Статті в журналах: "Trap-loss spectroscopy"

1

WANG Li, 王丽, 张好 ZHANG Hao, and 张临杰 ZHANG Lin-jie. "Trap Loss Spectroscopy of Ultracold Cesium Rydberg Atoms." Acta Sinica Quantum Optica 24, no. 2 (2018): 178–83. http://dx.doi.org/10.3788/jqo20182402.0009.

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2

WANG Li, 王丽, 张好 ZHANG Hao, and 张临杰 ZHANG Lin-jie. "Trap Loss Spectroscopy of Ultracold Cesium Rydberg Atoms." Acta Sinica Quantum Optica 24, no. 2 (2018): 178–83. http://dx.doi.org/10.3788/jqo20182402.0501.

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3

Wang, Xin, Xiaokai Hou, Feifei Lu, Rui Chang, Lili Hao, Wenjing Su, Jiandong Bai, Jun He, and Junmin Wang. "Autler–Townes splitting in the trap-loss fluorescence spectroscopy due to single-step direct Rydberg excitation of cesium cold atomic ensemble." AIP Advances 13, no. 3 (March 1, 2023): 035126. http://dx.doi.org/10.1063/5.0141479.

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We experimentally investigate trap-loss spectra of the cesium 6 S1/2( F = 4) → 71 P3/2 Rydberg transition by combining the cesium atomic magneto-optical trap with the narrow-linewidth, continuously tunable 318.6 nm ultraviolet laser. Specifically, the atoms in the magneto-optical trap are excited to the Rydberg state due to the ultraviolet laser single-step Rydberg excitation, which leads to the reduction of atomic fluorescence. Based on the trap-loss spectroscopy technology, the Autler–Townes (AT) splitting due to a strong cooling laser is observed, and the parameter dependence of the AT splitting interval of trap-loss spectroscopy is investigated. The effective temperature of cold atoms is measured by using simplified time-of-flight fluorescence imaging. In addition, closed-loop feedback power stabilization of 318.6 nm ultraviolet laser is carried out. This lays the foundation for further experimental research related to the Rydberg atoms using ultraviolet lasers, which is of great significance for the development of quantum computing and quantum information.

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4

Wang, L. R., J. Ma, W. B. Ji, G. P. Wang, L. T. Xiao, and S. T. Jia. "Ultra-high resolution trap-loss spectroscopy of ultracold 133Cs atom long-range states in a magnetooptical trap." Laser Physics 17, no. 9 (September 2007): 1171–75. http://dx.doi.org/10.1134/s1054660x07090113.

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5

Snyder, Dalton T., Lucas J. Szalwinski, Robert L. Schrader, Valentina Pirro, Ryan Hilger, and R. Graham Cooks. "Precursor and Neutral Loss Scans in an RF Scanning Linear Quadrupole Ion Trap." Journal of The American Society for Mass Spectrometry 29, no. 7 (March 9, 2018): 1345–54. http://dx.doi.org/10.1007/s13361-018-1920-3.

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Snyder, Dalton T., Lucas J. Szalwinski, Ryan Hilger, and R. Graham Cooks. "Implementation of Precursor and Neutral Loss Scans on a Miniature Ion Trap Mass Spectrometer and Performance Comparison to a Benchtop Linear Ion Trap." Journal of The American Society for Mass Spectrometry 29, no. 7 (March 13, 2018): 1355–64. http://dx.doi.org/10.1007/s13361-018-1922-1.

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7

Szalwinski, Lucas J., Dalton T. Snyder, J. Mitchell Wells, and R. Graham Cooks. "Triple Resonance Methods to Improve Performance of Ion Trap Precursor and Neutral Loss Scans." Journal of the American Society for Mass Spectrometry 31, no. 5 (April 13, 2020): 1123–31. http://dx.doi.org/10.1021/jasms.0c00048.

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8

Yang, Seung-Dong, Jun-Kyo Jung, Jae-Gab Lim, Seong-gye Park, Hi-Deok Lee, and Ga-Won Lee. "Investigation of Intra-Nitride Charge Migration Suppression in SONOS Flash Memory." Micromachines 10, no. 6 (May 29, 2019): 356. http://dx.doi.org/10.3390/mi10060356.

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In order to suppress the intra-nitride charge spreading in 3D Silicon-Oxide-Nitride-Oxide-Silicon (SONOS) flash memory where the charge trapping layer silicon nitride is shared along the cell string, N2 plasma treated on the silicon nitride is proposed. Experimental results show that the charge loss decreased in the plasma treated device after baking at 300 °C for 2 h. To extract trap density according to the location in the trapping layer, capacitance-voltage analysis was used and N2 plasma treatment was shown to be effective to restrain the interface trap formation between blocking oxide and silicon nitride. Moreover, from X-ray Photoelectron Spectroscopy, the reduction of Si-O-N bonding was observed.

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9

Du, Bin, Qian Liu, Yu Shi, and Yushun Zhao. "The Effect of Fe3O4 Nanoparticle Size on Electrical Properties of Nanofluid Impregnated Paper and Trapping Analysis." Molecules 25, no. 16 (August 6, 2020): 3566. http://dx.doi.org/10.3390/molecules25163566.

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This paper systematically studies the effect of Fe3O4 nanoparticle size on the insulation performance of nanofluid impregnated paper. Three kinds of Fe3O4 nanoparticles with different sizes and their nanofluid impregnated papers were prepared. Environmental scanning electron microscopy (ESEM) and infrared spectroscopy were used to analyze the combination of Fe3O4 nanoparticles and nanofluid impregnated paper. The effect of nanoparticle size on breakdown voltage and several dielectric characteristics, e.g., permittivity, dielectric loss, of the nanofluid impregnated paper were comparatively investigated. Studies show that the Fe3O4 nanoparticles were bound to impregnated paper fibers by O–H bonds, while the relative permittivity and dielectric loss of the nanofluid impregnated papers were increased. Meanwhile, the increase of trap depth, caused by the nanoparticles, can trap the electric charge and improve the breakdown strength. The test results show that the direct current (DC) and alternating current (AC) breakdown voltages of nanofluid impregnated paper increased by 9.1% and 10.0% compared to FR3 nanofluid impregnated paper, respectively.

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10

Qu, Xiangwei, and Xiaowei Sun. "Impedance spectroscopy for quantum dot light-emitting diodes." Journal of Semiconductors 44, no. 9 (September 1, 2023): 091603. http://dx.doi.org/10.1088/1674-4926/44/9/091603.

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Abstract Impedance spectroscopy has been increasingly employed in quantum dot light-emitting diodes (QLEDs) to investigate the charge dynamics and device physics. In this review, we introduce the mathematical basics of impedance spectroscopy that applied to QLEDs. In particular, we focus on the Nyquist plot, Mott−Schottky analysis, capacitance-frequency and capacitance-voltage characteristics, and the dC/dV measurement of the QLEDs. These impedance measurements can provide critical information on electrical parameters such as equivalent circuit models, characteristic time constants, charge injection and recombination points, and trap distribution of the QLEDs. However, this paper will also discuss the disadvantages and limitations of these measurements. Fundamentally, this review provides a deeper understanding of the device physics of QLEDs through the application of impedance spectroscopy, offering valuable insights into the analysis of performance loss and degradation mechanisms of QLEDs.

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11

Ito, Shinobu, Tomohisa Mori, Hideko Kanazawa, and Toshiko Sawaguchi. "Estimation of the Postmortem Duration of Mouse Tissue by Electron Spin Resonance Spectroscopy." Journal of Toxicology 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/973172.

