Anatomy Education Environment Measurement Inventory (AEEMI): a cross-validation study in Malaysian medical schools.

BACKGROUND: The Anatomy Education Environment Measurement Inventory (AEEMI) evaluates the perception of medical students of educational climates with regard to teaching and learning anatomy. The study aimed to cross-validate the AEEMI, which was previously studied in a public medical school, and proposed a valid universal model of AEEMI across public and private medical schools in Malaysia. METHODS: The initial 11-factor and 132-item AEEMI was distributed to 1930 pre-clinical and clinical year medical students from 11 medical schools in Malaysia. The study examined the construct validity of the AEEMI using exploratory and confirmatory factor analyses. RESULTS: The best-fit model of AEEMI was achieved using 5 factors and 26 items (χ 2 = 3300.71 (df = 1680), P < 0.001, χ 2/df = 1.965, Root Mean Square of Error Approximation (RMSEA) = 0.018, Goodness-of-fit Index (GFI) = 0.929, Comparative Fit Index (CFI) = 0.962, Normed Fit Index (NFI) = 0.927, Tucker-Lewis Index (TLI) = 0.956) with Cronbach's alpha values ranging from 0.621 to 0.927. Findings of the cross-validation across institutions and phases of medical training indicated that the AEEMI measures nearly the same constructs as the previously validated version with several modifications to the item placement within each factor. CONCLUSIONS: These results confirmed that variability exists within factors of the anatomy education environment among institutions. Hence, with modifications to the internal structure, the proposed model of the AEEMI can be considered universally applicable in the Malaysian context and thus can be used as one of the tools for auditing and benchmarking the anatomy curriculum.

A novel in vitro human microglia model: characterization of human monocyte-derived microglia.

Microglia are the innate immune cells of the central nervous system. They help maintaining physiological homeostasis and contribute significantly to inflammatory responses in the course of infection, injury and degenerative processes. To date, there is no standardized simple model available to investigate the biology of human microglia. The aim of this study was to establish a new human microglia model. For that purpose, human peripheral blood monocytes were cultured in serum free medium in the presence of M-CSF, GM-CSF, NGF and CCL2 to generate monocyte-derived microglia (M-MG). M-MG were clearly different in morphology, phenotype and function from freshly isolated monocytes, cultured monocytes in the absence of the cytokines and monocyte-derived dendritic cells (M-DC) cultured in the presence of GM-CSF and IL-4. M-MG acquired a ramified morphology with primary and secondary processes. M-MG displayed a comparable phenotype to the human microglia cell line HMC3, expressing very low levels of CD45, CD14 and HLA-DR, CD11b and CD11c; and undetectable levels of CD40, CD80 and CD83, and a distinct pattern of chemokine receptors (positive for CCR1, CCR2, CCR4, CCR5, CXCR1, CXCR3, CX3CR1; negative for CCR6 and CCR7). In comparison with M-DC, M-MG displayed lower T-lymphocyte stimulatory capacity, as well as lower phagocytosis activity. The described protocol for the generation of human monocyte-derived microglia is feasible, well standardized and reliable, as it uses well defined culture medium and recombinant cytokines, but no serum or conditioned medium. This protocol will certainly be very helpful for future studies investigating the biology and pathology of human microglia.