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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 103 (1981), S. 7102-7106 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1520-5827
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    s.l. ; Stafa-Zurich, Switzerland
    Key engineering materials Vol. 145-149 (Oct. 1997), p. 201-210 
    ISSN: 1013-9826
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 239-241 (Nov. 1996), p. 663-666 
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Key words Transgenic mice ; aldose reductase ; diabetic angiopathies ; diabetic retinopathy ; diabetic nephropathies.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the role of human aldose reductase (hAR) in the pathogenesis of diabetic complications, we generated transgenic mice carrying hAR cDNA driven by the murine MHC class I molecule promoter (hAR-Tg). Northern and Western blot analyses and immunoassay of hAR revealed that both hAR mRNA and the protein were expressed in all tissues tested. Thrombosis in renal vessels and fibrinous deposits in Bowman's capsule were observed in 6-week-old hAR-Tg mice fed a normal diet. Ingestion of a 30 % glucose diet for 5 days caused sorbitol concentrations in the liver, kidney, and muscle of hAR-Tg mice to be elevated significantly. Seven-week-old hAR-Tg mice fed a 20 % galactose diet for 7 days developed cataracts and occlusion of the retinochoroidal vessels, in addition to pathological changes in the kidney. Despite an elevated aldose reductase level in hAR-Tg mice and their intake of an aldose diet, no histopathological changes were found in other tissues, including the brain, lungs, heart, thymus, spleen, intestine, liver, muscle, spinal cord, or sciatic nerve. Results suggest that target organs of diabetic complications, such as the kidney, lens, and retina are sensitive to damage associated with a high level of AR expression, but other organs are not; the susceptibility of each organ to diabetic complications is determined by not only hAR but also other factors. [Diabetologia (1995) 38: 255–261]
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Transgenic mice ; aldose reductase ; diabetic angiopathies ; diabetic retinopathy ; diabetic nephropathies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the role of human aldose reductase (hAR) in the pathogenesis of diabetic complications, we generated transgenic mice carrying hAR cDNA driven by the murine MHC class I molecule promoter (hAR-Tg). Northern and Western blot analyses and immunoassay of hAR revealed that both hAR mRNA and the protein were expressed in all tissues tested. Thrombosis in renal vessels and fibrinous deposits in Bowman's capsule were observed in 6-week-old hAR-Tg mice fed a normal diet. Ingestion of a 30% glucose diet for 5 days caused sorbitol concentrations in the liver, kidney, and muscle of hAR-Tg mice to be elevated significantly. Seven-week-old hAR-Tg mice fed a 20% galactose diet for 7 days developed cataracts and occlusion of the retinochoroidal vessels, in addition to pathological changes in the kidney. Despite an elevated aldose reductase level in hAR-Tg mice and their intake of an aldose diet, no histopathological changes were found in other tissues, including the brain, lungs, heart, thymus, spleen, intestine, liver, muscle, spinal cord, or sciatic nerve. Results suggest that target organs of diabetic complications, such as the kidney, lens, and retina are sensitive to damage associated with a high level of AR expression, but other organs are not; the susceptibility of each organ to diabetic complications is determined by not only hAR but also other factors.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: Keywords Diabetes mellitus, islets of Langerhans, embryology, cell differentiation, transcription factors.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Both endocrine and exocrine cells of the pancreas differentiate from epithelial cells of primitive pancreatic ducts, and four types of pancreatic islet cells (alpha, beta, delta, and PP cells) are derived from the common pluripotent precursor cells. Although Pa × 6 is expressed in all islet cells, Pa × 4 is detected only in beta cells. In homozygous Pa × 4-null mice, beta cells are absent, whereas the number of alpha cells is increased. Therefore, we hypothesized that the balance of Pa × 4 and 6 is one of the determinants by which the common progenitor cells differentiate into alpha or beta cells.¶Methods. To change this balance, we generated transgenic mice overexpressing Pa × 6 driven by the insulin promoter or the PDX1 promoter.¶Results. In both types of transgenic mice, normal development of beta cells was disturbed, resulting in apoptosis of beta cells and diabetes. In Insulin/Pa × 6-Tg mice, beta cells were specifically affected, whereas in PDX/Pa × 6-Tg mice, developmental abnormalities involved the whole pancreas including hypoplasia of the exocrine pancreas. Furthermore, PDX/Pa × 6-Tg mice experienced proliferation of both ductal epithelia and islet cells and subsequent cystic adenoma of the pancreas.¶Conclusion/interpretation. These findings suggest that Pa × 6 promotes the growth of ductal epithelia and endocrine progenitor cells and that the suppression of Pa × 6 is necessary for the normal development of beta cells and the exocrine pancreas. [Diabetologia (2000) 43: 332–339]
