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- Bruun-Lundgren, Maria, 1949, et al.
(author)
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Industrial activities and personal adornments
- 2000
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In: The Greek-Swedish excavations at the Agia Aikaterini Square, Kastelli, Khania 1970-1987 : results of the excavations under the direction of Yannis Tzedakis and Carl-Gustaf Styrenius. Vol. 2, The Late Minoan IIIC settlement : text and plates. - 9179160417 ; 2, s. 175-183
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Book chapter (other academic/artistic)
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- Girnita, L., et al.
(author)
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Increased expression of insulin-like growth factor I receptor in malignant cells expressing aberrant p53 : Functional impact
- 2000
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In: Cancer Research. - 0008-5472 .- 1538-7445. ; 60:18, s. 5278-5283
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Journal article (peer-reviewed)abstract
- We investigated the functional impact of p53 on insulin-like growth factor I receptor (IGF-IR) expression in malignant cells. Using the BL-41tsp53-2 cell line, a transfectant carrying temperature-sensitive (ts) p53 and endogenous mutant p53 (codon 248), we demonstrated a drastic down-regulation of plasma membrane-bound IGF-IRs on induction of wild-type p53, However, a similar response was obtained by treatment of BL-41tsp53-2 cells expressing mutant ts p53 with a p53 antisense oligonucleotide. Thus, even if the negative effect of wild-type p53 predominates under a competitive condition, these data indicate that mutant p53 may be important for up-regulation of IGF-IR, To further elucidate this issue, three melanoma cell lines (BE, SK-MEL-5, and SK-MEL-28) that over expressed p53 were investigated. The BE cell line has a hot spot mutation (codon 248) and expresses only codon 248-mutant p53, SK-MEL-28 has a point mutation at codon 145. SK-MEL-5 cells did not exhibit any p53 mutations, but the absence of p21(Waf1) expression suggested functionally aberrant p53. Our data suggest that interaction with Mdm-2 may underlie p53 inactivation in these cells, Using p53 antisense oligonucleotides, we demonstrated a substantial down-regulation of cell surface expression of IGF-IR proteins in all melanoma cell lines after 24 h, This was paralleled by decreased tyrosine phosphorylation of IGF-IR and growth arrest, and, subsequently, massive cell death was observed (this was also seen in BL-41tsp53-2 cells with mutant conformation of ts p53). Taken together, our results suggest that up-regulation of IGF-IR as a result of expression of aberrant p53 may be important for the growth and survival of malignant cells.
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- Leander, K, et al.
(author)
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The G-455A polymorphism of the fibrinogen Bbeta-gene relates to plasma fibrinogen in male cases, but does not interact with environmental factors in causing myocardial infarction in either men or women.
- 2002
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In: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 252:4, s. 332-41
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Journal article (peer-reviewed)abstract
- OBJECTIVES: To elucidate the association between a genetic polymorphism of the fibrinogen Bbeta-gene (G-455A) and plasma fibrinogen levels and myocardial infarction (MI), respectively. In addition, to explore potential synergistic gene-environment interactions involving this polymorphism--until now, these data were unavailable. DESIGN SETTING AND SUBJECTS: This case-referent study of subjects aged 45-70 and living in Stockholm includes 834 men and 346 women with first-time MI and 1034 men and 494 women randomly chosen as referents from the population. The cases were identified between 1992 and 1994 at the 10 emergency hospitals in Stockholm County. MAIN OUTCOME MEASURES: MI and plasma fibrinogen levels. RESULTS: Crude analyses associated a high level of plasma fibrinogen with an increased risk of MI in both men and women. However, the relative risk decreased after controlling for other risk factors. The multivariate-adjusted odds ratio (OR) (95% confidence interval) was 1.6 (1.2-2.3) for men and 1.5 (0.9-2.6) for women. Presence of the A allele at the G-455A polymorphic site indicated higher plasma fibrinogen levels than the presence of the G allele, but the difference was only statistically significant for male cases. The -455A allele was not associated with an increased risk of MI. Furthermore, there were no strong indications of synergistic interaction between the G-455A polymorphism and any of the environmental exposures considered. CONCLUSIONS: In this large number of MI cases and referents, a high level of plasma fibrinogen was independently associated with increased risk of MI in men but not in women. The presence of the A allele at the G-455A polymorphism of the fibrinogen Bbeta-gene was not associated with increased risk of MI, and no synergistic gene-environment interactions were detected.
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- Sui, GC, et al.
