2013-2014 Graduate Fellows
Kilan Ashad-Bishop
I am a second year graduate student in the Sylvia and David Fuente Graduate Program for Cancer Biology. I work in the laboratory of Dr. Marc Lippman, studying molecular mechanisms underlying breast cancer metastasis. I am specifically interested in a new direction in the lab which involves host contributions to metastasis, specifically the accumulation of myeloid-derived suppressor cells in the tumor microenvironment.

Winter Beckles
As a member of the Uy lab on the Coral Gables campus, my research focuses on the relationship between ecology and evolution. I seek to understand how environmental changes brought on by urban development can influence natural selection among organisms, thereby shaping the biotic landscape of the future. To assess the evolutionary responses of organisms to the pressures of urbanization, I will study the morphological and behavioral differences that exist between the members of a species who have established populations in urban, suburban, and natural environments. Using an invasive species for this study will be a key factor, because it will allow me to compare the unique traits found among populations living in varying degrees of urbanization to the typical morphologies and behaviors found within populations living in their native environments. By identifying the traits that are most unique to populations living in urban environments, I can potentially determine the urban factors that are most influential to the development of these organisms, thereby increasing our understanding of how the environment influences evolution.

Yvonne Puplampu-Dove
I am currently in the lab of Eli Gilboa, PhD in the Department of Microbiology and Immunology. Our lab focuses on cancer immunotherapy, a rapidly developing field aimed at stimulating the immune system to eliminate tumor cells. Currently, most pharmacological agents used in cancer immunotherapy elicit undesirable effects reflecting their broad range of action on many cellular targets. Targeting the drugs to the desired cells in vivo would, therefore, reduce drug toxicity. Recent studies have shown that oligonucleotide aptamers are an excellent platform for drug targeting to specific cells. Aptamers are short single-stranded nucleic acid molecules, or oligonucleotides, that bind to specific targets with exquisite specificity and avidity comparable to or exceeding that of antibodies. My project involves the use of aptamer-siRNA conjugates specifically targeting components of the TGFβ signaling pathway in CD8+ T cells, to counteract immune suppression by tumor cells.

Andre Jordan
I am a first year graduate student. I have previous undergraduate research experience in the development of gene therapy to treat neuropathic pain in spinal cord injury patients. I have also been involved in drug development research aimed at assessing the binding affinity of potential cancer therapeutic agents to quadruplex DNA. Although I have not officially joined a department of study, I have general interest in cancer research and will most likely be joining the Cancer Biology Department. I am interested in the development and implementation of better diagnostics and therapeutics in the treatment of cancer.

Nelson Salgado
I'm a first year graduate student at the Miller School of Medicine. There are many areas of biomedical research that have drawn my attention over the years I spent in undergrad. This is actually one of the reasons I decided to join UM's PIBS program; they offer many research options. I am currently in the process of completing my lab rotations, which I have chosen in very different fields. Since starting at UM I have been exposed to research in nano-biotechnology, cancer, and diabetes. It has been a great opportunity to not only broaden my horizons, but to also help narrow my choice of which specific department to join. This coming semester I will be taking courses from the Biochemistry and Molecular Biology department.

2010-2011 Graduate Fellows
Natalia Borrego
I am interested in the link between intelligence and sociality, specifically predictions of social intelligence theory. My dissertation research focuses on kinship, cooperation, and social intelligence in Panthera. My research has two components: a field study in Africa and a series of local captive studies. For the captive study, I am investigating the cooperative problem solving abilities of African lions (Panthera leo),Tigers (Panthera tigris), and Leopards (Panthera pardus), which exhibit varying degrees of sociality. For the field study, I will be examining cooperative hunting and kinship in African lions. I am currently working with Lion Country Safari and conducting cooperative problem solving trials using their captive pride of lions.