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Electron spin resonance (ESR) method is a simple method for detecting various free radicals simultaneously and directly. However, ESR spin trap method is unsuited to analyze weak ESR signals in organs because of water-induced dielectric loss (WIDL). To minimize WIDL occurring in biotissues and to improve detection sensitivity to free radicals in tissues, ESR cuvette was modified and used with 5,5-dimethtyl-1-pyrroline N-oxide (DMPO). The tissue samples were mouse brain, hart, lung, liver, kidney, pancreas, muscle, skin, and whole blood, where various ESR spin adduct signals including DMPO-ascorbyl radical (AsA∗), DMPO-superoxide anion radical (OOH), and DMPO-hydrogen radical (H) signal were detected. Postmortem changes in DMPO-AsA∗and DMPO-OOH were observed in various tissues of mouse. The signal peak of spin adduct was monitored until the 205th day postmortem. DMPO-AsA∗in liver (y=113.8–40.7 log (day),R1=-0.779,R2=0.6,P<.001) was found to linearly decrease with the logarithm of postmortem duration days. Therefore, DMPO-AsA∗signal may be suitable for detecting an oxidation stress tracer from tissue in comparison with other spin adduct signal on ESR spin trap method.

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12

Aoshima, Keito, Masahiro Horita, and Jun Suda. "Correlation between non-ionizing energy loss and production rate of electron trap at E_C − (0.12–0.20) eV formed in gallium nitride by various types of radiation." Applied Physics Letters 122, no. 1 (January 2, 2023): 012106. http://dx.doi.org/10.1063/5.0128709.

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Production rate (PR = trap concentration/incident fluence) of traps formed by energetic particles is important for predicting device degradation caused by radiation when developing radiation-resistant devices. We demonstrate a clear correlation between non-ionizing energy loss (NIEL) and PR of an electron trap at about 0.12–0.20 eV below the conduction band edge [ EC − (0.12–0.20) eV] for various types of energetic particles in gallium nitride (GaN). NIEL values in GaN for electrons, protons, and [Formula: see text]-rays were calculated using a screened-relativistic treatment, and NIEL values for gamma-rays were calculated by simulating slowed-down spectra due to shielding material. To obtain the PRs of the electron trap, 60Co gamma-rays with an average photon energy of 1.25 MeV and electron beams with energies from 137 keV to 2 MeV were irradiated onto n-type GaN Schottky barrier diodes. We measured the concentration of an electron trap at EC − (0.13–0.14) eV using deep-level transient spectroscopy. We also used the PRs of electron traps with similar energy levels of EC − (0.12–0.20) eV from previous studies on electrons, protons, and [Formula: see text]-rays irradiated on GaN. All the trap PRs were proportional to the NIEL in a range of eight orders of magnitude, which confirms that the energy levels formed by various energetic particles have the same origin of being generated by atomic displacements. The obtained relationship coefficient between the NIEL and PRs of the trap is useful for predicting the degradation of GaN-based devices due to traps formed by various kinds of radiation.

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13

Pan, Su, Kathryn Verhoeven, and Jeehiun K. Lee. "Investigation of the initial fragmentation of oligodeoxynucleotides in a quadrupole ion trap: Charge level-related base loss." Journal of the American Society for Mass Spectrometry 16, no. 11 (November 2005): 1853–65. http://dx.doi.org/10.1016/j.jasms.2005.07.009.

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14

Ma, Jie, Jizhou Wu, Yanting Zhao, Liantuan Xiao, and Suotang Jia. "Determination of the rotational constant of the Cs_2 0_g ^- (6s + 6p_3/2) state by trap loss spectroscopy." Optics Express 18, no. 16 (July 28, 2010): 17089. http://dx.doi.org/10.1364/oe.18.017089.

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15

Comparat, D., C. Drag, A. Fioretti, O. Dulieu, and P. Pillet. "Photoassociative Spectroscopy and Formation of Cold Molecules in Cold Cesium Vapor: Trap–Loss Spectrum versus Ion Spectrum." Journal of Molecular Spectroscopy 195, no. 2 (June 1999): 229–35. http://dx.doi.org/10.1006/jmsp.1999.7764.

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16

Gonokami, Mio, Yoshimasa Yamamoto, Oraphin Chaikumpollert, Yoshito Ohtake, and Seiichi Kawahara. "ANTIOXIDANTS FOR EPDM SEALS EXPOSED TO CHLORINATED TAP WATER." Rubber Chemistry and Technology 87, no. 1 (March 1, 2014): 1–9. http://dx.doi.org/10.5254/rct.13.87963.

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ABSTRACT A suitable antioxidant for a poly(ethylene-co-propylene-co-5-ethylidene-2-norbornene) (EPDM) seal in tap water applications was determined with respect to volatilization and decomposition of the antioxidants. Seals were prepared by mixing EPDM with 1 phr antioxidant and other ingredients followed by vulcanizing the mixture at 433 K for 20 min. The resulting EPDM seals were immersed into chlorinated water to investigate accelerated degradation. The change in antioxidant content was measured by gas chromatography/mass spectroscopy (GC/MS) and high-performance liquid chromatography (HPLC). The weight loss of amine antioxidants during vulcanization was quite low due to their low volatility and decomposition. Antioxidant weight loss during accelerated degradation depended on both the antioxidant's ability to trap radicals and solubility in chlorinated water.

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17

Bai, Jiandong, Shuo Liu, Jieying Wang, Jun He, and Junmin Wang. "Single-Photon Rydberg Excitation and Trap-Loss Spectroscopy of Cold Cesium Atoms in a Magneto-Optical Trap by Using of a 319-nm Ultraviolet Laser System." IEEE Journal of Selected Topics in Quantum Electronics 26, no. 3 (May 2020): 1–6. http://dx.doi.org/10.1109/jstqe.2019.2941483.

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18

Chang, Yuhan, Yi-min Hsiao, Chih-Chien Hu, Chih-Hsiang Chang, Cai-Yan Li, Steve W. N. Ueng, and Mei-Feng Chen. "Synovial Fluid Interleukin-16 Contributes to Osteoclast Activation and Bone Loss through the JNK/NFATc1 Signaling Cascade in Patients with Periprosthetic Joint Infection." International Journal of Molecular Sciences 21, no. 8 (April 21, 2020): 2904. http://dx.doi.org/10.3390/ijms21082904.

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Because of lipopolysaccharide (LPS)-mediated effects on osteoclast differentiation and bone loss, periprosthetic joint infection (PJI) caused by Gram-negative bacteria increases the risk of aseptic loosening after reimplantation. Synovial fluid interleukin-16 (IL-16) expression was higher in patients with PJI than in patients without joint infection. Thus, we explored the effects of IL-16 on bone. We investigated whether IL-16 modulates osteoclast or osteoblast differentiation in vitro. An LPS-induced bone loss mice model was used to explore the possible advantages of IL-16 inhibition for the prevention of bone loss. IL-16 directly activated p38 and c-Jun N-terminal kinase (JNK)/mitogen-activated protein kinase (MAPK) signaling and increased osteoclast activation markers, including tartrate-resistant acid phosphatase (TRAP), cathepsin K, and nuclear factor of activated T cells 1 (NFATc1). IL-16 directly caused monocytes to differentiate into TRAP-positive osteoclast-like cells through NFATc1 activation dependent on JNK/MAPK signaling. Moreover, IL-16 did not alter alkaline phosphatase activity or calcium deposition during osteoblastic differentiation. Finally, IL-16 inhibition prevented LPS-induced trabecular bone loss and osteoclast activation in vivo. IL-16 directly increased osteoclast activation through the JNK/NFATc1 pathway. IL-16 inhibition could represent a new strategy for treating infection-associated bone loss.

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19

Marmet, L., and A. A. Madej. "Optical Ramsey spectroscopy and coherence measurements of the clock transition in a single trapped Sr ion." Canadian Journal of Physics 78, no. 5-6 (April 5, 2000): 495–507. http://dx.doi.org/10.1139/p00-027.

