Recent reports describe the antenatal sonographic diagnosis of placenta accreta based on failure to visualize a hypoechoic zone at the placental margin. This finding was confirmed in our series of seven cases. New observations in this series include prominent large or multiple placental venous lakes and periuterine vascularity in six of seven cases, and progressive thinning and disappearance of the retroplacental hypoechoic zone on sequential examinations in two of seven cases. Loss of normal venous flow pattern on Doppler interrogation of the peripheral placental margin also appeared to be of value in two patients. Histologic correlates for these findings are suggested on the basis of the primary histopathologic feature of placenta accreta: deficiency of the decidua basalis. Differential diagnostic considerations, including abdominal pregnancy and trophoblastic disease, also are discussed.

E. coli releases a 33 amino acid peptide melanocortin-like peptide of E. coli (MECO-1) that is identical to the C-terminus of the E. coli elongation factor-G (EF-G) and has interesting similarities to two prominent mammalian melanocortin hormones, alpha-melanocyte-stimulating hormone (alpha-MSH) and adrenocorticotropin (ACTH). Note that MECO-1 lacks HFRW, the common pharmacophore of the known mammalian melanocortin peptides. MECO-1 and the two hormones were equally effective in severely blunting release of cytokines (HMGB1 and TNF) from macrophage-like cells in response to (i) endotoxin (lipopolysaccharide) or (ii) pro-inflammatory cytokine HMGB-1. The in vitro anti-inflammatoty effects of MECO-1 and of alpha-MSH were abrogated by (i) antibody against melanocortin-1 receptor (MC1R) and by (ii) agouti, an endogenous inverse agonist of MC1R. In vivo MECO-1 was even more potent than alpha-MSH in rescuing mice from death due to (i) lethal doses of LPS endotoxin or (ii) cecal ligation and puncture, models of sterile and infectious sepsis, respectively.