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Search Results: 1 - 10 of 1172 matches for " Shinji Kume "
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Peroxisome Proliferator-Activated Receptors in Diabetic Nephropathy
Shinji Kume,Takashi Uzu,Keiji Isshiki,Daisuke Koya
PPAR Research , 2008, DOI: 10.1155/2008/879523
Abstract: Diabetic nephropathy is a leading cause of end-stage renal disease, which is increasing in incidence worldwide, despite intensive treatment approaches such as glycemic and blood pressure control in patients with diabetes mellitus. New therapeutic strategies are needed to prevent the onset of diabetic nephropathy. Peroxisome proliferator-activated receptors (PPARs) are ligand-activated nuclear transcription factors that play important roles in lipid and glucose homeostases. These agents might prevent the progression of diabetic nephropathy, since PPAR agonists improve dyslipidemia and insulin resistance. Furthermore, data from murine models suggest that PPAR agonists also have independent renoprotective effects by suppressing inflammation, oxidative stress, lipotoxicity, and activation of the renin-angiotensin system. This review summarizes data from clinical and experimental studies regarding the relationship between PPARs and diabetic nephropathy. The therapeutic potential of PPAR agonists in the treatment of diabetic nephropathy is also discussed.
Autophagy as a Therapeutic Target in Diabetic Nephropathy
Yuki Tanaka,Shinji Kume,Munehiro Kitada,Keizo Kanasaki,Takashi Uzu,Hiroshi Maegawa,Daisuke Koya
Experimental Diabetes Research , 2012, DOI: 10.1155/2012/628978
Abstract: Diabetic nephropathy is a serious complication of diabetes mellitus, and its prevalence has been increasing worldwide. Therefore, there is an urgent need to identify a new therapeutic target to prevent diabetic nephropathy. Autophagy is a major catabolic pathway involved in degrading and recycling macromolecules and damaged organelles to maintain intracellular homeostasis. The study of autophagy in mammalian systems is advancing rapidly and has revealed that it is involved in the pathogenesis of various metabolic or age-related diseases. The functional role of autophagy in the kidneys is also currently under intense investigation although, until recently, evidence showing the involvement of autophagy in the pathogenesis of diabetic nephropathy has been limited. We provide a systematic review of autophagy and discuss the therapeutic potential of autophagy in diabetic nephropathy to help future investigations in this field.
The Role of Autophagy in the Pathogenesis of Diabetic Nephropathy
Kosuke Yamahara,Mako Yasuda,Shinji Kume,Daisuke Koya,Hiroshi Maegawa,Takashi Uzu
Journal of Diabetes Research , 2013, DOI: 10.1155/2013/193757
Abstract: Diabetic nephropathy is a leading cause of end-stage renal disease worldwide. The multipronged drug approach targeting blood pressure and serum levels of glucose, insulin, and lipids fails to fully prevent the onset and progression of diabetic nephropathy. Therefore, a new therapeutic target to combat diabetic nephropathy is required. Autophagy is a catabolic process that degrades damaged proteins and organelles in mammalian cells and plays a critical role in maintaining cellular homeostasis. The accumulation of proteins and organelles damaged by hyperglycemia and other diabetes-related metabolic changes is highly associated with the development of diabetic nephropathy. Recent studies have suggested that autophagy activity is altered in both podocytes and proximal tubular cells under diabetic conditions. Autophagy activity is regulated by both nutrient state and intracellular stresses. Under diabetic conditions, an altered nutritional state due to nutrient excess may interfere with the autophagic response stimulated by intracellular stresses, leading to exacerbation of organelle dysfunction and diabetic nephropathy. In this review, we discuss new findings showing the relationships between autophagy and diabetic nephropathy and suggest the therapeutic potential of autophagy in diabetic nephropathy. 1. Introduction The increasing prevalence of diabetes mellitus and its vascular complications has become a major health problem worldwide. Diabetic nephropathy is a serious complication of diabetes and is a common cause of end-stage renal disease. Diabetes induces glomerular damage, along with proteinuria, and subsequent tubulointerstitial lesions, leading to end-stage renal disease [1–3]. Initially, the patient shows hyperfiltration, represented by high glomerular filtration rates (GFRs) and occasional occurrence of microalbuminuria. Later, the patient shows a gradual decline in the GFR and persistence of microalbuminuria that comes before mild and subsequently moderate proteinuria. Urinary protein seems to be almost entirely reabsorbed in early and late proximal tubules and may induce tubulointerstitial damage [3]. Reducing proteinuria by keeping blood pressure and blood glucose levels under control is therefore a primary therapeutic goal with diabetic nephropathy [4, 5]. Unfortunately, however, some patients develop treatment-resistant proteinuria, resulting in end-stage renal disease. There is now an urgent need to identify new therapeutic target molecules or cellular processes that underlie the pathogenesis of diabetic nephropathy to establish additional
The Role of FoxC2 Transcription Factor in Tumor Angiogenesis
Tsutomu Kume
Journal of Oncology , 2012, DOI: 10.1155/2012/204593
Abstract: Much has been learned about the mechanisms underlying tumor angiogenesis, and therapies that target vascular endothelial growth factor (VEGF) to limit tumor angiogenesis and subsequent disease progression have recently been approved. However, the transcriptional mechanisms that regulate pathological angiogenesis remain largely unknown. FoxC2, a member of the Forkhead box (Fox) transcription factor family, is critical for vascular formation during development, and recent studies have shown that FoxC2 is expressed in the endothelium of tumors in both humans and mice. In a B16 mouse melanoma model, Foxc2 deficiency reduced tumor growth and neovascularization and was associated with impairments in mural-cell coverage and increases in endothelial-cell apoptosis in tumor blood vessels. FoxC2 is also expressed by tumor cells in human breast, colonic, and esophageal cancer and participates in the epithelial-mesenchymal transition (EMT), a key process that leads to the invasion and metastasis of aggressive tumors. Collectively, these observations suggest that FoxC2 is essential for tumor angiogenesis and disease progression and that FoxC2 may be a viable target for cancer therapy.
