From medical doctor to medical director: leadership style matters.

Leadership is a skill to be developed by all doctors from the foundation trainee to the director of the board. This article explores the impact of leadership style on performance and considers techniques to develop doctors' leadership skills and personal effectiveness.

Increased prevalence of gallbladder polyps in acromegaly.

INTRODUCTION: Several studies have suggested an increased prevalence of benign and malignant tumors in acromegaly, particularly colonic neoplasms. The gallbladder's epithelial similarity to the colon raises the possibility that gallbladder polyps (GBP) may occur more frequently in acromegaly. PATIENTS AND METHODS: Thirty-one patients with newly diagnosed acromegaly (14 females, 17 males; mean age 54.7 yr, range 27-76 yr) were referred to our center between 2004 and 2008. All had pituitary adenomas and were treated with somatostatin analogs prior to transsphenoidal surgery. Biliary ultrasonography was performed at the time of referral. In a retrospective case-cohort study, we compared the prevalence of GBP in these scans with those of 13,234 consecutive patients (age range 20-80 yr) presenting at the hospital for abdominal/biliary ultrasound during the same time interval. Associations between GH and IGF-I levels and GBP in acromegaly were also examined. RESULTS: There was a higher prevalence of GBP in patients with acromegaly compared with controls (29.03 vs 4.62%, P = 0.000008); relative risk was 6.29 (95% confidence interval 3.61-10.96). Eight of nine patients with acromegaly and GBP were older than 50 yr of age. GH levels were higher in those with GBP (median 30.8 µg/liter, interquartile range 10.9-39.1) than those without (8.2 µg/liter, interquartile range 6.0-16.0), but IGF-I levels were comparable. CONCLUSIONS: This is the first study to demonstrate an increased prevalence of GBP in patients with newly diagnosed acromegaly. Further studies are required to determine whether these patients are at increased risk of developing gallbladder carcinoma and to define the role, if any, of biliary ultrasound surveillance.

Effects of maternal administration of vitamins C and E on ethanol neurobehavioral teratogenicity in the guinea pig.

Consumption of ethanol during human pregnancy can produce a wide spectrum of teratogenic effects, including neurobehavioral dysfunction. This study, in the guinea pig, tested the hypothesis that chronic maternal administration of antioxidant vitamins C plus E, together with ethanol, mitigates ethanol neurobehavioral teratogenicity. Pregnant guinea pigs received one of the following four chronic oral regimens: ethanol and vitamins C plus E; ethanol and vitamin vehicle; isocaloric-sucrose/pair-feeding and vitamins C plus E; or isocaloric-sucrose/pair-feeding and vehicle. Vitamins C (250 mg) plus E (100mg) or vehicle were given daily, and ethanol (4 g/kg maternal body weight/day) (E) or isocaloric-sucrose/pair-feeding was given for 5 consecutive days followed by 2 days of no treatment each week throughout gestation. One neonate from selected litters was studied on postnatal day (PD) 0. Neurobehavioral function was determined by measuring task acquisition and task retention using an 8-day moving-platform version of the Morris water-maze task, starting on PD 45. Thereafter, in vivo electrophysiologic assessment of changes in hippocampal synaptic plasticity was conducted. There was an ethanol-induced decrease in neonatal brain weight compared with sucrose. The vitamins C plus E regimen protected hippocampal weight relative to brain weight in ethanol offspring, and mitigated the ethanol-induced deficit in the task-retention component of the water-maze task. However, in the sucrose group, this Vit regimen produced deficits in both task acquisition and task retention. The vitamins C plus E regimen did not mitigate the ethanol-induced impairment of hippocampal long-term potentiation. These results indicate that maternal administration of this high-dose vitamins C plus E regimen throughout gestation has limited efficacy and potential adverse effects as a therapeutic intervention for E neurobehavioral teratogenicity.