Exact Drude weight for the one-dimensional Hubbard model at finite temperatures

The Drude weight for the one-dimensional Hubbard model is investigated at finite temperatures by using the Bethe ansatz solution. Evaluating finite-size corrections to the thermodynamic Bethe ansatz equations, we obtain the formula for the Drude weight as the response of the system to an external gauge potential. We perform low-temperature expansions of the Drude weight in the case of half-filling as well as away from half-filling, which clearly distinguish the Mott-insulating state from the metallic state.Comment: 9 pages, RevTex, To appear in J. Phys.

Report on Distribution and Spawning of Small-scale Sillago, Sillago parvisquamis (family Sillaginidae), Based on Specimens from Yamaguchi Bay in Western Seto Inland Sea, Japan. <Article>

瀬戸内海山口湾で2005 ～ 2008 年に,絶滅危惧種アオギスSillago parvisquamis 8 標本(SP-YB1 ～ 8)を採集した。全長226.5 ～ 320.1mm,体長197.7 ～ 281.0mm,いずれも雌で,年齢はSP-YB1 ～ 6 が1才,SP-YB7 が3才,およびSP-YB8 は4才で,全個体が2004年級であった。卵巣の組織学的検討より,SP-YB1 ～ 7 では,最も発達した正常な卵母細胞は第三次卵黄球期か胚胞移動期で,排卵後濾胞細胞を有し,活発な産卵活動が確認された。釣りCPUE(個体数/3時間/ 人)は,2005 ～ 2012年では,5 ～ 7月は0.2(n=24),通年では0.1(n=49)であった。2004年級を主な対象とした2005 ～ 2006年の2年間では,5 ～ 7月は0.3(n=14),通年では0.2(n=23)であった。今回,標本に基づき山口湾を生息地および繁殖地として記載した。Small-scale sillago, Sillago parvisquamis, were collected from Yamaguchi Bay, western Seto Inland Sea, Japan. This species has been evaluated as an endangered species in Japan. Eight specimens (sample no. SPYB1-8) collected in 2005-2008 were 226.5-320.1 mm TL, 197.7-281.0 mm SL and were all adult females. The ages of SPYB1-6, 7, and 8 were 1, 3, and 4 years, respectively, and all individuals were of the 2004 class. Judging from ovarian histological samples, the most developed stage of normal oocytes in SPYB1-7 was the tertiary yolk globule stage or the migratory nucleus stage. All individuals had a lot of post-ovulatory follicles. Therefore, these two evidences indicate spawning. The catch per unit effort (CPUE) (indiv. / 3 hours / person) by fishing in 2005-2012 was 0.2 for the spawning season (n=24) and 0.1 for the whole year (n=49). For the 2004 class, CPUE in 2005-2006 was 0.3 for the spawning season (n=14) and 0.2 for the whole year (n=23). This is the detailed report of the distribution and spawning of Sillago parvisquamis based on specimens from Yamaguchi Bay

SKF-10047, a prototype Sigma-1 receptor agonist, augmented the membrane trafficking and uptake activity of the serotonin transporter and its C-terminus-deleted mutant via a Sigma-1 receptor-independent mechanism

The serotonin transporter (SERT) is functionally regulated via membrane trafficking. Our previous studies have demonstrated that the SERT C-terminal deletion mutant (SERTΔCT) showed a robust decrease in its membrane trafficking and was retained in the endoplasmic reticulum (ER), suggesting that SERTΔCT is an unfolded protein that may cause ER stress. The Sigma-1 receptor (SigR1) has been reported to attenuate ER stress via its chaperone activity. In this study, we investigated the effects of SKF-10047, a prototype SigR1 agonist, on the membrane trafficking and uptake activity of SERT and SERTΔCT expressed in COS-7 cells. Twenty-four hours of SKF-10047 treatment (>200 μM) accelerated SERT membrane trafficking and robustly upregulated SERTΔCT activity. Interestingly, these effects of SKF-10047 on SERT functions were also found in cells in which SigR1 expression was knocked down by shRNA, suggesting that SKF-10047 exerted these effects on SERT via a mechanism independent of SigR1. A cDNA array study identified several candidate genes involved in the mechanism of action of SKF-10047. Among them, Syntaxin3, a member of the SNARE complex, was significantly upregulated by 48 h of SKF-10047 treatment. These results suggest that SKF-10047 is a candidate for ER stress relief. Keywords: Serotonin transporter, Sigma-1 receptor, Membrane trafficking, SKF-1004

Recurrent CCND3 mutations in MLL-rearranged acute myeloid leukemia

急性骨髄性白血病の新規遺伝子変異を発見 --乳がんの既存薬が治療に有効である可能性--. 京都大学プレスリリース. 2018-11-01.In acute myeloid leukemia (AML), MLL (KMT2A) rearrangements are among the most frequent chromosomal abnormalities; however, knowledge of the genetic landscape of MLL-rearranged AML is limited. In this study, we performed whole-exome sequencing (n = 9) and targeted sequencing (n = 56) of samples from pediatric MLL-rearranged AML patients enrolled in the Japanese Pediatric Leukemia/Lymphoma Study Group AML-05 study. Additionally, we analyzed 105 pediatric t(8;21) AML samples and 30 adult MLL-rearranged AML samples. RNA-sequencing data from 31 patients published in a previous study were also reanalyzed. As a result, we identified 115 mutations in pediatric MLL-rearranged AML patients (2.1 mutations/patient), with mutations in signaling pathway genes being the most frequently detected (60.7%). Mutations in genes associated with epigenetic regulation (21.4%), transcription factors (16.1%), and the cohesin complex (8.9%) were also commonly detected. Novel CCND3 mutations were identified in 5 pediatric MLL-rearranged AML patients (8.9%) and 2 adult MLL-rearranged AML patients (3.3%). Recurrent mutations of CCND1 (n = 3, 2.9%) and CCND2 (n = 8, 7.6%) were found in pediatric t(8;21) AML patients, whereas no CCND3 mutations were found, suggesting that D-type cyclins exhibit a subtype-specific mutation pattern in AML. Treatment of MLL-rearranged AML cell lines with CDK4/6 inhibitors (abemaciclib and palbociclib) blocked G1 to S phase cell-cycle progression and impaired proliferation. Pediatric MLL-MLLT3–rearranged AML patients with coexisting mutations (n = 16) had significantly reduced relapse-free survival and overall survival compared with those without coexisting mutations (n = 9) (P = .048 and .046, respectively). These data provide insights into the genetics of MLL-rearranged AML and suggest therapeutic strategies