Magic™ Anti-Cytokeratin, WSS polyclonal antibody

Most patients with papillary thyroid carcinoma have good prognosis; however, recurrence rates and the need of salvage treatment remain a significant problem for 5-40% of patients. Although several risk classifications based on clinicopathological prognostic factors are used, it is not possible to predict which patients will have a higher risk of recurrence. The objective of the study is to analyse the impact of cytokeratin-19 and Ki-67 immunoexpression as predictive markers of the risk of recurrence in papillary thyroid carcinoma. This is a retrospective case-control study, including 42 patients with papillary thyroid carcinoma and 42 controls. The groups were matched by gender, age and pathological staging T and N. Slides were made by the microarray tissue system. Multivariate logistic regression was applied to identify an independent risk factor for recurrence. Of the 42 selected cases, 30 patients (71.4%) were female and 12 (28.6%) were male, ranging in age from 10 to 80 years (median of 39 years). Most patients (64.3%) had tumors at initial T staging (T1-T2). Half of the sample was classified as low risk according to the American Thyroid Association (ATA) risk stratification. Follow-up time ranged from 46 to 196 months, with time to recurrence from 2 to 106 months (median, 30 months). CK-19 and Ki-67 immunoexpression had a statistically significant association with the risk of recurrence (p = 0.029 and p = 0.007, respectively). In multivariate logistic regression analysis, immunoexpression for these markers was an independent risk factor for locoregional recurrence (OR-9,64; CI-1.14-81.01 and OR-3,21; CI-1.32-7.94, respectively). The immunohistochemical analysis of the Ki-67 and CK-19 markers is useful to predict tumour recurrence in patients with papillary thyroid carcinoma.

Aims Myocardial infarction (MI) leads to activation of cardiac fibroblasts (aCFs) and at the same time induces the formation of epicardium-derived cells at the heart surface. To discriminate between the two cell populations, we elaborated a fast and efficient protocol for the simultaneous isolation and characterization of aCFs and epicardial stromal cells (EpiSCs) from the infarcted mouse heart. Methods and results For the isolation of aCFs and EpiSCs, infarcted hearts (50 min ischaemia/reperfusion) were digested by perfusion with a collagenase-containing medium for only 8 min, while EpiSCs were enzymatically removed from the outside by applying mild shear forces via a motor driven device. Cardiac fibroblasts (CFs) isolated from unstressed hearts served as control. Viability of isolated cells was >90%. Purity of EpiSCs was confirmed by immunofluorescence staining and qPCR of various mesenchymal markers including Wilms-tumor-protein-1. Microarray analysis of CFs, aCFs, and EpiSCs on day 5 post-MI revealed a unique gene expression pattern in the EpiSC fraction, which was enriched for epithelial markers and epithelial to mesenchymal transition-related genes. Compared to aCFs, 336 significantly altered gene entities were identified in the EpiSC fraction. qPCR analysis showed high expression of Serpinb2, Cxcl13, Adora2b, and Il10 in EpiSCs relative to CFs and aCFs. Furthermore, microarray data identified Ddahl and Cemip to be highly up-regulated in aCFs compared to CFs. Immunostaining of the infarcted heart revealed a unique distribution of Dermokine, Aquaporin-1, Cytokeratin, Lipocalin2, and Periostin within the epicardial cell Layer. Conclusions We describe the simultaneous isolation of viable, purified fractions of aCFs and EpiSCs from the infarcted mouse heart. In this study, several differentially expressed markers for aCFs and EpiSCs were identified, underlining the importance of cell separation to study heterogeneity of stromal cells in the heating process after MI.