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Kim, Heonjo,Chae, Youngjoo,Lee, Duck Hyun,Kim, Minsik,Huh, Jiyoung,Kim, Youngki,Kim, Hyunjin,Kim, Hyun Jung,Kim, Sang Ouk,Baik, Hionsuck,Choi, Kihang,Kim, Jong Seung,Yi, Gi-Ra,Lee, Kwangyeol WILEY-VCH Verlag 2010 Angewandte Chemie Vol.49 No.33
<B>Graphic Abstract</B> <P>Playing a dual role as a catalyst that destabilizes Fe nanoparticles to form soluble precursors in situ and as a catalytic center for nanorod growth allows Pd nanoparticles to transform Fe nanoparticles and a P source into Fe<SUB>2</SUB>P nanorods (see scheme). The diameter and length of the Fe<SUB>2</SUB>P nanorods can be fine-tuned by means of the diameter of the Pd nanoparticles and the Fe/Pd ratio, respectively. <img src='wiley_img_2010/14337851-2010-49-33-ANIE201001822-content.gif' alt='wiley_img_2010/14337851-2010-49-33-ANIE201001822-content'> </P>
Kim, Heonjo,Chae, Youngjoo,Lee, Duck Hyun,Kim, Minsik,Huh, Jiyoung,Kim, Youngki,Kim, Hyunjin,Kim, Hyun Jung,Kim, Sang Ouk,Baik, Hionsuck,Choi, Kihang,Kim, Jong Seung,Yi, Gi-Ra,Lee, Kwangyeol WILEY-VCH Verlag 2010 Angewandte Chemie Vol.122 No.33
<B>Graphic Abstract</B> <P>Eine doppelte Rolle spielen Pd-Nanopartikel bei der Umwandlung von Fe-Nanopartikeln und einer P-Quelle in Fe<SUB>2</SUB>P-Nanostäbchen: als Katalysatoren, die Fe-Nanopartikel unter Bildung löslicher Vorstufen destabilisieren, und als Katalysezentren für das Wachstum von Nanostäbchen (siehe Bild). Durchmesser und Länge der Nanostäbchen lassen sich über den Durchmesser der Pd-Nanopartikel bzw. das Fe/Pd-Verhältnis einstellen. <img src='wiley_img_2010/00448249-2010-122-33-ANGE201001822-content.gif' alt='wiley_img_2010/00448249-2010-122-33-ANGE201001822-content'> </P>
<P>A superparamagnetic iron oxide nanoparticle (SPION) was coupled to 2-aminoethyl-trimethyl ammonium (TMA) in a 2-step ligand exchange reaction to produce TMA–SPION. This particle, which has a strong positive charge, was investigated as the basis for a simple and efficient method for labelling human mesenchymal stem cells (hMSCs) for noninvasive monitoring by magnetic resonance imaging (MRI). TMA–SPION has a <I>ζ</I> potential of +40 mV and a hydrodynamic size of 101 nm. In addition to its long-term stability in an aqueous solution, TMA–SPION has a low cytotoxicity and favourable magnetic properties as a <I>T</I><SUB>2</SUB> contrast agent due to its high relaxivity. The <I>T</I><SUB>2</SUB> relaxivity of TMA–SPION is 4.4 times greater than the commercially available Feridex® I.V. magnetic resonance agent. Despite a short labelling time of 4 h, hMSCs are efficiently labelled with TMA–SPION without the need for a transfection agent. An <I>in vivo</I> MRI study of a brain infarction model confirmed the utility of TMA–SPION as an MRI tracking marker of administered hMSCs.</P> <P>Graphic Abstract</P><P>Superparamagnetic magnetite nanoparticle with high r2 relaxivity (728.23 mM<SUP>-1</SUP> s<SUP>-1</SUP>) and zeta potential (+40 mV) was synthesized and evaluated <I>in vitro</I> and <I>in vivo</I>. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c1jm10247h'> </P>
Kim, Tae-Hyeong,Lim, Minji,Park, Juhee,Oh, Jung Min,Kim, Hyeongeun,Jeong, Hyunjin,Lee, Sun Ju,Park, Hee Chul,Jung, Sungmok,Kim, Byung Chul,Lee, Kyusang,Kim, Mi-Hyun,Park, Do Youn,Kim, Gwang Ha,Cho, Yo American Chemical Society 2017 ANALYTICAL CHEMISTRY - Vol.89 No.2
