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BACKGROUND: Permanent stoma (PS) is common following treatment of anastomotic leakage (AL) after anterior resection (AR) and ways of predicting successful treatment outcome are missing. PURPOSE: To explore radiological variables in rectal contrast studies in their relation to end-result of PS following treatment for AL after AR. MATERIAL AND METHODS: The Swedish Cancer Registry (SCRCR) was explored for AL cases after AR for rectal cancer in patients operated in the region of Skåne from 1 January 2001 to 31 December 2011. Among identified AL cases, patients subjected to radiological imaging consistent with AL were evaluated according to a predetermined set of radiological variables. Information of PS as the end-result after AL treatment were retrieved from medical records. RESULTS: Thirty-two patients had radiological imaging available for analysis confirming AL after AR; PS rate after a median follow-up of 87 months (range = 21-165) after AR was 62%. Radiological findings compatible with abscess (P = 0.023) and a leak size ≤6 mm (P = 0.049) were significantly associated with PS. CONCLUSION: In this limited explorative study, our findings suggest that abscess status and leak size could correspond to outcome of PS in treatment for AL after AR. Additional studies are warranted to further explore this subject.
RESUMO
AIMS: Alternative transcription and splicing of the allograft inflammatory factor-1 (AIF-1) gene results in the expression of two different proteins: AIF-1 and interferon responsive transcript-1 (IRT-1). Here, we explore the impact of AIF-1 and IRT-1 on vascular smooth muscle cell (VSMC) activation and neointima formation, the mechanisms underlying their alternative splicing, and associations of AIF-1 and IRT-1 mRNA with parameters defining human atherosclerotic plaque phenotype. METHODS AND RESULTS: Translation of AIF-1 and IRT-1 results in different products with contrasting cellular distribution and functions. Overexpression of AIF-1 stimulates migration and proliferation of human VSMCs, whereas IRT-1 exerts opposite effects. Adenoviral infection of angioplasty-injured rat carotid arteries with AdAIF-1 exacerbates intima hyperplasia, whereas infection with AdIRT-1 reduces neointima. Expression of these variants is modulated by changes in nuclear factor of activated T-cells (NFAT) activity. Pharmacological inhibition of NFAT or targeting of NFATc3 with small interfering RNA (siRNA) lowers the AIF-1/IRT-1 ratio and favours an anti-proliferative outcome. NFAT acts as a repressor on the IRT-1 transcriptional start site, which is also sensitive to interferon-γ stimulation. Expression of AIF-1 mRNA in human carotid plaques associates with less extracellular matrix and a more pro-inflammatory plaque and plasma profile, features that may predispose to plaque rupture. In contrast, expression of IRT-1 mRNA associates with a less aggressive phenotype and less VSMCs at the most stenotic region of the plaque. CONCLUSION: Inhibition of NFAT signalling, by shifting the AIF-1/IRT-1 ratio, may be an attractive target to regulate the VSMC response to injury and manipulate plaque stability in atherosclerosis.