What is public relations to society? Toward an economically informed understanding of public relations

The notion of public relations contributing to the fabric of society is heavily contested in the public sphere and under-researched by the academy. The authors of this paper propose that the study of the relevance of public relations to society can be enlightened by turning to economics. Using information asymmetry as a framework, the argument is that public relations can be analyzed as a social institution that both helps to mitigate market imperfections and consequently increases the efficiency with which society’s resources are allocated as well as the chances for more market participants to derive value out of economic transaction

What is public relations to society? Toward an economically informed understanding of public relations

The notion of public relations contributing to the fabric of society is heavily contested in the public sphere and under-researched by the academy. The authors of this paper propose that the study of the relevance of public relations to society can be enlightened by turning to economics. Using information asymmetry as a framework, the argument is that public relations can be analyzed as a social institution that both helps to mitigate market imperfections and consequently increases the efficiency with which society’s resources are allocated as well as the chances for more market participants to derive value out of economic transaction

Liver transplantation for the Budd-Chiari syndrome

A retrospective study was performed that analyzed 23 patients who had an orthotopic liver transplantation for the Budd-Chiari syndrome with end-stage liver disease. Patient follow-up was as long as 14 years. The technical considerations relevant to the Budd-Chiari syndrome were discussed. There have been no serious complications of postoperative anticoagulation. Three patients, all of whom died, had recurrence of the Budd-Chiari syndrome. No other patient has had evidence of recurrent Budd-Chiari syndrome on postoperative liver biopsies. One-, 3-, and 5-year actuarial survival was 68.8%, 44.7%, and 44.7%, respectively. It was concluded that orthotopic liver transplantation is the most effective treatment for patients with the Budd-Chiari syndrome and end-stage liver disease

Nicotinic control of glutamate receptor trafficking

Nicotinic cholinergic signaling acting through nicotinic acetylcholine receptors influences numerous cognitive functions including learning and memory. Critical for these higher brain functions are basic attributes of excitatory transmission that depend on proper trafficking and lateral mobility of glutamate receptors to and from synapses. The link between nicotinic signaling and glutamate receptor trafficking, however, remains unclear. Here we measure the effect of nicotine on the surface expression and lateral mobility of AMPA receptors on hippocampal neurons in culture. We find that a short exposure to nicotine for only a few hours leads to the stabilization and accumulation of GluR1-containing AMPA receptors on dendritic spines. This process occurs through direct action on postsynaptic nicotinic acetylcholine receptors, independent of coincident fast, excitatory synaptic transmission, and results in increased synaptic efficacy. The pathway relies on intracellular calcium signaling, PDZ interactions, and the lateral diffusion, but not exocytosis, of GluR1-containing AMPA receptors. Prolonging the nicotine exposure by a few days, however, leads to the destabilization of AMPA receptors on spines. This is measured as an increase in the mobility of GluR2- containing AMPA receptors. Surprisingly, we find that nicotinic agonists alone, in the absence of nicotine, have the same effect on GluR2-containing AMPA receptor mobility, suggesting a non-canonical nicotinic mechanism. Our results demonstrate that varied nicotinic manipulations can have profound effects on glutamate receptor trafficking and offer insight into the possible mechanisms underlying the cognitive effects of nicotinic signalin

Miro proteins coordinate microtubule- and actin-dependent mitochondrial transport and distribution

In the current model of mitochondrial trafficking, Miro1 and Miro2 Rho-GTPases regulate mitochondrial transport along microtubules by linking mitochondria to kinesin and dynein motors. By generating Miro1/2 double-knockout mouse embryos and single- and double-knockout embryonic fibroblasts, we demonstrate the essential and non-redundant roles of Miro proteins for embryonic development and subcellular mitochondrial distribution. Unexpectedly, the TRAK1 and TRAK2 motor protein adaptors can still localise to the outer mitochondrial membrane to drive anterograde mitochondrial motility in Miro1/2 double-knockout cells. In contrast, we show that TRAK2-mediated retrograde mitochondrial transport is Miro1-dependent. Interestingly, we find that Miro is critical for recruiting and stabilising the mitochondrial myosin Myo19 on the mitochondria for coupling mitochondria to the actin cytoskeleton. Moreover, Miro depletion during PINK1/Parkin-dependent mitophagy can also drive a loss of mitochondrial Myo19 upon mitochondrial damage. Finally, aberrant positioning of mitochondria in Miro1/2 double-knockout cells leads to disruption of correct mitochondrial segregation during mitosis. Thus, Miro proteins can fine-tune actin- and tubulin-dependent mitochondrial motility and positioning, to regulate key cellular functions such as cell proliferation

SNX27-Mediated Recycling of Neuroligin-2 Regulates Inhibitory Signaling

GABAA receptors mediate fast inhibitory transmission in the brain, and their number can be rapidly up- or downregulated to alter synaptic strength. Neuroligin-2 plays a critical role in the stabilization of synaptic GABAA receptors and the development and maintenance of inhibitory synapses. To date, little is known about how the amount of neuroligin-2 at the synapse is regulated and whether neuroligin-2 trafficking affects inhibitory signaling. Here, we show that neuroligin-2, when internalized to endosomes, co-localizes with SNX27, a brain-enriched cargo-adaptor protein that facilitates membrane protein recycling. Direct interaction between the PDZ domain of SNX27 and PDZ-binding motif in neuroligin-2 enables membrane retrieval of neuroligin-2, thus enhancing synaptic neuroligin-2 clusters. Furthermore, SNX27 knockdown has the opposite effect. SNX27-mediated up- and downregulation of neuroligin-2 surface levels affects inhibitory synapse composition and signaling strength. Taken together, we show a role for SNX27-mediated recycling of neuroligin-2 in maintenance and signaling of the GABAergic synapse