Methods. In this study, we differentiated hUC-MSCs with in vitro synthesized pancreatic-duodenal homebox 1 (PDX1) messenger (m)RNA into islet-like cell clusters. hUC-MSCs were confirmed by both biomarker detection and functional differentiation. In vitro synthesized PDX1 messenger RNA can be transfected into hUC-MSCs efficiently. The upregulated expression of PDX1 protein can be detected 4 h after transfection and remains detectable for 36 h. Results.

The induction of islet-like structures was confirmed by means of morphology and dithizone staining. Reverse transcriptase polymerase chain reaction results revealed the expression of some key pancreatic transcription factors, such as PDX1, NeuroD, NKX6.1, Glut-2 and insulin in islet-like AZD4547 cell clusters. Immunofluorescence analysis showed that differentiated cells express both insulin and C-peptide. Enzyme-linked immunosorbent assay analysis validated the insulin secretion of islet-like cell clusters in response to the glucose stimulation. Conclusions. Our results demonstrate the use of in vitro synthesized PDX1 messenger RNA to differentiate hUC-MSCs into islet-like

cells and pave the way toward the development of reprogramming and directed-differentiation methods for Z-DEVD-FMK inhibitor the expression of encoded proteins.”
“Left-ventricular end-systolic elastance (Ees) is an index of cardiac contractility, but the invasive nature of its assessment has limited perioperative application. We explored the feasibility of a minimally invasive method of Ees estimation for perioperative assessment of cardiac function and evaluated the suitability of phenylephrine as a loading intervention.\n\nIn 17 surgical patients, Ees was

determined as the slope of the end-systolic pressurevolume relation, which was obtained from non-invasive or invasive continuous arterial Emricasan pressure measurements and left-ventricular volume determinations using transoesophageal echocardiography (TOE). Ees was determined using as loading interventions preload reduction by inferior vena cava compression (IVCC) and afterload increase by phenylephrine administration.\n\nMedian invasive Ees determined with phenylephrine estimated 1.05 (0.591.21) mm Hg ml(1) and with IVCC 0.58 (0.311.13) mm Hg ml(1). BlandAltman analysis to evaluate the level of agreement between minimally invasive and invasive Ees estimation revealed a bias of 0.03 (0.12) mm Hg ml(1) with limits of agreement from 0.27 to 0.21 mm Hg ml(1) and the percentage error was 33. Agreement between Ees obtained with phenylephrine and IVCC revealed a bias of 0.15 (0.69) mm Hg ml(1) with limits of agreement from 1.21 to 1.51 mm Hg ml(1) and a percentage error of 149.\n\nIt is feasible to determine Ees combining continuous non-invasive arterial pressure measurements and left-ventricular volume determinations with TOE.