2013-2015 MARC Cohort

Julio Flores is a third-year undergraduate student majoring in molecular and cellular biology. Following his expected graduation in May 2014, he intends to matriculate to a medical or doctoral program. Julio has been investigating protein redistribution on cells with inclusion body myopathy under Professor Kitazawa for one year before becoming involved with the MARC program. Since the summer of 2012, Julio has also been part of the Center of Excellence on Health Disparities Program at UC Merced, where he contributes to the number of educated underrepresented students competent in addressing the increasing health disparities of the Central Valley. In addition to being involved in research, Julio — president of Phi Delta Epsilon CA Lambda — expects to continue serving his community by organizing events to help the underserved people of Merced. Growing up in Mexicali, Mexico, Julio experienced the benefits of helping unprivileged populations by taking care of his ill grandparents, who, like many others in the area, did not have access to adequate health care. In 2010, Julio moved to Montclair to attend high school and eventually earn an education at UC Merced. In his spare time, Julio enjoys playing soccer for the UC Merced team as well as volunteering in the emergency department at the local hospital. Julios's research project was made possible by funding from MARC and the UPSTaRT Programs.

 

 

Julio Flores¹, Mohammed Abdelsaid Ph.D.² and Adviye Ergul M.D., Ph.D.², ¹School of Natural Sciences and ²physiology, Georgia Regents University

 

Diabetes increases the incidence of ischemic stroke as well as worsens outcomes and increases bleeding into the brain. We have previously shown that diabetic Goto-Kakizaki (GK) rats have increased yet dysfunctional angiogenesis, profuse bleeding into the brain and poor vascular repair if subjected to stroke. The effect of bleeding on endothelial cell survival and repair is unknown. Here, we test the hypothesis that iron exposure reduces brain microvascular endothelial cell (BMVEC) viability and plasticity after ischemia/reperfusion in diabetes. To test this hypothesis, BMVECs isolated from Wistar (non-diabetic) and GK (diabetic) rats were treated with 0.1 mM iron (III) sulfate, incubated six hours in hypoxia (0.1 percent O2), and reoxygenated overnight. The cells were subjected to cell proliferation, migration and tube formation assays. GK BMVECs showed increased cell proliferation, migration and tube length under normoxia. Hypoxia reduced all three measures of angiogenesis for GK BMVECs. Additionally, treatment with iron further reduced the migration and tube length of GK BMVECs exposed to hypoxia while it did not have an effect on control cells. These results suggest that iron has a deleterious effect on survival and angiogenic properties of diabetic BMVECs. More work is needed to investigate the exact mechanism of iron-induced impairments but our work identifies iron chelation as a novel therapy to improve recovery after stroke.

Debby Lee is a junior majoring in human biology. She will be the first of her five siblings to graduate college. She recently competed nationwide and won a fellowship awarded by the American Physiological Society jumpstarting her first summer (2013) research experience. She is currently collaborating with Professor Rudy Ortiz in analyzing thyroid hormone activities in natural-fasting and metabolically active adult male northern elephant seals. This research contributes to the understanding of evolutionary development and thyroid hormone-mediated cellular signaling mechanisms in a lipid-based metabolism. Aside from research, she is a part of Lift While You Lead where she mentors high school students to promote, enlighten and empower the well being of women. Debby spends her Friday nights volunteering in the emergency room of a local hospital. She is also a part of the Hmong Student Association of UC Merced and affiliated with an organization called Project Prevention where she does outreaching about health disparities in the Hmong community. She is determined to obtain her MD/PhD and come back to the Central Valley to serve the underserved. Debby's research project was made possible by funding from MARC and the American Physiological Society Scholars programs.​

 

 

Debby Lee¹, Bridget Martinez¹, Daniel E. Crocker² and Rudy M. Ortiz¹; ¹Cellular and Molecular Biology Unit, University of California, Merced; ²Department of Biology, Sonoma State

 

During food deprivation, deiodinase type 1(DI1) is increased to raise the mono-deiodination of the inner ring to promote the production of reverse T3, which suppresses cellular metabolism to protect the organism from energetic burdens imposed during periods of reduced energy intake. Thyroid hormones (TH) thyroxine (T4) and triiodthyronine (T3) promote basal metabolism in mammals but its levels are typically suppressed with prolonged fasting. TH plasma concentrations were measured in male northern elephant seals to better understand DI1. To address our hypothesis that natural fasting in elephant seals stimulate an increase in DI1, we measured plasma concentrations of rT3, free T3 (fT3), free T4 (fT4), total T3 (tT3), and total T4 (tT4) in male elephant seals (n=10) over 10 weeks of fasting. Fasting did not alter the concentrations of plasma thyroid hormone rT3, fT3, tT4. However fT4 increased (0.25± 0.03ng/dL to 0.78 ± 0.08ng/dL) suggesting that there is an increased potential for TH-mediated cellular effects. Conversely, tT3 decreased (63± 5 ng/mL to 50 ± 4ng/mL) between early and late fasting suggesting that DI2 or DI3 may be contributing to the dynamic changes in TH metabolism. Overall these findings reveal unconventional mechanisms of TH activity, regulation and metabolism associated with prolonged food deprivation in a fasting-adapted mammal.

