We thank Ministerio de Educación y Ciencia and FECYT (Spain) for a postdoctoral fellowship to O. Palomares. Conflict of interest: The authors declare no financial or commercial conflict of interest. “
“Citation Rosenberg VA, Buhimschi IA, Dulay AT, Abdel-Razeq SS, Oliver EA, Duzyj CM, Lipkind H, Pettker CM, Buhimschi CS. Modulation of amniotic fluid activin-A and inhibin-A in women with preterm premature rupture of the membranes and infection-induced preterm birth. Am J Reprod Immunol 2012; 67: 122–131 Problem  Activins and inhibins are important modulators of inflammatory processes. We explored activation of amniotic fluid (AF) activin-A and inhibin-A system in women with intra-amniotic

infection and preterm

premature rupture of the membranes (PPROM). Method of study  We analyzed 78 AF samples: ‘2nd trimester-control’ (n = 12), ‘3rd trimester-control’ Idasanutlin nmr (n = 14), preterm labor with intact membranes [positive-AF-cultures (n = 13), negative-AF-cultures (n = 13)], and PPROM [positive-AF-cultures (n = 13), negative-AF-cultures (n = 13)]. Activin-A levels were evaluated ex-vivo following incubation of amniochorion and placental villous explants with Gram-negative lipopolysaccharide (LPS) or Gram-positive (Pam3Cys) bacterial mimics. Ability of recombinant activin-A and inhibin-A to modulate inflammatory reactions in fetal membranes was explored through explants’ IL-8 release. Selleck Bortezomib Results  Activin-A and inhibin-A were present in human AF and were gestational age-regulated. Activin-A

was significantly upregulated by infection. Lower inhibin-A levels were seen in PPROM. LPS elicited release of activin-A from amniochorion, but not from villous explants. Recombinant activin-A stimulated IL-8 release from amniochorion, an effect that was not reversed by inhibin-A. Conclusion  Human AF activin-A and inhibin-A are involved in biological processes linked to intra-amniotic infection/inflammation-induced PRKD3 preterm birth. “
“National Institute for Medical Research, London, UK Cancer Research UK London Research Institute, London, UK The early growth response (Egr) transcription factor family regulates multiple steps during T-cell development. We examine here the role played by Egr2 in positive selection. In double-positive cells, Egr2 is upregulated immediately following TCR ligation, and its expression requires both the MAPK and calcineurin signaling pathways. Inducible transgenic and knockout mice were generated to cause gain- or loss-of-function of Egr2 in double-positive cells, and had reciprocal effects; more mature single-positive cells were made when Egr2 was overexpressed, and fewer when Egr2 was absent. These defects were associated with changes in the survival of positively selected cells rather than perturbation of positive selection or immediate post-selection signaling.