Revealing power dynamics and staging conflicts in agricultural system transitions : Case studies of innovation platforms in New Zealand

Innovation platforms (IPs) that support agricultural innovation to enable transition processes towards more sustainable agriculture provide a space where conflicts of interest among actors in the existing agricultural system (the so called incumbent regime) may play out. Sometimes these conflicts over how actors will benefit from an action are not revealed until actors are brought together. However, a barrier to change occurs when IP actors use their existing power to mobilise resources to influence if and how individual and collective interests are aligned. In the context of agricultural innovation and transitions, this paper uses the power in transitions framework (Avelino and Wittmayer, 2016), along with analytical perspectives on conflicts and role perceptions, to understand how consciously staging or revealing conflicts of interest among IP actors changed role perceptions and power relations among these actors. The paper explores this topic in two IPs addressing agricultural production and sustainability challenges in New Zealand's agricultural sector. Conflicts were staged in IPs when one group of actors mobilised resources that enabled them to move existing power relations from one-sided, to synergistic or a mutual dependency. This enabled conflicts to be acknowledged and solved. In contrast, conflicts were not staged when actors mobilised resources to maintain antagonostic power relations. Our cases demontrate that staging conflicts to change actors' role perceptions is an important intermediary step to forming new power relations in the agricultural system. Our findings highlight the need for IP theory to conceptualise power relations in IPs as context specific, dynamic and a force shaping outcomes, rather than solely a force exerted by actors in the incumbent regime over IP actors.</p

Human Amygdala Sensitivity to the Pupil Size of Others

Stimulation of the amygdala produces pupil dilation in animal and human subjects. The present study examined whether the amygdala is sensitive to variations in the pupil size of others. Male subjects underwent event-related functional magnetic resonance imaging while passively viewing unfamiliar female faces whose pupils were either unaltered (natural variations in large and small pupils) or altered to be larger or smaller than their original size. Results revealed that the right amygdala and left amygdala/substantia innominata were sensitive to the pupil size of others, exhibiting increased activity for faces with relatively large pupils. Upon debrief, no subject reported being aware that the pupils had been manipulated. These results suggest a function for the amygdala in the detection of changes in pupil size, an index of arousal and/or interest on the part of a conspecific, even in the absence of explicit knowledge

The velocity potential and the interacting force for two spheres moving perpendicularly to the line joining their centers

The velocity potential around two spheres moving perpendicularly to the line joining their centers is given by a series of spherical harmonics. The appropriateness of the truncation is evaluated by determining the residual normal surface velocity on the spheres. In evaluating the residual normal velocity, a recursive procedure is constructed to evaluate the spherical harmonics to reduce computational effort and truncation error as compared to direct transformation or numerical integration. We estimate the lift force coefficient for touching spheres to be 0.577771, compared to the most accurate earlier estimate of 0.51435 by Miloh (1977).Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42701/1/10665_2004_Article_BF00127479.pd

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)

The central melanocortin system affects the hypothalamo-pituitary thyroid axis and may mediate the effect of leptin

Prolonged fasting is associated with a downregulation of the hypothalamo-pituitary thyroid (H-P-T) axis, which is reversed by administration of leptin. The hypothalamic melanocortin system regulates energy balance and mediates a number of central effects of leptin. In this study, we show that hypothalamic melanocortins can stimulate the thyroid axis and that their antagonist, agouti-related peptide (Agrp), can inhibit it. Intracerebroventricular (ICV) administration of Agrp (83-132) decreased plasma thyroid stimulating hormone (TSH) in fed male rats. Intraparaventricular nuclear administration of Agrp (83-132) produced a long-lasting suppression of plasma TSH, and plasma T4. ICV administration of a stable α-MSH analogue increased plasma TSH in 24-hour–fasted rats. In vitro, α-MSH increased thyrotropin releasing hormone (TRH) release from hypothalamic explants. Agrp (83-132) alone caused no change in TRH release but antagonized the effect of α-MSH on TRH release. Leptin increased TRH release from hypothalami harvested from 48-hour–fasted rats. Agrp (83-132) blocked this effect. These data suggest a role for the hypothalamic melanocortin system in the fasting-induced suppression of the H-P-T axis