Probing the electrical impedance of thin films on a quartz crystal microbalance (QCM), making use of frequency shifts and piezoelectric stiffening.

Using a temperature-responsive polymer film as an example, it was shown that a conventional quartz crystal microbalance (QCM) can probe a sample's electrical properties in addition to its thickness and softness. The film's electrical impedance was accessed by alternating between the driving voltage being applied to the front electrode and the back electrode. The opposing electrode was grounded in both cases. In the first configuration, the electrical properties of the sample do have an influence on the resonance frequency because of piezoelectric stiffening. In the second, they do not. Using this scheme, it was monitored how the electrical impedance of a film composed of a mixture of poly-N-isopropylacrylamide and polyvinylalcohol changes when the film swells and deswells.

Two suppressors of sel-12 encode C2H2 zinc-finger proteins that regulate presenilin transcription in Caenorhabditis elegans.

Mutations in presenilin genes are associated with familial Alzheimer's disease in humans and affect LIN-12/Notch signaling in all organisms tested so far. Loss of sel-12 presenilin activity in Caenorhabditis elegans results in a completely penetrant egg-laying defect. In screens for extragenic suppressors of the sel-12 egg-laying defect, we have isolated mutations in at least five genes. We report the cloning and characterization of spr-3 and spr-4, which encode large basic C(2)H(2) zinc-finger proteins. Suppression of sel-12 by spr-3 and spr-4 requires the activity of the second presenilin gene, hop-1. Mutations in both spr-3 and spr-4 de-repress hop-1 transcription in the early larval stages when hop-1 expression is normally nearly undetectable. As sel-12 and hop-1 are functionally redundant, this suggests that mutations in spr-3 and spr-4 bypass the need for one presenilin by stage-specifically de-repressing the transcription of the other. Both spr-3 and spr-4 code for proteins similar to the human REST/NRSF (Re1 silencing transcription factor/neural-restrictive silencing factor) transcriptional repressors. As other Spr genes encode proteins homologous to components of the CoREST co-repressor complex that interacts with REST, and the INHAT (inhibitor of acetyltransferase) co-repressor complex, our data suggest that all Spr genes may function through the same mechanism that involves transcriptional repression of the hop-1 locus.