In vitro study of the biological interface of Bio-Oss: implications of the experimental setup.

Objectives: To systematically investigate the biological interface of Bio-Oss by analysing dissolution-precipitation behaviour and osteogenic responses using in vitro experimental systems.

Material And Methods: Different concentrations (1-100 mg/ml) of Bio-Oss were incubated in cell culture medium for 24 h before elemental concentrations for calcium, phosphorus and silicon in the medium were analysed with inductive coupled plasma-optical emission spectroscopy. Radioactive calcium-45 isotope labelling technique was used to study possible precipitation of calcium on the Bio-Oss particle.

Efficient internalization of silica-coated iron oxide nanoparticles of different sizes by primary human macrophages and dendritic cells.

Engineered nanoparticles are being considered for a wide range of biomedical applications, from magnetic resonance imaging to "smart" drug delivery systems. The development of novel nanomaterials for biomedical applications must be accompanied by careful scrutiny of their biocompatibility. In this regard, particular attention should be paid to the possible interactions between nanoparticles and cells of the immune system, our primary defense system against foreign invasion.

Toxicology of engineered nanomaterials: focus on biocompatibility, biodistribution and biodegradation.

Background: It is widely believed that engineered nanomaterials will be increasingly used in biomedical applications. However, before these novel materials can be safely applied in a clinical setting, their biocompatibility, biodistribution and biodegradation needs to be carefully assessed.

Scope Of Review: There are a number of different classes of nanoparticles that hold promise for biomedical purposes.

Acquisition of cisplatin-resistance in malignant mesothelioma cells abrogates Na+,K+,2Cl(-)-cotransport activity and cisplatin-induced early membrane blebbing.

Aims: Resistance mechanisms are important limiting factors in the treatment of solid malignancies with cis-diamminedichloroplatinum(II) (cisplatin). To gain further understanding of the effects of acquired cisplatin-resistance, we compared a human malignant pleural mesothelioma cell line (p31) to a sub-line (p31res1.2) with acquired cisplatin-resistance.

Pharmacological modulation of lung cancer cells for potassium ion depletion.

Background: Depletion of intracellular potassium ions (K+) is necessary for cells to shrink, induce DNA fragmentation and activate caspases, events which are features of apoptosis.

Materials And Methods: We used 86Rb+ as a K+ analogue to evaluate the possibility of pharmacologically depleting human pulmonary mesothelioma (P31) and small cell lung cancer (U1690) cells of K+, for future use in studies of apoptosis induction.

Results: The Na+, K+, 2CI(-)-cotransport inhibitor bumetanide transiently inhibited 86Rb+ influx, but when combined with the Na+, K+, ATPase pump inhibitor ouabain there was a marked and lasting (up to 6 h) 86Rb+ influx inhibition.

Cellular potassium ion deprivation enhances apoptosis induced by cisplatin.

The anticancer drug cisplatin induces cell death by apoptosis. Apoptosis is dependent on cellular loss of potassium ions (K+). We have recently shown that the antifungal drug amphotericin B (enhancing K+ efflux), combined with the Na+, K+, 2Cl(-)-cotransport blocker bumetanide (decreasing K+ influx), augmented cisplatin-induced apoptosis in vitro.