Temperature Sensors Based on Organic Field-Effect Transistors

The rapid growth of wearable electronics, Internet of Things, smart packaging, and advanced healthcare technologies demand a large number of flexible, thin, lightweight, and ultralow-cost sensors. The accurate and precise determination of temperature in a narrow range (~0–50 °C) around ambient temperatures and near-body temperatures is critical for most of these applications. Temperature sensors based on organic field-effect transistors (OFETs) have the advantages of low manufacturing cost, excellent mechanical flexibility, easy integration with other devices, low cross-sensitivity, and multi-stimuli detectability and, therefore, are very suitable for the above applications. This article provides a timely overview of research progress in the development of OFET-based temperature sensors. First, the working mechanism of OFETs, the fundamental theories of charge transport in organic semiconductors, and common types of OFET temperature sensors based on the sensing element are briefly introduced. Next, notable advances in the development of OFET temperature sensors using small-molecule and polymer semiconductors are discussed separately. Finally, the progress of OFET temperature sensors is summarized, and the challenges associated with OFET temperature sensors and the perspectives of research directions in this field are presented

Evidence for post-translational processing of vascular endothelial (VE)-cadherin in brain tumors: towards a candidate biomarker

Vessel abnormalities are among the most important features in malignant glioma. Vascular endothelial (VE)-cadherin is of major importance for vascular integrity. Upon cytokine challenge, VE-cadherin structural modifications have been described including tyrosine phosphorylation and cleavage. The goal of this study was to examine whether these events occurred in human glioma vessels. We demonstrated that VE-cadherin is highly expressed in human glioma tissue and tyrosine phosphorylated at site Y685, a site previously found phosphorylated upon VEGF challenge, via Src activation. In vitro experiments showed that VEGF-induced VE-cadherin phosphorylation, preceded the cleavage of its extracellular adhesive domain (sVE, 90 kDa). Interestingly, metalloproteases (MMPs) secreted by glioma cell lines were responsible for sVE release. Because VEGF and MMPs are important components of tumor microenvironment, we hypothesized that VE-cadherin proteolysis might occur in human brain tumors. Analysis of glioma patient sera prior treatment confirmed the presence of sVE in bloodstream. Furthermore, sVE levels studied in a cohort of 53 glioma patients were significantly predictive of the overall survival at three years (HR 0.13 [0.04; 0.40] p≤0.001), irrespective to histopathological grade of tumors. Altogether, these results suggest that VE-cadherin structural modifications should be examined as candidate biomarkers of tumor vessel abnormalities, with promising applications in oncolog

The tyrosine-kinase inhibitor sunitinib targets vascular endothelial (VE)-cadherin: a marker of response to antitumoural treatment in metastatic renal cell carcinoma

International audienceVascular endothelial (VE)-cadherin is an endothelial cell-specific protein responsible for endothelium integrity. Its adhesive properties are regulated by post-translational processing, such as tyrosine phosphorylation at site Y685 in its cytoplasmic domain, and cleavage of its extracellular domain (sVE). In hormone-refractory metastatic breast cancer, we recently demonstrated that sVE levels correlate to poor survival. In the present study, we determine whether kidney cancer therapies had an effect on VE-cadherin structural modifications and their clinical interest to monitor patient outcome