ABSTRACT
The low thermal conductivity of polymers is a barrier to their use in applications requiring high thermal conductivity such as electronic packaging, heat exchangers, and thermal management devices. Polyolefins represent about 55% of global thermoplastic production, and therefore improving their thermal conductivity is essential for many applications. This review analyzes the advances in enhancing the thermal conductivity of polyolefin composites. First, the mechanisms of thermal transport in polyolefin composites and the key parameters that govern conductive heat transfer through the interface between the matrix and the filler are discussed. Then, the advantage and limitations of the current methods for measuring thermal conductivity are analyzed. Moreover, the progress in predicting the thermal conductivity of polymer composites using modeling and simulation is discussed. Furthermore, polyolefin composites and nanocomposites with different thermally conductive fillers are reviewed and analyzed. Finally, the key challenges and future directions for developing thermally enhanced polyolefin composites are outlined.
ABSTRACT
17 beta-estradiol induces rapid effects on cells of the immune system via plasma membrane surface receptor but the ways in which delayed signals involving intracellular receptors affect the same functions are not well understood. To study the delayed but sustained events in estradiol signaling, we have investigated macrophage Ca(2+) signaling, detected specific Ca(2+) ion channel activated and found a relationship between intracellular calcium [Ca(2+)](i) and macrophage release of reactive oxygen species (ROS) and nitric oxide (NO) during delayed 17 beta-estradiol activity. We found evidence of additional effect of estradiol on capacitative entry of Ca(2+), Ca(2+) entry through L-type channel and a direct relationship between [Ca(2+)](i) and generation of ROS and NO. This study demonstrates that 17 beta-estradiol exhibits a delayed phase of Ca(2+) influx involving L-type channel and regulates macrophage immune redox function.
Subject(s)
Calcium Channels, L-Type/metabolism , Calcium Signaling/drug effects , Estradiol/pharmacology , Macrophages/drug effects , Macrophages/metabolism , Nitric Oxide/metabolism , Reactive Oxygen Species/metabolism , Animals , Cell Line , Dose-Response Relationship, Drug , Mice , Oxidation-Reduction/drug effects , Time FactorsABSTRACT
OBJECTIVES: Despite an efficient macrophage immune capability, Chlamydia pneumoniae infects host cells and causes chronic diseases. To gain better insights into C. pneumoniae survival mechanisms in macrophages, its growth in regular RAW-264.7 cells (nitric oxide sufficient NO (+)) and RAW-264.7 cells (nitric oxide insufficient NO (-)) were studied. METHODS: Role of Ca(2+), NO and reactive oxygen species (ROS) during C. pneumoniae infection in macrophages were determined. RESULTS: RAW-264.7 NO (-) cells supported significantly Chlamydia growth, showing an upregulation of ROS, superoxide dismutase (SOD) and catalase activities as compared with RAW-264.7 NO (+) cell. Ascorbic acid, inducible nitric oxide synthase inhibitor and glutathione significantly prompted Chlamydia inclusion formation. Cytosolic Ca(2+) had regulatory effect on organism growth, NO generation, SOD and catalase activities in both cell types. CONCLUSIONS: These findings suggest that minimal Ca(2+) signaling in macrophages at early stages of infection, NO and ROS release have modulatory effects onC. pneumoniae survival, onset of persistence and chronicity, processes which are needed for the initiation of diseases in which C. pneumoniae has been implicated as a possible etiologic agent.
