This T32 application seeks support for a Graduate Research in Immunology Program (GRIP) at the University of Texas Health Science Center San Antonio (UTHealthSA). GRIP will train three PhD, DDS/PhD and MD/PhD students per year for successful careers in academia, industry or government.

Discretionary control of renal Na+ transport matches renal Na+ excretion with dietary Na+ intake. Because Na+excretion can influence blood pressure, disordered renal Na+ transport in many instances causes abnormalblood pressure. Moreover, as we know from the actions of most diuretics and many tubulopathies interdictionof normal renal Na+ transport changes blood pressure. Renal sodium excretion is fine-tuned in response tohormonal signaling in the aldosterone-sensitive distal nephron (ASDN).

Aberrant intracellular calcium ([Ca2+]i) homeostasis has been implicated in cardiovascular diseases (CVD) which contributes to endothelial dysfunction. Ca2+ acts as a second messenger and is known to regulate several cell functions. Despite the available evidence of a link between Ca2+ signaling and endothelial dysfunction, mechanisms underlying the development of vascular disease remain incompletely understood. Besides Ca2+, reactive oxygen species have also been implicated in endothelial cell (EC) dysfunction.

Fungal infections constitute a major threat to an ever expanding spectrum of immune- and medically-compromised patients. The opportunistic pathogenic fungi Candida spp., Aspergillus spp. and Cryptococcus neoformans are among the most common etiologic agents of mycoses; but infections caused by other yeasts and moulds are on the rise as advances in modern medicine prolongs lives resulting in increasingly susceptible and vulnerable patients.

Fellowship for Colwyn Headley.