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We report on the observation of coherent excitation and spectroscopy performed using Ramsey's method of separated excitation fields on a single trapped and laser cooled ion of strontium. Single pulse Rabi excitation studies of the ion have shown linewidths approaching the transform limited value. Studies of transition rate versus pulse duration have shown a quadratic initial increase in transition rate with a duration consistent with coherent excitation and a rapid loss of Rabi oscillations, consistent with the concept of a dephasing of the thermally populated trap oscillator states as the excitation evolves. When two-pulse Ramsey excitation is applied to the single ion, fringe widths down to a linewidth of 840 Hz (FWHM) were observed with measured fringe contrasts consistent with a probe laser linewidth of 500 Hz.PACS Nos.: 32.80Qk, 32.30Jc, 06.30Ft

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20

Kuhn, Fabian, Michael Oehme, Fernando Romero, Eliane Abou-Mansour, and Raffaele Tabacchi. "Differentiation of isomeric flavone/isoflavone aglycones by MS2 ion trap mass spectrometry and a double neutral loss of CO." Rapid Communications in Mass Spectrometry 17, no. 17 (2003): 1941–49. http://dx.doi.org/10.1002/rcm.1138.

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Li, Liang, Ming Yang, Saroj Kumar Shrestha, Hyoungsu Kim, William H. Gerwick, and Yunjo Soh. "Kalkitoxin Reduces Osteoclast Formation and Resorption and Protects against Inflammatory Bone Loss." International Journal of Molecular Sciences 22, no. 5 (February 25, 2021): 2303. http://dx.doi.org/10.3390/ijms22052303.

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Osteoclasts, bone-specified multinucleated cells produced by monocyte/macrophage, are involved in numerous bone destructive diseases such as arthritis, osteoporosis, and inflammation-induced bone loss. The osteoclast differentiation mechanism suggests a possible strategy to treat bone diseases. In this regard, we recently examined the in vivo impact of kalkitoxin (KT), a marine product obtained from the marine cyanobacterium Moorena producens (previously Lyngbya majuscula), on the macrophage colony-stimulating factor (M-CSF) and on the receptor activator of nuclear factor κB ligand (RANKL)-stimulated in vitro osteoclastogenesis and inflammation-mediated bone loss. We have now examined the molecular mechanism of KT in greater detail. KT decreased RANKL-induced bone marrow-derived macrophages (BMMs) tartrate-resistant acid phosphatase (TRAP)-multinucleated cells at a late stage. Likewise, KT suppressed RANKL-induced pit area and actin ring formation in BMM cells. Additionally, KT inhibited several RANKL-induced genes such as cathepsin K, matrix metalloproteinase (MMP-9), TRAP, and dendritic cell-specific transmembrane protein (DC-STAMP). In line with these results, RANKL stimulated both genes and protein expression of c-Fos and nuclear factor of activated T cells (NFATc1), and this was also suppressed by KT. Moreover, KT markedly decreased RANKL-induced p-ERK1/2 and p-JNK pathways at different time points. As a result, KT prevented inflammatory bone loss in mice, such as bone mineral density (BMD) and osteoclast differentiation markers. These experiments demonstrated that KT markedly inhibited osteoclast formation and inflammatory bone loss through NFATc1 and mitogen-activated protein kinase (MAPK) signaling pathways. Therefore, KT may have potential as a treatment for destructive bone diseases.

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22

Zeng, Yun, Yimin Xu, Chee-Leong Kee, Min-Yong Low, and Xiaowei Ge. "Analysis of 40 weight loss compounds adulterated in health supplements by liquid chromatography quadrupole linear ion trap mass spectrometry." Drug Testing and Analysis 9, no. 2 (December 28, 2016): 334. http://dx.doi.org/10.1002/dta.2141.

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23

Tajima, Susumu, Low Foon Siang, Masao Fujishige, Satoshi Nakajima, and Osamu Sekiguchi. "Collision-induced dissociation spectra versus collision energy (collision-induced dissociation curve) using a quadrupole ion trap mass spectrometer. II.1 Loss of CO from ionizedo-,m- andp-anisoyl fluoride, CH3OC6H4COF+�." Journal of Mass Spectrometry 35, no. 9 (2000): 1144–46. http://dx.doi.org/10.1002/1096-9888(200009)35:9<1144::aid-jms43>3.0.co;2-q.

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24

Bi, Qi-rui, Jin-jun Hou, Min Yang, Yao Shen, Peng Qi, Rui-hong Feng, Zhuo Dai, et al. "A Strategy Combining Higher Energy C-Trap Dissociation with Neutral Loss- and Product Ion-Based MSn Acquisition for Global Profiling and Structure Annotation of Fatty Acids Conjugates." Journal of The American Society for Mass Spectrometry 28, no. 3 (December 6, 2016): 443–51. http://dx.doi.org/10.1007/s13361-016-1558-y.

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25

Yan, Zhixiang, Ge Lin, Yang Ye, Yitao Wang, and Ru Yan. "Triterpenoid saponins profiling by adducts-targeted neutral loss triggered enhanced resolution and product ion scanning using triple quadrupole linear ion trap mass spectrometry." Analytica Chimica Acta 819 (March 2014): 56–64. http://dx.doi.org/10.1016/j.aca.2014.02.019.

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26

Cheng, Jack, Bor-Tsang Wu, Hsin-Ping Liu, and Wei-Yong Lin. "Tyrosine Metabolism Pathway Is Downregulated in Dopaminergic Neurons with LRRK2 Overexpression in Drosophila." International Journal of Molecular Sciences 24, no. 21 (October 25, 2023): 15587. http://dx.doi.org/10.3390/ijms242115587.

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LRRK2 mutations are the leading cause of familial Parkinson’s disease (PD) and are a significant risk factor for idiopathic PD cases. However, the molecular mechanisms underlying the degeneration of dopaminergic (DA) neurons in LRRK2 PD patients remain unclear. To determine the translatomic impact of LRRK2 expression in DA neurons, we employed gene set enrichment analysis (GSEA) to analyze a translating ribosome affinity purification (TRAP) RNA-seq dataset from a DA-neuron-specific-expressing Drosophila model. We found that the tyrosine metabolism pathway, including tyrosine hydroxylase (TH), is downregulated in DA neurons with LRRK2 overexpression; in contrast, the Hippo signaling pathway is downregulated in the G2019S mutant compared to wild-type LRRK2 in the DA neurons. These results imply that the downregulation of tyrosine metabolism occurs before pronounced DA neuron loss and that LRRK2 may downregulate the tyrosine metabolism in a DA-neuron-loss-independent way.

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27

Gonçalves, Vinícius de Paiva, Marta Liliana Musskopf, Angeliz Rivera-Concepcion, Christina Yu, Sing Wai Wong, Stephen A. Tuin, Yizu Jiao, Cristiano Susin, Luís Carlos Spolidorio, and Patricia Almeida Miguez. "Systemic Dietary Hesperidin Modulation of Osteoclastogenesis, Bone Homeostasis and Periodontal Disease in Mice." International Journal of Molecular Sciences 23, no. 13 (June 26, 2022): 7100. http://dx.doi.org/10.3390/ijms23137100.

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This study aimed to evaluate the effects of hesperidin (HE) on in vitro osteoclastogenesis and dietary supplementation on mouse periodontal disease and femoral bone phenotype. RAW 264.7 cells were stimulated with RANKL in the presence or absence of HE (1, 100 or 500 µM) for 5 days, and evaluated by TRAP, TUNEL and Western Blot (WB) analyses. In vivo, C57BL/6 mice were given HE via oral gavage (125, 250 and 500 mg/kg) for 4 weeks. A sterile silk ligature was placed between the first and second right maxillary molars for 10 days and microcomputed tomography (μCT), histopathological and immunohistochemical evaluation were performed. Femoral bones subjected or not to dietary HE (500 mg/kg) for 6 and 12 weeks were evaluated using μCT. In vitro, HE 500 µM reduced formation of RANKL-stimulated TRAP-positive(+) multinucleated cells (500 µM) as well as c-Fos and NFATc1 protein expression (p < 0.05), markers of osteoclasts. In vivo, dietary HE 500 mg/kg increased the alveolar bone resorption in ligated teeth (p < 0.05) and resulted in a significant increase in TRAP+ cells (p < 0.05). Gingival inflammatory infiltrate was greater in the HE 500 mg/kg group even in the absence of ligature. In femurs, HE 500 mg/kg protected trabecular and cortical bone mass at 6 weeks of treatment. In conclusion, HE impaired in vitro osteoclastogenesis, but on the contrary, oral administration of a high concentration of dietary HE increased osteoclast numbers and promoted inflammation-induced alveolar bone loss. However, HE at 500 mg/kg can promote a bone-sparing effect on skeletal bone under physiological conditions.

