http://repub.eur.nl/res/aut/24667/ List of Publications en http://repub.eur.nl/static-eur/img/logo.png http://repub.eur.nl http://repub.eur.nl/res/pub/39698/ 2013-03-25T00:00:00Z In the present article, we argue that the constant pressure that leaders face may limit the willpower required to behave according to ethical norms and standards and may therefore lead to unethical behavior. Drawing upon the ego depletion and moral self-regulation literatures, we examined whether self-regulatory depletion that is contingent upon the moral identity of leaders may promote unethical leadership behavior. A laboratory experiment and a multisource field study revealed that regulatory resource depletion promotes unethical leader behaviors among leaders who are low in moral identity. No such effect was found among leaders with a high moral identity. This study extends our knowledge on why organizational leaders do not always conform to organizational goals. Specifically, we argue that the hectic and fragmented workdays of leaders may increase the likelihood that they violate ethical norms. This highlights the necessity to carefully schedule tasks that may have ethical implications. Similarly, organizations should be aware that overloading their managers with work may increase the likelihood of their leaders transgressing ethical norms. http://repub.eur.nl/res/pub/20515/ 2010-08-01T00:00:00Z We report two novel α2-globin gene mutations found in the same Surinamese family. The proband, a newborn presenting during neonatal screening with 21.3 Hb Bart's (γ4), proved to be a carrier of the common α3.7 deletion and a novel codon 32 (ATG>AGG) transversion that we named Hb Rotterdam. The father carried the same point mutation with borderline hemoglobin (Hb), MCV and low MCH values. The mother presented with a significant microcytic hypochromic anemia and also carried the α3.7 deletion and a second novel TAT>TAG transversion generating a stop codon at position 24. Shortly thereafter, Hb Rotterdam was again found in two unrelated adult females and in a Canadian newborn, all of African origin, suggesting that Hb Rotterdam could be a frequently occurring αT determinant in the Black population. Screening and characterization of the mutations, phenotypegenotype correlation and the issue of reporting newborn carriers of α-thalassemia (α-thal) are discussed. http://repub.eur.nl/res/pub/32063/ 2002-12-18T00:00:00Z Leukemia is characterised by an accumulation in the bone marrow of non-functional blood cells arrested at a particular stage of differentiation. In the process of normal hematopoiesis, errors may occur as the result of mutations in the DNA of hematopoietic precursor cells. These genetic lesions may lead to activation of protooncogenes, inactivation of tumour suppressor genes or expression of aberrant gene products. The combination of different genetic lesions in a hematopoietic progenitor cell may ultimately result in the development of leukemia. An approach to find leukemia disease genes is the identification and cloning of common virus integration sites in murine leukemias. This approach has proven to be a sensitive tool to identify novel proto-oncogenes as well as tumour suppressor genes. We used the slow transforming retrovirus Cas-Br-M murine leukemia virus (Cas-BrM MuL V) in NIH/Swiss mice to establish a panel of leukemias (Chapter 2). All tumours found in leukemic animals were classified by gross pathology, morphology, and immunophenotype as well as the incidence of known common virus integration sites in murine leukemia virus-induced myeloid malignancies, i.e., Evil [ 1], Evill/C b 2 [2], Evi 12 [3], Flil [ 4] and c-Myb [5]. While most of the immunophenotyped Cas-Br-M MuLV induced tumours were of myeloid origin (58%), also numerous T -cell leukemias (21%) and mixed myeloid/T -cell leukemias (21%) were found. The myeloid leukemias and myeloid compartment of the mixed leukemias were further characterised by immunophenotyping with stem cell-, myeloid- and erythroid-specific antibodies. The known Cas-Br-M MuLV common vims integration sites Evil, Evill/Cb2 and Evil2 were demonstrated in 19%, 12% and 20% of the cases, respectively, whereas no Flil or c-Myb rearrangements were found. Integrations into Evil were restricted to myeloid leukemias, whereas those in Evill/Cb2 and Evil2 were identified in myeloid as well as T -lymphoid leukemias. This panel of well-characterised Cas-Br-M MuL V -induced hematopoietic tumours may be useful for the isolation and characterisation of new proto-oncogenes involved in murine myeloid or T -cell leukemias