Multi-player and multi-round auctions with severely bounded communication. ESA

Abstract. We study auctions in which bidders have severe constraints on the size of messages they are allowed to send to the auctioneer. In such auctions, each bidder has a set of k possible bids (i.e. he can send up to t = log(k) bits to the mechanism). This paper studies the loss of economic efficiency and revenue in such mechanisms, compared with the case of unconstrained communication. For any number of players, we present auctions that incur an efficiency loss and a revenue loss of O ( 1 k 2), and we show that this upper bound is tight. When we allow the players to send their bits sequentially, we can construct even more efficient mechanisms, but only up to a factor of 2 in the amount of communication needed. We also show that when the players ’ valuations for the item are not independently distributed, we cannot do much better than a trivial mechanism.

Auctions with Severely Bounded Communication

We study auctions with severe bounds on the communication allowed: each bidder may only transmit t bits of information to the auctioneer. We consider both welfare- and profit-maximizing auctions under this communication restriction. For both measures, we determine the optimal auction and show that the loss incurred relative to unconstrained auctions is mild. We prove non-surprising properties of these kinds of auctions, e.g., that in optimal mechanisms bidders simply report the interval in which their valuation lies in, as well as some surprising properties, e.g., that asymmetric auctions are better than symmetric ones and that multi-round auctions reduce the communication complexity only by a linear factor. 1

Auctions with Severely Bounded Communication

We study auctions with severe bounds on the communication allowed: each bidder may only transmit t bits of information to the auctioneer. We consider both welfare-maximizing and prot-maximizing auctions under this communication restriction. For both measures, we determine the optimal auction and show that the loss incurred relative to unconstrained auctions is mild. We prove non-surprising properties of these kinds of auctions, e.g., that in optimal mechanisms bidders simply report the interval in which their valuation lies in, as well as some surprising properties, e.g., that asymmetric auctions are better than symmetric ones and that multi round auctions reduce the communication complexity only by a linear factor

Dock10 Regulates Cardiac Function under Neurohormonal Stress

Dedicator of cytokinesis 10 (Dock10) is a guanine nucleotide exchange factor for Cdc42 and Rac1 that regulates the JNK (c-Jun N-terminal kinase) and p38 MAPK (mitogen-activated protein kinase) signaling cascades. In this study, we characterized the roles of Dock10 in the myocardium. In vitro: we ablated Dock10 in neonatal mouse floxed Dock10 cardiomyocytes (NMCMs) and cardiofibroblasts (NMCFs) by transduction with an adenovirus expressing Cre-recombinase. In vivo, we studied mice in which the Dock10 gene was constitutively and globally deleted (Dock10 KO) and mice with cardiac myocyte-specific Dock10 KO (Dock10 CKO) at baseline and in response to two weeks of Angiotensin II (Ang II) infusion. In vitro, Dock10 ablation differentially inhibited the α-adrenergic stimulation of p38 and JNK in NMCM and NMCF, respectively. In vivo, the stimulation of both signaling pathways was markedly attenuated in the heart. The Dock10 KO mice had normal body weight and cardiac size. However, echocardiography revealed mildly reduced systolic function, and IonOptix recordings demonstrated reduced contractility and elevated diastolic calcium levels in isolated cardiomyocytes. Remarkably, Dock10 KO, but not Dock10 CKO, exaggerated the pathological response to Ang II infusion. These data suggest that Dock10 regulates cardiac stress-related signaling. Although Dock10 can regulate MAPK signaling in both cardiomyocytes and cardiofibroblasts, the inhibition of pathological cardiac remodeling is not apparently due to the Dock10 signaling in the cardiomyocyte