Bonnie Blazer-Yost

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https://hdl.handle.net/1805/14068

Dr. Bonnie Blazer-Yost’s primary interest is in epithelial cell biology as it relates to ion transport. Recently she has been investigating treatments for polycystic kidney disease. These studies resulted from a serendipitous finding regarding the potential use of Pioglitazone, a commonly used diabetes drug, in polycystic kidney disease patients. This research has progressed from tissue culture, through preclinical animal models and is currently funded as an initial clinical trial in polycystic kidney disease patients.

Dr. Blazer-Yost and her team are also researching potential treatments for hydrocephalus or “water on the brain.” Hydrocephalus may develop as a consequence of trauma, infection, tumors, intracranial hemorrhage or as a result of a congenital birth defect. Elderly patients may suffer from a poorly understood and underdiagnosed form called “normal pressure hydrocephalus,” characterized by urinary incontinence, gait instability, and dementia. Post-traumatic hydrocephalus occurs as the result of traumatic brain injury. Regardless of the form, brain surgery is currently the only effective long-term treatment. Dr. Blazer-Yost and her collaborators recently obtained a three-year Department of Defense grant to conduct translational studies in animal models with a goal of developing a drug treatment for hydrocephalus.

Dr. Blazer-Yost’s work to treat polycystic kidney disease and hydrocephalus is another example of how IUPUI faculty are TRANSLATING RESEARCH INTO PRACTICE.

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Browsing Bonnie Blazer-Yost by Author "Baldwin, Kieron"

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    Time-dependent stimulation by aldosterone of blocker-sensitive ENaCs in A6 epithelia
    (1998-04) Helman, Sandy I.; Liu, Xuehong; Baldwin, Kieron; Blazer-Yost, Bonnie; Els, Willem J.
    To study and define the early time-dependent response (< or = 6 h) of blocker-sensitive epithelial Na+ channels (ENaCs) to stimulation of Na+ transport by aldosterone, we used a new modified method of blocker-induced noise analysis to determine the changes of single-channel current (iNa) channel open probability (Po), and channel density (NT) under transient conditions of transport as measured by macroscopic short-circuit currents (Isc). In three groups of experiments in which spontaneous baseline rates of transport averaged 1.06, 5.40, and 15.14 microA/cm2, stimulation of transport occurred due to increase of blocker-sensitive channels. NT varied linearly over a 70-fold range of transport (0.5-35 microA/cm2). Relatively small and slow time-dependent but aldosterone-independent decreases of Po occurred during control (10-20% over 2 h) and aldosterone experimental periods (10-30% over 6 h). When the Po of control and aldosterone-treated tissues was examined over the 70-fold extended range of Na+ transport, Po was observed to vary inversely with Isc, falling from approximately 0.5 to approximately 0.15 at the highest rates of Na+ transport or approximately 25% per 3-fold increase of transport. Because decreases of Po from any source cannot explain stimulation of transport by aldosterone, it is concluded that the early time-dependent stimulation of Na+ transport in A6 epithelia is due exclusively to increase of apical membrane NT.