Classical Aspects of the Abelian Higgs Model on the Light Front

We investigate canonical structure of the Abelian Higgs model within the framework of DLCQ. Careful boundary analysis of differential equations, such as the Euler-Lagrange equations, leads us to a novel situation where the canonical structure changes in a drastic manner depending on whether the (light-front) spatial Wilson line is periodic or not. In the former case, the gauge-field ZM takes discrete values and we obtain the so-called ``Zero-Mode Constraints'' (ZMCs), whose semiclassical solutions give a nonzero vev to the scalar fields. Contrary, in the latter case, we have no ZMC and the scalar ZMs remain dynamical as well as the gauge-field ZM. In order to give classically nonzero vev to the scalar field, we work in a background field which minimizes the light-front energy.Comment: 10 pages, reference modifie

Many-Brane Extention of the Randall-Sundrum Solution

Recently, Randall and Sundrum proposed a static solution to Einstein's equations in five spacetime dimensions with two 3-branes located at the fixed points of $S^1/Z_2$ to solve the hierarchy problem. We extend the solution and construct static and also inflationary solutions to Einstein's equations in five spacetime dimensions, one of which is compactified on $S^1$, with any number of 3-branes whose locations are taken to be arbitrary. We discuss how the hierarchy problem can be explained in our model.Comment: PTPTeX 1.0(preprint style), 8 pages, no figures, references and typos correcte

Spontaneous Supersymmetry Breaking from Extra Dimensions

We propose a new spontaneous supersymmetry breaking mechanism, in which extra compact dimensions play an important role. To illustrate our mechanism, we study a simple model consisting of two chiral superfields, where one spatial dimension is compactified on a circle $S^1$. It is shown that supersymmetry is spontaneously broken irrespective of the radius of the circle, and also that the translational invariance for the $S^1$-direction and a global symmetry are spontaneously broken when the radius becomes larger than a critical radius. These results are expected to be general features of our mechanism. We further discuss that our mechanism may be observed as the O'Raifeartaigh type of supersymmetry breaking at low energies.Comment: 10 pages, No figur

Spontaneously Broken Translational Invariance of Compactified Space

We propose a mechanism to break the translational invariance of compactified space spontaneously. As a simple model, we study a real $\phi^4$ model compactified on $M^{D-1}\otimes S^1$ in detail, where we impose a nontrivial boundary condition on $\phi$ for the $S^1$-direction. It is shown that the translational invariance for the $S^1$-direction is spontaneously broken when the radius $R$ of $S^1$ becomes larger than a critical radius $R^*$ and also that the model behaves like a $\phi^4$ model on a single kink background for $R \to \infty$. It is pointed out that spontaneous breakdown of translational invariance is accompanied by that of some global symmetries, in general, in our mechanism.Comment: 9 pages, No figur

Tracheal Stenosis Caused by Unnoticed Foreign Bodies

We describe an extremely rare case of tracheal stenosis caused by unnoticed microscopic fiber-like foreign bodies. A 66-year-old woman complained of dyspnea with inspiratory stridor. Magnifying electroendoscopy and computed tomography revealed stenosis involving the entire circumference of the tracheal lumen. Tracheotomy and biopsy were performed. Histologically, the lesion showed chronic inflammation with a deposition of fiber-like foreign bodies. The patient had no history of trauma or inhalation injury, but had undergone intratracheal intubation on 4 occasions. The lesion was incised using semiconductor laser photoresection, and the postoperative course was good. To the best of our knowledge, this represents the first report in the English literature of tracheal stenosis caused by unnoticed foreign bodies. The origin of these fiber-like foreign bodies remains unclear but might be related to chronic inflammation resulting from intratracheal intubations

Role of Macrophage Migration Inhibitory Factor in NLRP3 Inflammasome Expression in Otitis Media

Hypothesis: Macrophage migration inhibitory factor plays an important role in the expression of interleukin (IL)-1β and the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome in lipopolysaccharide-induced otitis media. Background: NLRP3 inflammasome and macrophage migration inhibitory factor are critical molecules mediating inflammation. However, the interaction between the NLRP3 inflammasome and macrophage migration inhibitory factor has not been fully examined. Methods: Wild-type mice and macrophage migration inhibitory factor gene-deficient (MIF−/−) mice received a transtympanic injection of either lipopolysaccharide or phosphate-buffered saline. The mice were sacrificed 24 hours after the injection. Concentrations of IL-1β, NLRP3, ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain and a pyrin domain), and caspase-1 in the middle ear effusions were measured by enzyme-linked immunosorbent assay. Temporal bones were processed for histologic examination and immunohistochemistry. Results: In the immunohistochemical study using the wild-type mice, positive staining of macrophage migration inhibitory factor, NLRP3, ASC, and caspase-1 were observed in infiltrating inflammatory cells induced by lipopolysaccharide in the middle ear. The number of inflammatory cells caused by lipopolysaccharide administration decreased remarkably in the MIF−/− mice as compared with the wild-type mice. The concentrations of IL-1β, NLRP3, ASC, and caspase-1 increased in the lipopolysaccharide-treated wild-type mice. The MIF−/− mice with lipopolysaccharide had decreased levels of IL-1β, NLRP3, ASC, and caspase-1 as compared with the wild-type mice. Conclusion: Macrophage migration inhibitory factor has an important role in the production of IL-1β and the NLRP3 inflammasome. Controlling the inflammation by modulating macrophage migration inhibitory factor and the NLRP3 inflammasome may be a novel therapeutic strategy for otitis media

