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Littérature scientifique sur le sujet « Fura2 »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 6 février 2022

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Articles de revues sur le sujet "Fura2"

Gao, Chun-Hui, Wen-Ping Wei, Hui-Ling Tao, Li-Kai Cai, Wan-Zhong Jia, Lihua Hu et Min Yang. « Cross-talk between the three furA orthologs in Mycobacterium smegmatis and the contribution to isoniazid resistance ». Journal of Biochemistry 166, n^o 3 (16 avril 2019) : 237–43. http://dx.doi.org/10.1093/jb/mvz030.

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Abstract The ferric uptake regulator A (FurA) plays an essential role in responding to oxidative stress in mycobacteria. The genome of Mycobacterium smegmatis harbours three FurA orthologs; however, the potential cross-talk and contribution to drug resistance of different furA operon remain underdetermined. In this study, we characterized the cross-regulation and effect in drug resistance of these orthologs from M. smegmatis. Cross-binding of FurA protein to furA promoter was observed. The binding of FurA1 to furA3p and FurA2 to furA1p or furA3p is even more pronounced than their self-binding. The three FurA proteins are all functional at repressing the expression of the peroxidase enzyme katG1/katG2 in vivo. When overexpressing any of the furA orthologs in M. smegmatis, the bacteria become more resistant to isoniazid (INH). This pattern is consistent with that in Mycobacterium bovis. However, the knockdown of furA does not affect the INH sensitivity. This is the first report of cross-talk and contribution to drug resistance of all three furA orthologs in M. smegmatis.

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Dubois, Christophe, Laurence Panicot-Dubois, Barbara C. Furie et Bruce Furie. « Direct Real Time Visualization of Platelet Calclium Signaling In Vivo : Role of Platelet Activation and Thrombus Formation in a Living Mouse. » Blood 104, n^o 11 (16 novembre 2004) : 325. http://dx.doi.org/10.1182/blood.v104.11.325.325.

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Abstract Intracellular calcium mobilization plays a critical role in platelet signaling. Upon platelet activation, an intracellular calcium mobilization leads to the activation of various intracellular and membrane proteins, including integrins involved in both platelet shape change and aggregation. The goal of the present study was to monitor platelet calcium mobilization in vivo in an intact animal and to determine which intracellular pathways are dominant in platelet accumulation into the developing thrombus. Platelets were isolated from mice, washed, loaded with a calcium-sensitive fluorochrome, Fura2-AM and then infused into a recipient mouse. We studied Fura2-AM loaded platelet incorporation during arterial thrombus development following laser injury of the vessel wall in the cremaster microcirculation of living mice using high speed intravital widefield digital microscopy. Fura-2 loaded platelets were monitored by excitation at 380 nm; this fluorescence reports the basal calcium levels in platelets. Calcium mobilization was monitored by excitation at 340 nm where the fluorescence intensity reflects Fura2-calcium complex formation. We observed that platelets bind to the growing thrombus independent of calcium mobilization. However, the stable incorporation of platelets into the thrombus correlated with a significant intracellular calcium increase. Once the thrombus reached maximal size at about 100 seconds, the calcium mobilization also reached maximal intensity. Subsequently, platelets that did not mobilize calcium dissociated from the thrombus. We confirmed these observations by using platelets treated with the calcium chelators, BAPTA-AM or EGTA-AM. We observed a significant inhibition of platelet accumulation into the thrombus, indicating that the intracellular calcium increase is necessary in vivo for the stable accumulation of the platelets into the thrombus. We also evaluated the involvement in vivo of two platelet agonists, ADP and thromboxane A2 (TxA2), on calcium mobilization and platelet incorporation into thrombi. When platelets were treated with aspirin or with the P2Y1 antagonist A3P5P (adenosine 3′-phosphate-5′-phosphate), we observed a partial decrease in both calcium mobilization and platelet accumulation into the thrombus. These results indicate that TxA2 and ADP via the P2Y1 receptor are involved in vivo in platelet activation upon vessel wall injury in this thrombosis model. When platelets were treated with both compounds, we completely inhibited the calcium increase and the incorporation of platelets into the thrombus. Altogether, our results directly show, for the first time in vivo, the importance of the calcium mobilization on platelet accumulation into the developing thrombus. The platelet agonists TxA2 and ADP both play an important and complementary role on platelet activation by acting on the mobilization of the intracellular calcium.

