2,097 research outputs found

    Quantum-based Mechanical Force Realization in Pico-Newton Range

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    We propose mechanical force realization based on flux quantization in the pico-Newton range. By controlling the number of flux quantum in a superconducting annulus, a force can be created as integer multiples of a constant step. For a 50 nm-thick Nb annulus with the inner and outer radii of 5 μ\mum and 10 μ\mum, respectively, and the field gradient of 10 T/m the force step is estimated to be 184 fN. The stability against thermal fluctuations is also addressed.Comment: 5 pages; 4 figure

    Optimalne potrebe juvenilnih morskih grgeča sebastes schlegeli u proteinima i lipidima

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    U ovom istraživanju su analizirane optimalne potrebe juvenilnih morskih grgeča Sebastes schlegeli u proteinima i lipidima. 810 juvenilnih riba je izabrano po principu slučajnosti i distribuirano u 27 tankova od po 50 L sa protočnih sistemom. Pripremljeno je 9 eksperimentalnih smeša u vidu 3x3 faktorijalne eksperimentalne postavke: tri nivoa proteina (45, 50 i 55%) x tri nivoa lipida (11, 15 i 19%). Nivo proteina je imao uticaj na prirast riba, dok nivo lipida nije. Prirast riba hranjenih smešom u odnosu 50P-15L (50% proteina i 15% lipida) je bio veći nego prirast riba hranjenih smešama sa 45% proteina, bez obzira na nivo lipida, ali je bio isti kao kod riba hranjenih sa smešama 50P-11L, 50P-19L, 55P-11L, 55P-15L i 55P-19L. Stopa efikasnosti hrane (FER) riba je bila pod uticajem proteina u hrani ali ne i nivoa lipida. Stopa efikasnosti proteina (PER) riba je takođe bila pod uticajem proteina u hrani ali ne i nivoa lipida. Može se zaključiti da je za juvenilne Sebastes schlegeli optimalan nivo proteina i lipida za dobar prirast i iskoristljivost hrane (PER and NRE) 50% i 15% odnosno 45% i 19%, dok je optimalan odnos proteina i energije 27.4 i 23.9 mg protein/kJ

    Synthetic chloride transporters with the binding mode observed in a ClC chloride channel

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    A series of synthetic molecules bearing the same hydrogen bonding mode observed in StClC were prepared and their transport ability of chloride ion across a lipid membrane was systematically optimized.close4

    Size distributions of atmospheric particulate matter and associated trace metals in the multi-industrial city of Ulsan, Korea

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    Particulate matter (PM) was collected using micro-orifice uniform deposit impactors from a residential (RES) site and an industrial (IND) site in Ulsan, South Korea, in September-October 2014. The PM samples were measured based on their size distributions (11 stages), ranging from 0.06 ??m to over 18.0 ??m. Nine trace metals (As, Se, Cr, V, Cd, Pb, Ba, Sb, and Zn) associated with PM were analyzed. The PM samples exhibited weak bimodal distributions irrespective of sampling sites and events, and the mean concentrations of total PM (TPM) measured at the IND site (56.7 ??g/m3) was higher than that measured at the RES site (38.2 ??g/m3). The IND site also showed higher levels of nine trace metals, reflecting the influence of industrial activities and traffic emissions. At both sites, four trace metals (Ba, Zn, V, and Cr) contributed to over 80% of the total concentrations in TPM. The modality of individual trace metals was not strong except for Zn; however, the nine trace metals in PM2.5 and PM10 accounted for approximately 50% and 90% of the total concentrations in TPM, respectively. This result indicates that the size distributions of PM and trace metals are important to understand how respirable PM affects public health

    Functional enhancement of neuronal cell behaviors and differentiation by elastin-mimetic recombinant protein presenting Arg-Gly-Asp peptides

