Incentive-Centered Design for User-Contributed Content

We review incentive-centered design for user-contributed content (UCC) on the Internet. UCC systems, produced (in part) through voluntary contributions made by non-employees, face fundamental incentives problems. In particular, to succeed, users need to be motivated to contribute in the first place ("getting stuff in"). Further, given heterogeneity in content quality and variety, the degree of success will depend on incentives to contribute a desirable mix of quality and variety ("getting \emph{good} stuff in"). Third, because UCC systems generally function as open-access publishing platforms, there is a need to prevent or reduce the amount of negative value (polluting or manipulating) content. The work to date on incentives problems facing UCC is limited and uneven in coverage. Much of the empirical research concerns specific settings and does not provide readily generalizable results. And, although there are well-developed theoretical literatures on, for example, the private provision of public goods (the "getting stuff in" problem), this literature is only applicable to UCC in a limited way because it focuses on contributions of (homogeneous) money, and thus does not address the many problems associated with heterogeneous information content contributions (the "getting \emph{good} stuff in" problem). We believe that our review of the literature has identified more open questions for research than it has pointed to known results.http://deepblue.lib.umich.edu/bitstream/2027.42/100229/1/icd4ucc.pdf7

Why leave wikipedia?

Extended abstract and poster.Among active editors, earlier adopters tend to stay for longer. Higher edit frequency leads to higher likelihood of quitting. For new users, on their first day, creators are more likely to stay than preservers, and destroyers are more likely to drop out.http://deepblue.lib.umich.edu/bitstream/2027.42/65118/1/wiki_poster_v1.pd

Why Share in Peer-to-Peer Networks?

Prior theory and empirical work emphasize the enormous free-riding problem facing peer-to-peer (P2P) sharing networks. Nonetheless, many P2P networks thrive. We explore two possible explanations that do not rely on altruism or explicit mechanisms imposed on the network: direct and indirect private incentives for the provision of public goods. The direct incentive is a traffic redistribution effect that advantages the sharing peer. We din this incentive is likely insufficient to motivate equilibrium content sharing in large networks. We then approach P2P networks as a graph-theoretic problem and present sufficient conditions for sharing and free-riding to co-exist due to indirect incentives we call generalized reciprocity.http://deepblue.lib.umich.edu/bitstream/2027.42/60443/1/p2p_icec08.pd

Why Share in Peer-to-Peer Networks

Prior theory and empirical work emphasize the enormous free-riding problem facing peer-to-peer (P2P) sharing networks. Nonetheless, many P2P networks thrive. We explore two possible explanations: private provision of public goods and generalized reciprocity. We investigate a particular form of private incentives to share content: redistributing traffic in the network to the advantage of the sharing peer. Our preliminary model suggests that this incentive is likely insufficient to motivate equilibrium content sharing in large networks. We then approach P2P networks as a graph-theoretic problem and derive sufficient conditions for sharing and free-riding to co-exist in the absence of direct sharing benefits or an explicit incentive mechanism.http://deepblue.lib.umich.edu/bitstream/2027.42/49504/1/NetEcon06-final.pd

Astrocyte- and neuron-derived CXCL1 drives neutrophil transmigration and blood-brain barrier permeability in viral encephalitis

Herpes simplex virus (HSV)-1 encephalitis has significant morbidity partly because of an over-exuberant immune response characterized by leukocyte infiltration into the brain and increased blood-brain barrier (BBB) permeability. Determining the role of specific leukocyte subsets and the factors that mediate their recruitment into the brain is critical to developing targeted immune therapies. In a murine model, we find that the chemokines CXCL1 and CCL2 are induced in the brain following HSV-1 infection. Ccr2 (CCL2 receptor)-deficient mice have reduced monocyte recruitment, uncontrolled viral replication, and increased morbidity. Contrastingly, Cxcr2 (CXCL1 receptor)-deficient mice exhibit markedly reduced neutrophil recruitment, BBB permeability, and morbidity, without influencing viral load. CXCL1 is produced by astrocytes in response to HSV-1 and by astrocytes and neurons in response to IL-1alpha, and it is the critical ligand required for neutrophil transendothelial migration, which correlates with BBB breakdown. Thus, the CXCL1-CXCR2 axis represents an attractive therapeutic target to limit neutrophil-mediated morbidity in HSV-1 encephalitis

Increased Drp1-mediated mitochondrial fission promotes proliferation and collagen production by right ventricular fibroblasts in experimental pulmonary arterial hypertension

