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Search Results: 1 - 10 of 477 matches for " Maki Murakoshi "
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Role of Mindin in Diabetic Nephropathy
Maki Murakoshi,Tomohito Gohda,Mitsuo Tanimoto,Kazuhiko Funabiki,Satoshi Horikoshi,Yasuhiko Tomino
Experimental Diabetes Research , 2011, DOI: 10.1155/2011/486305
Abstract: A number of studies have shown that proinflammatory cytokines have important roles in determining the development of microvascular diabetic complications, including nephropathy. Inflammatory biomarkers should be useful for diagnosis or monitoring of diabetic nephropathy. Mindin (spondin 2) is a member of the mindin-/F-spondin family of secreted extracellular matrix (ECM) proteins. Recent studies showed that mindin is essential for initiation of innate immune response and represents a unique pattern-recognition molecule in the ECM. Previously, we demonstrated that the levels of urinary mindin in patients with type 2 diabetes were higher than those in healthy individuals. We propose that urinary mindin is a potent biomarker for the development of diabetic nephropathy.
Role of Mindin in Diabetic Nephropathy
Maki Murakoshi,Tomohito Gohda,Mitsuo Tanimoto,Kazuhiko Funabiki,Satoshi Horikoshi,Yasuhiko Tomino
Journal of Diabetes Research , 2011, DOI: 10.1155/2011/486305
Abstract: A number of studies have shown that proinflammatory cytokines have important roles in determining the development of microvascular diabetic complications, including nephropathy. Inflammatory biomarkers should be useful for diagnosis or monitoring of diabetic nephropathy. Mindin (spondin 2) is a member of the mindin-/F-spondin family of secreted extracellular matrix (ECM) proteins. Recent studies showed that mindin is essential for initiation of innate immune response and represents a unique pattern-recognition molecule in the ECM. Previously, we demonstrated that the levels of urinary mindin in patients with type 2 diabetes were higher than those in healthy individuals. We propose that urinary mindin is a potent biomarker for the development of diabetic nephropathy. 1. Introduction Diabetic nephropathy is a major cause of end-stage kidney disease (ESKD) in the United States, Japan, and most of Europe [1]. Although the etiology of this insidious disorder is not well understood, hyperglycemia and hypertension may play pivotal roles in the pathogenesis of diabetic nephropathy. Actually, almost 30% of diabetic patients develop diabetic nephropathy despite strict blood glucose and/or blood pressure control [2]. Chronic low-grade inflammation (so-called microinflammation) has been found to play roles in the pathogenesis of diabetes [3, 4] and has been identified as a risk factor for the development of diabetes [5, 6]. Moreover, diabetes has been proposed as a disease of the innate immune system [7]. In addition, the studies in recent years have shown that inflammation and inflammatory cytokines are determinants in the development of microvascular diabetic complications such as neuropathy, retinopathy, and nephropathy [8–11]. In 1991, Hasegawa et al. reported that glomerular basement membranes from diabetic rats induced significantly greater amounts of tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) in cultured peritoneal macrophages than when these cells were incubated with basement membranes from nondiabetic rats [12]. Based on these findings, the authors suggested for the first time that inflammatory cytokines may participate in the pathogenesis of diabetic nephropathy [12]. At present, a number of clinical studies have suggested relationships between inflammatory cytokines and diabetic nephropathy [13, 14]. Inflammatory cytokines, that is, IL-1, interleukin-6 (IL-6), and interleukin-18 (IL-18) [15, 16], vascular endothelial growth factor (VEGF) [17, 18], monocyte chemoattractant protein-1 (MCP-1) [19, 20], and transforming growth factor-β (TGF-β)
Effect of Exercise on Kidney Function, Oxidative Stress, and Inflammation in Type 2 Diabetic KK-Ay Mice
Yuji Ishikawa,Tomohito Gohda,Mitsuo Tanimoto,Keisuke Omote,Masako Furukawa,Saori Yamaguchi,Maki Murakoshi,Shinji Hagiwara,Satoshi Horikoshi,Kazuhiko Funabiki,Yasuhiko Tomino
Experimental Diabetes Research , 2012, DOI: 10.1155/2012/702948
