Interaction between triblock copolymer surfactant and low-κ dielectric surfaces relevant to CMP

We examine the effects of the nonionic triblock copolymer surfactant Pluronic P103 on three surfaces of different wettability relevant to chemical mechanical planarization (CMP). Two of the surfaces are low-k organosilicate glass (OSG) films, Coral and Black Diamond; the third is a silica surface. Atomic force microscopy (AFM) force curves were used to probe the forces over each surface in solutions of P103. Each surface was also examined in potassium sulfate solutions to investigate the effect of ionic strengths. The AFM force curves show that both P103 and potassium sulfate eliminate adhesive forces at sufficiently high concentrations. DLVO theory was used to fit the AFM approach curves in order to calculate estimated surface potentials. Interestingly, the force curves suggest that molecular orientation of the P103 is different on surfaces of different wettability. The P103 was found to adopt a flat conformation on the hydrophilic silica surface while more extended structures formed on the more hydrophobic Coral and Black Diamond surfaces. These results provide a molecular-level understanding to aid the development of CMP formulations that will provide greater control on dielectric removal rate and reduce the overall non-uniformity in film thickness across the wafer

Herpes simplex virus type 1 infection induces oxidative stress and the release of bioactive lipid peroxidation by-products in mouse P19N neural cell cultures

To determine whether herpes simplex virus type 1 (HSV-1) infection causes oxidative stress and lipid peroxidation in cultured neural cells, mouse P19 embryonal carcinoma cells were differentiated into cells with neural phenotypes (P19N cells) by retinoic acid and were then infected with HSV-1. Cellular levels of reactive oxygen species (ROS) and the release of lipid peroxidation by-products into the tissue culture medium were then measured by the generation of fluorescent markers hydroxyphenyl fluorescein and a stable chromophore produced by lipid peroxidation products, malondialdehyde (MDA) and hydroxyalkenals (4-HAEs; predominantly 4-hydroxy-2-nonenal [HNE]), respectively. HSV-1 infection increased ROS levels in neural cells as early as 1 h post infection (p.i.) and ROS levels remained elevated at 24 h p.i. This viral effect required viral entry and replication as heat- and ultraviolet light-inactivated HSV-1 were ineffective. HSV-1 infection also was associated with increased levels of MDA/HAE in the culture medium at 2 and 4 h p.i., but MDA/HAE levels were not different from those detected in mock infected control cultures at 1, 6, and 24 h p.i. HSV-1 replication in P19N cells was inhibited by the antioxidant compound ebselen and high concentrations of HNE added to the cultures, but was increased by low concentrations of HNE. These findings indicate that HSV-1 infection of neural cells causes oxidative stress that is required for efficient viral replication. Furthermore, these observations raise the possibility that soluble, bioactive lipid peroxidation by-products generated in infected neural cells may be important regulators of HSV-1 pathogenesis in the nervous system