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Kelso, Celine, Juan Diego Rojas, Renata L. A. Furlan, Gabriel Padilla, and Jennifer L. Beck. "Characterisation of Anthracyclines from a Cosmomycin D-Producing Species of Streptomyces by Collisionally-Activated Dissociation and Ion Mobility Mass Spectrometry." European Journal of Mass Spectrometry 15, no. 2 (April 2009): 73–81. http://dx.doi.org/10.1255/ejms.948.

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Cultures of cosmomycin D-producing Streptomyces olindensis ICB20 that were propagated for many generations underwent mutations that resulted in production of a range of related anthracyclines by the bacteria. The anthracyclines that retained the two trisaccharide chains of the parent compound were separated by HPLC. Exact mass determination of these compounds revealed that they differed from cosmomycin D (CosD) in that they contained one to three fewer oxygen atoms (loss of hydroxyl groups). Some of the anthracyclines that were separated by HPLC had the same mass. The location from which the hydroxyl groups had been lost relative to CosD (on the aglycone and/or on the sugar residues) was probed by collisionally-activated dissociation using an electrospray ionisation linear quadrupole ion trap mass spectrometer. The presence of anthracyclines with the same mass, but different structure, was confirmed using an electrospray ionisation travelling wave ion mobility mass spectrometer.

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29

Zhang, Rui, Keith J. Fisher, Derek R. Smith, Gary D. Willett, J. Barrie Peel, Liangbing Gan, Yaru Shi, and Zhen Gao. "An Electrospray Ionization Fourier Transform Ion Cyclotron Resonance Mass Spectrometry Study of 1,6-Methano[60]Fullerene-61,61-Dicarboxylic Acid." European Journal of Mass Spectrometry 6, no. 2 (April 2000): 161–68. http://dx.doi.org/10.1255/ejms.336.

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1,6-Methano[60]fullerene-61,61-dicarboxylic acid was studied by electrospray ionization Fourier transform ion cyclotron resonance mass spectrometry. The deprotonated molecule, C60C(COOH)COO−, and the decarboxylated molecular anion C60CHCOO− were observed. Gas-phase ion–molecule reactions occurred when the ion accumulation time in an external rf/dc hexapole ion trap was extended. Cluster ions of the type [C60CHCOOH] n[C60CHCOO]− ( n = 1–2) were observed. Multiply-charged anions were observed for the dimer [C60CHCOOH][C60CHCOO]−. Collision-induced dissociation in the ion cyclotron resonance cell showed that C60C(COOH)COO− dissociated through the loss of two CO2 groups, with further fragmentation to produce C60−. A similar fragmentation pathway was also observed with capillary/skimmer collision-induced dissociation during the electrospray process. Semi-empirical calculations using the AM1 approximation with the MOPAC program have been performed on most of the neutral and ionic species related to this compound. Energy differences and charge distributions have been obtained for the possible geometry structures for these species.

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30

Grabitzki, Julia, Volker Sauerland, Rudolf Geyer, and Günter Lochnit. "Identification of Phosphorylcholine-Substituted Peptides by Their Characteristic Mass Spectrometric Fragmentation." European Journal of Mass Spectrometry 11, no. 3 (June 2005): 335–44. http://dx.doi.org/10.1255/ejms.728.

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Phosphorylcholine (PC)-substituted biomolecules are wide-spread, highly relevant antigens of parasites, since this small hapten has been found to be a potent immunomodulatory component which allows the establishment of long lasting infections of the host. Structural data, especially of protein bound PC-substituents, are still rare due to the observation that mass spectrometric analyses are mostly hampered by this zwitterionic substituent resulting in low sensitivities and unusual but characteristic fragmentation patterns. Here, we investigated the fragmentation behavior of synthetic PC-substituted peptides by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and electrospray ionization ion-trap mass spectrometry. We could show that the predominant neutral loss of a trimethylamine unit (Hoffmann elimination) leads to cyclic phosphate derivatives which prevent further fragmentation of the peptide backbone by stabilizing the positive charge at this particular side chain. Knowledge of this PC-specific fragmentation might help to identify PC-substituted biomolecules and facilitate their structural analysis.

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Hsu, Fong-Fu, and John Turk. "Studies on sulfatides by quadrupole ion-trap mass spectrometry with electrospray ionization: Structural characterization and the fragmentation processes that include an unusual internal galactose residue loss and the classical charge-remote fragmentation." Journal of the American Society for Mass Spectrometry 15, no. 4 (April 2004): 536–46. http://dx.doi.org/10.1016/j.jasms.2003.12.007.

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32

Scholz, Karoline, Wolfgang Dekant, Wolfgang Völkel, and Axel Pähler. "Rapid detection and identification of N-acetyl-L-cysteine thioethers using constant neutral loss and theoretical multiple reaction monitoring combined with enhanced product-ion scans on a linear ion trap mass spectrometer." Journal of the American Society for Mass Spectrometry 16, no. 12 (December 2005): 1976–84. http://dx.doi.org/10.1016/j.jasms.2005.08.003.

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Eisa, Nada H., Sakamuri V. Reddy, Ahmed M. Elmansi, Galina Kondrikova, Dmitry Kondrikov, Xing-Ming Shi, Chad M. Novince, et al. "Kynurenine Promotes RANKL-Induced Osteoclastogenesis In Vitro by Activating the Aryl Hydrocarbon Receptor Pathway." International Journal of Molecular Sciences 21, no. 21 (October 26, 2020): 7931. http://dx.doi.org/10.3390/ijms21217931.

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There is increasing evidence of the involvement of the tryptophan metabolite kynurenine (KYN) in disrupting osteogenesis and contributing to aging-related bone loss. Here, we show that KYN has an effect on bone resorption by increasing osteoclastogenesis. We have previously reported that in vivo treatment with KYN significantly increased osteoclast number lining bone surfaces. Here, we report the direct effect of KYN on receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclastogenesis in Raw 264.7 macrophage cells, and we propose a potential mechanism for these KYN-mediated effects. We show that KYN/RANKL treatment results in enhancement of RANKL-induced osteoclast differentiation. KYN drives upregulation and activation of the key osteoclast transcription factors, c-fos and NFATc1 resulting in an increase in the number of multinucleated TRAP+ osteoclasts, and in hydroxyapatite bone resorptive activity. Mechanistically, the KYN receptor, aryl hydrocarbon receptor (AhR), plays an important role in the induction of osteoclastogenesis. We show that blocking AhR signaling using an AhR antagonist, or AhR siRNA, downregulates the KYN/RANKL-mediated increase in c-fos and NFATc1 and inhibits the formation of multinucleated TRAP + osteoclasts. Altogether, this work highlights that the novelty of the KYN and AhR pathways might have a potential role in helping to regulate osteoclast function with age and supports pursuing additional research to determine if they are potential therapeutic targets for the prevention or treatment of osteoporosis.

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Chen, Zhihao, Eunjin Cho, Jinkyung Lee, Sunwoo Lee, and Tae-Hoon Lee. "Inhibitory Effects of N-[2-(4-acetyl-1-piperazinyl) phenyl]-2-(2-chlorophenoxy) acetamide on Osteoclast Differentiation In Vitro via the Downregulation of TRAF6." International Journal of Molecular Sciences 20, no. 20 (October 20, 2019): 5196. http://dx.doi.org/10.3390/ijms20205196.

