a-Melanocyteestimulating hormone (a-MSH) is an endogenous peptide hormone involved in cutaneous pigmentation in atopic dermatitis (AD) with severe itching. a-MSH elicits itch-related responses in mice. We, therefore, investigated whether a-MSH was involved in itching in AD. In the skin of AD patients and mice with atopy-like dermatitis, a-MSH and the prohormone convertase 2, which is the key processing enzyme for the production of a-MSH, were distributed mainly in keratinocytes. In the skin of mice with dermatitis, melanocortin receptors (MC1R and MC5R) were expressed at the mRNA level and were distributed in the dermis. In the dorsal root ganglion of mice with dermatitis, mRNAs encoding MC1R, MC3R, and MC5R were also expressed. MC1R antagonist agouti-signaling protein inhibited spontaneous scratching in mice with dermatitis. In healthy mice, intradermal a-MSH elicited itch-associated responses, which were inhibited by thromboxane (TX) A 2 receptor antagonist ONO-3708. In mouse keratinocytes, a-MSH increased the production of TXA 2 , which was inhibited by adenylyl cyclase inhibitor SQ-22536 and Ca 2þ chelator EGTA. In mouse keratinocytes treated with siRNA for MC1R and/or MC5R, a-MSHeinduced TXA 2 production was decreased. a-MSH increased intracellular Ca 2þ ion concentration in dorsal root ganglion neurons and keratinocytes. These results suggest that a-MSH is involved in itching during AD and may elicit itching through the direct action of primary afferents and TXA 2 production by keratinocytes.

Continuing the project described by Kato et al. (2009, PASJ, 61, S395), we collected the times of superhump maxima for 51 SU UMa-type dwarf novae, mainly observed during the 2010–2011 season. Although most of the new data for systems with short superhump periods basically confirmed the findings by Kato et al. (ibid.) and Kato et al. (2010, PASJ, 62, 1525), the long-period system GX Cas showed an exceptionally large positive-period derivative. An analysis of public Kepler data of V344 Lyr and V1504 Cyg yielded less-striking stage transitions. In V344 Lyr, there was a prominent secondary component growing during the late stage of superoutbursts, and this component persisted for at least two more cycles of successive normal outbursts. We also investigated the superoutburst of two conspicuous eclipsing objects: HT Cas and the WZ Sge-type object SDSS J080434.20$+$510349.2. Strong beat phenomena were detected in both objects, and late-stage superhumps in the latter object had an almost constant luminosity during repeated rebrightenings. The WZ Sge-type object SDSS J133941.11$+$484727.5 showed a phase reversal around the rapid fading from the superoutburst. The object showed a prominent beat phenomenon, even after the end of the superoutburst. A pilot study of superhump amplitudes indicated that the amplitude of superhumps is strongly correlated with the orbital period, and the dependence on the inclination is weak in systems with inclinations smaller than 80$^{\circ}$.

Toyamaα-Melanocyte-stimulating hormone (α-MSH) is an endogenous peptide hormone that is involved in cutaneous pigmentation. Recent our study has demonstrated that α-MSH elicits scratching, an itch-related response, in mice. In this study, we investigated whether α-MSH was involved in spontaneous scratching in mice with atopy-like dermatitis (AD-mice). α-MSH and the prohormone convertase 2, which is the key processing enzyme for the production of α-MSH, were distributed mainly in keratinocytes in AD-mice. In primary cultures of mouse keratinocytes and dorsal root ganglion (DRG) neurons, α-MSH receptors (MC1R and MC5R) mRNAs were expressed. MC1R antagonist agouti-signaling protein inhibited spontaneous scratching in mice with atopy-like dermatitis. In mice, α-MSH elicited itch-associated responses, which were inhibited by TP thromboxane (TX) receptor antagonist. In mouse keratinocytes, α-MSH increased the production of TXA 2 , which was decreased in mouse keratinocytes treated with siRNA for MC1R and/or MC5R. α-MSH increased intracellular Ca 2+ ion concentration in DRG neurons and keratinocytes. These results suggested that α-MSH-TXA 2 system is involved in spontaneous scratching in AD-mice.