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    Background: Integrin-mediated interaction of neuronal cells with extracellular matrix (ECM) is important for the control of cell adhesion, morphology, motility, and differentiation in both in vitro and in vivo systems. Arg-Gly-Asp (RGD) sequence is one of the most potent integrin-binding ligand found in many native ECM proteins. An elastin-mimetic recombinant protein, TGPG[VGRGD(VGVPG)6]20WPC, referred to as [RGD-V6]20, contains multiple RGD motifs to bind cell-surface integrins. This study aimed to investigate how surface-adsorbed recombinant protein can be used to modulate the behaviors and differentiation of neuronal cells in vitro. For this purpose, biomimetic ECM surfaces were prepared by isothermal adsorption of [RGD-V6]20 onto the tissue culture polystyrene (TCPS), and the effects of protein-coated surfaces on neuronal cell adhesion, spreading, migration, and differentiation were quantitatively measured using N2a neuroblastoma cells.Results: The [RGD-V6]20 was expressed in E. coli and purified by thermally-induced phase transition. N2a cell attachment to either [RGD-V6]20 or fibronectin followed hyperbolic binding kinetics saturating around 2 μM protein concentration. The apparent maximum cell binding to [RGD-V6]20 was approximately 96% of fibronectin, with half-maximal adhesion on [RGD-V6]20 and fibronectin occurring at a coating concentration of 2.4 × 10-7 and 1.4 × 10-7 M, respectively. The percentage of spreading cells was in the following order of proteins: fibronectin (84.3% ± 6.9%) > [RGD-V6]20 (42.9% ± 6.5%) > [V7]20 (15.5% ± 3.2%) > TCPS (less than 10%). The migration speed of N2a cells on [RGD-V6]20 was similar to that of cells on fibronectin. The expression of neuronal marker proteins Tuj1, MAP2, and GFAP was approximately 1.5-fold up-regulated by [RGD-V6]20 relative to TCPS. Moreover, by the presence of both [RGD-V6]20 and RA, the expression levels of NSE, TuJ1, NF68, MAP2, and GFAP were significantly elevated.Conclusion: We have shown that an elastin-mimetic protein consisting of alternating tropoelastin structural domains and cell-binding RGD motifs is able to stimulate neuronal cell behaviors and differentiation. In particular, adhesion-induced neural differentiation is highly desirable for neural development and nerve repair. In this context, our data emphasize that the combination of biomimetically engineered recombinant protein and isothermal adsorption approach allows for the facile preparation of bioactive matrix or coating for neural tissue regeneration. © 2012 Jeon et al.; licensee BioMed Central Ltd.1

    The C-terminal region of Bfl-1 sensitizes non-small cell lung cancer to gemcitabine-induced apoptosis by suppressing NF-κB activity and down-regulating Bfl-1

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    Gemcitabine is used to treat several cancers including lung cancer. However, tumor cells often escape gemcitabine-induced cell death via various mechanisms, which include modulating bcl-2 family members and NF-κB activation. We previously reported that the C-terminal region of Bfl-1 fused with GFP (BC) is sufficient to induce apoptosis in 293T cells. In the present study, we investigated the anti-tumor effect of combined BC gene therapy and gemcitabine chemotherapy in vitro and in vivo using non-small cell lung cancer cell lines and a xenograft model. Cell lines were resistant to low dose gemcitabine (4-40 ng/ml), which induced NF-κB activation and concomitant up-regulation of Bfl-1 (an NF-κB-regulated anti-apoptotic protein). BC induced the apoptosis of A549 and H157 cells with caspase-3 activation. Furthermore, co-treatment with BC and low dose gemcitabine synergistically and efficiently induced mitochondria-mediated apoptosis in these cells. When administered alone or with low dose gemcitabine, BC suppressed NF-κB activity, inhibited the nuclear translocation of p65/relA, and down-regulated Bfl-1 expression. Furthermore, direct suppression of Bfl-1 by RNA interference sensitized cells to gemcitabine-induced cell death, suggesting that Bfl-1 importantly regulates lung cancer cell sensitivity to gemcitabine. BC and gemcitabine co-treatment also showed a strong anti-tumor effect in a nude mouse/A549 xenograft model. These results suggest that lung cancer cells become resistant to gemcitabine via NF-κB activation and the subsequent overexpression of Bfl-1, and that BC, which has both pro-apoptotic and NF-κB inhibitory effects, could be harnessed as a gene therapy to complement gemcitabine chemotherapy in non-small cell lung cancer
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