Clinical Significance of Cytoplasmic IgE-Positive Mast Cells in Eosinophilic Chronic Rhinosinusitis

Cross-linking of antigen-specific IgE bound to the high-affinity IgE receptor (Fc epsilon RI) on the surface of mast cells with multivalent antigens results in the release of mediators and development of type 2 inflammation. Fc epsilon RI expression and IgE synthesis are, therefore, critical for type 2 inflammatory disease development. In an attempt to clarify the relationship between eosinophilic chronic rhinosinusitis (ECRS) and mast cell infiltration, we analyzed mast cell infiltration at lesion sites and determined its clinical significance. Mast cells are positive for c-kit, and IgE in uncinated tissues (UT) and nasal polyps (NP) were examined by immunohistochemistry. The number of positive cells and clinicopathological factors were analyzed. Patients with ECRS exhibited high levels of total IgE serum levels and elevated peripheral blood eosinophil ratios. As a result, the number of mast cells with membranes positive for c-kit and IgE increased significantly in lesions forming NP. Therefore, we classified IgE-positive mast cells into two groups: membrane IgE-positive cells and cytoplasmic IgE-positive cells. The amount of membrane IgE-positive mast cells was significantly increased in moderate ECRS. A positive correlation was found between the membrane IgE-positive cells and the radiological severity score, the ratio of eosinophils, and the total serum IgE level. The number of cytoplasmic IgE-positive mast cells was significantly increased in moderate and severe ECRS. A positive correlation was observed between the cytoplasmic IgE-positive cells and the radiological severity score, the ratio of eosinophils in the blood, and the total IgE level. These results suggest that the process of mast cell internalization of antigens via the IgE receptor is involved in ECRS pathogenesis

Computed Tomography Findings for Diagnosing Follicular Thyroid Neoplasms

Since no diagnostic method has been established to distinguish follicular thyroid carcinoma (FTC) from follicular thyroid adenoma (FTA), surgery has been the only way to reach a diagnosis of follicular neoplasm. Here we investigated the computed tomography (CT) features of follicular neoplasms, toward the goal of being able to identify specific CT features allowing the preoperative differentiation of FTC from FTA. We retrospectively analyzed the cases of 205 patients who underwent preoperative CT of the neck and were histopathologically diagnosed with FTC (n=31) or FTA (n=174) after surgery between January 2002 and June 2016 at several hospitals in Japan. In each of these 205 cases, non-enhanced and contrast-enhanced CT images were obtained, and we analyzed the CT features. On univariate analysis, inhomogeneous features of tumor lesions on contrast-enhanced CT were more frequently observed in FTC than in FTA (p=0.0032). A multivariate analysis identified inhomogeneous features of tumor lesions on contrast-enhanced CT images as an independent variable indicative of FTC (p=0.0023). CT thus offers diagnostic assistance in distinguishing FTC from FTA

Experimental Approach Reveals the Role of alx1 in the Evolution of the Echinoderm Larval Skeleton

AbstractOver the course of evolution, the acquisition of novel structures has ultimately led to wide variation in morphology among extant multicellular organisms. Thus, the origins of genetic systems for new morphological structures are a subject of great interest in evolutionary biology. The larval skeleton is a novel structure acquired in some echinoderm lineages via the activation of the adult skeletogenic machinery. Previously, VEGF signaling was suggested to have played an important role in the acquisition of the larval skeleton. In the present study, we compared expression patterns of Alx genes among echinoderm classes to further explore the factors involved in the acquisition of a larval skeleton. We found that the alx1 gene, originally described as crucial for sea urchin skeletogenesis, may have also played an essential role in the evolution of the larval skeleton. Unlike those echinoderms that have a larval skeleton, we found that alx1 of starfish was barely expressed in early larvae that have no skeleton. When alx1 overexpression was induced via injection of alx1 mRNA into starfish eggs, the expression patterns of certain genes, including those possibly involved in skeletogenesis, were altered. This suggested that a portion of the skeletogenic program was induced solely by alx1. However, we observed no obvious external phenotype or skeleton. We concluded that alx1 was necessary but not sufficient for the acquisition of the larval skeleton, which, in fact, requires several genetic events. Based on these results, we discuss how the larval expression of alx1 contributed to the acquisition of the larval skeleton in the putative ancestral lineage of echinoderms