Abstract: The invention provides compounds that inhibit epoxide hydrolase in therapeutic applications for treating hypertension. A preferred class of compounds for practicing the invention have the structure shown by Formula I wherein Z is oxygen or sulfur, W is carbon phosphorous or sulfur, X and Y is each independently nitrogen, oxygen, or sulfur, and X can further be carbon, at least one of R1—R4 is hydrogen, R2 is hydrogen when X is nitrogen but is not present when X is sulfur or oxygen, R4 is hydrogen when Y is nitrogen but is not present when Y is sulfur or oxygen, R1 and R3 is each independently C1-C20 substituted or unsubstituted alkyl, cycloalkyl, aryl, acyl, or heterocyclic.

Abstract: The present disclosure relates to RFX4_v3 protein and nucleic acids encoding the RFX4_v3 protein. The present disclosure provides non-human transgenic animals with altered RFX4_v3 genes, and provides assays for the detection of RFX4_v3 and RFX4_v3 polymorphisms associated with disease states. The present disclosure additionally provides methods of determining a subjects' risk of developing congenital hydrocephalus, and treating or inhibiting its development.

Abstract: Epoxyeicosatrienoic acids (EETs) are products of cytocrome P450 epoxygenases that have vasodilatory properties similar to endotheilum-derived hyperpolarizing factor (EDHF). The cytochrome P450 isoform CYP2J2 was cloned and identified as a source of EETs in human endothelial cells. Physiological concentrations of EETs or overexpression of CYP2J2 decreased cytolcine-induced endothelial cell adhesion molecule expression and prevented subsequent leukocyte adhesion to the vascular wall by a mechanism involving inhibition of transcription factor NF-?B and I?B kinase (IKK). The inhibitory effects of EETs were independent of their membrane hyporpolarizing effects suggesting that these molecules play an important non-vasodilatory role in vascular inflammation.