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Graphene Oxide Supercapacitors: A Computer Simulation Study
DeYoung, Andrew D.,Park, Sang-Won,Dhumal, Nilesh R.,Shim, Youngseon,Jung, YounJoon,Kim, Hyung J. American Chemical Society 2014 The Journal of Physical Chemistry Part C Vol.118 No.32
<P>Supercapacitors with graphene oxide (GO) electrodes in a parallel plate configuration are studied with molecular dynamics (MD) simulations. The full range of electrode oxidation from 0% (pure graphene) to 100% (fully oxidized GO) is investigated by decorating the graphene surface with hydroxyl groups. The ionic liquid 1-ethyl-3-methylimidazolium tetrafluoroborate (EMI<SUP>+</SUP>BF<SUB>4</SUB><SUP>−</SUP>) is examined as an electrolyte. Capacitance tends to decrease with increasing electrode oxidation, in agreement with several recent measurements. This trend is attributed to the decreasing reorganization ability of ions near the electrode and a widening gap in the double layer structures as the density of hydroxyl groups on the electrode surface increases.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/jpccck/2014/jpccck.2014.118.issue-32/jp5072583/production/images/medium/jp-2014-072583_0008.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/jp5072583'>ACS Electronic Supporting Info</A></P>
Mateo, Joaquin,Ganji, Gopinath,Lemech, Charlotte,Burris, Howard A.,Han, Sae-Won,Swales, Karen,Decordova, Shaun,DeYoung, M. Phillip,Smith, Deborah A.,Kalyana-Sundaram, Shanker,Wu, Jiuhua,Motwani, Monic American Association for Cancer Research 2017 Clinical Cancer Research Vol.23 No.19
<P><B>Background:</B> The PI3K/protein kinase B (AKT) pathway is commonly activated in several tumor types. Selective targeting of p110β could result in successful pathway inhibition while avoiding the on- and off-target effects of pan-PI3K inhibitors. GSK2636771 is a potent, orally bioavailable, adenosine triphosphate-competitive, selective inhibitor of PI3Kβ.</P><P><B>Methods:</B> We evaluated the safety, pharmacokinetics, pharmacodynamics and antitumor activity of GSK2636771 to define the recommended phase II dose (RP2D). During the dose-selection and dose-escalation stages (parts 1 and 2), patients with <I>PTEN</I>-deficient advanced solid tumors received escalating doses of GSK2636771 (25–500 mg once daily) using a modified 3+3 design to determine the RP2D; tumor type-specific expansion cohorts (part 3) were implemented to further assess tumor responses at the RP2D.</P><P><B>Results:</B> A total of 65 patients were enrolled; dose-limiting toxicities were hypophosphatemia and hypocalcemia. Adverse events included diarrhea (48%), nausea (40%), and vomiting (31%). Single- and repeat-dose exposure increased generally dose proportionally. GSK2636771 400 mg once daily was the RP2D. Phospho/total AKT ratio decreased with GSK2636771 in tumor and surrogate tissue. A castrate-resistant prostate cancer (CRPC) patient harboring <I>PIK3CB</I> amplification had a partial response for over a year; an additional 10 patients derived durable (≥24 weeks) clinical benefit, including two other patients with CRPC with <I>PIK3CB</I> alterations (≥34 weeks). GSK2636771 400 mg once daily orally induced sufficient exposure and target inhibition with a manageable safety profile.</P><P><B>Conclusions:</B> Genomic aberrations of <I>PIK3CB</I> may be associated with clinical benefit from GSK2636771. <I>Clin Cancer Res; 23(19); 5981–92. ©2017 AACR</I>.</P>