Journal articles: 'Nitrure de bore – Synthèse'

1

Haussonne, J. M., J. Lostec, J. P. Bertot, L. Lostec, and S. Sadou. "Nouveau procédé de synthèse du nitrure d'aluminium." Journal de Physique III 3, no. 4 (April 1993): 689–701. http://dx.doi.org/10.1051/jp3:1993157.

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Yallese, Mohamed Athmane, Lakhdar Boulanouar, and Kamel Chaoui. "Usinage de l'acier 100Cr6 trempé par un outil en nitrure de bore cubique." Mécanique & Industries 5, no. 4 (July 2004): 355–68. http://dx.doi.org/10.1051/meca:2004036.

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3

Greco, M., C. Guimon, M. Loudet, and G. Pfister-Guillouzo. "Étude par XPS et calculs ab initio de couches minces de nitrure de bore." Journal de Chimie Physique 91 (1994): 1711–27. http://dx.doi.org/10.1051/jcp/199491711.

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4

Matar, S., V. Gonnet, and G. Dernazeau. "Structure électronique du nitrure de bore cubique dans l'approximation de la densité électronique locale." Journal de Physique I 4, no. 2 (February 1994): 335–42. http://dx.doi.org/10.1051/jp1:1994141.

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BARONNET, J. M., H. AGEORGES, CHANG KUN, S. MEGY, E. MEILLOT, and A. SANON. "SYNTHÈSE DE POUDRES ULTRAFINES DE NITRURE D'ALUMINIUM DANS UN FOUR À PLASMA À ARC TRANSFÉRÉ." Le Journal de Physique Colloques 51, no. C5 (September 1990): C5–127—C5–136. http://dx.doi.org/10.1051/jphyscol:1990516.

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Bougoin, M., F. Thevenot, J. Dubois, and G. Fantozzi. "Synthèse et caracterisation de ceramiques denses en carbure de bore." Journal of the Less Common Metals 114, no. 2 (December 1985): 257–71. http://dx.doi.org/10.1016/0022-5088(85)90444-8.

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7

Djouadi, A., D. Bouchier, and M. Lambertin. "Effets thermiques et collisionnels sur les contraintes internes de films de nitrure de bore déposés sous assistance ionique." Revue de Métallurgie 91, no. 9 (September 1994): 1283. http://dx.doi.org/10.1051/metal/199491091283.

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Bayo-Bangoura, Mabinty, Karifa Bayo, and Mireille Mossoyan-Deneux. "Synthèse de la chlorosousphtalocyanine de bore à partir de l’acide 1,4-diboronique benzène." Comptes Rendus Chimie 14, no. 6 (June 2011): 530–33. http://dx.doi.org/10.1016/j.crci.2010.09.008.

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9

Pouget, M., JP Lecompte, and M. Billy†. "Étude des composés formés lors de la réaction entre les halogénures d’aluminium et l’ammoniac dans le cadre de la synthèse du nitrure d’aluminium." Journal de Chimie Physique 91 (1994): 457–71. http://dx.doi.org/10.1051/jcp/1994910457.

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Pouget, M., JP Lecompte, and M. Billy†. "Étude des composés formés lors de la réaction entre les halogénures d’aluminium et l’ammoniac dans le cadre de la synthèse du nitrure d’aluminium." Journal de Chimie Physique 91 (1994): 547–61. http://dx.doi.org/10.1051/jcp/1994910547.

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11

Subotički, Tijana, Olivera Mitrović Ajtić, Dragoslava Đikić, Juan F. Santibanez, Milica Tošić, and Vladan P. Čokić. "Nitric Oxide Synthase Dependency in Hydroxyurea Inhibition of Erythroid Progenitor Growth." Genes 12, no. 8 (July 27, 2021): 1145. http://dx.doi.org/10.3390/genes12081145.

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Hydroxyurea (HU) causes nitric oxide (NO) bioactivation, acting as both a NO donor and a stimulator of NO synthase (NOS). To examine whether HU effects are NO mediated by chemical degradation or enzymatic induction, we studied human and mouse erythroid cells during proliferation, apoptosis, and differentiation. The HU and NO donor demonstrated persisted versus temporary inhibition of erythroid cell growth during differentiation, as observed by γ- and β-globin gene expression. HU decreased the percentage of erythroleukemic K562 cells in the G2/M phase that was reversed by N-nitro l-arginine methyl ester hydrochloride (L-NAME). Besides activation of endothelial NOS, HU significantly increased apoptosis of K562 cells, again demonstrating NOS dependence. Administration of HU to mice significantly inhibited colony-forming unit-erythroid (CFU-E), mediated by NOS. Moreover, burst-forming-units-erythroid (BFU-E) and CFU-E ex vivo growth was inhibited by the administration of nitrate or nitrite to mice. Chronic in vivo NOS inhibition with L-NAME protected the bone marrow cellularity despite HU treatment of mice. NO metabolites and HU reduced the frequency of NOS-positive cells from CFU-E and BFU-E colonies that was reverted by NOS inhibition. HU regulation of the G2/M phase, apoptosis, differentiation, cellularity, and NOS immunoreactive cells was NOS dependent. Inhalation of NO therapy as well as strategies to increase endogenous NO production could replace or enhance HU activity.

