| 1. |
- Löfstrand, Magnus
(författare)
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A modelling and simulation approach for linking design activities to business decisions
- 2007
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The business environment of the manufacturing industry is changing from a hardware-based product focus to a process and function focus. A current industrial interest is the development and sale of functions. This function could be realised as a product based on hardware, software and services, and may be sold as a function rather than as hardware. This function view is referred to as Functional Products (FP). The new focus for the customer is on value rather than hardware. This presents new challenges for how engineering hardware design may best be carried out. Sale of functional products requires a changed business model in which the price of the functional product is related to the functionality of the product itself; hence the name functional product. The supplier can in such a scenario no longer sell maintenance and spare parts. Instead, these activities become a cost, thus motivating the supplier to increase process efficiency, decrease internal production cost by using less energy per produced unit and increase knowledge about use-cases. The researcher's challenge is how to create new knowledge regarding functional product development for academic as well as for industrial benefit. The research question was formulated as: How may methods or tools for design process modelling and simulation be developed to support functional product development? Four case studies were carried out in Swedish industry. Case study 1 was carried out in cooperation with Hägglunds Drives AB. Case study 2 was carried out in cooperation with companies Hägglunds Drives AB, Volvo Aero and Volvo Car Corporation. Case study 3 was carried out in cooperation Volvo Aero and Case study 4 was carried out in cooperation with nine industrial companies during the formation of the Faste Laboratory, Centre for Functional Product Innovation. Results include the need for integrating product development process and company strategy for functional product development and the identification of the need for new methods and tools to enable better understanding of technology and business processes. The research shows the possibility of evaluating cost and time of development before doing the actual product development work by modelling and simulating the design process. Thus, the knowledge that previously was implicit in the work process is made explicit and possible to manipulate for a desired outcome. Linking the future business cases to work processes by modelling and simulation enables knowledge re-use and work-process predictions concerning cost and time. Hence, modelling and simulation of work processes results in better knowledge of company development capacity earlier than before, thus allowing shorter reaction time to changes in the business domain.
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| 2. |
- Langrish, Jeremy, et al.
(författare)
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Contribution of endothelin-1 to the vascular effects of diesel exhaust inhalation in humans
- 2009
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Ingår i: Hypertension. - Dallas, Tex. : The Association. - 0194-911X .- 1524-4563. ; 54:4, s. 910-915
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Tidskriftsartikel (refereegranskat)abstract
- Diesel exhaust inhalation impairs vascular function, and, althoughthe underlying mechanism remains unclear, endothelin (ET) 1and NO are potential mediators. The aim of this study was toidentify whether diesel exhaust inhalation affects the vascularactions of ET-1 in humans. In a randomized, double-blind crossoverstudy, 13 healthy male volunteers were exposed to either filteredair or dilute diesel exhaust (331±13 µg/m3). Plasmaconcentrations of ET-1 and big-ET-1 were determined at baselineand throughout the 24-hour study period. Bilateral forearm bloodflow was measured 2 hours after the exposure during infusionof either ET-1 (5 pmol/min) or the ETA receptor antagonist,BQ-123 (10 nmol/min) alone and in combination with the ETB receptorantagonist, BQ-788 (1 nmol/min). Diesel exhaust exposure hadno effect on plasma ET-1 and big-ET-1 concentrations (P>0.05for both) or 24-hour mean blood pressure or heart rate (P>0.05for all). ET-1 infusion increased plasma ET-1 concentrationsby 58% (P<0.01) but caused vasoconstriction only after dieselexhaust exposure (–17% versus 2% after air; P<0.001).In contrast, diesel exhaust exposure reduced vasodilatationto isolated BQ-123 infusion (20% versus 59% after air; P<0.001)but had no effect on vasodilatation to combined BQ-123 and BQ-788administration (P>0.05). Diesel exhaust inhalation increasesvascular sensitivity to ET-1 and reduces vasodilatation to ETAreceptor antagonism despite unchanged plasma ET-1 concentrations.Given the tonic interaction between the ET and NO systems, weconclude that diesel exhaust inhalation alters vascular reactivityto ET-1 probably through its effects on NO bioavailability.
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| 3. |
- Lucking, Andrew J, et al.
(författare)
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Diesel exhaust inhalation increases thrombus formation in man
- 2008
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Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 29:24, s. 3043-3051
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: Although the mechanism is unclear, exposure to traffic-derived air pollution is a trigger for acute myocardial infarction (MI). The aim of this study is to investigate the effect of diesel exhaust inhalation on platelet activation and thrombus formation in men. METHODS AND RESULTS: In a double-blind randomized crossover study, 20 healthy volunteers were exposed to dilute diesel exhaust (350 microg/m(3)) and filtered air. Thrombus formation, coagulation, platelet activation, and inflammatory markers were measured at 2 and 6 h following exposure. Thrombus formation was measured using the Badimon ex vivo perfusion chamber. Platelet activation was assessed by flow cytometry. Compared with filtered air, diesel exhaust inhalation increased thrombus formation under low- and high-shear conditions by 24% [change in thrombus area 2229 microm(2), 95% confidence interval (CI) 1143-3315 microm(2), P = 0.0002] and 19% (change in thrombus area 2451 microm(2), 95% CI 1190-3712 microm(2), P = 0.0005), respectively. This increased thrombogenicity was seen at 2 and 6 h, using two different diesel engines and fuels. Diesel exhaust also increased platelet-neutrophil and platelet-monocyte aggregates by 52% (absolute change 6%, 95% CI 2-10%, P = 0.01) and 30% (absolute change 3%, 95% CI 0.2-7%, P = 0.03), respectively, at 2 h following exposure compared with filtered air. CONCLUSION: Inhalation of diesel exhaust increases ex vivo thrombus formation and causes in vivo platelet activation in man. These findings provide a potential mechanism linking exposure to combustion-derived air pollution with the triggering of acute MI.
