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- Landin-Olsson, Mona, et al.
(författare)
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Immunoreactive trypsin(Ogen) in the sera of children with recent-onset insulin-dependent diabetes and matched controls
- 1990
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Ingår i: Pancreas. - : Ovid Technologies (Wolters Kluwer Health). - 0885-3177. ; 5:3, s. 241-247
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Tidskriftsartikel (refereegranskat)abstract
- To evaluate the exocrine pancreatic function at the time of diagnosis of insulin-dependent diabetes mellitus, we determined immunoreactive an-odal and cathodal trypsin(ogen) levels in sera from almost all children (n = 375) 0-14 years of age in Sweden in whom diabetes developed during 1 year, and in sex-, age-, and geographically matched control subjects (n = 312). The median level of anodal trypsin(ogen) was 5 (quartile range, 3-7) µg/L in children with newly diagnosed diabetes, compared with a median level of 7 (quartile range, 4-8) µg/L in control subjects (p < 0.0001). Similarly, the median level of cathodal trypsin(ogen) was 8 (quartile range, 4-10) µg/L in children with diabetes, compared with a median level of 11 (quartile range, 7-15) µg/L in control subjects (p < 0.0001). The median of the individual ratios between cathodal and anodal trypsin(ogen) was 1.4 in the diabetic patients and 1.7 in the control children (p < 0.001). In a multivariate test, however, only the decrease in cathodal trypsin(ogen) concentration was associated with diabetes. The levels of trypsin(ogen)s did not correlate with levels of islet cell antibodies, present in 81% of the diabetic children. Several mechanisms may explain our findings, for example, similar pathogenetic factors may affect both the endocrine and exocrine pancreas simultaneously, a failing local trophic stimulation by insulin on the exocrine cells may decrease the trypsinogen production, and there may be an increased elimination of trypsin(ogen) because of higher filtration through the kidneys in the hyperglycemic state.
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| 2. |
- Svanberg, Sune, et al.
(författare)
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Applications of terawatt lasers
- 1994
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Ingår i: LASER SPECTROSCOPY - XITH INTERNATIONAL CONFERENCE. - : AIP. - 1551-7616 .- 0094-243X. - 1563962624 ; :290, s. 264-269
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Konferensbidrag (refereegranskat)
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| 4. |
- Babiker-Mohamed, H, et al.
(författare)
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Characterization of monoclonal anti-alpha 1-microglobulin antibodies : binding strength, binding sites, and inhibition of lymphocyte stimulation
- 1991
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Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 1365-3083 .- 0300-9475. ; 34:5, s. 655-666
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Tidskriftsartikel (refereegranskat)abstract
- Eleven monoclonal antibodies (MoAb) directed against the immunoregulatory plasma glycoprotein alpha 1-microglobulin were characterized. The MoAb were produced in mice immunized with a mixture of alpha 1-microglobulin homologues from man, guinea pig, rat and rabbit. Using radioimmunoassay, western blotting, affinity chromatography, and Scatchard analysis, the affinities and binding sites of the MoAb were analysed. All antibodies were more or less cross-reactive, but most showed a major specificity for one or two of the alpha 1-microglobulin homologues. None of the antibodies was directed against the carbohydrate moiety of alpha 1-microglobulin. Six of the MoAb had high affinity for the antigen and four of these were directed towards the same part of the molecule though differing in their species specificity. Five showed lower affinity for the antigen and were mainly directed towards epitopes on other parts of the molecule. Only some of the antibodies could block the proliferation of lymphocytes induced by human alpha 1-microglobulin. The blocking efficiency of the different antibodies was similar when tested on the stimulation of human or mouse lymphocytes, suggesting that the same part of the alpha 1-microglobulin molecule is responsible in both species. The magnitude of blocking by the different MoAb was not related to their affinities, emphasizing the importance of where on the alpha 1-microglobulin molecule, rather than how strongly, they bind. The binding of the strongest blocking antibody was shown to be directed to a C-terminal peptide of rat alpha 1-microglobulin, indicating that this part of alpha 1-microglobulin is important for the mitogenic effects. Thus the panel of anti-alpha 1-microglobulin MoAb should be a valuable tool for structural and functional studies of alpha 1-microglobulin.
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| 5. |
- Borg, A., et al.
