Previous studies have shown that extracapsular dissection (ECD) is an alternative approach to superficial parotidectomy (SP) for pleomorphic adenoma parotid tumours, associated with low recurrence rates equal to those following SP, but with significantly reduced morbidity. However, if a malignant tumour masquerades as a clinically benign lump, this approach may be inappropriate. This study addressed this question by analysing the outcome of 821 consecutive patients with parotid tumours treated at one centre over 40 years and with a median 12 (range 5 -30) years follow-up. Tumours were classified as 'simple' (discrete, mobile, o 4 cm: n ¼ 662) and 'complex' (deep, fixed, facial nerve palsy, X4 cm: n ¼ 159). Among the 'simple' or clinically benign tumours, 503 patients underwent ECD; 159 patients underwent SP. In all, 32 (5%) clinically benign cases were subsequently revealed as malignant histologies (ECD, 12; SP, 20). For each group, 5-and 10-year cancer-specific survival rates were 100 and 98%, respectively. There were no differences in recurrence rates when subanalysed by surgical groups, but ECD was associated with significantly reduced morbidity (P o 0.001). This study demonstrates that ECD is a viable alternative to superficial parotidectomy for the majority of parotid tumours, associated with reduced morbidity without oncological compromise.

The recent identification of SATB2 as a candidate gene responsible for the craniofacial dysmorphologies associated with deletions and translocations at 2q32-q33, one of only three regions of the genome for which haploinsufficiency has been significantly associated with isolated cleft palate, led us to investigate the in vivo functions of murine Satb2. We find that, similar to the way in which SATB2 is perceived to act in humans, craniofacial defects due to haploinsufficiency of Satb2, including cleft palate (in approximately 25% of cases), phenocopy those seen with 2q32-q33 deletions and translocations in humans. Full functional loss of Satb2 results in amplification of these defects and leads both to increased apoptosis in the craniofacial mesenchyme where Satb2 is usually expressed and to changes in the pattern of expression of three genes implicated in the regulation of craniofacial development in humans and mice: Pax9, Alx4, and Msx1. The Satb2-dosage sensitivity in craniofacial development is conspicuous--along with its control of cell survival, pattern of expression, and reversible functional modification by SUMOylation, it suggests that Satb2/SATB2 function in craniofacial development may prove to be more profound than has been anticipated previously. Because jaw development is Satb2-dosage sensitive, the regulators of Satb2 expression and posttranslational modification become of critical importance both ontogenetically and evolutionarily, especially since such regulators plausibly play undetected roles in jaw and palate development and in the etiology of craniofacial malformations.

One hundred fourteen heterosexual men with acute nongonococcal urethritis (NGU) and 64 patients without NGU were studied. We determined that Chlamydia trachomatis and Mycoplasma genitalium were strongly associated with acute NGU after controlling, by means of multivariate analysis, for age, race, sexual lifestyle, and coinfection (odds ratio [OR], 13.0, 95% confidence interval [CI], 2.6-64.5; and OR, 17.9, 95% CI, 2.0-160, respectively). Eighty-six men with acute NGU reattended at least once 10-92 days after treatment; 59 (69%) of these 86 men had urethritis. Seven men had M. genitalium detected during 10-92 days of follow-up, and all had urethritis. Ureaplasmas were not associated with acute NGU in multivariate analysis, but their detection was associated with the presence of urethritis during follow-up (P=.014). Ureaplasmas or M. genitalium were associated with both chronic NGU, which was defined as urethritis that occurred 30-92 days after the commencement of treatment (P=.028), and chronic NGU with symptoms or signs (P=.005).

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