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James-Kracke, M. R. « Calmodulin activation of the Ca2+ pump revealed by fluorescent chelator dyes in human red blood cell ghosts. » Journal of General Physiology 99, n^o 1 (1 janvier 1992) : 41–62. http://dx.doi.org/10.1085/jgp.99.1.41.

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Ca2+ transport in red blood cell ghosts was monitored with fura2 or quin2 incorporated as the free acid during resealing. This is the first report of active transport monitored by the fluorescent intensity of the chelator dyes fura2 (5-50 microM) or quin2 (250 microM) in hemoglobin-depleted ghosts. Since there are no intracellular compartments in ghosts and the intracellular concentrations of all assay chelator substances including calmodulin (CaM), the dyes, and ATP could be set, the intracellular concentrations of free and total Ca [( Cafree]i and [Catotal]i) could be calculated during the transport. Ghosts prepared with or without CaM rapidly extruded Ca2+ to a steady-state concentration of 60-100 nM. A 10(4)-fold gradient for Ca2+ was routinely produced in medium containing 1 mM Ca2+. During active Ca2+ extrusion, d[Cafree]i/dt was a second order function of [Cafree]i and was independent of the dye concentration, whereas d[Catotal]i/dt increased as a first order function of both the [Cafree]i and the concentration of the Ca:dye complex. CaM (5 microM) increased d[Catotal]i/dt by 400% at 1 microM [Cafree]i, while d[Cafree]i/dt increased by only 25%. From a series of experiments we conclude that chelated forms of Ca2+ serve as substrates for the pump under permissive control of the [Cafree]i, and this dual effect may explain cooperativity. Free Ca2+ is extruded, and probably also Ca2+ bound to CaM or other chelators, while CaM and the chelators are retained in the cell.

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Lee, Meng-Luen, Erna Sulistyowati, Jong-Hau Hsu, Bo-Yau Huang, Zen-Kong Dai, Bin-Nan Wu, Yu-Ying Chao et Jwu-Lai Yeh. « KMUP-1 Ameliorates Ischemia-Induced Cardiomyocyte Apoptosis through the NO–cGMP–MAPK Signaling Pathways ». Molecules 24, n^o 7 (8 avril 2019) : 1376. http://dx.doi.org/10.3390/molecules24071376.

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To test whether KMUP-1 (7-[2-[4-(2-chlorophenyl) piperazinyl]ethyl]-1,3-dimethylxanthine) prevents myocardial ischemia-induced apoptosis, we examined KMUP-1-treated H9c2 cells culture. Recent attention has focused on the activation of nitric oxide (NO)-guanosine 3', 5'cyclic monophosphate (cGMP)-protein kinase G (PKG) signaling pathway triggered by mitogen-activated protein kinase (MAPK) family, including extracellular-signal regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 in the mechanism of cardiac protection during ischemia-induced cell-death. We propose that KMUP-1 inhibits ischemia-induced apoptosis in H9c2 cells culture through these pathways. Cell viability was assessed using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and apoptotic evaluation was conducted using DNA ladder assay and Hoechst 33342 staining. The level of intracellular calcium was detected using - Fura2-acetoxymethyl (Fura2-AM) staining, and mitochondrial calcium with Rhod 2-acetoxymethyl (Rhod 2-AM) staining under fluorescence microscopic observation. The expression of endothelium NO synthase (eNOS), inducible NO synthase (iNOS), soluble guanylate cyclase α1 (sGCα1), PKG, Bcl-2/Bax ratio, ERK1/2, p38, and JNK proteins were measured by Western blotting assay. KMUP-1 pretreatment improved cell viability and inhibited ischemia-induced apoptosis of H9c2 cells. Calcium overload both in the intracellular and mitochondrial sites was attenuated by KMUP-1 pretreatment. Moreover, KMUP-1 reduced intracellular reactive oxygen species (ROS), increased plasma NOx (nitrite and nitrate) level, and the expression of eNOS. Otherwise, the iNOS expression was downregulated. KMUP-1 pretreatment upregulated the expression of sGCα1 and PKG protein. The ratio of Bcl-2/Bax expression was increased by the elevated level of Bcl2 and decreased level of Bax. In comparison with the ischemia group, KMUP-1 pretreatment groups reduced the expression of phosphorylated extracellular signal-regulated kinases ERK1/2, p-p38, and p-JNK as well. Therefore, KMUP-1 inhibits myocardial ischemia-induced apoptosis by restoration of cellular calcium influx through the mechanism of NO-cGMP-MAPK pathways.