<P>Circulating tumor cells (CTCs) have great potential to provide minimally invasive ways for the early detection of cancer metastasis and for the response monitoring of various cancer treatments. Despite the clinical importance and progress of CTC-based cancer diagnostics, most of the current methods of enriching CTCs are difficult to implement in general hospital settings due to complex and time-consuming protocols. Among existing technologies, size-based isolation methods provide antibody-independent, relatively simple, and high throughput protocols. However, the clogging issues and lower than desired recovery rates and purity are the key challenges. In this work, inspired by antifouling membranes with liquid-filled pores in nature, clog-free, highly sensitive (95.9 +/- 3.1% recovery rate), selective (>2.5 log depletion of white blood cells), rapid (>3 mL/min), and label-free isolation of viable CTCs from whole blood without prior sample treatment is achieved using a stand-alone lab-on-a-disc system equipped with fluid-assisted separation technology (FAST). Numerical simulation and experiments show that this method provides uniform, clog-free, ultrafast cell enrichment with pressure drops much less than in conventional size-based filtration, at 1 kPa. We demonstrate the clinical utility of the point-of-care detection of CTCs with samples taken from 142 patients suffering from breast, stomach, or lung cancer.</P>
Tumor Necrosis Factor Receptor-associated Protein 1 (<i>TRAP1</i>) Mutation and TRAP1 Inhibitor Gamitrinib-triphenylphosphonium (G-TPP) Induce a Forkhead Box O (FOXO)-dependent Cell Protective Signal from Mitochondria
Kim, Hyunjin,Yang, Jinsung,Kim, Min Ju,Choi, Sekyu,Chung, Ju-Ryung,Kim, Jong-Min,Yoo, Young Hyun,Chung, Jongkyeong,Koh, Hyongjong American Society for Biochemistry and Molecular Bi 2016 The Journal of biological chemistry Vol.291 No.4
<P>TRAP1 (tumor necrosis factor receptor-associated protein 1), a mitochondrial Hsp90 family chaperone, has been identified as a critical regulator of cell survival and bioenergetics in tumor cells. To discover novel signaling networks regulated by TRAP1, we generated Drosophila TRAP1 mutants. The mutants successfully developed into adults and produced fertile progeny, showing that TRAP1 is dispensable in development and reproduction. Surprisingly, mutation or knockdown of TRAP1 markedly enhanced Drosophila survival under oxidative stress. Moreover, TRAP1 mutation ameliorated mitochondrial dysfunction and dopaminergic (DA) neuron loss induced by deletion of a familial Parkinson disease gene PINK1 (Pten-induced kinase 1) in Drosophila. Gamitrinib-triphenylphosphonium, a mitochondria-targeted Hsp90 inhibitor that increases cell death in HeLa and MCF7 cells, consistently inhibited cell death induced by oxidative stress and mitochondrial dysfunction induced by PINK1 mutation in mouse embryonic fibroblast cells and DA cell models such as SH-SY5Y and SN4741 cells. Additionally, gamitrinib-triphenylphosphonium also suppressed the defective locomotive activity and DA neuron loss in Drosophila PINK1 null mutants. In further genetic analyses, we showed enhanced expression of Thor, a downstream target gene of transcription factor FOXO, in TRAP1 mutants. Furthermore, deletion of FOXO almost nullified the protective roles of TRAP1 mutation against oxidative stress and PINK1 mutation. These results strongly suggest that inhibition of the mitochondrial chaperone TRAP1 generates a retrograde cell protective signal from mitochondria to the nucleus in a FOXO-dependent manner.</P>
<P>Pathophysiological evidences of AD have indicated that aggregation of Aβ is one of the principal causes of neuronal dysfunction, largely by way of inducing oxidative stresses such as free radical formation. We hypothesized that the known antioxidative attribute of SFN could be harnessed in Alzheimer’s treatment. SFN is an indirect, potent antioxidant derived from broccoli that has previously been found to stimulate the Nrf2-ARE pathway and facilitate several other cytoprotective mechanisms. In this study, administration of SFN ameliorated cognitive function of Aβ-induced AD acute mouse models in Y-maze and passive avoidance behavior tests. Interestingly, we found that the therapeutic effect of SFN did not involve inhibition of Aβ aggregation. While the exact mechanism of interaction of SFN in AD has not yet been ascertained, our results suggest that SFN can aid in cognitive impairment and may protect the brain from amyloidogenic damages.