Resume

Education:

B.S., Biology – Howard University Washington, D.C. – May 2024

Awards and Achievements:

Dean’s List – Howard University College of Arts and Sciences – 3.73 GPA  – Fall 2020 to Fall 2023
GAAN’s Fellowship Recipient – Stony Brook University – Fall 2024 to Spring 2025

Courses:

Bacteriophages, Genetics, Biotechnology, Evolution, Microbiology, Physics I&II, Organic Chemistry I&II, Biochemistry I&II lectures and labs
Microfluidics, Contemporary Biotechnology, Engineering Principles in Cell Biology

Laboratory Skills:

  • Characterized, isolated, purified, amplified and extracted DNA, genomes and bacteriophages
  • Applied knowledge of biology of microorganisms and their impact on the biotic and abiotic world to analyze host-microbe interactions
  • Created and broke down chemical compounds, solutions and solvents
  • Applied Physics concepts to measure physical properties and quantities
  • Understand biotechnology applications and their design
  • Familiar with regulatory, intellectual property, legal, ethical and societal implications of biotechnology
  • Thorough knowledge in engineering concepts for quantitative analysis of physiochemical systems in context of cell biology
  • Versed in application and theory of special fluid handling conditions related to biological systems
  • Proficient in Gel electrophoresis, PCR, Infrared Spectroscopy, Thin Layer Chromatography
  • Databases: Phages-DB, BLAST, NCBI, PECAAN, Ingenuity Pathway Analysis

Research:

Presented at Howard University and Virginia State University Research Conferences Spring 2024

Decoding Latent Autoimmune Disease (LADA) in African American Adult: A Comprehensive Study on the Role of PFKFB3 Gene and Pathways in Type 2 Diabetes Mellitus Patients

LADA or Type 1.5 diabetes mellitus shares qualities of T1 diabetes by damaging insulin producing cells and symptoms of Type 2 diabetes (T2DM) such as weight loss, blurry vision, excessive thirst and frequent urination. Research shows that 10-25% of patients diagnosed with T2DM are misdiagnosed and actually have LADA. African American patients are two times more likely to die from diabetes than their white peers.  Misdiagnosis is very prevalent among African American patients….. Blood was collected from 68 African American adults (59 were T2DM patients at Howard University and 9 healthy) between 45-65 years of age. Their RNA was isolated from blood samples and three analyses were conducted: transcriptomic, microarray and Ingenuity Pathway Analysis. The transcriptome data displayed that there were a total of 135,750 transcripts with 217 genes showing significant (139 genes were downregulated and 78 were upregulated). The microarray data showed that PFKFB3 gene had inhibited expression in T2DM African American patients (Figure 1). The downregulation of the gene led to the upregulation of AMPK, Sirtuin-1 protein, and glucose metabolism disorder signaling pathways (Figure 2). The activated associated diseases and disorders were hypertension, hyperglycemia, insulin resistance and impaired glucose tolerance. The inhibited associated disorders during PFKFB3 gene downregulation were glycolysis of cells, weight gain, concentration of fructose-2,6-diphosphate and non-insulin dependent diabetes mellitus (Figure 3). This research permitted better comprehension of PFKFB3 in relation to T2DM, glycemic control for T2DM patients and that the inhibition of specific gene causes an increase in T2DM misdiagnosis. This research never recruited categorized LADA patients. Type 1.5 diabetes is fairly new disease, the relationship between PFKFB3 and the African American population was difficult to identify since most studies have been conducted in patients of European descent. Most PFKFB3 studies are done on rats and mice. My HU research lab and I were able to establish a new outlook on identifying LADA and separating it from T2DM in African American patients.

Figure 1: The status of PFKFB3 expression is inhibited or downregulated in T2DM AA patients compared to healthy patients (control)

Figure 2: The network was generated with Ingenuity Pathway Analysis incorporating the relative gene expression levels in the T2DM group. The construction of the networks relied on stored information in the IPA Knowledge Base and expression data. The network includes canonical pathways associated with the analyzed genes, represented with red oval shaped circles. Genes that are upregulated are shown in red and downregulation is depicted in green. The intensity of the color reflects the degree of up- or down- regulations in the respective expression dataset.

Figure 3: The IPA generated network incorporates diseases, disorders and canonical pathways measured in the T2DM group, depicted with red oval shaped circles. Pathways that are activated are displayed in orange while inhibited pathways are represented in blue. The intensity of the color reflects the degree of activation or inhibition.