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Sago, Haruhiko, et Kazuso linuma. « Cell Shape Change and Cytosolic Ca2+ in Human Umbilical-Vein Endothelial Cells Stimulated with Thrombin ». Thrombosis and Haemostasis 67, n^o 03 (1992) : 331–34. http://dx.doi.org/10.1055/s-0038-1648442.

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SummaryWe quantified thrombin-induced endothelial cells shape change and investigated the role of Ca2+ in such shape change. We used the fluorescent Ca2+ indicator, fura2, to measure both shape change as cell size and intracellular free Ca2+ ([Ca2+]i), in cultured human umbilical-vein endothelial cells (HUVEC). Thrombin induced concentration-dependent decreases in cell size (percentage of cell size at 6 min after stimulation with 0.01 U/ml, 0.1 U/ml, or 1 U/ml thrombin) was 90.1 ± 1.5%, 78.1 ± 2.4%, and 40.9 ± 2.4%, respectively. Thrombin also increased [Ca2+]i in a concentration-dependent manner. Both depletion of extracellular Ca2+, and also the addition of W5, a calmodulin antagonist, inhibited thrombin-induced size reduction. These results indicate an association between shape change and [Ca2+]i mobilization in human endothelial cells stimulated by thrombin.

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Morita, Mitsuhiro, Jinichi Susuki, Takanori Moto, Chitose Higuchi et Yoshihisa Kudo. « A Novel Method to Quantify Calcium Response Pattern and Oscillation Using Fura2 and Acridine Orange ». Journal of Pharmacological Sciences 94, n^o 1 (2004) : 25–30. http://dx.doi.org/10.1254/jphs.94.25.

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Schafer, AI, GB Zavoico, J. Loscalzo et AK Maas. « Synergistic inhibition of platelet activation by plasmin and prostaglandin I2 ». Blood 69, n^o 5 (1 mai 1987) : 1504–7. http://dx.doi.org/10.1182/blood.v69.5.1504.1504.

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Abstract Endothelial cell prostacyclin (PGI2) inhibits platelet activation by raising platelet cyclic AMP. Previously, platelet activation was also shown to be blocked by plasmin formed by endothelium-derived tissue plasminogen activator (TPA). We have now studied interactions between PGI2 and plasmin in the control of platelet function. PGI2 and plasmin cause synergistic inhibition of thrombin- and ADP-induced aggregation of washed platelets. Inhibition by PGI2 is similarly potentiated by TPA added to platelet-rich plasma to generate plasmin. Thrombin-stimulated rise in platelet cytosolic Ca2+, measured by fura2 fluorescence, and thromboxane A2 formation, measured by radioimmunoassay (RIA), are likewise synergistically inhibited by PGI2 and plasmin. Plasmin neither increases nor potentiates PGI2-stimulated increases in platelet cyclic AMP. Thus, PGI2 and plasmin cause synergistic inhibition of platelet activation by both cyclic AMP-dependent and independent mechanisms. This interaction between two different endothelium-derived products may play an important role in localizing the hemostatic plug to a site of vascular injury by preventing further thrombin-mediated accrual of platelets.

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Endothelial cell prostacyclin (PGI2) inhibits platelet activation by raising platelet cyclic AMP. Previously, platelet activation was also shown to be blocked by plasmin formed by endothelium-derived tissue plasminogen activator (TPA). We have now studied interactions between PGI2 and plasmin in the control of platelet function. PGI2 and plasmin cause synergistic inhibition of thrombin- and ADP-induced aggregation of washed platelets. Inhibition by PGI2 is similarly potentiated by TPA added to platelet-rich plasma to generate plasmin. Thrombin-stimulated rise in platelet cytosolic Ca2+, measured by fura2 fluorescence, and thromboxane A2 formation, measured by radioimmunoassay (RIA), are likewise synergistically inhibited by PGI2 and plasmin. Plasmin neither increases nor potentiates PGI2-stimulated increases in platelet cyclic AMP. Thus, PGI2 and plasmin cause synergistic inhibition of platelet activation by both cyclic AMP-dependent and independent mechanisms. This interaction between two different endothelium-derived products may play an important role in localizing the hemostatic plug to a site of vascular injury by preventing further thrombin-mediated accrual of platelets.

