Raising collective agency is key to successful place-based development approaches. Existing policy arrangements have, however, been criticised, suggesting a need to effectuate more collaborative modes of governance. This paper shall contribute to a better understanding of how public support can best be arranged to raise collective agency for a more collaborative mode of governance in rural areas. The paper elaborates on findings of empirical investigations conducted within the EU FP7 project DERREG. It will be shown that differences in effectuating more collaborative modes of governance can partly be ascribed to different political dynamics, economic and demographic situations as well as the presence of a shared sense of place. To raise collective agency effectively requires a joint reconsideration and restructuring of the division of roles and tasks, including those of public administration. This can be supported by facilitating joint reflexivity among development actors and giving room for collaborative leadership and operational flexibility within policy arrangements.
We have reported that 5,6-epoxyeicosatrienoic acid (5,6-EET) was the only cytochrome P-450-dependent arachidonic acid (AA) epoxide to dilate the isolated, perfused caudal artery of the rat. We have investigated the mechanisms by which 5,6-EET dilates the rat-tail artery by studying the effect of deendothelialization and inhibition of AA metabolic pathways (cyclooxygenase, lipoxygenase, and cytochrome P-450 monooxygenase) on the vascular action of the epoxide. Rat isolated caudal arteries were perfused with Krebs-Henseleit solution at 370 C, pH 7.4, and gassed with 95% 02-5% CO2. Arterial tone was elevated with phenylephrine; acetylcholine (0.5 nmol) was used to detect the presence of intact, functional endothelium.Doses of 5,6-EET, from 6.25 to 25.0 nmol, were injected close-arterially. After obtaining control responses, the same doses were randomly retested after deendothelialization or in the presence of inhibitors of AA metabolism. Removal of the endothelium decreased by 70%o the vasodilator responses to 5,6-EET. The endothelial dependency was a function of the epoxide interacting with cyclooxygenase of the endothelium, because indomethacin (3 gM) and aspirin (50 ,iM) prevented the vasodilator response to 5,6-EET while not affecting the response to acetylcholine. SKF-525A (1.1 ,LM) and metyrapone (150 FM) did not affect the responses to the 5,6-EET, whereas clotrimazole (0.7 ,uM) and nordihydroguaiaretic acid (2.5 ,M) had nonspecific effects, decreasing responses to 5,6-EET and acetylcholine. Because 5,6-EET failed to stimulate detectable release of prostanoids into the effluent from the caudal artery, we conclude that 5,6-EET requires conversion by cyclooxygenase for expression of its vasoactivity. (Circulation Research 1990;67:1082-1088 T he cytochrome P-450 mixed-function oxidases metabolize arachidonic acid (AA) to biologically active products. This pathway of AA metabolism results in the formation of four epoxyeicosatrienoic acids (EETs or epoxides), their corresponding vicinal diols, the dihydroxyeicosatrienoic acids (DHETs), hydroxyeicosatetraenoic acids (HETEs), and wo and w-1 metabolites.' These AA metabolites have a wide range of biological activities.2-5 Importantly, some of the epoxides (5,6-EET; 8,9-EET; 11,12-EET; and 14,15-EET) are vasoactive. Thus, EETs differ in their capacity to dilate the intestinal microcirculation; 5,6-EET has an effect on intestinal blood flow far in excess of the other epoxides of AA.6 It is the only epoxide effective in relaxing precontracted rat aortic strips.7 One of the cytochrome P-450-AA metabolites released from a suspension of epithelial cells separated from the outer medulla of the rabbit kidney, tentatively identified as 5,6-EET, relaxes isolated blood vessels.4 This epoxide is labile, having a half-life of approximately 6 minutes; in aqueous solution it degrades to a y-lactone and 5,6-DHET. We have shown that 5,6-EET is the only epoxide that decreases vascular resistance in the isolated, perfused caudal artery of the rat.8 Other epoxides as well as 5,6-EE...
The electroadsorption on columnar Au electrodes (substrate) of pyridine from x M pyridine + 0.1 M HClO4 and x M pyridine + 0.1 M KClO4 aqueous solutions (10 -3 e x e 10 -2 ), at constant potential and 298 K, was studied using voltammetry, chronocoulometry, and ac impedance combined with scanning tunneling microscopy to characterize the substrate topography. For a constant pyridine concentration (c), the degree of surface coverage by pyridine adsorbate (θ) diminished as R was increased. The θ vs c plots, irrespective of R, were interpreted by a Frumkin adsorption isotherm including a constant standard adsorption free energy. The evaluation of adsorption isotherms reflects the existence of an excluded volume effect, which can be related to a barrier effect due to adsorbates at nanometer size pore entrances.
The roughness relaxation of thin columnar Au electrodeposits at constant potential and 25°C in 0.05 M NaF, 0.05 M KC1 and 0.05 M K,SO, has been studied. These measurements were taken in the -0.6 to 0.8 V (vs Hg/Hg,SO, reference electrode) potential range. The kinetic data were obtained from the roughness factor decay over 5 ~10~ s. The value of the surface diffusion coefficient D, of Au atoms was derived from the roughness decay law at constant potential and PH. At any potential, the value of D, increases in the order NaF < K,SO, < KCl. This sequence correlates with the specific adsorption of anions on Au. In K,SO, and NaF solutions, as the electroformation of AuOH species takes place, the effect of SO:-and F-ions is no longer observed. In contrast, in 0.05 M KCI solution, the value of D, increases steadily as the applied potential is increased positively. INTRODUCIIONSurface roughness relaxation phenomena on metals in the range 273-325 K offer the possibility of deriving quantitative information about the mobility of surface atoms either in vacua or at metal-aqueous solution interfaces [l-3].
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