Janice Dias
My research focus involves the application of Atomic Force Microscopy (AFM) to characterize the biomechanical properties of the cornea. Corneal biomechanics is an important ophthalmic field for designing, developing and improving diagnostic and treatment methods for corneal diseases, ranging from glaucoma to post-LASIK ectasia. However, corneal tissue mechanics is not fully understood, creating a subsequent impediment to the advancement of more improved and effective corneal refractive surgical procedures. Therefore, a need exists for the development of methodologies capable of accurately assessing corneal tissue responses in a non-destructive and reliable manner. My research strives to extend of the capability of the AFM technology to probe corneal mechanical responses and structure at the nanoscale and macroscale levels. Research projects I am currently involved with includes building custom atomic force microscopes capable of elastic and viscoelastic characterization and developing AFM techniques, such as tip modification, that will allow the characterization of corneal tissues at several length scales.
Michael Gonzalez
Development and application of Exome Sequencing and Bioinformatics Analytical strategies to identify disease causing mutations in high penetrant Mendelian disorders such as CMT Next-generation sequencing (NGS) technology is revolutionizing biomedical research. Due to the high costs of whole-genome sequencing, it is not pratical for most genomic studies. As of late, exome sequencing has surfaced as a cost effective application of NGS. Applying exome sequencing, NGS of the protein coding regions of the human genome, to monogenic Mendelian diseases has become increasingly popular. Due to the fact that Mendelian diseases have a highly penetrant phenotype, segregational analysis via targeted exome capture is extremely powerful. However, a technique to effectively and efficiently use this NGS tool for identifying disease variants is not available. Focusing on a highly penetrant disorder and only coding regions is important to reduce the amount of data produced by NGS and allowing meaningful results to be observed. Using Charcot-Marie-Tooth (CMT) disease, a Mendelian disease, I am proposing the application of exome sequencing in combination with various bioinformatics approaches to identify a subset of disease causing variants for CMT. By cross examining individuals from 100 unrelated families it will become clearer which mutations are shared amongst affected individuals. Next, the application of PolyPhen to predict nonsynonmous, missense, and short insertions/deletions in addition to GERP and PhastCons conservation scores will be used to define common “disease variants”. Through this study, development of molecular and bioinformatics analytical strategies will be defined that can be applied for genetic testing of Mendelian diseases.
Darrell Hardin
My research involves figuring out the mechanism in which CTLA-4 interacts with MDSC cells via CD80/86. I will be performing a Knock Down on the CTLA-4 protein in a mouse model and recording the effects that it has on the CD80/86 levels. I will be using the CD11b and Gr1 markers for this experiment as well.
Ashley Melchior
No Description Available
Monique Courtenay
I am a second year graduate student under Dr. William Scott in the department of Human Genetics and Genomics. My lab conducts research in the field of Computational Genomics, with a primary focus on genetic epidemiology. My current research involves deciphering the genetic associations between age-related macular degeneration and environmental factors such as smoking and estrogen exposure from hormone replacement therapy and birth control pills.
Santas Rosario
I recently joined Dr. Xiang-xi M. Xu's laboratory in the department of Medicine. Our laboratory investigates the molecular mechanims of epithelial differentiation during embryogenesis and the transformations that occur in epithelial cells that cause cancer, primarily ovarian cancer. Generally, nuclear morphology is used clinically to determine the degree of malignancy of a tumor and is characterized by a deformed nucleus and aneuploidy. A link has been established not only between nuclear morphology and oncogenic signalling, but also between aneuploidy and malignancy. Further, the nuclear lamina is part of the nuclear envelope and is comprised of a network of intermediate filament proteins called lamins. Mutations in genes encoding lamins and their protein product cause laminopathies and nuclear envelopathies. Interestingly, researchers studying the aforementioned diseases have shown an association between the nuclear envelope and sevaral pathways important in cancer. Therefore, I am exploring the role of nuclear lamina in cellular signaling in ovarian and breast cancer cells.
Nicole Salazar
I am investigating the role of CXCR7 in growth promotion in breast cancer models. CXCR7 has been found to be highly expressed in human breast, lung, and prostate cancers in a stage-and grade specific pattern. Unlike other CXCRs, ligand binding of CXCR7 does not activate typical GPCR response. The preliminary data generated for this project suggest that expression of CXCR7 does not correlate with aggressiveness of breast cancer cell lines, but down-modulation of CXCR7 in MCF-7 breast cancer cells reduces cell proliferation and cell cycle phase progression. CXCR7 depleted MCF-7 cells showed cell cycle arrest and several proliferation-associated proteins were down regulated, while some several S-phase inhibitory proteins, were increased. Understanding the mechanism by which CXCR7 affects proliferation can provide a powerful tool for improved design of agents to attack cancers with high expression of this protein.
Alexandria Scott
No Description Available
2009-2010 Graduate Fellows
Kahlilia Morris
I am in the Neuroscience PhD program and work in the lab of Dr. Perez-Pinzon in the Cerebral Vascular Disease Research Center. Mitochondrial dysfunction is a major source of neuronal injury after cardiac arrest or stroke. My research uses both in vitro and in vivo models to investigate cellular and molecular pathways by which mitochondria may be protected after ischemic injury. Specifically, my research investigates the role of mitochondria localized sirtuin deacetylases in regulating mitochondrial metabolism, oxidative stress, and apoptosis.
Alexis Sloan
I currently work in the laboratory of Christian Faul, PhD in the department of Cell Biology and Anatomy. Our work focuses on the blood filtration barrier function of the kidney. This barrier is comprised of a specialized cell type within the glomerular structure of the kidney, the podocyte. Proper filtration of the blood is dependant on the highly ordered structure of the podocyte, which ensures its function. We study the loss of proper structure and function of these podocytes that results in loss of blood proteins in to the urine or proteinuria. Currently, we are looking into the calcium -mediated effects of the transcription factor NFAT and its downstream targets and their effects on podocyte structure and function. We hope to establish novel target genes for manipulation that may result in rescue of structure and function of the podocyte in disease settings.
2008-2009 Graduate Fellows
Melvys Valledor
In August, 2012 Melvys' project was featured on the cover of "IUBMB Life" journal. Melvys was selected to attend the Lindau Nobel Laureate Meeting in Germany in 2011. Nobel Laureates in Physiology or Medicine and 550 students and postdocs from around the world met from June 26 - July 1, 2011 at Lindau (Germany) to exchange ideas, discuss projects and build international networks. Says Melvys "My long-term goal is to adapt fundamental mechanisms of molecular cell biology to study and cure human diseases and develop a career as an independent research investigator. Currently, I am examining the hypothesis that Recombineering is host-specific and that viral recombinases co-evolved with host proteins. To test this hypothesis I am studying the interaction of a human viral recombinase and a bacteriophage recombinase with their respective host proteins and am working to reconstitute both viral recombinases in human cells and bacterial cells to evaluate host-specific effects on recombination efficiency. I predict that the human viral recombinase, having co-evolved with human cells, will be specific to human cells and will not function well in E. coli. In contrast, the bacteriophage system will be specific to E. coli and not function well in human cells. This innovative project integrates state-of-the-art knowledge of homologous recombination with recent advances in human stem cell biology. Recombination in human stem cells with high efficiency and specificity will transform science and medicine. With sharper tools, genome engineering will realize its potential to cure genetic diseases, create human disease models, and achieve the promises of the biotechnology revolution."
Maitee Urbieta
Working on the mechanisms of migration and recruitment of innate and adaptive immune system cells to the transplant site, these cells are at large responsible for rejecting the transplanted graft, so by manipulating/interfering with their migration to the site and their activation once at the site, we can hopefully promote the engraftment of the transplanted cornea, or at least delay the onset of rejection.

