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- Ivanell, Stefan S. A.
(författare)
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Numerical computations of wind turbine wakes
- 2005
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Licentiatavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Numerical simulations using CFD methods are performed for wind turbine applications. The aim of the project is to get a better understanding of the wake behaviour, which is needed since today’s industrial design codes for wind power applications are based on the BEM (Blade Element Momentum) method. This method has been extended with a number of empirical corrections not based on physical flow features. The importance of accurate design models does also increase as the turbines become larger. Therefore, the research is today shifting toward a more fundamental approach, aiming at understanding basic aerodynamic mechanisms. The result from the CFD simulation is evaluated and special interest is given to the circulation and the position of vortices. From these evaluations, it will hopefully be possible to improve the engineering methods and base them, to a greater extent, on physical features instead of empirical corrections. The simulations are performed using the program ”EllipSys3D” developed at DTU (The Technical University of Denmark). The Actuator Line Method is used, where the blade is represented by a line instead of a large number of panels. The forces on that line are introduced by using tabulated aerodynamic coefficients. In this way, the computer resource is used more efficiently since the number of node points locally around the blade is decreased, and they can instead be concentrated in the wake behind the blades. An evaluation method to extract values of the circulation from the wake flow field is developed. The result shows agreement with classical theorems from Helmholtz, from which it follows that the wake tip vortex has the same circulation as the maximum value of the bound circulation on the blade.
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- Mosén, Henrik, et al.
(författare)
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Defective glucose-stimulated insulin release in the diabetic Goto-Kakizaki (GK) rat coincides with reduced activity of the islet carbon monoxide signaling pathway
- 2005
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Ingår i: Endocrinology. - : The Endocrine Society. - 0013-7227 .- 1945-7170. ; 146:3, s. 1553-1558
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Tidskriftsartikel (refereegranskat)abstract
- The Goto-Kakizaki (GK) rat displays a markedly reduced insulin response to glucose, a defect that is thought to be coupled to an impaired glucose signaling in the beta-cell. We have examined whether carbon monoxide (CO), derived from beta-cell heme oxygenase (HO), might be involved in the secretory dysfunction. Immunocytochemical labeling of constitutive HO (HO-2) showed no overt difference in fluorescence pattern in islets from GK vs. Wistar controls. However, isolated islets from GK rats displayed a markedly impaired HO activity measured as CO production (-50%), and immunoblotting revealed an approximately 50% reduction of HO-2 protein expression compared with Wistar controls. Furthermore, there was a prominent expression of inducible HO (HO-1) in GK islets. Incubation of isolated islets showed that the glucose-stimulated CO production and the glucose-stimulated insulin response were considerably reduced in GK islets compared with Wistar islets. Addition of the HO activator hemin or gaseous CO to the incubation media brought about a similar amplification of glucose-stimulated insulin release in GK and Wistar islets, suggesting that distal steps in the HO-CO signaling pathway were not appreciably affected. We conclude that the defective insulin response to glucose in the GK rat can be explained, at least in part, by a marked impairment of the glucose-HO-CO signaling pathway as manifested by a prominent decrease in glucose stimulation of islet CO production and a reduced expression of HO-2. A possible role of HO-1 expression as a compensatory mechanism in the GK islets is presently unclear.
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- Mosén, Henrik, et al.
(författare)
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Impaired glucose-stimulated insulin secretion in the GK rat is associated with abnormalities in islet nitric oxide production.
- 2008
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Ingår i: Regulatory Peptides. - : Elsevier BV. - 1873-1686 .- 0167-0115. ; 151, s. 139-146
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Tidskriftsartikel (refereegranskat)abstract
- We investigated implications of nitric oxide (NO) derived from islet neuronal constitutive NO synthase (ncNOS) and inducible NOS (iNOS) on insulin secretory mechanisms in the mildly diabetic GK rat. Islets from GK rats and Wistar controls were analysed for ncNOS and iNOS by HPLC, immunoblotting and immunocytochemistry in relation to insulin secretion stimulated by glucose or l-arginine in vitro and in vivo. No obvious difference in ncNOS fluorescence in GK vs control islets was seen but freshly isolated GK islets displayed a marked iNOS expression and activity. After incubation at low glucose GK islets showed an abnormal increase in both iNOS and ncNOS activities. At high glucose the impaired glucose-stimulated insulin release was associated with an increased iNOS expression and activity and NOS inhibition dose-dependently amplified insulin secretion in both GK and control islets. This effect by NOS inhibition was also evident in depolarized islets at low glucose, where forskolin had a further amplifying effect in GK but not in control islets. NOS inhibition increased basal insulin release in perfused GK pancreata and amplified insulin release after glucose stimulation in both GK and control pancreata, almost abrogating the nadir separating first and second phase in controls. A defective insulin response to l-arginine was seen in GK rats in vitro and in vivo, being partially restored by NOS inhibition. The results suggest that increased islet NOS activities might contribute to the defective insulin response to glucose and l-arginine in the GK rat. Excessive iNOS expression and activity might be deleterious for the beta-cells over time.
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