Items of interest from the collection of Serizawa Keisuke： Ancient Andean textiles

染色家・芹沢銈介の集めた世界の民族工芸品の中から、東北福祉大学芹沢銈介美術工芸館で所蔵するアンデスの染織品93 点の目録を掲載し、その内の6 点について資料紹介を行う。2 世紀のナスカで作られた「シャチ魚文様飾り房 断片」は、水と豊穣と死を象徴するシャチの刺繍が施され、装飾として衣服の縁に用いられた。「幾何学文様貫頭衣 断片」は、小片布を組み替えて綴じ合わせることで配色と文様の妙を見せる。「神人文様貫頭衣」は、交易で入手したアマゾンの熱帯に住む鳥たちの鮮やかな羽毛を使っており、「ジャガー・鳥文様マント 断片」には、アンデスの人々が好んだ綴織の特性を示す斜めや階段状の線からなる文様を見ることができる。「海老・鳥文様衣服 断片」は獣毛を使った綴織と木綿による二重織という2 種類の織物が継ぎ合わされてできた衣服で、対照的な二つの布の対比が面白い。そして「鳥・波・獣面文髪覆い」は、チャンカイ文化特有の捩織で作られた、レースのように見える繊細な織物である。 アンデスにはほとんど全ての織物の種類が見られ、さらに独自に考案された技法もあるが、インカ帝国が滅びるまでの全時代を通じて、基本的構造の織機を使用していた。すなわち、これらの繊細な仕事は、複雑な織機の開発によるものではなく、指先の細やかな操作によって生み出されてきたのである。それは、芹沢を導いた柳宗悦の「心偈」の一首「糸の道　法の道」に通じる世界である。芹沢銈介の目と感覚によって選ばれ集まったこれらのコレクションには、作り手への共感のまなざしが感じられる。journal articl

Merging community assembly into the regime-shift approach for informing ecological restoration

生物個体数のわずかな変化から生態系崩壊の兆しを予測、理論を提案. 京都大学プレスリリース. 2017-12-06.Ecosystems that exhibit alternative stable states are a prominent challenge for ecological restoration. So far, alternative stable states have been addressed from two different angles: community assembly studies, which focus on species and their interactions, and regime shift studies, which focus on changes in ecosystem states following environmental change. Here, we propose a synthetic perspective that merges the community assembly with the regime shift approach to effectively inform restoration of ecosystems exhibiting alternative stable states. We show that the community assembly and the regime shift approaches have emphasized different aspects of alternative stable states (i.e., coarse vs fine resolutions of the focal state variable, different sets of feedback mechanisms, and small vs large spatial scales), and consequently have different limitations that influence restoration strategies. Using a simple mathematical model, we illustrate that a more explicit consideration of species identity and composition (i.e., the community assembly approach) can improve our ability to understand regime shifts and restore degraded ecosystems. Finally, we highlight two case studies in which such merging can bring novel insights into alternative stable states and ecological restoration. Understanding the relevant aspects of community assembly (biotic interactions and species identity) will lead to more informed decisions that target future restoration and the prediction of regime shifts in response to global environmental change

Complete mimicry: a case of alveolar rhabdomyosarcoma masquerading as acute leukemia

