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We induced differentiation of human amnion-derived mesenchymal stem cells (AMCs) and menstrual blood-derived mesenchymal stem cells (MMCs) into endometrial stroma-like cells, which could be useful for cell therapy to support embryo implantation. Interestingly, the expression patterns of surface markers were similar among AMCs, MMCs, and endometrial stromal cells. In addition, whereas treatment with estrogen and progesterone was not very effective for decidualizing AMCs and MMCs, treatment with 8-Br-cAMP prompted remarkable morphological changes in these cells as well as increased expression of decidualization markers (prolactin and insulin-like growth factor binding protein-1) and attenuated expression of surface markers unique to mesenchymal stem cells. These results demonstrated that bone marrow-derived stem cells, which are considered a potential source of endometrial progenitor cells, as well as AMCs and MMCs show in vitro decidualization potential, which is characteristic of endometrial stromal cells.

Summary Background : The incidence and severity of non‐steroidal anti‐inflammatory drugs (NSAIDs)‐induced gastro‐duodenal ulcer have not been extensively studied in Japan. Aim : We performed a prospective study to clarify NSAIDs‐induced gastro‐duodenal injury, focusing especially on low‐dose aspirin (L‐A). Methods : Two hundred and thirty‐eight patients with bleeding peptic ulcers admitted to our hospital. History of taking NSAIDs and anti‐ulcer drugs was obtained from all patients who underwent endoscopic examinations. The lesion scores of patients taking L‐A were classified numerically from zero (no lesion) to five (ulcer). Results : The NSAIDs were associated with 28.2% of hemorrhagic ulcers. The rates of patients using L‐A, loxoprofen, diclofenac, and combination of two of these drugs were 27, 16, 10 and 9%, respectively. Co‐administered anti‐ulcer drugs were cytoprotective anti‐ulcer drugs (27%), H2 receptor antagonists (16%), PPI (4%), and none (53%). In patients taking L‐A, H2 receptor antagonists were used most frequently. The HP was positive in 63% of L‐A‐induced ulcer cases and in 69% of NSAIDs other than low‐dose aspirin‐induced ulcer cases. The lesion scores of patients taking L‐A with H2 receptor antagonists or PPI were significantly lower than those of patients who were taking only L‐A (P < 0.05). Conclusions : Approximately one‐third of hospitalized patients with NSAIDs‐induced hemorrhagic ulcer showed an association with L‐A. Prospective randomized controlled trials including H2 receptor antagonists are required to establish preventive efforts aimed at L‐A‐induced gastro‐duodenal injury.

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