A Multimodal Sensing Device for Simultaneous Measurement of Dissolved Oxygen and Hydrogen Ions by Monolithic Integration of FET-Based Sensors.

We examined the possibility of measuring dissolved oxygen by using a potentiometric solid-state semiconductor sensor. Thin films of tin (IV) oxide (SnO2) are widely used in oxygen gas sensors. However, their ability to detect dissolved oxygen (DO) in solutions is still unknown. In this paper, we present a method for investigating the dissolved oxygen-sensing properties of SnO2 thin films in solutions by fabricating a SnO2-gate field-effect transistor (FET). A similarly structured hydrogen ion-sensitive silicon nitride (Si3N4)-gate FET was fabricated using the same method. The transfer characteristics and sensitivities were experimentally obtained and compared. The transfer characteristics of the FET show a shift in threshold voltage in response to a decrease in DO concentration. The SnO2-gate FET exhibited a sensitivity of 4 mV/ppm, whereas the Si3N4-gate FET showed no response to DO. Although the SnO2-gate FET responds to pH changes in the solution, this sensitivity issue can be eliminated by using a Si3N4-gate FET, which is capable of selectively sensing hydrogen ions without DO sensitivity. The experimental results indicate the promising properties of SnO2 thin films for multimodal sensing applications.

Ultrastructural evidence of early endothelial damage in coronary arteries of rat cardiac allografts.

BACKGROUND: Events that occur early after transplantation, particularly immune recognition of allo-endothelium, initiate transplant vascular disease (TVD). Previous work suggests an important compromise of endothelial integrity as the allo-immune milieu evolves, although mechanisms by which integrity is altered remain unclear. Increased vascular permeability caused by endothelial damage may allow inflammatory cells, lipoproteins, other proteins, and plasma fluid to enter the sub-endothelial space, thereby contributing to the initiation of atherosclerosis. In this study, we examined endothelial integrity in coronary arteries and the proximal aorta after cardiac transplantation in rats. METHODS: We used Lewis-to-Lewis and Lewis-to-F344 rat heterotopic cardiac transplant models. We studied the effects of cyclosporine (5mg/kg/day) therapy compared with saline-treated controls. En face silver nitrate staining was performed to demonstrate endothelial cell borders and gaps. We used scanning electron microscopy to extend silver nitrate findings and to further define the presence and nature of endothelial disruptions. We used transmission electron microscopy to further characterize immune cell identity and interaction with endothelium. RESULTS: Syngrafts and cyclosporine-treated allografts showed normal-looking endothelium similar to that observed in arteries from native hearts. However, saline-treated allografts displayed progressive endothelial destruction, including large intercellular gaps, missing cells, and areas of bare extracellular matrix. Exfoliated surfaces were covered by platelets at various stages of adhesion, activation, and spreading. Similarly, we observed numerous leukocytes as either adherent to the endothelial lining or transmigrating into the sub-endothelial space. Cessation of cyclosporine therapy was associated with the development of similar abnormalities. CONCLUSIONS: Our findings indicate that, especially when immunosuppression is insufficient, early endothelial damage may promote vascular permeability and thereby initiate TVD.