|2012 Summer Program IMSD Scholars. From Left: Hunter Mitchell, Anjanisse Collins, Pablo Abrante, Paola Barrios, Miguel Santiago Montana, Thomas Iglesias, Dr. Michael Gaines, Christian Trejo, Monica Izquierdo, Aleena Ali, Jisu Yu, Sara Marin and Gabrielle Petroka|
|Jisu Yu conducted research with Wei Li, Ph.D., Ophthalmology Department. Project Title: Cald1 as a New Mer-Fc Ligand in Age-Related Macular Degeneration|
I work with Dr. James Klaus in a project to characterize the bacterial community of the mudbanks in Florida Bay. I want to see how the types of soil bacteria change with depth and distance from shore. I will correlate this data with parameter of temperature, salinity, and concentration of different nutrient in the water. This information will be important to understand the impact humans have on this ecosystem.
|Juan Pablo Ruiz
For my research I am working with Adult Mesenchymal Stem Cells (MSCs). At the moment I am using Atomic Force Microscopy in order to determine the Young's Modulus of these cells. I measure both their cytoplasm and nuclear region in order to find how elastic these cells are. I am currently testing cells cultured with different concentrations of Nicotene. This preliminary data is essential for understanding how smoking might affect the Stem Cell lineages in adults.
|Betty Albo Obeso
Retinal ganglion cells (RGC) survival and neurite outgrowth are promoted by neuro-trophins, and extracellular matrix (ECM) molecules such as laminin. Degradation of laminin in the ECM of RGC in experimental animal models relevant to retinal disease contributes to RGC death. Since integrins are the major ECM receptors, we have recently identified 1 integrin, FAK, Akt, bclxL as important regulators of the integrin survival pathway in RGC, and showed that this pathway is disrupted in animal models of retinal disease. The purpose of this study is to further evaluate the role of Focal Adhesion Kinase (FAK) in RGC survival.
Ubiquitous arbuscular mycorrhizal fungi profusely produce a sticky glycoprotein called glomalin that both immobilizes carbon in soil and improves soil structure by stabilizing water-soluble aggregates. We measured the glomalin concentrations of soil within and without large-herbivore exclosures in northern and southern savannas of Krueger National Park, South Africa to see if grazing diminishes glomalin. We extracted glomalin from 1 g dried soil by autoclaving it for one hour in 50 mM sodium citrate repeatedly for five cycles, and then we measured the protein content of the extracts spectrophotometrically by Bradford protein assay. Analysis of variance showed no difference in putative glomalin concentrations within versus without exclosures. Our data suggests that interference with the Bradford protein assay by tannic and humic acids might have made our protein measurements inaccurate. Currently, we are testing the hypothesis that phenols such as tannic and humic acid interfere with protein measurements when using the Bradford protein assay.
A major focus of Dr. Athula Wikramanayake's developmental biology laboratory is to investigate the molecular basis for the evolution, specification and patterning of the animal-vegetal (AV) axis. I study the effects of drug treatments on AV axis specification and patterning using sea urchin embryos as a model system.
I work in the laboratory of Dr. Richard L. Rotundo in the department of Cell Biology and Anatomy at the University of Miami Miller School of Medicine. We study the role of Pumilio-2 (PUM2), an RNA-binding protein, in the regulation of gene expression at the neuromuscular junction. PUM2 is a translational repressor protein that has an important role during development, stem cell self-renewal, and dendritic morphogenesis. Since little is known about the regulation of PUM2 expression we are investigating whether PUM2 regulates its own expression by acting as a translational repressor of its own mRNA. Also, we are trying to understand the role of cell signaling in modulating PUM2 activity. In particular, we are investigating whether phosphorylation of PUM2 by Protein Kinase A is an important regulatory mechanism of PUM2 activity.
I am currently helping conduct two experiments. The first one that I am working on regards the epigenetic effects of cocaine on mice. The experimental mice were injected with samples of cocaine, and then by using high throughput programs we plan to try and detect any significant changes in the methylation of their DNA. The other project, which I have yet to start on, regards the epigenetics of heart disease. We will take heart tissue samples from individuals who lived unhealthy lifestyles and never developed heart disease and individuals who lived healthy lifestyles and developed heart disease and analyze the methylation of the DNA in both of these samples.