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12

Hauschildt, S., A. Lückhoff, A. Mülsch, J. Kohler, W. Bessler, and R. Busse. "Induction and activity of NO synthase in bone-marrow-derived macrophages are independent of Ca2+." Biochemical Journal 270, no. 2 (September 1, 1990): 351–56. http://dx.doi.org/10.1042/bj2700351.

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The aim of the present study was to analyse whether an increase in the intracellular free Ca2+ concentration ([Ca2+]i) plays a role as a signal mediating synthesis of nitric oxide (NO) in bone-marrow-derived macrophages, either by stimulating induction of NO synthase or by regulating the activity of the enzyme. Therefore we compared the effects of various synthetic analogues of bacterial lipopeptide and of lipopolysaccharide (LPS) on NO production (assessed as nitrite formation during an incubation for 24 h) and on [Ca2+]i [measured with the fluorescent probe indo-1 (1-[2-amino-5-(6-carboxyindol-2-yl)phenoxy]-2- 2-(2′-amino-5′-methylphenoxy)ethane-NNN′N′-tetra-acetic acid)]. Strongly dissociating effects were evoked on nitrite formation and on [Ca2+]i by the stimuli. LPS was preferentially effective on nitrite formation, whereas the Ca2+ ionophore ionomycin and AlF3 induced increases only in [Ca2+]i. The lipopeptides N-palmitoyl-(S)-[2,3-bis(palmitoyloxy)-(2RS)- propyl]-(R)-cysteinylalanylglycine, N-palmitoyl-(S)-[2,3-bis(palmitoyloxy)- (2RS)-propyl]-(R)-cysteinylseryl-lysyl-lysyl-lysine and (S)-(1,2- dicarboxyhexadecyl)ethyl-N-palmitoylcysteinylseryl-lysyl-lys yl-lysine stimulated both parameters, but the maximal effects on nitrite formation and the shape of the dose-response curves did not parallel the effects on [Ca2+]i. Reduction of extracellular Ca2+ with EGTA significantly inhibited increases in [Ca2+]i, but did not change nitrite formation. Furthermore, NO synthesis in the cytosolic fraction of stimulated macrophages was not affected by Ca2+ over the concentration range 10 nM-2 microM. We conclude that increases in [Ca2+]i are not required for NO production in bone-marrow-derived macrophages. Thus the cellular regulation of NO production strikingly differs from that in the vascular endothelium, brain and adrenal gland.

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Thozet, A., S. Allaoud, T. Zaïr, A. Karim, and B. Frange. "Synthèse d'hétérocycles bore-azote-carbone Structure cristallographique du diméthyl-2,4 o-tolyl-3 méthyl-8 dibora-2,4 diazaro-1,3 naphtaléne." Journal of Organometallic Chemistry 406, no. 3 (April 1991): 269–78. http://dx.doi.org/10.1016/0022-328x(91)83114-j.

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14

Angleraud, B., J. Aubreton, and A. Catherinot. "Étude de l'expansion du panache plasma formé lors de l'interaction entre un laser ultraviolet et une cible de nitrure de bore ; application à la réalisation de couches minces." Annales de Physique 22 (February 1997): C1–121—C1–122. http://dx.doi.org/10.1051/anphys/1997022.

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15

Kovalova, I. O., and V. O. Kostenko. "EFFECT OF TRANSCRIPTION FACTOR KAPPA B INHIBITORS ON METABOLIC AND STRUCTURAL DISORDERS IN BONE TISSUE UNDER COMBINED EXCESSIVE INTAKE OF FLUORIDE AND SODIUM NITRATE." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 19, no. 1 (April 26, 2019): 65–70. http://dx.doi.org/10.31718/2077-1096.19.1.65.

