Constraints on Unparticle Interactions from Invisible Decays of Z, Quarkonia and Neutrinos

Unparticles (\U) interact weakly with particles. The direct signature of unparticles will be in the form of missing energy. We study constraints on unparticle interactions using totally invisible decay modes of $Z$, vector quarkonia $V$ and neutrinos. The constraints on the unparticle interaction scale \Lambda_\U are very sensitive to the dimension d_\U of the unparticles. From invisible $Z$ and $V$ decays, we find that with d_\U close to 1 for vector \U, the unparticle scale \Lambda_\U can be more than $10^4$ TeV, and for d_\U around 2, the scale can be lower than one TeV. From invisible neutrino decays, we find that if d_\U is close to 3/2, the scale can be more than the Planck mass, but with d_\U around 2 the scale can be as low as a few hundred GeV. We also study the possibility of using V (Z)\to \gamma + \U to constrain unparticle interactions, and find that present data give weak constraints.Comment: 12 pages, 4 figures, version to appear in JHEP

Initial presentation of mesenteric venous thrombosis mimicking acute duodenitis: A true gastrointestinal vascular emergency

AbstractWe present a patient who had a 3-day history of epigastric pain and acid regurgitation and was found to have gastroesophageal reflux disease and duodenitis by esophagogastroduodenoscopy. His symptoms were refractory to treatment with a proton pump inhibitor. Peritonitis developed subsequently. Enhanced computed tomography (CT) confirmed a diagnosis of mesenteric venous thrombosis (MVT) with jejunum infarction. Emergency exploratory laparotomy with segmental resectioning of the jejunum was performed. We emphasize that emergency department (ED) physicians should always thoroughly re-evaluate patients with abdominal pain using serial physical examinations in accordance with the chronic nature of the disease. There is a need to be highly alert to pain that is out of the proportion to the physical examination results and/or endoscopic findings, the development of peritoneal irritation signs, the presence of fever, and the presence of leukocytosis among patients with nonspecific endoscopic findings. This will help to differentiate MVT as the true etiology of ischemic duodenitis in a timely manner. ED physicians should also be aware that hyperemic edematous duodenitis can be the finding for MVT using endoscopy

Quantum Speedup for the Maximum Cut Problem

Given an undirected, unweighted graph with $n$ vertices and $m$ edges, the maximum cut problem is to find a partition of the $n$ vertices into disjoint subsets $V_1$ and $V_2$ such that the number of edges between them is as large as possible. Classically, it is an NP-complete problem, which has potential applications ranging from circuit layout design, statistical physics, computer vision, machine learning and network science to clustering. In this paper, we propose a quantum algorithm to solve the maximum cut problem for any graph $G$ with a quadratic speedup over its classical counterparts, where the temporal and spatial complexities are reduced to, respectively, $O(\sqrt{2^n/r})$ and $O(m^2)$. With respect to oracle-related quantum algorithms for NP-complete problems, we identify our algorithm as optimal. Furthermore, to justify the feasibility of the proposed algorithm, we successfully solve a typical maximum cut problem for a graph with three vertices and two edges by carrying out experiments on IBM's quantum computer.Comment: 4 pages, 6 figures, The 28th Workshop on Compiler Techniques and System Software for High-Performance and Embedded Computing (CTHPC 2023), May 25-26 2023, National Cheng Kung University, Tainan, Taiwan. v2: indicated corresponding authors, included a link to the GitHub repository in Section "Code availability

Cyclooxygenase-2 enhances α2β1 integrin expression and cell migration via EP1 dependent signaling pathway in human chondrosarcoma cells

<p>Abstract</p> <p>Background</p> <p>Cyclooxygenase (COX)-2, the inducible isoform of prostaglandin (PG) synthase, has been implicated in tumor metastasis. Interaction of COX-2 with its specific EP receptors on the surface of cancer cells has been reported to induce cancer invasion. However, the effects of COX-2 on migration activity in human chondrosarcoma cells are mostly unknown. In this study, we examined whether COX-2 and EP interaction are involved in metastasis of human chondrosarcoma.</p> <p>Results</p> <p>We found that over-expression of COX-2 or exogenous PGE₂increased the migration of human chondrosarcoma cells. We also found that human chondrosarcoma tissues and chondrosarcoma cell lines had significant expression of the COX-2 which was higher than that in normal cartilage. By using pharmacological inhibitors or activators or genetic inhibition by the EP receptors, we discovered that the EP1 receptor but not other PGE receptors is involved in PGE₂-mediated cell migration and α2β1 integrin expression. Furthermore, we found that human chondrosarcoma tissues expressed a higher level of EP1 receptor than normal cartilage. PGE₂-mediated migration and integrin up-regulation were attenuated by phospholipase C (PLC), protein kinase C (PKC) and c-Src inhibitor. Activation of the PLCβ, PKCα, c-Src and NF-κB signaling pathway after PGE₂treatment was demonstrated, and PGE₂-induced expression of integrin and migration activity were inhibited by the specific inhibitor, siRNA and mutants of PLC, PKC, c-Src and NF-κB cascades.</p> <p>Conclusions</p> <p>Our results indicated that PGE₂enhances the migration of chondrosarcoma cells by increasing α2β1 integrin expression through the EP1/PLC/PKCα/c-Src/NF-κB signal transduction pathway.</p