Suppression of electroacupuncture(EA)-induced beta-endorphin and ACTH release by hydrocortisone in man. Absence of effects on EA-induced anaesthesia

Auricular electroacupuncture (EA) increased plasma ACTH and beta-endorphin levels significantly in 10 patients receiving EA as an analgesic aid during surgery. Pre-treatment with iv hydrocortisone (200 mg) completely suppressed both ACTH and beta-endorphin release in response to EA without significantly affecting EA anaesthesia in 6 other patients and in a patient with Addison's disease.     

Evaluating the landscape of gene cooperativity with receptor tyrosine kinases in liver tumorigenesis using transposon-mediated mutagenesis

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Correlates of HIV Testing Refusal Among Emergency Department Patients in the Opt-Out Testing Era

Opt-out HIV screening is recommended by the CDC for patients in all healthcare settings. We examined correlates of HIV testing refusal among urban emergency department (ED) patients. Confidential free HIV screening was offered to 32,633 ED patients in an urban tertiary care facility in Washington, DC, during May 2007–December 2011. Demographic differences in testing refusals were examined using χ² tests and generalized linear models. HIV testing refusal rates were 47.7 % 95 % CI (46.7–48.7), 11.7 % (11.0–12.4), 10.7 % (10.0–11.4), 16.9 % (15.9–17.9) and 26.9 % (25.6–28.2) in 2007, 2008, 2009, 2010 and 2011 respectively. Persons 33–54 years of age [adjusted prevalence ratio (APR) 1.42, (1.36–1.48)] and those ≥55 years [APR 1.39 (1.31–1.47)], versus 33–54 years; and females versus males [APR 1.07 (1.02–1.11)] were more likely to refuse testing. Opt-out HIV testing is feasible and sustainable in urban ED settings. Efforts are needed to encourage testing among older patients and women.     

EMILIN2 down‐modulates the Wnt signalling pathway and suppresses breast cancer cell growth and migration

EMILIN2 is an extracellular matrix (ECM) protein that exerts contradictory effects within the tumour microenvironment: it induces apoptosis in a number of tumour cells, but it also enhances tumour neo‐angiogenesis. In this study, we describe a new mechanism by which EMILIN2 attenuates tumour cell viability. Based on sequence homology with the cysteine‐rich domain (CRD) of the Frizzled receptors, we hypothesized that EMILIN2 could affect Wnt signalling activation and demonstrate direct interaction with the Wnt1 ligand. This physical binding leads to decreased LRP6 phosphorylation and to the down‐modulation of β‐catenin, TAZ and their target genes. As a consequence, EMILIN2 negatively affects the viability, migration and tumourigenic potential of MDA‐MB‐231 breast cancer cells in a number of two‐ and three‐dimensional in vitro assays. EMILIN2 does not modulate Wnt signalling downstream of the Wnt–Frizzled interaction, since it does not affect the activation of the pathway following treatment with the GSK3 inhibitors LiCl and CHIR99021. The interaction with Wnt1 and the subsequent biological effects require the presence of the EMI domain, as there is no effect with a deletion mutant lacking this domain. Moreover, in vivo experiments show that the ectopic expression of EMILIN2, as well as treatment with the recombinant protein, significantly reduce tumour growth and dissemination of cancer cells in nude mice. Accordingly, the tumour samples are characterized by a significant down‐regulation of the Wnt signalling pathway. Altogether, these findings provide further evidence of the complex regulations governed by EMILIN2 in the tumour microenvironment, and they identify a key extracellular regulator of the Wnt signalling pathway. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.