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This experiment carried on 40 white Wistar rats aimed at studying the effect produced by inhibitors of the nuclear transcriptional factor kappa B (NF-κB) activation on the mechanisms of metabolic and structural disorders in the femoral bones and vertebrae under combined surplus fluoride and sodium nitrate intake. It has been found out that co-administration of sodium fluoride (10 mg/kg body weight) and sodium nitrate (500 mg/kg of body weight) for 30 days disrupts the autoregulation mechanism of nitrogen monoxide (NO) level in the femoral bones of the test rats that is manifested by an increase in the activity of total NO synthase and its inducible isoform against the background of a decrease in the total arginase activity and the activity of the constitutive NO synthase isoenzymes. Under these conditions, there has been observed the growth in the concentration of free hydroxyproline, N-acetylneuraminic and hexuronic acids in the femoral bones and vertebrae that is indicative of depolymerization of collagen, sialoglycoproteins and proteoglycans, decrease in bone mass, their density, mineral saturation, strength (the Simon index elevated). Inhibitors of NF-κB activation (ammonium pyrolidine dithiocarbamate and a water-soluble form of quercetin) restore the autoregulation mechanism of the NO level in the rats’ femoral bones that is accompanied by a decrease in the total activity of NO synthase, the activity of its inducible isoform, an increase in the total arginase activity and by limited peroxinitrite formation. Ammonium pyrolidine dithiocarbamate and a water-soluble form of quercetin have been shown to result in lowering in the content of free hydroxyproline, N-acetylneuraminic and hexuronic acids in bones that confirms their effectiveness as a means for correcting depolymerization of collagen, sialoglycoproteins and proteoglycans. There has been found their property to promote the growth of bone mass and density of the femurs and vertebrae.

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Jain, Mili, Ashutosh Kumar, Uma Shankar Singh, Rashmi Kushwaha, Abhishek Kumar Singh, Madhu Dikshit, and Anil Kumar Tripathi. "Cellular and plasma nitrite levels in myeloid leukemia: a pathogenetic decrease." Biological Chemistry 398, no. 11 (October 26, 2017): 1259–65. http://dx.doi.org/10.1515/hsz-2017-0143.

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AbstractNitric oxide (NO) has a contributory role in hemopoietic cell growth and differentiation. The effects of NO on leukemic cell growth have been predominantly studied inin vitrosettings. This study was done to assess the alterations in nitrite level in myeloid leukemias. Thirty-six newly diagnosed cases of myeloid leukemia (16 AML and 20 CML) were enrolled in the study. Neutrophil precursors from the marrow aspirate and peripheral blood were separated into cell bands using the Percoll density gradient method of Borregard and Cowland. The blood plasma and marrow fluid was also collected. Nitrite (stable non-volatile end product of NO) was estimated in the cell bands, blood plasma and marrow fluid using Griess reagent. The mean nitrite level in all cell bands from peripheral blood, bone marrow, blood plasma, and marrow fluid of cases was significantly lower as compared to corresponding value in the controls. No significant difference between AML and CML was seen. On follow-up, analysis of 13 CML patients higher nitrite levels were seen (p>0.05). The significant decrease in nitrite levels in myeloid leukemia suggests a decrease in nitric oxide synthase (NOS) activity. Further work may unfold molecular targets for therapeutic role of NO modulators.

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Hadjur, Suzana, and Frank R. Jirik. "Increased sensitivity of Fancc-deficient hematopoietic cells to nitric oxide and evidence that this species mediates growth inhibition by cytokines." Blood 101, no. 10 (May 15, 2003): 3877–84. http://dx.doi.org/10.1182/blood-2002-10-3147.

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AbstractFanconi anemia complementation group C (Fancc)–deficient murine bone marrow progenitors demonstrate increased sensitivity to growth inhibition by interferon γ (IFNγ), tumor necrosis factor α (TNFα), and macrophage inflammatory protein 1α (MIP-1α). This property has been proposed as a possible pathogenic factor in the marrow failure seen in Fanconi anemia. Supporting our hypothesis that nitric oxide (NO) production might be a common effector in this sensitivity, we found that cytokine-mediated growth inhibition ofFancc−/− bone marrow cells was prevented by inhibiting NO synthase activity. Interestingly,Fancc−/− hematopoietic cells also exhibited increased growth inhibition on exposure to 2 distinct NO-generating agents, S-nitroso-N-acetyl-D, L-penicillamine (SNAP) and diethylenetriamine nitric oxide adduct (DETA/NO). In keeping with the sensitivity of Fancc−/− cells to IFNγ, inducible nitric oxide synthase (iNOS) levels and nitrite release were both increased following stimulation ofFancc−/− macrophages with this cytokine, either alone or in combination with bacterial lipopolysaccharide. Suggesting a plausible mechanism for the increased expression of iNOS, IFNγ-stimulated Fancc−/− macrophages generated higher levels of phospho-Stat1, a positive regulator ofinos (nos2) gene expression. These observations, while confined to C57BL/6 Fancc−/−hematopoietic cells, raise the possibility that nitric oxide has a role in the pathogenesis of Fanconi anemia.

