Testing the single-pass VOC removal efficiency of an active green wall using methyl ethyl ketone (MEK)

© 2017, The Author(s). In recent years, research into the efficacy of indoor air biofiltration mechanisms, notably living green walls, has become more prevalent. Whilst green walls are often utilised within the built environment for their biophilic effects, there is little evidence demonstrating the efficacy of active green wall biofiltration for the removal of volatile organic compounds (VOCs) at concentrations found within an interior environment. The current work describes a novel approach to quantifying the VOC removal effectiveness by an active living green wall, which uses a mechanical system to force air through the substrate and plant foliage. After developing a single-pass efficiency protocol to understand the immediate effects of the system, the active green wall was installed into a 30-m3 chamber representative of a single room and presented with the contaminant 2-butanone (methyl ethyl ketone; MEK), a VOC commonly found in interior environments through its use in textile and plastic manufacture. Chamber inlet levels of MEK remained steady at 33.91 ± 0.541 ppbv. Utilising a forced-air system to draw the contaminated air through a green wall based on a soil-less growing medium containing activated carbon, the combined effects of substrate media and botanical component within the biofiltration system showed statistically significant VOC reduction, averaging 57% single-pass removal efficiency over multiple test procedures. These results indicate a high level of VOC removal efficiency for the active green wall biofilter tested and provide evidence that active biofiltration may aid in reducing exposure to VOCs in the indoor environment

Induction melt thermoforming of advanced multi-axial thermoplastic composite laminates

The viability of using induction heating to facilitate the wrinkle-free forming of multi-axial pre-consolidated advanced thermoplastic composites over complex geometries is explored. The research focuses on the use of tin as a medium to both heat and lubricate the forming laminate. Initial tests demonstrate the viability of the fundamental ideas of the process; induction heating is used to melt the tin sheet, which is then shown to melt the matrix phase of carbon-nylon composite laminates when stacked in a hybrid composite/tin layup. A novel low-cost reconfigurable multi-step forming tool is used to demonstrate how most of the tin can be squeezed out of the layup prior to consolidation. The multi-step tool can be augmented with segmented tooling to rapidly manufacture composite parts of high geometric complexity. In this investigation, a 'ripple' geometry containing three 'cavities' is used to demonstrate the technique. Tests demonstrated that at least three sheets of inter-laminar tin can be simultaneously melted using the induction heating system. Initial results indicate complex geometries can be formed with minimal wrinkling while removing interlaminar tin

DNA topoisomerases participate in fragility of the oncogene RET

Fragile site breakage was previously shown to result in rearrangement of the RET oncogene, resembling the rearrangements found in thyroid cancer. Common fragile sites are specific regions of the genome with a high susceptibility to DNA breakage under conditions that partially inhibit DNA replication, and often coincide with genes deleted, amplified, or rearranged in cancer. While a substantial amount of work has been performed investigating DNA repair and cell cycle checkpoint proteins vital for maintaining stability at fragile sites, little is known about the initial events leading to DNA breakage at these sites. The purpose of this study was to investigate these initial events through the detection of aphidicolin (APH)-induced DNA breakage within the RET oncogene, in which 144 APHinduced DNA breakpoints were mapped on the nucleotide level in human thyroid cells within intron 11 of RET, the breakpoint cluster region found in patients. These breakpoints were located at or near DNA topoisomerase I and/or II predicted cleavage sites, as well as at DNA secondary structural features recognized and preferentially cleaved by DNA topoisomerases I and II. Co-treatment of thyroid cells with APH and the topoisomerase catalytic inhibitors, betulinic acid and merbarone, significantly decreased APH-induced fragile site breakage within RET intron 11 and within the common fragile site FRA3B. These data demonstrate that DNA topoisomerases I and II are involved in initiating APH-induced common fragile site breakage at RET, and may engage the recognition of DNA secondary structures formed during perturbed DNA replication

Inositol Phosphate Recycling Regulates Glycolytic and Lipid Metabolism That Drives Cancer Aggressiveness

