5,5′-Bis[(1H-imidazol-1-yl)meth­yl]-2,2′-bipyridine methanol disolvate

The title compound, C18H16N6·2CH3OH, was prepared by the reaction of 5,5′-bis­(bromo­meth­yl)-2,2′-bipyridine with imidazole. The main mol­ecule lies on an inversion center located at the mid-point of the C—C bond joining the two pyridine rings. The asymmetric unit therefore contains one half-mol­ecule and one methanol solvent mol­ecule. The dihedral angle between the pyridine and imidazole rings is 72.32 (5)°. In the crystal, weak inter­molecular O—H⋯N, C—H⋯N and C—H⋯O hydrogen bonds contribute to the stabilization of the packing

3,3′-Dimethyl-1,1′-[2,2′-bipyridine-5,5′-diylbis(methyl­ene)]diimidazol-3-ium bis­(hexa­fluoro­phosphate)

The title compound, C20H22N6 2+·2PF6 −, was prepared by the reaction of 5,5′-bis­(bromo­meth­yl)-2,2′-bipyridine with 1-methyl­imidazole. The main mol­ecule lies on an inversion center located at the mid-point of the C—C bond joining the two pyridine rings. The asymmetric unit therefore contains one half-mol­ecule and one hexa­fluoro­phosphate anion. The dihedral angle between the pyridine and imidazole rings is 76.93 (7)°. In the crystal, weak inter­molecular C—H⋯F hydrogen bonds contribute to the stabilization of the packing

Novel superconducting structures of BH2 under high pressure

The crystal structures of boron hydrides in a pressure range of 50–400 GPa were studied using the genetic algorithm (GA) method combined with first-principles density functional theory calculations. BH4 and BH5 are predicted to be thermodynamically unstable. Two new BH2 structures with Cmcm and C2/c space group symmetries, respectively, were predicted, in which the B atoms tend to form two-dimensional sheets. The calculated band structures showed that in the pressure range of 50–150 GPa, the Cmcm-BH2 phase has very small gaps, while the C2/c-BH2 phase at 200–400 GPa is metallic. The superconductivity of the C2/c-BH2 structure was also investigated, and electron–phonon coupling calculations revealed that the estimated Tc values of C2/c-BH2 are about 28.18–37.31 K at 250 GPa

α-Tocopheryl Succinate Inhibits Osteoclast Formation by Suppressing Receptor Activator of Nuclear Factor-kappaB Ligand (RANKL) Expression and Bone Resorption

Objective: Osteoclasts are bone-resorbing multinucleated cells derived from the monocyte/macrophage lineage during normal and pathological bone turnover. Recently, several studies revealed that alpha-tocopheryl succinate (αTP-suc) have demonstrated potent anti-cancer activities in vitro and in vivo. However, the effects of αTP-suc on osteoclast formation and bone resorption remain unknown. Thus, in this study, we examined the effects of αTP-suc on osteoclast differentiation and bone resorbing activity in inflammatory bone loss model. Methods: Osteoclast differentiation assay was performed by cocultures of mouse bone marrow cells and calvarial osteoblasts in culture media including interleukin-1 (IL-1). Osteoclasts were stained for tartrate-resistant acid phosphatase (TRAP). The level of receptor activator of nuclear factor-kappaB ligand (RANKL) mRNA was determined by reverse transcriptase-polymerase chain reaction (RT-PCR). ICR mice were administered an intraperitoneal injections of αTP-suc or dimethyl sulfoxide (DMSO) 1 day before the implantation of a freeze-dried collagen sponge loaded with phosphate-buffered saline (PBS) or IL-1 over the calvariae and every other day for 7 days. The whole calvariae were obtained and analyzed by micro-computed tomography (CT) scanning, and stained for TRAP. Results: αTP-suc inhibits osteoclast formation in cocultures stimulated by IL-1 and decreased the level of expression of RANKL mRNA in osteoblasts. In addition, administered intraperitoneal injections of αTP-suc prevented IL-1-mediated osteoclast formation and bone loss in vivo. Conclusion: Our findings suggest that αTP-suc may have therapeutic value for treating and preventing bone-resorptive diseases, such as osteoporosis.OAIID:oai:osos.snu.ac.kr:snu2012-01/102/0000026258/9SEQ:9PERF_CD:SNU2012-01EVAL_ITEM_CD:102USER_ID:0000026258ADJUST_YN:NEMP_ID:A076310DEPT_CD:861CITE_RATE:0FILENAME:골대사학회지-TP-succinate.pdfDEPT_NM:치의학과EMAIL:[email protected]_YN:NCONFIRM:

Ambient particulate matter (PM10) concentrations in major urban areas of Korea during 1996–2010

AbstractIn this study, ambient particulate matter pollution was investigated using monthly PM10 concentration data collected from seven major cities in Korea from 1996 to 2010. The highest mean value for the whole study period is seen from the capital city, Seoul (63.2±17.9μg m–3), while the lowest is from Ulsan (46.7±14.8μg m–3). The concentrations of PM10 in all cities exhibited seasonal variations with the peak values occurring consistently in spring (March or April). The PM10 data in each city consistently exhibited strong correlations (p<0.01) with gaseous pollutants (SO2, NO2, and CO), except for O3 (p>0.05). The analysis of long term trends of PM10 levels indicates a weak but consistent decline in concentrations in most cities with the relative average annual reductions of between 0.4 and 2.8% y–1