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18

Kovalova, I. O., and V. O. Kostenko. "EFFECT OF AP-1 TRANSCRIPTION FACTOR INHIBITOR ON STRUCTURAL, METABOLIC AND BIOMECHANICAL CHANGES IN BONE TISSUE DURING COMBINED EXCESSIVE INTAKE OF SODIUM FLUORIDE AND SODIUM NITRATE." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 19, no. 2 (July 19, 2019): 123–28. http://dx.doi.org/10.31718/2077-1096.19.2.123.

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This article highlights the effect produced by the inhibitor of the AP-1 transcription factor activation on the mechanisms of structural, metabolic and biomechanical disorders in the femoral bones and vertebrae during combined excessive intake of sodium fluoride and sodium nitrate. The experiment was conducted on 30 white rats divided into 4 groups: the 1st included the intact animals, the 2nd group involved the rats subjected to the co- administration of sodium fluoride (10 mg / kg body weight) and sodium nitrate (500 mg / kg body weight) for 30 days, the 3rd group included the animals, which starting from the 15th day of intoxication, were injected SR 11302 ((E, E, Z, E) -3-Methyl-7- (4-methylphenyl) - 9- (2,6,6-trimethyl-1-cyclohexen-1-yl) -2,4,6,8-nonatetraenoic acid), an inhibitor of AP-1 activation in a dose of 1 mg / kg intraperitoneally 3 times a week. It has been revealed that the SR 11302 administration restores the mechanism of NO autoregulation in the femoral bones during the sodium fluoride and sodium nitrate co- administration, reducing the total activity of NO synthase and activity of its inducible isoform under a reciprocal increase in total arginase activity, and suppresses the peroxynitrite production. This is accompanied by a decrease in the activity of enzymes, which are known as markers of bone resorption (acid phosphatase and its bone isoform) and restriction of the depolymerization of collagen, proteoglycans and sialoglycoproteins of the connective (bone) tissue in the femurs and vertebrae. Moreover, the introduction of SR 11302 under the experimental conditions is accompanied by an increase in the density and mineral saturation of the femurs and vertebrae, and an improvement in the biomechanical characteristics of the femurs (their strength and elasticity).

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Clérigues, Victoria, Maria Isabel Guillén, Francisco Gomar, and Maria José Alcaraz. "Haem oxygenase-1 counteracts the effects of interleukin-1β on inflammatory and senescence markers in cartilage–subchondral bone explants from osteoarthritic patients." Clinical Science 122, no. 5 (November 8, 2011): 239–51. http://dx.doi.org/10.1042/cs20100519.

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IL (interleukin)-1β plays an important role in cartilage extracellular matrix degradation and bone resorption in OA (osteoarthritis) through the induction of degradative enzymes and pro-inflammatory mediators. In the present study, we have determined the consequences of HO-1 (haem oxygenase-1) induction on markers of inflammation and senescence in the functional unit cartilage–subchondral bone stimulated with IL-1β. Cartilage–subchondral bone specimens were obtained from the knees of osteoarthritic patients. Treatment with the HO-1 inducer CoPP (cobalt protoporphyrin IX) counteracted the stimulatory effects of IL-1β on IL-6, nitrite, PGE2 (prostaglandin E2), TGF (transforming growth factor) β2, TGFβ3 and osteocalcin. Immunohistochemical analyses indicated that CoPP treatment of explants down-regulated iNOS (inducible nitric oxide synthase), COX-2 (cyclooxygenase-2) and mPGES-1 (microsomal prostaglandin E synthase-1) induced by IL-1β. In contrast, the expression of HMGB1 (high-mobility group box 1) was not significantly modified. In addition, CoPP decreased the expression of iNOS and mPGES-1 in cells isolated from the explants and stimulated with IL-1β, which was counteracted by an siRNA (small interfering RNA) specific for human HO-1. In isolated primary chondrocytes, we determined senescence-associated β-galactosidase activity and the expression of senescence markers by real-time PCR. We have found that HO-1 induction could regulate senescence markers in the presence of IL-1β and significantly affected telomerase expression, as well as β-galactosidase activity and hTERT (human telomerase reverse transcriptase) and p21 expression in chondrocytes. The findings of the present study support the view that HO-1 induction results in the down-regulation of inflammatory and senescence responses in OA articular tissues.

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Wood, Katherine C., Virginia B. Liu, Audrey Noguchi, Xunde Wang, Nalini Raghavachari, and Mark T. Gladwin. "Blood Cell Versus Vascular Endothelial Cell Contributions to Nitrite Homeostasis and Blood Pressure Regulation." Blood 112, no. 11 (November 16, 2008): 4601. http://dx.doi.org/10.1182/blood.v112.11.4601.4601.