Future Research

My extensive knowledge and skills in microbiology, biochemistry and prior research at Howard
gives a route to enhancing Dr. SuFeng Zhang’s lab. I am a first year graduate student at Stony
Brook University Biomedical Engineering Program, working in Dr. SuFeng Zhang’s lab where
tissue engineering and targeted drug delivery is combined to create new technologies. In her
previous research she characterized the physicochemical properties of heparin coated human
serum albumin nanoparticles (3) and evaluated the microenvironment at the inflammation site of IBD (4). I find this work to be very fascinating. There is a strong correlation found between IBD and T2DM, whereas the severity of one increases the risk of the other. (5) Through
experimentation, the severity and risk of not just these but more chronic diseases and conditions can be established.

I can use techniques of inoculation, gel electrophoresis, centrifugation, enzyme kinetics, protein
purification and microscopy to identify inflammation in colonic mucosa as well as cause a
decrease in inflammation with drug delivery. Broadly, the creation of new and improved devices
that reduce inflammation will come about through drugs and other chemical interactions. The lab will use different protein drug based nanoparticle formulations to see the in vivo effects against inflamed vs healthy colonic tissue. Comparisons will be done between single, double and triple drug loaded formulations to find the most efficient one to treat inflammation.

My research plan would be to not only continue with Dr. Zhang but to include more chronic
conditions and medical isotopes in the discovery of drug delivery for various treatments. The key is collaboration between SBU and BNL to enable my growth. Brookhaven’s Linac Isotope
Producer (BLIP) is one of very few across the US. The device is able to use a high energy
particle accelerator to create enough energy and space to generate select isotopes. BLIP and their Relativistic Heavy Ion Collider facilities have capabilities to engineer radioisotopes and targeted cancer therapy, detect and track disease, and maximize production and use of the materials. The consideration of cancer and heart disease are the tip of the disease iceberg that BNL resources can be essential in.

Utilizing my established knowledge, new found knowledge of tissue engineering and BNL
resource of medical isotopes I can create new medicines necessary to challenge various chronic
diseases and inflammation everywhere in the body, not just to colonic tissue. Considering the
major differences and similarities between certain tissues so fixed combinations can be
developed. The created biomarkers may be able to also enhance my previous research in LADA
along with other misdiagnosed diseases. Personally combating and closing the aforementioned
healthcare gap for underprivileged patients. I will learn and experiment on different nanoparticle delivery systems finding out the best combinations of single, dual or triple drug loaded nanoparticles. Next, by using these nanoparticle formulations, radioisotopes can be encapsulated with specific chelating agents for binding. There are many different methods to create therapeutic medicine with radioactive isotopes. Systemic radiation therapy is major realization but has many limitations such as having suitable biomarkers for direct delivery, finding drug carrier that can hold optimal amount of radioisotopes for favorable pharmacokinetics, choosing radioisotope with proper half-life and inexpensively producing specific targeting ligands that can be conjugated to the drug carrier (2).

As we know radiation can cause radiation inflammation through activating the immune system
and damaging cells. Overcoming these limits will be a challenge but not unsolvable. One way
would be through low dosages to dissolve the issue. Other ways to decrease inflammation caused by radioactive materials will be creating more distance between patient and radiation source, antioxidants, shielding and medicine like Prussian Blue, Potassium iodide and Neupogen (1). Surely, I will find that some nanoparticle formulations may work better in certain tissues and diseases than in others. I plan on combining all of my resources to experiment, observe, collaborate and create the safest and most effective pathway to implement treatment.\

References (Nature)
1 CDC, US. G. Treatment of Radiation Exposure and Contamination, CDC
https://www.cdc.gov/radiation-emergencies/treatment/index.html (2024).
2 Longijang Zhang, H. C., Liya Wang, Tian Liu, Julie Yeh, Guangming Lu, Lily Yang and Hui
Mao. Delivery of therapeutic radioisotopes using nanoparticle platforms: potential benefit in systemic radiation therapy. PubMed Nanotechnology Science Application, 159-170 (2010).
https://doi.org/10.2147/NSA.S7462
3 SuFeng Zhang, J. C., Amy T. Jin, Lie Yun Kok, Yunhua Shi, David E. Heller, Young-Ah
Lucy Lee, Yixuan Zhou, Xi Xie, Joshua R. Korzenik, Jochen K. Lennerz, and Giovanni
Traverso. Heparin-Coated Albumin Nanoparticles for Drug Combination in Targeting
Inflamed Intestine. Advanced Healthcare Materials 9, 11 (2020).
4 SuFeng Zhang, R. L. a. G. T. Nanoparticle drug delivery systems targeting inflammation for
treatment of inflammatory bowel disease. Elsevier, 15 (2017).
https://doi.org/10.1016/j.nantod.2017.08.006
5 Xu, G., Xu, Y., Zheng, T. et al. Type 2 diabetes and inflammatory bowel disease: a
bidirectional two-sample Mendelian randomization study. Sci Rep 14, 5149 (2024).
https://doi.org/10.1038/s41598-024-55869-x