| 1. |
- Anderson, Arne M., 1925, et al.
(författare)
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Industriell ekonomi
- 2003
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Bok (övrigt vetenskapligt/konstnärligt)
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| 2. |
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| 3. |
- Anderson, Per, et al.
(författare)
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Differential activation of signal transducer and activator of transcription (STAT)3 and STAT5 and induction of suppressors of cytokine signalling in T(h)1 and T(h)2 cells
- 2003
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Ingår i: International Immunology. - : Oxford University Press (OUP). - 1460-2377. ; 15:11, s. 1309-1317
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Tidskriftsartikel (refereegranskat)abstract
- Cytokines direct the differentiation of naive CD4(+) T cells into either IFN-gamma-producing T(h)1 cells or IL-4-producing T(h)2 cells. In this study, we analyzed the activation of signal transducer and activator of transcription (STAT)1, STAT3 and STAT5 (together with STAT4 and STAT6), and the expression of the recently identified suppressor of cytokine signalling (SOCS) proteins, in differentiated T(h)1 and T(h)2 cells, both before and after re-stimulation with anti-CD3 and anti-CD28. In addition to the polarized activation of STAT4 in T(h)1 cells and STAT6 in T(h)2 cells, we found that STAT3 and STAT5 are selectively activated in T(h)1 cells after differentiation. This activation of STAT3 and STAT5 was maintained after TCR re-stimulation. The selective activation of STAT3 and STAT5 in T(h)1 cells was associated with differential induction of SOCS molecules. After restimulation, SOCS1 expression was significantly increased in T(h)2 cells, but not in T(h)1 and nonpolarized 'T-h' cells. Additionally, the level of CIS was higher in T(h)2 cells compared with T(h)1 and T-h cells. In contrast, the expression of SOCS3 was higher in T(h)1 cells. The differential induction of SOCS proteins was paralleled by the differential expression of cytokines in re-stimulated T(h)1 and T(h)2 cells (IFN-gamma and IL-4/IL-13 respectively). Our results suggests that STAT3 and STAT5, possibly regulated by the SOCS proteins, may play a role in the differentiation of T-h cells, and in the maintenance of the T(h)1 and T(h)2 phenotype.
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| 4. |
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| 5. |
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| 6. |
- Cederbrant, Karin, et al.
(författare)
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Cytokine production, lymphocyte proliferation and T-cell receptor Vbeta expression in primary peripheral blood mononuclear cell cultures from nickel-allergic individuals
- 2003
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Ingår i: International Archives of Allergy and Immunology. - : S. Karger AG. - 1018-2438 .- 1423-0097. ; 132:4, s. 373-379
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Tidskriftsartikel (refereegranskat)abstract
- Background: Clinical history and patch test constitute the two cornerstones in the diagnosis of nickel (Ni) allergy. Due to technical and interpretative limits of the patch test, the in vitro lymphocyte transformation test (LTT) has been developed for confirming contact allergy, however, most studies show an overlap in lymphocyte proliferation between Ni-allergic and nonallergic subjects using the LTT. The aim of this study was to see if the secretion of cytokines, especially interleukin (IL)-10 and IL-17, or the use of T-cell receptor (TCR) V▀ families in Ni-stimulated primary peripheral blood mononuclear cell (PBMC) cultures might be more useful for discriminating between allergic and nonallergic subjects. Methods: Ni2+-stimulated primary PBMC cultures derived from female subjects diagnosed as Ni-allergic (n = 5) or nonallergic (n = 5) on the basis of a positive or negative patch test were assessed for cell proliferation by tritiated thymidine incorporation and for production of interferon-?, IL-4, IL-10 and IL-17 in the culture supernatant by ELISA. The immunophenotype and TCR-V▀ family affiliation of the Ni2+-induced lymphoblasts were determined by flow cytometry. Results: Lymphocytes from Ni-allergic individuals challenged with a high and a low concentration of Ni showed significantly higher cell proliferation than lymphocytes from nonallergic individuals, but all subjects showed a positive LTT result (stimulation index>2). We found a significantly higher release of IL-10 in Ni2+-treated cultures from Ni-allergic compared with nonallergic subjects that provided better separation between individuals in the two groups than did lymphocyte proliferation. The proliferating lymphoblasts were predominantly CD4+, and in 2 of the 5 Ni-allergic subjects, but in none of the 5 nonallergic subjects, the CD4+ lymphoblasts showed a dominance of TCR-V▀17. Conclusions: Determination of IL-10 production in primary PBMC cultures is a potentially promising in vitro method for discrimination of Ni allergy in females, as compared with cell proliferation. Copyright ⌐ 2003 S. Karger AG, Basel.