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Abstract Mice genetically deficient in constitutive nitric oxide synthase (eNOS) are hypertensive compared to normal C57Bl6 (wild type) mice, indicating the importance of constitutively produced nitric oxide (NO•) to blood pressure regulation and vascular homeostasis. The objective of this study was to use molecular methodologies to determine the contribution of eNOS in circulating blood cells to the intravascular pool of nitrite, a metabolite and storage form of nitric oxide (NO•) with powerful vasorelaxant activity, and to the regulation of blood pressure under physiological conditions. We used bone marrow transplant to create chimeric mice genetically deficient in eNOS in either circulating blood cells (−/+) or vascular endothelium (+/−), confirmed by flow cytometry, western blot, RT-PCR and immunohistochemistry. Nitrite concentrations in whole blood and plasma of chimeras were quantified using ozone-based reductive chemiluminescence. Mean arterial and diastolic blood pressures of chimeras were assessed in the absence/presence of NOS stimulation with oral L-Arginine or NOS inhibition with oral L-Name. A highly significant inverse correlation between plasma nitrite concentrations and blood pressures was noted across all groups of chimeric mice. Importantly, in agreement with higher blood pressures in −/+ chimeras compared to eNOS positive controls (+/+ chimeras globally competent for eNOS), significantly reduced whole blood and plasma nitrite concentrations were also measured. Blood pressure responses to NOS inhibition or stimulation were intact in all chimera groups except eNOS negative controls (−/− chimeras globally deficient for eNOS) and, importantly, blunted in −/+ chimeras compared to eNOS positive controls. These findings indicate a functional blood cell eNOS that is a major contributor to circulating nitrite concentrations and plays a critical role in vascular homeostasis.

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Rao, Deviyani M., Della T. Phan, Michelle J. Choo, Amie L. Owen, Anne-Laure Perraud, and Fabienne Gally. "Mice Lacking Fatty Acid-Binding Protein 5 Are Resistant to Listeria monocytogenes." Journal of Innate Immunity 11, no. 6 (2019): 469–80. http://dx.doi.org/10.1159/000496405.

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To investigate the role of fatty acid-binding protein 5 (FABP5) in infectious diseases, FABP5-deficient mice were challenged with Listeria monocytogenes, a facultative intracellular bacterial pathogen. Interestingly, FABP5-deficient animals were able to clear the infection within 3 days whereas control wild-type (WT) animals showed comparatively higher bacterial burdens in the liver and spleen. Sections of infected tissues showed an increase in inflammatory foci in WT mice compared to FABP5-deficient mice. FABP5-deficient mice had lower circulating inflammatory cytokines and increased inducible nitric oxide synthase production. FABP5-deficient mouse bone marrow-derived macrophages produced higher levels of nitrite anion than their WT counterparts in response to various stimuli. Additionally, in contrast to FABP5–/– mice, transgenic mice overexpressing FABP5 in myeloid cells (LysM-Cre driven) showed decreased survival rates and increased bacterial burden and inflammatory cytokines. Overall, these findings suggest that increased FABP5 levels correlate with a higher L. monocytogenes bacterial burden and elevated subsequent inflammation.

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Liu, Jun, Jiqing Tang, Xiuting Li, Qiaojuan Yan, Junwen Ma, and Zhengqiang Jiang. "Curdlan (Alcaligenes faecalis) (1→3)-β-d-Glucan Oligosaccharides Drive M1 Phenotype Polarization in Murine Bone Marrow-Derived Macrophages via Activation of MAPKs and NF-κB Pathways." Molecules 24, no. 23 (November 22, 2019): 4251. http://dx.doi.org/10.3390/molecules24234251.

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Functional oligosaccharides, particularly curdlan (1→3)-β-d-glucan oligosaccharides (GOS), play important roles in modulating host immune responses. However, the molecular mechanisms underlying the immunostimulatory effects of GOS on macrophage polarization are not clear. In this work, GOS (5–1000 µg/mL) were non-toxic to bone marrow-derived macrophages (BMDMs) with improved pinocytic and bactericidal capacities. Incubation with GOS (100 µg/mL) induced M1 phenotype polarization of BMDMs as evidenced by increased CD11c+/CD86+ (10.1%) and M1 gene expression of inducible nitric oxide synthase, interleukin (IL)-1β, and chemokine C-C-motif ligand 2. Accordingly, the secretion of cytokines IL-1β, IL-6, monocyte chemotactic protein-1, and tumor necrosis factor-α, as well as the nitrite release of BMDMs were increased by GOS (100 µg/mL). Expression of mitogen-activated protein kinases (MAPKs) of phosphorylated (p)-c-Jun amino-terminal kinase, p-extracellular signal regulated kinase, and p-p38 in BMDMs were increased by GOS, as well as the p-Stat1. Moreover, nuclear factor-kappa B (NF-κB) p-p65 expression in BMDMs was promoted by GOS while it suppressed IκBα expression. Receptor blocking with anti-CR3 (CD11b/CD18) and anti-toll-like receptor (TLR) 2 antibodies diminished GOS induced M1 phenotype polarization with reduced mRNA expression of M1 genes, decreased cytokine and nitrite releases, and suppressed signaling pathway activation. Thus, CR3 (CD11b/CD18) and TLR2 mediated activation of MAPKs and NF-κB pathways are responsible for GOS induced polarization of BMDMs.

