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Fundamentals and Application of Porous Media Filtration for the Removal of Nanoparticles from Industrial Wastewater
Increasing use of engineered nanomaterials presents concerns as some nanoparticles appear to be harmful to both human health and the environment. Effective treatment methods are required to remove problematic nanoparticles from (waste)water streams. Porous media filtration, commonly used for the removal of particulate matter, shows promise for nanoparticle treatment. The goal of this work is to investigate the potential of porous media filtration for the abatement of nanoparticles from aqueous waste streams. To this end, an automated method was developed that allows real-time and in-situ monitoring of nanoparticle transport and retention in porous media using online measurement of UV-visible absorbance or fluorescence. Development of fluorescent-core nano-silica (n-SiO₂) in controllable sizes provided an excellent tracer for nanoparticle transport in porous media. Measurement of n-SiO₂ by destructive techniques is complicated by high natural Si background levels. Fluorescence monitoring enables real-time measurement, facilitating rapid evaluation of n-SiO₂ transport. Synthesized n-SiO₂ remain in their primary sizes making an evaluation of the behavioral change of particles due to transition into the "nano" range possible. A comparison of the role of particle size on transport in porous media displayed the importance of particle number concentration as the dominance of site-specific adsorption may be obscured by simple mass concentration evaluation.T he effectiveness of different bed materials, namely, sand, activated carbon (AC), and diatomaceous earth (DE), for the removal of TiO₂ nanoparticles (n-TiO₂) from aqueous streams was investigated. DE proved promising for n-TiO₂ capture shown by its high bed capacity (33.8 mg TiO₂ g⁻¹(medium)) compared to AC (0.23 mg TiO₂ g⁻¹(medium)) or sand (0.004 mg TiO₂ g⁻¹(medium)). The presence of organic and synthetic contaminants produced varying effects on n-TiO₂ retention, mostly due to either enhanced electrostatic or steric interactions. Application of a process simulator combining physical straining with site-specific interactions, delineating physisorption from chemisorption and diffusion limited interactions, enabled the accurate fit of n-TiO₂ transport in sand, AC and DE. The fitting process revealed the advantage of DE due to increased physisorption and physical straining of n-TiO₂. Modeling of this system afforded the elucidation of controlling retention mechanisms and provides a basis for future scaling and system design
Expression of an LMNA-N195K variant of A-type lamins results in cardiac conduction defects and death in mice
An Uncommon Presentation for Cardiac Melanoma
A 66-year-old man with locally advanced malignant melanoma, which was surgically resected, presented with a 3-week history of dizziness, recurrent near-syncopal episodes and generalized weakness. He was found to have sustained polymorphic ventricular tachycardia in the setting of cardiac melanoma. We draw attention to an unusual presentation of malignant melanoma with cardiac metastasis and discuss both its etiology and treatment options
Heart-type fatty acid-binding protein reciprocally regulates glucose and fatty acid utilization during exercise
First published September 30
. Abnormal mitochondrial bioenergetics and heart rate dysfunction in mice lacking very-long-chain acyl-CoA dehydrogenase. Am J Physiol Heart Circ Physiol 290: H1289 -H1297, 2006. First published September 30, 2005 doi:10.1152/ajpheart.00811.2005.-Mitochondrial very-long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is associated with severe hypoglycemia, cardiac dysfunction, and sudden death in neonates and children. Sudden death is common, but the underlying mechanisms are not fully understood. We report on a mouse model of VLCAD deficiency with a phenotype induced by the stresses of fasting and cold, which includes hypoglycemia, hypothermia, and severe bradycardia. The administration of glucose did not rescue the mice under stress conditions, but rewarming alone consistently led to heart rate recovery. Brown adipose tissue (BAT) from the VLCAD Ϫ/Ϫ mice showed elevated levels of the uncoupling protein isoforms and peroxisome proliferator-activated receptor-␣. Biochemical assessment of the VLCAD Ϫ/Ϫ mice BAT showed increased oxygen consumption, attributed to uncoupled respiration in the absence of stress. ADP-stimulated respiration was 23.05 (SD 4.17) and 68.24 (SD 6.3) nmol O2⅐min Ϫ1 ⅐mg mitochondrial protein Ϫ1 for VLCAD ϩ/ϩ and VLCAD Ϫ/Ϫ mice, respectively (P Ͻ 0.001), and carbonyl cyanide p-trifluoromethoxyphenylhydrazone-stimulated respiration was 35.9 (SD 3.6) and 49.3 (SD 9) nmol O2⅐min Ϫ1 ⅐mg mitochondrial protein Ϫ1 for VLCAD ϩ/ϩ and VLCAD Ϫ/Ϫ mice, respectively (P Ͻ 0.20), but these rates were insufficient to protect them in the cold. We conclude that disturbed mitochondrial bioenergetics in BAT is a critical contributing factor for the cold sensitivity in VLCAD deficiency. Our observations provide insights into the possible mechanisms of stress-induced death in human newborns with abnormal fat metabolism and elucidate targeting of specific substrates for particular metabolic needs. genetics; inborn errors; acyl-coenzyme A dehydrogenase; cardiomyopathy; hypothermia; hypoglycemia; bradycardia INBORN ERRORS OF METABOLISM affecting mitochondrial fatty acid oxidation are recessively inherited and account for a substantial number of cases of sudden infant death There are a number of theorized mechanisms proposed as the causes of death in VLCAD deficiency. These include energy starvation, metabolic acidosis, generalized or organspecific metabolic failure, lipotoxicity, and cardiac rhythm abnormalities. Previous work has shown that mice lacking the mitochondrial acyl-CoA dehydrogenases are cold sensitive MATERIALS AND METHODS VLCAD-deficient mice. VLCAD-deficient mice were generated as described previously (11). The VLCAD gene was inactivated by homologous recombination such that exons 1 through 7 were replaced with a neomycin resistance gene. Male 129sv/C57/BL6 VLCADdeficient mice 2 mo of age were used in this study. These experiments Address for reprint requests and other correspondence: V. Exil, Vanderbil