36 research outputs found

    Empirical evidence on vertical foreclosure

    Get PDF
    Recent papers have shown conditions under which vertical, mergers can result in anticompetitive foreclosure of unintegrated rivals. These models imply that a necessary but not sufficient condition for anticompetitive foreclosure is that unintegrated rivals are less profitable after a vertical merger. We test this hypothesis by examining the stock prices of unintegrated rivals at the time of a vertical merger announcement and at the time of a government antitrust complaint. We find no evidence to support the foreclosure hypothesis.Consolidation and merger of corporations

    De Novo Truncating Mutations in WASF1 Cause Intellectual Disability with Seizures.

    Get PDF
    Next-generation sequencing has been invaluable in the elucidation of the genetic etiology of many subtypes of intellectual disability in recent years. Here, using exome sequencing and whole-genome sequencing, we identified three de novo truncating mutations in WAS protein family member 1 (WASF1) in five unrelated individuals with moderate to profound intellectual disability with autistic features and seizures. WASF1, also known as WAVE1, is part of the WAVE complex and acts as a mediator between Rac-GTPase and actin to induce actin polymerization. The three mutations connected by Matchmaker Exchange were c.1516C>T (p.Arg506Ter), which occurs in three unrelated individuals, c.1558C>T (p.Gln520Ter), and c.1482delinsGCCAGG (p.Ile494MetfsTer23). All three variants are predicted to partially or fully disrupt the C-terminal actin-binding WCA domain. Functional studies using fibroblast cells from two affected individuals with the c.1516C>T mutation showed a truncated WASF1 and a defect in actin remodeling. This study provides evidence that de novo heterozygous mutations in WASF1 cause a rare form of intellectual disability

    Biallelic Mutation of ARHGEF18, Involved in the Determination of Epithelial Apicobasal Polarity, Causes Adult-Onset Retinal Degeneration

    Get PDF
    Mutations in more than 250 genes are implicated in inherited retinal dystrophy; the encoded proteins are involved in a broad spectrum of pathways. The presence of unsolved families after highly parallel sequencing strategies suggests that further genes remain to be identified. Whole-exome and -genome sequencing studies employed here in large cohorts of affected individuals revealed biallelic mutations in ARHGEF18 in three such individuals. ARHGEF18 encodes ARHGEF18, a guanine nucleotide exchange factor that activates RHOA, a small GTPase protein that is a key component of tight junctions and adherens junctions. This biological pathway is known to be important for retinal development and function, as mutation of CRB1, encoding another component, causes retinal dystrophy. The retinal structure in individuals with ARHGEF18 mutations resembled that seen in subjects with CRB1 mutations. Five mutations were found on six alleles in the three individuals: c.808A>G (p.Thr270Ala), c.1617+5G>A (p.Asp540Glyfs∗63), c.1996C>T (p.Arg666∗), c.2632G>T (p.Glu878∗), and c.2738_2761del (p.Arg913_Glu920del). Functional tests suggest that each disease genotype might retain some ARHGEF18 activity, such that the phenotype described here is not the consequence of nullizygosity. In particular, the p.Thr270Ala missense variant affects a highly conserved residue in the DBL homology domain, which is required for the interaction and activation of RHOA. Previously, knock-out of Arhgef18 in the medaka fish has been shown to cause larval lethality which is preceded by retinal defects that resemble those seen in zebrafish Crumbs complex knock-outs. The findings described here emphasize the peculiar sensitivity of the retina to perturbations of this pathway, which is highlighted as a target for potential therapeutic strategies

    Telomerecat: A ploidy-agnostic method for estimating telomere length from whole genome sequencing data (vol 8, 1300, 2018)

    Get PDF

    Antitrust policy and vertical mergers

    No full text
    Recently, federal regulators responsible for enforcing the antitrust laws have shown a renewed interest in the potential anticompetitive effects of vertical mergers--mergers between two independent firms in successive stages of production. This greater activism in vertical merger cases is in striking contrast to the permissive policies that prevailed throughout the 1980s, which, in turn, were a response to the Justice Department's and the Federal Trade Commission's open hostility to vertical mergers during the 1960s and 1970s.> The cyclical antitrust treatment of vertical mergers over the past three and one-half decades has been strongly influenced by the theoretical research of academic economists and lawyers. This article examines the empirical evidence of anticompetitive foreclosure in vertical mergers challenged by the Justice Department and the Federal Trade Commission during the period from 1963 to 1982. The authors find no evidence of anticompetitive market foreclosure for the sample of vertical merger cases challenged by the antitrust agencies during this period. They suggest that a more permissive policy towards vertical mergers be maintained until the theory can spell out more clearly the circumstances when vertical mergers result in anticompetitive foreclosure.Antitrust law ; Consolidation and merger of corporations

    Response to Coyne et al

    No full text
    The Coyne, Issacs, and Schwartz comment appears to rest on a fundamental misunderstanding of the difference between a critique and an original work.discrimination; baseball

    Business failures in New England

    No full text
    During the 1980s, the New England economy prospered relative to the nation as a whole, with lower unemployment rates, more rapidly rising real estate prices, and lower rates of business failures. As the economic tide turned against New England at the end of the decade, the rate of business failures soared, in absolute terms as well as relative to nationwide statistics. This recent wave of business failures appears to have been far in excess of that attributable to the decline in New England economic activity. Moreoever, it has undesirable implications for the regional economy and can be expected to slow economic recovery in the area. The authors explore several explanations for the increase in business failures, including employment losses, industry mix effects, and credit availability. Their findings suggest that difficulties in the banking sector have contributed significantly to the very high rate of business failures in New England.Business failures ; New England
    corecore