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- Junestav, Malin, 1971-
(författare)
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Arbetslinjer i svensk socialpolitisk debatt och lagstiftning 1930-2001
- 2004
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The purpose of this thesis has been to analyse the conception of the Swedish “work strategy” (arbetslinjen). This principle, or political idea, has been central in Sweden’s economic, employment as well as social policy since (at least) the inter war era. The purpose has been to detangle and dissect the ideas behind an almost sacred political principle, hardly ever questioned or challenged by political actors or scholars. Through studies of political debates and decision- and policy-making, the issue has been to reach an insight into how this particular set of ideas, gathered together in the conception of “the work strategy”, has been understood and how this influenced policy-making. In this thesis it has been shown the conception of “the work strategy” and its realisation is linked to Social Democratic economic policy since the 1930s and the full employment programs designed in the 1950s. The political ideas included in this principle, though, have deeper roots in the history of social and poor relief policy institutions. The theoretical assumption is that certain political ideas have such a strong position among politicians, no matter what their ideological residence, that it is broadly speaking impossible to implement political proposals that challenge these ideas.
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- Levin, Malin, 1973, et al.
(författare)
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A novel polymorphism in the gene coding for the beta(1)-adrenergic receptor associated with survival in patients with heart failure.
- 2000
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Ingår i: European heart journal. - : Oxford University Press (OUP). - 0195-668X. ; 21:22, s. 1853-8
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: The adrenergic nervous system is of major importance in congestive heart failure. No genetic polymorphism has previously been identified in the beta(1)-adrenergic receptor gene. The aim of this study was to find possible mutations in this gene and to relate such findings to morbidity and prognosis in heart failure. METHODS AND RESULTS: Genomic DNA was extracted from blood leukocytes from patients with congestive heart failure (n=184) and from age-matched controls (n=77). The part of the beta(1)-adrenergic receptor gene corresponding to nucleotide 1-255 was amplified by polymerase chain reaction and analysed by automated sequencing. The patients were investigated by echocardiography and followed regarding symptoms and survival for 5 years. A missense mutation was identified at nucleotide position 145 in the beta(1)-adrenergic receptor gene, which predicted an amino acid substitution at position 49 (Ser49Gly). The allele frequency of the Gly49 variant was 0.13 in controls and 0.18 in patients (P=0.19). At the time of the 5-years follow-up, 62% of the patients with the wild type gene and 39% of the patients with the Ser49Gly variant had died or had experienced hospitalization (P=0.005). Patients without the mutation had significantly poorer survival compared to those with the mutation, risk ratio 2.34 (95% CI 1.30-4.20), P=0.003. In a mulivariate analysis, the risk ratio was 2.03 (95% CI 0.99-4.16) P=0.05. CONCLUSION: A novel missense mution in the beta(1)-adrenergic receptor gene was associated with a decreased mortality risk in patients with congestive heart failure. These data suggest that the beta(1)-receptor Ser49Gly variant might be associated with altered receptor function, resulting in myocardial protection in patients with heart failure.
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- Levin, Malin, 1973, et al.
(författare)
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The myocardium-protective Gly-49 variant of the beta 1-adrenergic receptor exhibits constitutive activity and increased desensitization and down-regulation.
- 2002
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Ingår i: The Journal of biological chemistry. - 0021-9258. ; 277:34, s. 30429-35
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Tidskriftsartikel (refereegranskat)abstract
- The beta(1)-adrenergic receptor (beta(1)AR) is a major mediator of catecholamine effects in human heart. Patients with heart failure who were hetero- or homozygous for the Gly-49 variant of the beta(1)AR (Gly-49-beta(1)AR) showed improved long-term survival as compared with those with the Ser-49 genotype. Here, the functional consequences of this polymorphism were studied in cells expressing either variant. The Gly-49-beta(1)AR demonstrated characteristic features of constitutively active receptors. In cells expressing the Gly-49-beta(1)AR, both basal and agonist-stimulated adenylyl cyclase activities were higher than in cells expressing the Ser-49 variant (Ser-49-beta(1)AR). The Gly-49-beta(1)AR was more sensitive to the inhibitory effect of the inverse agonist metoprolol and displayed increased affinity for agonists. Isoproterenol potency for adenylyl cyclase activation was higher on membranes expressing the Gly-49-beta(1)AR than on those expressing the Ser-49-beta(1)AR. After incubation with saturating concentrations of catecholamines or sustained stimulation, the Gly-49 variant showed a much higher desensitization, which largely prevailed over constitutive activity in terms of cAMP accumulation. The Gly-49-beta(1)AR also displayed a more profound agonist-promoted down-regulation than the Ser-49 variant. The stronger regulation of the Gly-49-beta(1)AR could explain the beneficial effect of the Gly-49 genotypes on survival, further supporting the concept that beta(1)AR desensitization is protective in heart failure.
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