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Qian, Zhong Ming, De Sheng Xiao, Ya Ke, and Qin Kue Liao. "Increased nitric oxide is one of the causes of changes of iron metabolism in strenuously exercised rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 3 (March 1, 2001): R739—R743. http://dx.doi.org/10.1152/ajpregu.2001.280.3.r739.

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This study was carried out to investigate the possible role of increased nitric oxide (NO) production in the development of the low iron status in strenuously exercised rats. Female Sprague-Dawley rats were randomly assigned to four groups: sedentary (S1), sedentary + nitro-l-arginine methyl ester (l-NAME; S2), exercise (E1), and exercise + l-NAME (E2). Animals in the E1 and E2 groups swam for 2 h/day for 3 mo. l-NAME in the drinking water (1 mg/ml) was administrated to rats in the S2 and E2 groups for the same period. At the end of third month, hematological indexes and nitrite and nitrate (NOx) contents in the plasma and non-heme iron and NOx levels in the liver, spleen, and bone marrow cells were measured. Three months of exercise induced a significant increase in NOx content and a decrease in iron level both in plasma and tissues. Treatment with l-NAME, an inhibitor of NO synthase (NOS), led to a significant decrease in NOx and an increase in iron level both in plasma and tissues in the exercised rats. The E2 group had a significantly lower NOx content as well as a higher iron level both in plasma and tissues than the E1 group. However, the iron contents in the plasma and tissues of the E2 group were still significantly lower than those found in S1. No difference was found in NOx levels between E2 and S1. These findings showed that exercise was associated with elevation in NOx and reduction in iron in plasma and the tissues. Treatment with l-NAME was able to completely inhibit the effect of exercise on NOx as well as partly recover the decreased iron contents in plasma and tissues resulting from exercise. This suggests that the increased production of NO might be one of the causes of the lower iron status in exercised rats.

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Drobyski, WR, CA Keever, GA Hanson, T. McAuliffe, and OW Griffith. "Inhibition of nitric oxide production is associated with enhanced weight loss, decreased survival, and impaired alloengraftment in mice undergoing graft-versus-host disease after bone marrow transplantation." Blood 84, no. 7 (October 1, 1994): 2363–73. http://dx.doi.org/10.1182/blood.v84.7.2363.2363.

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Abstract The pathophysiologic role of nitric oxide (NO) in graft-versus-host disease (GVHD) was investigated in a murine bone marrow (BM) transplantation model where donor and recipient were H-2-matched but differed at multiple minor histocompatibility antigens. Host AKR/J (H- 2K) mice received lethal total body irradiation as pretransplant conditioning followed by transplantation of donor B10.BR (H-2K) BM cells with or without spleen cells as a source of GVH-reactive T cells. NO production, as assessed by serum nitrate and nitrite levels, was increased for up to 3 weeks posttransplant in animals undergoing both moderate and severe GVHD. Administration of NG-methyl-L-arginine (L- NMA), an inhibitor of nitric oxide synthase, to animals undergoing GVHD resulted in effective suppression of NO production when compared with saline-treated GVHD control animals. Suppression of NO production by L- NMA in GVHD animals was associated with enhanced weight loss early posttransplant and decreased overall survival. Histologic analysis of tissues from L-NMA-treated and saline-treated GVHD animals showed that early weight loss was not because of an exacerbation of GVHD, indicating that NO did not appear to play an immunosuppressive role in this experimental model. L-NMA-treated animals with enhanced weight loss were observed to have splenic atrophy, decreased extramedullary hematopoiesis, and a reduction in BM cellularity when compared with GVHD control mice that were weight-matched before transplant. Analysis of T-cell chimerism in the spleen showed that L-NMA treatment impaired donor T-cell repopulation. In vitro colony-forming unit (CFU) assays were performed to further assess the role of NO on BM progenitor cell growth. L-NMA added directly into culture had no effect on CFU- granulocyte/macrophage (CFU-GM) formation in normal murine BM. In contrast, total CFU-GM from L-NMA-treated animals were significantly reduced when compared with GVHD controls or BM control animals who did not develop GVHD. Collectively, these data indicate that inhibition of NO impairs hematopoietic reconstitution and support the premise that NO appears to play a novel role in the facilitation of alloengraftment posttransplant.