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Li, Shu, Jingyi Xue, Zhipeng Sun, Tiantian Liu, Lane Zhang, Limin Wang, Hongjie You, Zheng Fan, Yuanyuan Zheng et Dali Luo. « CaMKII Potentiates Store-Operated Ca2+ Entry Through Enhancing STIM1 Aggregation and Interaction with Orai1 ». Cellular Physiology and Biochemistry 46, n^o 3 (2018) : 1042–54. http://dx.doi.org/10.1159/000488835.

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Background/Aims: Upon Ca2+ store depletion, stromal interaction molecule 1 (STIM1) oligomerizes, redistributes near plasmalemma to interact with Ca2+ selective channel-forming subunit (Orai1) and initiates store-operated Ca2+ entry (SOCE). Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a regulator of SOCE, but how CaMKII regulates SOCE remains obscure. Methods: Using Fura2, confocal microscopy, co-immunoprecipitation, specific blocker and overexpression/knockdown approaches, we evaluated STIM1 aggregation and its interaction with Orai1, and SOCE upon Ca2+ store depletion in thapsigargin (TG) treated HEK293 and HeLa cells. Results: Overexpression of CaMKIIδ enhanced TG-induced STIM1 co-localization and interaction with Orai1 as well as SOCE. In contrast, CaMKIIδ knockdown and a specific inhibitor of CaMKII suppressed them. In addition, overexpression or knockdown of CaMKIIδ in TG treated cells exhibited increased or reduced STIM1 clustering and plasmalemma redistribution, respectively. Conclusion: CaMKII up-regulates SOCE by increasing STIM1 aggregation and interaction with Orai1. This study provides an additional insight into SOCE regulation and a potential mechanism for CaMKII involvement in some pathological situations through crosstalk with SOCE.

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Marchetti, C., C. Amico et C. Usai. « Functional characterization of the effect of nimodipine on the calcium current in rat cerebellar granule cells ». Journal of Neurophysiology 73, n^o 3 (1 mars 1995) : 1169–80. http://dx.doi.org/10.1152/jn.1995.73.3.1169.

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1. We investigated the effect of nimodipine on the calcium current in dissociated cerebellar granule cells from 8-day-old rats. We measured the whole cell current and the depolarization-induced internal calcium elevation in Fura2-loaded cells exposed to high-potassium solutions. 2. Nimodipine maximally depressed the peak calcium current from holding potential (Vh) = -80 mV by 25% and the inactivation resistant residual current from Vh = -50 mV by 44%. The nimodipine-sensitive current had the same amplitude under both conditions and the half-maximal inhibition concentration (IC50) was close to 50 nM. 3. In contrast to other components of the calcium current, the nimodipine-sensitive current did not inactivate significantly during 1-s depolarization and it was weakly sensitive to the holding potential and to depolarizing conditioning prepulses. The effect of nimodipine was higher on the current elicited by small depolarizations and the current at -30 mV was depressed by < or = 70%. Depolarizing prepulses enhanced the effect of 1 nM (but not that of 1 microM) nimodipine. 4. In Fura2-loaded cells, nimodipine strongly antagonized the internal calcium rise due to superfusion with 15-75 mM potassium. The effect was significantly more potent on the internal calcium rise determined by lower depolarizations, with 80% inhibition of the peak response to 25 mM KCl. The dose dependence of this depression was best approximated by a two-site curve with IC50(1) = 0.27 nM and IC50(2) = 65 nM. The time course of recovery was dependent on the duration of treatment, suggesting a close interaction between nimodipine and the lipid membrane. 5. The effect of 1 microM nimodipine was not influenced by predepolarizations determined by treatments with calcium-free elevated potassium solutions, but when doses as low as 1 nM were applied the fast decay of the calcium level suggested a voltage dependence of the effect. Nimodipine also depressed < or = 90% of the plateau phase of the depolarization-induced internal calcium rise at different depolarizations. 6. Incubation in omega-conotoxin, fraction GVIA (5 microM) did not cause any significant decrease in the calcium response, whereas omega-agatoxin, fraction IVA (0.5 microM) depressed the calcium peak by 40-60% and its effect was additive with that of nimodipine. 7. We conclude that the nimodipine-sensitive current is a persistent, inactivation-resistant current that activates at a membrane potential lower than the other components and is likely to be responsible for the elevation of calcium determined by nonovershooting, prolonged depolarizations in these cells.(ABSTRACT TRUNCATED AT 400 WORDS)

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Thèses sur le sujet "Fura2"

Wang, Yamin. « Novel synthetic routes to furan fatty acids and their analogues ». Thesis, Loughborough University, 2016. https://dspace.lboro.ac.uk/2134/23486.