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Osteoclasts are poly-nuclear cells that resorb mineral components from old or damaged bone tissue. Primary mononuclear cells are activated by receptor activator of nuclear factor kappa-Β ligand (RANKL) and differentiate into large multinucleated cells. Dysregulation of osteoclast differentiation can lead to pathological bone loss and destruction. Many studies have focused on the development of new molecules to regulate RANKL-mediated signaling. In this study, N-[2-(4-acetyl-1-piperazinyl)phenyl]-2-(2-chlorophenoxy) acetamide (PPOA-N-Ac-2-Cl) led to a significant decrease in the formation of multinucleated tartrate-resistant acid phosphatase (TRAP)-positive cells in a dose-dependent manner, without inducing significant cytotoxicity. PPOA-N-Ac-2-Cl affected the expression of osteoclast-specific marker genes, such as TRAF6, c-fos, DC-STAMP, NFATc1, MMP9, CtsK, and TRAP (Acp5), during RANKL-mediated osteoclastogenesis. Moreover, PPOA-N-Ac-2-Cl significantly attenuated the protein levels of CtsK, a critical protease involved in bone resorption. Accordingly, bone resorption activity and F-actin ring formation decreased in the presence of PPOA-N-Ac-2-Cl. In conclusion, this study shows that PPOA-N-Ac-2-Cl acts as an inhibitor of osteoclast differentiation and may serve as a potential candidate agent for the treatment of osteoclast-related bone diseases by virtue of attenuating bone resorption.

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35

Lee, Chang Gun, Jeonghyun Kim, Seung Hee Yun, Seokjin Hwang, Hyoju Jeon, Eunkuk Park, and Seon-Yong Jeong. "Anti-Osteoporotic Effect of Morroniside on Osteoblast and Osteoclast Differentiation In Vitro and Ovariectomized Mice In Vivo." International Journal of Molecular Sciences 22, no. 19 (September 30, 2021): 10642. http://dx.doi.org/10.3390/ijms221910642.

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Bone remodeling is a continuous process of bone synthesis and destruction that is regulated by osteoblasts and osteoclasts. Here, we investigated the anti-osteoporotic effects of morroniside in mouse preosteoblast MC3T3-E1 cells and mouse primary cultured osteoblasts and osteoclasts in vitro and ovariectomy (OVX)-induced mouse osteoporosis in vivo. Morroniside treatment enhanced alkaline phosphatase activity and positively stained cells via upregulation of osteoblastogenesis-associated genes in MC3T3-E1 cell lines and primary cultured osteoblasts. However, morroniside inhibited tartrate-resistant acid phosphatase activity and TRAP-stained multinucleated positive cells via downregulation of osteoclast-mediated genes in primary cultured monocytes. In the osteoporotic animal model, ovariectomized (OVX) mice were administered morroniside (2 or 10 mg/kg/day) for 12 weeks. Morroniside prevented OVX-induced bone mineral density (BMD) loss and reduced bone structural compartment loss in the micro-CT images. Taken together, morroniside promoted increased osteoblast differentiation and decreased osteoclast differentiation in cells, and consequently inhibited OVX-induced osteoporotic pathogenesis in mice. This study suggests that morroniside may be a potent therapeutic single compound for the prevention of osteoporosis.

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36

Kim, Su-Jin, Yun-Ho Hwang, Seul-Ki Mun, Seong-Gyeol Hong, Kwang-Jin Kim, Kyung-Yun Kang, Young-Jin Son та Sung-Tae Yee. "Protective Effects of 2,3,5,4′-Tetrahydroxystilbene-2-O-β-d-glucoside on Ovariectomy Induced Osteoporosis Mouse Model". International Journal of Molecular Sciences 19, № 9 (28 серпня 2018): 2554. http://dx.doi.org/10.3390/ijms19092554.

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2,3,5,4′-Tetrahydroxystilbene-2-O-β-d-glucoside (TSG), an active polyphenolic component of Polygonum multiflorum, exhibits many pharmacological activities including antioxidant, anti-inflammation, and anti-aging effects. A previous study demonstrated that TSG protected MC3T3-E1 cells from hydrogen peroxide (H2O2) induced cell damage and the inhibition of osteoblastic differentiation. However, no studies have investigated the prevention of ovariectomy-induced bone loss in mice. Therefore, we investigated the effects of TSG on bone loss in ovariectomized mice (OVX). Treatment with TSG (1 and 3 μg/g; i.p.) for six weeks positively affected body weight, uterine weight, organ weight, bone length, and weight change because of estrogen deficiency. The levels of the serum biochemical markers of calcium (Ca), inorganic phosphorus (IP), alkaline phosphatase (ALP), and total cholesterol (TCHO) decreased in the TSG-treated mice when compared with the OVX mice. Additionally, the serum bone alkaline phosphatase (BALP) levels in the TSG-treated OVX mice were significantly increased compared with the OVX mice, while the tartrate-resistant acid phosphatase (TRAP) activity was significantly reduced. Furthermore, the OVX mice treated with TSG showed a significantly reduced bone loss compared to the untreated OVX mice upon micro-computed tomography (CT) analysis. Consequently, bone destruction in osteoporotic mice as a result of ovariectomy was inhibited by the administration of TSG. These findings indicate that TSG effectively prevents bone loss in OVX mice; therefore, it can be considered as a potential therapeutic for the treatment of postmenopausal osteoporosis.

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Gierlikowska, Barbara, Albert Stachura, Wojciech Gierlikowski, and Urszula Demkow. "The Impact of Cytokines on Neutrophils’ Phagocytosis and NET Formation during Sepsis—A Review." International Journal of Molecular Sciences 23, no. 9 (May 3, 2022): 5076. http://dx.doi.org/10.3390/ijms23095076.

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Sepsis is an overwhelming inflammatory response to infection, resulting in multiple-organ injury. Neutrophils are crucial immune cells involved in innate response to pathogens and their migration and effector functions, such as phagocytosis and neutrophil extracellular trap (NET) formation, are dependent on cytokine presence and their concentration. In the course of sepsis, recruitment and migration of neutrophils to infectious foci gradually becomes impaired, thus leading to loss of a crucial arm of the innate immune response to infection. Our review briefly describes the sepsis course, the importance of neutrophils during sepsis, and explains dependence between cytokines and their activation. Moreover, we, for the first time, summarize the impact of cytokines on phagocytosis and NET formation. We highlight and discuss the importance of cytokines in modulation of both processes and emphasize the direction of further investigations.

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38

Auvray, Mihai, Lundberg, and Olsson. "Deactivation of Cu/SSZ-13 NH3-SCR Catalyst by Exposure to CO, H2, and C3H6." Catalysts 9, no. 11 (November 6, 2019): 929. http://dx.doi.org/10.3390/catal9110929.

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Lean nitric oxide (NOx)-trap (LNT) and selective catalytic reduction (SCR) are efficient systems for the abatement of NOx. The combination of LNT and SCR catalysts improves overall NOx removal, but there is a risk that the SCR catalyst will be exposed to high temperatures and rich exhaust during the LNTs sulfur regeneration. Therefore, the effect of exposure to various rich conditions and temperatures on the subsequent SCR activity of a Cu-exchanged chabazite catalyst was studied. CO, H2, C3H6, and the combination of CO + H2 were used to simulate rich conditions. Aging was performed at 800 °C, 700 °C, and, in the case of CO, 600 °C, in a plug-flow reactor. Investigation of the nature of Cu sites was performed with NH3-temperature-programed desorption (TPD) and diffuse reflectance infrared Fourier transform spectroscopy (DRIFT) of probe molecules (NH3 and NO). The combination of CO and H2 was especially detrimental to SCR activity and to NH3 oxidation. Rich aging with low reductant concentrations resulted in a significantly larger deactivation compared to lean conditions. Aging in CO at 800 °C caused SCR deactivation but promoted high-temperature NH3 oxidation. Rich conditions greatly enhanced the loss of Brønsted and Lewis acid sites at 800 °C, indicating dealumination and Cu migration. However, at 700 °C, mainly Brønsted sites disappeared during aging. DRIFT spectroscopy analysis revealed that CO aging modified the Cu2+/CuOH+ ratio in favor of the monovalent CuOH+ species, as opposed to lean aging. To summarize, we propose that the reason for the increased deactivation observed for mild rich conditions is the transformation of the Cu species from Z2Cu to ZCuOH, possibly in combination with the formation of Cu clusters.

