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  • 1
    Electronic Resource
    Electronic Resource
    Acute onset of diabetic pathological changes in transgenic mice with human aldose reductase cDNA (1995)
    Springer
    Diabetologia 38 (1995), S. 255-261 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00400627
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Molecular cloning of a group of mouse pancreatic islet beta-cell-related genes by random cDNA sequencing (1995)
    Springer
    Diabetologia 38 (1995), S. 381-386 
    Details
    ISSN: 1432-0428
    Keywords: Key words Random cDNA sequencing ; MIN6 ; pancreatic islet beta cell.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To understand the molecular basis of glucose concentration-responsive insulin synthesis and secretion from pancreatic islet beta cells, a group of pancreatic islet beta-cell-related cDNAs was cloned. A pair of cDNA libraries was constructed from a mouse pancreatic islet beta-cell line of MIN6, which was cultured in either high glucose or low glucose media. By applying a random cDNA sequencing approach, 503 and 395 independent species were obtained from a total of 1,011 and 762 clones in the high glucose and low glucose library, respectively. The unknown genes comprised the majority of about 70 % independent clones in both libraries. In Northern blot analysis, 311 (69.4 %) of 448 independent clones showed positive signals within 72 h of autoradiographic exposure. Surprisingly, 150 (48.2 %) out of 311 positive clones showed positive signals to MIN6 cells, but not to NIH/3T3 fibroblasts. The expression level of three unknown clones were glucose-concentration dependent. Combination of a random cDNA sequencing approach and Northern blot analysis is useful to obtain a large number of novel genes and islet beta-cell-related genes. [Diabetologia (1995) 38: 381–386]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00410274
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    GGAAAT motifs play a major role in transcriptional activity of the human insulin gene in a pancreatic islet beta-cell line MIN6 (1996)
    Springer
    Diabetologia 39 (1996), S. 1462-1468 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin gene ; GG motif ; transcription ; pancreatic islet ; MIN6.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The insulin gene is specifically expressed in pancreatic islet beta cells. Various cis-acting DNA elements in the 5 ′-flanking region of the human insulin gene were examined for their contribution to the transcriptional activity using sensitive human growth hormone (hGH) reporter plasmids. The hGH constructs, having successively deleted human insulin promoter sequences, were transfected to a pancreatic islet beta-cell line MIN6. The deletion of two GGAAAT (GG) motifs, GG2 at –145 to –140 bp and GG1 at –134 to –129 bp, decreased the transcriptional activity to 6.5 % of that of the promoter sequence from –156 to + 1 bp. The selective mutations in both GG motifs also decreased the transcriptional activity to 5.5 %. One-base mutations of GG2 and GG1 decreased the transcriptional activity to 82 and 11 %, respectively. The two-base mutations between GG2 and GG1 affected the transcriptional activity more strongly than those just outside the GG motifs. A single set of GG motifs in the upstream of thymidine kinase promoter increased the transcriptional activity to 216 % compared to that of thymidine kinase promoter alone in MIN6 cells. With an electrophoretic mobility shift assay (EMSA), a nuclear factor in MIN6 cells was shown to bind the DNA fragments containing two GG motifs. This factor did not bind to another GGAAAT-like sequence at –313 to –305 bp in the human insulin gene. These results suggested that the GG motifs contributed to the cell-specific transcription of the human insulin gene in association with the binding of the sequence-specific nuclear factor. [Diabetologia (1996) 39: 1462–1468]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050599
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Acute onset of diabetic pathological changes in transgenic mice with human aldose reductase cDNA (1995)
    Springer
    Diabetologia 38 (1995), S. 255-261 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00400627
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Molecular cloning of a group of mouse pancreatic islet beta-cell-related genes by random cDNA sequencing (1995)
    Springer
    Diabetologia 38 (1995), S. 381-386 
    Details
    ISSN: 1432-0428
    Keywords: Random cDNA sequencing ; MIN6 ; pancreatic islet beta cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To understand the molecular basis of glucose concentration-responsive insulin synthesis and secretion from pancreatic islet beta cells, a group of pancreatic islet beta-cell-related cDNAs was cloned. A pair of cDNA libraries was constructed from a mouse pancreatic islet beta-cell line of MIN6, which was cultured in either high glucose or low glucose media. By applying a random cDNA sequencing approach, 503 and 395 independent species were obtained from a total of 1,011 and 762 clones in the high glucose and low glucose library, respectively. The unknown genes comprised the majority of about 70% independent clones in both libraries. In Northern blot analysis, 311 (69.4%) of 448 independent clones showed positive signals within 72 h of autoradiographic exposure. Surprisingly, 150 (48.2%) out of 311 positive clones showed positive signals to MIN6 cells, but not to NIH/3T3 fibroblasts. The expression level of three unknown clones were glucose-concentration dependent. Combination of a random cDNA sequencing approach and Northern blot analysis is useful to obtain a large number of novel genes and islet beta-cell-related genes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00410274
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Diabetes and pancreatic tumours in transgenic mice expressing Pa × 6 (2000)
    Springer
    Diabetologia 43 (2000), S. 332-339 
    Details
    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
    URL: http://dx.doi.org/10.1007/s001250050051
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    Paper (German National Licenses)
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  • 7
    Electronic Resource
    Electronic Resource
    Apoptosis and remodelling of beta cells by paracrine interferon-γ without insulitis in transgenic mice (1999)
    Springer
    Diabetologia 42 (1999), S. 566-573 
    Details
    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
    URL: http://dx.doi.org/10.1007/s001250051196
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    Paper (German National Licenses)
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  • 8
    Electronic Resource
    Electronic Resource
    Microstructure of Anisotropic Nd-Fe-B Film Magnets Prepared by Pulsed Laser Deposition (2007)
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 561-565 (Oct. 2007), p. 1131-1134 
    Details
    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
    Notes: Microstructure of the anisotropic Nd-Fe-B thick-film magnets has been investigated bytransmission electron microscopy. Specimens of the thick-film magnets were prepared by thehigh-speed pulsed laser deposition method with a substrate heating system. It was revealed that thefilm deposited on a Ta substrate has a three-layer structure of Nd2Fe14B: The lower layer is composedof isotropic grains about 50-300 nm in diameter, the middle one has a columnar structure of 1 3m inheight, and the upper one is again composed of small isotropic grains about several ten nm indiameter. The three-layer-structure is explained to result from a partial recrystallization ofmicro-crystalline Nd2Fe14B that are formed at the moment of deposition. In the middle layer, thec-axis of columnar grains is fairly aligned in the direction perpendicular to the substrate surface. Thepreferred orientation of c-axis produces the magnetic anisotropy of the thick-films
    Type of Medium: Electronic Resource
    URL: http://www.tib-hannover.de/fulltexts/2011/0528/02/17/transtech_doi~10.4028%252Fwww.scientific.net%252FMSF.561-565.1131.pdf
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    Paper (German National Licenses)
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  • 9
    Electronic Resource
    Electronic Resource
    Angiotensin Converting Enzyme Inhibitor But Not Calcium Blocker Down-Regulates Gene Expression of Vascular Natriuretic Peptide Receptor in Hypertensive Rats
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 205 (1994), S. 1595-1600 
    Details
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1006/bbrc.1994.2849
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    Paper (German National Licenses)
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  • 10
    Electronic Resource
    Electronic Resource
    Molecular Cloning of Human Amidophosphoribosyltransferase
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 190 (1993), S. 192-200 
    Details
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1006/bbrc.1993.1030
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    Paper (German National Licenses)
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