Entrepreneurship education as human capital: implications for youth self-employment and conflict mitigation in sub-Saharan Africa

Previous research has focused on stable developed economies to predict that human capital and entrepreneurship education (EE) provision at the higher education (HE) level will positively affect entrepreneurial success. This article draws on the outcome of recent EE projects in two HE institutions in a conflict-torn northern Nigeria as a proxy to advocate the introduction of entrepreneurship as a compulsory component into the secondary school curriculum in Sub-Saharan Africa. Using semi-structured interview data, it is found that the provision of EE at secondary education level could help to facilitate human capital development and assist efforts to curb youth unemployment. Specifically, the study suggests that EE comprises both generic and specific human capital that increases an individual’s ability to identify and exploit opportunities, particularly for young people, and in doing so helps to reduce their vulnerability to poverty and involvement in armed conflict. Suggestions for future research and policy considerations are provided

Risk factors for inhibitor formation in haemophilia: a prevalent case-control study.

Inhibitor formation is a major complication of haemophilia treatment. In a prevalent case-control study, we evaluated blood product exposure, genotype and HLA type on haemophilia A inhibitor formation. Product exposure was extracted from medical records. Genotype was determined on stored DNA samples by detection of virtually all mutations-SSCP (DOVAM-S) and subcycling PCR. HLA typing was performed by PCR amplification and exonuclease-released fluorescence. Cases experienced higher intensity factor, 455 vs. 200 U per exposure, P \u3c 0.005, more frequent central nervous system (CNS) bleeding, seven of 20 (35.0%) vs. one of 57 (1.7%), P = 0.001 and more commonly from inhibitor families, seven of 20 (35.0%) vs. zero of 57 (0%), P \u3c 0.001, and African-American, 12 of 63 (19.0%) vs. six of 117 (5.1%), P = 0.015. Among the latter, CNS bleeding was more commonly the initial bleed, 60% vs. 0%, P \u3c 0.001, and survival was shorter, 14 vs. 38 yr, P = 0.025. Inhibitor formation was uncommon in those with missense mutations, two of 65 (3.1%) vs. 31 of 119 (26.0%), P = 0.008, and unrelated to factor VIII immunogenic epitope, P = 0.388, or HLA type, P \u3e 0.100. Genotype was not associated with race. Time to immune tolerance was shorter for titresor = 120 BU/mL, six vs. 16 months, P \u3c 0.01, but unaffected by tolerizing dose regimen, P \u3e 0.50. Inhibitor formation is associated with high intensity product exposure, CNS bleeding, African-American race and low frequency of missense mutations. The ideal time to initiate prophylaxis to reduce CNS bleeding and inhibitor formation will require prospective studies

The canonical NF-κB pathway governs mammary tumorigenesis in transgenic mice and tumor stem cell expansion

The role of mammary tumor epithelial cell (MEC) NF-κB in tumor progression in vivo is unknown as murine NF-κB components and kinases are either required for murine survival or interfere with normal mammary gland development. As NF-κB inhibitors block both tumor-associated macrophages (TAM) and MEC NF-κB, the importance of MEC NF-κB to tumor progression in vivo remained to be determined. Herein, an MEC-targeted inducible transgenic inhibitor of NF-κB (IκBαSR) was developed in ErbB2 mammary oncomice. Inducible suppression of NF-κB in the adult mammary epithelium delayed the onset and number of new tumors. Within similar sized breast tumors, TAM and tumor neoangiogenesis was reduced. Co-culture experiments demonstrated MEC NF-κB enhanced TAM recruitment. Genome wide expression and proteomic analysis demonstrated IκBαSR inhibited tumor stem cell pathways. IκBαSR inhibited breast tumor stem cell markers in transgenic tumors, reduced stem cell expansion in vitro, and repressed expression of Nanog and Sox2 in vivo and in vitro. Mammary epithelial cell NF-κB contributes to mammary tumorigenesis. As we show NF-κB contributes to expansion of breast tumor stem cells and heterotypic signals that enhance TAM and vasculogenesis, these processes may contribute to NF-κB dependent mammary tumorigenesis