Cancer cells possess fundamentally altered metabolism that supports their pathogenic features, which includes a heightened reliance on aerobic glycolysis to provide precursors for synthesis of biomass. We show here that inositol polyphosphate phosphatase 1 (INPP1) is highly expressed in aggressive human cancer cells and primary high-grade human tumors. Inactivation of INPP1 leads to a reduction in glycolytic intermediates that feed into the synthesis of the oncogenic signaling lipid lysophosphatidic acid (LPA), which in turn impairs LPA signaling and further attenuates glycolytic metabolism in a feed-forward mechanism to impair cancer cell motility, invasiveness, and tumorigenicity. Taken together these findings reveal a novel mode of glycolytic control in cancer cells that can serve to promote key oncogenic lipid signaling pathways that drive cancer pathogenicity

Enhancement of Naringenin Bioavailability by Complexation with Hydroxypropoyl-β-Cyclodextrin

The abundant flavonoid aglycone, naringenin, which is responsible for the bitter taste in grapefruits, has been shown to possess hypolipidemic and anti-inflammatory effects both in vitro and in vivo. Recently, our group demonstrated that naringenin inhibits hepatitis C virus (HCV) production, while others demonstrated its potential in the treatment of hyperlipidemia and diabetes. However, naringenin suffers from low oral bioavailability critically limiting its clinical potential. In this study, we demonstrate that the solubility of naringenin is enhanced by complexation with β-cyclodextrin, an FDA approved excipient. Hydroxypropoyl-β-cyclodextrin (HPβCD), specifically, increased the solubility of naringenin by over 400-fold, and its transport across a Caco-2 model of the gut epithelium by 11-fold. Complexation of naringenin with HPβCD increased its plasma concentrations when fed to rats, with AUC values increasing by 7.4-fold and Cmax increasing 14.6-fold. Moreover, when the complex was administered just prior to a meal it decreased VLDL levels by 42% and increased the rate of glucose clearance by 64% compared to naringenin alone. These effects correlated with increased expression of the PPAR co-activator, PGC1α in both liver and skeletal muscle. Histology and blood chemistry analysis indicated this route of administration was not associated with damage to the intestine, kidney, or liver. These results suggest that the complexation of naringenin with HPβCD is a viable option for the oral delivery of naringenin as a therapeutic entity with applications in the treatment of dyslipidemia, diabetes, and HCV infection.National Institute of Diabetes and Digestive and Kidney Diseases (U.S.) (K01DK080241)Harvard Clinical Nutrition Research Center (P30-DK040561)European Research Council (Starting Grant (TMIHCV 242699))Massachusetts General Hospital (BioMEMS Resource Center (P41 EB-002503))Alexander Silberman Institute of Life Science

Temperature sensitive point mutations in fission yeast tropomyosin have long range effects on the stability and function of the actin- tropomyosin copolymer

The actin cytoskeleton is modulated by regulatory actin-binding proteins which fine- tune the dynamic properties of the actin polymer to regulate function. One such actin-binding protein is tropomyosin (Tpm), a highly-conserved alpha-helical dimer which stabilises actin and regulates interactions with other proteins. Temperature sensitive mutants of Tpm are invaluable tools in the study of actin filament dependent processes, critical to the viability of a cell. Here we investigated the molecular basis of the temperature sensitivity of fission yeast Tpm mutants which fail to undergo cytokinesis at the restrictive temperatures. Comparison of Contractile Actomyosin Ring (CAR) constriction as well as cell shape and size revealed the cdc8.110 or cdc8.27 mutant alleles displayed significant differences in their temperature sensitivity and impact upon actin dependent functions during the cell cycle. In vitro analysis revealed the mutant proteins displayed a different reduction in thermostability, and unexpectedly yield two discrete unfolding domains when acetylated on their amino-termini. Our findings demonstrate how subtle changes in structure (point mutations or acetylation) alter the stability not simply of discrete regions of this conserved cytoskeletal protein but of the whole molecule. This differentially impacts the stability and cellular organisation of this essential cytoskeletal protein