Institution
Tokyo University of Science
Education•Tokyo, Japan•
About: Tokyo University of Science is a education organization based out in Tokyo, Japan. It is known for research contribution in the topics: Thin film & Enantioselective synthesis. The organization has 15800 authors who have published 24147 publications receiving 438081 citations. The organization is also known as: Tōkyō Rika Daigaku & Science University of Tokyo.
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TL;DR: AeA1144 is the first known structure of this type among not only Fe-based superconductors but also other materials, which can be regarded as hybrid phases between AeFe 2As2 (Ae = Ca, Sr) and AFe2As2.
Abstract: Fe-based superconductors have attracted research interest because of their rich structural variety, which is due to their layered crystal structures. Here we report the new-structure-type Fe-based superconductors CaAFe4As4 (A = K, Rb, Cs) and SrAFe4As4 (A = Rb, Cs), which can be regarded as hybrid phases between AeFe2As2 (Ae = Ca, Sr) and AFe2As2. Unlike solid solutions such as (Ba1–xKx)Fe2As2 and (Sr1–xNax)Fe2As2, Ae and A do not occupy crystallographically equivalent sites because of the large differences between their ionic radii. Rather, the Ae and A layers are inserted alternately between the Fe2As2 layers in the c-axis direction in AeAFe4As4 (AeA1144). The ordering of the Ae and A layers causes a change in the space group from I4/mmm to P4/mmm, which is clearly apparent in powder X-ray diffraction patterns. AeA1144 is the first known structure of this type among not only Fe-based superconductors but also other materials. AeA1144 is formed as a line compound, and therefore, each AeA1144 has its own s...
217 citations
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TL;DR: The results suggest that IL-27 activates JAK1 and -2, tyrosine kinase-2, STAT1, - 2, -3, and -5 in naive CD4+ T cells and that STAT1 plays an indispensable role inIL-27-induced T-bet and subsequent IL-12Rβ2 expression and MHC class I expression as well but not proliferation, while STAT3 presumably plays an important role in IL- 27-induced proliferation.
Abstract: IL-27 is a novel IL-12 family member that plays a role in the early regulation of Th1 initiation, induces proliferation of naive CD4 + T cells, and synergizes with IL-12 in IFN-γ production. It has been recently reported that IL-27 induces T-bet and IL-12Rβ2 expression through JAK1/STAT1 activation. In the present study, we further investigated the JAK/STAT signaling molecules activated by IL-27 and also the role of STAT1 in IL-27-mediated responses using STAT1-deficient mice. In addition to JAK1 and STAT1, IL-27-activated JAK2, tyrosine kinase-2, and STAT2, -3, and -5 in naive CD4 + T cells. The activation of STAT2 and STAT5, but not of STAT3, was greatly diminished in STAT1-deficient naive CD4 + T cells. Comparable proliferative response to IL-27 was observed between STAT1-deficient and wild-type naive CD4 + T cells. In contrast, IL-27 hardly induced T-bet and subsequent IL-12Rβ2 expression, and synergistic IFN-γ production by IL-27 and IL-12 was impaired in STAT1-deficient naive CD4 + T cells. Moreover, IL-27 augmented the expression of MHC class I on naive CD4 + T cells in a STAT1-dependent manner. These results suggest that IL-27 activates JAK1 and -2, tyrosine kinase-2, STAT1, -2, -3, and -5 in naive CD4 + T cells and that STAT1 plays an indispensable role in IL-27-induced T-bet and subsequent IL-12Rβ2 expression and MHC class I expression as well but not proliferation, while STAT3 presumably plays an important role in IL-27-induced proliferation.
217 citations
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TL;DR: Epicutaneous sensitization on a disrupted skin barrier is associated with accumulation of TSLP-elicited basophils, which are necessary and sufficient to promote antigen-induced intestinal food allergy.