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| 7. |
- Chen, S, et al.
(författare)
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Functional association of cytokine-induced SH2 protein and protein kinase C in activated T cells
- 2003
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Ingår i: International Immunology. - : Oxford University Press (OUP). - 1460-2377. ; 15:3, s. 403-409
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Tidskriftsartikel (refereegranskat)abstract
- TCR signaling is mediated by intracellular signaling molecules and nuclear transcription factors, which are tightly regulated by interaction with regulatory proteins such as Grb2 and SLAP. We reported recently that TCR stimulation induces the expression of cytokine-induced SH2 protein (CIS). The expression of CIS promotes TCR-mediated activation. We have now found specific interactions between CIS and activated protein kinase C (PKC) alpha, beta and theta in TCR-stimulated T cells. CIS was shown by in vitro kinase assay to associate with activated PKC. In CIS-expressing T cells isolated from CIS-transgenic mice, the amount of activated PKC associated with CIS was found to increase following TCR stimulation. By immunohistochemical analysis, CIS was also found to co-localize with PKCtheta at the plasma membrane of activated T cells. In addition to the interaction and intracellular co-localization of the CIS and PKC, an increase in the activation of AP-1 and NF-kappaB was noted in CIS-expressing T cells, after stimulation by either anti-CD3/CD28 or phorbol myristate acetate + ionomycin. These results suggest that CIS regulates PKC activation, and that this may be important for the activation of both the AP-1 and NF-kappaB pathways in TCR signaling.
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| 8. |
- Grundstrom, S, et al.
(författare)
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Bcl-3 and NF kappa B p50-p50 homodimers act as transcriptional repressors in tolerant CD4(+) T cells
- 2004
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Ingår i: Journal of Biological Chemistry. - 1083-351X. ; 279:9, s. 8460-8468
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Tidskriftsartikel (refereegranskat)abstract
- The transcriptional events that control T cell tolerance are still poorly understood. To investigate why tolerant T cells fail to produce interleukin (IL)-2, we analyzed the regulation of NFkappaB-mediated transcription in CD4(+) T cells after tolerance induction in vivo. We demonstrate that a predominance of p50-p50 homodimers binding to the IL-2 promoter kappaB site in tolerant T cells correlated with repression of NFkappaB-driven transcription. Impaired translocation of the p65 subunit in tolerant T cells was a result from reduced activation of IkappaB kinase and poor phosphorylation and degradation of cytosolic IkappaBs. Moreover, tolerant T cells expressed high amounts of the p50 protein. However, the increased expression of p50 could not be explained by activation-induced de novo synthesis of the precursor p105, which was constitutively expressed in tolerant T cells. We also demonstrate the exclusive induction of the IkappaB protein B cell lymphoma 3 (Bcl-3) in tolerant T cells as well as its specific binding to the NFkappaB site. These results suggest that the cellular ratio of NFkappaB dimers, and thus the repression of NFkappaB activity and IL-2 production, are regulated at several levels in tolerant CD4(+) T cells in vivo.
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| 9. |
- Larsson, L C, et al.
