Differential Expression of Extracellular Matrix and Adhesion Molecules in Fetal-Origin Amniotic Epithelial Cells of Preeclamptic Pregnancy.

Preeclampsia is a common disease that can occur during human pregnancy and is a leading cause of both maternal and neonatal morbidity and mortality. Inadequate trophoblast invasion and deficient remodeling of uterine spiral arteries are associated with preeclampsia (PE). The development of this syndrome is thought to be related to multiple factors. Recently, we isolated patient-specific human amniotic epithelial cells (AECs) from the placentas of 3 women with normal pregnancy and 3 with preeclamptic pregnancy. Since the characteristics of human AECs in PE are different from those in normal pregnancy, we sought to confirm the genes differentially expressed between preeclamptic pregnancy and normal pregnancy. Therefore, we performed transcriptome analysis to investigate the candidate genes associated with the possible pathophysiology of preeclampsia. Pathway analysis was performed using the Database for Annotation, Visualization, and Integrated Discovery (DAVID) and Kyoto Encyclopedia of Genes and Genomes (KEGG) online resource. In this study, we selected a total of 12 pathways and focused on extracellular matrix-related and biological adhesion molecules. Using RT-PCR array and real-time PCR, we confirmed that COL16A1, ITGB2, and LAMA3 were significantly up-regulated, but ITGA1, ITGA3, ITGA6, MMP1, MMP3, MMP10 and MMP11 were significantly down-regulated in preeclamptic fetal origin cells. Taken together, we suggest that the genes and pathways identified here may be responsible for the occurrence and development of PE, and controlling their expression may play a role in communication with fetal-maternal placenta to keep normal pregnancy.

The ON-Q pain management system in elective gynecology oncologic surgery: Management of postoperative surgical site pain compared to intravenous patient-controlled analgesia.

OBJECTIVE: The goal of this study was to compare postoperative surgical site pain in gynecologic cancer patients who underwent elective extended lower midline laparotomy and managed their pain with either the ON-Q pain management system (surgical incision site pain relief system, ON-Q pump) or an intravenous patient-controlled analgesia pump (IV PCA). METHODS: Twenty gynecologic cancer patients who underwent elective extended lower midline laparotomy were divided into two groups. One group received a 72-hour continuous wound perfusion of the local anesthetic ropivacaine (0.5%, study group) into the supraperitoneal layer of the abdominal incision through the ON-Q pump. The other group received intravenous infusion pump of patient-controlled analgesia (fentanyl citrate 20 mg/mL · kg+ondansetron hydrochloride 16 mg/8 mL+normal saline). Postoperative pain was assessed immediately and at 6, 24, 48, 72, and 96 hours after surgery using the visual analogue scale. RESULTS: Postoperative surgical site pain scores at 24, 48, and 72 hours after surgery were lower in the ON-Q group than the IV PCA group. Pain scores at 24 hours and 48 hours after surgery were significantly different between the two groups (P=0.023, P<0.001). Overall painkiller administration was higher in the ON-Q group but this difference was not statistically significant (5.1 vs. 4.3, P=0.481). CONCLUSION: This study revealed that the ON-Q pain management system is a more effective approach than IV PCA for acute postoperative surgical site pain relief after extended lower midline laparotomy in gynecologic cancer patients.

Rupture of an unscarred uterus in a woman with long-term steroid treatment for systemic lupus erythematosus.

BACKGROUND: Unscarred uterine rupture in association with systemic lupus erythematosus (SLE) and long-term steroid treatment is rare. CASE: A 36-year-old primigravid woman conceived a twin gestation after in vitro fertilization therapy. At 23 weeks of gestation, she was found to have a spontaneous rupture of the uterus. Her medical history was significant for SLE for a duration of 19 years, and her condition had been maintained with prednisolone. She had no history of uterine scarring or other known risk factors for uterine rupture. The uterine fundus was the main location of the rupture and a subtotal hysterectomy was performed. CONCLUSION: Long-term treatment with systemic steroids and SLE may increase the risk of spontaneous rupture of an unscarred uterus.