Political opportunity and the rise and decline of interest group sectors

Interest group activity is always affected by the political environment in which groups operate. As a result, effective study of public interest groups must situate them in a larger political context. We propose a means of doing so by building on theoretical and empirical studies of both social movements and interest groups. We argue that groups can best be understood by changing the unit of analysis from an individual group to the set of groups pursuing common agendas, or an "interest group sector." Drawing from both empirical and theoretical literature, we establish both the necessity and the theoretical parameters for a sectoral analysis, and offer a basic framework for such an analysis. We demonstrate empirical support for a sectoral approach by looking at the periodicity of group formation in five public interest sectors. We then propose a six stage framework to describe a cyclic process of issue emergence, resource mobilization, organization building, and their relation to the policy process. We conclude by discussing the potential policy impact of interest group mobilization and institutionalization, and its relationship to democracy.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/31068/1/0000745.pd

AT(2) antagonist-sensitive potentiation of angiotensin II-induced constriction by NO blockade and its dependence on endothelium and P450 eicosanoids in rat renal vasculature

1. We showed earlier that NO inhibition caused a left-shift and augmented E(max) of the concentration-response curve of AT(1)-mediated (angiotensin II)-induced vasoconstrictions (AII-VC) in the rat kidney. The 0.01–0.1 nM AII-VC unmasked by the potentiating effect of NO inhibition, were sensitive not only to AT(1) (L158809), but also to AT(2) receptor (PD123319) antagonists. We now demonstrate the role of endothelium and eicosanoids in the NO-masked AT(1)/AT(2)-mediated component of the AII-VC in isolated indomethacin-perfused kidneys of the rat. 2. L-NAME increased 0.1 nM AII-VC 7.2 fold. Pretreatment of the kidneys with factor VIII antibody/complement or with the detergent CHAPS to damage endothelium, decreased carbachol-induced vasodilatation and blunted by 60 and 30% respectively, the enhancement of AII-VC during NO inhibition. 3. L-NAME also increased 3 μM noradrenaline (NA)-induced vasoconstriction (NA-VC) 8.1 fold. In contrast to AII-VC, endothelium damage was without effect on the enhancement of NA-VC by L-NAME, suggesting a dominant role of endothelium-derived NO in the enhancement of NA-VC. 4. During NO inhibition, ETYA (2 μM; an inhibitor of all arachidonic acid derived pathways) and α-naphtoflavone (10 μM; an inhibitor of the cytochrome P450 isozymes), decreased by 85% the 0.1 nM AII-VC. 5. In conclusion, during NO inhibition, the AT(1)-mediated constriction to low concentrations of AII, which is sensitive to AT(2) antagonists, depends on intact endothelium, and can be blocked by inhibition of eicosanoid synthesis. The results suggest that the AII-mediated vasoconstriction through AT(1) receptors is potentiated in the absence of NO, by the release of eicosanoids from the endothelium through AT(2) receptors

Spatial plasticity of the auditory cortex in single-sided deafness

Objectives/Hypothesis: To evaluate spatial plasticity of the auditory cortex in single-sided deafness (SSD). Study Design: Cross-sectional study comparing a cohort with adult-onset, idiopathic SSD to a cohort with normal hearing. Methods: Demographic, audiometric, magnetoencephalographic imaging, and magnetic resonance imaging data were collected for 13 SSD adult subjects and 13 normal-hearing controls. Locations of peak activation corresponding to the M100 response in auditory cortices ipsilateral and contralateral to tonal stimuli (0.5 kHz and 4 kHz) were extracted from advanced biomagnetic source imaging analyses. Spatial extent of frequency representation across the 0.5 kHz to 4 kHz zone was computed for the two hemispheres. Results: Spatial separation distance between peak locations for 0.5 kHz and 4 kHz stimuli in SSD showed increased activation spread distance in the hemisphere contralateral to the only hearing ear and decreased distance in the ipsilateral hemisphere. In contrast, normal hearing controls had nearly the same activation spread distance in the two hemispheres for ipsilateral and contralateral inputs. The difference between interhemispheric activation spread distance in SSD is significantly increased to 6.5 mm, when compared to 1.7 mm in normal controls (P \u3c.05). Conclusions: Loss of unilateral peripheral input in SSD is associated with spatial reorganization of the auditory cortex in both hemispheres. This change in central auditory functional organization may in turn lead to higher order hearing deficits that rely on interhemispheric processing. Hearing optimization in the only hearing ear may require remediation of both spatial and temporal central auditory changes in SSD. Level of Evidence: NA Laryngoscope, 126:2785–2791, 2016