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- Almqvist, Roland M, 1964-
(författare)
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Icons of New Public Management : four studies on competition, contracts and control
- 2004
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Public organizations have undergone major changes over the past few decades. The umbrella term used to characterize these changes in the style of public administration is ‘New Public Management’ (NPM). NPM is a cluster of ideas borrowed from the conceptual framework of private-sector administrative practice –– a multifarious concept, covering diverse ideas and theories about what the nature of public management and administration should be. Arguably, then, NPM is primarily not a practitioners’ product but, rather, a construct of the research community, which assembled the programmatic aspects of NPM. The impact of these programmatic aspects on public administrative routines, operations and everyday work is a matter of analysis at the technological level.This thesis studies both the programmatic and the technological aspects of NPM. It focuses on how the programmatic aspects of NPM transform into technological aspects and how we can understand the outcome of these transformations, i.e. NPM’s impact on public administrative practice. The four discrete papers of the thesis cover three aspects (‘Icons’) of NPM – ‘Competition’, ‘Contracts’ and ‘Control’ – in depth:1. Paper I presents a method for isolating effects of the competition threat, with three possible approaches. All three include cost-cutting with respect to full-time annual staff appointments, but combine it with a number of changing variables. The results indicate one plausible conclusion: that one effect of the threat of competition has been to boost savings. In the units concerned, this effect – in terms of a mean cost reduction – may be estimated between 4 and 6 per cent.2. Paper II seeks to study how quality issues have been managed by contract. First, it presents some of the conceptual (programmatic) arguments of ‘Management by Contract’, discussing the structural arguments generally used (the purchaser/ provider split) and a common method (competitive tendering). Second, it presents some technological effects based on empirical findings. The paper’s concluding statement is that there is a gap between the programmatic and technological dimensions. Five interpretations intended to explain this gap are put forward.3. Paper III investigates the existence and function of various mechanisms of internal change in relation to broader aspects of change and characteristics of management control systems. The findings indicate that organizations can continuously transform their management control systems by creating, and promoting the use of, specific transformation mechanisms. In the two organizations studied, these mechanisms include internal benchmarking and internal contracting.4. Paper IV evaluates the City of Stockholm’s decentralization reform, which resulted in 24 local suborganizations (district councils). The empirical findings do not appear to fit into a single, allembracing theory, and the kaleidoscopic nature of the reform demands a broad, multidisciplinary approach. This paper therefore contributes to knowledge of the organizational changes that took place by addressing them both in rational terms and as symbolic acts. Although reforms tend to be perceived as ways of shaking up an organization, it is suggested here that they may in fact have a cohesive function – serving to hold the organization together.One general conclusion of this thesis is that NPM cannot readily be described in terms of success or failure. Instead, the four papers provide widely varying perspectives on, and interpretations of, NPM’s practical impact and the technologies that are taking shape in the field. Based on the notion of NPM as a management doctrine, seven contradictory general observations are presented. Sometimes all goes according to plan. Alternatively, the outcome may deviate from the plan; the result may be ‘business as usual’, i.e. little may change; things may only get worse; programmes may have contradictory effects; change may be excessive; and, finally, there may be unexpected but positive effects. Here, the conclusion is that in some cases the solution is to develop the theories and concepts, i.e. the programmatic level, while in others the solution may, instead, involve developing the application and implementation of existing theories and concepts – i.e. the technological level.
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| 3. |
- Andrén, Maria, 1976-
(författare)
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The Role of Fc Gamma Receptors in Experimental Arthritis
- 2004
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Induction of collagen-induced arthritis (CIA), an animal model for human rheumatoid arthritis, is dependent on anti-collagen type II (CII) antibodies. The effector mechanism by which autoantibodies contribute to inflammatory reactions in autoimmune diseases is not well understood. In this thesis I have studied the effector pathways used by IgG anti-CII antibodies to initiate arthritis, namely the IgG Fc receptors (FcγRs) and the complement system. We have found that FcγRIII is crucial for development of CIA, as CII-immunized mice lacking this receptor do not develop arthritis and IgG1 and IgG2b anti-CII antibodies require FcγRIII to trigger arthritis when transferred to naïve mice. The antibody-mediated arthritis was further enhanced in mice deficient in the inhibitory FcγRIIB, indicating that FcγRIIB regulates the activation of FcγRIII. Furthermore, we demonstrate that FcγRIII exist as three distinct haplotypes in mice, FcγRIII:H, FcγRIII:V and FcγRIII:T. Mice expressing the FcγRIII:H haplotype are more susceptible to CIA than mice expressing the FcγRIII:V haplotype, indicating that certain FcγRIII haplotype predisposes for CIA. We also show that the most likely FcγRIII-expressing effector cell in CIA is the macrophage, since FcγRIII-expressing macrophages exclusively can induce arthritis in FcγRIII-deficient mice challenged for CIA.The complement system was also investigated in development of CIA. We found that this effector pathway is also necessary for onset of arthritis, as CIA was inhibited by treatment with anti-complement factor 5 (C5) antibodies. C5-deficient mice could neither develop CIA unless provided with C5-containing sera. Taken together, the work presented in this thesis indicates that FcγRs and the complement system are crucial for the induction of experimental arthritis. These findings are important for understanding the mechanisms behind rheumatoid arthritis and blocking of these effector pathways may in the future be used as treatment of rheumatoid arthritis.
