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  • 11
    Electronic Resource
    Electronic Resource
    Hepatocyte nuclear factor-1a gene and non-insulin-dependent diabetes mellitus in the Japanese population (1998)
    Springer
    Acta diabetologica 35 (1998), S. 150-153 
    Details
    ISSN: 1432-5233
    Keywords: Key words Non-insulin-dependent diabetes mellitus ; MODY ; Hepatocyte nuclear factor-1α ; Genetics ; Microsatellite polymorphism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recently, hepatocyte nuclear factor-1α (HNF-1α, which is encoded by the TCF1 gene) mutations were reported in a subset of patients with maturity onset diabetes of the young (MODY3). We studied the contribution of TCF1 to genetic susceptibility to common non-insulin-dependent diabetes mellitus (type 2) in Japanese subjects by investigating allelic association with type 2 diabetes use of three markers. We also studied the frequency of the G191D mutation, the only mutation of TCF1 reported so far in late-onset type 2 diabetes. A total of 356 subjects were studied. There were no significant differences in allele frequency of the three markers between patients with type 2 diabetes and control subjects. A G191D mutation was not found in the subjects studied, giving a frequency of less than 0.4% in common type 2 diabetes. The lack of association of type 2 diabetes with three markers in and near TCF1 suggests that mutations in TCF1 derived from a limited number of founders are not a major cause of common type 2 diabetes even in the genetically homogeneous Japanese population. The data also indicate that the G191D mutation in TCF1 plays little, if any, role in susceptibility to common type 2 diabetes in the Japanese.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s005920050120
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  • 12
    Electronic Resource
    Electronic Resource
    Detection of lysyl oxidase gene expression in rat skin during wound healing (1995)
    Springer
    Archives of dermatological research 288 (1995), S. 7-10 
    Details
    ISSN: 1432-069X
    Keywords: Key words Lysyl oxidase ; Gene expression ; Wound healing ; Type III collagen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Lysyl oxidase (LOX) initiates the crosslinking of the lysine-derived aldehyde and plays an essential role in maturation of collagen, for example in wound healing. Although the activity of this enzyme has been examined in various disorders, and a further intriguing aspect of the relationship between LOX and tumorigenesis has recently emerged, its gene expression pattern in tissues is still unknown. We examined LOX gene expression during wound healing in rat skin. In addition, type III collagen gene expression was studied to determine the formation of fibrils. The LOX mRNA level reached a peak by day 3 after injury, which was earlier than that of type III collagen, and continued at a high level until day 22. The type III collagen mRNA level began to rise from day 3 and had increased intensely by day 22. In situ hybridization revealed grains corresponding to LOX mRNA in the fibroblasts of the granulomatous tissue. These results suggest that LOX is produced before collagen synthesis in preparation for crosslinking in the early phase of wound healing.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004030050014
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  • 13
    Electronic Resource
    Electronic Resource
    The migration of luteinizing hormone-releasing hormone (LHRH) neurons from the medial alfactory placode into the medial basal forebrain (1990)
    Springer
    Cellular and molecular life sciences 46 (1990), S. 956-962 
    Details
    ISSN: 1420-9071
    Keywords: Terminalis nerve ; olfactory pit ; nasal placode
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Over the years, investigators have noticed, in a wide variety of species of vertebrates, large numbers of cells migrating from the olfactory placode to the forebrain. These cells were considered to be Schwann cells or ganglion cells of the terminalis nerve. Recently, immunocytochemical localization studies have shown that many of these migrating cells contain luteinizing hormone-releasing hormone (LHRH), a brain peptide that regulates reproductive functions by evoking the release of luteinizing hormone and follicle-stimulating hormone from the anterior pituitary gland. The origin of LHRH cells in the epithelium of the medial olfactory placode, their migration across the nasal septum and into the forebrain, with branches of the terminalis nerve, also a derivative of the medial part of the olfactory placode, has led to some interesting speculations, from evolutionary and physiological perspectives, about the origin of these cells and the role of the terminalis nerve in their migration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01939389
