Strategic Interaction in the Sex Market

There have been few attempts to empirically explain the pursuit of short term relationships and sex in a formal context. Previous work has lamented the paucity of empirical studies which utilize incentive driven behavior to draw conclusions and recommend policy. We develop a model of social network formation through sexual matching, provide an empirical approach derived from the model and apply it to a population of high interest. Specifically, we apply the approach to a population of sexually active men who have sex with men (MSM) in a large metropolitan area and derive qualitative conclusions regarding how individuals behave in the marketplace for sex

Left, Right, Left: Income and Political Dynamics in Transition Economies

The political left turn in Latin America, which lagged its transition to liberalized market economies by a decade or more, challenges conventional economic explanations of voting behavior. While the implications of upward mobility for the political preferences of forward-looking voters have been studied, neither the upward mobility model nor conventional myopic median voter models are well equipped to explain Latin America's political transformation. This paper generalizes the forward-looking voter model to consider a broad range of dynamic processes. When voters have full information on the nature of income dynamics in a transition economy, we show that strong support for redistributive policies will materialize rapidly if income dynamics offer few prospects of upward mobility for key sections of the electorate. In contrast, when voters have imperfect information, our model predicts a slow and politically polarizing shift toward redistributive voter preferences under these same non-concave income dynamics. Simulation using fitted income dynamics for two Latin American economies suggests that the imperfect information model better accounts for the observed shift back to the left in Latin America, and that this generalized, forward-looking voter approach may offer additional insights about political dynamics in other transition economies.income dynamics, redistributive politics, polarization, Bayesian learning, Latin America

Credit Derivatives

Credit derivatives are a useful tool for lenders who want to reduce their exposure to a particular borrower but are unwilling to sell their claims on that borrower. Without actually transferring ownership of the underlying assets, these contracts transfer risk from one counterparty to another. Commercial banks are the major participants in this growing market, using these transactions to diversify their portfolios of loans and other risky assets. The authors examine the size and workings of this relatively new market and discuss the potential of these transactions for distorting existing incentives for risk management and risk monitoring.

Benford's Law, families of distributions and a test basis

Benford's Law is used to test for data irregularities. While novel, there are two weaknesses in the current methodology. First, test values used in practice are too conservative and the test values of this paper are more powerful and hold for fairly small samples. Second, testing requires Benford's Law to hold, which it often does not. I present a simple method to transform distributions to satisfy the Law with arbitrary precision and induce scale invariance, freeing tests from the choice of units. I additionally derive a rate of convergence to Benford's Law. Finally, the results are applied to common distributions

Discovery and effects of pharmacological inhibition of the E3 ligase Skp2 by small molecule protein-protein interaction disruptors

Skp2 (S-phase kinase-associated protein 2), one component of the SCF E3 ubiquitin ligase complex, directly interacts with Skp1 and indirectly associates with Cullin1 and Rbx1 to bridge the E2 conjugating enzyme with its protein substrate to execute its E3 ligase activity. Skp2 is an Fbox protein (due to it containing an Fbox domain) and it is the rate-limiting component of the SCF complex. Skp2 targets several cell-cycle regulatory proteins for ubiquitination and degradation; most notable and significant for cancer are the cyclin-dependent kinase inhibitor, p27. Skp2 is an oncogene and studies have shown that over-expression of Skp2 leads to increased degradation of p27 and increased proliferation in several tumor types. Additionally, Skp2 is over-expressed in multiple human cancers. Clearly, Skp2 represents an attractive target for attenuating p27 ubiquitination and subsequent cell cycle progression. However, Skp2 does not have an easily identifiable and druggable “pocket” on which small molecules can bind; it interacts with Skp1 through the Fbox domain and binds to an accessory protein called Cks1 to bind to p27. Despite this hurdle, in this study, two selective small molecule inhibitors of the Skp2 SCF complex were discovered via an in silico screen that disrupt two places: the Skp1/Skp2 interaction site and the p27 binding site via targeting hot-spot residues. The Skp1/Skp2 inhibitor disruption resulted in restoring p27 levels in the nucleus and blocks cancer progression and cancer stem cell traits. Additionally, the inhibitors phenocopy the effects of genetic Skp2 deficiency. Two specific residues on Skp2 were predicted to bind to this Skp1/Skp2 inhibitor: Trp97 and Asp98. When these residues were mutated to alanine, the inhibitor lost its ability to bind to Skp2. To investigate the flexibility and understand the conformational change upon inhibitor binding and dynamics of the SCF complex, molecular dynamics simulations, homology models, and structural analysis was carried out on the complex with and without the inhibitors. These simulations showed that the contributions of the N-terminal tail region of Skp2 does not contribute directly to the binding of these inhibitors; but its conformation is important in the context of the other members of the SCF complex. Further dynamics analysis validated the mutagenesis results, showing that the two Skp2 mutants (Trp97Ala, Asp98Ala) that retained Skp1 binding but blocked inhibitor binding were stable, whereas the mutant that was unable to retain Skp1 binding (Trp127Ala) showed destabilization in the Fbox domain. Finally, active recruitment events after post-translational modifications are shown to be possible by the interaction of phosphorylated Ser256 on Skp2 with Lys104 loop region on Cul1 The model shows that this is due to the significant flexibility in the F-box domain of Skp2, making this interaction very likely. These results show that Skp2 is a promising target on which protein-protein interaction disruptors can be designed, and consideration of the dynamics of protein complexes is required to understand ligand binding

