Effects of the Zero-Mode Landau Level on Inter-Layer Magnetoresistance in Multilayer Massless Dirac Fermion Systems

We report on the experimental results of interlayer magnetoresistance in multilayer massless Dirac fermion system $\alpha$-(BEDT-TTF)$_2$I$_3$ under hydrostatic pressure and its interpretation. We succeeded in detecting the zero-mode Landau level (n=0 Landau level) that is epected to appear at the contact points of Dirac cones in the magnetic field normal to the two-dimensional plane. The characteristic feature of zero-mode Landau carriers including the Zeeman effect is clearly seen in the interlayer magnetoresistance.Comment: 2 pages, 2 figure

A Case of Nevoid Acanthosis Nigricans Successfully Treated with Topical Ketoconazole Plus Urea

Nevoid acanthosis nigricans (AN) is a rare form of benign AN that can be mostly found as a solitary lesion distributed along Blaschko’s lines (1). It is not associated with any known syndrome, endocrinopathy, drugs, or internal malignancy. Treatments include retinoid, calcipotriol, and laser treatments (2). Herein we report a case of nevoid AN successfully treated with topical ketoconazole plus ure

A Case of Dapsone-induced Mild Methemoglobinemia with Dyspnea and Cyanosis

Dapsone is a dual-function drug with antimicrobial and antiprotozoal effects and anti-inflammatory features (1). In dermatology, it is a first choice for conditions such as leprosy, IgA pemphigus, dermatitis herpetiformis, and linear IgA bullous dermatosis, or an adjunctive treatment for, e.g. bullous pemphigoid (BP) and pemphigus vulgaris (1). However, dapsone is associated with some adverse effects, including methemoglobinemia (1)

A novel control of human keratin expression: cannabinoid receptor 1-mediated signaling down-regulates the expression of keratins K6 and K16 in human keratinocytes in vitro and in situ

Cannabinoid receptors (CB) are expressed throughout human skin epithelium. CB1 activation inhibits human hair growth and decreases proliferation of epidermal keratinocytes. Since psoriasis is a chronic hyperproliferative, inflammatory skin disease, it is conceivable that the therapeutic modulation of CB signaling, which can inhibit both proliferation and inflammation, could win a place in future psoriasis management. Given that psoriasis is characterized by up-regulation of keratins K6 and K16, we have investigated whether CB1 stimulation modulates their expression in human epidermis. Treatment of organ-cultured human skin with the CB1-specific agonist, arachidonoyl-chloro-ethanolamide (ACEA), decreased K6 and K16 staining intensity in situ. At the gene and protein levels, ACEA also decreased K6 expression of cultured HaCaT keratinocytes, which show some similarities to psoriatic keratinocytes. These effects were partly antagonized by the CB1-specific antagonist, AM251. While CB1-mediated signaling also significantly inhibited human epidermal keratinocyte proliferation in situ, as shown by K6/Ki-67-double immunofluorescence, the inhibitory effect of ACEA on K6 expression in situ was independent of its anti-proliferative effect. Given recent appreciation of the role of K6 as a functionally important protein that regulates epithelial wound healing in mice, it is conceivable that the novel CB1-mediated regulation of keratin 6/16 revealed here also is relevant to wound healing. Taken together, our results suggest that cannabinoids and their receptors constitute a novel, clinically relevant control element of human K6 and K16 expression

Inflammatory Mediator TAK1 Regulates Hair Follicle Morphogenesis and Anagen Induction Shown by Using Keratinocyte-Specific TAK1-Deficient Mice

Transforming growth factor-β-activated kinase 1 (TAK1) is a member of the NF-κB pathway and regulates inflammatory responses. We previously showed that TAK1 also regulates keratinocyte growth, differentiation, and apoptosis. However, it is unknown whether TAK1 has any role in epithelial–mesenchymal interactions. To examine this possibility, we studied the role of TAK1 in mouse hair follicle development and cycling as an instructive model system. By comparing keratinocyte-specific TAK1-deficient mice (Map3k7fl/flK5-Cre) with control mice, we found that the number of hair germs (hair follicles precursors) in Map3k7fl/flK5-Cre mice was significantly reduced at E15.5, and that subsequent hair follicle morphogenesis was retarded. Next, we analyzed the role of TAK1 in the cyclic remodeling in follicles by analyzing hair cycle progression in mice with a tamoxifen-inducible keratinocyte-specific TAK1 deficiency (Map3k7fl/flK14-Cre-ERT2). After active hair growth (anagen) was induced by depilation, TAK1 was deleted by topical tamoxifen application. This resulted in significantly retarded anagen development in TAK1-deficient mice. Deletion of TAK1 in hair follicles that were already in anagen induced premature, apoptosis-driven hair follicle regression, along with hair follicle damage. These studies provide the first evidence that the inflammatory mediator TAK1 regulates hair follicle induction and morphogenesis, and is required for anagen induction and anagen maintenance