This fMRI study investigated the human somatosensory system, especially the secondary somatosensory cortex (SII), with respect to its potential somatotopic organization. Eight subjects received electrical stimulation on their right second finger, fifth finger and hallux. Within SII, the typical finding for both fingers was a representation site within the contralateral parietal operculum roughly halfway between the lip of the lateral sulcus and its fundus, whereas the representation site of the hallux was found more medially to this position at the fundus of the lateral sulcus, near the posterior pole of the insula. Somatotopy in SII seems to be less fine-grained than in primary somatosensory cortex (SI), as, in contrast to SI, no separate representations of the two fingers in SII were observed. A similar somatotopic representation pattern between fingers and the hallux was also observed within ipsilateral SII, indicating somatotopy of contra- as well as ipsilateral SII using unilateral stimulation. Further areas exhibiting activation were found in the superior and inferior parietal lobule, in the supplementary and cingulate motor area, and in the insula.

The vitamin D receptor participates in the control of IgE class-switch recombination in B cells. The physiologic vitamin D receptor agonist, 1,25(OH)D (calcitriol), is synthesized by the essential enzyme 25-hydroxyvitamin D-1α-hydroxylase (CYP27B1), which can be expressed by activated immune cells. The role of endogenous calcitriol synthesis for the regulation of IgE has not been proven. In this study, we investigated IgE-responses in -knockout (KO) mice following sensitization to OVA or intestinal infection with Specific Igs and plasmablasts were determined by ELISA and ELISpot, expression was measured by quantitative PCR. The data show elevated specific IgE and IgG1 concentrations in the blood of OVA-sensitizedKO mice compared with wild-type littermates (+898 and +219%). Accordingly, more OVA-specific IgG1-secreting cells are present in spleen and fewer in the bone marrow of -KO mice. Ag-specific mechanisms are suggested as the leucopoiesis is in general unchanged and activated murine B and T lymphocytes express Accordingly, elevated specific IgE concentrations in the blood of sensitized T cell-specific -KO mice support a lymphocyte-driven mechanism. In an independent IgE-inducing model, i.e., intestinal infection with, we validated the increase of total and specific IgE concentrations of -KO compared with wild-type mice, but not those of IgG1 or IgA. We conclude that endogenous calcitriol has an impact on the regulation of IgE in vivo. Our data provide genetic evidence supporting previous preclinical and clinical findings and suggest that vitamin D deficiency not only promotes bone diseases but also type I sensitization.

Induced pluripotent stem cells (iPSCs) are promising candidates for the study of disease models as well as for tissue engineering purposes. Part of a strategy to develop safe reprogramming technique is reducing the number of exogenous reprogramming factors. Some cells types are more prone to reprogramming than others. iPSC induction with less reprogramming factors has been described in cells with endogenous expression levels of pluripotency genes, such as neural stem cells. Because multipotent neural crest stem cells (NCSCs) from mammalian hair follicle bulges also express pluripotency genes, we argued that this property would facilitate reprogramming of hair follicle bulge NCSCs and could substitute for the use of exogenous reprogramming factors. Although we confirmed the expression of pluripotency genes in hair follicle bulge cells, our results show that these cells do require a full set of reprogramming factors for iPSC induction. Hair follicle bulge-derived iPSCs were created with efficiencies similar to fibroblasts. We conclude that high endogenous levels of pluripotency factors are no guarantee for facilitated induction of pluripotency.