Higher Berry curvature from matrix product states

The higher Berry curvature was introduced by Kapustin and Spodyneiko as an extension of the Berry curvature in quantum mechanical systems with finite degrees of freedom to quantum many-body systems in finite spatial dimensions. In this paper, we propose an alternative formulation of the higher Berry curvature using translationally invariant matrix product states. They are the ground states of a set of gapped Hamiltonians which are evolved adiabatically through a discretized parameter space. Because matrix product states transform under a projective representation, evaluating the Berry curvature on a closed loop through parameter space is not sufficient to fix all the gauge degrees of freedom. To obtain a gauge-invariant real quantity, the higher-dimensional Berry curvature is evaluated on small tetrahedra in parameter space. Our numerical calculations confirm that the higher Berry curvature varies continuously throughout an adiabatic evolution and becomes quantized over a closed 3-dimensional parameter space.Comment: Sec. V-B-2, numerical calculation for random J1 J2 adde

Prognostic utility of chromosomal instability detected by fluorescence in situ hybridization in fine-needle aspirates from oral squamous cell carcinomas

<p>Abstract</p> <p>Background</p> <p>Although chromosomal instability (CIN) has been detected in many kinds of human malignancies by means of various methods, there is no practical assessment for small clinical specimens. In this study, we evaluated CIN in fine-needle aspiration (FNA) biopsied oral squamous cell carcinomas (SCCs) using fluorescence <it>in situ </it>hybridization (FISH) analysis, and investigated its prognostic significance.</p> <p>Methods</p> <p>To evaluate CIN status of tumors, FISH with genomic probes for the centromeres of chromosomes 7, 9, and 11 was performed on specimens obtained by FNA from 77 patients with primary oral SCCs.</p> <p>Results</p> <p>High-grade CIN (CIN3) was observed in 11.7% (9/77) of patients with oral SCCs and was associated significantly with reduced disease-free survival (<it>p </it>= .008) and overall survival (<it>p </it>= .003). Multivariate Cox proportional hazards analysis showed that CIN status was significantly correlated with disease-free survival (<it>p </it>= .035) and overall survival (<it>p </it>= .041).</p> <p>Conclusion</p> <p>Analysis of CIN status using FISH on FNA biopsy specimens may be useful in predicting of recurrence and poor prognosis in patients with oral SCCs.</p

A reporter system evaluates tumorigenesis, metastasis, β-catenin/MMP regulation, and druggability

Cancer invasion, metastasis, and therapy resistance are the crucial phenomena in cancer malignancy. The high-expression of matrix metalloproteinase 9 (MMP9) is a biomarker as well as a causal factor of cancer invasiveness and metastatic activity. However, a regulatory mechanism underlying MMP9 expression in cancer is not clarified yet. Additionally, a new strategy for anti-cancer drug discovery is becoming an important clue. In the present study, we aimed (i) to develop a novel reporter system evaluating tumorigenesis, invasiveness, metastasis, and druggability with a combination of three-dimensional (3D) tumoroid model and Mmp9 promoter and (ii) to examine pharmacological actions of anti-cancer medications using this reporter system. High expression and genetic amplification of MMP9 were found in colon cancer cases. We found that proximal promoter sequences of MMP9 in murine and human contained conserved binding sites for transcription factors β-catenin/TCF/LEF, glucocorticoid receptor (GR), and NF-κB. The murine Mmp9 promoter (-569 to +19) was markedly activated in metastatic colon cancer cells and additionally activated by tumoroid formation and by β-catenin signaling stimulator lithium chloride (LiCl). The Mmp9 promoter-driven fluorescent reporter cells enabled the monitoring of activities of MMP9/gelatinase, tumorigenesis, invasion, and metastasis in allogeneic/syngenic transplantation experiments. We also demonstrated pharmacological actions as follows. ids Dexamethasone and hydrocortisone, steroidal medications binding to GR, inhibited the Mmp9 promoter but did not inhibit tumorigenesis. On the other hand, an antimetabolite 5-fluorouracil, a golden standard for colon cancer chemotherapy, inhibited tumoroid formation but did not inhibit Mmp9 promoter activity. Notably, anti-malaria medication artesunate inhibited both tumorigenesis and the Mmp9 promoter in vitro, potentially through inhibition of β-catenin/TCF/LEF signaling. Thus, this novel reporter system enabled monitoring tumorigenesis, invasiveness, metastasis, key regulatory signalings such as β-catenin/MMP9 axis, and druggability

