Late Pleistocene variation in lignin and fatty acids from core TKN-2004 in a small mountain basin in central Japan

We generated a record of lignin and fatty acid compositions from the TK-2004 core in Takano Basin, central Japan, during 39-162 ka by TMAH-thermochemolysis-GC/MS. We tested lignin and fatty acid compositions in the sediments of a small lake (1.88 km(2) watershed) as a paleovegetation proxy to understand the responses of terrestrial vegetation in central Japan to global climate change. Variation in terrestrial organic carbon contents estimated by C/N and Sigma 8 was parallel to the total organic content (TOC) variation, suggesting that the inflow of terrestrial organic matter was a major factor determining the TOC. The ratio of mid-chain C-20-C-24 n-fatty acids to short-chain C-14-C-18 n-fatty acids (MFA/SFA ratio) and the ratio of cinnamyl to vanillyl phenols (C/V ratio) of lignin gradually increased from mid-MIS 6 to early MIS 3. The increase in both parameters suggested increase in the contribution of submerged and floating plants as the flats were expanded in the lake margin. The ratio of syringyl to vanillyl phenols (S/V ratio) corresponded to the pollen vegetation index. This correspondence indicated that the S/V ratio reflected the relative abundance of angiosperms to gymnosperms in the Takano Basin. The consistency of the S/V ratio at the site of core TKN-2004 and the other two locations suggests that the S/V ratio in a small basin is a robust proxy for terrestrial vegetation on a regional scale.ArticleGEOCHEMICAL JOURNAL. 48(2):207-217 (2014)journal articl

The Effect of Incentives and Meta-incentives on the Evolution of Cooperation

Although positive incentives for cooperators and/or negative incentives for free-riders in social dilemmas play an important role in maintaining cooperation, there is still the outstanding issue of who should pay the cost of incentives. The second-order free-rider problem, in which players who do not provide the incentives dominate in a game, is a well-known academic challenge. In order to meet this challenge, we devise and analyze a meta-incentive game that integrates positive incentives (rewards) and negative incentives (punishments) with second-order incentives, which are incentives for other players' incentives. The critical assumption of our model is that players who tend to provide incentives to other players for their cooperative or non-cooperative behavior also tend to provide incentives to their incentive behaviors. In this paper, we solve the replicator dynamics for a simple version of the game and analytically categorize the game types into four groups. We find that the second-order free-rider problem is completely resolved without any third-order or higher (meta) incentive under the assumption. To do so, a second-order costly incentive, which is given individually (peer-to-peer) after playing donation games, is needed. The paper concludes that (1) second-order incentives for first-order reward are necessary for cooperative regimes, (2) a system without first-order rewards cannot maintain a cooperative regime, (3) a system with first-order rewards and no incentives for rewards is the worst because it never reaches cooperation, and (4) a system with rewards for incentives is more likely to be a cooperative regime than a system with punishments for incentives when the cost-effect ratio of incentives is sufficiently large. This solution is general and strong in the sense that the game does not need any centralized institution or proactive system for incentives. (authors' abstract

Regulatory T Cell-Mediated Control of Autoantibody-Induced Inflammation

Autoimmune inflammation including autoantibody-induced inflammation is responsible for the lethal organ damage. Autoantibody-induced inflammation can be separated in two components, autoantibody production, and local inflammatory responses. Accumulating evidence has suggested that regulatory T cells (Treg) control both antibody production and the numbers and functions of effector cells such as innate cells and T helper cells. Autoantibodies are produced by both the follicular and extrafollicular pathways. Recently, follicular regulatory T cells (TFR) and Qa-1 restricted CD8+ Treg were identified as populations that are capable of suppressing follicular T helper cell (TFH)-mediated antibody production. In local inflammation, CD4+CD25+Foxp3+ Treg have the capacity to control inflammation by suppressing cytokine production in T helper cells. Although complement proteins contribute to autoantibody-induced local inflammation by activating innate cells, Treg including CD4+CD25+Foxp3+ Treg are able to suppress innate cells, chiefly via IL-10 production. IL-10-secreting T cells such as T regulatory type I (Tr1) and Tr1-like cells might also play roles in the control of Th17 and innate cells. Therefore, several kinds of Tregs have the potential to control autoimmune inflammation by suppressing both autoantibody production and the local inflammatory responses induced by autoantibodies

植物に関する自由形式説明文からのJSON形式テキストの自動生成

Kanagawa Institute of Technology会議名: 言語資源活用ワークショップ2020, 開催地: オンライン, 会期: 2020年9月8日−9日, 主催: 国立国語研究所 コーパス開発センター電子図鑑等において柔軟な植物検索を可能とするため、日本語の自由形式による植物の特性記述から、コンピュータで処理しやすいJSON形式テキストを自動生成することを試みた。まず、それらの自由形式テキストに係り受け解析を施した。次に、葉と花と果実についてそれぞれ事前に設定した数種類のタグに対して、そのバリュー（値）を係り受け解析結果の木構造をたどりながら設定できる方式を考案した。さらに、自動生成されたJSONを、植物を表す（JAVAの）オブジェクトのストリームに変換して、マップやフィルタ処理を施すことにより、多様な検索を効率的に実行できることを示した

Interactions between IL-32 and tumor necrosis factor alpha contribute to the exacerbation of immune-inflammatory diseases

IL-32 is a newly described cytokine in the human found to be an in vitro inducer of tumor necrosis factor alpha (TNFα). We examined the in vivo relationship between IL-32 and TNFα, and the pathologic role of IL-32 in the TNFα-related diseases – arthritis and colitis. We demonstrated by quantitative PCR assay that IL-32 mRNA was expressed in the lymphoid tissues, and in stimulated peripheral T cells, monocytes, and B cells. Activated T cells were important for IL-32 mRNA expression in monocytes and B cells. Interestingly, TNFα reciprocally induced IL-32 mRNA expression in T cells, monocyte-derived dendritic cells, and synovial fibroblasts. Moreover, IL-32 mRNA expression was prominent in the synovial tissues of rheumatoid arthritis patients, especially in synovial-infiltrated lymphocytes by in situ hybridization. To examine the in vivo relationship of IL-32 and TNFα, we prepared an overexpression model mouse of human IL-32β (BM-hIL-32) by bone marrow transplantation. Splenocytes of BM-hIL-32 mice showed increased expression and secretion of TNFα, IL-1β, and IL-6 especially in response to lipopolysaccharide stimulation. Moreover, serum TNFα concentration showed a clear increase in BM-hIL-32 mice. Cell-sorting analysis of splenocytes showed that the expression of TNFα was increased in resting F4/80(+ )macrophages, and the expression of TNFα, IL-1β and IL-6 was increased in lipopolysaccharide-stimulated F4/80(+ )macrophages and CD11c(+ )dendritic cells. In fact, BM-hIL-32 mice showed exacerbation of collagen-antibody-induced arthritis and trinitrobenzen sulfonic acid-induced colitis. In addition, the transfer of hIL-32β-producing CD4(+ )T cells significantly exacerbated collagen-induced arthritis, and a TNFα blockade cancelled the exacerbating effects of hIL-32β. We therefore conclude that IL-32 is closely associated with TNFα, and contributes to the exacerbation of TNFα-related inflammatory arthritis and colitis