(author)
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The Bbeta-sheet in the PAI-1 molecule plays an important role for its stability
- 2000
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In: Thrombosis and haemostasis. - : Georg Thieme Verlag KG. - 0340-6245 .- 2567-689X. ; 83:6, s. 896-901
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Journal article (peer-reviewed)abstract
- We have investigated the B β-sheet in PAI-1 regarding its role for the stability of the molecule. The residues from His219 to Tyr241 (except for Gly230 and Pro240), covering the s2B and s3B strands, and in addition His185 and His190 were substituted by amino acids with opposite properties. The 23 generated single-site changed mutants and also wild type PAI-1 (wtPAI-1) were expressed in E. coli. Subsequently they were purified by heparin-Sepharose and anhydrotrypsin agarose affinity chromatographies. The stability of the purified PAI-1 variants was analyzed at 37° C and at different pHs (5.5, 6.5 or 7.5). At pH 7.5 and 37° C, single substitutions of the residues in the central portions of both strands 2 and 3 in the B β-sheet (Ile223 to Leu226 on s2B and Met235 to Ile237 on s3B), caused a significant decrease in stability, yielding half-lives of about 10–25% as compared to wtPAI-1. On the other hand, mutations at both sides of the central portion of the B β-sheet (Tyr221, Asp222, Tyr228 and Thr232) frequently resulted in an increased PAI-1 stability (up to 7-fold). While wtPAI-1 exhibited prolonged half-lives at pH 6.5 and 5.5, the PAI-1 variant Y228S was more stable at neutral pH (half-life of 9.6 h at pH 7.5) as compared to its half-life at pH 5.5 (1.1 h). One of the 4 modified histidine residues (His229) resulted in a variant with a clearly affected stability as a function of pH, suggesting that it may, at least in part, be of importance for the pH dependence of the PAI-1 stability. Thus, our data demonstrate that the B β-sheet is of great importance for the stability of the molecule. Modifications in this part causes decreased or increased stability in a certain pattern, suggesting effects on the insertion rate of the reactive center loop into the A β-sheet of the molecule.
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- Wiman, B, et al.
(author)
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Plasma levels of tissue plasminogen activator/plasminogen activator inhibitor-1 complex and von Willebrand factor are significant risk markers for recurrent myocardial infarction in the Stockholm Heart Epidemiology Program (SHEEP) study.
- 2000
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In: Arteriosclerosis, Thrombosis and Vascular Biology. - : Ovid Technologies (Wolters Kluwer Health). - 1079-5642 .- 1524-4636. ; 20:8, s. 2019-23
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Journal article (peer-reviewed)abstract
- An impaired fibrinolytic function due to elevated plasma levels of plasminogen activator inhibitor (PAI)-1 activity or tissue plasminogen activator (tPA) antigen is correlated with the development of myocardial infarction (MI) in patients with manifest coronary heart disease. Recently, methods for determining the specific tPA/inhibitor complexes constituting tPA antigen in plasma have become available. In the Stockholm Heart Epidemiology Program (SHEEP) study, 86 of 1212 MI patients, subjected to blood sampling in a metabolically stable period, suffered reinfarction before the end of 1996. These individuals have been compared with an approximately equal number of matched MI patients without recurrence and a group of matched healthy control subjects regarding the plasma concentrations of some hemostatic factors. The hemostatic compounds studied (fibrinogen, von Willebrand factor, tPA antigen, PAI-1, and the tPA/PAI-1 complex) were typically higher in the groups (men and women) with recurrence of MI compared with those without. The plasma concentrations were also typically higher in the pooled groups of patients compared with the groups of healthy control subjects. The largest between-group differences were found for the plasma tPA/PAI-1 complex. The crude odds ratio for reinfarction associated with higher concentration (>/=75th percentile among the control subjects) of tPA/PAI-1 was 1.8 (95% CI 1.1 to 3.1); the corresponding crude odds ratio for von Willebrand factor was 2.3 (1. 3 to 4.0). The tPA/PAI-1 complex correlated strongly with PAI-1 and tPA antigen in all groups and with serum triglycerides and body mass index in all groups except for women with reinfarction. An increased plasma level of tPA/PAI-1 complex is a novel risk marker for recurrent MI in men and women. Most likely, increased plasma levels of tPA/PAI-1 complex reflect impaired fibrinolysis, because the correlation with PAI-1 is strong. Further support is obtained indicating that the plasma concentration of von Willebrand factor is also an important risk marker for recurrent MI.
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