Background:The mechanism underlying the anabolic effect of estrogen on the skeleton is unclear. Results: We report that estrogen-induced bone formation in mice occurs through oxytocin (OT) produced by osteoblasts in bone marrow. Conclusion: Feed-forward OT release in bone marrow by a rising estrogen level may facilitate rapid skeletal recovery after lactation. Significance: The study highlights a novel mechanism for estrogen action on bone.

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In this paper, we present a Description Logic approach-fully compliant with the Semantic web vision and technologies to extended matchmaking between demands and supplies in a semantic-enabled Electronic Marketplace, which allows the semantic-based treatment of negotiable and strict requirements in the demand/supply descriptions. To this aim, we exploit two novel non-standard Description Logic inference services, Concept Contraction-which extends sat-isfiability-and Concept Abduction-which extends subsumption. Based on these services, we devise algorithms, which allow to find negotiation spaces and to determine the quality of a possible match, also in the presence of a distinction between strictly required and optional elements. Both the algorithms and the semantic-based approach are novel, and enable a mechanism to boost logic-based discovery and negotiation stages within an e-marketplace. A set of simple experiments confirm the validity of the approach.

The online version of this article has a Supplementary Appendix. BackgroundDivalent metal transporter 1 (DMT1) is a widely expressed metal-iron transporter gene encoding four variant mRNA transcripts, differing for alternative promoter at 5' (DMT1 1A and 1B) and alternative splicing at 3' UTR, differing by a specific sequence either containing or lacking an iron regulatory element (+IRE and -IRE, respectively). DMT1-IRE might be the major DMT1 isoform expressed in erythroid cells, although its regulation pathways are still unknown. Design and MethodsThe microRNA (miRNA) Let-7d (miR-Let-7d) was selected by the analysis of four miRNAs, predicted to target the DMT1-IRE gene in CD34+ hematopoietic progenitor cells, in K562 and in HEL cells induced to erythroid differentiation. Using a luciferase reporter assay we demonstrated the inhibition of DMT1-IRE by miR-Let-7d in K562 and HEL cells. The function of miRLet-7d in erythroid cells was evaluated by the flow cytometry analysis of erythroid differentiation markers, by benzidine staining and by iron flame atomic absorption for the evaluation of iron concentration in the endosomes from K562 cells over-expressing miR-Let-7d. ResultsWe show that in erythroid cells, DMT1-IRE expression is under the regulation of miR-Let-7d. DMT1-IRE and miR-Let-7d are inversely correlated with CD34 + cells, K562 and HEL cells during erythroid differentiation. Moreover, overexpression of miR-Let-7d decreases the expression of DMT1-IRE at the mRNA and protein levels in K562 and HEL cells. MiR-Let-7d impairs erythroid differentiation of K562 cells by accumulation of iron in the endosomes. ConclusionsOverall, these data suggest that miR-Let-7d participates in the finely tuned regulation of iron metabolism by targeting DMT1-IRE isoform in erythroid cells.Key words: iron metabolism, DMT1-IRE, miRNAs. Let-7d in erythroid cells. Haematologica 2010;95(8):1244-1252. doi:10.3324/haematol.2009 This is an open-access paper. Citation: Andolfo I, De Falco L, Asci R, Russo R, Colucci S, Gorrese M, Zollo M, and Iolascon A. Regulation of divalent metal transporter 1 (DMT1) non-IRE isoform by the microRNA Regulation of divalent metal transporter 1 (DMT1) non-IRE isoform by the microRNA Let-7d in erythroid cells

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