Quantum Field Theories with Tensor Renormalization Group

We report recent progress on the application of the tensor renormalization group (TRG) to quantum field theories pursued by the Tsukuba group. We explain how to treat the scalar, fermion, and gauge theories with the TRG method presenting the results for the phase transitions in the (3+1)-dimensional ((3+1)$d$) complex $\phi^4$ theory at finite density, (1+1)$d$ pure U(1) lattice gauge theory with a $\theta$ term, (3+1)$d$ Nambu--Jona-Lasinio model at finite density and (1+1)$d$ and (2+1)$d$ Hubbard models at an arbitrary chemical potential. It is demonstrated that the TRG method is free from the sign problem in practical calculations and applicable to the four-dimensional models.Comment: 25 pages, 20 figures, Proceedings of the 38th International Symposium on Lattice Field Theory, LATTICE2021 26th-30th July 2021, Zoom/Gather@Massachusetts Institute of Technolog

Detecting Train Delays using Railway Network Topology in Twitter

This paper presents a novel train delay detection method based on topic propagation analysis of geo-tagged tweets between railway stations. Our goal is to detect traffic accidents and to predict train delays in railway network topology by tracing how relevant tweets propagate in real space and cyberspace. In our method, we utilize railway network as the topology of real space, and extract the topology of social network that is mapped on the railway network. This permits observing the influence of delays on stations with a few tweets, or predicting related tweets of affected stations even if the tweets contain indirect topics about delays

Activation of an Estrogen/ Estrogen Receptor Signaling by BIG3 Through Its Inhibitory Effect on Nuclear Transport of PHB2/REA in Breast Cancer

Breast cancer is known to be a hormone-dependent disease, and estrogens through an interaction with estrogen receptor (ER) enhance the proliferative and metastatic activity of breast tumor cells. Here we show a critical role of transactivation of BIG3, brefeldin A-inhibited guanine nucleotide-exchange protein 3, in activation of the estrogen/ER signaling in breast cancer cells. Knocking-down of BIG3 expression with small-interfering RNA (siRNA) drastically suppressed the growth of breast cancer cells. Subsequent co-immunoprecipitation and immunoblotting assays revealed an interaction of BIG3 with prohibitin 2/repressor of estrogen receptor activity (PHB2/REA). When BIG3 was absent, stimulation of estradiol caused the translocation of PHB2/REA to the nucleus, enhanced the interaction of PHB2/REA and ER[alpha], and resulted in suppression of the ER[alpha]; transcriptional activity. On the other hand, when BIG3 was present, BIG3 trapped PHB2/REA in cytoplasm and inhibited its nuclear translocation, and caused enhancement of ER[alpha]; transcriptional activity. Our results imply that BIG3 overexpression is one of the important mechanisms causing the activation of the estrogen/ER[alpha]; signaling pathway in the hormone-related growth of breast cancer cells

Actin Family in INO80 Complex

Nuclear actin family proteins, comprising of actin and actin-related proteins (Arps), are essential functional components of the multiple chromatin remodeling complexes. The INO80 chromatin remodeling complex, which is evolutionarily conserved and has roles in transcription, DNA replication and repair, consists of actin and actin-related proteins Arp4, Arp5, and Arp8. We generated Arp5 knockout (KO) and Arp8 KO cells from the human Nalm-6 pre-B cell line and used these KO cells to examine the roles of Arp5 and Arp8 in the transcriptional regulation mediated by the INO80 complex. In both of Arp5 KO and Arp8 KO cells, the oxidative stress-induced expression of HMOX1 gene, encoding for heme oxygenase-1 (HO-1), was significantly impaired. Consistent with these observations, chromatin immunoprecipitation (ChIP) assay revealed that oxidative stress caused an increase in the binding of the INO80 complex to the regulatory sites of HMOX1 in wild-type cells. The binding of INO80 complex to chromatin was reduced in Arp8 KO cells compared to that in the wild-type cells. On the other hand, the binding of INO80 complex to chromatin in Arp5 KO cells was similar to that in the wild-type cells even under the oxidative stress condition. However, both remodeling of chromatin at the HMOX1 regulatory sites and binding of a transcriptional activator to these sites were impaired in Arp5 KO cells, indicating that Arp5 is required for the activation of the INO80 complex. Collectively, these results suggested that these nuclear Arps play indispensable roles in the function of the INO80 chromatin remodeling complex