I work in the lab of Dr. Michael Norenberg, investigating the pathways involved in the ammonia-induced neurotoxicity resulting from acute liver failure (ALF) and the activation of the Na-K-Cl cotransporter (NKCC) in the Thioacetamide (TAA) rat model of ALF. As part of our work we have explored the involvement of MAPK and JNK pathways in the activation of NKCC leading to astrocyte swelling. We have also examined the effects of several drugs in attenuating brain edema in the TAA rat model. Thus far, we have had success with the NKCC inhibitor Bumetanide and the anti-diabetic drug Glibenclamide which have significantly reduced the severity of brain edema in TAA treated rats. Our studies suggest the involvement of NKCC in the development of brain edema in experimental ALF, and that targeting NKCC may represent a useful therapeutic strategy in humans with ALF. Our work on NKCC was recently published in Journal of Hepatology. In addition, we have recently found activation of another ion channel NCCAP in ammonia-treated astrocytes and that inhibition of NCCAP activation blocked ammonia-induced astrocyte swelling. We are currently in the process of preparing the manuscript for publication in Neurobiology of Disease, and the abstract relating to this work was recently accepted into the Neuroscience 2011 conference in Washington, DC. Abstract: The atp dependent non-selective cation channel mediates astrocyte swelling/brain edema in acute liver failure" A.R. Jayakumar, V. Valdes, X.Y. Tong, N. Shamaladevi, W. Gonzalez, M.D. Norenberg.
I work under the mentorship of Dr. Jean-Marie Parel. The predominant focus of my research revolves around accommodation and presbyopia. I am working on investigating and designing a method to evaluate the dynamics of accommodation in an ex vivo accommodation simulator. The emphasis of this analysis is to determine the effectiveness of a specific accommodative restorative surgery by comparing tissue pre and post operation. The preliminary data is proving this method to be an effective means to evaluate the dynamics of accommodation.
Since January of 2009, I have been working at the Miami Project to Cure Paralysis with Dr. Shyam Gajavelli and his outstanding team of researchers, who have taught me essential skills to triumph in the field biomedical research. My work at the lab focuses on the elucidation of novel strategies to alleviate chronic pain caused by spinal cord injuries using rat models of pain. During my actual lab experience, I performed many DNA mini preps, bacterial transformations, and western blots. I also transplant cells with analgesic properties into the spinal cord to stop chronic pain; hence, a great extent of my work consists on cell culturing and engineering for the production and secretion of the analgesic peptide of interest. The DNA sequence for this analgesic peptide, the Cav2.2 inhibitor-conotoxin, is introduced into a DNA construct that contains a sequence coding for a red fluorescent protein and a viral vector. The construct is then transduced to a mammal cell. I use a fluorescence microscope to make sure these cells are making the peptide as they fluoresce in red. Then, I transplant these working cells to the spinal cord of the rat via intrathecal injection. Subsequent behavioral assessments measure pain and recovery levels for each animal.
I work at the Veterans Affairs Medical Center in Dr. Paul C. Schiller's laboratory mainly with Swine Marrow-Isolated Adult Multilineage Inducible cells (SwMIAMI) cells. I have been looking at the osteogenic differentiation potential of this cell lineage. These cells are maintained and expanded in conditions that mimic the in-vivo niche microenvironment. They are incubated at certain oxygen tensions and are with a supplemented aMEM-HG medium. We analyze the expression pattern of self-renewal markers and the osteoblastic differentiation potential using various techniques. We specifically target the osteoblastic lineage gene expression markers: osterix, bone sialoprotein, collagen 1a, alkaline-phosphatase and osteocalcein. And a histochemical staining is done to detect the presence of alkaline-phosphatase activity and mineral deposition. The cells showed a higher gene expression at 7, 14 and 21 days after induction, than the non-treated cells. We observed that SwMIAMI cells have the same main pluripotency and self renewal markers expression pattern, and osteoblastic differentiation potential when compared to Human MIAMI cells.
