Analyst vs. Market Forecasts of Earnings Management to Avoid Small Losses

Burgstahler and Eames (2003) present evidence that analysts commonly anticipate earnings management to avoid small losses, but often incorrectly predict its occurrence. Here we consider whether the market\u27s behavior mimics that of analysts. Our results suggest that analysts exhibit more forecast optimism in their zero earnings forecasts than in their other small earnings forecast levels, and markets exhibit less relative optimism at this point. At the 271-360 day forecast horizon, we find a reduction in the earnings response coefficient at analysts\u27 zero earnings forecasts and interpret this as reflecting less optimism in market earnings forecasts than in analyst forecasts when analysts forecast zero earnings. This evidence is consistent with the market not following analysts in erroneously predicting earnings management to avoid small losses. We do not find similar evidence for shorter forecast horizons, suggesting that market and analyst forecasts converge towards the end of the year. Finding differences in market and analyst earnings forecasts in this loss avoidance environment raises the possibility of differences in a variety of earnings management and other environments, and sends a general note of caution in using analyst forecasts issued early in the year to proxy market expectations. JEL Classification: M41, G14, G24

Germline Mutations in NFKB2 Implicate the Noncanonical NF-κB Pathway in the Pathogenesis of Common Variable Immunodeficiency

Common variable immunodeficiency (CVID) is a heterogeneous disorder characterized by antibody deficiency, poor humoral response to antigens, and recurrent infections. To investigate the molecular cause of CVID, we carried out exome sequence analysis of a family diagnosed with CVID and identified a heterozygous frameshift mutation, c.2564delA (p.Lys855Serfs∗7), in NFKB2 affecting the C terminus of NF-κB2 (also known as p100/p52 or p100/p49). Subsequent screening of NFKB2 in 33 unrelated CVID-affected individuals uncovered a second heterozygous nonsense mutation, c.2557C>T (p.Arg853∗), in one simplex case. Affected individuals in both families presented with an unusual combination of childhood-onset hypogammaglobulinemia with recurrent infections, autoimmune features, and adrenal insufficiency. NF-κB2 is the principal protein involved in the noncanonical NF-κB pathway, is evolutionarily conserved, and functions in peripheral lymphoid organ development, B cell development, and antibody production. In addition, Nfkb2 mouse models demonstrate a CVID-like phenotype with hypogammaglobulinemia and poor humoral response to antigens. Immunoblot analysis and immunofluorescence microscopy of transformed B cells from affected individuals show that the NFKB2 mutations affect phosphorylation and proteasomal processing of p100 and, ultimately, p52 nuclear translocation. These findings describe germline mutations in NFKB2 and establish the noncanonical NF-κB signaling pathway as a genetic etiology for this primary immunodeficiency syndrome

Expanded Instrument Comparison of Amplicon DNA Melting Analysis for Mutation Scanning and Genotyping,

purification and characterization of adiponectin multimer species fro