24 research outputs found
皮膚逆アルサス反応にはIntercellular Adhesion Molecule 1とL-Selectinの発現が必要である
取得学位 : 博士(医学), 学位授与番号 : 医博乙第1565号, 学位授与年月日 : 平成14年7月3日, 学位授与大学 : 金沢大
Eisenhart Lift of --Dimensional Mechanics
The Eisenhart lift is a variant of geometrization of classical mechanics with
degrees of freedom in which the equations of motion are embedded into the
geodesic equations of a Brinkmann-type metric defined on -dimensional
spacetime of Lorentzian signature. In this work, the Eisenhart lift of
-dimensional mechanics on curved background is studied. The corresponding
-dimensional metric is governed by two scalar functions which are just the
conformal factor and the potential of the original dynamical system. We derive
a conformal symmetry and a corresponding quadratic integral, associated with
the Eisenhart lift. The energy--momentum tensor is constructed which, along
with the metric, provides a solution to the Einstein equations. Uplifts of
-dimensional superintegrable models are discussed with a particular emphasis
on the issue of hidden symmetries. It is shown that for the -dimensional
Darboux--Koenigs metrics, only type I can result in Eisenhart lifts which
satisfy the weak energy condition. However, some physically viable metrics with
hidden symmetries are presented.Comment: 20 page
CD19-dependent B lymphocyte signaling thresholds influence skin fibrosis and autoimmunity in the tight-skin mouse
金沢大学大学院医学系研究科血管分子科学The tight-skin (TSK/+) mouse, a genetic model for human systemic sclerosis (SSc), develops cutaneous fibrosis and autoantibodies against SSc-specific target autoantigens. Although molecular mechanisms explaining the development of fibrosis and autoimmunity in SSc patients or TSK/+ mice remain unknown, we recently demonstrated that SSc patients overexpress CD19, an important regulatory molecule expressed by B lymphocytes. B cells from CD19-deficient mice are hyporesponsive to transmembrane signals, while B cells overexpressing CD19 are hyperresponsive and generate autoantibodies. In this study, TSK/+ B cells also exhibited a hyperresponsive phenotype with decreased surface IgM expression, enhanced serum Ig production, and spontaneous autoantibody production. Moreover, CD19 tyrosine phosphorylation was constitutively augmented in TSK/+ B cells. CD19-mediated [Ca2+]i responses, Vav phosphorylation, and Lyn kinase activity were similarly enhanced. Studies of TSK/+ mice deficient in CD19 expression demonstrated that CD19 deficiency significantly decreased skin fibrosis in TSK/+ mice. Additionally, CD19 loss in TSK/+ mice upregulated surface IgM expression and completely abrogated hyper-γ-globulinemia and autoantibody production. CD19 deficiency also inhibited IL-6 production by TSK/+ B cells. Thus, chronic B cell activation resulting from augmented CD19 signaling in TSK/+ mice leads to skin sclerosis possibly through IL-6 overproduction as well as autoimmunity
CXCR2 expression and postoperative complications affect long-term survival in patients with esophageal cancer
The cutaneous reverse arthus reaction requires intercellular adhesion molecule 1 and L-selectin expression
Low-Carbohydrate Diet Inhibits Different Advanced Glycation End Products in Kidney Depending on Lipid Composition but Causes Adverse Morphological Changes in a Non-Obese Model Mice
Low carbohydrate diets (LC diets) have been noted for adverse health effects. In addition, the effect of lipid composition on an LC diet is unclear. In this study, we used an LC diet containing two different lipids, lard (LC group) and medium-chain triglyceride oil (MCT-LC group), to examine the effect of an LC diet in non-obese mice. Male C57BL/6J mice were fed the control diet or one of the experimental diets ad libitum for 13 weeks. Increased renal weight and glomerular hypertrophy, as well as enlargement of intraglomerular small vessels with wall thickening, were seen in the LC and MCT-LC groups. Renal AMP-activated protein kinase activity was significantly decreased only in the LC diet group. On the other hand, epididymal adipose tissue weight and adipocyte area were markedly decreased only in the MCT-LC group. A positive effect was also observed in the kidney, where different advanced glycation end products, Nε-(carboxyethyl)-lysine and Nε-(carboxymethyl)-lysine, were inhibited depending on the lipid composition of the LC diet. Our findings suggest that, in non-obese conditions, low dietary intake of carbohydrates had both positive and negative impacts. The safety of diets low in carbohydrates, including the effects of fatty acid composition, requires further investigation
CD19-dependent B lymphocyte signaling thresholds influence skin fibrosis and autoimmunity in the tight-skin mouse
L-Selectin or ICAM-1 Deficiency Reduces an Immediate-Type Hypersensitivity Response by Preventing Mast Cell Recruitment in Repeated Elicitation of Contact Hypersensitivity
Alleviation of lipopolysaccharide/d-galactosamine-induced liver injury in leukocyte cell-derived chemotaxin 2 deficient mice
Leukocyte cell-derived chemotaxin 2 (LECT2) is a secreted pleiotropic protein that is mainly produced by the liver. We have previously shown that LECT2 plays an important role in the pathogenesis of inflammatory liver diseases. Lipopolysaccharide/d-galactosamine (LPS/d-GalN)-induced acute liver injury is a known animal model of fulminant hepatic failure. Here we found that this hepatic injury was alleviated in LECT2-deficient mice. The levels of TNF-α and IFN-γ, which mediate this hepatitis, had significantly decreased in these mice, with the decrease in IFN-γ production notably greater than that in TNF-α. We therefore analyzed IFN-γ-producing cells in liver mononuclear cells. Flow cytometric analysis showed significantly reduced IFN-γ production in hepatic NK and NKT cells in LECT2-deficient mice compared with in wild-type mice. We also demonstrated a decrease in IFN-γ production in LECT2-deficient mice after systemic administration of recombinant IL-12, which is known to induce IFN-γ in NK and NKT cells. These results indicate that a decrease of IFN-γ production in NK and NKT cells was involved in the alleviation of LPS/d-GalN-induced liver injury in LECT2-deficient mice