Pathogenic roles of CXCL10 signaling through CXCR3 and TLR4 in macrophages and T cells: relevance for arthritis

Abbreviations ACK: Ammonium–chloride–potassium; BMM: Bone marrow-derived macrophage; CAIA: Collagen antibody-induced arthritis; CIA: Collagen-induced arthritis; CsA: Cyclosporin A; CTX: C-terminal telopeptide; CXCL10: C-X-C motif chemokine 10; CXCR3: Chemokine receptor 3; DAPI: 4′,6-Diamidino-2- phenylindole; EDTA: Ethylenediaminetetraacetic acid; ELISA: Enzyme-linked immunosorbent assay; FITC: Fluorescein isothiocyanate; H&E: Hematoxylin and eosin; IFN-γ: Interferon gamma; IL: Interleukin; LPS: Lipopolysaccharide; NFATc1: Nuclear factor of activated T cells, cytoplasmic 1; PBS: Phosphatebuffered saline; RA: Rheumatoid arthritis; RANKL: Receptor activator of nuclear factor kappa-B; TLR4: Toll-like receptor 4; TNFα: Tumor necrosis factor alpha; TRAP: Tartrate-resistant acid phosphatase; WT: Wild-typeAbstract Background Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by uncontrolled joint inflammation and destruction of bone and cartilage. We previously reported that C-X-C motif chemokine 10 (CXCL10; also called IP-10) has important roles in joint inflammation and bone destruction in arthritis. However, the specific mechanisms by which CXCL10 regulates the recruitment of inflammatory cells and the production of osteoclastogenic cytokines in RA progression are not fully understood. Methods Bone marrow-derived macrophages and CD4+ T cells were isolated from wild-type (WT), Cxcl10 –/–, and Cxcr3 –/– mice. CXCL10-induced migration was performed using a Boyden chamber, and CXCL10-stimulated production of osteoclastogenic cytokines was measured by quantitative real-time PCR and ELISA. Collagen antibody-induced arthritis (CAIA) was induced by administration of collagen type II antibodies and lipopolysaccharide to the mice. Clinical scores were analyzed and hind paws were collected for high-resolution micro-CT, and histomorphometry. Serum was used to assess bone turnover and levels of osteoclastogenic cytokines. Results CXCL10 increased the migration of inflammatory cells through C-X-C chemokine receptor 3 (CXCR3)-mediated, but not toll-like receptor 4 (TLR4)-mediated, ERK activation. Interestingly, both receptors CXCR3 and TLR4 were simultaneously required for CXCL10-stimulated production of osteoclastogenic cytokines in CD4+ T cells. Furthermore, calcineurin-dependent NFATc1 activation was essential for CXCL10-induced RANKL expression. In vivo, F4/80+ macrophages and CD4+ T cells robustly infiltrated into synovium of WT mice with CAIA but were significantly reduced in both Cxcl10 –/– and Cxcr3 –/– mice. Serum concentrations of osteoclastogenic cytokines and bone destruction were also reduced in the knockout mice, leading to attenuated progression of arthritis. Conclusion These findings highlight the importance of CXCL10 signaling in the pathogenesis of RA and provide previously unidentified details of the mechanisms by which CXCL10 promotes the development of arthritis.This study was supported by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning (NRF-2014R1A2A2A01002531)

Finding Faint Intermediate-mass Black Holes in the Radio Band

We discuss the prospects for detecting faint intermediate-mass black holes, such as those predicted to exist in the cores of globular clusters and dwarf spheroidal galaxies. We briefly summarize the difficulties of stellar dynamical searches, then show that recently discovered relations between black hole mass, X-ray luminosity and radio luminosity imply that in most cases, these black holes should be more easily detected in the radio than in the X-rays. Finally, we show upper limits from some radio observations of globular clusters, and discuss the possibility that the radio source in the core of the Ursa Minor dwarf spheroidal galaxy might be a $\sim 10,000-100,000 M_\odot$ black hole.Comment: 10 pages, no figures, to appear in From X-ray Binaries to Quasars: Black Hole Accretion on All Mass Scales, ed. T. J. Maccarone, R. P. Fender, and L. C. Ho (Dordrecht: Kluwer

Braggoriton--Excitation in Photonic Crystal Infiltrated with Polarizable Medium

Light propagation in a photonic crystal infiltrated with polarizable molecules is considered. We demonstrate that the interplay between the spatial dispersion caused by Bragg diffraction and polaritonic frequency dispersion gives rise to novel propagating excitations, or braggoritons, with intragap frequencies. We derive the braggoriton dispersion relation and show that it is governed by two parameters, namely, the strength of light-matter interaction and detuning between the Bragg frequency and that of the infiltrated molecules. We also study defect-induced states when the photonic band gap is divided into two subgaps by the braggoritonic branches and find that each defect creates two intragap localized states inside each subgap.Comment: LaTeX, 8 pages, 5 figure