Russia as a factor of growing importance in the world economic structure

This item was digitized by the Internet Archive

Analysis of the LAT Promoter of Herpes Simplex Virus Type 1

A major feature of the biology of herpes simplex virus type 1 (HSV-1) is it's capacity to establish a latent infection in peripheral nervous system ganglionic neurons and to periodically reactivate to produce recrudescent disease. Until recently the extent and the nature of any expression from latent HSV genomes was unknown. In 1987, latency associated transcripts (LATs) were detected in murine ganglia which were latently infected with HSV-1. The LATs map to the long repeat region and are transcribed in the opposite direction to and partially overlap with IE-1 mRNA. Subsequent work has refined our knowledge of the HSV-1 LATs and shown that transcripts associated with latency are also encoded by a number of other herpesviruses including pseudorabies virus in swine and bovine herpes virus in rabbits. It is now known that the HSV-1 LATs comprise at least 3 overlapping non-polyadenylated RNAs which share common 5' and 3' ends, but differ in size through differential splicing. These LAT species are thought to be stable introns or stable processing products of a less stable 8.3 kb (m-LAT) polyadenylated primary transcript. Since LAT appears to be the only actively transcribed gene during latency, the control of LAT gene expression must differ considerably from that of any of the lytic cycle genes. A great deal of attention has thus been focussed on the LAT promoter in order to identify cis-acting sequences responsible for this unique pattern of transcription. In this study, in order to determine the location of the LAT promoter, various sequences upstream from the 2 kb LATs were cloned and examined for their ability to drive expression of an adjoining reporter gene in transient expression assays in a plasmid expression vector. The response of these sequences to the presence of HSV-1 trans- acting factors was also examined by infecting cells transfected with the various LAT promoter/CAT fusion constructs. Both the promoter and HSV-1 responsive elements mapped to a 137 bp region 800 bp upstream from the 5' end of the 2kb LATs. Sequence analysis of this region demonstrated that it contained several homologies to recognised promoter elememts including a TATA box, a CAAT box and two putative Sp1 binding sites. Comparison of this region to the corresponding region of the HSV-2 genome revealed that while the 2kb LAT transcription unit itself is completely unconserved, the putative LAT promoter region bears several interesting conserved loci, possibly indicative of the presence of enhancer like elements responsible for tissue-specific expression of the LAT gene. Several of the LAT promoter/CAT fusion constructs were examined in the context of the virus genome by use of a virus vector whereby DNA sequences of interest are introduced into the viral genome by direct ligation. To facilitate this analysis, the parental vector was modified by deletion of the endogenous LAT sequences, thereby preventing possible rearrangments of the viral genome by homologous recombination between the endogenous and introduced LAT promoter sequences. These recombinant viruses were subsequently used for analysis of the LAT promoter during infection of tissue culture cell lines. The most significant result to come from these studies was the finding that sequences upstream from the core LAT promoter, while not having any effect on LAT promoter strength in BHK cells, considerably enhanced LAT promoter strength in C1300 neuroblastoma cells, thereby suggesting that these sequences harbour neuronal specific enhancer elements. In addition to studying the LAT promoter, it was considered interesting to examine the behaviour of an endogenous neuronal specific promoter when introduced into the virus genome. To this end, the 5' flanking region of the human neurofilament-light chain gene was obtained, and two constructs, extending from -296 to +84 and -896 to +84 of the HNF-L promoter fused to the CAT reporter gene were made. Transient transfection assays showed that these constructs performed at least as well as the HSV-1 gD promoter, and were similarly strongly trans-activated upon infection of transfected cells with HSV-1. Introduction of the HNF-L/CAT fusions into the HSV-1 genome, and subsequent examination of these constructs during infection of tissue culture cell lines revealed that sequences upstream from -296, while only moderately enhancing promoter activity in BHK cells, had a greater effect in C1300 neuroblastoma cells, thereby suggesting that these sequences perhaps also containied neuronal specific enhancer elements. The original aim of these studies was to examine promoter/reporter gene activity of the various recombinant viruses in animal latency systems. However, due to lack of time and the necessity of replacing the CAT with the lacZ reporter gene for reasons of sensitivity, these studies were unable to be carried out. One virus which was available, (vFJ12) containing the HSV-2 IE-4/5 promoter fused to the lad reporter gene was used in animal latency studies. In situ analysis showed that the parental virus vector expressed LAT in latently infected murine sensory ganglia, thereby demonstrating that this virus could establish latency in this system. (Abstract shortened by ProQuest.)

Criminal Law - Due Process - Public Policy as Valid Grounds for Denying Recovery of Proceeds of Illegal Act

Plaintiff collected a $10 fee from a number of persons for the privilege of attending a farm outing and photographing female models, some of whom posed in the nude. The sheriff arrested all concerned. Plaintiff pleaded guilty to a charge of outraging public decency and was fined$50. The others were found guilty of disorderly conduct. Plaintiff brought a trover action against the sheriff who had kept the money ($149) which the plaintiff had collected, but the trial court dismissed the action. On appeal to the New York Court of Appeals, held, affirmed, one judge dissenting. Plaintiff could not invoke the aid of the courts to regain the proceeds of his illegal act. Carr v. Hoy, 2 N.Y. (2d) 185, 158 N.Y.S. (2d) 572 (1957)