Down-regulation of the transcription factor snail in the placentas of patients with preeclampsia and in a rat model of preeclampsia.

BACKGROUND: Placental malfunction in preeclampsia is believed to be a consequence of aberrant differentiation of trophoblast lineages and changes in utero-placental oxygenation. The transcription factor Snail, a master regulator molecule of epithelial-mesenchymal transition in embryonic development and in cancer, is shown to be involved in trophoblast differentiation as well. Moreover, Snail can be controlled by oxidative stress and hypoxia. Therefore, we examined the expression of Snail and its downstream target, e-cadherin, in human normal term, preterm and preeclamptic placentas, and in pregnant rats that developed preeclampsia-like symptoms in the response to a 20-fold increase in sodium intake. METHODS: Western blotting analysis was used for comparative expression of Snail and e- cadherin in total protein extracts. Placental cells expressing Snail and e-cadherin were identified by immunohistochemical double-labeling technique. RESULTS: The levels of Snail protein were decreased in human preeclamptic placentas by 30% (p < 0.01) compared to normal term, and in the rat model by 40% (p < 0.001) compared to control placentas. In preterm placentas, the levels of Snail expression varied, yet there was a strong trend toward statistical significance between preterm and preeclamptic placentas. In humans, e-cadherin protein level was 30% higher in preeclamptic (p < 0.05) placentas and similarly, but not significantly (p = 0.1), high in the preterm placentas compared to normal term. In the rat model of preeclampsia, e-cadherin was increased by 60% (p < 0.01). Immunohistochemical examination of human placentas demonstrated Snail-positive staining in the nuclei of the villous trophoblasts and mesenchymal cells and in the invasive trophoblasts of the decidua. In the rat placenta, the majority of Snail positive cells were spongiotrophoblasts of the junctional zone, while in the labyrinth, Snail-positive sinusoidal giant trophoblasts cells were found in some focal areas located close to the junctional zone. CONCLUSION: We demonstrated that human preeclampsia and the salt-induced rat model of preeclampsia are associated with the reduced levels of Snail protein in placenta. Down-regulation of the transcription factor Snail in placental progenitor cell lineages, either by intrinsic defects and/or by extrinsic and maternal factors, may affect normal placenta development and function and thus contribute to the pathology of preeclampsia.

5-millimeter trocar-site bowel herniation following laparoscopic surgery.

BACKGROUND AND OBJECTIVES: This is a case report of a 5-mm trocar-site large bowel herniation following laparoscopic tubal sterilization. During laparoscopic sterilization, the 5-mm port site was closed initially. Large bowel herniation was recognized at the end of the case and managed immediately by laparoscopically reducing the hernia and closing the port site without any short- or long-term complications. Trocar-site bowel hernia is a rare complication after laparoscopic surgery. It is usually associated with trocar size > 10 mm. We describe a case of bowel herniation through a 5-mm trocar site, which was managed after laparoscopic surgery. CASE REPORT: A 36-year-old multigravid patient underwent a laparoscopic tubal fulguration. Two 5-mm ports were used for the procedure. At the end of the procedure, the lateral trocar site was found to have fat protrusion that looked like appendices epiploicae. A laparoscopic camera was reintroduced into the abdominal cavity that showed a large bowel herniation through the 5-mm lateral port site. The hernia was reduced laparoscopically, and the fascial defect was repaired. CONCLUSION: Bowel herniation can occur through a 5-mm port. All port sites should be closed to avoid such complications.

Findings from a 10-year follow-up of bone mineral density in competitive perimenopausal runners.

OBJECTIVE: To evaluate bone mineral density (BMD) in perimenopausal competitive runners with long-term follow-up. STUDY DESIGN: Fifteen master female runners between 40 and 50 years old who ran at least 20 miles per week were evaluated. BMD was measured by dual-energy x-ray absorptiometry (DEXA) at baseline and at the 10-year follow-up. RESULTS: The median age was 46 and median miles run per week, 25. At baseline, after a median of 11 years of competitive running, hip BMD was above peak bone mass (T-score = 0.8) and that of age-matched controls (Z-score = 1.6), while lumbar spine BMD was below peak bone mass (T-score = -0.8) and equal to that of age-matched controls (Z-score = -0.1). At the 10-year follow-up, hip BMD fell below peak bone mass (T-score = -0.2, p = 0.0004) but was still above that of age-matched controls (Z-score = 0.5, p = 0.002), while there was little change in lumbar spine BMD. CONCLUSION: Competitive running prior to the perimenopausal period seems to be associated with improved hip BMD. However, continued competitive running during the perimenopausal period is not associated with prevention of a perimenopausal hip BMD decline. In contrast, competitive running had little effect on peri-menopausal lumbar spine BMD.