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  • 1
    Electronic Resource
    Electronic Resource
    Bone mineral density, collagen type 1 α 1 genotypes and bone turnover in premenopausal women with diabetes mellitus (1998)
    Springer
    Diabetologia 41 (1998), S. 1314-1320 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetes mellitus ; bone ; COL1A1 polymorphism ; vitamin D ; parathyroid hormone ; bone markers.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Osteopenia is a recognised complication of diabetes mellitus which could be due to abnormal bone turnover or disturbances in the calcium/parathyroid hormone/vitamin D axis or both. Genetic factors also play an important part in determining bone mass although this has not been studied in diabetes. Recently a polymorphism of the collagen type 1 α 1 (COL1A1) gene has been shown to be associated with low bone mass in British women. To identify subjects with diabetes who may be at risk of developing osteoporosis and fractures, we analysed bone mineral density in relation to the biochemical markers of bone turnover, calcium homeostasis and the COL1A1 genotype in a group of premenopausal women with Type I (insulin-dependent) diabetes mellitus (n = 31), Type II (non-insulin dependent) diabetes mellitus (n = 21) and control subjects (n = 20). Bone mineral density was lower at the femoral neck in the subjects with Type I diabetes (p = 0.08) as were serum 25-hydroxyvitamin D compared with control subjects (p = 0.023) and this was negatively correlated with serum collagen type 1 C-terminal propeptide (r = –0.56, p 〈 0.001). Bone mineral density in Type II diabetes was not different from control subjects, after correction for body mass index. Bone resorption was, however, raised in the Type II diabetic subjects as reflected by the higher urinary deoxypyridinoline values (p = 0.016) and lower collagen type 1 C-terminal propeptide:deoxypyridinoline ratio (p = 0.04). In the whole group studied, subjects with the COL1A1 ’s' genotype had lower bone mineral density at the femoral neck (p = 0.01) which was partly attributable to a lower body mass index. Following multiple regression analysis body mass index and collagen type 1 C-terminal propeptide concentrations remained determinants of bone mass at all three sites, whereas genotype appeared to be a predictor of bone mass at the femoral neck only. We conclude that measurement of these variables could prove useful in firstly identifying those diabetic women at risk of osteoporosis and secondly guiding therapeutic intervention. [Diabetologia (1998) 41: 1314–1320]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051071
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  • 2
    Electronic Resource
    Electronic Resource
    Lack of Influence of Collagen Type Iα1 Sp1 Binding Site Polymorphism on the Rate of Bone Loss in a Cohort of Postmenopausal Danish Women Followed for 18 Years (2000)
    Springer
    Calcified tissue international 66 (2000), S. 409-413 
    Details
    ISSN: 1432-0827
    Keywords: Key words: COLIA1 — Collagen — Sp1 — Polymorphism — Bone loss.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Abstract. A polymorphism in an Sp1 site in the collagen Iα1 (COLIA1) gene has recently been identified and the Ss and ss genotypes were shown to be potentially important determinants of low bone mass in postmenopausal women. Additionally, in a Dutch population, the association of the COLIA1 polymorphism with low bone mineral density (BMD) was more pronounced with increasing age, suggesting a genotype effect on the rate of bone loss. We have investigated the relationship between the COLIA1 Sp1 polymorphism and the rate of bone loss in a longitudinal study with a total of 133 postmenopausal women followed for 18 years. The frequencies of the genotypes were SS 70.7%, Ss 27.8%, ss 1.5% and were in Hardy-Weinberg equilibrium. No association of the COLIA1 genotype with rate of bone loss was detected and there was no difference between the genotype groups with respect to BMD at the femoral neck or lumbar spine. Women with the Ss or ss genotypes, who have been postulated to have low BMD, had even higher BMD at the lower forearm than women with the SS genotype. The levels of serum osteocalcin and urinary collagen type I degradation products were not found to be associated with the COLIA1 Sp1 polymorphism. In conclusion, this study does not support the hypothesis that the Ss COLIA1 genotype predisposes women to increased rate of bone loss or low BMD. However, because of a low absolute number of the ss genotype, it was not possible to reach a conclusion on this particular genotype with regard to an association with low BMD or rate of bone loss.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002230010083