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Wu, Chia-Hsin, Ching-Huei Ou, I.-Chuan Yen, and Shih-Yu Lee. "4-Acetylantroquinonol B Inhibits Osteoclastogenesis by Inhibiting the Autophagy Pathway in a Simulated Microgravity Model." International Journal of Molecular Sciences 21, no. 18 (September 22, 2020): 6971. http://dx.doi.org/10.3390/ijms21186971.

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Astronauts suffer from 1–2% bone loss per month during space missions. Targeting osteoclast differentiation has been regarded as a promising strategy to prevent osteoporosis in microgravity (μXg). 4-acetylantroquinonol B (4-AAQB), a ubiquinone from Antrodia cinnamomea, has shown anti-inflammatory and anti-hepatoma activities. However, the effect of 4-AAQB on μXg-induced osteoclastogenesis remains unclear. In this study, we aimed to explore the mechanistic impact of 4-AAQB on osteoclast formation under μXg conditions. The monocyte/macrophage-like cell line RAW264.7 was exposed to simulated μXg (Rotary Cell Culture System; Synthecon, Houston, TX, USA) for 24 h and then treated with 4-AAQB or alendronate (ALN) and osteoclast differentiation factor receptor activator of nuclear factor kappa-B ligand (RANKL). Osteoclastogenesis, bone resorption activity, and osteoclast differentiation-related signaling pathways were analyzed using tartrate-resistant acid phosphatase (TRAP) staining, actin ring fluorescent staining, bone resorption, and western blotting assays. Based on the results of TRAP staining, actin ring staining, and bone resorption assays, we found that 4-AAQB significantly inhibited μXg-induced osteoclast differentiation. The critical regulators of osteoclast differentiation, including nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), c-Fos, and dendritic cell-specific transmembrane protein (DC-STAMP), were consistently decreased. Meanwhile, osteoclast apoptosis and cell cycle arrest were also observed along with autophagy suppression. Interestingly, the autophagy inhibitors 3-methyladenine (3-MA) and chloroquine (CQ) showed similar effects to 4-AAQB. In conclusion, we suggest that 4-AAQB may serve as a potential agent against μXg-induced osteoclast formation.

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Liu, Cong-Jin, Xiao Yang, Shou-Hui Wang, Xin-Tong Wu, Yan Mao, Jing-Wen Shi, Yu-Bo Fan, and Lian-Wen Sun. "Preventing Disused Bone Loss through Inhibition of Advanced Glycation End Products." International Journal of Molecular Sciences 24, no. 5 (March 3, 2023): 4953. http://dx.doi.org/10.3390/ijms24054953.

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Bone loss occurs in astronauts during long-term space flight, but the mechanisms are still unclear. We previously showed that advanced glycation end products (AGEs) were involved in microgravity-induced osteoporosis. Here, we investigated the improvement effects of blocking AGEs formation on microgravity-induced bone loss by using the AGEs formation inhibitor, irbesartan. To achieve this objective, we used a tail-suspended (TS) rat model to simulate microgravity and treated the TS rats with 50 mg/kg/day irbesartan, as well as the fluorochrome biomarkers injected into rats to label dynamic bone formation. To assess the accumulation of AGEs, pentosidine (PEN), non-enzymatic cross-links (NE−xLR), and fluorescent AGEs (fAGEs) were identified in the bone; 8-hydroxydeoxyguanosine (8-OHdG) was analyzed for the reactive oxygen species (ROS) level in the bone. Meanwhile, bone mechanical properties, bone microstructure, and dynamic bone histomorphometry were tested for bone quality assessment, and Osterix and TRAP were immunofluorescences stained for the activities of osteoblastic and osteoclastic cells. Results showed AGEs increased significantly and 8-OHdG expression in bone showed an upward trend in TS rat hindlimbs. The bone quality (bone microstructure and mechanical properties) and bone formation process (dynamic bone formation and osteoblastic cells activities) were inhibited after tail-suspension, and showed a correlation with AGEs, suggesting the elevated AGEs contributed to the disused bone loss. After being treated with irbesartan, the increased AGEs and 8-OHdG expression were significantly inhibited, suggesting irbesartan may reduce ROS to inhibit dicarbonyl compounds, thus suppressing AGEs production after tail-suspension. The inhibition of AGEs can partially alter the bone remodeling process and improve bone quality. Both AGEs accumulation and bone alterations almost occurred in trabecular bone but not in cortical bone, suggesting AGEs effects on bone remodeling under microgravity are dependent on the biological milieu.

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Zhang, Zijiao, Juhan Song, Seung-Hee Kwon, Zhao Wang, Suk-Gyun Park, Xianyu Piao, Je-Hwang Ryu та ін. "Pirfenidone Inhibits Alveolar Bone Loss in Ligature-Induced Periodontitis by Suppressing the NF-κB Signaling Pathway in Mice". International Journal of Molecular Sciences 24, № 10 (12 травня 2023): 8682. http://dx.doi.org/10.3390/ijms24108682.

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There has been increasing interest in adjunctive use of anti-inflammatory drugs to control periodontitis. This study was performed to examine the effects of pirfenidone (PFD) on alveolar bone loss in ligature-induced periodontitis in mice and identify the relevant mechanisms. Experimental periodontitis was established by ligating the unilateral maxillary second molar for 7 days in mice (n = 8 per group), and PFD was administered daily via intraperitoneal injection. The micro-computed tomography and histology analyses were performed to determine changes in the alveolar bone following the PFD administration. For in vitro analysis, bone marrow macrophages (BMMs) were isolated from mice and cultured with PFD in the presence of RANKL or LPS. The effectiveness of PFD on osteoclastogenesis, inflammatory cytokine expression, and NF-κB activation was determined with RT-PCR, Western blot, and immunofluorescence analyses. PFD treatment significantly inhibited the ligature-induced alveolar bone loss, with decreases in TRAP-positive osteoclasts and expression of inflammatory cytokines in mice. In cultured BMM cells, PFD also inhibited RANKL-induced osteoclast differentiation and LPS-induced proinflammatory cytokine (IL-1β, IL-6, TNF-a) expression via suppressing the NF-κB signal pathway. These results suggest that PFD can suppress periodontitis progression by inhibiting osteoclastogenesis and inflammatory cytokine production via inhibiting the NF-κB signal pathway, and it may be a promising candidate for controlling periodontitis.

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MAZUMDAR, Abhijit, Subrata ADAK, Ratna CHATTERJEE, and Ranajit K. BANERJEE. "Mechanism-based inactivation of lacrimal-gland peroxidase by phenylhydrazine: a suicidal substrate to probe the active site." Biochemical Journal 324, no. 3 (June 15, 1997): 713–19. http://dx.doi.org/10.1042/bj3240713.

