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Kang, Yesol,Obaid, M.,Jang, Jaewon,Ham, Moon-Ho,Kim, In S. Elsevier 2018 CHEMOSPHERE - Vol.207 No.-
<P><B>Abstract</B></P> <P>A novel polysulfone (PSf) nanocomposite ultrafiltration (UF) membrane using sulfonated graphene oxide (SGO) as additives was fabricated and investigated. SGO nanoparticles were chemically synthesized from graphene oxide (GO) by using sulfuric acid (H<SUB>2</SUB>SO<SUB>4</SUB>) and were confirmed by Raman and Fourier transform infrared (FTIR) spectroscopy. The morphology of prepared membranes was characterized by scanning electron microscopy (SEM), energy dispersive x-ray (EDX) and atomic force microscopy (AFM). Results showed that adding small amount (less than 0.3 wt%) of SGO improved wettability, porosity and mean pore size of PSf/SGO membranes compared to the pristine PSf membrane and significantly enhanced the water flux of SGO incorporated PSf membranes. In UF performance, the nanocomposite membrane prepared by adding 1.5 w/w% SGO of PSf (designated as M1.5) showed the highest water flux result, which was 125% higher than the control PSf membrane (no SGO addition). Interestingly, there was no trade-off between water flux and bovine serum albumin (BSA) rejection, i.e more than 98% BSA rejection. The addition of SGO hydrophilic additives also showed better results in long-term BSA separation performance. The enhancement of hybrid membrane's properties was attributed to the hydrophilicity of sulfonic acid group (SO<SUB>3</SUB>H) on the surface of SGO additive. This study suggested that the SGO nanoparticle is a promising candidate to modify the PSf UF membranes.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Mixed matrix UF membranes by incorporating sulfonated GO into polysulfone matrix. </LI> <LI> Hydrophilicity, porosity and mean pore size were enhanced in SGO hybrid PSf membranes. </LI> <LI> SGO nanoparticles significantly improved the pure water flux of membranes. </LI> <LI> Over 98% BSA rejection rate exhibited for all membranes. </LI> </UL> </P>
Bak, Yesol,Kim, Heejong,Kang, Jeong-Woo,Lee, Dong Hun,Kim, Man Sub,Park, Yun Sun,Kim, Jung-Hee,Jung, Kang-Yeoun,Lim, Yoongho,Hong, Jintae,Yoon, Do-Young American Chemical Society 2011 Journal of agricultural and food chemistry Vol.59 No.18
<P>Naringenin, a well-known naturally occurring flavonone, demonstrates cytotoxicity in a variety of human cancer cell lines; its inhibitory effects on tumor growth have spurred interest in its therapeutic application. In this study, naringenin was derivatized to produce more effective small-molecule inhibitors of cancer cell proliferation, and the anticancer effects of its derivative, 5-hydroxy-7,4′-diacetyloxyflavanone-<I>N</I>-phenyl hydrazone (N101-43), in non-small-cell lung cancer (NSCLC) cell lines NCI-H460, A549, and NCI-H1299 were investigated. Naringenin itself possesses no cytotoxicity against lung cancer cells. In contrast, N101-43 inhibits proliferation of both NCI-H460 and A549 cell lines; this capacity is lost in p53-lacking NCI-H1299 cells. N101-43 induces apoptosis via sub-G<SUB>1</SUB> cell-cycle arrest in NCI-H460 and via G<SUB>0</SUB>/G<SUB>1</SUB> arrest in A549 cells. Expression of apoptosis and cell-cycle regulatory factors is altered: Cyclins A and D1 and phospho-pRb are down-regulated, but expression of CDK inhibitors such as p21, p27, and p53 is enhanced by N101-43 treatment; N101-43 also increases expression levels of the extrinsic death receptor Fas and its binding partner FasL. Furthermore, N101-43 treatment diminishes levels of cell survival factors such as PI3K and p-Akt dose-dependently, and N101-43 additionally induces cleavage of the pro-apoptotic factors caspase-3, caspase-8, and poly ADP-ribose polymerase (PARP). Cumulatively, these investigations show that the naringenin derivative N101-43 induces apoptosis via up-regulation of Fas/FasL expression, activation of caspase cascades, and inhibition of PI3K/Akt survival signaling pathways in NCI-H460 and A549 cells. In conclusion, these data indicate that N101-43 may have potential as an anticancer agent in NSCLC.</P>
