Human Computation and Economics

This article is devoted to economical aspects of Human Computation (HC) and to perspectives of HC in economics. As of economical aspects of HC, it is first observed that much of what makes HC systems effective is economical in nature suggesting that complexity being reconsidered as a “HC complexity” and the conception of efficient HC systems as a “HC economics”. This article also points to the relevance of HC in the development of standard software and to the importance of competition in HC systems. As of HC in economics, it is first argued that markets can be seen as HC systems avant la lettre. Looking more closely at financial markets, the article then points to a speed differential between transactions and credit risk awareness that compromises the efficiency of financial markets. Finally, a HCbased credit risk rating is proposed that, overcoming the afore mentioned speed differential, holds promise for better functioning financial markets

Observation of the ^1P_1 State of Charmonium

The spin-singlet P-wave state of charmonium, hc(1P1), has been observed in the decay psi(2S) -> pi0 hc followed by hc -> gamma etac. Inclusive and exclusive analyses of the M(hc) spectrum have been performed. Two complementary inclusive analyses select either a range of energies for the photon emitted in hc -> gamma etac or a range of values of M(etac). These analyses, consistent with one another within statistics, yield M(h_c) =[3524.9 +/- 0.7 (stat) +/- 0.4 (sys)]MeV/c^2 and a product of the branching ratios B_psi(psi(2S) -> pi0 hc) x B_h(hc -> gamma etac) = [3.5 +/- 1.0 (stat) +/- 0.7 (sys)] x 10^{-4}. When the etac is reconstructed in seven exclusive decay modes, 17.5 +/- 4.5 hc events are seen with an average mass M(hc) = [3523.6 +/- 0.9 (stat) +/- 0.5 (sys)] MeV/c^2, and B_psi x B_h = [5.3 +/- 1.5 (stat) +/- 1.0 (sys)] x 10^{-4}. Because the inclusive and exclusive data samples are largely independent they are combined to yield an overall mass M(hc) = [3524.4 +/- 0.6 (stat) +/- 0.4 (sys)]MeV/c^2 and product of branching ratios B_psi x B_h = [4.0 +/- 0.8 (stat) +/- 0.7 (sys)] x 10^{-4}. The hc mass implies a P-wave hyperfine splitting Delta M_{HF}(1P) \equiv M(1^3P)-M(1^1P_1) = [1.0 +/- 0.6 (stat) +/- 0.4 (sys)] MeV/c^2.Comment: 38 pages postscript,also available through http://www.lns.cornell.edu/public/CLNS/2005/, Submitted to PR

Non cell autonomous upregulation of CDKN2 transcription linked to progression of chronic hepatitis C disease

Chronic hepatitis C virus infection (C-HC) is associated with higher mortality arising from hepatic and extrahepatic disease. This may be due to accelerated biological aging; however, studies in C-HC have thus far been based solely on telomere length as a biomarker of aging (BoA). In this study, we have evaluated CDKN2 locus transcripts as alternative BoAs in C-HC. Our results suggest that C-HC induces non-cell-autonomous senescence and accelerates biological aging. The CDKN2 locus may provide a link between C-HC and increased susceptibility to age-associated diseases and provides novel biomarkers for assessing its impact on aging processes in man

Human collagen Krox up-regulates type I collagen expression in normal and scleroderma fibroblasts through interaction with Sp1 and Sp3 transcription factors.

Despite several investigations, the transcriptional mechanisms that regulate the expression of both type I collagen genes (COL1A1 and COL1A2) in either physiological or pathological situations, such as scleroderma, are not completely known. We have investigated the role of hc-Krox transcription factor on type I collagen expression by human dermal fibroblasts. hc-Krox exerted a stimulating effect on type I collagen protein synthesis and enhanced the corresponding mRNA steady-state levels of COL1A1 and COL1A2 in foreskin fibroblasts (FF), adult normal fibroblasts (ANF), and scleroderma fibroblasts (SF). Forced hc-Krox expression was found to up-regulate COL1A1 transcription through a -112/-61-bp sequence in FF, ANF, and SF. Knockdown of hc-Krox by short interfering RNA and decoy strategies confirmed the transactivating effect of hc-Krox and decreased substantially COL1A1 transcription levels in all fibro-blast types. The -112/-61-bp sequence bound specifically hc-Krox but also Sp1 and CBF. Attempts to elucidate the potential interactions between hc-Krox, Sp1, and Sp3 revealed that all of them co-immunoprecipitate from FF cellular extracts when a c-Krox antibody was used and bind to the COL1A1 promoter in chromatin immunoprecipitation assays. Moreover, hc-Krox DNA binding activity to its COL1A1-responsive element is increased in SF, cells producing higher amounts of type I collagen compared with ANF and FF. These data suggest that the regulation of COL1A1 gene transcription in human dermal fibroblasts involves a complex machinery that implicates at least three transcription proteins, hc-Krox, Sp1, and Sp3, which could act in concert to up-regulate COL1A1 transcriptional activity and provide evidence for a pro-fibrotic role of hc-Krox