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  • 14
    Electronic Resource
    Electronic Resource
    Association of Trp64Arg mutation of the β3-adrenergic-receptor with NIDDM and body weight gain (1996)
    Springer
    Diabetologia 39 (1996), S. 349-352 
    Details
    ISSN: 1432-0428
    Keywords: Β3-adrenergic-receptor gene ; susceptibility ; missense mutation ; non-insulin-dependent diabetes mellitus ; insulin resistance syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A possible pathogenic mutation in the Β3-adrenergic-receptor gene (Trp64Arg) has been reported to be associated with an earlier age of onset of non-insulin-dependent diabetes mellitus (NIDDM) and clinical features of the insulin resistance syndrome in Pima Indian, Finnish and French subjects. Since marked heterogeneity has been reported in the association of mutations of candidate genes with NIDDM between Japanese and other ethnic groups, we investigated the association of Trp64Arg with NIDDM in Japanese subjects. The allele frequency of the mutation (Arg) was slightly, but not significantly, higher in NIDDM than in control subjects (70 out of 342 alleles [20.5%] vs 40 out of 248 [16.1%], respectively, p〉0.2). When our data were combined with those of Pima Indian and Finnish subjects, however, the Arg/Arg genotype was significantly associated with NIDDM as compared with the other two genotypes (p〈0.005, relative risk [RR] 2.13, 95% confidence interval [CI] 1.28–3.55). The Arg allele was also associated with NIDDM (p〈0.05, RR 1.27, 95% CI 1.06–1.52). Japanese subjects homozygous for the mutation had a significantly higher body mass index (mean ± SD∶25.5±3.9 kg/ m2) than heterozygotes (22.6±4.1, p〈0.05) and normal homozygotes (22.8±3.8, p〈0.05). NIDDM patients homozygous for the mutation tended to have an earlier age of onset of NIDDM than those with other genotypes. These data suggest that the Trp64Arg mutation not only contributes to weight gain and age-at-onset of NIDDM but is also associated with susceptibility to NIDDM.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418352
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  • 15
    Electronic Resource
    Electronic Resource
    Reactive oxygen intermediates in autoimmune islet cell destruction of the NOD mouse induced by peritoneal exudate cells (rich in macrophages) but not T cells (1994)
    Springer
    Diabetologia 37 (1994), S. 22-31 
    Details
    ISSN: 1432-0428
    Keywords: NOD mice ; insulitis ; reactive oxygen intermediates ; superoxide dismutase ; peritoneal macrophages
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The non-obese diabetic (NOD) mouse spontaneously develops autoimmune Type 1 (insulin-dependent) diabetes mellitus. NOD mice exhibit massive infiltrates of T cells and macrophages into pancreatic islets (insulitis) prior to diabetes. The contribution of oxygen free radicals to the development of insulitis in NOD mice was examined by administration of its scavengers, such as superoxide dismutase and catalase. Bovine superoxide dismutase and catalase were each coupled to polyethylene glycol. The treatment with superoxide dismutase-polyethylene glycol reduced the number of islets with insulitis and increased the undamaged islet tissue, as compared with the control group. The treatment with catalase-polyethylene glycol showed a similar tendency which did not reach significance. Using a flow cytometric assay of the oxidation of 2′, 7′-dichlorofluorescein, the content of reactive oxygen intermediates in islet cells in the culture system was measured and the effect of peritoneal exudate cells and T cells on their production examined. Peritoneal exudate cells, but not T cells, from NOD mice increased the content of reactive oxygen intermediates in islet cells of either the NOD mouse or the ILI mouse (MHC-identical to NOD); the addition of superoxide dismutase to the culture medium suppressed this increase in NOD or ILI islet cells. The present data support the concept that production of oxygen free radicals mediated by macrophages can damage islet beta cells, directly resulting in autoimmune Type 1 diabetes in NOD mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00428773
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  • 16
    Electronic Resource
    Electronic Resource
    Reactive oxygen intermediates in autoimmune islet cell destruction of the NOD mouse induced by peritoneal exudate cells (rich in macrophages) but not T cells (1994)
    Springer
    Diabetologia 37 (1994), S. 22-31 
