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  • 1
    Electronic Resource
    Electronic Resource
    Osmotic Pressure Effect of the Red Blood Cells-Possible Physiological Significance (1961)
    [s.l.] : Nature Publishing Group
    Nature 190 (1961), S. 504-508 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] THE present concept of the net fluid volume transfer across the capillary wall rests mainly on the balance between the hydrostatic and colloid osmotic pressures as expressed in Starling's hypothesis1. The osmotic forces demonstrated in the conspicuous and well-known behaviour of the red blood cells ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/190504a0
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  • 2
    Electronic Resource
    Electronic Resource
    Organisation of the coding exons and mutational screening of the uncoupling protein 3 gene in subjects with juvenile-onset obesity (1998)
    Springer
    Diabetologia 41 (1998), S. 241-244 
    Details
    ISSN: 1432-0428
    Keywords: Keywords uncoupling protein 3 ; obesity ; genetics ; mutation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Uncoupling proteins (UCPs) are mitochondrial transporters that uncouple the cellular respiration releasing stored energy as heat. Recently a third member of the UCP family was identified. Human UCP3 is different from UCP1 and UCP2 by its high and preferential expression in skeletal muscle and consequently the UCP3 gene is an attractive candidate gene for obesity. In this study we have determined the intron/exon organization of the coding region of the UCP3 gene and performed single strand conformation polymorphism (SSCP) analysis and direct sequencing of variants of the gene in 60 Caucasian subjects with juvenile-onset obesity. We detected 4 nucleotide substitutions in the intron regions and 2 silent amino acid variants. During the identification of the intron/exon structure of the gene in a normal healthy male subject with a BMI of 23.5 kg/m2, a nucleotide substitution replacing a glycine with a serine was identified at codon 84. This variant was neither found among 156 subjects with juvenile-onset obesity nor among 205 control subjects. In a population based sample of 380 young healthy subjects the Gly/Ser84 variant was found in one female subject with a BMI of 25.5 kg/m2 and a fat mass of 23.7 kg. We conclude it is unlikely that variants in the coding region of the UCP3 gene contribute to the pathogenesis of juvenile-onset obesity among Danish Caucasians. [Diabetologia (1998) 41: 241–244]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050897
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  • 3
    Electronic Resource
    Electronic Resource
    Mutational analysis of the coding region of the uncoupling protein 2 gene in obese NIDDM patients: Impact of a common amino acid polymorphism on juvenile and maturity onset forms of obesity and insulin resistance (1997)
    Springer
    Diabetologia 40 (1997), S. 1227-1230 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Uncoupling protein 2 ; obesity ; genetics ; insulin resistance ; amino acid polymorphism.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recently, a gene encoding a novel human uncoupling protein, designated UCP2, was discovered. The murine UCP2 was mapped to a region on mouse chromosome 7 which in several models has been shown to be linked to obesity and hyperinsulinaemia. Single strand conformation polymorphism (SSCP) analysis and direct sequencing of the coding region of the UCP2 gene in 35 obese Caucasian NIDDM patients of Danish ancestry revealed one nucleotide substitution, replacing an alanine with a valine at codon 55. The amino acid polymorphism was present in 24 of the 35 (69 %) examined subjects. The allelic frequency of the A/V55 variant was 48.3 % (95 % CI: 42.5–54.1 %) among 144 subjects with juvenile onset obesity, 45.6 % (40.5–50.7 %) among 182 subjects randomly selected at the draft board examination, and 45.5 % (37.1–53.9 %) among lean control subjects selected from the same study cohort. Within these cohorts there were no differences in BMI values at different ages among wild-type carriers and A/V55 carriers. In a population-based sample of 369 young healthy Caucasians the variant showed no association with alterations in BMI, waist-to-hip ratio, fat mass or weight gain during childhood or adolescence. The A/V55 polymorphism was not related to alterations in fasting values of serum insulin and C-peptide or to an impaired insulin sensitivity index. We conclude that genetic variability in the human UCP2 gene is not a common factor contributing to NIDDM in obese Danish Caucasian subjects and the common A/V55 amino acid polymorphism of the gene is not implicated in the pathogenesis of juvenile or maturity onset obesity or insulin resistance in Caucasians. [Diabetologia (1997) 40: 1227–1230]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050811
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  • 4
    Electronic Resource
