Nonspecific binding is a frequently encountered problem with fluorescent labeling of tissue cultures when labeled with quantum dots. In these studies various cell lines were examined for nonspecific binding. Evidence suggests that nonspecific binding is related to cell type and may be significantly reduced by functionalizing quantum dots with poly(ethylene glycol) ligands (PEG). The length of PEG required to give a significant reduction in nonspecific binding may be as short as 12-14 ethylene glycol units.

Current approaches to the synthesis of metal oxides generally require harsh conditions. In contrast, many biological processes can produce intricate metal oxide nanostructures under ambient conditions. For example, the diatom Cylindrotheca fusiformis forms reproducible nanostructures from silicic acid using species specific peptides known as silaffins. Herein, we report that the R5 peptide a bioinspired analogue derived from the NatSil protein in C. fusiformis can form titanium dioxide (TiO2) in a concentration dependent manner from the non-natural substrate, titanium bis(ammonium lactato)dihydroxide. Additionally, the polypeptide poly(l-lysine) acts as a template for the biomimetic synthesis of TiO2. Subsequently, the nanoparticles were characterized using scanning electron microscopy, energy-dispersive X-ray spectrometry, and IR spectroscopy. A variable temperature X-ray diffraction study of the titanium dioxide phase transition from anatase to rutile was conducted. A delay in transition temperature was observed with titanium dioxide synthesized in the presence of phosphate buffer.

Hemoproteins, hemoglobin and myoglobin, once released from cells can cause severe oxidative damage as a consequence of heme redox cycling between ferric and ferryl states that generates radical species that induce lipid peroxidation. We demonstrate in vitro that acetaminophen inhibits hemoprotein-induced lipid peroxidation by reducing ferryl heme to its ferric state and quenching globin radicals. Severe muscle injury (rhabdomyolysis) is accompanied by the release of myoglobin that becomes deposited in the kidney, causing renal injury. We previously showed in a rat model of rhabdomyolysis that redox cycling between ferric and ferryl myoglobin yields radical species that cause severe oxidative damage to the kidney. In this model, acetaminophen at therapeutic plasma concentrations significantly decreased oxidant injury in the kidney, improved renal function, and reduced renal damage. These findings also provide a hypothesis for potential therapeutic applications for acetaminophen in diseases involving hemoproteinmediated oxidative injury.isoprostanes | oxidative damage | hemoglobin | myoglobin

While it is well known that the presence of lymphocytes and cytokines are important for fracture healing, the exact role of the various cytokines expressed by cells of the immune system on osteoblast biology remains unclear. To study the role of inflammatory cytokines in fracture repair, we studied tibial bone healing in wild-type and Rag1 −/− mice. Histological analysis, µCT stereology, biomechanical testing, calcein staining and quantitative RNA gene expression studies were performed on healing tibial fractures. These data provide support for Rag1 −/− mice as a model of impaired fracture healing compared to wild-type. Moreover, the pro-inflammatory cytokine, IL-17F, was found to be a key mediator in the cellular response of the immune system in osteogenesis. In vitro studies showed that IL-17F alone stimulated osteoblast maturation. We propose a model in which the Th17 subset of T-lymphocytes produces IL-17F to stimulate bone healing. This is a pivotal link in advancing our current understanding of the molecular and cellular basis of fracture healing, which in turn may aid in optimizing fracture management and in the treatment of impaired bone healing.