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Postbac Seminar Series: October 15, 2019

Series: Science Skills; Speaking

Oct 15, 2019

This event is recommended for: Postbacs.

Science isn't complete until the results have been shared with others, and talking about your results is one of the important ways of making them public. The Postbac Seminar Series provides a unique opportunity for two Postbacs each month to present their research to a diverse audience of their peers.  The atmosphere is relatively informal and non-threatening.  The series allows Postbacs who attend to learn about the different types of biomedical research being conducted at the NIH while meeting other postbacs.  Read more about the seminar series.

This month's presenters are:

Name: Risako Kimura


Research Title: Long-term NAD+ supplementation rescues high-frequency age-related hearing loss in mice

Research Summary: Hearing loss is the most common sensory impairment in elderly adults, affecting over one-third of adults beyond age 60. Age-related hearing loss (ARHL) is characterized by a progressive loss of sensitivity to sounds, starting with high-frequency stimuli. Our group has shown that mouse models of Cockayne Syndrome (CS), a premature aging disease with a major symptom resembling an accelerated form of ARHL, display high metabolic activity and mitochondrial dysfunction. Interestingly, a short-term 4-week intervention with nicotinamide riboside (NR), a precursor of a key metabolite nicotinamide adenine dinucleotide (NAD+), has preventative effects for high-frequency hearing loss in both CS and WT mice. Our recent long-term intervention data shows that NR treatment dramatically reduces ARHL, with 12-month-old NR-treated mice showing rescued auditory brainstem responses, intact neural processing, and high-frequency hearing comparable to that at 2 months of age. These results collectively support a model of metabolic deficit in ARHL and offer NAD+ supplementation as a promising therapeutic for this condition.

Bio: Risako graduated from Brown University with a B.S. in Neuroscience. Her thesis work with Dr. Edward Hawrot characterized the role of the alpha3 nicotinic acetylcholine receptor subunit in embryonic development. Currently, she works at the National Institute on Aging with Dr. Vilhelm Bohr to study how DNA repair deficiencies and mitochondrial dysfunction contribute to the process of neurodegeneration.


Name: Morgan Carter


Research Title: Targeting Mechanisms of Camptothecin Resistance in Ewing Sarcoma Using a High-Throughput Drug Screening Assay

Research Summary: Ewing sarcoma (EWS) is an aggressive malignancy of the bones and soft tissues that arises from a single chromosomal translocation – t(11;22)(q24;q12). A major problem for patients’ long-term survival is the development of refractory or relapsed disease after the standard regimen of chemotherapy, including camptothecin-based agents (topoisomerase I (TOP1) inhibitors). This study modeled camptothecin-based resistance in vitro by creating multiple isogenic cell lines deficient in TOP1 via CRISPR-Cas9. As a result, we identified novel molecular targets in camptothecin-resistant cells. Our findings offer a promising new therapeutic strategy for EWS, in addition to highlighting the varying degree of synergy within camptothecin-based combinations.

Bio: Morgan graduated from the University of Virginia in May 2018 with a B.Sc. in Biochemistry and a minor in Bioethics. She completed her thesis work with highest distinction in the lab of Dr. James Landers, developing a pharmacogenetic assay for detecting human sensitivity to warfarin. Her interest in cancer biology stems from her time at St. Jude Children’s Research Hospital, where she studied mouse mitochondrial mutations for single-cell lineage tracing in leukemia mutagenesis. Morgan began working in the Pediatric Oncology Branch in September 2018 with Dr. Jack Shern to explore novel molecular targets in treating Ewing Sarcoma.


Name: Margaret Smith


Research Title: Seeking Genes and Their Expression Profiles that Control Sexual Assignment in P. falciparum

Research Summary: The sexual stage of Plasmodium parasites is a bottleneck in the malaria life cycle and blocking the development process could potentially stop disease transmission. Although AP2-g transcription factor is known to be important for sexual stage commitment, what is not known is what genes or gene expression profiles control the sexual assignment of gametocytes (i.e., either developing to male or female gametocytes). We are addressing this question using two lines of P. falciparum NF54, SA and N1. N1 is a female gametocyte dominated strain with a female to male ratio of ~20 while SA has a ratio of ~2. Whole genomic sequencing and RNA-sequencing were performed to determine the factors which contribute to the different sex ratios. Data from DNA-sequencing and RNA transcriptomics will be presented.

Bio: Margaret graduated from Appalachian State University in 2018 with a B.S. in Biology. She completed her thesis in lab of Dr. Michael Opata, where she developed a mouse model that replicates childhood malaria. Margaret works for Dr. Carole Long exploring the genes that cause male/female assignments in malaria gametocytes.