Orbit,zygoma, and maxilla growth patterns in Crouzon syndrome

The facial malformations of Crouzon syndrome involve the entire cranio-orbito-zygomatic region. The detailed sequence of changes in orbit, zygoma, and maxilla over time, the mutual influence among these three anatomical structures, and their relationship with the cranial base were studied to determine the sequence and timing of deformity. Preoperative CT scans of 36 patients with Crouzon syndrome (mean age 10.84 ± 14.70 years; 14 male, 22 female) and CT scans of 54 control subjects (mean age 8.53 ± 13.22 years; 29 male, 25 female) were divided into five subgroups by age: 0–6 months, 6 months–2 years, 2–6 years, 6–18 years, and 18–62 years. Craniofacial morphometric cephalometrics were analyzed using Materialise software. Crouzon orbit anteroposterior length was shorter before 6 months (P = 0.021) and remained shorter into adulthood (P < 0.001). Globe projection was greater across all age subgroups (P < 0.001), reaching a peak at 6 months to 2 years (P < 0.001). The increased medial orbital width was the most remarkable and persistent secondary deformity (P < 0.001). The zygoma anterior protrusion was retruded before 6 months of age (P < 0.001), but then improved gradually. The width of maxilla was greater by 24% in the Crouzon cohort (P < 0.001), with a difference of 16% before 6 months (P = 0.024), and was developed earlier than the shortened anteroposterior length. Crouzon high and shallow orbital walls are distinctive. Maxillary widening developed before the malformation of sphenoid. The anteroposterior position of zygoma is likely a principal deformity, rather than a reflection of the intrinsic shape of the bone.Level of Evidence: II     

Effect of lamivudine on transmission of human T-cell lymphotropic virus type 1 to adult peripheral blood mononuclear cells in vitro

The effects of lamivudine (3TC) on in vitro infection of peripheral blood mononuclear cells (PBMC) from healthy donors with human T-cell lymphotropic virus type 1 (HTLV-1) were investigated. Direct measures of viral replication (viral DNA, RNA, and protein) all gave similar, very high 50% inhibitory concentrations in comparison with those previously reported for zidovudine. Nevertheless, 3TC inhibited HTLV-1-driven long-term growth of infected PBMC in vitro at concentrations (6.25 micro M) which had poor or no direct antiviral effects, suggesting that another mechanism may be playing a role.