(författare)
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Porcine neural xenografts in rats and mice : donor tissue development and characteristics of rejection
- 2001
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Ingår i: Experimental Neurology. - : Elsevier BV. - 0014-4886. ; 172:1, s. 14-100
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Tidskriftsartikel (refereegranskat)abstract
- Embryonic ventral mesencephalic tissue from the pig is a potential alternative donor tissue for neural transplantation to Parkinson's disease patients. For stable graft survival, the host immune response has to be prevented. This study was performed in order to analyze the mechanisms and dynamics of neural xenograft rejection, as well as neurobiological properties of the donor tissue. Adult normal mice and rats, and cyclosporin A-treated rats, received intrastriatal transplants of dissociated embryonic ventral mesencephalic pig tissue that was 27 or 29 embryonic days of age (E27 and E29). The animals were perfused at 2, 4, 6, and 12 weeks after grafting and the brains were processed for immunohistochemistry of dopaminergic (tyrosine hydroxylase positive) neurons, CD4(+) and CD8(+) lymphocytes, natural killer cells, macrophages, microglia, and astrocytes. Thirty-five rats received daily injections of BrdU for 5 consecutive days at different time points after transplantation and were perfused at 6 weeks. These animals were analyzed for proliferation of cells in the donor tissue, both in healthy and in rejecting grafts. No tyrosine hydroxylase-positive cells proliferated after grafting. Our results demonstrated that E27 was superior to E29 donor tissue for neurobiological reasons. Cyclosporin A immunosuppression was protective only during the first weeks and failed to protect the grafts in a long-term perspective. Grafts in mice were invariably rejected between 2 and 4 weeks after transplantation, while occasional grafts in untreated rats survived up to 12 weeks without signs of an ongoing rejection process. CD8(+) lymphocytes and microglia cells are most likely important effector cells in the late, cyclosporin A-resistant rejection process.
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| 10. |
- Li, Li, et al.
(författare)
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Insulin induces SOCS-6 expression and its binding to the p85 monomer of phosphoinositide 3-kinase, resulting in improvement in glucose metabolism
- 2004
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Ingår i: Journal of Biological Chemistry. - 1083-351X. ; 279:33, s. 34107-34114
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Tidskriftsartikel (refereegranskat)abstract
- The suppressors of cytokine signaling ( SOCS) family is thought to act largely as a negative regulator of signaling by cytokines and some growth factors. Surprisingly, the SOCS-6 transgenics had no significant defects in the cytokine signaling and hematopoietic system but displayed significant improvements in glucose metabolism. Insulin stimulation of Akt/protein kinase B was also potentiated. Biochemical analysis showed that, after insulin stimulation, SOCS-6 interacted with the monomeric p85 subunit of class-Ia phosphoinositide ( PI) 3-kinase but not with p85/p110 dimers. Furthermore, SOCS-6 expression is transiently increased by serum and insulin in normal fibroblasts. However, both the mRNA and protein of SOCS-6 were rapidly degraded after induction by insulin. The degradation of the SOCS-6 protein was partially inhibited by a proteasome inhibitor, suggesting a proteasome-mediated degradation mechanism. In contrast, SOCS-6- associated p85 was not degraded and could be recruited to the newly synthesized SOCS-6 molecules in the presence of insulin, suggesting that SOCS-6 expression and its interaction with p85, but not the degradation, is regulated by insulin. The phenotype of SOCS-6 transgenic mice bears a striking resemblance to p85 knock-out mouse models in which glucose metabolism stimulated by insulin is significantly improved despite reduced activation of PI 3-kinase. This suggests that monomeric p85 might play a physiologically important role in attenuating signaling through PI 3-kinase-dependent pathways in unstimulated cells. Therefore, our results indicate that SOCS-6 may provide a dynamically regulated mechanism by which insulin can transiently overcome the negative effects that p85 monomers have on signaling via PI 3-kinase-dependent signaling pathways.
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| 11. |
- Malmström, Per, et al.
(författare)
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Breast conservation surgery, with and without radiotherapy, in women with lymph node-negative breast cancer: a randomised clinical trial in a population with access to public mammography screening.