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0428
    Keywords: Keywords Type I diabetes ; interferon-γ ; transgenic mice ; apoptosis ; insulin secretion ; tumour necrosis factor.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. To examine whether interferon-γ destroys islet beta cells directly or indirectly through lymphocyte activation, or whether direct action of interferon-γ on beta cells by itself induces diabetes without insulitis. Methods. To avoid possible nonspecific breakdown of beta cells by transgenic overexpression of interferon-γ by the insulin promoter, we generated transgenic mice expressing interferon-γ under the control of rat glucagon promoter (RGP-IFN-γ-Tg mice). Results. The absence of insulitis in RGP-IFN-γ-Tg mice enabled us to investigate the direct effects of paracrine interferon-γ. In RGP-IFN-γ-Tg mice, serum concentrations of interferon-γ and tumour necrosis factor-α (TNF-α) were 50 and 6 times higher than those in their littermates, respectively, and glucose-responsive insulin secretion decreased to one-half the level of that in the littermates. Transgenic interferon-γ induced remodelling of beta cells where apoptosis of many beta cells was compensated by their vigorous regeneration and diabetes did not occur in most of the RGP-IFN-γ-Tg mice. Conclusion/interpretation. Interferon-γ alone is insufficient for the complete destruction of beta cells in vivo, and factors other than interferon-γ including activated lymphocytes or other cytokines, are necessary in addition to interferon-γ for the development of Type I (insulin-dependent) diabetes mellitus. [Diabetologia (1999) 42: 566–573]
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0509
    Keywords: Key words: Liver, neoplasms—Liver, ultrasound—Liver, computed tomography—Liver, magnetic resonance—Comparative studies.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Purpose: The purpose of this study was to assess the imaging findings of pathologically-proved small hepatic nodules 2 cm in size or smaller detected with ultrasonography in cirrhotic patients with suspected hepatocellular carcinoma (HCC). Materials and Methods: We evaluated sonographically detected 32 small hepatic nodules which were pathologically confirmed in 23 consecutive cirrhotic patients who were suspected of having HCC. Twenty-six lesions were confirmed with ultrasonographically-guided aspiration needle-core biopsy, and six with definitive surgery. Ultrasonographic examination records were retrospectively reviewed. CT, and MR images obtained with various imaging techniques were retrospectively reviewed by two radiologists in a blind fashion. Results: The 32 hepatic nodules were comprised of seven focal fatty changes, two large regenerative nodules, three low-grade dysplastic nodules, five high-grade dysplastic nodules, and fifteen HCCs. Ultrasonography showed various echogenicity for the hepatic nodules. The signal-intensity characteristics with T1-weighted spin-echo, in-phase gradient-recalled-echo, and dynamic MR imagings may be useful in distinguishing HCC from nonHCC nodules. Conclusions: Nearly half of small hepatic nodules detected with ultrasonography were nonHCC nodules. Ultrasonographic findings may not be reliable in characterizing small hepatic nodules in cirrhosis. CT and MR imaging obtained with the various techniques are still insensitive to these hepatic nodules. RID=""ID=""〈e5〉Correspondence to:〈/e5〉 M. Kanematsu
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0533
    Keywords: Parkinson's disease ; Substantia nigra ; Insulin receptor ; Immunochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Immunohistochemistry using both a newly developed polyclonal, and a commercially available monoclonal, anti-insulin receptor antibody was done on the midbrain from cases of idiopathic Parkinson's disease (PD), Alzheimer's disease, amyotrophic lateral sclerosis, vascular parkinsonism and non-neurological controls. Both antibodies gave indentical patterns of neuronal staining. The neurons of the oculomotor nucleus were immunopositive in all the brains. However, the neurons in the pars compacta of the substantia nigra, paranigral nucleus, parabrachial pigmental nucleus, tegmental pedunculopontine nucleus, supratrocheal nucleus, cuneiform nucleus, subcuneiform nucleus and lemniscus medialis, which were positive in other diseases and in non-neurological controls, were not stained by these antibodies in PD brains. These results suggest that, in PD, a dysfunction of the insulin/insulin receptor system may precede death of the dopaminergic neurons.
    Type of Medium: Electronic Resource
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