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Furan and its derivatives are commonly found in numerous compounds such as natural products, polymers and medicines. The furan ring system is not only the core component to many natural products, but also serves as a key synthetic intermediate to access other more complex molecules. Among furan derivatives, furan fatty acids (F-acids) are an important class of natural products which are widely distributed in nature, and occupy a unique place in the field of medicinal chemistry because of their potent biological and pharmacological activity. This thesis examines the development of novel approaches towards highly substituted furans, with the ultimate goal of applying novel and high efficiency methods to the synthesis of F-acids and their derivatives. The first total synthesis of a natural product, an F-acids metabolite originally isolated from shark (Lamna ditropis) bile, was accomplished by the utilisation of an iodocyclisation of the corresponding 3-alkyne-1,2-diol to construct the furan nucleus; the synthetic route will be discussed in this thesis. Through the study of palladium-catalysis of a formal cyclisation to construct the furan ring system, a general route to access different F-acids has been developed. Splitting the F-acids into relatively simple fragments allows for easy preparation and modification of two fragments to produce a range of F-acids. The synthetic route was then applied to the formal synthesis of a natural product, F-acid F6. After optimisation of the synthetic route, total synthesis of F-acids F4, F6 and their analogues was accomplished.

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Finlay, James William. « Applications of synthesis of furan oxidations ». Thesis, Queen's University Belfast, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263395.

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Surgenor, Avril E. « Copolymers of acrylonitrile with furan compounds ». Thesis, Queen's University Belfast, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334646.

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Brennan, Joseph J. « Applications in synthesis of furan oxidations ». Thesis, Queen's University Belfast, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239003.

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Demircan, Aydin. « Cascade reactions involving a furan core ». Thesis, University of Sussex, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297561.

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Rae, Robert Lammie. « Substitution effects in intramolecular furan cycloadditions ». Thesis, Heriot-Watt University, 2014. http://hdl.handle.net/10399/2829.

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The intramolecular Diels-Alder reaction of furan (IMDAF) provides a high degree of structural complexity in one step. However, reaction reversibility issues and the lower reactivity of furan in comparison to non-aromatic dienes prevent more widespread use of furan as a diene component in such reactions. Initial efforts to develop a new mode of organocatalysis which we hoped would facilitate IMDAF reaction was unfortunately unsuccessful, thus alternative means of IMDAF facilitation were investigated. For the first time, a comprehensive synthetic and computational study of the effect of halogen substitution on the IMDAF reaction has been undertaken. We have successfully demonstrated that halogenation of the furan moiety facilitates the IMDAF reaction (displaying increased reactivity to the non-halogenated analogue, regardless of halogen position), whereas dienophile halogenation hinders it. Additionally, careful selection of the position of the halogen on the furan can somewhat overcome the detrimental effect of having a halogen on the dienophile leading to highly functionalised cycloadducts with potential for further modification. Computational data produced by Martin Paterson and Justyna McKinlay support the idea that frontier molecular orbital effects cannot explain the experimental observations and we thus believe that the reactions are controlled by the interplay of three factors: positive charge stabilisation in the transition state and product, steric effects and a dipolar interaction term identified by the high level calculations. Finally, we have briefly demonstrated that nitro groups on the furan moiety also facilitate the IMDAF reaction whereas acyl groups appear to hinder the reaction. STEREOCHEMICAL ABSTRACT Any chiral compounds included in this thesis are racemic in nature. However, for clarity, such mixtures are schematically represented by drawings of only one of the enantiomers.

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Alakhras, Fadi. « Spectroelectrochemistry of Intrinsically Conducting Furan-Thiophenes Copolymers ». Doctoral thesis, Universitätsbibliothek Chemnitz, 2008. http://nbn-resolving.de/urn:nbn:de:bsz:ch1-200801350.