    Details
    ISSN: 1432-0428
    Keywords: Key words NOD mice, insulitis, reactive oxygen intermediates, superoxide dismutase, peritoneal macrophages.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The non-obese diabetic (NOD) mouse spontaneously develops autoimmune Type 1 (insulin-dependent) diabetes mellitus. NOD mice exhibit massive infiltrates of T cells and macrophages into pancreatic islets (insulitis) prior to diabetes. The contribution of oxygen free radicals to the development of insulitis in NOD mice was examined by administration of its scavengers, such as superoxide dismutase and catalase. Bovine superoxide dismutase and catalase were each coupled to polyethylene glycol. The treatment with superoxide dismutase-polyethylene glycol reduced the number of islets with insulitis and increased the undamaged islet tissue, as compared with the control group. The treatment with catalase-polyethylene glycol showed a similar tendency which did not reach significance. Using a flow cytometric assay of the oxidation of 2′, 7′-dichlorofluorescein, the content of reactive oxygen intermediates in islet cells in the culture system was measured and the effect of peritoneal exudate cells and T cells on their production examined. Peritoneal exudate cells, but not T cells, from NOD mice increased the content of reactive oxygen intermediates in islet cells of either the NOD mouse or the ILI mouse (MHC-identical to NOD); the addition of superoxide dismutase to the culture medium suppressed this increase in NOD or ILI islet cells. The present data support the concept that production of oxygen free radicals mediated by macrophages can damage islet beta cells, directly resulting in autoimmune Type 1 diabetes in NOD mice. [Diabetologia (1994) 37: 22–31]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050067
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  • 17
    Electronic Resource
    Electronic Resource
    A mutation in the glucagon receptor gene (Gly40Ser): heterogeneity in the association with diabetes mellitus (1995)
    Springer
    Diabetologia 38 (1995), S. 983-985 
    Details
    ISSN: 1432-0428
    Keywords: Key words Glucagon receptor gene ; susceptibility ; missense mutation ; non-insulin-dependent diabetes mellitus.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A possible pathogenic mutation in the glucagon receptor gene causing a Gly to Ser change at codon 40 (Gly40Ser) was reported to be associated and linked with non-insulin-dependent diabetes mellitus (NIDDM), in France and Sardinia. Since the frequency of the mutation (Gly40Ser), about 5 % in the French population of familial NIDDM and 8 % in randomly chosen diabetic patients in Sardinia, was much higher than that of any of the previously reported mutations in candidate genes, it is important to clarify whether the contribution of this mutation to NIDDM is universal. In this study, we investigated the association of this mutation with diabetes mellitus in a large number of Japanese diabetic patients (383 NIDDM and 53 insulin-dependent diabetic patients) by polymerase chain reaction-restriction fragment length polymorphism analysis. None of the Japanese diabetic patients showed Gly40Ser mutation and the association of this mutation with NIDDM was significantly different (p 〈 4 · 10−5 vs French, p 〈 3 · 10−6 vs Sardinian by Fisher's exact test). The results not only indicate that the mutation plays little, if any, role in susceptibility to diabetes in Japan, but also indicate the genetic heterogeneity in NIDDM and further emphasize the importance of studies on genetic susceptibility to NIDDM and other complex traits in different ethnic groups. [Diabetologia (1995) 38: 983–985]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400589
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  • 18
    Electronic Resource
    Electronic Resource
    Meta-analysis of association of insertion/deletion polymorphism of angiotensin I-converting enzyme gene with diabetic nephropathy and retinopathy (1998)
    Springer
