Vortex-actuated cell sorting: a new cell sorter, based on a transient microfluidic vortex generated by a thermal vapour bubble.

Traditionally, capacitive micromachined ultrasonic transducers (CMUTs) are modeled using the isotropic plate equation, and this leads to deviations between analytical calculations and finite element modeling (FEM). In this paper, the deflection is calculated for both circular and square plates using the full anisotropic plate equation. It is shown that the anisotropic calculations match excellently with FEM, whereas an isotropic approach causes up to 10% deviations in deflection. For circular plates, an exact solution can be found. For square plates using the Galerkin method, and utilizing the symmetry of the silicon crystal, a compact and accurate expression for the deflection can be obtained. The deviation from FEM in center deflection is <0.1%. The theory of multilayer plates is also applied to the CMUT. The deflection of a square plate was measured on fabricated CMUTs using a white light interferometer. Fitting the plate parameter for the anisotropic calculated deflection to the measurement, a deviation of 0.07% is seen. Electrostatic and small-signal dynamic analysis are performed using energy considerations including anisotropy. The stable position, effective spring constant, pullin distance, and pull-in voltage are found for both circular and square anisotropic plates, and the pressure dependence is included by comparison with the corresponding analysis for a parallel plate. Measurements on fabricated devices with both circular and square plates subjected to increasing bias voltage are performed, and it is observed that the models including anisotropic effects are within the uncertainty interval of the measurements. Finally, a lumped element small-signal model for both circular and square anisotropic plates is derived to describe the dynamics of the CMUT.

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Deterioration in mitochondrial function leads to hepatic ischemia and reperfusion injury (IRI) in liver surgery and transplantation. 3D optical cryoimaging was used to measure the levels of mitochondrial coenzymes NADH and FAD, and their redox ratio (NADH/FAD) gave a quantitative marker for hepatocyte oxidative stress during IRI. Using a rat model, five groups were compared: control, ischemia for 60 or 90 minutes (Isc60, Isc90), ischemia for 60 or 90 minutes followed by reperfusion of 24 hours (IRI60, IRI90). Ischemia alone did not cause a significant increase in the redox ratio; however, the redox ratio in both IRI60 and IRI90 groups was significantly decreased by 29% and 71%, respectively. A significant correlation was observed between the redox ratio and other markers of injury such as serum aminotransferase levels and the tissue ATP level. The mitochondrial redox state can be successfully measured using optical cryoimaging as a quantitative marker of hepatic IR injury.

Whole thoracic irradiation (WTI) is known to cause deterioration in cardiac function. Whether irradiation predisposes the heart to further ischemia and reperfusion (IR) injury is not well known. The aim of this study is to examine the susceptibility of rat hearts to IR injury following a single fraction of 15 Gy WTI and to investigate the role of mitochondrial metabolism in the differential susceptibility to IR injury. After day 35 of irradiation, ex vivo hearts from irradiated and nonirradiated rats (controls) were exposed to 25-min global ischemia followed by 60-min IR, or hearts were perfused without IR for the same protocol duration [time controls (TC)]. Online fluorometry of metabolic indices [redox state: reduced nicotinamide adenine dinucleotide (NADH), oxidized flavin adenine dinucleotide (FAD), and NADH/FAD redox ratio] and functional variables [systolic left ventricular pressure (LVP), diastolic LVP (diaLVP), coronary flow (CF), and heart rate were recorded in the beating heart; developed LVP (dLVP) and rate pressure product (RPP)] were derived. At the end of each experimental protocol, hearts were immediately snap frozen in liquid N2 for later three-dimensional imaging of the mitochondrial redox state using optical cryoimaging. Irradiation caused a delay in recovery of dLVP and RPP after IR when compared to nonirradiated hearts but recovered to the same level at the end of reperfusion. CF in the irradiated hearts recovered better than the control hearts after IR injury. Both fluorometry and 3-D cryoimaging showed that in WTI and control hearts, the redox ratio increased during ischemia (reduced) and decreased on reperfusion (oxidized) when compared to their respective TCs; however, there was no significant difference in the redox state between WTI and controls. In conclusion, our results show that although irradiation of rat hearts compromised baseline cardiovascular function, it did not alter cardiac mitochondrial redox state and induce greater susceptibility of these hearts to IR injury.