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Kobe, Japan

Kobe University , also known in the Kansai region as Shindai , is a leading national university located in Kobe, Hyōgo, Japan. It was established in 1949, but the academic origins of Kobe University trace back to the establishment of Kobe Higher Commercial School in 1902, which was renamed as Kobe University of Commerce, and Kobe University of Economics.Kobe University comprises 14 graduate schools and 11 undergraduate faculties. The university holds a total of about 16,000 students enrolled in undergraduate and graduate programs. The institution welcomes overseas students, which accounted for a total of 1,108 students, as of 2011. It also has 3,300 staff members, including professors, associate professors and administrative officials.Located beside the foothills of Mount Rokkō, the university provides a view of the city and port of Kobe, providing an environment for the pursuit of academic studies, especially social science areas. Kobe University is one of the oldest and largest national universities in Japan. It is consistently one of the highest ranking national universities in Japan that is not one of Japan's National Seven Universities.Kobe Higher Commercial School was one of the oldest institution with business and economics majors in Japan. Especially, the Graduate School of Economics benefits fully from a century of the history and the tradition. Kobe is also the first collegiate business school in Japan. Therefore, Kobe is called the birthplace of Japanese higher education in economics and business administration, and it has always been the center of Japanese business studies.Furthermore, the Graduate School of Law was also established with the legal studies section of the former Kobe University of Economics. It has become a leading institution of high academic institution in the field of legal and political studies, and has been successful in becoming a reputable academic center.The Research Institute for Economics and Business Administration, founded in 1919, has a history as a high-level research institution for international economics and international management. The Institute has been highly regarded internationally for its outstanding achievements in theoretical, historical, empirical, and quantitative research.In the meantime, Kobe Hospital was established in 1869; it was a training center for medical practitioners, which was one of the oldest institutions in the modern medical education in Japan.In 1990, they made new changes as one of the major universities specializing in graduate research and education.Under the Japanese Ministry of Education and Science, it has started a new Center of Excellence projects, the "Research and Education Center of New Japanese Economic Paradigms", "Development and Education Center for Advanced Business Systems", and "Research Center for Dynamic Legal Processes of Advanced Market Societies". Wikipedia.

Aikawa Y.,Kobe University
Chemical Reviews | Year: 2013

Cores are subject to gravitational instability; they are massive enough to collapse due to their own gravity. The cores are supported against collapse by a pressure gradient due to the combination of thermal, magnetic, and turbulent pressure. The cores start collapse to form stars, once the gravity overwhelms the pressure gradient. The core before star formation is called a prestellar core, whereas the core harboring protostar(s) are called a protostellar core. Molecular line observations in radio wavelength is a very powerful tool to investigate the core structure, since millimeter radiation suffer much less attenuation than shorter wavelength. High spectral resolution of radio telescopes also enable us to investigate dynamics of the core. Source

Kamisawa T.,Tokyo Metropolitan Komagome Hospital | Zen Y.,Kobe University | Pillai S.,Harvard University | Stone J.H.,Harvard University
The Lancet | Year: 2015

IgG4-related disease is a protean condition that mimics many malignant, infectious, and inflammatory disorders. This multi-organ immune-mediated condition links many disorders previously regarded as isolated, single-organ diseases without any known underlying systemic condition. It was recognised as a unified entity only 10 years ago. Histopathology is the key to diagnosis. The three central pathology features of IgG4-related disease are lymphoplasmacytic infiltration, storiform fibrosis, and obliterative phlebitis. The extent of fibrosis is an important determinant of responsiveness to immunosuppressive therapies. IgG4-related disease generally responds to glucocorticoids in its inflammatory stage, but recurrent or refractory cases are common. Important mechanistic insights have been derived from studies of patients treated by B-cell depletion. Greater awareness of this disease is needed to ensure earlier diagnoses, which can prevent severe organ damage, disabling tissue fibrosis, and even death. Identification of specific antigens and T-cell clones that drive the disease will be the first steps to elucidate the pathogenesis of IgG4-related disease. Source

Furuse M.,Kobe University
Cold Spring Harbor perspectives in biology | Year: 2010

The morphological feature of tight junctions (TJs) fits well with their functions. The core of TJs is a fibril-like proteinaceous structure within the lipid bilayer, the so-called TJ strands. TJ strands in apposing plasma membranes associate with each other to eliminate the intercellular space. A network of paired TJ strands generates a continuous belt that circumscribes each cell to establish the diffusion barrier to the solutes in the paracellular pathway throughout the cellular sheet. Identification and characterization of TJ-associated proteins during the last two decades has unveiled the nature of TJ strands and how they are spatially organized. The interplay between integral membrane proteins, claudins, and cytoplasmic plaque proteins, ZO-1/ZO-2, is critical for TJ formation and function. Source

Approximately 20% of breast cancers are characterized by overexpression of human epidermal growth factor receptor 2 (HER2) protein and associated gene amplification, and the receptor tyrosine kinase is believed to play a critical role in the pathogenesis of these tumors. The development and implementation of trastuzumab, a humanized monoclonal antibody against the extracellular domain of HER2 protein, has significantly improved treatment outcomes in patients with HER2-overexpressing breast cancer. However, despite this clinical usefulness, unmet needs for better prediction of trastuzumab's response and overcoming primary and acquired resistance remain. In this review, we discuss several potential mechanisms of resistance to trastuzumab that have been closely studied over the last decade. Briefly, these mechanisms include: impaired access of trastuzumab to HER2 by expression of extracellular domain-truncated HER2 (p95 HER2) or overexpression of MUC4; alternative signaling from insulin-like growth factor-1 receptor, other epidermal growth factor receptor family members, or MET; aberrant downstream signaling caused by loss of phosphatase and tensin homologs deleted from chromosome 10 (PTEN), PIK3CA mutation, or downregulation of p27; or FCGR3A polymorphisms. In addition, we discuss potential strategies for overcoming resistance to trastuzumab. Specifically, the epidermal growth factor receptor/HER2 tyrosine kinase inhibitor lapatinib partially overcame trastuzumab resistance in a clinical setting, so its efficacy results and limited data regarding potential mechanisms of resistance to the drug are also discussed. © 2010 Japanese Cancer Association. Source

Sugasawa K.,Kobe University
Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis | Year: 2010

Nucleotide excision repair operating throughout the mammalian genome plays a crucial role in the suppression of mutagenesis and carcinogenesis, which can arise from DNA lesions induced by a wide variety of genotoxic agents, such as ultraviolet light and chemical compounds. A key process of this DNA repair pathway, damage recognition, is accomplished through multiple steps including concerted actions of the damaged DNA binding factors XPC and UV-DDB, both of which are implicated in a human cancer-prone genetic disorder, xeroderma pigmentosum. Accumulating evidence indicates that the expression and functions of these damage recognition factors are subject to exquisite regulation at diverse levels, including transcriptional activation, post-translational modification, complex formation, and protein degradation through ubiquitination. © 2009 Elsevier B.V. All rights reserved. Source

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