Regression of Nevi After Candida Injection for the Treatment of Verruca Vulgaris.

The most common treatment methods for verruca vulgaris are destructive methods that are often painful and treat individual verruca. Thus immune modulators, including Candida immunotherapy, are used to treat persistent recalcitrant and multiple verrucas simultaneously. Very few side effects are reported with Candida immunotherapy; they include vitiligo and now halo nevi. Physicians need to be aware of and discuss side effects with patients undergoing Candida immunotherapy.

Effect of micellar and reverse micellar interface on solute location: 2,6-pyridinedicarboxylate in CTAB micelles and CTAB and AOT reverse micelles.

The interface-solute interactions, including solute location, surfactant charge, and geometry of solute interactions were studied in CTAB micelles and reverse micelles and were found to be similar as measured using (1)H NMR spectroscopy and a pH-sensitive probe. (1)H NMR spectra were recorded in the presence and absence of 2,6-pyridinedicarboxylate probe at CTAB concentrations above and below the critical micelle concentration showing interaction between dipic-probe and the micellar self-assembled structure. Downfield chemical shifts are observed for the CTAB surfactant signals upon aggregation and micelle formation. The effect of micelle formation on CTAB chemical shifts was quantitated, and simple ion pairing was ruled out. No significant change in CTAB surfactant signals are observed in the presence of monoanionic probe, whereas significant shifts are observed in the presence of the dianionic probe. The (1)H NMR spectra of the dipic-probe are diagnostic of the protonation state and isomeric form of the dipic-probe. The (1)H NMR chemical shifts in micelles are sensitive to the location of the dipic-probe, and the downfield chemical shift suggests location of part of the molecule in the Stern layer near the charged interface. Other parts of the probe show an upfield chemical shifts consistent with a deeper penetration of the dipic-probe into the surfactant layer. Probe location was confirmed using the 2D ROESY. Spectra recorded of the dipic-probe at various pH values demonstrate that both CTAB micellar and CTAB/pentanol/cyclohexane reverse micellar interfaces are different than those reported in aqueous solution and in AOT/isooctane reverse micelles (Crans et al. J. Org. Chem. 2008, 73, 9633-9640) and suggest interface penetration by dipic(2-). Together these observations and comparisons provide guidelines for future interpretation of chemical shift changes in both micelles and reverse micelles and point to headgroup charge as being a key factor determining the direction of chemical shift change and the depth of solute penetration.

Fibroblast growth factor controls the timing of Scl, Lmo2, and Runx1 expression during embryonic blood development.

To program pluripotent cells into blood, a knowledge of the locations of precursors during their journey through the embryo and the signals they experience would be informative. The anterior (a) and posterior (p) ventral blood islands (VBIs) in Xenopus are derived from opposite sides of the pregastrula embryo. The aVBI goes through a "hemangioblast" state, characterized by coexpression of blood and endothelial genes at neurula stages, whereas the pVBI expresses these genes in a nonoverlapping fashion several hours later, after commitment to either a blood or an endothelial fate. We describe a novel role for fibroblast growth factor (FGF) in controlling the timing of Scl, Lmo2, and Runx1 expression in the 2 VBI compartments. Blocking FGF signaling during gastrulation expands expression at neurula stages into posterior regions. We show, by lineage labeling, explant analysis, and targeted blocking of FGF signaling, that this is due to the pVBI prematurely expressing these genes with the timing of the aVBI. In contrast, overexpression of FGF in aVBI precursors eliminates the anterior hemangioblast program. Using this information, we have recapitulated the anterior hemangioblast program in pluripotent cells in vitro by inhibiting FGF signaling in anterior mesoderm induced by activin and exposed to bone morphogenetic protein (BMP) signaling.