- 2003
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Ingår i: European journal of cancer (Oxford, England : 1990). - 0959-8049. ; 39, s. 1690-
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Tidskriftsartikel (refereegranskat)abstract
- The effect of postoperative radiotherapy after sector resection for stage I-II lymph node-negative breast cancer was evaluated in a patient population with access to public mammographical screening. 1187 women were randomised to no further treatment or postoperative radiotherapy following a standardised sector resection and axillary dissection. Radiation was administered to a dose of 48-54 Gy. Median age was 60 years, and median size of the detected tumours was 12 mm. Of the women 65% had their tumours detected by mammographical screening. The relative risk (RR) of ipsilateral breast recurrence was significantly higher in the non-irradiated patients compared with the irradiated patients, RR=3.33 (95% Confidence Interval (CI) 2.13-5.19, P<0.001). The corresponding cumulative incidence at 5 years was 14% versus 4%, respectively. Overall survival (OS) was similar, RR=1.16 (95% CI 0.81-1.65, P=0.41), with 5 year probabilities of 93 and 94%, respectively. Recurrence-free survival (RFS) at 5 years was significantly lower in the non-irradiated women, 77% versus 88% (P<0.001). Although women above 49 years of age, whose tumours were detected with mammographical screening, had the lowest rate of ipsilateral breast recurrence in this study, the cumulative incidence of such event amounted to 10% at 5 years if radiotherapy was not given. Such a recurrence rate has been considered as unacceptably high, but is, however, in the same range as that reported after lumpectomy and postoperative radiotherapy in published series.
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| 12. |
- Paulsson, Kajsa M, et al.
(författare)
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Association of tapasin and COPI provides a mechanism for the retrograde transport of major histocompatibility complex (MHC) class I molecules from the Golgi complex to the endoplasmic reticulum
- 2002
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Ingår i: Journal of Biological Chemistry. - 1083-351X. ; 277:21, s. 18266-18271
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Tidskriftsartikel (refereegranskat)abstract
- Tapasin is a subunit of the transporter associated with antigen processing (TAP). It associates with the major histocompatibility complex (MHC) class I. We show that tapasin interacts with beta- and gamma-subunits of COPI coatomer. COPI retrieves membrane proteins from the Golgi network back to the endoplasmic reticulum (ER). The COPI subunit-associated tapasin also interacts with MHC class I molecules suggesting that tapasin acts as the cargo receptor for packing MHC class I molecules as cargo proteins into COPI-coated vesicles. In tapasin mutant cells, neither TAP nor MHC class I are detected in association with the COPI coatomer. Interestingly, tapasin-associated MHC class I molecules are antigenic peptide-receptive and detected in both the ER and the Golgi. Our data suggest that tapasin is required for the COPI vesicle-mediated retrograde transport of immature MHC class I molecules from the Golgi network to the ER.
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| 13. |
- Sandell, A, et al.
(författare)
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Titanium dioxide thin-film growth on silicon(111) by chemical vapor deposition of titanium(IV) isopropoxide
- 2002
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Ingår i: Applied Physics Reviews. - : AIP Publishing. - 1931-9401. ; 92:6, s. 3381-3387
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Tidskriftsartikel (refereegranskat)abstract
- The initial stages of TiO2 growth on Si(111) under ultra-high vacuum conditions is studied using core level photoelectron spectroscopy, x-ray absorption spectroscopy, and scanning tunneling microscopy. The TiO2 film was formed by means of chemical vapor deposition of titanium(IV) isopropoxide at a sample temperature of 500 degreesC. The thickness and composition of the amorphous interface layer and its subsequent transition to crystalline anatase TiO2 are discussed. Three different stages are identified: In the initial stage (film thickness <10 Angstrom), the oxygen atoms are coordinated mainly to Si atoms giving rise to Ti atoms with oxidation states lower than 4+. At this stage, a small amount of carbon (0.15 ML) is observed. The next stage (<25 Angstrom) is best described as an amorphous TiSixOy compound in which the oxidation state of Ti is 4+ and the x and y values vary monotonically with the film thickness, from 2 to 0 and 4 to 2, respectively. Finally (>30 Angstrom) a stoichiometric TiO2 layer starts to form. The TiO2 phase is anatase and the layer consists of particles similar to10 nm wide.