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| 4. |
- Lundbäck, David, et al.
(författare)
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Molecular epidemiology of Neisseria gonorrhoeae- identification of the first presumed Swedish transmission chain of an azithromycin-resistant strain
- 2006
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Ingår i: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS). - : Wiley. - 0903-4641 .- 1600-0463. ; 114:1, s. 67-71
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Tidskriftsartikel (refereegranskat)abstract
- In the present study, 10 azithromycin-resistant Neisseria gonorrhoeae isolates from 6 Swedish male patients in 2004, 3 sporadic Swedish azithromycin-resistant N. gonorrhoeae isolates from recent years and one Swedish N. gonorrhoeae isolate from 2003 that was susceptible to azithromycin but assigned the same serological variant (serovar), i.e. IB-37, as the isolates from 2004 were included. The isolates were characterized phenotypically using antibiograms and serovar determination and genetically with pulsed-field gel electrophoresis (PFGE), entire porB gene sequencing and N. gonorrhoeae multiantigen sequence typing (NG-MAST). The epidemiological information and the results of the thorough phenotypic characterisation and genetic characterisation identified the first presumed domestic transmission of one azithromycin-resistant N. gonorrhoeae strain in Sweden in 2004. This stresses the need for continuous surveillance of the antibiotic susceptibility of N. gonorrhoeae in order to identify emergence of new resistance, monitor the changing patterns of the susceptibility, and be able to update treatment recommendations on a regular basis.
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| 5. |
- Lundbäck, Magnus, 1976-
(författare)
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Cardiovascular effects of diesel exhaust : mechanistic and interventional studies
- 2009
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Background: Air pollution is associated with negative health effects. Exposure to combustion-derived particulate matter (PM) air pollution has been related to increased incidence of cardiovascular and respiratory morbidity and mortality, specifically in susceptible populations. Ambient particles, with a diameter of less than 2.5 mm, have been suggested to be the strongest contributor to these health effects. Diesel exhaust (DE) is a major source of small combustion-derived PM air pollution world wide. In healthy volunteers, exposure to DE, has been associated with airway inflammation and impaired vasomotor function and endogenous fibrinolysis. The aims of this thesis were to further elucidate the underlying mechanisms to the reported cardiovascular effects following exposure to DE, with specific focus on endothelin-1 (ET-1). Additionally, the vascular effects of the major gaseous component of DE, nitrogen dioxide (NO2), were assessed together with the impact of an exhaust particle trap to reduce the observed negative vascular effects after DE exposure. Methods: In all studies healthy, non-smoking male volunteers were included and exposed for one hour during intermittent exercise in a randomised double-blind crossover fashion. In studies I-III, subjects were exposed to DE at a particulate matter concentration of approximately 300 μg/m3 and filtered air, on two different occasions. In study V an additional exposure was employed, during which DE was filtered through an exhaust particle trap. In study IV subjects were exposed to nitrogen dioxide (NO2) at 4 ppm or filtered air. In study I, thrombus formation and platelet activation were assessed using the Badimon ex vivo perfusion chamber and flow cytometry. Study II comprised the determination of arterial stiffness including pulse wave analysis and velocity. In studies III-V, vascular assessment was performed using venous occlusion plethysmography. In studies IV and V, the vascular responses to intra-arterially infused endothelial-dependent and endothelial-independent vasodilatators were registered. In study III, vascular responses to intra-arterial infusion of Endothelin-1 (ET-1) and ET-1-receptor antagonists were assessed. Venous occlusion phlethysmography was in all cases performed 4-6 hours following exposures. Blood samples for markers of inflammation, coagulation and platelet activation were collected before and throughout the study periods in studies III and V. Results: Exposure to DE increased ex vivo thrombus formation and arterial stiffness, in terms of augmentation index. DE inhalation impaired vasomotor function and endogenous fibrinolysis. The exhaust particle trap reduced the particle concentration by 98% and abolished the effects on vasomotor function, endogenous fibrinolysis and ex vivo thrombus formation. Plasma concentrations of ET-1 and its precursor big-ET-1 were unchanged following exposure. Dual endothelial receptor antagonism caused similar vasodilatation after both exposures, although vasodilatation to the endothelin-A receptor alone was blunted after DE exposure. ET-1 infusion induced vasoconstriction only following DE exposure. Exposure to nitrogen dioxide did not affect vascular function. Conclusion: Inhalation of diesel exhaust in young healthy men impaired important and complementary aspects of vascular function in humans; regulation of vascular tone and endogenous fibrinolysis as well as increased ex vivo thrombus formation. The use of an exhaust particle trap significantly reduced particle emissions and abolished the DE-induced vascular and prothrombotic effects. The adverse vascular effects following DE exposure do not appear to be directly mediated through the endothelin system. Neither is NO2 suggested to be a major arbiter of the DE-induced cardiovascular responses. Arterial stiffness is a non-invasive and easily accessible method and could thus be employed to address vascular function in larger field studies. Taken together, this thesis has given further knowledge about the mechanisms underlying the DE-induced vascular effects.
