Periprosthetic Fluid Analysis in the Diagnosis of Breast Implant Infections Using Cell Count and Differential.

Background: One of the most devastating complications following implant-based breast reconstruction is periprosthetic infection. Making a prompt and accurate diagnosis has been a challenge as plastic surgeons are limited by nonspecific systemic markers of infection, clinical examination findings, or imaging modalities.

Objectives: The aim of this study is to evaluate the use of periprosthetic fluid using cell count and differential as an aid in the diagnosis of infection.

Role of transcriptional coregulator GRIP1 in the anti-inflammatory actions of glucocorticoids.

Inhibition of cytokine gene expression by the hormone-activated glucocorticoid receptor (GR) is the key component of the anti-inflammatory actions of glucocorticoids, yet the underlying molecular mechanisms remain obscure. Here we report that glucocorticoid repression of cytokine genes in primary macrophages is mediated by GR-interacting protein (GRIP)1, a transcriptional coregulator of the p160 family, which is recruited to the p65-occupied genomic NFκB-binding sites in conjunction with liganded GR. We created a mouse strain enabling a conditional hematopoietic cell-restricted deletion of GRIP1 in adult animals.

Glucocorticoid-dependent phosphorylation of the transcriptional coregulator GRIP1.

Much of the regulatory diversity in eukaryotic transcription is provided by coregulators, which are recruited by DNA-binding factors to propagate signaling to basal machinery or chromatin. p160 family members, including the glucocorticoid receptor (GR)-interacting protein 1 (GRIP1), function as coactivators for GR, a ligand-dependent transcription factor of the nuclear receptor superfamily. Unlike other p160s, GRIP1 also potentiates GR-mediated repression of AP1 and NF-κB targets and, surprisingly, transcriptional activation by interferon regulatory factors.