    Electronic Resource
    Insulin-gene flanking sequences, diabetes mellitus and atherosclerosis: a review (1985)
    Springer
    Diabetologia 28 (1985), S. 556-564 
    Details
    ISSN: 1432-0428
    Keywords: Insulin-gene ; DNA-polymorphisms ; diabetes mellitus ; atherosclerosis ; genetic markers ; molecular genetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A highly polymorphic locus flanking the human insulin gene contains two major size classes of DNA restriction fragments, which segregate in families as stable genetic elements. The L-allele, i.e. fragments with an average size of about 600 base-pairs seems to be a weak genetic marker for Type 1 (insulin-dependent) diabetes mellitus, whereas the Uallele, i. e. fragments of an average size of about 2500 basepairs hitherto has been associated with Type 2 (non-insulin-dependent) diabetes mellitus and diabetic hypertriglyceridaemia. The most recent reports on this subject do not confirm an association between the U-allele and Type 2 diabetes. Our own studies indicate that the U-allele is a fairly strong marker for the development of atherosclerosis (relative risk for U-carriers 3.36). The putative functions of the polymorphic region in atherogenesis and the relation of this region to other genetic markers for atherosclerosis are not known.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00281989
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  • 5
    Electronic Resource
    Electronic Resource
    Multipoint linkage analysis of the short arm of chromosome 11 in non-insulin dependent diabetes including maturity onset diabetes of youth (1992)
    Springer
    Human genetics 〈Berlin〉 89 (1992), S. 207-212 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Members of three families with maturity onset diabetes of youth (MODY) and seven with “common” type 2 diabetes were typed for six DNA markers (H-RAS, INS, HBBC, PTH, CALC1, CAT) on the short arm of chromosome 11. Using conventional pairwise linkage analysis, close linkage in the MODY families was excluded for all six markers. By multipoint analysis and a genetic map of the short arm of chromosome 11, MODY was excluded from a region of at least 35 and up to 60 centiMorgans (cM) on the short arm of chromosome 11. Multipoint analysis in the type 2 families also excludes linkage to the INS, H-RAS region of at least 3 and up to 30 cM. This study using multipoint linkage analysis in non-insulin dependent diabetes provides strong evidence against a role for mutations in or around the insulin gene in the causation of MODY or type 2 diabetes in the families studied.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00217125
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  • 6
    Electronic Resource
    Electronic Resource
    IDL, VLDL, chylomicrons and atherosclerosis (1992)
    Springer
    European journal of epidemiology 8 (1992), S. 92-98 
    Details
    ISSN: 1573-7284
    Keywords: Lipoprotein lipase deficiency ; Familial combined hyperlipidemia ; Dysbetalipoproteinemia ; The St. Thomas' Hospital rabbit strain ; Atherosclerosis ; Lipoprotein permeability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In humans with the lipoprotein lipase deficiency disorder large amounts of chylomicrons and large very low-density lipoprotein (VLDL) accumulate in plasma. In spite of this, atherosclerosis does not seem to develop at an accelerated rate, suggesting that these lipoproteins do not promote atherogenesis. In humans with dysbetalipoproteinemia remnant lipoproteins (intermediate density lipoprotein (IDL) plus B-VLDL) accumulate in plasma and these particles may therefore be the factor causing accelerated atherosclerosis in this disorder. Epidemiological studies in humans suggest that IDL or remnant lipoproteins are predictors of the severity or progression of atherosclerosis. Similar studies in the St. Thomas' Hospital rabbit strain, an animal model with genetically elevated plasma levels of VLDL, IDL and low-density lipoprotein (LDL), showed that IDL or remnant lipoproteins were better predictors of the extent of atherosclerosis than were LDL or VLDL. Studies of lipoprotein/arterial wall interactions have demonstrated that the larger the lipoprotein particle, the lower the influx into intima. Very large VLDL and chylomicrons do not seem to enter intima. Although high-density lipoprotein (HDL) enters intima faster than other lipoproteins, the small HDL particles seem to penetrate the entire arterial wall and leave via lymphatics and vasa vasorum in the outer media and adventitia. In contrast, LDL, and possibly also IDL and smaller VLDL, may only leave the intima via the lumen of the artery. In conclusion, a substantial body of evidence suggests that remnant lipoproteins (IDL and smaller VLDL) share with LDL the potential for promoting atherosclerosis, whereas very large VLDL and chylomicrons do not seem to have this effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00145358
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