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| 6. |
- Lundbäck, Magnus, et al.
(författare)
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Decision-making in conditions of constant change - a case within the automotive industry
- 2005
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Ingår i: Management Decision. - Bradford : MCB University Press. - 0025-1747 .- 1758-6070. ; 43:2, s. 220-235
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Tidskriftsartikel (refereegranskat)abstract
- PurposeTo analyse how differences in decision-making affected the integration of the R&D functions after Ford's acquisition of Volvo Cars. Design/methodology/approachThe analysis is carried out in two steps. Step one analyses which type of approach Ford employed to integrate Volvo into the company. Step two analyses how R&D decisions are made by both firms and the consequences of found differences in decision-making on the success of the integration process.FindingsFord's approach to the integration of Volvo Cars follows a symbiosis approach, combining a high need of both organizational autonomy and strategic interdependence. A symbiosis acquisition integration approach demands that the decision-making processes are given special attention. The acquired firm's specific decision-making processes need to remain intact in order to preserve its embedded unique R&D value creation capabilities. The decision-making processes should be kept separate in order to prevent disruption. Originality/valueThe paper relates theories about firm acquisition processes and aspects of organization theory to establish a bridge between these research areas.
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| 7. |
- Lundbäck, Magnus, 1976-, et al.
(författare)
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Exposure to diesel exhaust increases arterial stiffness in man
- 2009
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Ingår i: Particle and Fibre Toxicology. - : Springer Science and Business Media LLC. - 1743-8977. ; 6:7
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Tidskriftsartikel (refereegranskat)abstract
- Introduction Exposure to air pollution is associated with increased cardiovascular morbidity, although the underlying mechanisms are unclear. Vascular dysfunction reduces arterial compliance and increases central arterial pressure and left ventricular after-load. We determined the effect of diesel exhaust exposure on arterial compliance using a validated non-invasive measure of arterial stiffness.Methods In a double-blind randomized fashion, 12 healthy volunteers were exposed to diesel exhaust (approximately 350 μg/m3) or filtered air for one hour during moderate exercise. Arterial stiffness was measured using applanation tonometry at the radial artery for pulse wave analysis (PWA), as well as at the femoral and carotid arteries for pulse wave velocity (PWV). PWA was performed 10, 20 and 30 min, and carotid-femoral PWV 40 min, post-exposure. Augmentation pressure (AP), augmentation index (AIx) and time to wave reflection (Tr) were calculated.Results Blood pressure, AP and AIx were generally low reflecting compliant arteries. In comparison to filtered air, diesel exhaust exposure induced an increase in AP of 2.5 mmHg (p = 0.02) and in AIx of 7.8% (p = 0.01), along with a 16 ms reduction in Tr (p = 0.03), 10 minutes post-exposure.Conclusion Acute exposure to diesel exhaust is associated with an immediate and transient increase in arterial stiffness. This may, in part, explain the increased risk for cardiovascular disease associated with air pollution exposure. If our findings are confirmed in larger cohorts of susceptible populations, this simple non-invasive method of assessing arterial stiffness may become a useful technique in measuring the impact of real world exposures to combustion derived-air pollution.
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| 8. |
- Lundbäck, Magnus, et al.
(författare)
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Inter-firm product platform development in the automotive industry
- 2005
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Ingår i: International Journal of Innovation Management. - 1363-9196 .- 1757-5877. ; 9:2, s. 155-181
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Tidskriftsartikel (refereegranskat)abstract
- The product platform development process becomes critical and of general interest when different brand name products are developed from inter-firm developed product platforms. The inter-firm platform adds perspectives not considered in previous research. In this article areas related to the inter-firm product platform integration process are described. The study is a longitudinal, deep, explorative study aimed at identifying managerial challenges to inter-firm platform development and how they can be dealt with. Analysis shows that the factory sequence is a critical factor when developing inter-firm platform architecture. Also, making architectural concessions without jeopardising brand uniqueness places new demands on managers involved in the development processes. Further, we found a reciprocal interdependence between technological and managerial factors that created a need for innovative organisational and managerial solutions. Finally, reciprocal interdependences add complementary theoretical knowledge on how to better control and understand areas that hamper inter-firm product development projects from attaining cost-effective solutions and economies of scale.
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