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Search Results: 1 - 10 of 477 matches for " Mitsuo Tanimoto "
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Podocyte loss and albuminuria of KK-Ay mouse: A spontaneous animal model for human type 2 diabetic nephropathy  [PDF]
Yuji Ishikawa, Takamichi Ito, Mitsuo Tanimoto, Shinji Hagiwara, Masako Furukawa, Saori Yamaguchi, Keisuke Omote, Katsuhiko Asanuma, Tomohito Gohda, Yoshio Shimizu, Kazuhiko Funabiki, Satoshi Horikoshi, Yasuhiko Tomino
Journal of Diabetes Mellitus (JDM) , 2012, DOI: 10.4236/jdm.2012.23054
Abstract: Podocyte loss was well known in type 2 diabetic nephropathy patients. The objective of the present study was to determine the number of podocytes and the degree of albuminuria in diabetic KK-Ay/Ta (KK-Ay) mice which had been reported as diabetic nephropathy model. Diabetic KK-Ay mice, diabetic KK/Ta mice and non-diabetic BALB/cA Jcl (BALB/cA) mice were studied. We analyzed glomerular lesions in all mice by morphometric analysis and immunofluorescence to determine the number of podocytes. Level of urinary albumin was also measured. Glomerular enlargement and mesangial expansion were observed in KK-Ay mice. Mean number of podocytes per glomerulus (NG pod) in diabetic KK-Ay mice was significantly lower than that in non-diabetic BALB/cA mice. Mean NG pod/glomerular area (GA) per glomerulus was also significantly decreased in diabetic KK-Ay mice. The level of urinary albumin/creatinine ratio (ACR) in diabetic KK-Ay mice was significantly higher than that in non-diabetic BALB/cA mice. These data suggest that podocyte loss might induce albuminuria in KK-Ay mice. This finding confirmed our previous report that KK-Ay mice, especially in terms of histological findings, are a suitable animal model for glomerular injury in type 2 diabetic nephropathy.
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 the Direct Renin Inhibitor Aliskiren on Urinary Albumin Excretion in Spontaneous Type 2 Diabetic KK- Mouse
Masako Furukawa,Tomohito Gohda,Shinji Hagiwara,Mitsuo Tanimoto,Satoshi Horikoshi,Kazuhiko Funabiki,Yasuhiko Tomino
International Journal of Nephrology , 2013, DOI: 10.1155/2013/519130
Abstract: Objective. Although angiotensin II-mediated inflammation and extracellular matrix accumulation are considered to be associated with the progression of diabetic nephropathy, these processes have not yet been sufficiently clarified. The objective of this study was to determine whether the correction of the abnormal renal expression of MMPs and its inhibitors (MMPs/TIMPs) and cytokines following the administration of aliskiren to KK- mice results in a renoprotective effect. Methods. KK- mice were divided into two groups, that is, untreated (saline) and treated (aliskiren) groups. Systolic BP, HbA1c levels, and the albumin-creatinine ratio (ACR) were measured. The renal expression of MMPs/TIMPs, fibronectin, type IV collagen, MCP-1, and (pro)renin receptor ((P)RR) was examined using real-time PCR and/or immunohistochemical staining. Renal MAPK and NF-κB activity were also examined by Western blot analyses and ELISA, respectively. Results. Significant decreases in systolic BP and ACR levels were observed in treated KK- mice compared with the findings in untreated KK- mice. Furthermore, increases in MMPs/TIMPs, fibronectin, type IV collagen, MCP-1, and (P)RR expression, in addition to MAPK and NF-κB activity, were significantly attenuated by aliskiren administration. Conclusions. It appears that aliskiren improves albuminuria and renal fibrosis by regulating inflammation and the alteration of collagen synthesis and degradation. 1. Introduction Recent studies suggest that chronic inflammation and extracellular matrix (ECM) accumulation promote the progression of diabetic nephropathy (DN) [1, 2]. We have also reported the increased renal expression of monocyte chemotactic protein (MCP)-1, fibronectin, and type IV collagen in KK- mice [3–5], a frequently used animal model of type 2 diabetes (T2D) [6]. Furthermore, angiotensin (Ang) II induces the phosphorylation of mitogen-activated protein kinase (MAPK) and increases nuclear factor (NF)-κB binding activity in this mouse model [5]. Several studies have suggested that the renin-angiotensin system (RAS) is one of the major mediators of the progression of glomerular hypertension, inflammation, and tubulointerstitial fibrosis, which leads to the progression of DN [7–9]. Aliskiren is the first agent in a new class of orally effective direct renin inhibitors approved for hypertension treatment [10, 11]. In contrast to conventional RAS blockers, angiotensin-converting enzyme (ACE) inhibitors and Ang II type 1 receptor blockers (ARBs), aliskiren blocks RAS by directly inhibiting plasma renin activity and preventing the
Dual Band MIMO Antenna Composed of Two Low Profile Unbalanced Fed Inverted L Antennas for Wireless Communications  [PDF]