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Detection of nitric oxide and nitric oxide synthases in psoriasis (1998)
    Springer
    Archives of dermatological research 290 (1998), S. 3-8 
    Details
    ISSN: 1432-069X
    Keywords: Key words Nitric oxide ; Nitric oxide synthase ; Immunohistochemistry ; Psoriasis ; Chemiluminescence
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Biopsies from psoriasis lesions and clinically uninvolved skin of eight patients and five normal subjects were studied by immunocytochemistry with computerized image analysis for the presence of endothelial, neuronal and inducible isoforms of nitric oxide synthase. Endothelial nitric oxide synthase was expressed in the endothelium and weakly in some keratinoctyes. Its expression was not significantly different in psoriasis. Inducible nitric oxide synthase, however, was absent from normal skin but was significantly upregulated in psoriatic lesional skin, focally in keratinocytes but to the greatest extent in the papillary dermis and to a lesser extent in clinically uninvolved psoriatic skin. Inducible nitric oxide synthase staining was greatest in the more severe lesions and correlated with the inflammatory infiltrate (CD3-positive cells) and with keratinocyte proliferation (Ki-67-positive cells). In normal skin, neuronal nitric oxide synthase was expressed only in keratinocytes in the granular layer and eccrine sweat glands. However, in psoriasis and clinically uninvolved skin the neuronal form was present through all levels of the epidermis. Direct measurement of nitric oxide production from the skin surface revealed a tenfold increase in the lesions of 16 psoriatic patients compared with their nonlesional skin, and this nitric oxide production was inhibited by topical betamethasone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004030050268
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Susceptibility to Osteoporotic Fracture is Determined by Allelic Variation at the Sp1 Site, Rather than Other Polymorphic Sites at the COL1A1 Locus (2000)
    Springer
    Osteoporosis international 11 (2000), S. 338-343 
    Details
    ISSN: 1433-2965
    Keywords: Key words:COL1A1 – Collagen – Fracture – Genetic – Osteoporosis – Polymorphism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: Previous studies have identified an association between osteoporotic fracture and a polymorphism affecting a Sp1 binding site in the first intron of the collagen type I alpha 1 gene (COL1A1). It is currently unclear, however, whether this association is direct or the result of linkage disequilibrium with other polymorphisms situated nearby. In this study we analyzed the relationship between four well-characterized single-nucleotide polymorphisms at the COL1A1 locus and osteoporotic fracture in 93 patients with vertebral fracture and 88 age-matched controls randomly selected from the community. We studied a Msp I polymorphism 26 kb upstream of the COLIA1 gene, the Sp1 binding site polymorphism in intron 1, a Rsa I polymorphism in intron 5 and a Mnl I polymorphism in exon 52. The Sp1 and Rsa I polymorphisms were in strong linkage disequilibrium (χ2=77.87, p〈0.001) and weaker linkage disequilibrium was detected between the Sp1 and Mnl I polymorphisms (χ2=5.54, p〈0.025). There was a significant association between COL1A1 haplotypes that included the Sp1 and Rsa I polymorphisms and fracture (p〈0.05–0.001), but no association with haplotypes that included only the Msp I and Mnl I polymorphisms. This association with fracture was strongest when haplotypes were grouped by Sp1 alleles (χ2=11.15, d.f. = 1; p= 0.001). Furthermore, logistic regression analysis showed that of all the polymorphisms tested, only the Sp1 binding site polymorphism acted as an independent predictor of fracture: odds ratio [95% CI] = 2.26 [1.09–4.69]. These data suggest that it is the Sp1 polymorphism rather than other polymorphisms at the COL1A1 locus which act as a marker for osteoporotic fractures.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001980070123
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