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| 5. |
- Johansson, Åsa, et al.
(författare)
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The genetic control of sialadenitis versus arthritis in a NOD.QxB10.Q F2 cross.
- 2002
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Ingår i: European Journal of Immunology. - 1521-4141 .- 0014-2980. ; 32:1, s. 243-250
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Tidskriftsartikel (refereegranskat)abstract
- The non-obese diabetic (NOD) mouse spontaneously develops diabetes and sialadenitis. The sialadenitis is characterized by histopathological changes in salivary glands and functional deficit similar to Sjögren's syndrome. In humans, Sjögren's syndrome could be associated with other connective tissue disorders, such as rheumatoid arthritis. In the present study the genetic control of sialadenitis in mice was compared to that of arthritis. We have previously reported a NOD locus, identified in an F2 cross with the H2(q) congenic NOD (NOD.Q) and C57BL/10.Q (B10.Q) strains, that promoted susceptibility to collagen-induced arthritis. The sialadenitis in NOD.Q showed a similar histological phenotype as in NOD, whereas no submandibular gland infiltration was found in B10.Q. The development of sialadenitis was independent of immunization with type II collagen and established arthritis. To identify the genetic control of sialadenitis, a gene segregation experiment was performed on an (NOD.QxB10.Q)F2 cross and genetic mapping of 353 F2 mice revealed one significant locus associated with sialadenitis on chromosome 4, LOD score 4.7. The NOD.Q allele-mediated susceptibility under a recessive inheritance pattern. The genetic control of sialadenitis seemed to be unique in comparison to diabetes and arthritis, as no loci associated with these diseases have been identified at the same location.
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| 6. |
- Lord, John, et al.
(författare)
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The Luleå ball and disc apparatus
- 2001
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Ingår i: Bench testing of industrial fluid lubrication and wear properties used in machinery applications. - West Conshohocken, Pa : ASTM International. - 0803128673 ; , s. 53-67
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Konferensbidrag (refereegranskat)abstract
- The ability to measure lubricant film thickness in elastohydrodynamic point contacts was greatly improved when the method of interferometry was introduced in the late 1960s. Constant refinements of the technique have made it possible to measure the thickness of thin films with an accuracy of a few nanometers. In order to further develop the technique and provide a tool for advanced lubricant experiments, a Ball and Disc Apparatus was developed. The aim was to accomplish an apparatus with an open architecture for easy expansion and the ability to use several sub-methods for film thickness determination.
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| 7. |
- Prokunina, Ludmila, et al.
(författare)
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A regulatory polymorphism in PDCD1 is associated with susceptibility to systemic lupus erythematosus in humans
- 2002
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 32:4, s. 666-669
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Recension (övrigt vetenskapligt/konstnärligt)abstract
- Systemic lupus erythematosus (SLE, OMIM 152700) is a complex autoimmune disease that affects 0.05% of the Western population, predominantly women. A number of susceptibility loci for SLE have been suggested in different populations, but the nature of the susceptibility genes and mutations is yet to be identified. We previously reported a susceptibility locus (SLEB2) for Nordic multi-case families. Within this locus, the programmed cell death 1 gene (PDCD1, also called PD-1) was considered the strongest candidate for association with the disease. Here, we analyzed 2,510 individuals, including members of five independent sets of families as well as unrelated individuals affected with SLE, for single-nucleotide polymorphisms (SNPs) that we identified in PDCD1. We show that one intronic SNP in PDCD1 is associated with development of SLE in Europeans (found in 12% of affected individuals versus 5% of controls; P = 0.00001, r.r. (relative risk) = 2.6) and Mexicans (found in 7% of affected individuals versus 2% of controls; P = 0.0009, r.r. = 3.5). The associated allele of this SNP alters a binding site for the runt-related transcription factor 1 (RUNX1, also called AML1) located in an intronic enhancer, suggesting a mechanism through which it can contribute to the development of SLE in humans.
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