Conservative Finite Element Modeling of EEG and MEG on Unstructured Grids.

For interpretation of electroencephalography (EEG) and magnetoencephalography (MEG) data, multiple solutions of the respective forward problems are needed. In this paper, we assess performance of the mixed-hybrid finite element method (MHFEM) applied to EEG and MEG modeling. The method provides an approximate potential and induced currents and results in a system with a positive semi-definite matrix. The system thus can be solved with a variety of standard methods (e.g. the preconditioned conjugate gradient method). The induced currents satisfy discrete charge conservation law making the method conservative. We studied its performance on unstructured tetrahedral grids for a layered spherical head model as well as a realistic head model. We also compared its accuracy versus the conventional nodal finite element method ( P1 FEM). To avoid modeling singular sources, we completed our computations with a subtraction approach; the derived expression for the MEG response different from earlier published and involves integration of finite quantities only. We conclude that although the MHFEM is more computationally demanding than the P1 FEM, its use is justified for EEG and MEG modeling on low-resolution head models where P1 FEM loses accuracy.

Formaldehyde Induces Mesenteric Artery Relaxation via a Sensitive Transient Receptor Potential Ankyrin-1 (TRPA1) and Endothelium-Dependent Mechanism: Potential Role in Postprandial Hyperemia.

Formaldehyde (FA), the smallest aldehyde, is generated endogenously, and is widespread in the environment in foods, beverages and as a gas phase product of incomplete combustion. The main metabolite of FA, formate, was increased significantly in murine urine (∼3×) after overnight feeding. Because feeding increases mesenteric blood flow, we explored the direct effects of FA in isolated murine superior mesenteric artery (SMA). Over the concentration range of 30-1,200 µM, FA strongly and reversibly relaxed contractions of SMA induced by three different agonists: phenylephrine (PE), thromboxane A2 analog (U46,619) and high potassium (60K, 60 mM K+). Formate (to 1.5 mM) induced a modest relaxation. FA (>1,500 µM) irreversibly depressed vascular function in SMA indicating vasotoxicity. The sensitivity (EC50) but not the efficacy (% relaxation) of FA-induced relaxations was dependent on blood vessel type (SMA << aorta) and contractile agonist (PE, EC50= 52 ± 14 µM; U46,619, EC50= 514 ± 129 µM; 60K, EC50= 1,093 ± 87 µM). The most sensitive component of FA vasorelaxation was within physiological levels (30-150 µM) and was inhibited significantly by: (1) mechanically impaired endothelium; (2) Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME); (3) transient receptor potential ankyrin-1 (TRPA1) antagonist (A967079); (4) guanylyl cyclase (GC) inhibitor (ODQ); and, (5) K+ channel inhibitor (BaCl2). A similar mechanism of SMA vasorelaxation was stimulated by the TRPA1 agonist cinnamaldehyde. Positive TRPA1 immunofluorescent staining and gene-specific sequence were present in SMA but not in aorta. These data indicate FA, but not formate, robustly relaxes SMA via a sensitive TRPA1- and endothelium-dependent mechanism that is absent in aorta. Thus, as FA levels increase with feeding, FA likely contributes to the physiological reflex of post-prandial hyperemia via SMA vasodilatation.