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Анотація:

Humans are exposed to various hydrazine derivatives for therapeutic control of several diseases, and mammalian peroxidases are implicated in the oxidative metabolism of many drugs. The results presented here indicate that lacrimal-gland peroxidase is irreversibly inactivated in a mechanism-based way by phenylhydrazine, which acts as a suicidal substrate in the presence of H2O2. The pseudo-first-order kinetic constants for inactivation at pH 5.5 are Ki=18 μM, kinact=0.25 min-1 and τ50=2.75 min, with a second-order rate constant of 0.75×104 M-1·min-1. Approx. 27 mol of phenylhydrazine and 54 mol of H2O2 are required per mol of enzyme for complete inactivation. The pH-dependent inactivation kinetics indicate the involvement of an ionizable group on the enzyme with a pKa value of 5.4, protonation of which favours inactivation. SCN-, the plausible physiological electron donor of the enzyme, protects it from inactivation. Binding studies by optical difference spectroscopy indicate that phenylhydrazine interacts with the enzyme with a KD value of 60 μM, and its binding is prevented by the presence of SCN-. The enzyme is also protected by 5,5-dimethyl-1-pyrroline N-oxide, a free-radical trap, suggesting the involvement of a radical species in the inactivation. ESR studies indicate the formation of a spin-trapped phenyl radical (aN=15.9 G and aβH=24.8 G) generated on incubation of phenylhydrazine with the enzyme and H2O2. A 75% loss of the Soret spectrum is observed when the enzyme is completely inactivated. However, in the presence of the spin trap, spectral loss is prevented and the enzyme compound II is readily reduced to the native state by phenylhydrazine. The phenylhydrazine-inactivated enzyme reacts with H2O2 or CN- to form compound II or the cyanide complex with a characteristic spectrum, indicating that haem iron is protected from attack by the radical species. The inactivated enzyme binds SCN- with a KD value similar to that of the native enzyme (15±3 mM), suggesting that the donor-binding site remains unaffected. CD studies of the inactive enzyme show complete disappearance of the Soret band at 409 nm with the appearance of a new band at 275 nm. This indicates that the haem environment of the enzyme is perturbed in the inactive form. As benzene, the end product of phenylhydrazine oxidation, has no effect on the enzyme, we suggest that the phenyl radical formed by one-electron oxidation by catalytically active enzyme inactivates it by incorporation in the vicinity of its haem moiety. The data support the use of phenylhydrazine as a probe for structural and mechanistic analysis of the active site of the lacrimal-gland peroxidase.

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Heinemann, Christiane, Josephine Adam, Benjamin Kruppke, Vera Hintze, Hans-Peter Wiesmann, and Thomas Hanke. "How to Get Them off?—Assessment of Innovative Techniques for Generation and Detachment of Mature Osteoclasts for Biomaterial Resorption Studies." International Journal of Molecular Sciences 22, no. 3 (January 29, 2021): 1329. http://dx.doi.org/10.3390/ijms22031329.

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The fusion process of mononuclear monocytes into multinuclear osteoclasts in vitro is an essential process for the study of osteoclastic resorption of biomaterials. Thereby biomaterials offer many influencing factors such as sample shape, material composition, and surface topography, which can have a decisive influence on the fusion and thus the entire investigation. For the specific investigation of resorption, it can therefore be advantageous to skip the fusion on samples and use mature, predifferentiated osteoclasts directly. However, most conventional detachment methods (cell scraper, accutase), lead to a poor survival rate of osteoclasts or to a loss of function of the cells after their reseeding. In the present study different conventional and novel methods of detachment in combination with different culture surfaces were investigated to obtain optimal osteoclast differentiation, yield, and vitality rates without loss of function. The innovative method—using thermoresponsive surfaces for cultivation and detachment—was found to be best suited. This is in particular due to its ability to maintain osteoclast activity, as proven by TRAP 5b-, CTSK-activity and resorption pits on dentin discs and decellularized osteoblast-derived matrix plates. In conclusion, it is shown, that osteoclasts can be predifferentiated on cell culture dishes and transferred to a reference biomaterial under preservation of osteoclastic resorption activity, providing biomaterial researchers with a novel tool for material characterization.

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Nasulewicz-Goldeman, Anna, Waldemar Goldeman, Anna Nikodem, Marcin Nowak, Diana Papiernik, Tomasz M. Goszczyński, and Joanna Wietrzyk. "Aromatic Bis[aminomethylidenebis(phosphonic)] Acids Prevent Ovariectomy-Induced Bone Loss and Suppress Osteoclastogenesis in Mice." International Journal of Molecular Sciences 22, no. 17 (September 3, 2021): 9590. http://dx.doi.org/10.3390/ijms22179590.

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Osteoporosis is a skeletal disease associated with excessive bone turnover. Among the compounds with antiresorptive activity, nitrogen-containing bisphosphonates play the most important role in antiosteoporotic treatment. In previous studies, we obtained two aminomethylidenebisphosphonates—benzene-1,4-bis[aminomethylidene(bisphosphonic)] (WG12399C) acid and naphthalene-1,5-bis[aminomethylidene(bisphosphonic)] (WG12592A) acid—which showed a significant antiproliferative activity toward J774E macrophages, a model of osteoclast precursors. The aim of these studies was to evaluate the antiresorptive activity of these aminobisphosphonates in ovariectomized (OVX) Balb/c mice. The influence of WG12399C and WG12592A administration on bone microstructure and bone strength was studied. Intravenous injections of WG12399C and WG12592A bisphosphonates remarkably prevented OVX-induced bone loss; for example, they sustained bone mineral density at control levels and restored other bone parameters such as trabecular separation. This was accompanied by a remarkable reduction in the number of TRAP-positive cells in bone tissue. However, a significant improvement in the quality of bone structure did not correlate with a parallel increase in bone strength. In ex vivo studies, WG12399C and WG12592A remarkably bisphosphonates reduced osteoclastogenesis and partially inhibited the resorptive activity of mature osteoclasts. Our results show interesting biological activity of two aminobisphosphonates, which may be of interest in the context of antiresorptive therapy.

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Kim, Eun-Nam, Ga-Ram Kim, Jae Sik Yu, Ki Hyun Kim та Gil-Saeng Jeong. "Inhibitory Effect of (2R)-4-(4-hydroxyphenyl)-2-butanol 2-O-β-d-apiofuranosyl-(1→6)-β-d-glucopyranoside on RANKL-Induced Osteoclast Differentiation and ROS Generation in Macrophages". International Journal of Molecular Sciences 22, № 1 (28 грудня 2020): 222. http://dx.doi.org/10.3390/ijms22010222.

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Анотація:

In bone homeostasis, bone loss due to excessive osteoclasts and inflammation or osteolysis in the bone formation process cause bone diseases such as osteoporosis. Suppressing the accompanying oxidative stress such as ROS in this process is an important treatment strategy for bone disease. Therefore, in this study, the effect of (2R)-4-(4-hydroxyphenyl)-2-butanol 2-O-β-d-apiofuranosyl-(1→6)-β-d-glucopyranoside (BAG), an arylbutanoid glycoside isolated from Betula platyphylla var. japonica was investigated in RANKL-induced RAW264.7 cells and LPS-stimulated MC3E3-T1 cells. BAG inhibited the activity of TRAP, an important marker of osteoclast differentiation and F-actin ring formation, which has osteospecific structure. In addition, the protein and gene levels were suppressed of integrin β3 and CCL4, which play an important role in the osteoclast-induced bone resorption and migration of osteoclasts, and inhibited the production of ROS and restored the expression of antioxidant enzymes such as SOD and CAT lost by RANKL. The inhibitory effect of BAG on osteoclast differentiation and ROS production appears to be due to the inhibition of MAPKs phosphorylation and NF-κβ translocation, which play a major role in osteoclast differentiation. In addition, BAG inhibited ROS generated by LPS and effectively restores the mineralization of lost osteoblasts, thereby showing the effect of bone formation in the inflammatory situation accompanying bone loss by excessive osteoclasts, suggesting its potential as a new natural product-derived bone disease treatment.

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46

Kouranti, Ilektra, Waed Abdel-Khalek, Stephani Mazurkiewicz, Irmine Loisel-Ferreira, Alexis M. Gautreau, Lionel Pintard, Xavier Jeunemaitre, and Eric Clauser. "Cullin 3 Exon 9 Deletion in Familial Hyperkalemic Hypertension Impairs Cullin3-Ring-E3 Ligase (CRL3) Dynamic Regulation and Cycling." International Journal of Molecular Sciences 23, no. 9 (May 5, 2022): 5151. http://dx.doi.org/10.3390/ijms23095151.

