Investigation of 6TSWCNT by Cs-Corrected Transmission Electron Microscopy

Extended abstract of a paper presented at Microscopy and Microanalysis 2009 in Richmond, Virginia, USA, July 26 - July 30, 200

Imaging of GaAs Nanowire Using Combined Aberration-corrected TEM/STEM and Exit Wave Restoration

Extended abstract of a paper presented at Microscopy and Microanalysis 2009 in Richmond, Virginia, USA, July 26 - July 30, 200

Targeting low-cost type-II heterostructures: Synthesis, structure and photoreactivity

One design strategy by which to iterate the photocatalytic efficiency of semiconducting nanomaterials for harvesting solar energy involves the synthesis of type-II heterostructured materials. In this article, a straightforward, facile and environmentally benign route to heterostructures in which SnO₂ nanospheres are capped by PbS nanocubes is reported. It offers to address current limitations to photocatalytic efficiency brought about by electron-hole recombination and narrow photoresponsive ranges in many existing systems. PbS nanocubes are grown in the presence of preformed SnO₂ nanospheres by functionalizing the surface of the latter using cetyltrimethylammonium bromide (CTAB). Heterostructure formation is confirmed by X-ray diffraction (XRD), Raman spectroscopy, X-ray photoelectron spectroscopy (XPS), Brunauer-Emmett-Teller (BET) surface area analysis, and transmission electron microscopy (TEM) analysis. Rietveld refinement has been exploited to simultaneously elucidate the atomic and microstructures of these materials, allowing the quantitative determination of particle structure and stability. The combination of narrow band-gap semiconductor (PbS) and wide band-gap semiconductor (SnO₂) endows the heterostructured nanomaterial with potential as a photocatalyst and, in the degradation of Rhodamine B (RhB) dye under solar simulation, it showed superior photocatalytic activity to that of its separate SnO₂ and PbS components. A strong type-II interaction is demonstrated by the heterostructure and a charge separation mechanism has been utilized to clarify this behaviour.A. K. acknowledges support from the Royal Society's Newton International Fellowship scheme (NF130808). B. R. K. thanks the UK EPSRC for financial support (EP/J500380/1)

Plasticity of Adult Human Pancreatic Duct Cells by Neurogenin3-Mediated Reprogramming

AIMS/HYPOTHESIS: Duct cells isolated from adult human pancreas can be reprogrammed to express islet beta cell genes by adenoviral transduction of the developmental transcription factor neurogenin3 (Ngn3). In this study we aimed to fully characterize the extent of this reprogramming and intended to improve it. METHODS: The extent of the Ngn3-mediated duct-to-endocrine cell reprogramming was measured employing genome wide mRNA profiling. By modulation of the Delta-Notch signaling or addition of pancreatic endocrine transcription factors Myt1, MafA and Pdx1 we intended to improve the reprogramming. RESULTS: Ngn3 stimulates duct cells to express a focused set of genes that are characteristic for islet endocrine cells and/or neural tissues. This neuro-endocrine shift however, is incomplete with less than 10% of full duct-to-endocrine reprogramming achieved. Transduction of exogenous Ngn3 activates endogenous Ngn3 suggesting auto-activation of this gene. Furthermore, pancreatic endocrine reprogramming of human duct cells can be moderately enhanced by inhibition of Delta-Notch signaling as well as by co-expressing the transcription factor Myt1, but not MafA and Pdx1. CONCLUSIONS/INTERPRETATION: The results provide further insight into the plasticity of adult human duct cells and suggest measurable routes to enhance Ngn3-mediated in vitro reprogramming protocols for regenerative beta cell therapy in diabetes

Targeted agents and immunotherapies: optimizing outcomes in melanoma

Treatment options for patients with metastatic melanoma, and especially BRAF-mutant melanoma, have changed dramatically in the past 5 years, with the FDA approval of eight new therapeutic agents. During this period, the treatment paradigm for BRAF-mutant disease has evolved rapidly: the standard-of-care BRAF-targeted approach has shifted from single-agent BRAF inhibition to combination therapy with a BRAF and a MEK inhibitor. Concurrently, immunotherapy has transitioned from cytokine-based treatment to antibody-mediated blockade of the cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) and, now, the programmed cell-death protein 1 (PD-1) immune checkpoints. These changes in the treatment landscape have dramatically improved patient outcomes, with the median overall survival of patients with advanced-stage melanoma increasing from approximately 9 months before 2011 to at least 2 years - and probably longer for those with BRAF-V600-mutant disease. Herein, we review the clinical trial data that established the standard-of-care treatment approaches for advanced-stage melanoma. Mechanisms of resistance and biomarkers of response to BRAF-targeted treatments and immunotherapies are discussed, and the contrasting clinical benefits and limitations of these therapies are explored. We summarize the state of the field and outline a rational approach to frontline-treatment selection for each individual patient with BRAF-mutant melanoma