Take a look at what our trainees are doing!

The trainees’ clinical experiences brought forth a range of emotions and insights. They encountered diverse patient cases, highlighting the importance of empathy and patience in healthcare. Some found motivation and a renewed interest in pursuing biomedicine careers, while others grappled with the emotional complexities of the profession. Despite their individual reflections, all trainees gained valuable insights into patient care and the challenges of the medical field.

Research, mentored by Dr. Joel Spencer, focused on the role of Vhl in bone marrow cells contributing to the dysregulation in the bone marrow microenvironment. I measured the cell density, location and size measurements in the bone marrow of mice using intravital and ex vivo imaging data obtained from a new inducible VhlcKO mouse model. and analyzed the data using the implementation of negative contrast imaging. The data was analyzed creating a bone mask as well as a vessel mask for every single stack of data using Fiji. Once the masks were created, a MATLAB script was adjusted and used to generate a centroid of each cell and from there preliminary data about the cell density, location and size was generated. Further analysis as well as future results will grow our understanding for how deletion of Vhl in specific bone marrow cells dysregulates the bone marrow microenvironment.

With PI, Dr. Stephanie Woo, I examined the immunofluorescence of wild type, septin9a heterozygous mutant, and homozygous mutant fish. The gene that was changed in the mutant fish was. Septin9a is the only septin protein with a microtubule binding domain, exhibited as tail blistering in the homozygous mutant fish. The goal of staining the fish was to see what ECM proteins (laminin and fibronectin) and microtublues were impacted by the genetic mutation. The ECM proteins were relatively unaffected in mutant fish, while the microtubules were very disorganized in those homozygous fish, compared to the wild-type and heterozygous fish.

My research project in Dr. Kara McCloskey’s laboratory is to grow and characterize the different endothelial cells (ECs), as well as to investigate in vitro differentiation from embryonic stem cells. The McCloskey laboratory previously generated highly angiogenic EC subpopulations that exhibit distinct surface markers, gene expression profiles, and positional affinities during sprouting. I work alongside mentor and graduate student Maria Mendoza, generating and collecting data of these specialized ECs from stem cells.

My project, with Drs. Manilay and Spencer, consists of determine if knocking out the sclerostin (Sost) gene would results in the acceleration of aging in mice. In this project I learned different techniques such as histology, flow cytometer, wet lab training, hemacytometer, fluorescent microscope, light microscope, and dissection of mice.  I used techniques such FACS (Fluorescent Activated Cell Sorting) to analyze different type of cells and microscopy and histology to look at specific tissues like the bones (femur and tibia), and the liver to see any type of evidence in aging in these tissues.

I am working in Dr. Ge’s lab on cell signaling pathways in the primary cilium, with an emphasis on Hedgehog signaling. Our goal is to learn the molecular mechanisms behind these pathways during neural development. Over the summer I conducted research to identify the localization of ciliary proteins and determine signaling levels under different experimental conditions to determine if these proteins play a role in neural stem cell proliferation and cilium-mediated signal transduction in the developing brain. 

Allyzza works with Dr. Manilay examines the function and the structure of the bone marrow (BM) and spleen in sclerostin knockout (SOSTKO) mice. Sclerostin is an important regulator of bone homeostasis and, Romosozumab, is a new treatment for osteogenesis, but also blocks sclerostin. They hypothesize that sclerostin deficiency, a side effect of Romosozumab, may accelerate aging of the hematopoietic system in the BM and could lead to increases in RBC production on patients taking Romosozumab – an indication of extramedullary hematopoiesis (EMH), that of hematopoietic maturity taking place outside the BM.

Cynthia works with Dr. Manilay on hematopoietic stem cells (HSCs) influenced by specific microenvironments located within the bone marrow. Sclerostin, a protein encoded by the SOST gene, is involved in bone homeostasis and its depletion has been associated with increased bone mass which disrupts HSC development. Changes in the bone marrow may cause HSCs to migrate to different locations outside the bone marrow and contribute to age-related decline in hematopoiesis. They use SOST knock-out mice to investigate the effects of blocking sclerostin on various immune cells and flow cytometry to analyze these targeted cell types. By analyzing the consequences of sclerostin inhibition, they aim to gain insight into the potential influence of sclerostin on immune cell distribution and organ functionality.

Laura is working in Dr. McCloskey’s research laboratory.  She is culturing mouse embryonic stem cell-derived tip and non tip-containing endothelial cells and examining their differential roles in angiogenesis and responses to antiangiogenic compounds.  She is also working on deriving more tip-specific endothelial cells for our planned mouse studies and converting human umbilical vein endothelial cells into tip endothelial cells.

Jose is working in Dr. McCloskey’s cardiovascular tissue engineering laboratory. He is learning how to design and fabricate microfluidic chips for generating the perfusable vasculature. Eventually, he will examine the role of stem cell-derived smooth muscle cells and pericytes in these chips, specifically the matrix production for each cell type within the neovessels. Jose is also directing human pluripotent stem cells into pericytes and smooth muscle cells for generating perfusable vasculature in vitro. 

Nathan is working in Dr. Materna’s research laboratory on the syne1b gene in the signaling pathways of the zebrafish. It was found to be the highest differentially expressed gene in the dorsal forerunner cells that eventually control left right asymmetry. By treating zebrafish embryos with different cell signaling inhibitors and then using qPCR to see the syne1b expression rates they strive to better understand what is activating this gene that is important for left right asymmetry in these fish.