Louis Gonzalez
The NOD.SCID γc-/- humanized mouse model NOD.SCID γc-/- (NSG) mice lack functional adaptive immunity due to two key genomic changes: The first is the SCID mutation which is characterized by a non-functional pkrdc gene, resulting in the inability to repair double stranded DNA breaks. This leads to a block in both B and T cell development, since both B cell receptors (BCR) and T cell receptors (TCR) must undergo germ line rearrangement during lymphopoiesis in order to fully mature. The IL-2 receptor common gamma chain deletion (γc-/-) prevents all members of the IL-2 family from signaling. IL-2 family members provide critical survival and developmental signals to B, T and NK cells; a lack of proper signaling therefore, leads to a severe impairment in their ability to survive. In addition, the NOD background is characterized by a variety of unique polymorphisms, the most significant for this model being the sirpa polymorphism. The NOD sirpa polymorphism has been shown to allow greater interaction between mouse cells and human cells, leading to a greater degree of xenopermissiveness when compared to other inbred lab strains of mice. In order to generate a humanized mouse we have chosen to use hematopoietic stem cells (HSC) that have been harvested from human fetal liver tissue between 12 and 20 weeks of gestation. This gestational period, in human development, is before the final wave of hematopoietic progenitors leaves the liver to take up residence in the bone marrow, the adult source of blood cells. HSC are purified on the basis of CD34 expression yielding a population of cells highly enriched primitive progenitors as well as some committed progenitors. HSC are then transplanted intrahepatically into irradiated NSG pups where they go on to seed the bone marrow and give rise to all the members of the hematopoietic lineage. Any cells of the adaptive immune system isolated from the mouse are of human origin whereas myeloid derived cells are human/mouse chimeras. Upon weaning, the pups are screened via flow cytometry and evaluated for human/mouse chimerism on the basis of human CD45 and mouse CD45 expression in the peripheral blood. We use humanized NOD.SCID γc-/- mice as a model to test our cell secreted heat shock protein gp96 based HIV vaccine. Gp96 is an ER-resident, ubiquitously expressed cellular chaperone protein. The Podack lab has reengineered the protein, replacing its KDEL ER-retention sequence with an IgG tail. The, now secreted, chaperone can be readily detected outside the cell along with its associated peptides. Extracellular gp96 serves as a danger signal to antigen presenting cells (APCs), binding toll-like receptors 2/4 and CD91, maturing and activating them. Activated APCs cross-present antigen and are capable of activating CD8 T cells that recognize cognate antigen, in addition to secreting IL-12 and activating NK cells. By transfecting into vaccine cells plasmids encoding for HIV proteins (gag, env and ReTaNef) we are able to generate an HIV-specific CD8 T cell response. What remains to be seen, however, is how vaccination is able to prevent or alter the kinetics of HIV infection and disease progression.

Dawn Seales
I am a student of the Cancer Biology Program, currently working in the lab of Dr. Eli Gilboa. The main focus of the lab is to find novel therapeutic approaches to augmenting anti-tumoral immunity. There are several mechanisms employed by a developing tumor to subvert the immune system. Although initially tumor-specific T cells may be generated and become activated, they later on become anergized when they reach the microenvironment. My project specifically involves targeted delivery of siRNA to activated T helper cells to knock down inhibitors of activation and mediators of anergy. Co-stimulation of T cells by ligation of specific TNF superfamily members can then enhance their activation, proliferation and survival, leading to a longer-lasting and effective anti-tumor response.

Albert Hayward
Molecular signaling is a key component of many developmental processes. However, considering the vast array of developmental processes, there are a relatively small number of signaling pathways involved. I am interested in how cell competence allows these signaling pathways to be used in different contexts of neural development.