Medical records of 32 women with abdominal incision endometriosis who underwent surgical treatment in the Obstetrics and Gynaecology Hospital at Fudan University between September 1999 and March 2006 were reviewed retrospectively. All cases concerning the diagnosis of endometriosis were confirmed by two gynaecological pathologists. The median age was 32 years (range from 25 to 45). A total of 31 patients had a history of caesarean section, and one case underwent ovarian endometrioid cystectomy. All abdominal incision endometriosis presented with a mass in the abdominal scar. Among them, there were 30 patients who complained of cyclical pain during menses. All of the 32 cases underwent surgical treatment and had follow-up from 10 months to 6 years; there was no recurrence of endometriosis in 31 cases. Abdominal incision endometriosis is rare in women and most cases present following caesarean section. It is suggested that during caesarean section, precautions need to be taken to avoid transplantation of endometrium into the abdominal incision. Surgical treatment is recommended to excise the lesion completely. The frozen section is performed during the operation due to the possibility of malignancy in abdomen incision endometriosis.
Preeclampsia (PE) is a risk factor for autism spectrum disorder (ASD) in offspring. However, the exact mechanisms underlying the impact of PE on progeny ASD are not fully understood, which hinders the development of effective therapeutic approaches. This study shows the offspring born to a PE mouse model treated by Nω-nitro-L-arginine methyl ester (L-NAME) exhibit ASD-like phenotypes, including neurodevelopment deficiency and behavioral abnormalities. Transcriptomic analysis of the embryonic cortex and adult offspring hippocampus suggested the expression of ASD-related genes was dramatically changed. Furthermore, the level of inflammatory cytokines TNFα in maternal serum and nuclear factor kappa B (NFκB) signaling in the fetal cortex were elevated. Importantly, TNFα neutralization during pregnancy enabled to ameliorate ASD-like phenotypes and restore the NFκB activation level in the offspring exposed to PE. Furthermore, TNFα/NFκB signaling axis, but not L-NAME, caused deficits in neuroprogenitor cell proliferation and synaptic development. These experiments demonstrate that offspring exposed to PE phenocopies ASD signatures reported in humans and indicate therapeutic targeting of TNFα decreases the likelihood of bearing children with ASD phenotypes from PE mothers.
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