University of Oregon (UO) Summer Program for Undergraduate Research (SPUR)https://scholarsbank.uoregon.edu/xmlui/handle/1794/225322024-03-29T11:07:44Z2024-03-29T11:07:44ZEffects of histamine-receptor blockade and exercise on blood-glucose concentrationRaqueno-Angel, SabrinaEly, MattSieck, DylanHalliwell, Johnhttps://scholarsbank.uoregon.edu/xmlui/handle/1794/228132018-10-23T20:36:35Z2017-01-01T00:00:00ZEffects of histamine-receptor blockade and exercise on blood-glucose concentration
Raqueno-Angel, Sabrina; Ely, Matt; Sieck, Dylan; Halliwell, John
Histamine has been found to be an important component during the
exercise recovery period, particularly in mediating vasodilation,
hyperemia, and hypotension. Blocking H1/H2 histamine receptors
produced altered outcomes during recovery, including a decrease in
interstitial glucose concentrations and reductions in blood flow and
whole-body insulin sensitivity. It is unknown if blood glucose
concentrations change with histamine receptor blockades, specifically
during the exercise period. PURPOSE: To determine if H1/H2
histamine receptor blockades decrease blood glucose concentrations
during exercise. HYPOTHESIS: It was hypothesized that histamine
receptor blockade would decrease blood glucose concentrations
during exercise. METHODS: Nine competitive cyclists performed 120
minutes of cycling exercise at 50% VO2 peak. 60 minutes prior to
exercise, subjects were given either a placebo or histamine receptor
blockades (540 mg Fexofenadine and 300 mg Ranitidine). Blood
glucose concentrations were measured using a handheld Precision
Xtra Blood Glucose Monitoring System (Abbot Diabetes Care INC,
Alameda CA). Measurements were taken from the earlobe pre-exercise
and three times during exercise at 15, 60, and 120 minutes.
A repeated-measures two-way ANOVA (RM ANOVA, Group X Time)
was used for statistical analysis. RESULTS: No differences were
found between placebo and histamine receptor blockades groups (p =
0.801), and no Group X Time Interaction was determined (p = 0.881).
Blood glucose levels at 15, 60, and 105 minutes were lower than the
pre-exercise levels (p<0.001). CONCLUSION: No significant
differences in blood glucose concentrations were found between
placebo and histamine receptor blockade groups.
Single page poster pdf.
2017-01-01T00:00:00ZQuantification of Synapse Number for Identification of Molecules Influencing Cholinergic Synapse Formation in DrosophilaSweet, SerenaAckerman, SarahSales, EmilyDoe, Chris Q.https://scholarsbank.uoregon.edu/xmlui/handle/1794/228022017-09-28T07:34:01Z2017-01-01T00:00:00ZQuantification of Synapse Number for Identification of Molecules Influencing Cholinergic Synapse Formation in Drosophila
Sweet, Serena; Ackerman, Sarah; Sales, Emily; Doe, Chris Q.
Synapses are chemical junctions between neurons that allow signals to be transmitted from one neuron to another. Although disruptions to synapse structure and function contribute to symptoms of most neurological disorders, not much is known about the molecular mechanisms that are responsible for synapse formation and maintenance. Glial cells are a group of non-neuronal cells in the nervous system known for protecting neurons and mediating neuronal function. Astrocytes are glial cells that secrete synaptogenic compounds required for synapse formation. Here, we combine the reverse genetic technique of RNAi and light microscopy to identify novel secreted and cell surface molecules from astrocytes that influence understudied cholinergic synapses in Drosophila melanogaster. I studied two established techniques for labeling the active-zone protein Bruchpilot (Brp) in cholinergic dorsal bipolar dendritic (Dbd) neurons to quantify synapses: 1) Brp-short and 2) Synaptic tagging with recombination (STaR). I used light microscopy to quantify Dbd-synapse number at three larval (L) stages: L1, L2, and L3. We will use this information to identify novel regulators of synapse development by performing an astrocyte-specific RNAi screen choosing genes that are predicted as cell surface or secreted, are highly conserved in humans, and are highly expressed by astrocytes. This screen will allow us to identify new genes that instruct synapse formation and maintenance that could ultimately contribute to the establishment of therapies for neurological disorders.
Single page poster.
2017-01-01T00:00:00ZEvolution of a photoactivatable GFP-like proteinHernandez, Jocelynehttps://scholarsbank.uoregon.edu/xmlui/handle/1794/226132017-09-02T07:59:53Z2017-01-01T00:00:00ZEvolution of a photoactivatable GFP-like protein
Hernandez, Jocelyne
Understanding how new protein functions evolve is crucial to rationally engineering proteins with desired functions. One way we can begin to understand this is to compare the biochemical properties of ancestral and extant proteins whose functions have changed over an evolutionary interval. An evolutionary interval
in green fluorescent protein-like (GFP-like) proteins from corals has been identified where an ancestral green state evolved to an extant photoconvertible red state. Irradiation of photoconvertible fluorescent proteins with light of a specific wavelength, intensity, and duration causes distinct changes in their fluorescence properties. I developed experimental photoconversion assays and biochemically characterized the photoconversion process for a natural evolutionary transition in the Kaede GFP-like protein family. Developing a deeper understanding of the biochemical properties that lead to the natural evolution of a photoconvertible protein will allow better design of markers that can be used in imaging and microscopy.
Single page poster.
2017-01-01T00:00:00ZAssessing the role of the SMC-5/6 complex in meiotic double strand DNA break repairClark, Cordellhttps://scholarsbank.uoregon.edu/xmlui/handle/1794/226122017-09-02T07:59:53Z2017-01-01T00:00:00ZAssessing the role of the SMC-5/6 complex in meiotic double strand DNA break repair
Clark, Cordell
Meiosis is the specialized cell division used to form haploid gametes. During meiosis, endogenous double strand DNA breaks (DSBs) are induced. A subset of these DSBs must be repaired as crossovers with the homologous chromosome to ensure proper chromosome segregation. Although repair is required for proper chromosome segregation, use of the homologs as a repair template for DSB repair is restricted to a specific time window during meiotic prophase I. DSBs incurred outside of this window must be repaired to ensure genomic integrity. Multiple lines of evidence have suggested that these homolog-independent repair events utilize the sister chromatid as a template in repairing DSBs. Utilizing Caenorhabidits elegans, the Libuda lab has developed a genetic assay for intersister repair, directly demonstrating the occurrence of intersister repair events during meiosis; however, the molecular mechanism of intersister repair remains unknown. Previous studies have implicated multiple proteins in promoting homolog-independent DNA repair during meiosis, including the structural maintenance of chromosomes (SMC) 5/6 complex. Utilizing this assay, I will determine whether the SMC-5/6 complex is required for intersister repair during meiosis. Specifically, I will place an smc-5 null mutation in the intersister repair assay and examine the frequency of intersister repair events at a specific locus in the genome. If SMC-5 is required for intersister repair, I expect to observe a lowered frequency or elimination of intersister repair events compared to wild type controls. Determining the precise role of smc-5 and other candidate genes in DSB repair will provide insight into the mechanisms underlying DNA repair decisions during meiosis.
Single page poster
2017-01-01T00:00:00Z