| Mileydis Zambrana
The effect of the perfluorocarbon Oxycyte™ on brain tissue oxygenation and survival of hippocampal cells after traumatic brain injury in a rat model
Each year, about 1.5 million Americans suffer from traumatic brain injury and their fate depends on the medical care, however, there is no treatment available yet to protect and salvage neuronal tissue post TBI. In our study we tested the effect of Oxycyte™, a perfluorocarbon compound that promises to deliver oxygen to those tissues that are compromised of blood flow and especially oxygen delivery due to brain swelling, hemorrhage and other mechanisms post trauma. Ocyxyte™ has shown to in several other studies to protect neuronal tissue in a TBI model in rats and in middle cerebral artery occlusion in the rat. Currently, this compound is in phase II clinical testing for a single dose administration in Switzerland and Israel. It is not known whether a second dose would show better superior results. In our laboratory, we used the lateral fluid percussion injury model in the rat and administered two doses of this compound. The first dose of Ocyxyte™ was administered the day of the injury and the second, 24 hours later followed by a 30 min hypoxic period to simulate secondary injury as it is seen in clinical patiens. This was decided after knowing that Oxycyte™ has a half-life of around 20 hours in the blood and that around 30-40% of severe TBI patients experience a secondary hypoxic/ischemic event in this period. We monitored Oxycyte’s safety and efficacy of two doses after TBI and searched for higher oxygen levels and better histopathological outcome compared to single- dose studies.
| Julio Diaz
I study changes in brain volume due to decompressive craniectomies in brain-injured patients, with the guidance of doctors Jose Sanchez and Ross Bullock at the Miami Project to Cure Paralysis and the Department of Neurological Surgery, Miller School of Medicine, University of Miami. Decompressive craniectomy (DC) is the removal of a skull flap to stabilize intracranial pressure (ICP) after a severe traumatic brain injury (TBI). It is performed after sedation, hyperventilation, hypothermia, and cerebrospinal fluid (CSF) drainage have failed to reduce ICP levels below 20mmHg. Sustained ICP above this threshold is the primary cause of death after TBI, and results from brain swelling, hemorrhages and/or CSF accumulation. However, DC may also cause important complications, such as transcranial herniation, hydrocephalus, brain infarction and subdural collections. Understanding the mechanisms elicited by DC is crucial for optimizing the surgery and reducing complication incidence. Our current objective is to quantify the changes in brain volume that occur after DC in cases of severe TBI. For volumetric analyses, we use the software Analyze 10.0 and CT scans of decompressed (severe-TBI) patients with herniation syndrome. We expect to gain insights that may help improve the outcome of patients with severe TBI.
| Angel Gabriel Leiva
I work in the Department of Dermatology and Cutaneous Surgery at the Miller School of Medicine and my main focus of study has been on a type of skin cancer called Squamous Cell Carcinoma (SCC). In the summer 2009, I had the honor of working with Dr. Keyvan Nouri on the predictive factors that determine wound healing after cutaneous surgery of skin cancer. We examined patients that underwent the removal of skin cancer after three months from the initial date of surgery to establish which factors influenced wound healing. Patients that smoked during the three month wound healing period experienced poor recovery of the lesion. After conducting clinical research with Dr. Nouri in 2009, in January 2010 I decided to work in a lab setting with Dr. Tongyu Cao Wikramanayake. At Dr. Wikramanayake’s lab, I have conducted research on a novel immunoglobulin protein gene, Mpzl3, which plays an important role in keratinocyte differentiation; found in the skin epidermal layer. Mice carrying a missense mutation in Mpzl3 developed severe skin abnormalities. We studied the expression of Mpzl3 in human SCC by collecting skin samples carrying this cancer and tagging the protein using immunofluorescent staining. We hypothesized that Mpzl3 expression was decreased in the tumor mass of SCC, in comparison to normal human skin. After analyzing the expression of keratinocyte differentiation of the epidermis for 20 samples, we obtained significant results that Mpzl3 gene expression is decreased in the presence of SCC. We are now studying the roles of an autosomal recessive mutation of the Mpzl3 gene on mice, which develop rough coat texture and severe skin and hair abnormalities two weeks after birth. Further studies will lead to a better understanding of the Mpzl3 gene.
| Juan Torres
I work with Zhibin Chen MD, PhD at the department of Microbiology and Immunology at the University of Miami. I am studying the role of the calcium bingding protein S100A8 in the breast cancer cell line 4T1. Previous studies have shown this protein to be highly expressed in different tumors and I hypothesize that S100A8 plays an important role in cancer cell pathogenesis and its expression may be influenced by antitumor cytokines.