Stability and welfare of 'merit-based' group-matching mechanisms in voluntary contribution game

We study the stability and welfare properties of merit-based (meritocratic) group-matching mechanisms in voluntary contribution games. Meritocratic matching in this context means that players tend to be assortatively grouped according to their contributions. We let regimes di ffer from one another with respect to their matching fidelity. The stability analysis summarizes as follows. When there is not enough meritocracy, the only equilibrium state is universal free-riding. Above a first threshold, several Nash equilibria above free-riding emerge, but only the free-riding equilibrium is stochastically stable. There exists a second meritocratic threshold, above which an equilibrium with high contributions becomes the unique stochastically stable state. This operationalization of meritocracy sheds light on critical transitions, that are enabled by contribution-assortative matching, between equilibria related to "tragedy of the common

Meritocratic matching can dissolve the efficiency-equality tradeoff: the case of voluntary contributions

One of the fundamental tradeoffs underlying society is that between efficiency and equality. The challenge for institutional design is to strike the right balance between these two goals. Game-theoretic models of public-goods provision under ‘meritocratic matching’ succinctly capture this tradeoff: under zero meritocracy (society is randomly formed), theory predicts maximal inefficiency but perfect equality; higher levels of meritocracy (society matches contributors with contributors) are predicted to improve efficiency but come at the cost of growing inequality. We conduct an experiment to test this tradeoff behaviorally and make the astonishing finding that, notwithstanding theoretical predictions, higher levels of meritocracy increase both efficiency and equality, that is, meritocratic matching dissolves the tradeoff. Fairness considerations can explain the departures from theoretical predictions including the behavioral phenomena that lead to dissolution of the efficiency-equality tradeoff

Observation of playa salts as nuclei in orographic wave clouds

During the Ice in Clouds Experiment-Layer Clouds (ICE-L), dry lakebed, or playa, salts from the Great Basin region of the United States were observed as cloud nuclei in orographic wave clouds over Wyoming. Using a counterflow virtual impactor in series with a single-particle mass spectrometer, sodium-potassium-magnesium-calcium-chloride salts were identified as residues of cloud droplets. Importantly, these salts produced similar mass spectral signatures to playa salts with elevated cloud condensation nuclei (CCN) efficiencies close to sea salt. Using a suite of chemical characterization instrumentation, the playa salts were observed to be internally mixed with oxidized organics, presumably produced by cloud processing, as well as carbonate. These salt particles were enriched as residues of large droplets (>19 μm) compared to smaller droplets (>7 μm). In addition, a small fraction of silicate-containing playa salts were hypothesized to be important in the observed heterogeneous ice nucleation processes. While the high CCN activity of sea salt has been demonstrated to play an important role in cloud formation in marine environments, this study provides direct evidence of the importance of playa salts in cloud formation in continental North America has not been shown previously. Studies are needed to model and quantify the impact of playas on climate globally, particularly because of the abundance of playas and expected increases in the frequency and intensity of dust storms in the future due to climate and land use changes

Primordial Helium-3 Redux: The Helium Isotope Ratio of the Orion Nebula*

We report the first direct measurement of the helium isotope ratio, 3He/4He, outside of the Local Interstellar Cloud, as part of science-verification observations with the upgraded CRyogenic InfraRed Echelle Spectrograph. Our determination of 3He/4He is based on metastable He i* absorption along the line of sight toward Θ2A Ori in the Orion Nebula. We measure a value 3He/4He = (1.77 ± 0.13) × 10−4, which is just ∼40% above the primordial relative abundance of these isotopes, assuming the Standard Model of particle physics and cosmology, (3He/4He)p = (1.257 ± 0.017) × 10−4. We calculate a suite of galactic chemical evolution simulations to study the Galactic build up of these isotopes, using the yields from Limongi & Chieffi for stars in the mass range M = 8–100 M⊙ and Lagarde et al. for M = 0.8–8 M⊙. We find that these simulations simultaneously reproduce the Orion and protosolar 3He/4He values if the calculations are initialized with a primordial ratio ${\left({}^{3}\mathrm{He}{/}^{4}\mathrm{He}\right)}_{{\rm{p}}}=(1.043\pm 0.089)\times {10}^{-4}$. Even though the quoted error does not include the model uncertainty, this determination agrees with the Standard Model value to within ∼2σ. We also use the present-day Galactic abundance of deuterium (D/H), helium (He/H), and 3He/4He to infer an empirical limit on the primordial 3He abundance, ${\left({}^{3}\mathrm{He}/{\rm{H}}\right)}_{{\rm{p}}}\leqslant (1.09\pm 0.18)\times {10}^{-5}$, which also agrees with the Standard Model value. We point out that it is becoming increasingly difficult to explain the discrepant primordial 7Li/H abundance with nonstandard physics, without breaking the remarkable simultaneous agreement of three primordial element ratios (D/H, 4He/H, and 3He/4He) with the Standard Model values