Abstract: Exercise is recommended for the management of type 2 diabetes, but its effects on diabetic nephropathy (DN) are still unknown. We hypothesized that appropriate exercise improves early DN via attenuation of inflammation and oxidative damage. Type 2 diabetic KK- mice, a spontaneous DN model, underwent two different kinds of exercise (i.e., moderate and low intensity). Sedentary mice or those undergoing an exercise regimen causing no significant body weight loss were used. We examined the urinary excretion of albumin, number of podocytes and macrophages, renal expressions of HIF-1α and MCP-1, and biomarkers of oxidative stress such as urinary 8-OHdG and serum SOD. Exercise reduced urinary levels of albumin and also maintained the number of podocytes in the exercised KK- mice independently of improvements of overweight and hyperglycemia, although moderate-intensity exercise increased expression of HIF-1α. Sedentary KK- mice showed increased expression of MCP-1 and infiltration of macrophage, increased urinary 8-OhdG, and decreased serum SOD levels compared with exercised KK- mice. On the whole, low-intensity exercise attenuates progression of early DN without affecting marked renal ischemia. Reduction rates of urinary albumin and maintained podocyte numbers, with parallel improvements in oxidative damage and inflammation, are related to beneficial effects of exercise in diabetic kidney disease.
Effect of Exercise on Kidney Function, Oxidative Stress, and Inflammation in Type 2 Diabetic KK-Ay Mice
Yuji Ishikawa,Tomohito Gohda,Mitsuo Tanimoto,Keisuke Omote,Masako Furukawa,Saori Yamaguchi,Maki Murakoshi,Shinji Hagiwara,Satoshi Horikoshi,Kazuhiko Funabiki,Yasuhiko Tomino
Journal of Diabetes Research , 2012, DOI: 10.1155/2012/702948
Abstract: Exercise is recommended for the management of type 2 diabetes, but its effects on diabetic nephropathy (DN) are still unknown. We hypothesized that appropriate exercise improves early DN via attenuation of inflammation and oxidative damage. Type 2 diabetic KK- mice, a spontaneous DN model, underwent two different kinds of exercise (i.e., moderate and low intensity). Sedentary mice or those undergoing an exercise regimen causing no significant body weight loss were used. We examined the urinary excretion of albumin, number of podocytes and macrophages, renal expressions of HIF-1α and MCP-1, and biomarkers of oxidative stress such as urinary 8-OHdG and serum SOD. Exercise reduced urinary levels of albumin and also maintained the number of podocytes in the exercised KK- mice independently of improvements of overweight and hyperglycemia, although moderate-intensity exercise increased expression of HIF-1α. Sedentary KK- mice showed increased expression of MCP-1 and infiltration of macrophage, increased urinary 8-OhdG, and decreased serum SOD levels compared with exercised KK- mice. On the whole, low-intensity exercise attenuates progression of early DN without affecting marked renal ischemia. Reduction rates of urinary albumin and maintained podocyte numbers, with parallel improvements in oxidative damage and inflammation, are related to beneficial effects of exercise in diabetic kidney disease. 1. Introduction Recent studies suggest that a chronic inflammatory process and oxidative stress promote the progression of diabetic nephropathy (DN) [1–4]. We have also showed the presence of macrophage infiltration and increased MCP-1 expressions and levels in glomeruli and urine of KK- mice, a frequently used animal model of type 2 diabetes (T2D) [5, 6]. Furthermore, urinary 8-OHdG, a marker of oxidative DNA damage, was also increased in this mouse model [7]. Lifestyle modification, especially appropriate exercise, is recommended for the management of T2D through improvements of metabolic risk factors such as blood pressure, blood glucose, plasma lipids, and oxidative stress markers. On the other hand, this also consumes considerable amounts of oxygen, leading to production of high levels of reactive oxygen species (ROS). There is also evidence that ROS and high glucose exposure contribute to podocyte apoptosis in experimental DN [8]. It is considered that exercise-induced proteinuria is usually not permanent but evanescent [9, 10]. Moreover it is little known that moderate exercise has adverse effect on the renal function [11–14]. Several studies reported that
Properties of Time-Varying Causality Tests in the Presence of Multivariate Stochastic Volatility  [PDF]
Daiki Maki
Open Journal of Statistics (OJS) , 2016, DOI: 10.4236/ojs.2016.65064
Abstract: This paper compares the statistical properties of time-varying causality tests when errors of variables have multivariate stochastic volatility (SV). The time-varying causal-ity tests in this paper are based on a logistic smooth transition autoregressive model. The compared time-varying causality tests include asymptotic tests, heteroskedasticity-robust tests, and tests using wild bootstrap. Our simulation results show that asymptotic tests and heteroskedasticity-robust counterparts have size distortions under multivariate SV, whereas tests using wild bootstrap have better size properties regardless of type of error. In particular, the time-varying causality test with first-order Taylor approximation using wild bootstrap has better statistical properties.
