505 research outputs found

    Auctioned IPOs: The U.S. Evidence

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    Between 1999 and 2007, WR Hambrecht has completed 19 IPOs in the U.S. using an auction mechanism. We analyze investor behavior and mechanism performance in these auctioned IPOs using detailed bidding data. The existence of some bids posted at high prices suggests that some investors (mostly retail) try to free-ride on the mechanism. But institutional demand in these auctions is very elastic, suggesting that institutional investors reveal information in the bidding process. Investor participation is largely predictable based on deal size, and demand is dominated by institutions. Flipping is equally prevalent in auctions as in bookbuilt deals – but unlike in bookbuilding, investors in auctions tend to flip their shares more in cold deals. Finally, we find that institutional investors, who provide more information, are rewarded by obtaining a larger share of the deals that have higher initial returns. Our results therefore suggest that auctioned IPOs could be an effective alternative to traditional bookbuilding.Initial public offerings;investment banking;auctions

    Auctioned IPOs:The U.S. Evidence

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    Artificial Intelligence Approach to the Determination of Physical Properties of Eclipsing Binaries. I. The EBAI Project

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    Achieving maximum scientific results from the overwhelming volume of astronomical data to be acquired over the next few decades will demand novel, fully automatic methods of data analysis. Artificial intelligence approaches hold great promise in contributing to this goal. Here we apply neural network learning technology to the specific domain of eclipsing binary (EB) stars, of which only some hundreds have been rigorously analyzed, but whose numbers will reach millions in a decade. Well-analyzed EBs are a prime source of astrophysical information whose growth rate is at present limited by the need for human interaction with each EB data-set, principally in determining a starting solution for subsequent rigorous analysis. We describe the artificial neural network (ANN) approach which is able to surmount this human bottleneck and permit EB-based astrophysical information to keep pace with future data rates. The ANN, following training on a sample of 33,235 model light curves, outputs a set of approximate model parameters (T2/T1, (R1+R2)/a, e sin(omega), e cos(omega), and sin i) for each input light curve data-set. The whole sample is processed in just a few seconds on a single 2GHz CPU. The obtained parameters can then be readily passed to sophisticated modeling engines. We also describe a novel method polyfit for pre-processing observational light curves before inputting their data to the ANN and present the results and analysis of testing the approach on synthetic data and on real data including fifty binaries from the Catalog and Atlas of Eclipsing Binaries (CALEB) database and 2580 light curves from OGLE survey data. [abridged]Comment: 52 pages, accepted to Ap

    Neurology

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    Contains reports on six research projects.U. S. Public Health Service (B-3055-4, B-3090-4, MH-06175-02)U. S. Air Force (AF49(638)-1313)U.S. Navy. Office of Naval Research (Nonr-1841(70)

    Gαi2- and Gαi3-Specific Regulation of Voltage-Dependent L-Type Calcium Channels in Cardiomyocytes

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    BACKGROUND: Two pertussis toxin sensitive G(i) proteins, G(i2) and G(i3), are expressed in cardiomyocytes and upregulated in heart failure. It has been proposed that the highly homologous G(i) isoforms are functionally distinct. To test for isoform-specific functions of G(i) proteins, we examined their role in the regulation of cardiac L-type voltage-dependent calcium channels (L-VDCC). METHODS: Ventricular tissues and isolated myocytes were obtained from mice with targeted deletion of either Gα(i2) (Gα(i2) (-/-)) or Gα(i3) (Gα(i3) (-/-)). mRNA levels of Gα(i/o) isoforms and L-VDCC subunits were quantified by real-time PCR. Gα(i) and Ca(v)α(1) protein levels as well as protein kinase B/Akt and extracellular signal-regulated kinases 1/2 (ERK1/2) phosphorylation levels were assessed by immunoblot analysis. L-VDCC function was assessed by whole-cell and single-channel current recordings. RESULTS: In cardiac tissue from Gα(i2) (-/-) mice, Gα(i3) mRNA and protein expression was upregulated to 187 ± 21% and 567 ± 59%, respectively. In Gα(i3) (-/-) mouse hearts, Gα(i2) mRNA (127 ± 5%) and protein (131 ± 10%) levels were slightly enhanced. Interestingly, L-VDCC current density in cardiomyocytes from Gα(i2) (-/-) mice was lowered (-7.9 ± 0.6 pA/pF, n = 11, p<0.05) compared to wild-type cells (-10.7 ± 0.5 pA/pF, n = 22), whereas it was increased in myocytes from Gα(i3) (-/-) mice (-14.3 ± 0.8 pA/pF, n = 14, p<0.05). Steady-state inactivation was shifted to negative potentials, and recovery kinetics slowed in the absence of Gα(i2) (but not of Gα(i3)) and following treatment with pertussis toxin in Gα(i3) (-/-). The pore forming Ca(v)α(1) protein level was unchanged in all mouse models analyzed, similar to mRNA levels of Ca(v)α(1) and Ca(v)β(2) subunits. Interestingly, at the cellular signalling level, phosphorylation assays revealed abolished carbachol-triggered activation of ERK1/2 in mice lacking Gα(i2). CONCLUSION: Our data provide novel evidence for an isoform-specific modulation of L-VDCC by Gα(i) proteins. In particular, loss of Gα(i2) is reflected by alterations in channel kinetics and likely involves an impairment of the ERK1/2 signalling pathway
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