrolein concentrations started at 1 μg/ml and increased to 243 μg/ml, and PO started at 100 μg/ml and increased to 24300 μg/ml. Results from Experiment 1 showed Acrolein cell death between 1-to-10 μg/ml. PO didn’t cause any deaths. Results from Experiment 2 showed Acrolein causing cell death at beyond 3 μg/ml. PO reacted at beyond 8100 μg/ml. To find a lethal range for both chemicals, further experimentation is needed. These results show changes in morphology, supporting the hypothesis, Acrolein and PO can damage endothelial cells even at nonlethal doses. This study has far-reaching applications as scientists hope to learn more about the dangers of vaping and communicate findings to the public. This study shows both chemicals could be responsible for morphological changes in HUVECs and Acrolein contributing to cell death. Flagella-Mediated Antibiotic Persistence: A Scientific Enigma Jacob Egelberg New Rochelle High School New Rochelle, New York Supervising Scientist: Michael Gates Northeastern University Persister cells are mutli-drug tolerant bacterial subpopulations likely responsible for the recalcitrance of chronic infections. It is unclear what population heterogeneities encourage individual cells to become persistent or which molecular pathways confer tolerance. The current study addressed the latter by elucidating the relationship between flagellar gene expression and persister formation. A variety of Escherichia coli deletion mutants constructed via P1 phage transductions, as well as transformants containing an inducible ycgR expression vector, were subjected to persister assays. It was found that any inhibition of cellular motility significantly reduced persister formation, whether facilitated by the knockout of genes necessary for movement or the induction of ycgR. This was observed independent of proton-motive force (PMF) utilization by flagellar rotation. However, when the two methyl-accepting chemotaxis receptor genes tsr and trg were knocked out, persister frequencies increased. While it is unclear how trg is related to persistence, the knockout of tsr likely enables antibiotic survival by inhibiting chemotaxis towards serine, thereby starving cells of serine and conferring tolerance. The current study concludes that stochastic cellular motility promotes persister formation, while chemotactic motility mediated by tsr and trg acts as a moderate persister repressor. Loss of Hippocampal Day-Time Inhibition in Alzheimer’s Disease and its Contribution to Cognitive Impairment and Amyloid-β Pathogenesis Rachael S. George Alabama School of Fine Arts Birmingham Alabama High School Mentor: Rebecca Thrash University of Alabama At Birmingham (UAB) PI: Dr. Karen Gamble Lab Mentor: Allison Fusilier When diagnosing Alzheimer’s disease, doctors look for pathogenic amyloid-β (Aβ) plaque accumulation, tau tangles, and cognitive impairment. In the early stages of Alzheimer's disease, subclinical epileptiform activity or seizures, which are typical of network hyperexcitability, can be detected. Circadian rhythms are intrinsic predictable changes in physiology and behavior occurring over a 24-hour period. During the inactive phase of the circadian cycle, seizure thresholds are lower and epileptiform activity is greater in general in Alzheimer’s disease. Previous literature suggests that decreased inhibition during the day plays a role in observed hyperexcitability and cognitive impairment, but the role of loss of day-night differences in hippocampal inhibition in cognitive impairment and Aβ pathology has not been studied. To begin this study, the point at which plaque buildup is seen in the J-20 mouse model must be determined. From the preliminary findings of the project, we see that by the age of 4 months, Aβ pathology is not detectable in the J20 mouse model of Alzheimer’s disease. By 12 months of age, hAPP(+) J20 mice exhibit Aβ plaque pathology.

Awards (1)

• 1st Place Environmental Science

Competition history

• JSHS 2020 Category not listed

Resources

• National JSHS abstract book ↗

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