Kang, Jeong-Woo,Park, Yun Sun,Lee, Dong Hun,Kim, Jung-hee,Kim, Man Sub,Bak, Yesol,Hong, Jintae,Yoon, Do-Young American Society for Biochemistry and Molecular Bi 2012 The Journal of biological chemistry Vol.287 No.42
<P>IL-32α is known as a proinflammatory cytokine. However, several evidences implying its action in cells have been recently reported. In this study, we present for the first time that IL-32α plays an intracellular mediatory role in IL-6 production using constitutive expression systems for IL-32α in THP-1 cells. We show that phorbol 12-myristate 13-acetate (PMA)-induced increase in IL-6 production by IL-32α-expressing cells was higher than that by empty vector-expressing cells and that this increase occurred in a time- and dose-dependent manner. Treatment with MAPK inhibitors did not diminish this effect of IL-32α, and NF-κB signaling activity was similar in the two cell lines. Because the augmenting effect of IL-32α was dependent on the PKC activator PMA, we tested various PKC inhibitors. The pan-PKC inhibitor Gö6850 and the PKCϵ inhibitor Ro-31-8220 abrogated the augmenting effect of IL-32α on IL-6 production, whereas the classical PKC inhibitor Gö6976 and the PKCδ inhibitor rottlerin did not. In addition, IL-32α was co-immunoprecipitated with PMA-activated PKCϵ, and this interaction was totally inhibited by the PKCϵ inhibitor Ro-31-8220. PMA-induced enhancement of STAT3 phosphorylation was observed only in IL-32α-expressing cells, and this enhancement was inhibited by Ro-31-8220, but not by Gö6976. We demonstrate that IL-32α mediated STAT3 phosphorylation by forming a trimeric complex with PKCϵ and enhanced STAT3 localization onto the IL-6 promoter and thereby increased IL-6 expression. Thus, our data indicate that the intracellular interaction of IL-32α with PKCϵ and STAT3 promotes STAT3 binding to the IL-6 promoter by enforcing STAT3 phosphorylation, which results in increased production of IL-6.</P>
Obaid, M.,Kang, Yesol,Wang, Sungrok,Yoon, Myung-Han,Kim, Chang-Min,Song, Jun-ho,Kim, In S. The Royal Society of Chemistry 2018 Journal of Materials Chemistry A Vol.6 No.25
<P>Although forward osmosis (FO) technology is considered to be a sustainable solution for the water and energy shortage, it has not been commercialized yet due to a few factors. Internal concentration polarization (ICP) is one of the most important barriers preventing the commercialization of the technology. To overcome the ICP obstacle, novel high-performance thin-film nanocomposite (TFN) membranes were successfully fabricated <I>via</I> interfacial polymerization on robust freestanding graphene oxide (GO) incorporated polyvinylidene fluoride (PVDF) nanofiber substrates. Compared to the pristine PVDF nanofiber substrate, the incorporation of GO (ranging from 0.1-15 wt%) significantly alters the chemical structure, porosity, wettability, morphology, and mechanical properties of the substrate, leading to an enhancement in the TFN membrane performance. The results showed that TFN5 (containing 5% GO) membrane possesses the lowest structural parameter of 85.5 μm (one of the best values in the literature), indicating a low internal concentration polarization (ICP) effect, resulting in a remarkably heightened water permeability (<I>A</I>; 2.96 L m<SUP>−2</SUP> h<SUP>−1</SUP> bar<SUP>−1</SUP>, enhanced by 167% compared to TFC). As a result, the membrane achieved the highest FO water flux at all draw solution concentrations (0.5-2 M NaCl), and the maximum FO water flux was 80.9 L m<SUP>−2</SUP> h<SUP>−1</SUP> (LMH) with a comparable specific salt flux (<I>J</I>s/<I>J</I>v) of 0.41 g L<SUP>−1</SUP> in the active layer facing the deionized feed water (AL-FS) when 2 M NaCl was applied as a draw solution. Interestingly, TFN5 was found to be the strongest material, with outstanding flexibility and strength over that of the TFC membrane. Furthermore, it showed high stability and durability during long-term FO operation. More importantly, the interaction mechanism between PVDF and GO was proposed schematically. Overall, the obtained results show highly efficient and promising TFN membranes that may overcome the drawbacks of the aforementioned FO membranes.</P>