Ectopic Varices Rupture in the Gastroduodenal Anastomosis Successfully Treated with N-butyl-2-cyanoacrylate Injection

The term &#34;ectopic varices&#34; is used to describe dilated portosystemic collateral veins in unusual locations other than the gastroesophageal region. We recently experienced a rare case of ectopic varices that developed in the gastroduodenal anastomosis after subtotal gastrectomy. A 70-year-old male with liver cirrhosis due to hepatitis C virus infection was admitted for hematemesis and tarry stool. He had received a subtotal gastrectomy with the Billroth-I method for gastric ulcer at 46 years of age. Although emergency endoscopy revealed esophageal and gastric fundal varices, there were no obvious bleeding points. After removal of the coagula, ectopic varices and a fibrin plug were observed on the gastroduodenal anastomosis. During the observation, blood began to spurt from the fibrin plug. N-butyl-2-cyanoacrylate with lipiodol injection succeeded in hemostasis. Splenic angiography showed gastric varices feeding from a short gastric vein and the posterior gastric vein. The blood flow around the bleeding point, as indicated by lipiodol deposition, had decreased, and no feeding vein was observed. Endoscopic and angiographic findings are shown and the treatment for such lesions is discussed.</p

Nociceptive interneurons control modular motor pathways to promote escape behavior in Drosophila.

Rapid and efficient escape behaviors in response to noxious sensory stimuli are essential for protection and survival. Yet, how noxious stimuli are transformed to coordinated escape behaviors remains poorly understood. In Drosophila larvae, noxious stimuli trigger sequential body bending and corkscrew-like rolling behavior. We identified a population of interneurons in the nerve cord of Drosophila, termed Down-and-Back (DnB) neurons, that are activated by noxious heat, promote nociceptive behavior, and are required for robust escape responses to noxious stimuli. Electron microscopic circuit reconstruction shows that DnBs are targets of nociceptive and mechanosensory neurons, are directly presynaptic to pre-motor circuits, and link indirectly to Goro rolling command-like neurons. DnB activation promotes activity in Goro neurons, and coincident inactivation of Goro neurons prevents the rolling sequence but leaves intact body bending motor responses. Thus, activity from nociceptors to DnB interneurons coordinates modular elements of nociceptive escape behavior

Nociceptive interneurons control modular motor pathways to promote escape behavior in Drosophila

Rapid and efficient escape behaviors in response to noxious sensory stimuli are essential for protection and survival. Yet, how noxious stimuli are transformed to coordinated escape behaviors remains poorly understood. In Drosophila larvae, noxious stimuli trigger sequential body bending and corkscrew-like rolling behavior. We identified a population of interneurons in the nerve cord of Drosophila, termed Down-and-Back (DnB) neurons, that are activated by noxious heat, promote nociceptive behavior, and are required for robust escape responses to noxious stimuli. Electron microscopic circuit reconstruction shows that DnBs are targets of nociceptive and mechanosensory neurons, are directly presynaptic to pre-motor circuits, and link indirectly to Goro rolling command-like neurons. DnB activation promotes activity in Goro neurons, and coincident inactivation of Goro neurons prevents the rolling sequence but leaves intact body bending motor responses. Thus, activity from nociceptors to DnB interneurons coordinates modular elements of nociceptive escape behavior