May 23 - July 1, 2016
The application for
SURF 2016 is now available.
Participants in the SURF program work in an active research
laboratory under the guidance of a faculty member with the goal of
exposing students to the challenges, excitement and satisfaction of
Selection is based on academic records and the appropriateness of
the applicant’s scientific interests. Students about to begin their
senior year of college studies are preferred, but promising juniors
and recent graduates will be considered.
Participants are provided with room, board and a $600 stipend.
Six undergraduate credit hours in biology are also available
tuition-free to all program participants. In addition, those program
participants who meet minimum requirements for admission to OU-HCOM,
including having taken the MCAT, will be offered an opportunity to
interview during the summer.
* Important note to those who may have already applied
to our medical school through AACOMAS*
You will need to use
the same email address for your SURF application as you did on your
The link above will take you to our application log
in screen. Select the New Applicant Registration link at the
bottom to set up your account. Once your account has been set
up, you can select the link to apply to SURF.
Once you are in the application portal, you will be able to complete
the application at your own pace and you may save and come back to
the form as needed. The portal will also be the place to check on
the status of your application.
SURF 2016 Faculty Mentors:
You will be able to select up to five
faculty mentors below with whom you would like to work. Please
rank them in order of preference on your application essay.
Control of toxin production and secretion in Staphylococcus
aureus and methicillin resistant S. aureus (MRSA).
Identification and characterization of small RNAs and their role in
S. aureus infection.
overall goal of my research is to develop effective and
implementable interventions that increase muscle function (e.g.,
muscle strength, motor control, fatigue-resistance) and physical
performance in older adults, and/or patients with orthopedic and
neurologic disabilities for preventative and rehabilitation
medicine. I have expertise and experience with basic and applied
science human physiology experiments as well as randomized
controlled trials (including phase 1 and 2 trials). As such, my work
is in the area of ‘translational physiology’, as it sits at the
intersection of the bench and bedside. Within this scope my
laboratory maintains programmatic efforts in two focused areas: 1)
the causes of low back pain and non-surgical strategies to alleviate
low back pain, and 2) the causes of impaired muscle function (e.g.,
muscle weakness, fatigue, unsteadiness) in the elderly and
interventional strategies to enhance muscle and physical function in
elders. The research across these foci has an overarching aim of
developing interventions that remove barriers to independent
physical mobility and ultimately reduce disability.
research is focused on delineating the molecular mechanisms
underlying the neurodegeneration that occurs in a variety of
disorders such as cerebral ischemia and Alzheimer's Disease. Zinc is
quite abundant in the brain. It is an essential trace element
required as a co-factor for several metalloproteins (e.g.,
transcription factors, metalloenzymes), but may also have signaling
functions too. Like most other things in life, too much zinc is not
good for cell survival. High levels of zinc inside cells, kill them,
so there are several cellular mechanisms for maintaining
intracellular zinc concentrations within a narrow range. One
important mechanism is zinc transporters, but very little is known
about these proteins. Elevations of intracellular zinc may
contribute to glutamate excitotoxicity (a mechanism of neuron death
in stroke) and play a role in Alzheimer's disease pathology. We are
using several different techniques to study zinc transport. These
include direct measurement of the zinc transport function in primary
cell culture and various imaging techniques using fluorescent dyes.
Karen Coschigano, Ph.D.
main research focus of my laboratory is the identification of genes,
proteins and regulatory pathways involved in the development of
diabetic nephropathy, or kidney damage, with an emphasis on the
roles of growth hormone, STAT5 and inflammation. My group uses mouse
models, cell culture and gene expression assays including real-time
RT/PCR, western blot and immunohistochemical analyses. We are also
using bioinformatics to evaluate gene expression.
Molecular basis of aging, growth hormone action, obesity and
Kevin Lee, Ph.D.
Defining the Intrinsic Heterogeneity of Adipose Tissue
The global increase in obesity is a major force driving the epidemic
of type 2 diabetes. Over the past decade it has become clear
that both obesity and adipose tissue are more complex than
originally believed. Recent research from my laboratory has found
that adipocytes are heterogeneous in nature, arise from different
developmental lineages, and have distinct phenotypic properties.
The central goal of my laboratory is to understand at a molecular
and cellular level what accounts for heterogeneity between white
adipocyte subpopulations and to study the effect these different
adipocyte subpopulations have on systemic metabolism. To this
end, we have developed novel cell and mouse models to study
adipocyte biology. Knowledge gained from this research will
aid in the identification of specific markers and the development of
therapeutic approaches to combat the metabolic disorders associated
In addition to critical thinking and experimental design,
students participating in the laboratory would learn standard
molecular biology techniques (gel electrophoresis, PCR, western
blot, immunohistochemistry), as well as cell culture, mouse
genetics, state of the art confocal microscopy, and lineage tracing
Chunmin Lo, Ph.D.
My research interest focuses on control of energy intake and
expenditure, glucose homeostasis, and lipid transport / metabolism.
I have investigated that cholecystokinin (CCK) and
apolipoprotein AIV (ApoAIV) are involved in the regulation of
insulin sensitivity, insulin secretion, and glucose homeostasis and
I have also studied the effect of ApoAIV and CCK
on the control of energy homeostasis and the neuronal activation in
I have extensive experience in the study of lipid
transport and metabolism, especially in chylomicrons and
lipoproteins, and secretion of gut peptides and incretins.
Don Miles, Ph.D.
Responses of ectothermic (“cold-blooded) organisms to climate
warming, thermal and biophysical ecology of lizards, Diversity in
mating systems and alternative mating strategies, evolution of
adaptive phenotypic plasticity as a strategy for coping with
fluctuating environments, ecological opportunity, habitat variation
and adaptive radiations.
research focuses on understanding how bacteria control the
production of disease-associated factors in response to specific
environmental conditions encountered within the human host. We are
particularly interested in Shigella dysenteriae and how this
disease causing bacterium utilizes regulatory RNA molecules to
control the production and/or activity of disease-associated
factors. Research in my laboratory utilizes many standard molecular
biology techniques including, but not limited to, DNA cloning, gene
mutation, Real-time PCR as well as western and northern blot
Allan Showalter, Ph.D.
Molecular and cellular biology approaches to the structure,
biosynthesis and function of plant cell surface proteins, including
the use of genetic mutants and transgenics in Arabidopsis.
DNA barcoding of medicinal plants to authenticate plant material and
detect potential adulterants.
We are studying the mechanisms of DNA homologous recombination, DNA
repair, and mutagenesis. By using purified proteins and model DNA
substrates, we are investigating the details of biochemical
processes of DNA repair/recombination. We are also working on the
mechanisms of repair error, which cause mutations.
of research projects in my lab is to elucidate genetic relationships
of Clic5a to genes involved in remodeling actin cytoskeleton in
mice. Clic5a is one of essential proteins to link actin bundles to
plasma membrane of stereocilia of hair cells in the inner ear.
Thus, loss of Clic5a leads to deafness in mice as well as humans.
To understand how Clic5a works with other actin cytoskeleton
modulators, I am planning to create Clic5a mutants with mutations of
these modulators for their genetic interaction. Morphologies of
stereoscilia will be examined by staining of actin with confocal
use genetic, molecular and bioinformatics analyses to identify
components of plant signaling pathways responsible for responses to
gravitropism on Earth and the space flight environment.