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| 14. |
- Shiao, Y. H., et al.
(författare)
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VHL down-regulation and differential localization as mechanisms in tumorigenesis
- 2003
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Ingår i: Kidney International. - Malden, USA : Blackwell Publishing. - 0085-2538 .- 1523-1755. ; 64:5, s. 1671-1674
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Tidskriftsartikel (refereegranskat)abstract
- Background: The von Hippel-Lindau (VHL) gene has been widely analyzed in many tumors. Early studies in animal tumors suggest that changes in VHL protein level and localization may be also important in tumorigenesis. In this study, we determined the role of VHL protein in human renal cell carcinomas. METHODS: Seventy-five human renal cell carcinomas, predominantly of clear cell type (60 of 75), were examined for VHL protein by immunohistochemistry. The level and pattern of protein expression were then compared to VHL mutations and tumor characteristics.Results: An apparent decline of VHL level (positive in <50% of tumor cells) was observed in 49 (65%) tumors, a change more frequent than VHL mutations (28 of 75) (37%). In tumors, VHL was localized to the cytoplasm and/or the cell membrane. The occurrence of a predominantly membranous signal was significantly associated with missense mutations (9 of 14 tumors with missense mutations versus 14 of 61 tumors with no or nonmissense mutations, P = 0.0025) and tumor stage (23 of 60 tumors with stage TI versus 0 of 15 tumors with TII and TIII, P = 0.0034).Conclusion: This study provides the first evidence of the role of VHL protein level and intracellular localization in tumorigenesis in humans.
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| 15. |
- Ståhl, Per, et al.
(författare)
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A note on tailbiting codes and their feedback encoders
- 2002
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Ingår i: IEEE Transactions on Information Theory. - : Institute of Electrical and Electronics Engineers (IEEE). - 0018-9448. ; 48:2, s. 529-534
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Tidskriftsartikel (refereegranskat)abstract
- Tailbiting codes encoded by feedback convolutional encoders are studied. A condition for when tailbiting will work is given and it Is described how the encoder starting state can be obtained for feedback encoders in both controller and observer canonical forms. Finally, results from a search for systematic feedback encoders that encode tailbiting codes with good decoding bit error probabilities are presented.
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| 16. |
- Ståhl, Per, et al.
(författare)
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The effect of the tailbiting restriction on feedback encoders
- 2000
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Ingår i: [Host publication title missing]. - 0780358570 ; , s. 343-343
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Konferensbidrag (refereegranskat)abstract
- It is shown that, for short and moderate relative tailbiting lengths and high signal-to-noise ratios, systematic feedback encoders have better bit error performance than nonsystematic feedforward encoders. Conditions for when tailbiting will fail are given and it is described how the encoder starting state can be obtained for feedback encoders in both controller and observer canonical form
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| 17. |
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| 18. |
- Stålbrand, Henrik, et al.
(författare)
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Isolation, characterization, and enzymatic hydrolysis of acetyl-galactoglucomannan from spruce (Picea abies)
- 2004
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Ingår i: Hemicelluloses. Science and Technology (ACS Symposium Series). - 0097-6156. - 9780841238428 - 0841238421 ; 864, s. 66-78
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Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- Water-soluble hemicelluloses were extracted from spruce chips by heat-fractionation using microwave treatment. A screening of conditions (pH, temperature and residence time) was performed for the extraction of O-acetyl-galactoglucomannan (AcGGM). The yield and the average molecular weight of the extracted mannan were analysed using HPLC, size-exclusion chromatography (SEC) and mass-spectrometry. The pH during heat fractionation influenced the yield and the structure of AcGGM. The highest yield (78%) of AcGGM (average molecular weight 3800) was achieved with heat-fractionation in water at 190degrees C for 5 minutes. With 0.025% NaOH, an average molecular weight of 9500 was obtained at a yield of 30%. AcGGM molecular weight standard molecules were prepared using SEC. The structure of the AcGGM was determined using H-1-NMR. The enzymatic hydrolysis of AcGGM was studied using beta-mannanase and alpha-galactosidase.
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