Luminescent quantum dots (QDs) are colloidal semiconductor nanocrystals consisting of an inorganic core covered by a molecular layer of organic surfactants. Although QDs have been known for more than thirty years, they are still attracting the interest of researchers because of their unique size‐tunable optical and electrical properties arising from quantum confinement. Moreover, the controlled decoration of the QD surface with suitable molecular species enables the rational design of inorganic‐organic multicomponent architectures that can show a vast array of functionalities. This minireview highlights the recent progress in the use of surface‐modified QDs – in particular, those based on cadmium chalcogenides – as supramolecular platforms for light‐related applications such as optical sensing, triplet photosensitization, photocatalysis and phototherapy.

Heterometallic Anderson wheels of formula [(VIVO)2MII5(hmp)10Cl2](ClO4)2·2MeOH (M = Ni, 1; Co, 2) have been synthesised from the solvothermal reaction of M(ClO4)2·6H2O and VCl3 with hmpH (2-(hydroxymethyl)pyridine). The metallic skeleton describes...

We report the synthesis and characterization of four new tetranuclear Ni(II) complexes, C1-C4, all of which exhibit defective dicubane cores. The complexes C1-C4 are derived from the same salicylaldoxime derived...

Given the emerging epidemic of renal disease in HIV+ patients and the fact that HIV DNA and RNA persist in the kidneys of HIV+ individuals despite therapy, it is necessary to understand the role of direct HIV-1 infection of the kidney. HIV-associated kidney disease pathogenesis is attributed in large part to viral proteins. Expression of vpr in renal tubule epithelial cells (RTECs) induces G2 arrest, apoptosis and polyploidy.The ability of a subset of cells to overcome the G2 block and progress to polyploidy is not well understood. Polyploidy frequently associates with a bypass of cell death and disease pathogenesis. Given the ability of the kidney to serve as a unique compartment for HIV-1 infection, and the observed occurrence of polyploid cells in HIV+ renal cells, it is critical to understand the mechanisms and consequences of Vpr-induced polyploidy.Here I determined the effects of HIV-1 Vpr expression in renal cells using highly efficient transduction with VSV.G pseudotyped lentiviral vectors expressing vpr in the HK2 human tubule epithelial cell line. Using FACS, fluorescence microscopy, and live cell imaging I determined that G2 escape immediately precedes a critical junction between two distinct outcomes in Vpr+ RTECs: mitotic cell death and polyploidy. Vpr+ cells that evade aberrant mitosis and become polyploid have a substantially higher survival rate than those that undergo complete mitosis, and this survival correlates with enrichment for polyploidy in cell culture over time. Further, I identified a novel role for ATM kinase in promoting G2 arrest escape and polyploidy in Vpr+ RTECs. In summary, my work identifies ATM-dependent override of Vpr-mediated G2 arrest as a critical determinant of cell fate Vpr+ RTECs. Further, my work highlights how a poorly understood HIV mechanism, ploidy increase, may offer insight into key processes of reservoir establishment and disease pathogenesis in HIV+ kidneys.v researcher, but also her dedication to maintaining a fulfilling family life, and I aspire to achieve similar successes going forward. Dedication List of Tables List of FiguresI would like to thank my committee member and unofficial co---mentor, Dr.Donald Fox, for introducing me to the fascinating phenomenon of polyploidy. Dr. Fox's enthusiasm for science is unparalleled, and his mentorship and expertise were invaluable to the development and execution of my project. I also want to thank, Dr.David Howell, Dr. Micah Luftig and Dr. Robin Bachelder for serving on my committee.Their support, questions and feedback have made me a stronger scientist and contributed greatly to the completion of my dissertation.