Gunma University | Date: 2017-02-08
An existing ultrasonic diagnostic device is used to obtain a color flow image of a target object whose stiffness is to be measured. At this time, a vibration exciter applies a micro vibration with a frequency of n/4 (n represents an odd number equal to or larger than 1) to the target object with respect to a burst frequency of an ultrasonic pulse to generate a shear elastic wave. As a result, a striped pattern corresponding to the stiffness of the target object caused by the shear elastic wave appears on a display of the ultrasonic diagnostic device as a shear elastic wave detection image.
Tohoku University, Gunma University and Fuso Pharmaceutical Industries Ltd. | Date: 2017-01-04
The present invention provides a useful medicament for the treatment and/or prophylaxis of a disease associated with the enhancement of OPN production including cancer, which comprises a compound of formula:^(1), R^(2), R^(3), R^(4), R^(5), R^(6), R^(7), m, n, p, X, and Y are as defined in the specification, or a pharmaceutically acceptable salt thereof.
Tohoku University, Gunma University and Fuso Pharmaceutical Industries Ltd. | Date: 2016-01-13
Disclosed herein is an osteopontin production inhibitor capable of preventing a disease resulting from increased production of osteopontin. The osteopontin production inhibitor contains a dictyopyrone derivative or a dihydrodictyopyrone derivative as an active ingredient. The dictyopyrone derivative is preferably a compound represented by Chemical Formula 1 or 2, and the dihydrodictyopyrone derivative is preferably a compound represented by Chemical Formula 3 or 4.
Mizuno-Yamasaki E.,Gunma University |
Rivera-Molina F.,Yale University |
Novick P.,University of California at San Diego
Annual Review of Biochemistry | Year: 2012
Members of the Rab or ARFSar branches of the Ras GTPase superfamily regulate almost every step of intracellular membrane traffic. A rapidly growing body of evidence indicates that these GTPases do not act as lone agents but are networked to one another through a variety of mechanisms to coordinate the individual events of one stage of transport and to link together the different stages of an entire transport pathway. These mechanisms include guanine nucleotide exchange factor (GEF) cascades, GTPase-activating protein (GAP) cascades, effectors that bind to multiple GTPases, and positive-feedback loops generated by exchange factor-effector interactions. Together these mechanisms can lead to an ordered series of transitions from one GTPase to the next. As each GTPase recruits a unique set of effectors, these transitions help to define changes in the functionality of the membrane compartments with which they are associated. © 2012 by Annual Reviews. All rights reserved.
Ito K.,Gunma University
Nature Reviews Urology | Year: 2014
Prostate cancer incidence and mortality in most native Asian populations have gradually increased, but are around one-third lower than in corresponding Asian-American cohorts, which are themselves lower than the rates observed in other American cohorts. Although genetic and environmental factors, particularly a Western diet, could partially explain these differences, lower exposure to PSA screening in Asian individuals might be a major contributing factor. Genetic features and diet are, however, unlikely to differ substantially within the same region of Asia, and age-stratified PSA levels in men from various Asian countries are almost identical; therefore, variation in the epidemiology of prostate cancer among native Asian populations might be attributable to differences in access to PSA testing, urology clinics, and available therapies. Conversely, the proportion of patients with metastatic prostate cancer is substantially higher even in the more developed Asian countries than in migratory Asian populations residing in Western countries and in Westerners. Consequently, the most appropriate approaches to the management of prostate cancer in Asian countries probably also differ, and therefore individualized prostate cancer screening and treatment strategies based on the epidemiological features and socioeconomic status of each country are needed. © 2014 Macmillan Publishers Limited. All rights reserved.
