Research
I was born in Valencia, Spain in 1985. Four years ago
I graduated with distinction at High School and I joined the
Medical School at the University of Valencia. Nowadays, I am
pursuing my forth year of Medical Studies.
For the past years, I have attended some basic science
courses at places such as Harvard University, in Boston (MA)
or Phillips Exeter Academy, in Exeter (NH).
Recently, I have been working at the Ocular Surface Center (Miami, FL) under the instruction of Prof.
Dr. Scheffer C. G. Tseng, in the “Isolation and expansion
of human corneal endothelial cells”. Currently, and supported by
Prof. Dr. Jose Viña (University of Valencia), we are
developing a new method for isolating and expanding these
cells in vitro.
At the
present time, I am Member of the Research Commission at the Medical School, in the University of Valencia.
I am also a Founding Member of Universitas
Foundation, a non-lucrative Foundation created by students
from the University of Valencia, which promotes scientific
and social events, like meetings, lectures or debates.
Research
Background
The
corneal endothelium is a single layer of cells at the
posterior surface of the cornea facing the anterior chamber.
The endothelium has two major functions: it provides a
significant pathway for corneal nutrient uptake and waste
removal via simple and facilitated diffusion and secondary
active transport mechanisms, and it generates fluid
secretion, through the actions of ion transport mechanisms,
that counterbalances a continuous leak of fluid into the
corneal stroma (Bonnano JA 2003). It
is generally believed that the entire population of human corneal
endothelial cells (HCEC) declines with age (Hanna
C et al. 1978), and that dysfunction and a low
density of HCEC represent a major cause of sight-threatening
bullous keratopathy (McCartney et al 1987).
Because
it has been long and widely held that HCEC possess a limited
proliferative capacity in vivo (Laing et al. 1984),
treatments toward bullous keratopathy caused by corneal
endothelial dysfunction resort to transplantation of the
corneal endothelium via penetrating keratoplasty (Padmanabhan
P et al. 2001). Several mechanisms have been advanced to
explain why HCEC have a limited proliferative capacity in
vivo. They include the relative lack of positive mitogenic
stimulation, the potential negative regulation by
transforming growth factor-b2 (TGF-b2) in aqueous humor, and
maintenance of the endothelial monolayer in a
contact-inhibited state
(Joyce
2003)
.
Exogenous
transforming growth factor-beta (TGF-b) and TGF-b in aqueous
humor suppress S-phase entry in cultured endothelial cells,
suggesting that this cytokine could inhibit proliferation in
vivo. In addition, cell–cell contact appears to inhibit
endothelial cell proliferation during corneal development
and to help maintain the mature endothelial monolayer in a
non-proliferative state, in part, via the activity of
p27kip1, a known G1-phase inhibitor
(Joyce
2003)
.
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