Lessons learned during establishment of the college of health sciences of the University of Zimbabwe 1995-2001

Background: The five year training of medical doctors has been conducted through the Faculty of Medicine of the University of Zimbabwe since 1963 in two physical sites in Harare; Mount Pleasant Campus for Basic Sciences and Mazowe Street Campus for Clinical Sciences. Annual student enrolment has gradually increased from less than 30 in the early stages to 200 currently. The continuing brain drain of doctors from the country necessitated the Government to instruct the Faculty of Medicine to double its student intake by enrolling a new student intake within three months to address this shortage. Methods: This descriptive longitudinal study is largely complemented by desk review and reflections from the authors who oversaw the evolution of the Faculty into the College. Authors experienced the transition of the institution over most of the study period and shared first-hand information. Results: Instruction from Government was used as an opportunity to develop. The Faculty of Medicine developed and began implementation of its inaugural five year strategic plan 1995-2001. The key tenets of the plan were to be a semi-autonomous institution (in relation to the University of Zimbabwe) comprising five Faculties with a designated teaching hospital under joint administration with Government where academicians were to receive similar emoluments. Clinicians were entitled to additional remuneration from Government for the clinical work delivered. The infrastructure was expanded to accommodate 200 medical students annually at the two sites. A government loan secured from the Spanish Protocol was used to purpose build the Health Sciences Building and equipment to accommodate and equip the five faculties. Discussion: The directive by Government to double medical student intake in order to address the doctor shortages was used as opportunity to address some of the Faculty of Medicine’s academic needs, including infrastructure, professional development and additional academic provisions in line with international trends. The realization of some of the outcomes is on course with the exception of ownership of a teaching hospital, autonomy of the College from the University and additional emoluments for clinicians from government, which are work in progress

Adrenaline suppression of the macrophage nitric oxide response to lipopolysaccharide is associated with differential regulation of tumour necrosis factor-α and interleukin-10

Adrenaline is a catecholamine hormone secreted by the adrenal medulla in response to acute stress. Previous studies have shown that adrenaline suppresses the nitric oxide (NO) response of murine macrophages (Mφs) stimulated in vitro with lipopolysaccharide (LPS). We have now extended these studies to examine the effects of adrenaline on the production of tumour necrosis factor alpha (TNF-α) and interleukin-10 (IL-10). Our results showed that NO, TNF-α and IL-10 were concurrently produced following in vitro LPS (10 µg/ml) stimulation of murine peritoneal Mφs. Adrenaline suppressed both NO and TNF-α with concomitant up-regulation of the IL-10 response above that seen with LPS alone. In this in vitro model of LPS stimulation we demonstrated that TNF-α was required for NO production, as the TNF-α neutralizing monoclonal antibody, TN3.19.12, abolished the response; in contrast, IL-10 suppressed NO. In order to determine any functional consequence of adrenaline-mediated IL-10 augmentation on NO production, Mφs were stimulated with LPS and specific neutralizing anti-IL-10 antibodies were added to the cultures. The LPS NO response was suppressed to 43% of the control value by adrenaline (10(−8) m) and an irrelevant control antibody had no effect on the adrenaline-mediated inhibition of NO, but anti-IL-10 treatment restored the NO response to levels similar to those observed with LPS alone. Furthermore, we demonstrated that exogenous TNF-α, at a dose range of 1·9–50 ng per ml, also restored the nitrite response to LPS in the presence of adrenaline. Together, the observations that neutralization of IL-10 and addition of TNF-α abrogate adrenaline's inhibition of NO, suggest that this hormone suppresses NO partly through up-regulation of IL-10 which, in turn, may suppress TNF-α that is required for NO production. Finally, we also observed that the Mφ-activating cytokine, interferon-γ (IFN-γ), attenuated the inhibitory effect of adrenaline on the LPS NO response