Occupational depression in a Spanish-speaking sample: Associations with cognitive performance and work-life characteristics

This 386-participant study investigated the structural and psychometric properties of the Spanish version of the Occupational Depression Inventory (ODI). Exploratory structural equation modeling bifactor analysis revealed that the ODI meets the requirements for essential unidimensionality. Measurement invariance held across our sample and the English- and French-speaking samples used in the ODI’s initial validation study. Mokken scale analysis indicated that (a) the scalability of the instrument was strong, (b) no violations of monotonicity or local independence were present, and (c) invariant item ordering was sufficiently accurate. The ODI’s reliability was optimal. The ODI exhibited both convergent validity and discriminant validity vis-à-vis a job-unrelated measure of depression. Furthermore, occupational depression correlated substantially, and in the expected direction, with objective cognitive performance and 10 widely studied worklife characteristics. This study suggests that the ODI’s Spanish version has excellent structural and psychometric properties and can be confidently employed by occupational health specialists

Lung adenocarcinomas induced in mice by mutant EGF receptors foundin human lung cancers respondto a tyrosine kinase inhibitor orto down-regulation of the receptors

Somatic mutations in exons encoding the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) gene are found in human lung adenocarcinomas and are associated with sensitivity to the tyrosine kinase inhibitors gefitinib and erlotinib. Nearly 90% of the EGFR mutations are either short, in-frame deletions in exon 19 or point mutations that result in substitution of arginine for leucine at amino acid 858 (L858R). To study further the role of these mutations in the initiation and maintenance of lung cancer, we have developed transgenic mice that express an exon 19 deletion mutant (EGFR(ΔL747–S752)) or the L858R mutant (EGFR(L858R)) in type II pneumocytes under the control of doxycycline. Expression of either EGFR mutant leads to the development of lung adenocarcinomas. Two weeks after induction with doxycycline, mice that express the EGFR(L858R) allele show diffuse lung cancer highly reminiscent of human bronchioloalveolar carcinoma and later develop interspersed multifocal adenocarcinomas. In contrast, mice expressing EGFR(ΔL747–S752) develop multifocal tumors embedded in normal lung parenchyma with a longer latency. With mice carrying either EGFR allele, withdrawal of doxycycline (to reduce expression of the transgene) or treatment with erlotinib (to inhibit kinase activity) causes rapid tumor regression, as assessed by magnetic resonance imaging and histopathology, demonstrating that mutant EGFR is required for tumor maintenance. These models may be useful for developing improved therapies for patients with lung cancers bearing EGFR mutations