Physio-chemical and antibacterial characteristics of pressure spun nylon nanofibres embedded with functional silver nanoparticles

© 2015 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). Date of Acceptance: 05/06/2015A novel and facile approach to prepare hybrid nanoparticle embedded polymer nanofibers using pressurised gyration is presented. Silver nanoparticles and nylon polymer were used in this work. The polymer solution's physical properties, rotating speed and the working pressure had a significant influence on the fibre diameter and the morphology. Fibres in the range of 60–500 nm were spun using 10 wt.%, 15 wt.% and 20 wt.% nylon solutions and these bead-free fibres were processed under 0.2 MPa and 0.3 MPa working pressure and a rotational speed of 36,000 rpm. 1–4 wt.% of Ag was added to these nylon solutions and in the case of wt.% fibres in the range 50–150 nm were prepared using the same conditions of pressurised gyration. Successful incorporation of the Ag nanoparticles in nylon nanofibres was confirmed by using a combination of advanced microscopical techniques and Raman spectrometry was used to study the bonding characteristics of nylon and the Ag nanoparticles. Inductively coupled plasma mass spectroscopy showed a substantial concentration of Ag ions in the nylon fibre matrix which is essential for producing effective antibacterial properties. Antibacterial activity of the Ag-loaded nanofibres shows higher efficacy than nylon nanofibres for Gram-negative Escherichia coli and Pseudomonas aeruginosa microorganisms, and both Ag nanoparticles and the Ag ions were found to be the reason for enhanced cell death in the bacterial solutionPeer reviewe

Apoptin Induces Tumor specific Apoptosis as a Globular Multimer

Biofysische structuurchemi

Importance of nuclear localization of apoptin for tumor-specific induction of apoptosis

Biofysische structuurchemi

Recombinant apoptin multimers kill tumor cells but are nontoxic and epitope-shielded in a normal-cell-specific fashion

Biophysical Structural Chemistr

Apoptin's functional N- and C-termini independently bind DNA

AbstractApoptin induces apoptosis specifically in tumour cells, where Apoptin is enriched in the DNA-dense heterochromatin and nucleoli. In vitro, Apoptin interacts with dsDNA, forming large nucleoprotein superstructures likely to be relevant for apoptosis induction. Its N- and C-terminal domains also have cell-killing activity, although they are less potent than the full-length protein. Here, we report that both Apoptin’s N- and C-terminal halves separately bound DNA, indicating multiple independent binding sites. The reduced cell killing activity of both truncation mutants was mirrored in vitro by a reduced affinity compared to full-length Apoptin. However, none of the truncation mutants cooperatively bound DNA or formed superstructures, which suggests that cooperative DNA binding by Apoptin is required for the formation of nucleoprotein superstructures. As Apoptin’s N- and C-terminal fragments not only share apoptotic activity, but also affinity for DNA, we propose that both properties are functionally linked

Pre-TCR-triggered ERK signalling-dependent downregulation of E2A activity in Notch3-induced T-cell lymphoma

Notch and basic helix–loop–helix E2A pathways specify cell fate and regulate neoplastic transformation in a variety of cell types. Whereas Notch enhances tumorigenesis, E2A suppresses it. However, whether and how Notch and E2A interact functionally in an integrative mechanism for regulating neoplastic transformation remains to be understood. It has been shown that Notch3-induced T-cell leukaemia is abrogated by the inactivation of pTα/pre-T-cell antigen receptor (pre-TCR). We report here that Notch3-induced transcriptional activation of pTα/pre-TCR is responsible for the downregulation of E2A DNA binding and transcriptional activity. Further, the E2A messenger RNA and protein levels remain unaltered but the E2A inhibitor Id1 expression is augmented in thymocytes and T lymphoma cells derived from Notch3 transgenic mice. The increase in Id1 expression is achieved by pre-TCR-induced extracellular-signalling-regulated kinase 1/2. These observations support a model in which the upregulation of pre-TCR signalling seems to be the prerequi-site for Notch3-induced inhibition of E2A, thus leading to the development of lymphoma in Notch3 transgenic mice