| 1. |
- Brodow, Bengt, et al.
(author)
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Retoriken kring grammatiken : Didaktiska perspektiv på skolgrammatik
- 2000
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Other publication (pop. science, debate, etc.)abstract
- Grammatikundervisningen har en lång tradition inom grundskolans och gymnasiets svenskundervisning, men dess innehåll och uppföljning problematiseras sällan. Tvärtom uppfattas den gärna som självklar och utgör inte sällan ett centralt inslag i svenskämnet. I Grammatiken kring retoriken granskar författarna olika argument som under historien framförts för att legitimera den skolgrammatiska traditionen. I ett kritiskt perspektiv diskuterar de också dagens grammatikundervisning som den kommer till uttryck i olika läromedel samt genom intervjuer med lärare. De argumenterar för en funktionellt inriktad språkundervisning, i vilken språkbeskrivning och metareflektion kan koppas samman med elevers processinriktade skrivande.
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| 2. |
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| 3. |
- Jönsson, Daniel, et al.
(author)
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Immunocytochemical demonstration of estrogen receptor beta in human periodontal ligament cells.
- 2004
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In: Archives of Oral Biology. - 1879-1506 .- 0003-9969. ; 49:1, s. 85-88
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Journal article (peer-reviewed)abstract
- Two transcription associated estrogen receptor (ER) subtypes have been identified and named ERα and ERβ. In the present study we investigate the expression of these ER subtypes in cultured human periodontal ligament (PDL) cells by immunocytochemistry. ERβ immunoreactivity was observed in the nuclei of about 40% of the PDL cells, while no ERα immunoreactivity was detected. In human breast cancer MCF-7 cells, serving as positive controls, both ERα and ERβ immunoreactivities were demonstrated. No immunoreactivity was observed after omission of the primary antibodies. This study suggests that estrogen acts on gene transcription preferentially via ERβ in human PDL cells.
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| 4. |
- Liang, Min, et al.
(author)
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Combined lack of estrogen receptors alpha and beta affects vascular iNOS protein expression.
- 2003
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In: Cell and Tissue Research. - : Springer Science and Business Media LLC. - 1432-0878 .- 0302-766X. ; 313:1, s. 63-70
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Journal article (peer-reviewed)abstract
- Endothelial and vascular smooth muscle cells express both estrogen receptor (ER) agr and beta. Recent findings indicate that vascular ERbeta and ERagr may substitute for one another. Here, we investigate vascular morphology, contractility and protein expression in intact aorta from adult (4 months old) female mice lacking both ERagr and ERbeta (DERKO). The body weights were 17% higher (P<0.01) in DERKO than in wild-type mice. Vascular morphology, investigated in paraffin sections from aorta stained with hematoxylin-eosin or van Gieson, was identical in DERKO and wild-type mice. Endothelial cells were clearly visible in aorta of both DERKO and wild-type animals. Morphometric analysis of media thickness and wall to lumen ratio using a computerized image analyzing system demonstrated no differences between the two groups of mice. The vascular expression of endothelial nitric oxide synthase (eNOS, NOS III) and inducible nitric oxide synthase (iNOS, NOS II) was investigated using Western blotting. Aorta from both DERKO and wild-type mice expressed iNOS protein, but the iNOS expression was 3 times lower (P<0.05) in DERKO compared to wild-type mice. No difference in eNOS protein level between the two groups of animals was observed. Force responses to noradrenaline, determined either in the absence or in the presence of the nitric oxide synthase inhibitor l-NAME and the cyclo-oxygenase inhibitor indomethacin, were unaffected by the lack of functional ERagr/ERbeta. In summary, combined lack of functional ERagr and ERbeta lowers the vascular expression of iNOS but has no effects on morphology, eNOS expression, and noradrenaline sensitivity in the intact aorta.
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| 5. |
- Liang, Min, et al.
(author)
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Polyamine Synthesis Inhibition Attenuates Vascular Smooth Muscle Cell Migration.
