Development of fast-response PPAC with strip-readout for heavy-ion beams

A strip-readout parallel-plate avalanche counter (SR-PPAC) has been developed aiming at the high detection efficiency and good position resolution in high-intensity heavy-ion measurements. The performance was evaluated using 115 MeV/u $^{132}$Xe, 300 MeV/u $^{132}$Sn, and 300 MeV/u $^{48}$Ca beams. A detection efficiency beyond 99% for these beams is achieved even at an incident beam intensity of 0.7 billion particles per second. The best position resolution achieved is 235 um (FWHM).Comment: 16 pages, 18 figures, 2 table

Periostin Contributes to the Pathogenesis of Atopic Dermatitis by Inducing TSLP Production from Keratinocytes

Background: Atopic dermatitis (AD) is a chronic inflammatory skin disease where Th2-type immune responses are dominant. Keratinocytes persistently secrete proinflammatory cytokines and chemokines, amplifying Th2-type responses in AD. We have recently reported that periostin, an extracellular matrix protein induced by Th2 cytokines, plays a critical role in AD. In the present study, we have further investigated the characteristics of our allergen-induced AD model mice and the role of periostin in the pathogenesis of AD. Methods: The ears of C57BL/6 mice, BALB/c mice, and Rag-2−/− γc−/− mice (BALB/c background) were epicutaneously sensitized repeatedly with HDM. Mice were analyzed after the final sensitization. To examine the direct role of periostin, we reconstituted skin in vitro by coculture of keratinocytes with wild-type or periostin-deficient fibroblasts. Results: Epicutaneous sensitization with HDM induced AD-like phenotypes and accumulation of periostin in dermis in C57BL/6 mice but not in Rag-2−/− γc−/− mice. In vitro organotypic coculture systems revealed that periostin promoted survival and proliferation of keratinocytes and directly induced production of thymic stromal lymphopoietin (TSLP). Conclusions: Our results suggest that periostin exacerbates the pathogenesis of AD through TSLP production from keratinocytes

Periostin contributes to epidermal hyperplasia in psoriasis common to atopic dermatitis

AbstractBackgroundEpidermal hyperplasia is a histological hallmark observed in both atopic dermatitis (AD) and psoriasis, although the clinical features and the underlying immunological disorders of these diseases are different. We previously showed that periostin, a matricellular protein, plays a critical role in epidermal hyperplasia in AD, using a mouse model and a 3-dimensional organotypic coculture system. In this study, we explore the hypothesis that periostin is involved in epidermal hyperplasia in psoriasis.MethodsTo examine expression of periostin in psoriasis patients, we performed immunohistochemical analysis on skin biopsies from six such patients. To investigate periostin's role in the pathogenesis of psoriasis, we evaluated periostin-deficient mice in a psoriasis mouse model induced by topical treatment with imiquimod (IMQ).ResultsPeriostin was substantially expressed in the dermis of all investigated psoriasis patients. Epidermal hyperplasia induced by IMQ treatment was impaired in periostin-deficient mice, along with decreased skin swelling. However, upon treatment with IMQ, periostin deficiency did not alter infiltration of inflammatory cells such as neutrophils; production of IL-17, −22, or −23; or induction/expansion of IL-17– and IL-22–producing group 3 innate lymphoid cells.ConclusionsPeriostin plays an important role during epidermal hyperplasia in IMQ-induced skin inflammation, independently of the IL-23–IL-17/IL-22 axis. Periostin appears to be a mediator for epidermal hyperplasia that is common to AD and psoriasis

Periostin promotes chronic allergic inflammation in response to Th2 cytokines

Allergic inflammation triggered by exposure of an allergen frequently leads to the onset of chronic inflammatory diseases such as atopic dermatitis (AD) and bronchial asthma. The mechanisms underlying chronicity in allergic inflammation remain unresolved. Periostin, a recently characterized matricellular protein, interacts with several cell surface integrin molecules, providing signals for tissue development and remodeling. Here we show that periostin is a critical mediator for the amplification and persistence of allergic inflammation using a mouse model of skin inflammation. Th2 cytokines IL-4 and IL-13 stimulated fibroblasts to produce periostin, which interacted with αv integrin, a functional periostin receptor on keratinocytes, inducing production of proinflammatory cytokines, which consequently accelerated Th2-type immune responses. Accordingly, inhibition of periostin or αv integrin prevented the development or progression of allergen-induced skin inflammation. Thus, periostin sets up a vicious circle that links Th2-type immune responses to keratinocyte activation and plays a critical role in the amplification and chronicity of allergic skin inflammation

Isotope-production cross sections of residual nuclei in proton- and deuteron-induced reactions on

The isotope-production cross sections in p- and d-induced reactions on 93Zr at approximately 50 MeV/nucleon were measured by using the inverse-kinematics method at RIKEN RI Beam Factory. The measured data were compared with the previous experimental 93Zr + p, d at 105 and 209 MeV/nucleon data. This comparison represents that the isotopic distribution of production cross sections at 51 MeV p-induced reaction is appreciably different from those at 105 and 209 MeV. On the other hand, these three data sets show that the shape of isotopic distribution is similar in the case of the d-induced reaction. Also, the measured production cross sections were compared with the theoretical model calculations with Particle and Heavy Ion Transport code System (PHITS) version 3.10 in order to investigate the reproducibility of the models implemented in PHITS. The calculations well reproduced the experimental data even in such low incident energy, while several discrepancies were still seen as in the p- and d-induced reactions at 105 and 209 MeV/nucleon