Postdoctoral scholar
Division of Research

Research interests:

Traumatic brain injury (TBI) is the leading cause of death and long-term disability in industrialized countries for people under the age of 45.  TBI is a complex time-dependent series of pathological events, including brain swelling, decreased cerebral blood flow and ischemia, leading to brain damage accompanied by cognitive and motor deficit.  The blood-brain barrier (BBB), specifically the brain vascular endothelium, is a crucial protective barrier against cerebral edema and ensuing events leading to brain damage.  I am interested in the mechanisms of cerebral edema formation during TBI, and the roles of deleterious compounds that accumulate in the brain following TBI on BBB function (e.g. glutamate and inflammatory cytokines).  My goals are to 1) define the effects of glutamate and inflammatory cytokines on BBB function in the context of TBI; 2) identify signaling molecules and pathways that mediate BBB dysfunction during TBI; and 3) propose strategies for therapeutic intervention based on rational design to prevent cerebral edema formation and thereby improve survival and long-term recovery following TBI.

Ortiz-Acevedo A, Rigor RR, Maldonado HM, Cala PM. Activation of Na+/H+ and K+/H+ exchange by calyculin A in Amphiuma tridactylum red blood cells: implications for the control of volume-induced ion flux activity. Am J Physiol Cell Physiol. 2008 Nov;295(5):C1316-25. Epub 2008 Sep 17.

Pedersen SF, King SA, Nygaard EB, Rigor RR, Cala PM. NHE1 inhibition by amiloride- and benzoylguanidine-type compounds. Inhibitor binding loci deduced from chimeras of NHE1 homologues with endogenous differences in inhibitor sensitivity. J Biol Chem. 2007 Jul 6;282(27):19716-27. Epub 2007 May 10.

Pedersen SF, King SA, Rigor RR, Zhuang Z, Warren JM, Cala PM. Molecular cloning of NHE1 from winter flounder RBCs: activation by osmotic shrinkage, cAMP, and calyculin A. Am J Physiol Cell Physiol. 2003 Jun;284(6):C1561-76. Epub 2003 Jan 29.