Integrating knowledge management in the context of evidence based learning: two concept models for facilitating the assessment and acquisition of job knowledge

Within the field of Human Resource Management (HRM), the role of individual knowledge has received limited research attention despite offering the promise of superior job performance and improved managerial decision-making. In part, this lack of research may be attributed to the difficulty and laboriousness inherent to the adequate and accurate modeling of job relevant knowledge, particularly since such knowledge by definition varies from job to job. Despite this caveat, there is much to be gained from a knowledge based approach to (managing) human resources. The current paper presents two ontology based concepts for modeling job relevant knowledge, namely Meta-Practitioner and Med-Assess. The former focuses on availing to a practitioner audience the evidence that has accumulated in the academic literature, whereas the latter focuses on the facilitation of personnel selection and training in the medical field through a detailed assessment of individual job knowledge and general mental ability. Ultimately both concepts are aimed at knowledge provision to job applicants and incumbents alike. Having discussed the concepts, the paper summarizes the gains that may be expected from their implementation by presenting an integrated framework. The framework focuses on integrating aspects of Knowledge Management (KM) in the context of Evidence Based Learning (EBL) for business organizations. The paper concludes by addressing the challenges that lie ahead, highlighting some of the limitations of this approach and offering suggestions for further research

Contribution of c-erbB-2 and topoisomerase IIalpha to chemoresistance in ovarian cancer

Overexpression of the c-erbB-2 (HER-2/neu) oncogene, which encodes a transmembrane receptor tyrosine kinase, has been shown to be associated with poor prognosis in ovarian and breast cancer. Recent studies indicate that c-erbB-2 may also be involved in determining the chemosensitivity of human cancers. In the present study, we examined the role of c-erbB-2 for chemoresistance in ovarian cancer. Overexpression of c-erbB-2 mRNA in tumor tissue was associated with a shorter survival of patients with primary ovarian cancer (P = 0.0001; n = 77) and was an independent prognostic factor in the proportional-hazard model adjusted for International Federation of Gynecologists and Obstetricians stage, residual disease, chemotherapy, and age (P = 0.035). A significant association between expression of c-erbB-2 mRNA and survival was obtained for the subgroup of patients who received a standard chemotherapy with carboplatin or cisplatin and cyclophosphamide (P = 0.0003), whereas only a nonsignificant trend was observed for patients who did not receive a standard chemotherapy (P = 0.124). In addition, the application of a standard chemotherapy improved the survival of patients with relatively low c-erbB-2 expression (P = 0.013) but not of patients with overexpression of c-erbB-2 (P = 0.359). Expression of c-erbB-2 mRNA correlated with expression of topoisomerase IIalpha mRNA determined by a reverse semiquantitative PCR technique (P = 0.009), whereas expression of c-erbB-2 and topoisomerase IIbeta mRNA did not correlate (P = 0.221). To examine the hypothesis that coamplified and/or coregulated topoisomerase IIalpha contributes to the resistance of c-erbB-2-overexpressing carcinomas, we established a chemosensitivity assay using primary cells from an ovarian carcinoma that overexpressed both c-erbB-2 and topoisomerase IIalpha. The combination of carboplatin with nontoxic concentrations of the topoisomerase II inhibitors etoposide or novobiocin enhanced the toxicity of carboplatin. In contrast, the tyrosine kinase inhibitor emodin exhibited no chemosensitizing effect in cells of this individual carcinoma. In conclusion, overexpression of c-erbB-2 was associated with poor prognosis and poor response to chemotherapy. The data suggest that topoisomerase IIlalpha, which correlates with c-erbB-2 expression, contributes to the resistance of c-erbB-2-overexpressing carcinomas