Fabrication of stable Pd nanowire assisted by hydrogen in solution
Manabu Kiguchi,Kei Murakoshi
Physics , 2006, DOI: 10.1063/1.2216029
Abstract: We have mechanically fabricated a Pd nanowire in solution under electrochemical potential control. A clear feature appeared in the conductance histogram when the electrochemical potential of the Pd wire was kept at the hydrogen evolution potential. Conductance traces showed the Pd wire was stretched 0.4 nm in length just before breaking, suggesting that at least two Pd atoms might contribute to the formation of the Pd wire. The results indicate that a certain atomic configuration of the Pd nanowire is stabilized by hydrogen. We discuss the stabilization mechanism due to changes in bond strengths caused by hydrogen adsorption or incorporation.
Angiotensinogen Expression Is Enhanced in the Progression of Glomerular Disease  [PDF]
Maki Urushihara, Hiroyuki Kobori
International Journal of Clinical Medicine (IJCM) , 2011, DOI: 10.4236/ijcm.2011.24064
Abstract: Intrarenal renin-angiotensin system (RAS) activation plays a critical role in the development and progression of renal injury. In the kidney, all of the RAS components are present and intrarenal angiotensin II (Ang II) is formed by multiple independent mechanisms. Angiotensinogen (AGT) is the only known substrate for renin that is a rate-limiting enzyme of the RAS. Recently, enhanced intrarenal AGT levels have been shown to reflect the intrarenal RAS status in hypertension, chronic glomerular disease and diabetic nephropathy. In this review, we focus on AGT expression of the diseased glomeruli in the progression of glomerular disease. An anti-glomerular basement membrane nephritis rat model developed progressive proteinuria and glomerular crescent formation, accompanied by increased macrophage infiltration and glomerular expression of AGT and Ang II. The addition of Ang II type 1 receptor blocker to CC-chemokine recaptor 2 antagonist markedly attenuated the induction of macrophage infiltration, AGT and Ang II, and reduced glomerular crescent formation. Next, the levels of glomerular AGT expression and marker of reactive oxygen species in Zucker diabetic fatty (ZDF) obese rats were higher than those in ZDF lean rats. Hydrogen peroxide (H2O2) induced an increase in the AGT expression in primary rat mesangial cells. Furthermore, the H2O2-induced upregulation of AGT was inhibited by a mitogen-activated protein kinase kinase and a c-Jun N-terminal kinase inhibitor. These data suggest the potential contribution of enhanced AGT expression in glomeruli to the intrarenal RAS activation for the development of glomerular disease.
