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P Ciarmela and P Florio contributed equally to this work AbstractObjective: Activin A is a multifunctional growth and cell differentiation factor produced by normal endometrium, and secreted in high amounts by endometrial adenocarcinoma. In the present study we evaluated the expression of two inhibitory activin A ligands, follistatin and follistatin-related gene (FLRG), in endometrial adenocarcinoma and in age-matched healthy human endometrium. Design and methods: Atropic menopausal (n ¼ 13) and tumoral (n ¼ 9 adenocarcinoma) tissues were processed to evaluate mRNA expression levels (by semiquantitative RT-PCR) and peptide localization (by immunohistochemistry). Differences were evaluated by the unpaired t-test and assumed to be statistically significant when P , 0.05. Results: Both control and tumoral endometrial samples express and localize follistatin and FLRG. However, whereas follistatin mRNA expression did not differ significantly, FLRG was significantly lower in endometrial adenocarcinoma than in healthy endometrial specimens (P , 0.0001). With respect to the localization of proteins, follistatin was immunolocalized in endometrial epithelial and vascular cells both in tumoral and healthy endometrium without any significant difference in intensity. Nuclear and cytoplasmic FLRG immunolocalization was seen in glands, and only nuclear immunolocalization was found in stroma and vessels of healthy endometrium. FLRG was weakly immunostained in endometrial adenocarcinoma. Conclusions: Whilst follistatin expression is unchanged, FLRG is down-regulated in endometrial carcinoma. As activin A is a differentiation factor of human endometrium, the present findings support an imbalance between increased activin A and decreased FLRG expression in endometrial cancer, so that the failure of the activin A pathway through FLRG may be pivotal in endometrial tumorigenesis.

Physical interaction with the fetus through a 3D model may reduce maternal stress.

Growing evidence is demonstrating that several peptides (corticotrophin-releasing factor, urocortins, ghrelin), proteins (leptin, adiponectin) and growth factors (vascular endothelial growth factor; epidermal growth factor family of growth factors and receptors, fibroblast growth factor, insulin like growth factor and insulin like growth factor-binding proteins, transforming growth factor-β and, activin A and related proteins) are expressed in endometriotic implants, and locally play a relevant role in affecting the biological mechanisms leading to endometriosis. They establish a complex network of interactions by which they are therefore able to stimulate angiogenesis, inflammatory cell recruitment and reaction, the growth of endometriotic tissue and its survival through the modulation of the narrow immune system. This review will evaluate the role played by several regulatory peptides, proteins and growth factors in affecting endometrial physiology and the putative mechanisms advocated to explain endometriosis (angiogenesis, cellular and humoral immunity, inflammatory response, endometrial cell proliferation, activation, motility, adhesion and invasion).

Front Cover: In article 2200259 by Katja Loos and Aldo Altomare, the light‐catalyzed atom transfer radical polymerization (ATRP) of PVDF‐based block copolymers with methyl methacrylate using five different organic photoredox catalysts (OPRC) is reported. The authors prove how the three OPRC operating through an oxidative quenching pathway offer a good control over the process. They also achieve successful chain‐extension and external temporal control through light ON‐light OFF process. Cover design by Dina Maniar.