Abstract: Background Exposure to food allergens through a disrupted skin barrier has been recognized as a potential factor in the increasing prevalence of food allergy. Objective We sought to test the immunologic mechanisms by which epicutaneous sensitization to food allergens predisposes to intestinal food allergy. Methods Mice were epicutaneously sensitized with ovalbumin or peanut on an atopic dermatitis–like skin lesion, followed by intragastric antigen challenge. Antigen-specific serum IgE levels and T H 2 cytokine responses were measured by ELISA. Expression of type 2 cytokines and mast cell proteases in the intestine were measured by using real-time PCR. Accumulation of basophils in the skin and mast cells in the intestine was examined by using flow cytometry. In vivo basophil depletion was achieved by using diphtheria toxin treatment of Baso-DTR mice. For cell-transfer studies, the basophil population was expanded in vivo by means of hydrodynamic tail vein injection of thymic stromal lymphopoietin (TSLP) cDNA plasmid. Results Sensitization to food allergens through an atopic dermatitis–like skin lesion is associated with an expansion of TSLP-elicited basophils in the skin that promote antigen-specific T H 2 cytokine responses, increased antigen-specific serum IgE levels, and accumulation of mast cells in the intestine, promoting the development of intestinal food allergy. Critically, disruption of TSLP responses or depletion of basophils reduced the susceptibility to intestinal food allergy, whereas transfer of TSLP-elicited basophils into intact skin promoted disease. Conclusion Epicutaneous sensitization on a disrupted skin barrier is associated with accumulation of TSLP-elicited basophils, which are necessary and sufficient to promote antigen-induced intestinal food allergy.
216 citations
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TL;DR: The potential for bioengineered organ replacement to functionally restore the lacrimal gland is demonstrated, including tear production in response to nervous stimulation and ocular surface protection.
Abstract: The lacrimal gland has a multifaceted role in maintaining a homeostatic microenvironment for a healthy ocular surface via tear secretion. Dry-eye disease, which is caused by lacrimal gland dysfunction, is one of the most prevalent eye diseases that cause corneal epithelial damage and results in significant loss of vision and a reduction in the quality of life. Here we demonstrate orthotopic transplantation of bioengineered lacrimal gland germs into adult mice with an extra-orbital lacrimal gland defect, a mouse model that mimics the corneal epithelial damage caused by lacrimal gland dysfunction. The bioengineered lacrimal gland germs and harderian gland germs both develop in vivo and achieve sufficient physiological functionality, including tear production in response to nervous stimulation and ocular surface protection. This study demonstrates the potential for bioengineered organ replacement to functionally restore the lacrimal gland.
215 citations
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University of Utah1, Saitama University2, Tokyo Institute of Technology3, Ewha Womans University4, Hanyang University5, Tokyo University of Science6, Kindai University7, Yonsei University8, University of Tokyo9, Osaka City University10, Kanagawa University11, University of Yamanashi12, Tokyo City University13, Waseda University14, Chiba University15, Kōchi University16, Ritsumeikan University17, Sungkyunkwan University18, Moscow State University19, Université libre de Bruxelles20, Rutgers University21, Hiroshima City University22, National Institute of Radiological Sciences23, Ehime University24
TL;DR: In this paper, the authors compare the results of the HiRes and PAO UHECR measurements to the results obtained by the QGSJetII-03 and QGS jet-01c models.
215 citations
Authors
Showing all 15878 results
Name | H-index | Papers | Citations |
---|---|---|---|
Kazunori Kataoka | 138 | 908 | 70412 |
Yoichiro Iwakura | 129 | 705 | 64041 |
Kouji Matsushima | 124 | 590 | 56995 |
Masaki Ishitsuka | 103 | 624 | 39383 |
Shinsuke Tanabe | 98 | 722 | 37445 |
Tatsumi Koi | 97 | 411 | 50222 |
Hirofumi Akagi | 94 | 618 | 43179 |
Clifford A. Lowell | 91 | 258 | 23538 |
Teruo Okano | 91 | 605 | 28346 |
László Á. Gergely | 89 | 426 | 60674 |
T. Sumiyoshi | 88 | 855 | 62277 |
Toshinori Nakayama | 86 | 405 | 25275 |
Akihiko Kudo | 86 | 328 | 39475 |
Hans-Joachim Gabius | 85 | 699 | 28085 |
Motohide Tamura | 85 | 1007 | 32725 |