Adriana Lopez is majoring in human biology and is currently working in the lab of Dr. Rudy Ortiz. She is studying the effects of oxidative stress in the liver of insulin resistant rats. She plans to attend graduate school and receive a Ph.D. She is the first in her family to graduate from college. She hopes to be an example, not only to her younger siblings, but to those whom are first generation college students. On her free time, Adriana enjoys reading and exercising.

 

 

Adriana Lopez¹, Antonio De Maio² Ph.D., ¹School of Natural Sciences, University of California, Merced; ²Department of Surgery, University of California, San Diego, La Jolla, Ca

 

Heat shock proteins (hsp) are chaperones that participate in protein folding as well as the repair of damage after stressful conditions. Hsp are also present in the extracellular milieu where they signal other cells to avoid the propagation of the stress. In particular, Hsp70 has been shown to increase survival in critically ill patients and is essential to relieve cell stress. Past research has shown that hsp70 is released in vesicles or in membrane-bound form (Vega et al. 2008), although the signaling mechanism is unknown. To induce stress in HepG2 cells (human liver cells), cells are exposed to a 43˚C temperature for 1.5 hours, which has been shown to induce increased levels of Hsp70 in these cells. In order to better understand the signaling mechanism, we isolated extracellular vesicles from either control or heat shocked cells, and added to non-stressed HepG2 cells. These cells were analyzed for Hsp70 expression and compared to non-treated cells and cells treated with recombinant Hsp70 to evaluate whether the membrane-bound Hsp70 could induce a stress response. These studies will provide us with a better understanding of the Hsp70 signaling mechanism.

Emmanuel Villanueva is a third-year undergraduate student and a psychology major. He expects to graduate in the Spring 2015. However, before Emmanuel graduates, he will delve into researching the way various emotions influence the human immune system. Emmanuel has a special interest in the elderly population and hopes to gear his research toward this population, which he feels is often neglected. As a UC LEADS scholar, Emmanuel combines immunology, neuroscience and psychology to contribute to the emerging field of psychoneuroimmunology (PNI). If it seems as though Emmanuel is nowhere to be found because he is not volunteering at a senior home, working out at the gym or on the soccer field, then he is most likely nourishing himself well at his local cafeteria. Emmanuel's research project was made possible by funding from MARC and the UC LEADS programs.

 

 

Emmanuel Villanueva and Professor Jitske Tiemensma, School of Social Sciences, Humanities and Arts

 

There is growing and compelling evidence of emotions having the potential to significantly influence the immune system. However, there appear to be inconsistencies in the literature with some studies showing an effect of positive or negative mood states on immune markers while other studies do not observe any effect of emotions on the immune system. Moreover, the specific pathways through which emotions might influence the immune system remain unclear. The present structured literature review was performed to highlight the findings of previous studies with regard to the relation between emotions and the immune system, as well as to explore the possible pathways through which emotions might influence immune functioning. Databases Pubmed, EBSCO, and Science Direct were surveyed using specific keywords in order to carry out the present structured literature review. This review shows the importance of emotion regulation and underscores its elusive pathway. Evidence in some of the literature highlights the benefits positive emotions can have on an individual’s immune responsiveness; whereas other studies show incongruent results. There is inclusively evidence in animal research for a reverse relation between cytokines and the immune system. Further research is needed to determine the existence of a single or multiple neurochemical pathway(s) that give(s) rise to the interaction between emotion regulation and the immune system.

Major: Biological Sciences  Home City: Alliance, OH Contact: chawkins2@ucmerced.edu Faculty Mentor: Professor Masashi Kitazawa

Charlesice Hawkins is pursing bachelor's degrees in both cognitive science and human biology. She expects to graduate in Spring 2015 and continue on to obtain her Ph.D. in neuroscience. She has had experience working in a computational cognitive neuroscience lab and is involved in a molecular biology lab. She intends to examine the molecular mechanisms of different neurological disorders. In her spare time, she enjoys quad skating as a roller derby referee. Charlesice's research project was made possible by funding from the UC LEADS Program. 

 

 

Charlesice C. Hawkins, Carlos Rodriguez-Ortiz, Ph.D., Ruben Rodriguez, Professor Rudy Ortiz and Professor Masashi Kitazawa, School of Natural Sciences

 

Type II diabetes mellitus (T2DM) is a fast growing disease, as more than 20 million people are affected in the U.S. It occurs when the body develops a resistance against insulin and does not properly utilize glucose. Insulin resistance and other comorbidities of T2DM such as hypertension, inflammation and increased oxidative stress may damage blood vessels in the brain. Approximately 60-70 percent of T2DM patients develop neuropathic conditions, and it has also been listed as a risk factor for Alzheimer’s disease (AD). However, the exact molecular link between T2DM and AD has not been fully elucidated. To investigate this connection, brains from a Cholecystokinin-1 (CCK1) receptor mutant rat model for type II diabetes and obesity were examined using biochemical and histological techniques in search of features of AD-like neuropathology. This rat model develops a metabolic syndrome characteristic of T2DM in an age-dependent manner. In the present study, oxidative stress, amyloid-precursor protein (APP), inflammation and synaptic markers were examined. There were slight increases in inflammation and APP in the brain of T2DM rat model, suggesting that T2DM phenotypes may trigger AD-like neuropathology at later ages. In perspective of such trends, longitudinal examinations of brain pathology of this model will further provide insights into the molecular link between T2DM and AD.