- 2004
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In: Journal of Vascular Research. - : S. Karger AG. - 1423-0135 .- 1018-1172. ; 41:2, s. 141-147
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Journal article (peer-reviewed)abstract
- Vascular smooth muscle cell migration, occurring after intimal injury, is a substantial clinical problem in atherosclerosis and restenosis after stenting. Here we investigate the effects of polyamine synthesis inhibition on vascular smooth muscle cell migration after maximal and submaximal growth stimulation with PDGF-AB or FCS. Vascular smooth muscle cells were obtained from mouse aorta explants. These cells coexpressed smooth muscle alpha-actin, PDGFRalpha and PDGFRbeta as demonstrated by immunocytochemistry. Treatment with a high (100 ng/ ml) concentration of PDGF-AB stimulated DNA synthesis 6-fold and markedly elevated cell migration. PDGF-AB (100 ng/ml) increased cellular spermidine concentration 2-fold, but had no effect on spermine or putrescine levels. Treatment with the polyamine synthesis inhibitors CGP48664 (1 µM) and DFMO (5 mM) prevented the PDGF-AB-induced increase in spermidine and reduced spermine concentrations, but had no effect on PDGF-AB-stimulated DNA synthesis or cell migration. Cell migration after submaximal stimulation with either PDGF-AB (8 ng/ml) or FCS (8%) was, however, inhibited by the polyamine synthesis blockers. In summary, these data show that polyamine synthesis inhibition attenuates vascular smooth muscle cell migration under submaximal growth-stimulating conditions, suggesting that polyamines participate in regulation of cell migration and that treatment with polyamine synthesis inhibitors might reduce vascular smooth muscle cell migration after intimal injury.
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| 6. |
- Liang, Min, et al.
(author)
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Proteasome-dependent degradation of ERalpha but not ERbeta in cultured mouse aorta smooth muscle cells.
- 2004
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In: Molecular and Cellular Endocrinology. - : Elsevier BV. - 1872-8057 .- 0303-7207. ; 224:1-2, s. 65-71
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Journal article (peer-reviewed)abstract
- Here we investigate ERα and ERβ expression and regulation in vascular smooth muscle cells from mouse aorta. Immunocytochemistry showed nuclear staining for both ERα and ERβ. Double stainings revealed co-expression of ERα and ERβ in vascular smooth muscle cells. ERα (66 kDa) and ERβ (54 kDa) expression determined by Western blotting was unchanged within 7 h after inhibition of protein synthesis with cycloheximide in the absence of 17β-estradiol (E2), showing that both proteins are stable without ligand-binding. Treatment with 10 nM E2 for 7 h in the presence of cycloheximide increased ERα, suggesting that E2 causes a conformational change in the ERα protein. The ERβ was not affected by E2. Treatment with the proteasome inhibitor epoxomicin (100 nM) for 3 days caused a prominent upregulation of ERα both in the absence and in the presence of E2, while ERβ was unaffected, suggesting that ERα but not ERβ is degraded by ubiquitin–proteasome system in vascular smooth muscle cells. In summary, we disclose a short-term regulation of ERα protein by estrogen and that ERα but not ERβ is degraded via the ubiquitin–proteasome pathway in vascular smooth muscle cells.
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| 7. |
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| 8. |
- Liang, M, et al.
(author)
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Stimulation of vascular protein synthesis by activation of oestrogen receptor beta
- 2001
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In: Journal of Endocrinology. - : Bioscientifica. - 1479-6805 .- 0022-0795. ; 171:3, s. 417-423
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Journal article (peer-reviewed)abstract
- The objective of this study was to investigate the effects of oestrogen receptor (ER) beta activation on vascular protein synthesis and protein expression. Nuclear immunoreactivity towards ER beta was observed abundantly in vascular smooth muscle and endothelial cells of mouse aorta. No ER alpha-positive cell nuclei were observed. In aorta from ovariectomized mice, treatment with the selective ER beta agonist genistein (100 nM) for 24 h increased [(3)H]leucine incorporation by about 30%. This effect was prevented by the ER blocker ICI 182780 (10 microM). Although genistein treatment stimulated protein synthesis, it caused no change in total protein determined either by the Lowry method on tissue homogenate or by densitometric scanning of protein bands (10-220 kDa) separated by SDS-PAGE. Separation of [(35)S]methionine-labelled proteins by SDS-PAGE did not reveal the protein(s) stimulated by genistein. DNA synthesis was not affected by 100 nM genistein, suggesting that genistein-induced stimulation of protein synthesis is not part of a growth response. Protein expression, determined by SDS-PAGE, was similar in aorta from ER beta-knockout and wild-type mice, suggesting that expression of vascular proteins does not depend solely on a functional ER beta gene. We suggest that activation of vascular ER beta stimulates synthesis of proteins and that this response is not associated with vascular growth.