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Die elektrochemische Copolymerisation von Furan und Thiophen oder 3-Chlorothiophen wurde erfolgreich realisiert in einer Elektrolytlösung von Bortrifluorid-Diethylether + Ethylether (Verhältnis 1:2) bei konstantem Elektrodenpotenzial. Die Zugabe von Trifluoroessigsäure (TFA) (10 Vol-%) zu Bortrifluorid-Diethylether + Ethylether (Verhältnis 1:2) erniedrigte das Oxidationspotenzial der Monomere; die Polymerisationsgeschwindigkeit erhöhte sich, da TFA die Ionenleitfähigkeit des Elektrolyts vergrößert. Die Homopolymere zeigen nur einen Redoxpeak, verursacht durch Polymeroxidation und - reduktion. Die elektrochemische Copolymerisation wird bei verschiedenen Potenzialen und mit unterschiedlichen Thiophen- oder 3-Chlorothiophenkonzentrationen untersucht. Die Copolymere zeigen ein Redoxpeakpaar, dessen Position sich wesentlich von der der Homopolymere unterscheidet. Mit zunehmendem Polymerisationspotenzial und/oder zunehmender Konzentration an Thiophen- oder 3-Chlorothiophen werden auch mehr Thiophen- oder 3-Chlorothiopheneinheiten in den Copolymerfilm eingebaut. Ein Elektropolymerisationmechanismus wird für die Copolymere vermutet und die Copolymere weisen eine recht gute Langzeitstabilität der Redoxaktivität nach Zyklen in Acetonitril auf. In situ UV-Vis-Spektren der Homo- und Copolymerfilme wurden gemessen und λ1max, welches dem π → π*- Übergang entspricht, wurde bestimmt. Der optische Übergang bei λ2max vom Valenzband in das höhere Bipolaronband wurde ebenfalls bestimmt. Die Bandlücke für die Homo- und Copolymerfilme beim direkten Übergang wurde von der Kante im Absorptionsspektrum abgeschätzt. Die elektrochemische Thermodynamik für die Homo- und Copolymerfilme deutet darauf hin, dass jeweils ein Elektron von den Polymersegmenten, bestehend aus 4 Monomereinheiten, entfernt wird. Die untersuchten leitfähigen Filme zeigen einen Leitfähigkeitssprung mit einer stabilen Leitfähigkeit bis EAg/AgCl= 2 V. Diese Leitfähigkeitsänderung ist reversibel. Polyfuran hat verglichen mit Polythiophen eine geringere Leitfähigkeit und die Leitfähigkeit von Poly(3-chlorothiophen) ist rund eine Zehnerpotenz niedriger als die von Polythiophen. Da das in situ Leitfähigkeitsverhalten der Copolymere nicht die Summe der einzelnen Homopolymere bildet, kann man ausschließen, dass es sich bei den abgeschiedenen Copolymeren um Blockcopolymere handelt. Mit Hilfe der FTIR-Spektroskopie wurden Schwingungsspektren der Homo- und Copolymerfilme aufgenommen. Die Ergebnisse zeigen, dass es zur α-α'-Verknüpfung zwischen den Radikalkationen während der Copolymerisation kommt, was charakteristisch ist für α-substituierte fünfgliedrige heterozyklische Verbindungen. Der Mechanismus der elektrochemischen Degradation von Furan-Thiophen-Copolymeren wird ebenfalls mit Hilfe der gemessenen Spektren beschrieben. Die in situ Resonanz-Raman-Spektroskopie ergab, dass die spektroskopischen Eigenschaften der Copolymere zwischen denen der Homopolymere lagen. Bei höheren Polymerisationspotenzialen und höheren Konzentrationen an Thiophen oder 3-Chlorothiophen werden mehr Thiophen- oder 3- Chlorothiopheneinheiten in die Copolymerketten eingebaut. Es ist offensichtlich, dass die Ramanspektren der Copolymere wesentlich komplexer sind als die der Homopolymere, wodurch die Auswertung erschwert wird. Dennoch erinnern die Ramanspektren der Copolymere an die der Homopolymere. Die spektroelektrochemischen Eigenschaften der Copolymere haben bestätigt, dass deren Charakteristika zwischen denen der Homopolymere liegen, was deutlich macht, dass die Oxidation von Monomeren möglich ist und dass die Copolymerketten demnach aus Furan- und Thiophen- bzw. 3- Chlorothiopheneinheiten bestehen können
Electrochemical copolymerization of furan and thiophene or 3-chlorothiophene was successfully realized in a solvent system consisting of boron trifluoride ethyl ether (BFEE) + ethyl ether (EE) (ratio 1:2) at constant electrode potential. The addition of trifluoroacetic acid (TFA) (10 % by volume) to BFEE + EE (ratio 1:2) decreased the oxidation potential of the monomers; the polymerization rate was also accelerated because TFA increases the ionic conductivity of the electrolyte. The homopolymers have only one redox peak caused by polymer oxidation and reduction. Electrochemical copolymerization both at different potentials and with different thiophene or 3-chlorothiophene concentrations is investigated. The copolymers show one anodic/cathodic peak couple that appears at a position quite different from the positions observed with homopolymers. More thiophene or 3-chlorothiophene units are incorporated into the copolymer film with an increasing polymerization potential of the copolymer and/or with an increasing concentration of thiophene or 3- chlorothiophene in the feed. An electropolymerization mechanism of copolymers has been proposed, and the copolymers show a fairly good long-term stability of the redox activity after cycling in acetonitrile. In situ UV-Vis spectra of the homo- and copolymer films were measured and λ1max which corresponds to the π → π* transition is determined. The optical transition with λ2max from the valence band into the higher bipolaron band is also assigned. The band gap (Eg) for homo- and copolymer films from a direct interband transition is estimated from the absorption edge of the spectrum. The redox thermodynamics of the homo- and copolymer films suggest that one electron is removed from polymer segments containing four monomer units. The studied conducting films show a single conductivity change with a stable conductivity up to EAg/AgCl= 2 V. The conductivity of these films is almost restored when the potential shift direction is reversed. Polyfuran compared to polythiophene, has a lower conductivity and the conductivity of poly(3-chlorothiophene) is around one order of magnitude lower than that of polythiophene. The in situ conductivity properties of the copolymers are not the sum of those of the individual homopolymers. This result may eliminate the possibility that the copolymers can be considered as block copolymers. Vibrational spectra of homo- and copolymer films investigated in this study have been obtained using FTIR spectroscopy. The results indicate that α-α' coupling of radical cations has taken place in the copolymerization. This is a characteristic of α-substituted five-membered heterocyclic compounds. The electrochemical degradation mechanism of furan-thiophene copolymers is also described using the obtained spectra. The in situ resonance Raman spectroscopy of the copolymers shows spectroscopic properties intermediate between those of homopolymers. At higher polymerization potentials and at higher concentrations of thiophene or 3-chlorothiophene in the feed more thiophene or 3-chlorothiophene units are incorporated into the copolymer chains. It is obvious that the Raman spectra of the copolymers are more complex than those of homopolymers, which makes the assignment difficult. However, the in situ Raman spectra of the copolymers are reminiscent of those of the homopolymers. The spectroelectrochemical properties of the copolymers confirmed that the copolymers show intermediate characteristics between the homopolymers, implying that oxidation of monomers is possible and the copolymer chains may accordingly be composed of furan and thiophene or 3-chlorothiophene units