CNV Workshop: an integrated platform for high-throughput copy number variation discovery and clinical diagnostics

<p>Abstract</p> <p>Background</p> <p>Recent studies have shown that copy number variations (CNVs) are frequent in higher eukaryotes and associated with a substantial portion of inherited and acquired risk for various human diseases. The increasing availability of high-resolution genome surveillance platforms provides opportunity for rapidly assessing research and clinical samples for CNV content, as well as for determining the potential pathogenicity of identified variants. However, few informatics tools for accurate and efficient CNV detection and assessment currently exist.</p> <p>Results</p> <p>We developed a suite of software tools and resources (CNV Workshop) for automated, genome-wide CNV detection from a variety of SNP array platforms. CNV Workshop includes three major components: detection, annotation, and presentation of structural variants from genome array data. CNV detection utilizes a robust and genotype-specific extension of the Circular Binary Segmentation algorithm, and the use of additional detection algorithms is supported. Predicted CNVs are captured in a MySQL database that supports cohort-based projects and incorporates a secure user authentication layer and user/admin roles. To assist with determination of pathogenicity, detected CNVs are also annotated automatically for gene content, known disease loci, and gene-based literature references. Results are easily queried, sorted, filtered, and visualized via a web-based presentation layer that includes a GBrowse-based graphical representation of CNV content and relevant public data, integration with the UCSC Genome Browser, and tabular displays of genomic attributes for each CNV.</p> <p>Conclusions</p> <p>To our knowledge, CNV Workshop represents the first cohesive and convenient platform for detection, annotation, and assessment of the biological and clinical significance of structural variants. CNV Workshop has been successfully utilized for assessment of genomic variation in healthy individuals and disease cohorts and is an ideal platform for coordinating multiple associated projects.</p> <p>Availability and Implementation</p> <p>Available on the web at: <url>http://sourceforge.net/projects/cnv</url></p

MicroRNA-184 inhibits neuroblastoma cell survival through targeting the serine/threonine kinase AKT2

BACKGROUND: Neuroblastoma is a paediatric cancer of the sympathetic nervous system. The single most important genetic indicator of poor clinical outcome is amplification of the MYCN transcription factor. One of many down-stream MYCN targets is miR-184, which is either directly or indirectly repressed by this transcription factor, possibly due to its pro-apoptotic effects when ectopically over-expressed in neuroblastoma cells. The purpose of this study was to elucidate the molecular mechanism by which miR-184 conveys pro-apoptotic effects. RESULTS: We demonstrate that the knock-down of endogenous miR-184 has the opposite effect of ectopic up-regulation, leading to enhanced neuroblastoma cell numbers. As a mechanism of how miR-184 causes apoptosis when over-expressed, and increased cell numbers when inhibited, we demonstrate direct targeting and degradation of AKT2, a major downstream effector of the phosphatidylinositol 3-kinase (PI3K) pathway, one of the most potent pro-survival pathways in cancer. The pro-apoptotic effects of miR-184 ectopic over-expression in neuroblastoma cell lines is reproduced by siRNA inhibition of AKT2, while a positive effect on cell numbers similar to that obtained by the knock-down of endogenous miR-184 can be achieved by ectopic up-regulation of AKT2. Moreover, co-transfection of miR-184 with an AKT2 expression vector lacking the miR-184 target site in the 3\u27UTR rescues cells from the pro-apoptotic effects of miR-184. CONCLUSIONS: MYCN contributes to tumorigenesis, in part, by repressing miR-184, leading to increased levels of AKT2, a direct target of miR-184. Thus, two important genes with positive effects on cell growth and survival, MYCN and AKT2, can be linked into a common genetic pathway through the actions of miR-184. As an inhibitor of AKT2, miR-184 could be of potential benefit in miRNA mediated therapeutics of MYCN amplified neuroblastoma and other forms of cancer