Room-Temperature Routes Toward the Creation of Zinc Oxide Films from Molecular Precursors

The fabrication of “flexible” electronics on plastic substrates with low melting points requires the development of thin-film deposition techniques that operate at low temperatures. This is easily achieved with vacuum- or solution-processed molecular or polymeric semiconductors, but oxide materials remain a significant challenge. Here, we show that zinc oxide (ZnO) can be prepared using only room-temperature processes, with the molecular thin-film precursor zinc phthalocyanine (ZnPc), followed by UV-light treatment in vacuum to elicit degradation of the organic components and transformation of the deposited film to the oxide material. The degradation mechanism was assessed by studying the influence of the atmosphere during the reaction: it was particularly sensitive to the oxygen pressure in the chamber and optimal degradation conditions were established as 3 mbar with 40% oxygen in nitrogen. The morphology of the film remained relatively unchanged during the reaction, but a detailed analysis of its composition using both scanning transmission electron microscopy and secondary ion mass spectrometry revealed that a 40 nm thick layer containing ZnO results from the 100 nm thick precursor after complete reaction. Our methodology represents a simple route for the fabrication of oxides and multilayer structures that can be easily integrated into current molecular thin-film growth setups, without the need for a high-temperature step

Enhanced activation of an amino-terminally truncated isoform of the voltage-gated proton channel HVCN1 enriched in malignant B cells

The final published version can be found here: http://dx.doi.org/10.1073/pnas.1411390111M.C. is the recipient of a Bennett Fellowship from Leukaemia and Lymphoma Research (ref. 12002). M.A.B. is supported by a GlaxoSmithKline Oncology–Biotechnology and Biological Sciences Research Council Collaborative Awards in Science and Engineering PhD studentship. This work was supported by National Institutes of Health Grants GM087507 and GM102336 (to T.E.D.)

Room temperature routes towards the creation of zinc oxide films from molecular precursors

The advent of “flexible” electronics on plastic substrates with low melting points requires the development of thin film deposition techniques that operate at low temperatures. This is easily achieved with vacuum or solution - processed molecular or polymeric semiconductors, but oxide materials remain a significant challenge. Here we show that zinc oxide (ZnO) can be prep ared using only room - temperature processes, using the molecular thin film precursor zinc phthalocyanine (ZnPc), follow ed by vacuum ultra - violet light treatment to elicit degradation of the organic components and transformation of the deposited film to oxide mate rial. The degradation mechanism was assessed by studying the influence of the atmosphere during the reaction: i t was particularly sensitive to oxygen pressure in the chamber and optimal degradation conditions were established as 3 mbar with 40% oxygen in nitrogen. The morphology of the film was relatively unchanged during the reaction, but detailed analysis of its composition using both scanning transmission electron microscopy (STEM) and secondary ion mass spectrometry (SIMS) revealed that a 40 nm thick layer containing ZnO results from the 100 nm thick precursor after complete reaction. Our methodology represent s a simple route for the fabrication of oxides and multilayer structures that can be easily integrated into current molecular thin film growth setups, without the n eed for a high temperature step

HVCN1 modulates BCR signal strength via regulation of BCR-dependent generation of reactive oxygen species

Voltage-gated proton currents regulate generation of reactive oxygen species (ROS) in phagocytic cells. In B cells, stimulation of the B cell antigen receptor (BCR) results in the production of ROS that participate in B cell activation, but the involvement of proton channels is unknown. We report here that the voltage-gated proton channel HVCN1 associated with the BCR complex and was internalized together with the BCR after activation. BCR-induced generation of ROS was lower in HVCN1-deficient B cells, which resulted in attenuated BCR signaling via impaired BCR-dependent oxidation of the tyrosine phosphatase SHP-1. This resulted in less activation of the kinases Syk and Akt, impaired mitochondrial respiration and glycolysis, and diminished antibody responses in vivo. Our findings identify unanticipated functions for proton channels in B cells and demonstrate the importance of ROS in BCR signaling and downstream metabolism