The purpose of this Theory to Practice article is to present a systematic, cross‐disciplinary, and accessible synthesis of relevant research and to offer explicit evidence‐based design guidelines to help practitioners design better participation processes. From the research literature, the authors glean suggestions for iteratively creating, managing, and evaluating public participation activities. The article takes an evidence‐based and design science approach, suggesting that effective public participation processes are grounded in analyzing the context closely, identifying the purposes of the participation effort, and iteratively designing and redesigning the process accordingly.
This article argues that participation and inclusion are independent dimensions of public engagement and elaborates the relationships of inclusion with deliberation and diversity. Inclusion continuously creates a community involved in defining and addressing public issues; participation emphasizes public input on the content of programs and policies. Features of inclusive processes are coproducing the process and content of decision making, engaging multiple ways of knowing, and sustaining temporal openness. Using a community of practice lens, we compare the consequences of participatory and inclusive practices in four processes, finding that inclusion supports an ongoing community with capacity to address a stream of issues.
This article is a theoretical contribution to reconsidering the boundaries that are central features of collaborative public management. We identify two contrasting ways of doing boundary work: one oriented to treating them as barriers that promote separation and the other to treating them as junctures that enable connecting. We describe three general practices for creating junctures: translating across, aligning among, and decentering differences. We argue that orienting boundary work in collaboration to making connections supports efficient resilience, making it possible for systems to work even when they are disrupted or when resources are constrained. We illustrate the practices and their benefits with examples from collaborative public management.This article is a theoretical contribution to reconceptualizing boundaries in public management and the implications of public managers' boundary work practices for resilience. Collaborative management, a central feature of modern public management, is commonly defined as a "boundary-spanning" endeavor (
SummaryTransient receptor potential (TRP) channels TRPC3 and TRPC6 are expressed in both sensory neurons and cochlear hair cells. Deletion of TRPC3 or TRPC6 in mice caused no behavioural phenotype, although loss of TRPC3 caused a shift of rapidly adapting (RA) mechanosensitive currents to intermediateadapting currents in dorsal root ganglion sensory neurons. Deletion of both TRPC3 and TRPC6 caused deficits in light touch and silenced half of smalldiameter sensory neurons expressing mechanically activated RA currents. Double TRPC3/TRPC6 knock-out mice also showed hearing impairment, vestibular deficits and defective auditory brain stem responses to highfrequency sounds. Basal, but not apical, cochlear outer hair cells lost more than 75 per cent of their responses to mechanical stimulation. FM1-43-sensitive mechanically gated currents were induced when TRPC3 and TRPC6 were co-expressed in sensory neuron cell lines. TRPC3 and TRPC6 are thus required for the normal
Blood platelet aggregation must be tightly controlled to promote clotting at injury sites but avoid inappropriate occlusion of blood vessels. Thrombin, which cleaves and activates Gq-coupled protease-activated receptors, and collagen-related peptide, which activates the receptor glycoprotein VI, stimulate platelets to aggregate and form thrombi. Coincident activation by these two agonists synergizes, causing the exposure of phosphatidylserine on the cell surface, which is a marker of cell death in many cell types. Phosphatidylserine exposure is also essential to produce additional thrombin on platelet surfaces, which contributes to thrombosis. We found that activation of either thrombin receptors or glycoprotein VI alone produced a calcium signal that was largely dependent only on store-operated Ca(2+) entry. In contrast, experiments with platelets from knockout mice showed that the presence of both ligands activated nonselective cation channels of the transient receptor potential C (TRPC) family, TRPC3 and TRPC6. These channels principally allowed entry of Na(+), which coupled to reverse-mode Na(+)/Ca(2+) exchange to allow calcium influx and thereby contribute to Ca(2+) signaling and phosphatidylserine exposure. Thus, TRPC channels act as coincidence detectors to coordinate responses to multiple signals in cells, thereby indirectly mediating in platelets an increase in intracellular calcium concentrations and exposure of prothrombotic phosphatidylserine.
Mendelian heritable pain disorders have provided insights into human pain mechanisms and suggested new analgesic drug targets. Interestingly, many of the heritable monogenic pain disorders have been mapped to mutations in genes encoding ion channels. Studies in transgenic mice have also implicated many ion channels in damage sensing and pain modulation. It seems likely that aberrant peripheral or central ion channel activity underlies or initiates many pathological pain conditions. Understanding the mechanistic basis of ion channel malfunction in terms of trafficking, localization, biophysics, and consequences for neurotransmission is a potential route to new pain therapies.
Transient receptor potential (TRP) channels act as sensors for a range of stimuli as diverse as light, sound, touch, pheromones, and tissue damage. Their role in mechanosensation in the animal kingdom, identified by gene ablation studies, has raised questions about whether they are directly mechanically gated, whether they act alone or in concert with other channels to transduce mechanical stimuli, and their relative importance in various functions and disease states in humans. The ability of these channels to form heteromultimers and interact with other ion channels underlies a range of cell-specific functions in different cell types. Here we overview recent advances in this rapidly expanding field, focusing on somatosensation, hearing, the cardiovascular system, and interactions between TRP channels and other proteins involved in mechanoelectrical signaling.
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