Virtual surgical planning (VSP) is becoming more widely used in maxillofacial reconstruction and can be surgeon-based or industry-based. Surgeon-based models require software training but allow surgeon autonomy. We evaluate the learning curve for VSP through a prospective cohort study in which planning times and accuracy of 7 otolaryngology residents with no prior VSP experience were compared to that of a proficient user after a single training protocol and 6 planning sessions for orbital fractures. The average planning time for the first session was 21 minutes 41 seconds ± 6 minutes 11 seconds with an average maximum deviation of 2.5 ± 0.8 mm in the lateral orbit and 2.3 ± 0.6 mm in the superior orbit. The average planning time for the last session was 13 minutes 5 seconds ± 10 minutes and 7 seconds with an average maximum deviation of 1.4 ± 0.5 mm in the lateral orbit and 1.3 ± 0.4 mm in the superior orbit. Novice users reduced planning time by 40% and decreased maximum deviation of plans by 44% and 43% in the lateral and superior orbits, respectively, approaching that of the proficient user. Virtual surgical planning has a quick learning curve and may be incorporated into surgical training.

The mycobacterial cell wall component lipoarabinomannan (LAM) has been described as one of the key virulence factors of Mycobacterium tuberculosis. Modification of the terminal arabinan residues of this lipoglycan with mannose caps in M. tuberculosis or with phosphoinositol caps in Mycobacterium smegmatis results in distinct host immune responses. Given that M. tuberculosis typically persists in the phagosomal vacuole after being phagocytosed by macrophages, we performed a proteomic analysis of that organelle after treatment of macrophages with LAMs purified from the two mycobacterial species. The quantitative changes in phagosomal proteins suggested a distinct role for mannose-capped LAM in modulating protein trafficking pathways that contribute to the arrest of phagosome maturation. Enlightened by our proteomic data, we performed further experiments to show that only the LAM from M. tuberculosis inhibits accumulation of autophagic vacuoles in the macrophage, suggesting a new function for this virulence-associated lipid.