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Drobyski, WR, CA Keever, GA Hanson, T. McAuliffe, and OW Griffith. "Inhibition of nitric oxide production is associated with enhanced weight loss, decreased survival, and impaired alloengraftment in mice undergoing graft-versus-host disease after bone marrow transplantation." Blood 84, no. 7 (October 1, 1994): 2363–73. http://dx.doi.org/10.1182/blood.v84.7.2363.bloodjournal8472363.

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The pathophysiologic role of nitric oxide (NO) in graft-versus-host disease (GVHD) was investigated in a murine bone marrow (BM) transplantation model where donor and recipient were H-2-matched but differed at multiple minor histocompatibility antigens. Host AKR/J (H- 2K) mice received lethal total body irradiation as pretransplant conditioning followed by transplantation of donor B10.BR (H-2K) BM cells with or without spleen cells as a source of GVH-reactive T cells. NO production, as assessed by serum nitrate and nitrite levels, was increased for up to 3 weeks posttransplant in animals undergoing both moderate and severe GVHD. Administration of NG-methyl-L-arginine (L- NMA), an inhibitor of nitric oxide synthase, to animals undergoing GVHD resulted in effective suppression of NO production when compared with saline-treated GVHD control animals. Suppression of NO production by L- NMA in GVHD animals was associated with enhanced weight loss early posttransplant and decreased overall survival. Histologic analysis of tissues from L-NMA-treated and saline-treated GVHD animals showed that early weight loss was not because of an exacerbation of GVHD, indicating that NO did not appear to play an immunosuppressive role in this experimental model. L-NMA-treated animals with enhanced weight loss were observed to have splenic atrophy, decreased extramedullary hematopoiesis, and a reduction in BM cellularity when compared with GVHD control mice that were weight-matched before transplant. Analysis of T-cell chimerism in the spleen showed that L-NMA treatment impaired donor T-cell repopulation. In vitro colony-forming unit (CFU) assays were performed to further assess the role of NO on BM progenitor cell growth. L-NMA added directly into culture had no effect on CFU- granulocyte/macrophage (CFU-GM) formation in normal murine BM. In contrast, total CFU-GM from L-NMA-treated animals were significantly reduced when compared with GVHD controls or BM control animals who did not develop GVHD. Collectively, these data indicate that inhibition of NO impairs hematopoietic reconstitution and support the premise that NO appears to play a novel role in the facilitation of alloengraftment posttransplant.

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Harrington, Jane C., Sandy M. S. Wong, Charles V. Rosadini, Oleg Garifulin, Victor Boyartchuk, and Brian J. Akerley. "Resistance of Haemophilus influenzae to Reactive Nitrogen Donors and Gamma Interferon-Stimulated Macrophages Requires the Formate-Dependent Nitrite Reductase Regulator-Activated ytfE Gene." Infection and Immunity 77, no. 5 (March 16, 2009): 1945–58. http://dx.doi.org/10.1128/iai.01365-08.

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ABSTRACT Haemophilus influenzae efficiently colonizes and persists at the human nasopharyngeal mucosa, causing disease when it spreads to other sites. Nitric oxide (NO) represents a major antimicrobial defense deployed by host cells in locations colonized by H. influenzae during pathogenesis that are likely to vary in oxygen levels. Formate-dependent nitrite reductase regulator (FNR) is an oxygen-sensitive regulator in several bacterial pathogens. We report that fnr of H. influenzae is required for anaerobic defense against exposure to NO donors and to resist NO-dependent effects of gamma interferon (IFN-γ)-activated murine bone marrow-derived macrophages. To understand the mechanism of resistance, we investigated the role of FNR-regulated genes in defense against NO sources. Expression analysis revealed FNR-dependent activation of nrfA, dmsA, napA, and ytfE. Nonpolar deletion mutants of nrfA and ytfE exhibited sensitivity to NO donors, and the ytfE gene was more critical for survival. Compared to the wild-type strain, the ytfE mutant exhibited decreased survival when exposed to macrophages, a defect that was more pronounced after prior stimulation of macrophages with IFN-γ or lipopolysaccharide. Complementation restored survival of the mutant to the level in the parental strain. Increased sensitivity of the ytfE mutant relative to that of the parent was abrogated by treatment of macrophages with a NO synthase inhibitor, implicating YtfE in resistance to a NO-dependent pathway. These results identify a requirement for FNR in positive control of ytfE and indicate a critical role for ytfE in resistance of H. influenzae to reactive nitrogen species and the antibacterial effects of macrophages.