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| 9. |
- Lindqvist, A, et al.
(author)
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Platelet-derived growth factor receptors expressed in response to injury of differentiated vascular smooth muscle in vitro: effects on Ca2+ and growth signals
- 2001
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In: Acta Physiologica Scandinavica. - 0001-6772. ; 173:2, s. 175-175
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Journal article (peer-reviewed)abstract
- Vascular smooth muscle cells (VSMCs) in the intact vascular wall are differentiated for contraction, whereas the response to vascular injury involves transition towards a synthetic phenotype, with increased tendency for proliferation. Platelet-derived growth factor (PDGF) is thought to be important for this process. We investigated expression and functional coupling of PDGF receptors (PDGFRs) alpha and beta in rat tail arterial rings kept in organ culture, in order to capture early events in the phenotypic transition. In freshly dissected rings no PDGFR immunoreactivity was found in medial VSMCs, whereas PDGFR alpha was detected in nerve fibres. After organ culture for 1-4 days PDGFR alpha and beta as well as phospholipase Cgamma2 (PLCgamma2), known to couple to PDGFR, were expressed in VSMCs within 100 microm of the cut ends. Calponin, a marker for the contractile phenotype, was decreased near the injured area, suggesting that cells were in transition towards synthetic phenotype. In these cells, which showed functional Ca2+-release from the sarcoplasmic reticulum, PDGF-AB (100 ng x mL(-1)) had no effect on [Ca2+]i, whereas cultured VSMCs obtained from explants of rat tail arterial rings responded to PDGF-AB with an increase in [Ca2+]i. However, PDGFR within the cultured rings coupled to growth signalling pathways, as PDGF-AB caused a tyrphostin AG1295-sensitive activation of extracellular signal-regulated kinases 1 and 2 and of [3H]-thymidine incorporation. Thus, early expression of PDGFR in VSMC adjacent to sites of vascular injury coincides with signs of dedifferentiation. These receptors couple to growth signalling, but do not activate intracellular Ca2+ release.
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| 10. |
- Mai, Xiaomei, 1969-, et al.
(author)
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Asthma, lung function and allergy in 12-year-old children with very low birth weight : a prospective study
- 2003
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In: Pediatric Allergy and Immunology. - : Wiley. - 0905-6157 .- 1399-3038. ; 14:3, s. 184-192
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Journal article (peer-reviewed)abstract
- We assessed the relationship between very low birth weight (VLBW) (≤1500 g) and the development of asthma, lung function and atopy. The study groups comprised 74 of all 86 (86%) VLBW and 64 of all 86 (74%) matched term children who were prospectively followed for 12 years. A questionnaire on asthmatic and allergic symptoms was completed and skin prick tests, spirometry and hypertonic saline provocation tests were performed at 12 years of age. Cytokine secretion was analysed in stimulated blood leukocyte cultures in 28 VLBW and 23 term children. A history of asthma was more frequent among the VLBW children, as compared with the term children at age 12 (22% vs. 9%, p = 0.046). Among the VLBW children, very preterm birth (gestational age: week 25 to 29) (RR 2.5, 95%CI 1.1–5.8), neonatal mechanical ventilation (RR 2.8, 95%CI 1.2–6.4) and neonatal oxygen supplementation (RR 4.3, 95%CI 1.3–14.0) were significantly associated with a history of asthma by the age of 12 years in univariate analyses. In multivariate logistic regression, neonatal oxygen supplementation ≥ 9 days was the only remaining significant risk factor for a history of asthma (adjusted OR 6.7, 95%CI 1.0–44). The VLBW children who required mechanical ventilation during the neonatal period were more likely to have bronchial hyperresponsiveness than those not requiring mechanical ventilation (60% vs. 28%, p = 0.050). The spirometric values were similar among the VLBW and the term children at 12 years. Very low birth weight was not significantly related to allergic rhinoconjunctivitis, eczema or positive skin prick tests. Furthermore, the levels of IL-4, IL-5 and IFN-γ in stimulated cell cultures were similar in the VLBW and the term children. A history of asthma by 12 years of age was twice as common among the VLBW as the term children, and neonatal oxygen supplementation seemed to be associated with the increased risk. Furthermore, mechanical ventilation during the neonatal period was associated with bronchial hyperresponsiveness at age 12. Very low birth weight per se was not, however, related to atopy.
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