Photonic-crystal nano-photodetector with ultrasmall capacitance for on-chip light-to-voltage conversion without an amplifier

The power consumption of a conventional photoreceiver is dominated by that of the electric amplifier connected to the photodetector (PD). An ultralow-capacitance PD can overcome this limitation, because it can generate sufficiently large voltage without an amplifier when combined with a high-impedance load. In this work, we demonstrate an ultracompact InGaAs PD based on a photonic crystal waveguide with a length of only 1.7 μm and a capacitance of less than 1 fF. Despite the small size of the device, a high responsivity of 1 A/W and a clear 40 Gbit/s eye diagram are observed, overcoming the conventional trade-off between size and responsivity. A resistor-loaded PD was actually fabricated for light-to-voltage conversion, and a kilo-volt/watt efficiency with a gigahertz bandwidth even without amplifiers was measured with an electro-optic probe. Combined experimental and theoretical results reveal that a bandwidth in excess of 10 GHz can be expected, leading to an ultralow energy consumption of less than 1 fJ/bit for the photoreceiver. Amplifier-less PDs with attractive performance levels are therefore feasible and a step toward a densely integrated photonic network/processor on a chip

MMP-9 Inhibition Suppresses Interferon-γ-Induced CXCL10 Production in Human Salivary Gland Ductal Cells

Gene expression profiling of lip salivary gland (LSG) has shown that C-X-C motif chemokine 10 (CXCL10) and matrix metalloproteinase 9 (MMP9) expression is up-regulated in primary Sjögren's syndrome (pSS) patients. Although CXCL10 and MMP-9 are both associated with pSS pathogenesis, the potential relationship between these two factors has not been investigated. In this study, we used LSG sections from pSS patients and human salivary gland cell lines to investigate the relationship between CXCL10 and MMP-9. Immunofluorescence analyses revealed that CXCL10 and MMP-9 were co-expressed in the LSG of pSS patients, particularly in expanded ductal cells. Furthermore, RT-qPCR analyses on human salivary gland ductal NS-SV-DC cells confirmed that CXCL10 expression was induced by interferon (IFN)-γ, whereas that of MMP9 was stimulated by IFN-α, tumor necrosis factor-α, and interleukin 1β. Remarkably, MMP-9 inhibition in IFN-γ-stimulated NS-SV-DC cells significantly decreased CXCL10 mRNA and secreted protein levels. Further analyses established that MMP-9 inhibition in IFN-γ-stimulated NS-SV-DC cells decreased STAT1 phosphorylation and hence suppressed IFN-γ signaling. Collectively, these results suggest that in addition to its reported role in the destruction of acinar structures, MMP-9 is involved in the IFN-γ-induced production of CXCL10 in pSS lesions. We believe that our findings open the door to the development of novel treatments for pSS, based on the modulation of MMP-9 activity

自然災害と兵乱 ― 九世紀の奥羽地方を中心に ―

　二〇一一年三月十一日に発生した東日本大震災は甚大なる被害を生み出し、自然災害の脅威を我々に見せつけることとなった。この震災を機に、歴史学がどのような役割を果たすべきかを考え直す動きが生まれ、地震史・災害史という分野の重要性が再確認されるとともに、研究の深化が求められている。　東日本大震災によって注目されることになった貞観地震を含め、九世紀には日本列島の各地で地震・火山活動が発生している。これは現在の日本列島と共通点が多く、将来に向けての教訓を得ることができる重要な時代とされている。　本論では、九世紀の奥羽地方を中心に地震・火山活動などの自然災害が、当時の社会や兵乱にどのような影響を及ぼしたかについて考察する。特に「征夷」終結後の奥羽地方では九世紀段階で中央政府の支配領域の縮小が起こっていたとの指摘があるが、その要因・時期についての特定がなされておらず、その点について自然災害の影響がどの程度あったかについて考察した。また、この前後、奥羽地方や坂東で兵乱が発生した際の中央政府の対応についても併せて考察を行った。　その結果、陸奥国では斉衡～貞観年間にかけて奥郡住民の反乱が激化し、北部四郡の離脱問題が生じたのに対して、中央政府は鎮守将軍に坂東諸国の権介を兼任させ、離脱阻止の活動をさせる方策を実施したが、貞観地震（津波）の発生による陸奥国の疲弊化を契機として、北部四郡の完全放棄につながったのではないかという結論に達した

摂津源氏の東国進出 ― 下総国を中心として ―

　本論は十一世紀から十二世紀にかけて東国を舞台に発生した兵乱を中心に、河内源氏・大和源氏・摂津源氏の源氏諸流の東国進出の動きを概観したうえで、摂津源氏である源頼綱・仲正父子が国守に任じられた下総国における摂津源氏と現地勢力である下河辺・千葉氏との関係を明らかにすることで、摂津源氏の東国進出における下総国の様相について考察した。　前九年合戦以後の源氏諸流（河内源氏・大和源氏・摂津源氏）の東国進出の動きのなかで、摂津源氏の動向が注目されることはあまりなかったが、元永元年の下総守源仲正による常陸国侵攻は、摂津源氏による東国進出の契機となる事件と位置付けることが出来るとの結論に達した。　また、摂津源氏が下総国に進出する際、摂津源氏に登用されたとみられる下河辺・千葉氏は、その本拠地である下河辺荘・千葉荘・相馬御厨を開発・維持するうえで、摂津源氏の働きかけがあったことも明らかにした。　源仲正の下総・下野国を中心とした東国進出は、ある一定の成果を挙げたと考えられ、特に下総国での摂津源氏の勢力および摂津源氏と下河辺・千葉氏の関係は、頼政の挙兵時まで継続していることが確認できた。　しかしながら、頼政の挙兵失敗により摂津源氏が失脚すると、下河辺・千葉氏共に次の後ろ盾を求めて行動を起こし、下河辺・千葉氏共に河内源氏である源頼朝の許へ参陣することとなるのである

Baricitinib Inhibits CXCL10 Production in Salivary Gland Cells

Sjögren's syndrome (SS) is a chronic autoimmune disease targeting salivary and lacrimal glands. C-X-C motif chemokine ligand 10 (CXCL10) expression is upregulated in lip salivary glands (LSGs) of primary SS (pSS) patients, and CXCL10 involved in SS pathogenesis via immune-cell accumulation. Moreover, interferon (IFN)-γ enhances CXCL10 production via the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway. We investigated the effects of baricitinib, a selective JAK1/2 inhibitor, on both IFN-γ-induced CXCL10 production and immune-cell chemotaxis. We used immunohistochemical staining to determine the expression levels and localization of JAK1 and JAK2 in LSGs of SS patients (n=12) and healthy controls (n=3). We then evaluated effect of baricitinib in an immortalized normal human salivary gland ductal (NS-SV-DC) cell line. Immunohistochemical analysis of LSGs from pSS patients revealed strong JAK1 and JAK2 expression in ductal and acinar cells, respectively. Baricitinib significantly inhibited IFN-γ-induced CXCL10 expression as well as the protein levels in an immortalized human salivary gland ductal-cell clone in a dose-dependent manner. Additionally, western blot analysis showed that baricitinib suppressed the IFN-γ-induced phosphorylation of STAT1 and STAT3, with a stronger effect observed in case of STAT1. It also inhibited IFN-γ-mediated chemotaxis of Jurkat T cells. These results suggested that baricitinib suppressed IFN-γ-induced CXCL10 expression and attenuated immune-cell chemotaxis by inhibiting JAK/STAT signaling, suggesting its potential as a therapeutic strategy for pSS