Failing Companies and the Antitrust Laws

This article will examine two areas in which the courts have given financially-troubled companies special treatment under the antitrust laws. Part I discusses the acquisition of a failing company, which may constitute a judicially-created exemption from section 7 of the Clayton Act. Part II considers certain cases involving failing companies whose conduct is challenged under section 1 of the Sherman Act

Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

We identified rare coding variants associated with Alzheimer’s disease (AD) in a 3-stage case-control study of 85,133 subjects. In stage 1, 34,174 samples were genotyped using a whole-exome microarray. In stage 2, we tested associated variants (P<1×10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, an additional 14,997 samples were used to test the most significant stage 2 associations (P<5×10-8) using imputed genotypes. We observed 3 novel genome-wide significant (GWS) AD associated non-synonymous variants; a protective variant in PLCG2 (rs72824905/p.P522R, P=5.38×10-10, OR=0.68, MAFcases=0.0059, MAFcontrols=0.0093), a risk variant in ABI3 (rs616338/p.S209F, P=4.56×10-10, OR=1.43, MAFcases=0.011, MAFcontrols=0.008), and a novel GWS variant in TREM2 (rs143332484/p.R62H, P=1.55×10-14, OR=1.67, MAFcases=0.0143, MAFcontrols=0.0089), a known AD susceptibility gene. These protein-coding changes are in genes highly expressed in microglia and highlight an immune-related protein-protein interaction network enriched for previously identified AD risk genes. These genetic findings provide additional evidence that the microglia-mediated innate immune response contributes directly to AD development

A novel Alzheimer disease locus located near the gene encoding tau protein

This is the author accepted manuscript. The final version is available from the publisher via the DOI in this recordAPOE ε4, the most significant genetic risk factor for Alzheimer disease (AD), may mask effects of other loci. We re-analyzed genome-wide association study (GWAS) data from the International Genomics of Alzheimer's Project (IGAP) Consortium in APOE ε4+ (10 352 cases and 9207 controls) and APOE ε4- (7184 cases and 26 968 controls) subgroups as well as in the total sample testing for interaction between a single-nucleotide polymorphism (SNP) and APOE ε4 status. Suggestive associations (P<1 × 10-4) in stage 1 were evaluated in an independent sample (stage 2) containing 4203 subjects (APOE ε4+: 1250 cases and 536 controls; APOE ε4-: 718 cases and 1699 controls). Among APOE ε4- subjects, novel genome-wide significant (GWS) association was observed with 17 SNPs (all between KANSL1 and LRRC37A on chromosome 17 near MAPT) in a meta-analysis of the stage 1 and stage 2 data sets (best SNP, rs2732703, P=5·8 × 10-9). Conditional analysis revealed that rs2732703 accounted for association signals in the entire 100-kilobase region that includes MAPT. Except for previously identified AD loci showing stronger association in APOE ε4+ subjects (CR1 and CLU) or APOE ε4- subjects (MS4A6A/MS4A4A/MS4A6E), no other SNPs were significantly associated with AD in a specific APOE genotype subgroup. In addition, the finding in the stage 1 sample that AD risk is significantly influenced by the interaction of APOE with rs1595014 in TMEM106B (P=1·6 × 10-7) is noteworthy, because TMEM106B variants have previously been associated with risk of frontotemporal dementia. Expression quantitative trait locus analysis revealed that rs113986870, one of the GWS SNPs near rs2732703, is significantly associated with four KANSL1 probes that target transcription of the first translated exon and an untranslated exon in hippocampus (P≤1.3 × 10-8), frontal cortex (P≤1.3 × 10-9) and temporal cortex (P≤1.2 × 10-11). Rs113986870 is also strongly associated with a MAPT probe that targets transcription of alternatively spliced exon 3 in frontal cortex (P=9.2 × 10-6) and temporal cortex (P=2.6 × 10-6). Our APOE-stratified GWAS is the first to show GWS association for AD with SNPs in the chromosome 17q21.31 region. Replication of this finding in independent samples is needed to verify that SNPs in this region have significantly stronger effects on AD risk in persons lacking APOE ε4 compared with persons carrying this allele, and if this is found to hold, further examination of this region and studies aimed at deciphering the mechanism(s) are warranted

Failing Companies and the Antitrust Laws

This article will examine two areas in which the courts have given financially-troubled companies special treatment under the antitrust laws. Part I discusses the acquisition of a failing company, which may constitute a judicially-created exemption from section 7 of the Clayton Act. Part II considers certain cases involving failing companies whose conduct is challenged under section 1 of the Sherman Act

High-dose vitamin C supplement use is associated with self-reported histories of breast cancer and other illnesses in the UK Women's Cohort Study.

To determine whether frequent vitamin C supplement use is associated with healthier behaviours, and a history of cancer and other illnesses in UK women

Post-Merger Product Repositioning

Abstract We study mergers among firms that compete by simultaneously choosing price and location. The merged firm moves its two products away from each other to reduce cannibalization, and the nonmerging firms move their products in between the merging firm&apos;s products. Post-merger repositioning increases product variety, which benefits consumers, but repositioning also affects post-merger prices in two ways: There is upward pressure on price as products spread out, but the merged firm&apos;s incentive to raise prices is reduced as its products are moved away from each other. Either effect can dominate, although the latter is likely to be the more important. We use a novel technique known as the stochastic response dynamic to find equilibria, which does not require the computation of first-order conditions. * The University of Chicago. The authors acknowledge useful comments from Simo

Ohio Child and Adolescent Sexual Abuse Protocol

Since development of the first protocol in 2000 developed by the Ohio American Academy of Pediatrics Committee on Child Abuse and Neglect in collaboration with the Ohio Department of Health and the Ohio Attorney General’s office, the field of child abuse pediatrics and the development of coordinated efforts to provide comprehensive, standardized, non-judgmental, equitable treatment of pediatric sexual abuse/assault has changed and improved. This protocol is a modification of the Ohio Department of Health Protocol For The Treatment Of Sexual Assault Survivors, and addresses many of the complex services necessary to facilitate consistent, comprehensive health care treatment to include emotional, social, and crisis intervention as well as provide information about available follow up services in the community

Ohio Child and Adolescent Sexual Abuse Protocol

Since development of the first protocol in 2000 developed by the Ohio American Academy of Pediatrics Committee on Child Abuse and Neglect in collaboration with the Ohio Department of Health and the Ohio Attorney General’s office, the field of child abuse pediatrics and the development of coordinated efforts to provide comprehensive, standardized, non-judgmental, equitable treatment of pediatric sexual abuse/assault has changed and improved. This protocol is a modification of the Ohio Department of Health Protocol For The Treatment Of Sexual Assault Survivors, and addresses many of the complex services necessary to facilitate consistent, comprehensive health care treatment to include emotional, social, and crisis intervention as well as provide information about available follow up services in the community