Energy Functions in Box Ball Systems

The box ball system is studied in the crystal theory formulation. New conserved quantities and the phase shift of the soliton scattering are obtained by considering the energy function (or $H$-function) in the combinatorial $R$-matrix.Comment: 15 pages, LaTeX2e: one paragraph replaced and reference added in Introduction, a paragraph added in Section 2.5, remark 2) after Th 4.6 adde

Algorithms for finding attribute value group for binary segmentation of categorical databases

科研費報告書収録論文(課題番号:13680387・基盤研究(C)(2)・H13～H15/研究代表者:徳山, 豪/パラメトリック最適化を用いた幾何学データ処理の研究

Mining Optimized Association Rules for Numeric Attributes

AbstractGiven a huge database, we address the problem of finding association rules for numeric attributes, such as(Balance∈I)⇒(CardLoan=yes),which implies that bank customers whose balances fall in a rangeIare likely to use card loan with a probability greater thanp. The above rule is interesting only if the rangeIhas some special feature with respect to the interrelation betweenBalanceandCardLoan. It is required that the number of customers whose balances are contained inI(called thesupportofI) is sufficient and also that the probabilitypof the conditionCardLoan=yesbeing met (called theconfidence ratio) be much higher than the average probability of the condition over all the data. Our goal is to realize a system that finds such appropriate ranges automatically. We mainly focus on computing twooptimized ranges: one that maximizes the support on the condition that the confidence ratio is at least a given threshold value, and another that maximizes the confidence ratio on the condition that the support is at least a given threshold number. Using techniques from computational geometry, we present novel algorithms that compute the optimized ranges in linear time if the data are sorted. Since sorting data with respect to each numeric attribute is expensive in the case of huge databases that occupy much more space than the main memory, we instead apply randomized bucketing as the preprocessing method and thus obtain an efficient rule-finding system. Tests show that our implementation is fast not only in theory but also in practice. The efficiency of our algorithm enables us to compute optimized rules for all combinations of hundreds of numeric and Boolean attributes in a reasonable time

Crystal interpretation of Kerov-Kirillov-Reshetikhin bijection

The Kerov-Kirillov-Reshetikhin (KKR) bijection is the crux in proving fermionic formulas. It is defined by a combinatorial algorithm on rigged configurations and highest paths. We reformulate the KKR bijection as a vertex operator by purely using combinatorial R in crystal base theory. The result is viewed as a nested Bethe ansatz at q=0 as well as the direct and the inverse scattering (Gel'fand-Levitan) map in the associated soliton cellular automaton.Comment: 28 page

Tau functions in combinatorial Bethe ansatz

We introduce ultradiscrete tau functions associated with rigged configurations for A^{(1)}_n. They satisfy an ultradiscrete version of the Hirota bilinear equation and play a role analogous to a corner transfer matrix for the box-ball system. As an application, we establish a piecewise linear formula for the Kerov-Kirillov-Reshetikhin bijection in the combinatorial Bethe ansatz. They also lead to general N-soliton solutions of the box-ball system.Comment: 52 page

Notch3-dependent β-catenin signaling mediates EGFR TKI drug persistence in EGFR mutant NSCLC

EGFR tyrosine kinase inhibitors cause dramatic responses in EGFR-mutant lung cancer, but resistance universally develops. The involvement of β-catenin in EGFR TKI resistance has been previously reported, however, the precise mechanism by which β-catenin activation contributes to EGFR TKI resistance is not clear. Here, we show that EGFR inhibition results in the activation of β-catenin signaling in a Notch3-dependent manner, which facilitates the survival of a subset of cells that we call “adaptive persisters”. We previously reported that EGFR-TKI treatment rapidly activates Notch3, and here we describe the physical association of Notch3 with β-catenin, leading to increased stability and activation of β-catenin. We demonstrate that the combination of EGFR-TKI and a β-catenin inhibitor inhibits the development of these adaptive persisters, decreases tumor burden, improves recurrence free survival, and overall survival in xenograft models. These results supports combined EGFR-TKI and β-catenin inhibition in patients with EGFR mutant lung cancer

頸部リンパ節転移が嚢胞を呈した甲状腺不顕性癌の1例

頸部リンパ節転移が,嚢胞を呈した甲状腺不顕性癌の1例を経験したので報告した.症例31歳男性,左側頸部腫瘤を主訴として来院.側頸部嚢胞と診断したが,摘出腫瘤を組織学的に検討した結果,甲状腺癌のリンパ節転移と判明した.The purpose of this paper is to report a case of minimal carcinoma of the thyroid manifested by a cystic metastasis to the cervical lymph nodes which mimicked a lateral cervical cyst in a 31-year-old male and to discuss the clinical significance of cystic metastasis from papillary adenocarcinoma of the thyroid

Brown adipose tissue dysfunction promotes heart failure via a trimethylamine N-oxide-dependent mechanism.