Trends in age distribution of participants in a self-covered and a public expense-covered health check-up programs in Japan  [PDF]
Maki Ogawa, Atsushi Imai
Health (Health) , 2012, DOI: 10.4236/health.2012.49088
Abstract: Objective: In Japan, there are unique facilities (namely Ningen Dock) of health check-up, where asymptomatic participants undergo a medical examination at their own expense. The earlier occurrence of cervical cancer and the concern on screening prompted us compare to the age distribution in the self-covered system with that of free physical check-up programs at public expense. Methods: We analyzed medical records of Japanese women, who underwent gynecological examinations at self-covered expense and at public expense between for the periods 2002-2011 and 2005-2009, respectively, restricting examinee’s age group. Results: For self-covered system, approximately 80% of the overall examinee population was occupied with three age groups 30-39, 40-49 and 50-59. The participants was extremely fewer in the over 60 years age group accounting for 10%, compared to those for the public expense-covered system, the over 60 years age group being 25%. Participant under the age of 30 years seemed to increase in chronological order in both systems. Conclusion: The level of knowledge on sexually transmitted infections may contribute to screening promotion for the younger women, while the elderly over 60 years’ attitudes toward screening may be mainly related to social-economic status and/or public expense support.
Comparative Interactions of Anesthetic Alkylphenols with Lipid Membranes  [PDF]
Hironori Tsuchiya, Maki Mizogami
Open Journal of Anesthesiology (OJAnes) , 2014, DOI: 10.4236/ojanes.2014.412044
Abstract: Objective: While substituted phenols have a variety of pharmacological activity, the mechanism underlying their anesthetic effects remains uncertain especially about the critical target. We characterized the lipid membrane-interacting properties of different phenols by comparing with general anesthetic propofol and local anesthetics. Based on the results, we also studied the pharmacological effects possibly associated with their membrane interactivities. Methods: 1,6-Diphenyl-1,3,5-hexatriene-labeled lipid bilayer membranes were prepared with 1,2-dipalmitoyl-phosphatidylcholine as model membranes and with different phospholipids and cholesterol to mimic neuronal membranes. These membrane preparations were treated with phenols and anesthetics at 1 - 200 μM, followed by measuring the fluorescence polarization to determine the membrane interactivities to change membrane fluidity. Antioxidant effects were fluorometrically determined using diphenyl-1-pyrenylphosphine-incorporated liposomes which were treated with 10 - 100 μM phenols, and then peroxidized with 10 μM peroxynitrite. Results: Several phenols interacted with the model membranes and the neuronal mimetic membranes to increase their fluidity at 1 - 10 μM as well as lidocaine and bupivacaine did at 50 - 200 μM. Their comparative potencies were propofol > thymol > isothymol > guaiacol > phenol > eugenol, and bupivacaine > lidocaine, consistent with the rank order of neuro-activity. These phenols inhibited membrane lipid peroxidation at 10 and 100 μM with the potencies correlating to their membrane interactivities. Conclusion: The structure-specific membrane interaction is at least in part responsible for the pharmacology of anesthetic alkylphenols. Membrane-interacting antioxidant alkylphenols may be protective against the peroxynitrite-relating ischemia/reperfusion injury.
Contact Urticaria Syndrome from Tofu  [PDF]
Maki Kitakawa, Tokio Nakada
Case Reports in Clinical Medicine (CRCM) , 2016, DOI: 10.4236/crcm.2016.56038
Abstract: A-52-year-old woman ate dinner after preening roses in her garden. Immediately, she developed oralaryngeal malaise and pruritic rash. Nasal obstruction and increase of cutaneous lesions were seen although she took betamethasone, 2 mg, orally. Physical examination revealed geographic wheal on trunk and extremities, and no overt mucosal lesions. History demonstrated that she had developed such reactions four times before: three of the four were seen shortly after eating soybean. Tofu was examined by prick-by-prick testing, and prick testing was performed with a petal, a piece of stem and rose leaf, positive and negative control. Positive reactions to tofu (wheal, 5 × 7 mm) and positive control (wheal 5 × 5 mm) and negative ones to others were noted. Although sensitization to soybean seemed to antedate pollen allergy on the basis of interview, oral allergy syndrome could be complicated because of various pollens-specific IgE. Since soy-bean specific IgE was class 2, such titer was not an effective predictor of clinical severity. This case should be classified into stage 3 of contact urticaria syndrome (CUS). Since CUS can be fatal, we must be careful in management for such patients.
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