Novel insights into the differential functions of Notch ligands in vascular formation
Tsutomu Kume
Vascular Cell , 2009, DOI: 10.1186/2040-2384-1-8
Abstract: Notch signaling is evolutionarily conserved and critical for cell-fate determination, differentiation, and many other biological processes [1]. The mammalian Notch signaling pathway is composed of four Notch receptors (Notch1-4) and five ligands (Jagged1 and 2 and Delta-like [Dll] 1, 3, and 4). All of the ligands are transmembrane-type proteins and, consequently, Notch signaling is often mediated by cell-cell interactions. Transmission generally occurs between neighboring cells that express high levels of either the receptor or the ligand, although receptor-ligand coexpression occurs in some cells, such as vascular endothelial cells. Over the last decade, numerous studies have demonstrated that Notch signaling is critically involved in vascular development and disease [2-6]. For example, Notch signaling is required for arterial cell-fate determination during embryonic development, and the Notch pathway controls both developmental and pathological angiogenesis by modulating the selection of endothelial tip and stalk cells in newly sprouting blood vessels. Regulation of the Notch pathway in blood vessels has been well characterized; however, the specific roles of each Notch ligand during vascular formation and morphogenesis are unknown. Recent studies provide insight into the distinct functions of Notch ligands in blood vessels, and this review summarizes the current understanding of how several ligands differentially activate Notch signaling in the vasculature.Notch signaling is initiated by interactions between a Notch ligand expressed on the surface of one cell (the signaling cell) and a Notch receptor expressed on the surface of a neighboring cell (the receiving cell). Upon ligand binding, Notch is sequentially cleaved, and the Notch intracellular domain (NICD) is released into the cytoplasm. The NICD enters the nucleus, where it interacts with the transcription factor CSL (named after mammalian CBF1, Drosophila Su(H), and Caenorhabditis elegans LAG1) to form a tr
Legal issues on subsidies of endangered animal breeds in Albania and their need for improvement in light of international and EU legislations
Andon Kume
Albanian Journal of Agricultural Sciences , 2013,
Abstract: The Albanian legislation treats partially and as separate matters issues related to subsidies for endangered animal breeds. In order to approximate this legislation with the international and EU member states one, these issues are to be treated and developed as integral part of agriculture and sustainable rural development legislation. This legislation should clarify specifically the concept of animal breed that may be subject to subsidise. A legal framework should be developed in order to create and update the “Red Book” for endangered animal breeds. The legislation should define the criteria and the methodological principles, according to which the subsidy measures for animal breeds at risk are to be assessed. The subsidy should aim to reduce financial losses caused by raising these breeds.
Endoscopic mucosal resection and endoscopic submucosal dissection for early gastric cancer: Current and original devices
Keiichiro Kume
World Journal of Gastrointestinal Endoscopy , 2009,
Abstract: Compared with endoscopic submucosal dissection (ESD), endoscopic mucosal resection (EMR) is easier to perform and requires less time for treatment. However, EMR has been replaced by ESD, because achieving en bloc resection of specimens > 20 mm in diameter is difficult with EMR. The technique of ESD was introduced to resect large specimens of early gastric cancer in a single piece. ESD can provide precise histological diagnosis and can also reduce the rate of recurrence, but has a high level of technical difficulty, and is consequently associated with a high rate of complications, a need for advanced endoscopic techniques, and a lengthy procedure time. To overcome disadvantages in both EMR and ESD, various advances have been made in submucosal injections, knives, other accessories, and in electrocoagulation systems.
NEW MEMBERS OF EDITORIAL BOARD
Vasilika Kume
Serbian Journal of Management , 2013,
Abstract:
HAS THE BOLOGNA PROCESS IMPROVED MASTER’S EDUCATION STANDARDS? PERSPECTIVES OF ALBANIAN EMPLOYERS
Vasilika Kume
Serbian Journal of Management , 2013, DOI: 10.5937/sjm8-3038
Abstract: In this research the professional innovation of the Master studies as per Bologna Process standards, observed from the possible buyers of such product, the Albanian Employers is studied.With the help of a survey, it has been tried to reflect the opinion of the employers about the quality of a Master degree according to the standarts of the Bologna Process. Around 53% of the employersthink that the Bologna system can qualitatively improve the employee’s qualification, but this should be observed in a long-term horizon. About 87% of employers would not pay more a prospective employee given the fact that he/she has earned a master degree according the Bologna Process standards. This individual, in the majority of Albanian companies, would not be considered as more qualified than other colleagues who are educated in another system. Moreover, 20% of employers with work experience 11-15 years believe that the Bologna Process worsens the quality of education in Albania.
Solvability of the Economic Input-Output Equation by Time Irreversibility  [PDF]
Shinji Miura
Advances in Linear Algebra & Matrix Theory (ALAMT) , 2014, DOI: 10.4236/alamt.2014.43013
Abstract:
This paper reinterprets the economic input-output equation as a description of a realized situation without considering decision making. This paper uses the equation that the self-sufficiency rate is added to the Leontief type, and discusses its solvability. The equation has a unique solution if and only if each part of the relevant society satisfies the space-time openness condition. This condition means that commodities which a part of the relevant society possesses are not all inputted to its inside. Moreover, if the process of input and output is time irreversible, each part of the relevant society satisfies the space-time openness condition. Therefore, the solvability of the equation is guaranteed by time irreversibility. This proposition seems to be relevant to the grandfather paradox which is a type of time paradox.
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