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McGuigan, Peter. « New uses of furan in organic synthesis ». Thesis, Queen's University Belfast, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282255.

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Annis, Michael Colin. « Free radical cascade reactions involving furan rings ». Thesis, University of Sussex, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394991.

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King, Ian Stephen Charles. « On the synthesis of furan-containing fragrance compounds ». Thesis, Cardiff University, 2011. http://orca.cf.ac.uk/55118/.

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This thesis describes the use of both silver nitrate, and iodine, to promote 5-endo-dig cyclisations for the formation of furans. The synthesis of kahweofuran and other furan-containing fragrance compounds is described, along with an investigation into the selectivity of the 5-endo-dig cyclisation process. Chapter 2 describes the synthesis of furan-containing analogues of known fragrance compounds using a silver-catalysed cyclisation methodology. The analysis of some of these compounds by an "expert nose" is discussed. Chapter 3 describes the synthesis of kahweofuran, a furan-containing compound reported to be one of the major odour constituents of roasted coffee. Chapter 4 describes an investigation into the cyclisation of triols upon exposure to silver nitrate or iodine when more than one cyclisation pathway is possible.

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Livres sur le sujet "Fura2"

Furai, dadī, furai. Tōkyō : Kōdansha, 2003.

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Haq, Husainul. Furat. Delgi : Takhleeqkar, 1992.

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Hussain-ul-Haq. Furat. Delhi : Takhliqkar, 1992.

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Casals, Joaquim Ripoll i. La fura. Argentona : [s.n.], 1994.

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Aid, Timor. Timor-Leste furak. Dili, Timor-Leste : Timor Aid, 2014.

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Zaidi, Baqir. Furat-i sukhan. Laurel, Md : Idara-e-Faiz-e-Adab, 2004.

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Naqvī, Muḥsin. Furat-i fikr. