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  • 1
    Language: English
    In: Journal of Vascular Surgery, 2011, Vol.54(6), pp.1753-1759
    Description: Intimal hyperplasia is a major obstacle to patency after vein grafting. Several clinical trials revealed that pioglitazone, a peroxisome proliferator-activated receptor-γ ligand, exerts beneficial actions on cardiovascular complications. We investigated whether pioglitazone modulates intimal hyperplasia in experimental rabbit autologous vein grafts. Male Japanese White rabbits were randomly divided into two groups: one group received pioglitazone as food admixture at a concentration of 0.01%, and the other did not (control). One week later, each group underwent reversed autologous vein bypass grafting of the right common carotid artery using ipsilateral external jugular vein. Pioglitazone therapy was continued after surgery and until harvest. Intimal hyperplasia of the grafted vein was assessed at 28 days. Two weeks after implantation, proliferative cells in the neointima were identified by immunohistochemical staining with Ki-67 monoclonal antibody. To determine apoptotic cells, we performed terminal deoxynucleotidyl transferase-mediated deoxyuride-5′-triphosphate nick-end labeling (TUNEL) staining. Blood samples were collected at 28 days after implantation for measuring metabolic parameters such as plasma glucose and total cholesterol. Adiponectin levels were determined by Western blot analysis. Finally, we assessed adiponectin-related signaling pathway, 5′ adenosine monophosphate-activated protein kinase (AMPK), and extracellular signal-regulated kinase (ERK) in the grafted vein by Western blot analysis. Treatment with pioglitazone markedly inhibited intimal hyperplasia of carotid interposition-reversed jugular vein grafts in the pioglitazone group (0.54 ± 0.04 mm ) vs control (0.93 ± 0.04 mm ; n = 7; 〈 .01). Pioglitazone treatment reduced the number of Ki-67-positive proliferating cells in the neointima of the vein grafts at 14 days after implantation in the pioglitazone group (4.1% ± 1.1%) vs the controls (16.8% ± 1.7%; 〈 .05). The frequency of TUNEL-positive apoptotic cells was enhanced by pioglitazone (3.5% ± 0.5%) vs the controls (1.2% ± 0.1%; 〈 .05). Pioglitazone treatment also increased plasma levels of adiponectin, a vascular protective hormone, and led to an increase in phosphorylation of AMPK and a decrease in phosphorylation of ERK in the grafted vein. Pioglitazone attenuates intimal hyperplasia of the vein graft after autologous bypass grafting by its ability to suppress cell proliferation and enhance apoptosis. Pioglitazone could represent a therapeutic target for the prevention of graft failure after bypass grafting. Intimal hyperplasia is a major obstacle to patency after vein grafting. Various treatments to reduce neointimal hyperplasia have been examined; however, a standard clinical treatment has not yet been established. We report that pioglitazone, a peroxisome proliferator-activated receptor-γ ligand, inhibits intimal hyperplasia of autologous vein grafts. Pioglitazone also increased adiponectin, an adipose-derived hormone. Obesity-related complications, such as diabetes, are closely associated with autologous vein graft stenosis after bypass surgery. The findings reported here suggest that pharmacologic approaches aimed at increasing adiponectin production, such as pioglitazone, can contribute to the prevention of autologous vein graft stenosis in obese individuals.
    Keywords: Medicine
    ISSN: 0741-5214
    E-ISSN: 1097-6809
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  • 2
    Language: English
    In: Environmental Health, 01 October 2008, Vol.7(1), p.47
    Description: Abstract Background The Yusho poisoning incident, which was caused by rice bran oil contaminated with polychlorinated biphenyls (PCBs), polychlorinated quarterphenyls (PCQs) and polychlorinated dibenzofurans (PCDFs) generated by heat denaturation of PCB, occurred in 1968 in western Japan. Annual...
    Keywords: Medicine
    ISSN: 1476-069X
    E-ISSN: 1476-069X
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  • 3
    Language: Japanese
    In: Rinsho byori. The Japanese journal of clinical pathology, February 2008, Vol.56(2), pp.95-100
    Description: Quantitative measurement of hepatitis C virus (HCV) has been performed by PCR method. However, PCR method has problems such as a special instrument, a complicated manual skill and a high cost. Recently, simple and highly sensitive HCV core antigen (Ag) method has been developed. We performed fundamental evaluation of HCV core Ag method, and compared HCV core Ag method with HCV PCR high-range method. The intra-assay and inter-assay variation coefficients for HCV core Ag were calculated to be within the ranges of 1.0-11.3% and 0.8-9.3%, respectively. The test of dilution linearity revealed the unstableness in the vicinity of a cut-off level of 50 fmol/L. Based on the result of the high-range method; sensitivity, specificity, positive predictive value, negative predictive value, and agreement rate were 97.0%, 100%, 100%, 82.0%, and 96.5%, respectively. The correlation between the HCV core Ag method and the high-range method was r = 0.87. Cost per sample and time from sample preparation to final report for HCV core Ag were cheaper and shorter than those of HCV PCR method, respectively. We consider that the HCV core Ag method seems to be useful as the quantitative measurement of HCV with respect to rapidness, easiness and low cost.
    Keywords: Hepatitis C Antigens -- Analysis ; Nucleic Acid Amplification Techniques -- Methods ; Viral Core Proteins -- Analysis
    ISSN: 0047-1860
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 4
    Language: English
    In: The Journal of nutrition, February 2002, Vol.132(2), pp.145-51
    Description: The relationship between nutritional status and insulin-like growth factor binding protein-2 (IGFBP-2) gene expression in chickens was studied. Chickens (6 wk old) were food deprived for 2 d and then refed. IGFBP-2 mRNA in the brain was significantly decreased by food deprivation and levels did not increase when birds were refed for 24 h. Gizzard and hepatic IGFBP-2 mRNA levels were significantly increased by food deprivation and decreased by refeeding. Any nutrients tested decreased hepatic IGFBP-2 gene expression. In kidney, IGFBP-2 mRNA was detected but not influenced by food deprivation and refeeding. In another study, the influence of dietary protein source [isolated soybean protein vs. casein; crude protein (CP) 20%] and the supplementation of essential amino acids on IGFBP-2 gene expression of young chickens (5 wk old) was examined. The influence of feeding a low soybean protein diet (CP 5%) on tissue IGFBP-2 gene expression was also investigated. Hepatic IGFBP-2 mRNA was not detected in any group. Feeding the low protein diet for 7 d decreased brain IGFBP-2 mRNA level and increased gizzard IGFBP-2 level compared with chickens fed 20% protein diets. A significant interaction between protein source and amino acid supplementation was observed in gizzard IGFBP-2 mRNA level. In both casein-fed groups and in chickens fed 20% soybean protein diet without supplemental amino acids, the levels did not differ from one another or from the low protein diet-fed birds. The level was lower in chickens fed the amino acid-supplemented, 20% soybean protein diet. In conclusion, the response of IGFBP-2 gene expression to variations in nutritional status was rapid and different in several tissues of young chickens, which would help modulate the growth-promoting effect of circulating IGF-I by making the IGF-IGFBP complex.
    Keywords: Gene Expression Regulation, Developmental ; Chickens -- Metabolism ; Food Deprivation -- Physiology ; Insulin-Like Growth Factor Binding Protein 2 -- Genetics
    ISSN: 0022-3166
    E-ISSN: 15416100
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  • 5
    Language: English
    In: Biomaterials, April 2015, Vol.47, pp.62-71
    Description: The nanoscale structure-function relationship is a key determinant of bone toughness or micro-fragility. The loss of bone toughness during the aging process has been accepted based on empirical evidence, but this concept has not yet been fully supported by evidence at the material level. Here, we demonstrate a reduction in bone toughening mechanism in mimetic aged cortical bone obtained from deficient ( ) mice and assessed by dynamic mechanical analysis. The strain-rate nanoindentation tests showed enhanced stiffening of the wild-type calvarial bone and a large dimensional recovery during rapid loading following the constant displacement test. Such strain-dependent stiffening was likely associated with nanoscale dilatational bands and subsequent strain-energy transfer to the superior wild-type cross-linked collagen matrix network. The absence of dilatational bands formed by hydroxyapatite crystals and non-collagenous proteins in the bone samples likely diminished the intrinsic bone toughening mechanisms almost independent of viscoelastic behaviors. Such nanoscale structural alternations that occur during aging processes lead to crack propagation and result in overall bone fractures under large external stresses. In addition, dynamic mechanical analysis using instrumented nanoindentation was useful for the evaluation of bone mechanical properties in this pathological model of a genetic knockout mouse.
