The effect of reusable versus disposable draping material on infection rates in implant-based breast reconstruction: a prospective randomized trial.

BACKGROUND: Clinical infection remains a significant problem in implant-based breast reconstruction and is a physical and emotional strain to the breast reconstruction patient. Bacterial strikethrough of draping and gown material is a likely source of infection. Strategies to reduce infection in implant-based breast reconstruction are essential to improve patient outcomes. OBJECTIVE: The aim of this study is to determine if a disposable draping system is superior to reusable draping materials in the prevention of implant-based breast reconstruction infection. METHODS: This single-institution, prospective, randomized, single-blinded, IRB-approved study enrolled women with breast cancer who were eligible for implant-based breast reconstruction. The primary endpoint was clinical infection by postoperative day 30. Secondary endpoints included all other complications encountered throughout the follow-up period and culture data. Demographic data recorded included patient age, body mass index, diabetes, smoking, chemotherapy, radiation, and follow-up. Procedural data recorded included procedure type, procedure length, estimated blood loss, use of acellular dermal matrix, use of muscle flap, and inpatient versus outpatient setting. RESULTS: From March 2010 through January 2012, 107 women were randomized and 102 completed the study. Five patients were determined not to be candidates for reconstruction after randomization. There were 43 patients in the Reusable Group and 59 patients in the Disposable Group. There were no significant differences in patient demographic data, procedural data, or the type of procedure performed between groups. In the Reusable Group, there were 5 infections (12%) within 30 days compared to 0 (0%) infections in the Disposable Group (P = 0.012). There was no significant difference in secondary complications. There was a trend for positive wound cultures (11% vs. 3%, P = 0.10) and positive drape cultures (17% vs.4%, P = 0.08) in patients with clinical infection. There were no differences in the number of colony-forming units or positive cultures between groups. CONCLUSIONS: Disposable draping material is superior to a reusable draping system in the prevention of clinical infection within the immediate postoperative period. This study did not demonstrate a clear link between intraoperative culture data and the development of clinical infection. A completely disposable gown and draping system is recommended during implant-based breast reconstruction.

Influence of frontosphenoidal suture synostosis on skull dysmorphology in unicoronal suture synostosis.

Severity of the Harlequin deformity seen in unicoronal synostosis may be augmented when frontoparietal suture synostosis has an associated fusion of the frontosphenoidal suture or in cases of isolated frontosphenoidal synostosis. The purpose of the current study is to characterize various suture fusion patterns along the coronal ring using a modified orbital index (MOI), orbital angle (OA), and endocranial base (EB) angle.This study is a retrospective single institution cohort study. Charts were reviewed over the past 12 years; patients with isolated UCS were included. MOI, OA, and EB were used to identify 3 groups of UCS patients.Twenty-one patients were identified for inclusion in skeletal dysmorphology analysis using MOI, OA, and EB measures. Frontoparietal synostosis patients were diagnosed at significantly younger ages than frontoparietal + frontosphenoidal patients (P = 0.0001). Ipsilateral MOI measures were more severe for frontoparietal patients compared with frontoparietal + frontosphenoidal patients (P = 0.0239). There was a trend for more severe ipsilateral OA measures in frontoparietal patients compared with frontoparietal + frontosphenoidal patients (P = 0.181).Modified orbital index, OA, and EB measurements are useful in the diagnosis of suture fusion patterns in UCS patients. Frontoparietal synostosis has more severe Harlequin deformity compared with frontoparietal + frontosphenoidal patients. Frontosphenoidal fusion coinciding with frontoparietal synostosis may blunt the severity of skeletal dysmorphology in UCS patients and be associated with a delayed diagnosis. Attention must be paid to assessing the frontosphenoidal suture to assure adequate surgical release.

Downstream of tyrosine kinases-1 and Src homology 2-containing inositol 5'-phosphatase are required for regulation of CD4+CD25+ T cell development.

The adaptor protein, downstream of tyrosine kinases-1 (Dok-1), and the phosphatase SHIP are both tyrosine phosphorylated in response to T cell stimulation. However, a function for these molecules in T cell development has not been defined. To clarify the role of Dok-1 and SHIP in T cell development in vivo, we compared the T cell phenotype of wild-type, Dok-1 knockout (KO), SHIP KO, and Dok-1/SHIP double-knockout (DKO) mice. Dok-1/SHIP DKO mice were runted and had a shorter life span compared with either Dok-1 KO or SHIP KO mice. Thymocyte numbers from Dok-1/SHIP DKO mice were reduced by 90%. Surface expression of both CD25 and CD69 was elevated on freshly isolated splenic CD4(+) T cells from SHIP KO and Dok-1/SHIP DKO, suggesting these cells were constitutively activated. However, these T cells did not proliferate or produce IL-2 after stimulation. Interestingly, the CD4(+) T cells from SHIP KO and Dok-1/SHIP DKO mice produced higher levels of TGF-beta, expressed Foxp3, and inhibited IL-2 production by CD3-stimulated CD4(+)CD25(-) T cells in vitro. These findings suggest Dok-1 and SHIP function in pathways that influence regulatory T cell development.

Early growth response-1 regulates lipopolysaccharide-induced suppressor of cytokine signaling-1 transcription.

Suppressor of cytokine signaling (SOCS)-1 is a critical regulator of lipopolysaccharide (LPS) tolerance and LPS-induced cytokine production. The mechanisms regulating the transcription of SOCS-1 in response to LPS are not entirely understood. Functional analysis of the SOCS-1 promoter demonstrates that early growth response-1 (Egr-1) is an important transcriptional regulator of SOCS-1. Two Egr-1 binding sites are present within the SOCS-1 promoter as shown by EMSA and supershift analysis. Further, mutation of the Egr-1 binding sites significantly reduces both the basal and LPS-induced transcriptional activity of the promoter. Chromatin immunoprecipitation experiments confirm LPS-induced binding of Egr-1 to the SOCS-1 promoter in vivo. Additionally, Egr-1(-/-) macrophages show reduced levels of LPS-induced SOCS-1 expression in comparison with macrophages derived from Egr-1(+/+) littermate controls. These results demonstrate an important role for Egr-1 in regulating both the basal and LPS-induced activity of the SOCS-1 promoter.

SOCS-1 localizes to the microtubule organizing complex-associated 20S proteasome.

The regulation of cytokine signaling is critical for controlling cellular proliferation and activation during an immune response. SOCS-1 is a potent inhibitor of Jak kinase activity and of signaling initiated by several cytokines. SOCS-1 protein levels are tightly regulated, and recent data suggest that SOCS-1 may regulate the protein levels of some signaling proteins by the ubiquitin proteasome pathway; however, the cellular mechanism by which SOCS-1 directs proteins for degradation is unknown. In this report, SOCS-1 is found to colocalize and biochemically copurify with the microtubule organizing complex (MTOC) and its associated 20S proteasome. The SOCS-1 SH2 domain is required for the localization of SOCS-1 to the MTOC. Overexpression of SOCS-1 targets Jak1 in an SH2-dependent manner to a perinuclear distribution resembling the MTOC-associated 20S proteasome. Analysis of MTOCs fractionated from SOCS-1-deficient cells demonstrates that SOCS-1 may function redundantly to regulate the localization of Jak1 to the MTOC. Nocodazole inhibits the protein turnover of SOCS-1, demonstrating that the minus-end transport of SOCS-1 to the MTOC-associated 20S proteasome is required to regulate SOCS-1 protein levels. These data link SOCS-1 directly with the proteasome pathway and suggest another function for the SH2 domain of SOCS-1 in the regulation of Jak/STAT signaling.