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Träfflista för sökning "WFRF:(Marcus J. C.) srt2:(2000-2004)"

Sökning: WFRF:(Marcus J. C.) > (2000-2004)

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1.
  • Eliman, A., et al. (författare)
  • Totalparenteral nutrition after surgery rapidly increases serum leptin levels
  • 2001
  • Ingår i: European Journal of Endocrinology. - Bristol, NQ, USA : Bioscientifica. - 0804-4643 .- 1479-683X. ; 144:2, s. 123-128
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: In humans, leptin is regulated by long-term changes in energy intake. However, short-term regulation of serum leptin by nutrients has been difficult to show. The aim of this study was to investigate whether short periods of fasting and stress sensitise the leptin response to nutrients.Subjects and experimental protocol: Fourteen patients of normal weight undergoing elective open cholecystectomy were randomised into two groups. One group received saline infusion during surgery and for 24 h postoperatively. The other group also received saline during the surgical procedure, but total parenteral (TPN) was started immediately after surgery. Blood samples were drawn before as well as 2, 4, 8, 16, and 24 h after the start of surgery to determine the serum levels of leptin and other hormones.Results: Postoperative TPN induced a significant rise in serum leptin within 6 h, reaching a more than fourfold increase within 14 h (P < 0.001). Serum glucose and insulin levels increased within 2 h. Growth hormone and IGF-1 serum levels also increased significantly in the group receiving TPN. Serum cortisol levels increased postoperatively in both groups, which may explain why no significant reduction in serum leptin was observed in the group receiving saline. Free tri-iodothyronine (T3) decreased in both groups, while catecholamines were similar in the groups.Conclusion: During fasting and surgical stress, nutrients rapidly increased the serum leptin levels in humans in a manner similar to that previously reported in rodents. This may be mediated by increases in serum glucose, insulin and cortisol.
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  • Ohrn, K, et al. (författare)
  • Craniofacial morphology in obese adolescents
  • 2002
  • Ingår i: Acta odontologica Scandinavica. - : Informa UK Limited. - 0001-6357 .- 1502-3850. ; 60:4, s. 193-197
  • Tidskriftsartikel (refereegranskat)
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  • Tay, GK, et al. (författare)
  • PERB11 (MIC) : a polymorphic MHC gene is expressed in skin and single nucleotide polymorphisms are associated with psoriasis.
  • 2000
  • Ingår i: Clinical and Experimental Immunology. - : John Wiley & Sons. - 0009-9104 .- 1365-2249. ; 119:3, s. 553-558
  • Tidskriftsartikel (refereegranskat)abstract
    • The susceptibility genes for psoriasis remain to be identified. At least one of these must be in the major histocompatibility complex (MHC) to explain associations with alleles at human leucocyte antigen (HLA)-A, -B, -C, -DR, -DQ and C4. In fact, most of these alleles are components of just two ancestral haplotypes (AHs) designated 13.1 and 57.1. Although relevant MHC gene(s) could be within a region of at least 4 Mb, most studies have favoured the area near HLA-B and -C. This region contains a large number of non-HLA genes, many of which are duplicated and polymorphic. Members of one such gene family, PERB11.1 and PERB11.2, are expressed in the skin and are encoded in the region between tumour necrosis factor and HLA-B. To investigate the relationship of PERB11.1 alleles to psoriasis, sequence based typing was performed on 97 patients classified according to age of onset and family history. The frequency of the PERB11.1*06 allele is 44% in type I psoriasis but only 7% in controls (Pc = 0.003 by Fisher's exact test, two-tailed). The major determinant of this association is a single nucleotide polymorphism (SNP) within intron 4. In normal and affected skin, expression of PERB11 is mainly in the basal layer of the epidermis including ducts and follicles. PERB11 is also present in the upper keratin layers but there is relative deficiency in the intermediate layers. These findings suggest a possible role for PERB11 and other MHC genes in the pathogenesis of psoriasis.
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