Okajima F.,Gunma University
Cellular Signalling | Year: 2013
Under ischemic and inflammatory circumstances, such as allergic airway asthma, rheumatoid arthritis, atherosclerosis, and tumors, extracellular acidification occurs due to the stimulation of anaerobic glycolysis. An acidic microenvironment has been shown to modulate pro-inflammatory or anti-inflammatory responses, including cyclooxygenase-2 (COX-2) expression, prostaglandin synthesis, and cytokine expression, in a variety of cell types, and thereby to exacerbate or ameliorate inflammation. However, molecular mechanisms underlying extracellular acidic pH-induced actions have not been fully understood. Recent studies have shown that ovarian cancer G protein-coupled receptor 1 (OGR1)-family G protein-coupled receptors (GPCRs) can sense extracellular pH or protons, which in turn stimulates intracellular signaling pathways and subsequent diverse cellular responses. In the present review, I discuss extracellular acidic pH-induced inflammatory responses and related responses in inflammatory cells, such as macrophages and neutrophils, and non-inflammatory cells, such as smooth muscle cells and endothelial cells, focusing especially on proton-sensing GPCRs. © 2013 Elsevier Inc.
Gunma University | Date: 2016-11-02
Provided is an implantable spacer that can be placed in a body and can be easily removed after placement. The implantable spacer includes a tube which is folded or bent at one or a plurality of positions to form partial sections adjacent to each other; fixing threads which are disposed along a direction transverse to the partial sections in order to maintain the shape of the tube; and a trigger thread for catching the fixing threads being in a releasable state.
Japan National Institute of Advanced Industrial Science, Technology, Gunma University and Alps Electric | Date: 2016-03-22
An electroconductive film for an actuator is formed from a gel composition including carbon nanofibers, an ionic liquid, and a polymer. The carbon nanofibers are produced with an aromatic mesophase pitch by melt spinning.
Tokunaga F.,Gunma University
Journal of Biochemistry | Year: 2013
Ubiquitination is a post-translational modification involved in the regulation of a broad variety of cellular functions, such as protein degradation and signal transduction, including nuclear factor-κB (NF-κB) signalling. NF-κB is crucial for inflammatory and immune responses, and aberrant NF-κB signalling is implicated in multiple disorders. We found that linear ubiquitin chain assembly complex (LUBAC), composed of HOIL-1L, HOIP and SHARPIN, generates a novel type of Met1 (M1)-linked linear polyubiquitin chain and specifically regulates the canonical NF-κB pathway. Moreover, specific deubiquitinases, such as CYLD, A20 (TNFAIP3) and OTULIN/gumby, inhibit LUBAC-induced NF-κB activation by different molecular mechanisms, and several M1-linked ubiquitin-specific binding domains have been structurally defined. LUBAC and these linear ubiquitination-regulating factors contribute to immune and inflammatory processes and apoptosis. Functional impairments of these factors are correlated with multiple disorders, including autoinflammation, immunodeficiencies, dermatitis, B-cell lymphomas and Parkinson's disease. This review summarizes the molecular basis and the pathophysiological implications of the linear ubiquitination-mediated NF-κB activation pathway regulation by LUBAC. © 2013 The Authors. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved.
Kitamura T.,Gunma University
Nature Reviews Endocrinology | Year: 2013
Over the past two decades, insulin resistance has been considered essential to the aetiology of type 2 diabetes mellitus (T2DM). However, insulin resistance does not lead to T2DM unless it is accompanied by pancreatic β-cell dysfunction, because healthy β cells can compensate for insulin resistance by increasing in number and functional output. Furthermore, β-cell mass is decreased in patients with diabetes mellitus, suggesting a primary role for β-cell dysfunction in the pathogenesis of T2DM. The dysfunction of β cells can develop through various mechanisms, including oxidative, endoplasmic reticulum or hypoxic stress, as well as via induction of cytokines; these processes lead to apoptosis, uncontrolled autophagy and failure to proliferate. Transdifferentiation between β cells and α cells occurs under certain pathological conditions, and emerging evidence suggests that β-cell dedifferentiation or transdifferentiation might account for the reduction in β-cell mass observed in patients with severe T2DM. FOXO1, a key transcription factor in insulin signalling, is implicated in these mechanisms. This Review discusses advances in our understanding of the contribution of FOXO1 signalling to the development of β-cell failure in T2DM. © 2013 Macmillan Publishers Limited. All rights reserved.