Abstract Background A small number of rhabdomyosarcoma (RMS) cases involve the bone marrow. A leukemic presentation of RMS has been reported in a few case series, although almost all cases of leukemic RMS are not completely mimicking leukemia. We encountered a case with RMS cell infiltration of the bone marrow that resembled floating hematological cells. Case presentation We encountered a rare case of a 15-year-old boy with a 2-week history of left femoral pain. Upon admission, he was afebrile with no other symptoms. No apparent cause of femoral pain was detected on an initial examination. Laboratory findings revealed normal white blood cell (WBC) count and hemoglobin concentration, with a platelet count of 10.3 × 104/μL. WBCs included 2.0% metamyelocytes, 4.5% myelocytes, and 0.5% blasts. Lactate dehydrogenase concentration was 1299 U/L, creatine kinase was 437 U/L, and C-reactive protein was 1.25 mg/dL. Bone marrow aspiration demonstrated hypercellular marrow (nucleated cell count 1.84 × 104/μL) and 89.0% of blast-like cells of all nucleated cells. The proliferating cells were negative for myeloperoxidase and esterase, and strongly positive for CD56. Positron emission tomography exhibited extensive accumulation of 18F–fludeoxyglucose with a SUVmax of 7.09. Magnetic resonance imaging revealed T1-low intensity, gadolinium-enhanced, diffuse, and irregular lesions on his pelvis and bilateral femurs. These laboratory and imaging findings suggested hematological malignancy with diffuse bone involvement, suggestive of acute leukemia. However, the pathological diagnosis of bone marrow and basal penile muscle biopsy was alveolar RMS. Karyotype analysis of bone marrow cells revealed the characteristic translocation of t(2;13)(q35;q14). The final diagnosis was alveolar RMS with massive involvement of the bone marrow and the primary site in the perineal muscles. The tumor cells both of the primary site and bone marrow were positive for myogenin. Conclusions A literature review found a misdiagnosed case of completely mimicking leukemic RMS as natural-killer (NK)-cell leukemia. Such a misdiagnosis can have critical consequences. We experienced a rare case of alveolar RMS with symmetrical diffuse bone marrow involvement completely masquerading as acute leukemia. The results of a surface marker study showing that the tumor cells had a near NK-cell phenotype were misleading

Defining HIV-1 Vif residues that interact with CBFβ by site-directed mutagenesis

AbstractVif is essential for HIV-1 replication in T cells and macrophages. Vif recruits a host ubiquitin ligase complex to promote proteasomal degradation of the APOBEC3 restriction factors by poly-ubiquitination. The cellular transcription cofactor CBFβ is required for Vif function by stabilizing the Vif protein and promoting recruitment of a cellular Cullin5-RING ubiquitin ligase complex. Interaction between Vif and CBFβ is a promising therapeutic target, but little is known about the interfacial residues. We now demonstrate that Vif conserved residues E88/W89 are crucial for CBFβ binding. Substitution of E88/W89 to alanines impaired binding to CBFβ, degradation of APOBEC3, and virus infectivity in the presence of APOBEC3 in single-cycle infection. In spreading infection, NL4-3 with Vif E88A/W89A mutation replicated comparably to wild-type virus in permissive CEM-SS cells, but not in multiple APOBEC3 expressing non-permissive CEM cells. These results support a model in which HIV-1 Vif residues E88/W89 may participate in binding CBFβ

CKIP-1 Is an Intrinsic Negative Regulator of T-Cell Activation through an Interaction with CARMA1

<div><p>The transcription factor NF-κB plays a key regulatory role in lymphocyte activation and generation of immune response. Stimulation of T cell receptor (TCR) induces phosphorylation of CARMA1 by PKCθ, resulting in formation of CARMA1-Bcl10-MALT1 (CBM) complex at lipid rafts and subsequently leading to NF-κB activation. While many molecular events leading to NF-κB activation have been reported, it is less understood how this activation is negatively regulated. We performed a cell-based screening for negative regulators of TCR-mediated NF-κB activation, using mutagenesis and complementation cloning strategies. Here we show that casein kinase-2 interacting protein-1 (CKIP-1) suppresses PKCθ-CBM-NF-κB signaling. We found that CKIP-1 interacts with CARMA1 and competes with PKCθ for association. We further confirmed that a PH domain of CKIP-1 is required for association with CARMA1 and its inhibitory effect. CKIP-1 represses NF-κB activity in unstimulated cells, and inhibits NF-κB activation induced by stimulation with PMA or constitutively active PKCθ, but not by stimulation with TNFα. Interestingly, CKIP-1 does not inhibit NF-κB activation induced by CD3/CD28 costimulation, which caused dissociation of CKIP-1 from lipid rafts. These data suggest that CKIP-1 contributes maintenance of a resting state on NF-κB activity or prevents T cells from being activated by inadequate signaling. In conclusion, we demonstrate that CKIP-1 interacts with CARMA1 and has an inhibitory effect on PKCθ-CBM-NF-κB signaling.</p></div