Introduction: Right ventricular (RV) fibrosis contributes to RV failure in pulmonary arterial hypertension (PAH). The mechanisms underlying RV fibrosis in PAH and the role of RV fibroblasts (RVfib) are unknown. Activation of the mitochondrial fission mediator dynamin-related protein 1 (Drp1) contributes to dysfunction of RV myocytes in PAH through interaction with its binding partner, fission protein 1 (Fis1). However, the role of mitochondrial fission in RVfib and RV fibrosis in PAH is unknown. Objective: We hypothesize that mitochondrial fission is increased in RVfib of rats with monocrotaline (MCT)-induced PAH. We evaluated the contribution of Drp1 and Drp1–Fis1 interaction to RVfib proliferation and collagen production in culture and to RV fibrosis in vivo. Methods: Vimentin (+) RVfib were enzymatically isolated and cultured from the RVs of male Sprague–Dawley rats that received MCT (60 mg/kg) or saline. Mitochondrial morphology, proliferation, collagen production, and expression of Drp1, Drp1 binding partners and mitochondrial fusion mediators were measured. The Drp1 inhibitor mitochondrial division inhibitor 1 (Mdivi-1), P110, a competitive peptide inhibitor of Drp1–Fis1 interaction, and siRNA targeting Drp1 were assessed. Subsequently, prevention and regression studies tested the antifibrotic effects of P110 (0.5 mg/kg) in vivo. At week 4 post MCT, echocardiography and right heart catheterization were performed. The RV was stained for collagen. Results: Mitochondrial fragmentation, proliferation rates and collagen production were increased in MCT-RVfib versus control-RVfib. MCT-RVfib had increased expression of activated Drp1 protein and a trend to decreased mitofusin-2 expression. Mdivi-1 and P110 inhibited mitochondrial fission, proliferation and collagen III expression in MCT-RVfib. However, P110 was only effective at high doses (1 mM). siDrp1 also reduced fission in MCT-RVfib. Despite promising results in cell therapy, in vivo therapy with P110 failed to prevent or regress RV fibrosis in MCT rats, perhaps due to failure to achieve adequate P110 levels or to the greater importance of interaction of Drp1 with other binding partners. Conclusion: PAH RVfib have increased Drp1-mediated mitochondrial fission. Inhibiting Drp1 prevents mitochondrial fission and reduces RVfib proliferation and collagen production. This is the first description of disordered mitochondrial dynamics in RVfib and suggests that Drp1 is a potential new antifibrotic target

I Scratched Yours: The Prevalence of Reciprocation in Feedback Provision on eBay

Many online systems for bilateral transactions elicit performance feedback from both transacting partners. Such bilateral feedback giving introduces strategic considerations. We focus on reciprocity in the giving of feedback: how prevalent a strategy of giving feedback is only if feedback is first received from one’s trading partner. The overall level of feedback activity clearly depends on the prevalence of the reciprocation strategy: in a market with many reciprocators and few unconditional feedback providers, the equilibrium quantity of feedback can be quite low. We estimate the prevalence of such reciprocation in one market, eBay. Reciprocation cannot be directly distinguished from late feedback that was not conditioned on the partner having provided feedback. We develop a model that distinguishes the two by exploiting information about the timing of feedback provision when the partner does not provide feedback. We find that buyers and sellers on eBay used the “reciprocate only” strategy about 20-23% of the time. We also measure the extent to which the prevalence of these strategies changes with the experience levels of the two parties and with the item price.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/78401/1/prevalence_of_reciprocation.pd

Ischemia-induced Drp1 and Fis1-mediated mitochondrial fission and right ventricular dysfunction in pulmonary hypertension

Right ventricular (RV) function determines prognosis in pulmonary arterial hypertension (PAH). We hypothesize that ischemia causes RV dysfunction in PAH by triggering dynamin-related protein 1 (Drp1)-mediated mitochondrial fission. RV function was compared in control rats (n = 50) versus rats with monocrotaline-induced PAH (MCT-PAH; n = 60) both in vivo (echocardiography) and ex vivo (RV Langendorff). Mitochondrial membrane potential and morphology and RV function were assessed before or after 2 cycles of ischemia-reperfusion injury challenge (RV-IR). The effects of Mdivi-1 (25 μM), a Drp1 GTPase inhibitor, and P110 (1 μM), a peptide inhibitor of Drp1-Fis1 interaction, were studied. We found that MCT caused RV hypertrophy, RV vascular rarefaction, and RV dysfunction. Prior to IR, the mitochondria in MCT-PAH RV were depolarized and swollen with increased Drp1 content and reduced aconitase activity. RV-IR increased RV end diastolic pressure (RVEDP) and mitochondrial Drp1 expression in both control and MCT-PAH RVs. IR depolarized mitochondria in control RV but did not exacerbate the basally depolarized MCT-PAH RV mitochondria. During RV IR mdivi-1 and P110 reduced Drp1 translocation to mitochondria, improved mitochondrial structure and function, and reduced RVEDP. In conclusion, RV ischemia occurs in PAH and causes Drp1-Fis1-mediated fission leading to diastolic dysfunction. Inhibition of mitochondrial fission preserves RV function in RV-IR

How well do local relations predict gas-phase metallicity gradients? : results from SDSS-IV MaNGA

Gas-phase metallicity gradients in galaxies provide important clues to those galaxies’ formation histories. Using SDSS-IV MaNGA data, we previously demonstrated that gas metallicity gradients vary systematically and significantly across the galaxy mass–size plane: at stellar masses beyond approximately 1010 M , more extended galaxies display steeper gradients (in units of dex/Re) at a given stellar mass. Here, we set out to develop a physical interpretation of these findings by examining the ability of local ∼kpc-scale relations to predict the gradient behaviour along the mass–size plane. We find that local stellar mass surface density, when combined with total stellar mass, is sufficient to reproduce the overall mass–size trend in a qualitative sense. We further find that we can improve the predictions by correcting for residual trends relating to the recent star formation histories of star-forming regions. However, we find as well that the most extended galaxies display steeper average gradients than predicted, even after correcting for residual metallicity trends with other local parameters. From these results, we argue that gas-phase metallicity gradients can largely be understood in terms of known local relations, but we also discuss some possible physical causes of discrepant gradients