The goal of this surgical protocol is to expose the facial nerve, which innervates the facial musculature, at its exit from the stylomastoid foramen and either cut or crush it to induce peripheral nerve injury. Advantages of this surgery are its simplicity, high reproducibility, and the lack of effect on vital functions or mobility from the subsequent facial paralysis, thus resulting in a relatively mild surgical outcome compared to other nerve injury models. A major advantage of using a cranial nerve injury model is that the motoneurons reside in a relatively homogenous population in the facial motor nucleus in the pons, simplifying the study of the motoneuron cell bodies. Because of the symmetrical nature of facial nerve innervation and the lack of crosstalk between the facial motor nuclei, the operation can be performed unilaterally with the unaxotomized side serving as a paired internal control. A variety of analyses can be performed postoperatively to assess the physiologic response, details of which are beyond the scope of this article. For example, recovery of muscle function can serve as a behavioral marker for reinnervation, or the motoneurons can be quantified to measure cell survival. Additionally, the motoneurons can be accurately captured using laser microdissection for molecular analysis. Because the facial nerve axotomy is minimally invasive and well tolerated, it can be utilized on a wide variety of genetically modified mice. Also, this surgery model can be used to analyze the effectiveness of peripheral nerve injury treatments. Facial nerve injury provides a means for investigating not only motoneurons, but also the responses of the central and peripheral glial microenvironment, immune system, and target musculature. The facial nerve injury model is a widely accepted peripheral nerve injury model that serves as a powerful tool for studying nerve injury and regeneration. Video LinkThe video component of this article can be found at

The oxidation of [Co(edta)](2-) by [IrCl(6)](2-) proceeds by both inner-sphere and outer-sphere electron-transfer pathways. In the presence of added [Co(en)(3)](3+), the outer-sphere pathway is enhanced. When optically active [Co(en)(3)](3+) is used, the [Co(edta)](-) formed is optically active, reflecting a 1.5% DeltaLambda selectivity. It is proposed that the selectivity arises from preferential formation and reactivity of the DeltaLambda ion pair, {[Co(edta)](2-),[Co(en)(3)](3+)}. Direct reaction of [Co(edta)](-) with [Co(en)(3)](2+) has also been investigated in the optically active solvent, (S)-(-)-1,2-propylene carbonate. The induction is small, forming 0.75% Delta-[Co(en)(3)](3+), consistent with the important role for hydrogen bonding in determining the precursor stereoselectivity to the exclusion of solvent.

Cytosolic phospholipase A2‐alpha (cPLA2α) has been a protein of interest for over 16 years because of its presence in inflammatory diseases, including asthma and rheumatoid arthritis. cPLA2α is composed of two domains, a catalytic domain that generates arachidonic acid by cleaving phospholipids, and a C2 domain responsible for anchoring the protein to the lipid membrane. Ceramide‐1‐phosphate (C1P) is a sphingolipid found in inflamed tissue that previous research demonstrates to significantly upregulate the activity of cPLA2α. cPLA2α's C2 domain contains a debated binding site for C1P, and the goal of this study is to culture 15N‐tagged cPLA2α C2 domain for structural investigation by NMR. In addition, binding studies utilizing large unilamellar vesicles (LUV) and increasing concentrations of C1P will help us construct a binding curve, thus better understand C2 binding to C1P. Preliminary results of the NMR study and LUV assay support our hypothesis that C1P and cPLA2α interact. This interaction is likely significant in inflammatory disease processes and is potentially a novel drug target. Funding provided by American Heart Association SDG0735350N.

Previous facial motoneuron (MN) survival studies have identified a facial MN population that is resilient to axotomy. Examination of the literature suggests two distinct populations of MN: one population vulnerable to axotomy and another population potentially resilient to axotomy. To identify potential differences in MN survival levels after target disconnection, we performed a facial nerve transection at the stylomastoid foramen in a number of different mouse strains, as well as models of immunodeficiency and MN disease. All mice were monitored for facial MN survival for up to 26 weeks post‐axotomy (wpa). We observed an 85% survival of facial MN at 4 wpa that was reduced to about 50% at 10 wpa in WT mice. In contrast, facial MN survival significantly dropped at 4 wpa to approximately 62% and 50% in immunodeficient and MN disease mice, respectively. Similar to WT mice, facial MN survival levels remained at about 50% for up to 18 wpa in both the immunodeficient and MN disease mice. Collectively, these data suggest that, despite target disconnection of similar MN populations by either axotomy or disease, there are inherent differences that may be exploited for therapeutic applications in the future.