    Keywords: Bone ; Mechanical Properties ; Ageing ; Dynamic Mechanical Analysis ; Nanoindentation ; Medicine ; Engineering
    ISSN: 0142-9612
    ISSN: 20452322
    E-ISSN: 1878-5905
    E-ISSN: 20452322
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  • 6
    Language: English
    In: Diabetic Medicine, 10/16/2017
    Description: To purchase or authenticate to the full-text of this article, please visit this link: http://onlinelibrary.wiley.com/doi/10.1111/dme.13524/abstract Byline: K. Iseri, M. Iyoda, Y. Shikida, T. Inokuchi, T. Morikawa, N. Hara, T. Hirano, T. Shibata Abstract Background Type B insulin resistance syndrome is a rare disease characterized by refractory transient hyperglycaemia and severe insulin resistance associated with circulating anti-insulin receptor antibodies. A standardized treatment regimen for type B insulin resistance syndrome has yet to be established. Case report We report the case of a 64-year-old man undergoing haemodialysis for antineutrophil cytoplasmic antibody-associated vasculitis and diabetic nephropathy, who developed rapid onset of hyperglycaemia (glycated albumin 52.1%). Type B insulin resistance syndrome was diagnosed, on the basis of positivity for anti-insulin receptor antibodies and the man's autoimmune history of antineutrophil cytoplasmic antibody-associated vasculitis and idiopathic thrombocytopenic purpura. Although severe hyperglycaemia persisted in spite of corticosteroids and high-dose insulin therapy, rituximab treatment resulted in remarkable improvement of the man's severe insulin resistance and disappearance of anti-insulin receptor antibodies without any adverse effects. Conclusions According to a literature review of 11 cases in addition to the present case, rituximab appears to be a safe and effective strategy for the treatment of corticosteroid-resistant type B insulin resistance syndrome.
    Keywords: Hyperglycemia – Development and Progression ; Hyperglycemia – Care and Treatment ; Insulin Resistance – Development and Progression ; Insulin Resistance – Care and Treatment ; Diabetic Nephropathies – Development and Progression ; Diabetic Nephropathies – Care and Treatment;
    ISSN: Diabetic Medicine
    E-ISSN: 07423071
    E-ISSN: 14645491
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  • 7
    In: PLoS ONE, 2014, Vol.9(3)
    Description: Oral phosphate loading and calcitriol stimulate Fibroblast growth factor 23 (FGF23) secretion, but the mechanisms underlying the stimulation of FGF23 remain to be studied. We compared the effect of intravenous phosphate loading with that of oral loading on FGF23 levels in normal and 5/6 nephrectomized uremic rats. Uremic rats (Nx) and sham-operated rats were fed a normal phosphate diet for 2 weeks and then divided into 3 groups: 1) with the same phosphate diet (NP), 2) with a high phosphate diet (HP), and 3) NP rats with intravenous phosphate infusion using a microinfusion pump (IV). Blood and urine were obtained 1 day (early phase) and 7 days (late phase) after the interventions. In the early and late phases, serum phosphate levels and fractional excretion of phosphate (FEP) were comparable in the HP and IV groups in both Sham and Nx rats. Serum phosphate levels in the HP and IV groups were equally and significantly higher than those in the NP group only in the late phase in Nx rats. In the early phase, FGF23 levels were comparable in the NP, HP, and IV groups, but were significantly higher in the HP and IV groups compared to the NP group in the late phase in Nx rats. 1α-hydroxylase and sodium dependent phosphate co-transporter 2a expression levels in the kidney in Nx rats were equally and significantly decreased in the HP and IV groups compared with the NP group, while 24-hydroxylase expression was equally and significantly increased. These results show that chronic intravenous phosphate loading increases bioactive FGF23, indicating that an alternative pathway for FGF23 regulation, in addition to the dietary route, may be present. This pathway is clearer under conditions produced by a kidney injury in which phosphate is easily overloaded.
    Keywords: Research Article ; Biology ; Medicine ; Veterinary Science
    E-ISSN: 1932-6203
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  • 8
    Language: English
    In: Nanomedicine: Nanotechnology, Biology, and Medicine, October 2013, Vol.9(7), pp.1036-1047
    Description: Bone morphogenetic protein-2 (BMP2) is among the most popular anabolic agents and substantially increase bone volume related to enhanced osteoblast differentiation. Here we demonstrate a remarkable deterioration in the nanomechanical properties of mineralized tissue induced from osteoblasts solely by the function of BMP2. Mineralized tissue of primary osteoblasts cultured with BMP2 shows molecular features of both bone and cartilage, but depletion of lysyl oxidase family members leads to poor nanomechanical properties of the mineralized tissue. Lysyl oxidase like-2 supplementation reinforces the inferior mineralized tissue induced from osteoblasts by BMP2 through intermolecular cross-linking of type II or type X collagen-rich extracellular matrix. This may also mimic a consolidation of bone fracture gaps, despite the fact that the distribution of the bone properties in such microenvironments has been poorly elucidated. These findings confirm the importance of testing newly induced bone down to the microscale and nanoscale in bone tissue engineering. Bone morphogenetic protein-2 is known to substantially increase bone volume related to enhanced osteoblast differentiation; however, this team of investigators report a remarkable deterioration in the nanomechanical properties of mineralized tissue induced from osteoblasts solely by the function of BMP2. Five indentation tests on an mineralize tissue. With the loading/partial unloading test, we can obtain constant hardness and elastic modulus on mineralized tissue along with indenter penetration.