Low body temperature predicts a poor outcome in patients with heart failure, but the underlying pathological mechanisms and implications are largely unknown. Brown adipose tissue (BAT) was initially characterised as a thermogenic organ, and recent studies have suggested it plays a crucial role in maintaining systemic metabolic health. While these reports suggest a potential link between BAT and heart failure, the potential role of BAT dysfunction in heart failure has not been investigated. Here, we demonstrate that alteration of BAT function contributes to development of heart failure through disorientation in choline metabolism. Thoracic aortic constriction (TAC) or myocardial infarction (MI) reduced the thermogenic capacity of BAT in mice, leading to significant reduction of body temperature with cold exposure. BAT became hypoxic with TAC or MI, and hypoxic stress induced apoptosis of brown adipocytes. Enhancement of BAT function improved thermogenesis and cardiac function in TAC mice. Conversely, systolic function was impaired in a mouse model of genetic BAT dysfunction, in association with a low survival rate after TAC. Metabolomic analysis showed that reduced BAT thermogenesis was associated with elevation of plasma trimethylamine N-oxide (TMAO) levels. Administration of TMAO to mice led to significant reduction of phosphocreatine and ATP levels in cardiac tissue via suppression of mitochondrial complex IV activity. Genetic or pharmacological inhibition of flavin-containing monooxygenase reduced the plasma TMAO level in mice, and improved cardiac dysfunction in animals with left ventricular pressure overload. In patients with dilated cardiomyopathy, body temperature was low along with elevation of plasma choline and TMAO levels. These results suggest that maintenance of BAT homeostasis and reducing TMAO production could be potential next-generation therapies for heart failure.We thank Kaori Yoshida, Keiko Uchiyama, Satomi Kawai, Naomi Hatanaka, Yoko Sawaguchi, Runa Washio, Takako Ichihashi, Nanako Koike, Keiko Uchiyama, Masaaki Nameta (Niigata University), Kaori Igarashi, Kaori Saitoh, Keiko Endo, Hiroko Maki, Ayano Ueno, Maki Ohishi, Sanae Yamanaka, Noriko Kagata (Keio University) for their excellent technical assistance, C. Ronald Kahn (Joslin Diabetes Center and Harvard Medical School) for providing the BAT cell line, Evan Rosen (Harvard Medical School) for providing us Ucp-Cre mice, Kosuke Morikawa (Kyoto University), Tomitake Tsukihara (University of Hyogo) and Shinya Yoshikawa (University of Hyogo) for their professional opinions and suggestions. Tis work was supported by a Grant-in-Aid for Scientifc Research (A) (20H00533) from MEXT, AMED under Grant Numbers JP20ek0210114, and AMED-CREST under Grant Number JP20gm1110012, and Moonshot Research and Development Program (21zf0127003s0201), MEXT Supported Program for the Strategic Research Foundation at Private Universities Japan, Private University Research Branding Project, and Leading Initiative for Excellent Young Researchers, and grants from the Takeda Medical Research Foundation, the Vehicle Racing Commemorative Foundation, Ono Medical Research Foundation, and the Suzuken Memorial Foundation (to T.M.). Support was also provided by a Grants-in-Aid for Young Scientists (Start-up) (26893080), and grants from the Uehara Memorial Foundation, Kowa Life Science Foundation, Manpei Suzuki Diabetes Foundation, SENSHIN Medical Research Foundation, ONO Medical Research Foundation, Tsukada Grant for Niigata University Medical Research, Te Nakajima Foundation, SUZUKEN memorial foundation, HOKUTO Corporation, Mochida Memorial Foundation for Medical & Pharmaceutical Research, Grants-in-Aid for Encouragement of Young Scientists (A) (16H06244), Daiichi Sankyo Foundation of Life Science, AMED Project for Elucidating and Controlling Mechanisms of Aging and Longevity under Grant Number JP17gm5010002, JP18gm5010002, JP19gm5010002, JP20gm5010002, JP21gm5010002, Astellas Foundation for Research on Metabolic Disorders, Research grant from Naito Foundation, Te Japan Geriatrics Society (to I.S.); by a Grant-in-Aid for Scientifc Research (C) (19K08974), Yujin Memorial Grant, Sakakibara Memorial Research Grant from Te Japan Research Promotion Society for Cardiovascular Diseases, TERUMO Life Science Foundation, Kanae Foundation (to Y.Y.), JST ERATO (JPMJER1902), AMED-CREST (JP20gm1010009), the Takeda Science Foundation, the Food Science Institute Foundation (to S.F.), and by a grant from Bourbon (to T.M., I.S. and Y.Y.).S