(författare)
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Association of int2/hst1 coamplification in primary breast cancer with hormone-dependent phenotype and poor prognosis
- 1991
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Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 63:1, s. 136-142
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Tidskriftsartikel (refereegranskat)abstract
- The human proto-oncogene INT2 (homologous to the mouse INT2 gene, implicated in proviral induced mammary carcinoma) has been mapped to chromosome llql3 and found to share band localisation with, among others, the HST1 proto-oncogene. Both genes are members of the fibroblast growth factor family. In the present study, coamplification (2-15 copies) of the INT2/HST1 genes was found in 27 (9%) of 311 invasive human breast carcinomas using slot blot and Southern blot analyses. Amplification was not correlated to tumour size, axillary lymph node status or stage of disease, neither to patient age nor menopausal status. However, 26 (96%) of the 27 amplified tumours were, often strongly, Oestrogen receptor positive compared to 65% of the unamplified cases (P = 0. 001). These findings are in sharp contrast to the strong correlations of HER-2/neu proto-oncogene amplification with advanced stage and steroid receptor negativity, previously observed in the same series of tumours. Patients with INT2/HSTI amplified breast cancer had a significantly shorter disease-free survival compared to those with unamplified genes (P = 0. 015, median follow up 45 months). This correlation was confined to node-negative patients and persisted in multivariate analysis. No significant correlation to survival from breast cancer was found. It is concluded that amplification of the 1 lql3 region in breast cancer occurs in a particular subset of aggressive tumours, quite different from that identified by HER-2/neu amplification. It still remains to be shown that the selection for amplified genes at llql3 is due to the activity of INT2, HSTl or yet another, still unidentified, neighbouring gene. However, the results are potentially of clinical value in separating a group of node-negative breast cancer for more intense treatment.
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| 6. |
- Fernö, Mårten, et al.
(författare)
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Cathepsin D, both a prognostic factor and a predictive factor for the effect of adjuvant tamoxifen in breast cancer. South Sweden Breast Cancer Group
- 1994
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Ingår i: European Journal of Cancer. - 1879-0852. ; 30a:14, s. 2042-2048
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Tidskriftsartikel (refereegranskat)abstract
- Cathepsin D is a lysosomal protease implicated in cancer metastasis. Its concentration in breast tumours has also been shown to be of prognostic importance, although to what extent this is subject to lymph node status, the use of adjuvant therapy and menopausal status has not been clearly evaluated. At a cut-off level of 45 pmol/mg protein (61% of the 623 samples were classified as high cathepsin D tumours; immunoradiometric assay), we found cathepsin D to be of prognostic importance only among breast cancer patients with lymph node-positive (N+) disease not treated with adjuvant tamoxifen. When the series was stratified according to cathepsin D content of their tumours, progesterone receptor (PgR) status and lymph node involvement, adjuvant tamoxifen was found to have a significant beneficial effect only among patients with N+ and PgR-positive breast cancer whose tumours had a high cathepsin D content.
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| 10. |
- Sairenji, T., et al.
(författare)
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Relating homology between the Epstein-Barr virus BOLF1 molecule and HLA-DQw8 β chain to recent onset Type 1 (insulin-dependent) diabetes mellitus
- 1991
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Ingår i: Diabetologia. - 0012-186X. ; 34:1, s. 33-39
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Tidskriftsartikel (refereegranskat)abstract
- A role for the Epstein-Barr virus in initiating Type 1 (insulin-dependent) diabetes mellitus has been proposed since Epstein-Barr virus BOLF1(497-513) AVTPL RIFIVP PAAEY has an 11 amino acid identity with HLA-DQw8 β (49-60) AVTPL GPPAAEY. Rabbit antisera to the BOLF1 (496-515) peptide crossreacted with the homologous DQw8 β (44-63) peptide but not with the related DQw7 β(44-63) peptide, which differed from the DQw8 peptide only in an ALA to ASP substitution in position 57. Antisera to DQw8 β(49-60) reacted with the DQw8 β(44-63) peptide and BOLF1 (496-515), but not with DQw7 β (44-63). The antiserum to the BOLF1 peptide bound to denatured class II major histocompatibility complex β chains from Epstein-Barr virus-transformed DQw8-positive lymphocytes in an immunoblotting analysis. Epstein-Barr virus antibodies were detected at equal frequencies and similar titres in sera of 30 patients with Type 1 diabetes (16 of 30;63%) and in sera of 20 non-diabetic control subjects (13 of 20;65%). Sera from diabetic patients did not bind to DQw8 β (44-63) or BOLF1(496-515) peptides. From these data we conclude that there is no simple relationship between serological evidence of Epstein-Barr virus infection and crossreactions between homologous Epstein-Barr virus and class II major histocompatibility complex peptides.
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