Erfan Rohadi, Mitsuo Taguchi
Wireless Engineering and Technology (WET) , 2014, DOI: 10.4236/wet.2014.53007
Abstract:
A low profile dual-band multiple-input-multiple-output (MIMO) antenna system is proposed. The proposed MIMO antenna consists of two low profile unbalanced fed inverted L antennas with parasitic elements to resonate at 2.45 GHz and 5 GHz. The structure is uncomplicated by locating two ultra low profile inverted L antennas on the finite conducting plane. The proposed MIMO antenna is numerically and experimentally analyzed. When the size of conducting plane is 55 mm by 55 mm and the height of antenna is 9 mm, the directive gain of 4.11 dBi and the S11 bandwidth of 5.71% are achieved for lower frequency of 2.45 GHz. At the upper frequency of 5 GHz, the directive gain of 8.22 dBi and the S11 bandwidth of 6% are obtained. The proposed antenna has good diversity gain, shown by the correlation coefficient becomes less than 0.005 at the frequency of 2.45 GHz and 5 GHz band when the distance between inverted L elements is 41 mm. A good agreement between calculated and measured results is obtained. The results show that the weak mutual coupling of the proposed antenna and this feature enables it to cover the required bandwidths for WLAN operation at the 2.4 GHz band and 5 GHz band.
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
Challenging for cartilage repair
Mitsuo Ochi
Sports Medicine, Arthroscopy, Rehabilitation, Therapy & Technology , 2009, DOI: 10.1186/1758-2555-1-13
Abstract: The next contribution to our variety of cartilage repair methods, was the minimally invasive approach using a tissue-engineered chondral plug. New scaffolds, consisting of a type I collagen sponge and surrounding PLLA mesh [4] or interconnected porous calcium hydroxyapatite ceramic [5], were demonstrated to comprise an effective minimally invasive approach.The bone marrow stimulating technique under arthroscopy is another minimally invasive technique which is a well accepted procedure for large osteochondral defects. However, there are two potential weak points when inducing hyaline cartilage. One is a compressive overload on the drilled or microfractured area in the early stage after surgery. In order to reduce this early stage overload, we have developed external fixators which allow almost full ROM with joint distraction for clinical cases, based on an animal study [6]. This apparatus has been successfully used for 12 patients, each with a large cartilage defect [7]. Another weak point is a small number of mesenchymal stem cells obtained from drilled holes which are used for chondrogenesis. An injection of cultured MSCs into the joint has been demonstrated to be effective for cartilage defects in rats [8]. The combined approach should be adopted for large defects in the near future.However, the most optimal procedure for the repair cartilage defects is simply an injection of cytokines or growth factors and cells. Our planned novel approach for the future is to use a cell delivery system using an external magnetic field. Our procedure involves using autologous bone marrow mesenchymal stem cells attached to small-sized magnetic beads and an external magnetic field. For successful cartilage repair, it is ideal to effectively attract injected mesenchymal stem cells to a desired portion in the knee joint (osteochondral defect) using an external magnet force [9]. We believe that this novel system is also effective in the treatment of brain or spinal cord injury and for
Automatic Production System for Circuit Boards With Universal Hybrid Integrated Circuits
Mitsuo Ohsawa
Active and Passive Electronic Components , 1981, DOI: 10.1155/apec.8.37
Abstract:
Recent research and development in titanium alloys for biomedical applications and healthcare goods
Mitsuo Niinomi
Science and Technology of Advanced Materials , 2003,
Abstract: Nb, Ta and Zr are the favorable non-toxic alloying elements for titanium alloys for biomedical applications. Low rigidity titanium alloys composed of non-toxic elements are getting much attention. The advantage of low rigidity titanium alloy for the healing of bone fracture and the remodeling of bone is successfully proved by fracture model made in tibia of rabbit. Ni-free super elastic and shape memory titanium alloys for biomedical applications are energetically developed. Titanium alloys for not only implants, but also dental products like crowns, dentures, etc. are also getting much attention in dentistry. Development of investment materials suitable for titanium alloys with high melting point is desired in dental precision castings. Bioactive surface modifications of titanium alloys for biomedical applications are very important for achieving further developed biocompatibility. Low cost titanium alloys for healthcare goods, like general wheel chairs, etc. has been recently proposed.
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