Objective To evaluate our experience with the diagnosis and treatment of Cesarean scar pregnancy. Methods

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Background: Although death rates are often used to monitor the quality of health care, in industrialized countries maternal deaths have become rare. Severe maternal morbidity has therefore been proposed as a supplementary indicator for surveillance of the quality of maternity care. Our purpose in this study was to describe severe maternal morbidity in Canada over a 10-year period, among women with or without major pre-existing conditions. Methods: We carried out a retrospective cohort study of severe maternal morbidity involving 2 548 824 women who gave birth in Canadian hospitals between 1991 and 2000. Thirteen conditions that may threaten the life of the mother (e.g., eclampsia) and 11 major pre-existing chronic conditions (e.g., diabetes) that could be identified from diagnostic codes were noted. Results: The overall rate of severe maternal morbidity was 4.38 per 1000 deliveries. The fatality rate among these women was 158 times that of the entire sample. Rates of venous thromboembolism, uterine rupture, adult respiratory distress syndrome, pulmonary edema, myocardial infarction, severe postpartum hemorrhage requiring hysterectomy, and assisted ventilation increased substantially from 1991 to 2000. The presence of major pre-existing conditions increased the risk of severe maternal morbidity to 6-fold. Interpretation: Severe maternal morbidity occurs in about 1 of 250 deliveries in Canada, with marked recent increases in certain morbid conditions such as pulmonary edema, myocardial infarction, hemorrhage requiring hysterectomy, and the use of assisted ventilation.Cite this article as CMAJ 2005;173(7).

BackgroundMesenchymal stem cells (MSCs) promote tumor growth by differentiating into carcinoma-associated fibroblasts (CAFs) and composing the tumor microenvironment. However, the mechanisms responsible for the transition of MSCs to CAFs are not well understood. Exosomes regulate cellular activities by mediating cell-cell communication. In this study, we aimed to investigate whether cancer cell-derived exosomes were involved in regulating the differentiation of human umbilical cord-derived MSCs (hucMSCs) to CAFs.Methodology/Principal FindingsWe first showed that gastric cancer cell-derived exosomes induced the expression of CAF markers in hucMSCs. We then demonstrated that gastric cancer cell-derived exosomes stimulated the phosphorylation of Smad-2 in hucMSCs. We further confirmed that TGF-β receptor 1 kinase inhibitor attenuated Smad-2 phosphorylation and CAF marker expression in hucMSCs after exposure to gastric cancer cell-derived exosomes.Conclusion/SignificanceOur results suggest that gastric cancer cells triggered the differentiation of hucMSCs to CAFs by exosomes-mediated TGF-β transfer and TGF-β/Smad pathway activation, which may represent a novel mechanism for MSCs to CAFs transition in cancer.