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Jouni, Dima, Yanyan Zhang, Hakim Bouamar, Monika Wittner, William Vainchenker, and Fawzia Louache. "Stromal Microenvironment Regulates Progenitor Survival through Nitric Oxide Production." Blood 114, no. 22 (November 20, 2009): 1440. http://dx.doi.org/10.1182/blood.v114.22.1440.1440.

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Abstract Abstract 1440 Poster Board I-463 Nitric oxide (NO) is a small gaseous molecule with diverse roles including the regulation of cell proliferation, differentiation, apoptosis, adhesion and migration. NO is derived from L-arginine by the nitric oxide synthase (NOS) family of enzymes. At least three distinct NOS isoforms have been identified in mammalian cells including the endothelial (eNOS), neuronal (nNOS) and inducible (iNOS). Recently, we have shown that NO donors induce CXCR4 expression in human CD34 positive cells suggesting that NO production may regulate the migration and adhesion of hematopoietic progenitors. To determine the in vivo relevance of these findings and define the role of NO in the biology of hematopoietic progenitor cells, we first investigated NOS expression in hematopoietic and non-hematopoietic cells. Using quantitative reverse transcription-PCR analysis, we demonstrate that nNOS, and eNOS isoforms are highly expressed in Human Umbilical Vein Endothelial Cells (HUVEC) and osteoblastic cell lines, but there was no or low expression of NOS in hematopoietic cells including cell lines and mature blood cells except macrophages that express high level of iNOS. In agreement with RNA analysis, we found large amounts of nitrite (a stable derivative of NO) in the culture medium of stromal (MS-5) and osteoblasic (MG-63) cell lines. To determine the effects of NO on hematopoietic progenitor cells survival, cord blood CD34+ were cultured on MS-5 cells in the presence/absence of NOS inhibitor (L-NAME) for three days, then hematopoietic progenitor numbers were determined by culture in a semi-solid medium and colonies were quantified 14 days later. Treatment with L-NAME reduced colony number by 33, 42 and 54% with 10, 100 and 500 μM L-NAME concentrations, respectively. This effect is NO specific since the diminution of progenitor number was reverted by adding NO donor in the culture medium. These results indicate that NO is produced by bone marrow stromal cells. This production regulates the survival of hematopoietic progenitors in vitro. Further experiments are needed to determine if these effects are dependent on the regulation of CXCR4/SDF-1 signaling. Disclosures Jouni: Région IDF: Employment. Bouamar: Association pour la Recherche sur le Cancer: Employment; Cancéropôle IDF: Employment.

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Ayoub, Abeer J., Layal Hariss, Nehme El-Hachem, Ghewa A. El-Achkar, Sandra E. Ghayad, Oula K. Dagher, Nada Borghol, et al. "gem-Difluorobisarylic derivatives: design, synthesis and anti-inflammatory effect." BMC Chemistry 13, no. 1 (October 31, 2019). http://dx.doi.org/10.1186/s13065-019-0640-5.

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Abstract Introduction New fluorinated diaryl ethers and bisarylic ketones were designed and evaluated for their anti-inflammatory effects in primary macrophages. Methods The synthesis of the designed molecules started from easily accessible and versatile gem-difluoro propargylic derivatives. The desired aromatic systems were obtained using Diels–Alder/aromatization sequences and this was followed by Pd-catalyzed coupling reactions and, when required, final functionalization steps. Both direct inhibitory effects on cyclooxygenase-1 or -2 activities, protein expression of cyclooxygenase-2 and nitric oxide synthase-II and the production of prostaglandin E2, the pro-inflammatory nitric oxide and interleukin-6 were evaluated in primary murine bone marrow-derived macrophages in response to lipopolysaccharide. Docking of the designed molecules in cyclooxygenase-1 or -2 was performed. Results Only fluorinated compounds exerted anti-inflammatory activities by lowering the secretion of interleukin-6, nitric oxide, and prostaglandin E2, and decreasing the protein expression of inducible nitric oxide synthase and cyclooxygenase-2 in mouse primary macrophages exposed to lipopolysaccharide, as well as cyclooxygenase activity for some inhibitors with different efficiencies depending on the R-groups. Docking observation suggested an inhibitory role of cyclooxygenase-1 or -2 for compounds A3, A4 and A5 in addition to their capacity to inhibit nitrite, interleukin-6, and nitric oxide synthase-II and cyclooxygenase-2 expression. Conclusion The new fluorinated diaryl ethers and bisarylic ketones have anti-inflammatory effects in macrophages. These fluorinated compounds have improved potential anti-inflammatory properties due to the fluorine residues in the bioactive molecules.

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Journal articles on the topic 'Nitrure de bore – Synthèse'

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