    Diabetologia 41 (1998), S. 47-53 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Angiotensin I-converting enzyme gene ; I/D polymorphism ; meta-analysis ; diabetic nephropathy ; diabetic retinopathy ; genetic susceptibility.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene has repeatedly been shown to be associated with ischaemic heart disease, but the association of this genetic marker with diabetic microangiopathy is controversial. To assess the association of the genotypes with the development of diabetic nephropathy or retinopathy, we performed a meta-analysis of data from the literature, using Mantel-Haenszel method followed by the Breslow-Day test for assessing homogeneity among data. In a total of 4773 diabetic patients from 18 studies with (n = 2495) and without (n = 2278) renal complications, the D allele was significantly associated with diabetic nephropathy (p 〈 0.0001) in a dominant model (summary odds ratio 1.32, 95 % confidence interval: 1.15 to 1.51). There was no significant evidence against homogeneity of the odds ratios (χ 2 = 18.9, 20 df; p = 0.53). The association was significant both in non-insulin-dependent (p 〈 0.005) and in insulin-dependent diabetes mellitus (p 〈 0.05). Likewise, in a total of 2010 diabetic patients with (n = 1008) and without (n = 1002) retinopathy, there was no association of the I/D polymorphism with diabetic retinopathy. These data suggest that the ACE I/D polymorphism affects the risk for diabetic nephropathy, but not for diabetic retinopathy. [Diabetologia (1998) 41: 47–53]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050865
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  • 19
    Electronic Resource
    Electronic Resource
    Cystic acoustic neurinomas: Studies of 14 cases (1996)
    Springer
    Acta neurochirurgica 138 (1996), S. 695-699 
    Details
    ISSN: 0942-0940
    Keywords: Acoustic neurinoma ; computerized tomography ; cystic tumour ; magnetic resonance imaging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cystic acoustic neurinomas (ANs) are less frequent and are different from solid ANs in clinical and radiological features. We had 14 cystic ANs (13.5% of 104 cases) in the last 17 years. Computerized tomographic or magnetic resonance images allowed for the classification of these cystic ANs into three types: Type A being large single cysts with a thin tumourous wall (7 cases); type B single cysts with a thick tumourous wall (3 cases); type C multicystic (4 cases). Half of the cystic ANs were not accompanied by enlargement of the internal auditory canal, despite the largeness of the cysts. The mean size of the tumours was 29 mm in diameter. Type A cysts had a shorter clinical history than types B and C. One patient had intact hearing. In five cases, an atypical initial symptom such as facial pain, dysgeusia, facial palsy, unsteadiness or vertigo presented. The trigeminal nerve was involved in 12 cases, the facial nerve in nine. The characteristic features of cystic ANs are largeness of the tumour, a short clinical history, an atypical initial symptom, facial nerve involvement, and/or no enlargement of the internal auditory canal. In addition, the histological features are a lobular growth pattern, high nuclear atypia, and numerous macro phages.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01411474
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  • 20
    Electronic Resource
    Electronic Resource
    A mutation in the glucagon receptor gene (Gly40Ser): heterogeneity in the association with diabetes mellitus (1995)
    Springer
    Diabetologia 38 (1995), S. 983-985 
    Details
    ISSN: 1432-0428
    Keywords: Glucagon receptor gene ; susceptibility ; missense mutation ; non-insulin-dependent diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A possible pathogenic mutation in the glucagon receptor gene causing a Gly to Ser change at codon 40 (Gly40Ser) was reported to be associated and linked with non-insulin-dependent diabetes mellitus (NIDDM), in France and Sardinia, Since the frequency of the mutation (Gly40Ser), about 5% in the French population of familial NIDDM and 8% in randomly chosen diabetic patients in Sardinia, was much higher than that of any of the previously reported mutations in candidate genes, it is important to clarify whether the contribution of this mutation to NIDDM is universal. In this study, we investigated the association of this mutation with diabetes mellitus in a large number of Japanese diabetic patients (383 NIDDM and 53 insulin-dependent diabetic patients) by polymerase chain reaction-restriction fragment length polymorphism analysis. None of the Japanese diabetic patients showed Gly40Ser mutation and the association of this mutation with NIDDM was significantly different (p〈4·10−5 vs French, p〈3·10−6 vs Sardinian by Fisher's exact test). The results not only indicate that the mutation plays little, if any, role in susceptibility to diabetes in Japan, but also indicate the genetic heterogeneity in NIDDM and further emphasize the importance of studies on genetic susceptibility to NIDDM and other complex traits in different ethnic groups.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400589
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    Paper (German National Licenses)
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