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Cullin 3 (CUL3) is the scaffold of Cullin3 Ring E3-ligases (CRL3s), which use various BTB-adaptor proteins to ubiquitinate numerous substrates targeting their proteasomal degradation. CUL3 mutations, responsible for a severe form of familial hyperkalemia and hypertension (FHHt), all result in a deletion of exon 9 (amino-acids 403-459) (CUL3-∆9). Surprisingly, while CUL3-∆9 is hyperneddylated, a post-translational modification that typically activates CRL complexes, it is unable to ubiquitinate its substrates. In order to understand the mechanisms behind this loss-of function, we performed comparative label-free quantitative analyses of CUL3 and CUL3-∆9 interactome by mass spectrometry. It was observed that CUL3-∆9 interactions with COP9 and CAND1, both involved in CRL3 complexes’ dynamic assembly, were disrupted. These defects result in a reduction in the dynamic cycling of the CRL3 complexes, making the CRL3-∆9 complex an inactive BTB-adaptor trap, as demonstrated by SILAC experiments. Collectively, the data indicated that the hyperneddylated CUL3-∆9 protein is inactive as a consequence of several structural changes disrupting its dynamic interactions with key regulatory partners.

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Wu, Chao-Yi, Huang-Yu Yang, and Jenn-Haung Lai. "Anti-Citrullinated Protein Antibodies in Patients with Rheumatoid Arthritis: Biological Effects and Mechanisms of Immunopathogenesis." International Journal of Molecular Sciences 21, no. 11 (June 4, 2020): 4015. http://dx.doi.org/10.3390/ijms21114015.

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Анотація:

Individuals with high anti-citrullinated protein antibody (ACPA) titers have an increased risk of developing rheumatoid arthritis (RA). Although our knowledge of the generation and production of ACPAs has continuously advanced during the past decade, our understanding on the pathogenic mechanisms of how ACPAs interact with immune cells to trigger articular inflammation is relatively limited. Citrullination disorders drive the generation and maintenance of ACPAs, with profound clinical significance in patients with RA. The loss of tolerance to citrullinated proteins, however, is essential for ACPAs to exert their pathogenicity. N-linked glycosylation, cross-reactivity and the structural interactions of ACPAs with their citrullinated antigens further direct their biological functions. Although questions remain in the pathogenicity of ACPAs acting as agonists for a receptor-mediated response, immune complex (IC) formation, complement system activation, crystallizable fragment gamma receptor (FcγR) activation, cross-reactivity to joint cartilage and neutrophil extracellular trap (NET)-related mechanisms have all been suggested recently. This paper presents a critical review of the characteristics and possible biological effects and mechanisms of the immunopathogenesis of ACPAs in patients with RA.

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48

Lee, Chang-Gun, Do-Wan Kim, Jeonghyun Kim, Laxmi Prasad Uprety, Kang-Il Oh, Shivani Singh, Jisu Yoo, et al. "Effects of Loganin on Bone Formation and Resorption In Vitro and In Vivo." International Journal of Molecular Sciences 23, no. 22 (November 16, 2022): 14128. http://dx.doi.org/10.3390/ijms232214128.

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Osteoporosis is a disease caused by impaired bone remodeling that is especially prevalent in elderly and postmenopausal women. Although numerous chemical agents have been developed to prevent osteoporosis, arguments remain regarding their side effects. Here, we demonstrated the effects of loganin, a single bioactive compound isolated from Cornus officinalis, on osteoblast and osteoclast differentiation in vitro and on ovariectomy (OVX)-induced osteoporosis in mice in vivo. Loganin treatment increased the differentiation of mouse preosteoblast cells into osteoblasts and suppressed osteoclast differentiation in primary monocytes by regulating the mRNA expression levels of differentiation markers. Similar results were obtained in an osteoblast–osteoclast co-culture system, which showed that loganin enhanced alkaline phosphatase (ALP) activity and reduced TRAP activity. In in vivo experiments, the oral administration of loganin prevented the OVX-induced loss of bone mineral density (BMD) and microstructure in mice and improved bone parameters. In addition, loganin significantly increased the serum OPG/RANKL ratio and promoted osteogenic activity during bone remodeling. Our findings suggest that loganin could be used as an alternative treatment to protect against osteoporosis.

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Burgers, Peter C., John L. Holmes, and Johan K. Terlouw. "Metal Ion Hydrocarbon Bidentate Bonding in Alkyl Acetates, Methyl Alkanoates, Alcohols and 1-Alkenes: A Comparative Study." European Journal of Mass Spectrometry 22, no. 6 (December 2016): 297–305. http://dx.doi.org/10.1255/ejms.1440.

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The relative affinity of the monovalent metal ions Li+, Na+, Cu+ and Ag+ towards a series of aliphatic alkyl acetates and some selected 1-alkenes (P) was examined using the kinetic method. A detailed analysis of the dissociation characteristics of a series of mixed metal-bound dimer ions of the type P1-M+-P2 and the evaluated proton affinities (PAs) of the monomers shows that the affinity of the cation towards long-chain alkyl acetates and alkenes (having a chain length ? C4) is markedly enhanced. In line with recent studies of nitriles, alcohols and methyl alkanoates, this is attributed to a bidentate interaction of the metal ion with the functional group or double bond and the aliphatic chain. In particular, the longer chain alkyl acetates, methyl alkanoates and alcohols show a remarkably similar behaviour with respect to silver ion hydrocarbon bonding. The Ag+ adducts of the alkyl acetates dissociate by loss of CH3COOH. This reaction becomes more pronounced at longer chain lengths, which points to metal ion bidentate formation in [Ag+···1-alkene] product ions having a long hydrocarbon chain. In the same vein, the heterodimers [1-hexene···Ag+···1-heptene] and [1-heptene·Ag+···1-octene] dissociate primarily into [Ag+···1-heptene] and [Ag+···1-octene] ions, respectively. Hydrocarbon bidentate formation in [Ag+···1-octene] also reveals itself by the reluctance of this ion to react with water in an ion trap, as opposed to [Ag+···1-hexene] which readily undergoes hydration.

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Kim, Kwang-Jin, Jusung Lee, Weihong Wang, Yongjin Lee, Eunseok Oh, Kyu-Hyung Park, Chanyoon Park, Gee-Eun Woo, Young-Jin Son, and Heonjoong Kang. "Austalide K from the Fungus Penicillium rudallense Prevents LPS-Induced Bone Loss in Mice by Inhibiting Osteoclast Differentiation and Promoting Osteoblast Differentiation." International Journal of Molecular Sciences 22, no. 11 (May 23, 2021): 5493. http://dx.doi.org/10.3390/ijms22115493.

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Osteoporosis is a chronic disease that has become a serious public health problem due to the associated reduction in quality of life and its increasing financial burden. It is known that inhibiting osteoclast differentiation and promoting osteoblast formation prevents osteoporosis. As there is no drug with this dual activity without clinical side effects, new alternatives are needed. Here, we demonstrate that austalide K, isolated from the marine fungus Penicillium rudallenes, has dual activities in bone remodeling. Austalide K inhibits the receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation and improves bone morphogenetic protein (BMP)-2-mediated osteoblast differentiation in vitro without cytotoxicity. The nuclear factor of activated T cells c1 (NFATc1), tartrate-resistant acid phosphatase (TRAP), dendritic cell-specific transmembrane protein (DC-STAMP), and cathepsin K (CTSK) osteoclast-formation-related genes were reduced and alkaline phosphatase (ALP), runt-related transcription factor 2 (Runx2), osteocalcin (OCN), and osteopontin (OPN) (osteoblast activation-related genes) were simultaneously upregulated by treatment with austalide K. Furthermore, austalide K showed good efficacy in an LPS-induced bone loss in vivo model. Bone volume, trabecular separation, trabecular thickness, and bone mineral density were recovered by austalide K. On the basis of these results, austalide K may lead to new drug treatments for bone diseases such as osteoporosis.

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