32 research outputs found
Standing waves for acoustic levitation
Standing waves are the most popular method to achieve acoustic trapping. Particles with greater acoustic impedance than the propagation medium will be trapped at the pressure nodes of a standing wave. Acoustic trapping can be used to hold particles of various materials and sizes, without the need of a close-loop controlling system. Acoustic levitation is a helpful and versatile tool for biomaterials and chemistry, with applications in spectroscopy and lab-on-a-droplet procedures. In this chapter, multiple methods are presented to simulate the acoustic field generated by one or multiple emitters. From the acoustic field, models such as the Gor'kov potential or the Flux Integral are applied to calculate the force exerted on the levitated particles. The position and angle of the acoustic emitters play a fundamental role, thus we analyse commonly used configurations such as emitter and reflector, two opposed emitters, or arrangements using phased arrays
Mass Spectrometric Sampling of a Liquid Surface by Nanoliter Droplet Generation from Bursting Bubbles and Focused Acoustic Pulses: Application to Studies of Interfacial Chemistry
In vitro function of the human liver ABC transporter MDR3 and its extended X loop mutant
Phase II trial of gemcitabine, paclitaxel, and cisplatin in advanced transitional cell carcinoma
Phase II trial of gemcitabine, paclitaxel, and cisplatin in advanced transitional cell carcinoma
An Environmental Management Information System for Improving Reverse Logistics Decision-Making
A reverse logistics chain mathematical model for a sustainable production system of perishable goods based on demand optimization
Functional interplay between MDM2, p63/p73 and mutant p53
Many cancers express mutant p53 proteins that have lost wild-type tumor suppressor activity and, in many cases, have acquired oncogenic functions that can contribute to tumor progression. These activities of mutant p53 reflect interactions with several other proteins, including the p53 family members p63 and p73. Mutations in p53 that affect protein conformation (such as R175H) show strong binding to p63 and p73, whereas p53 mutants that only mildly affect the conformation (such as R273H) bind less well. A previously described aggregation domain of mutant p53 is not required for p63 or p73 binding; indeed, mutations within this region lead to the acquisition of a mutant p53 phenotype—including a conformational shift, p63/p73 binding and the ability to promote invasion. The activity of wild-type p53 is regulated by an interaction with MDM2 and we have investigated the potential role of MDM2 in the mutant p53/p63/p73 interactions. Both mutant p53 and p73 bind MDM2 well, whereas p63 binds much more weakly. We found that MDM2 can inhibit p63 binding to p53R175H but enhances the weaker p53R273H/p73 interaction. These effects on the interactions are reflected in an ability of MDM2 to relieve the inhibition of p63 by p53R175H, but enhance the inhibition of p73 activity by p53R175H and R273H. We propose a model in which MDM2 competes with p63 for binding to p53R175H to restore p63 activity, but forms a trimeric complex with p73 and p53R273H to more strongly inhibit p73 function