We hypothesize that if individual auditors possess unique audit styles that they consistently apply to different audit engagements, then client firms with a common signing auditor will exhibit higher earnings comparability. Using a large sample of Chinese firms, we find that client firms report more comparable earnings when they are audited by the same individual auditor than when they are audited by (1) different audit firms, (2) the same audit firm, but different audit offices, and (3) the same audit office, but different individual auditors. The individual auditor style effect is stronger for larger audit firms, senior signing auditors, and signing auditors with more stable teamwork experience. We also document that having a common signing auditor is associated with lower analyst earnings forecast error and dispersion for client firms. This study contributes to the literature by showing that individual auditors have a significant impact on client firms' earnings comparability.

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myoblast city (mbc), a member of the CDM superfamily, is essential in the Drosophila melanogaster embryo for fusion of myoblasts into multinucleate fibers. Using germ line clones in which both maternal and zygotic contributions were eliminated and rescue of the zygotic loss-of-function phenotype, we established that mbc is required in the fusion-competent subset of myoblasts. Along with its close orthologs Dock180 and CED-5, MBC has an SH3 domain at its N terminus, conserved internal domains termed DHR1 and DHR2 (or "Docker"), and C-terminal proline-rich domains that associate with the adapter protein DCrk. The importance of these domains has been evaluated by the ability of MBC mutations and deletions to rescue the mbc loss-of-function muscle phenotype. We demonstrate that the SH3 and Docker domains are essential. Moreover, ethyl methanesulfonate-induced mutations that change amino acids within the MBC Docker domain to residues that are conserved in other CDM family members nevertheless eliminate MBC function in the embryo, which suggests that these sites may mediate interactions specific to Drosophila MBC. A functional requirement for the conserved DHR1 domain, which binds to phosphatidylinositol 3,4,5-triphosphate, implicates phosphoinositide signaling in myoblast fusion. Finally, the proline-rich C-terminal sites mediate strong interactions with DCrk, as expected. These sites are not required for MBC to rescue the muscle loss-of-function phenotype, however, which suggests that MBC's role in myoblast fusion can be carried out independently of direct DCrk binding.In Drosophila melanogaster, formation of multinucleate muscle fibers occurs between two distinct myoblast populations, termed founder and fusion-competent cells, and is mediated by cell adhesion molecules specific to each of these cell types (1,3,38,41). Genes such as myoblast city (mbc) encode proteins that appear to function downstream of these cell surface receptors to regulate intracellular and cytoskeletal events through the activation of small GTPases (8). Embryos homozygous for mutations in the mbc locus exhibit severe defects in myoblast fusion, with a large number of unfused mononucleate myoblasts in place of multinucleate muscle fibers (14, 39).MBC was a founding member of the CDM superfamily, which includes human Dock180 (20), Caenorhabditis elegans CED-5 (43), and almost 20 additional members in a wide variety of species (13, 17). Dock180 was originally identified as a major binding partner for the adapter protein Crk (20), while CED-5 and MBC were identified on the basis of their loss-offunction phenotypes. All three proteins are characterized by an SH3 domain at their N terminus, internal dock homology region 1 (DHR1) and dock homology region 2 (DHR2) (or Docker) domains, and proline-rich sites in their C termini that bind to the SH2-SH3 adapter protein Crk. Vertebrate Dock180 binds to Rac1 in a nucleotide-independent manner and increases the amount of GTP-bound Rac1 (24). Deletion of the Docker domain results in loss of Rac binding and ...

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Dissatisfaction with body image, greater symptom severity, and hypopharyngeal and laryngeal cancer are predictive of the amount HNC patients speak, as compared with the amount they spoke before having HNC. Clinicians should be aware of and systematically assess communication problems of HNC patients to promote their social function. Further research on interventions that facilitate the development of a positive body image and communication is strongly suggested.