</P><P><B>Abbreviations:</B> Aβ, amyloid-β; AD, Alzheimer’s disease; PBS, phosphate buffered saline; DMSO, dimethyl sulfoxide; ROS, reactive oxygen species; SFN, sulforaphane; DMEM, Dulbecco’s modified eagle medium; FBS, fetal bovine serum; ICR, imprinting control region; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; DW, deionized water; ThT, thioflavin T; PA, passive avoidance; ARE, antioxidant response element.</P>
<P><B>Purpose</B></P><P>This study determined the effects of oleoresin capsicum (OC) and nanoemulsion OC (NOC) on obesity in obese rats fed a high-fat diet.</P><P><B>Methods</B></P><P>The rats were randomly separated into three groups: a high-fat (HF) diet group, HF + OC diet group, and HF + NOC diet group. All groups were fed the diet and water ad libitum for 14 weeks.</P><P><B>Results</B></P><P>NOC reduced the body weight and adipose tissue mass, whereas OC did not. OC and NOC reduced mRNA levels of adipogenic genes, including peroxisome proliferator-activated receptor (<I>PPAR</I>)-γ, sterol regulatory element-binding protein-1c, and fatty acid-binding protein in white adipose tissue. The mRNA levels of genes related to β-oxidation or thermogenesis including <I>PPAR</I>-<I>α</I>, palmitoyltransferase-1α, and uncoupling protein-2 were increased by the OC and NOC relative to the HF group. Both OC and NOC clearly stimulated AMP-activated protein kinase (AMPK) activity. In particular, <I>PPAR</I>-<I>α</I>, palmitoyltransferase-1α, uncoupling protein-2 expression, and AMPK activity were significantly increased in the NOC group compared to in the OC group. NOC decreased glycerol-3-phosphate dehydrogenase activity whereas OC did not.</P><P><B>Conclusion</B></P><P>From these results, NOC could be suggested as a potential anti-obesity agent in obese rats fed a HF diet. The effects of the NOC on obesity were associated with changes of multiple gene expression, activation of AMPK, and inhibition of glycerol-3-phosphate dehydrogenase in white adipose tissue.</P>
Kim, Hyunjin,Lee, Hyunpyo,Kim, Mokwon,Bae, Youngjoon,Baek, Woonjoong,Park, Kwangjin,Park, Seongyong,Kim, Taeyoung,Kwon, Hyukjae,Choi, Wonsung,Kang, Kisuk,Kwon, Soonchul,Im, Dongmin Elsevier 2017 Carbon Vol.117 No.-
<P>Li-O-2 batteries have been proposed as next-generation energy-storage devices, but this technology is hindered by serious problems including parasitic reactions, degradation, and leakage of the electrolyte. Li-O-2 batteries are also currently designed to have a rigid bulky structure, which cannot satisfy the flexibility demands of modern electronics. Herein, we report the significant enhancement of the electrochemical performance and flexibility of a Li-O-2 battery by introducing a free-standing, binder-free carbon nanotube cathode with a bimodal pore architecture. This electrode structure imparted stability to active sites during the recovery of discharge products to the initial state, providing long-term cyclability of more than 100 cycles in a tetraethylene glycol dimethyl ether electrolyte system. The O-2 transportation and conductivity were also improved, yielding an increased discharge capacity of 5500 mAh g(-1) (nearly twice that of a non-porous cathode) and minimizing parasitic reactions. This novel bimodal-pore cathode exhibited an increased tri-phase boundary for the Li-O-2 reactive zone in the interconnected CNT network. The small pore structures (similar to 50 nm) accommodated Li2O2, and the large pore structures (similar to 385 nm) enabled effective oxygen diffusion without clogging the pores. Moreover, Li+ and oxygen diffusion were facilitated by the two independent channels provided by the pore structures. (C) 2017 Elsevier Ltd. All rights reserved.</P>