    Keywords: Nanoindentation ; Raman Spectroscopy ; Osteoblasts ; Bone Morphogenetic Protein-2 ; Lysyl Oxidase Like-2 ; DNA Microarray ; Medicine
    ISSN: 1549-9634
    E-ISSN: 1549-9642
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  • 9
    Language: English
    In: Journal of Vascular Surgery, February 2015, Vol.61(2), pp.489-496
    Description: As first-line treatment for type 2 diabetes, metformin has gained a strong position. In addition, type 2 diabetics benefit from the fact that metformin is associated with a reduction in cardiovascular events. Nevertheless, there is a dearth of information concerning the functional role of metformin in regulating angiogenesis. Our present study explores whether metformin is involved in the modulation of the revascularization processes in vivo by employing a hindlimb mice model of ischemia-induced angiogenesis. For comparative purposes, randomly selected wild-type (WT) mice or endothelial nitric oxide synthase (eNOS) deficient mice were assigned to one of two groups. One group was orally administered a daily dose of metformin through a gastric tube whereas the other group served as a control with no metformin administered. Both groups were subjected to unilateral hindlimb ischemia. Laser Doppler analysis coupled with capillary density staining with CD31was the method employed to determine revascularization. Adenosine monophosphate-activated protein kinase (AMPK) and eNOS phosphorylation levels were assessed using Western blot analysis. Subsequent to hindlimb ischemic surgery, in comparison to the nontreated mice, metformin-treated WT mice showed accelerated limb perfusion, which was substantiated by laser Doppler blood-flow measurements and the presence of increased capillary density in the ischemic adductor muscle. Treatment with metformin significantly enhanced the increase in AMPK and eNOS phosphorylation levels of muscle tissues in WT mice induced by ischemia. In eNOS- deficient knockout mice, there was a significant increase in ischemic tissue AMPK phosphorylation induced by metformin; however, blood flow recovery in ischemic limb after surgery was unaffected. Metformin promoted revascularization in the presence of tissue ischemia through an AMPK/eNOS-related mechanism. Our study indicates that, in addition to its glucose-lowering effect, metformin fosters improved revascularization, which is responsible for its positive effect on patients with critical limb ischemia. In patients with peripheral arterial disease, the incidence of the diabetes mellitus is high. One of the comorbidities that affect wound healing is diabetes. In Japan, in particular, the complication rates of diabetes mellitus and end-stage renal disease are high in patients with critical limb ischemia. Metformin is a widely used first-line drug for the treatment of type2 diabetes. The present study indicates that, in addition to its glucose-lowering effect, metformin has beneficial effects on the improvement of revascularization, which produce positive effects on the patient with critical limb ischemia.
    Keywords: Medicine
    ISSN: 0741-5214
    E-ISSN: 1097-6809
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  • 10
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 28 May 2002, Vol.99(11), pp.7367-72
    Description: Prostaglandin D(2) (PGD(2)), a major cyclooxygenase product in a variety of tissues and cells, readily undergoes dehydration to yield the bioactive cyclopentenone-type PGs of the J(2)-series, such as 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)). The observation that the level of 15d-PGJ(2) increased in the tissue cells from patients with sporadic amyotrophic lateral sclerosis suggested that the formation of 15d-PGJ(2) may be closely associated with neuronal cell death during chronic inflammatory processes. In vitro experiments using SH-SY5Y human neuroblastoma cells revealed that 15d-PGJ(2) induced apoptotic cell death. An oligonucleotide microarray analysis demonstrated that, in addition to the heat shock-responsive and redox-responsive genes, the p53-responsive genes, such as gadd45, cyclin G1, and cathepsin D, were significantly up-regulated in the cells treated with 15d-PGJ(2). Indeed, the 15d-PGJ(2) induced accumulation and phosphorylation of p53, which was accompanied by a preferential redistribution of the p53 protein in the nuclei of the cells and by a time-dependent increase in p53 DNA binding activity, suggesting that p53 accumulated in response to the treatment with 15d-PGJ(2) was functional. The 15d-PGJ(2)-induced accumulation of p53 resulted in the activation of a death-inducing caspase cascade mediated by Fas and the Fas ligand.
    Keywords: Apoptosis -- Drug Effects ; Immunologic Factors -- Pharmacology ; Neurons -- Physiology ; Prostaglandin D2 -- Analogs & Derivatives
    ISSN: 0027-8424
    E-ISSN: 10916490
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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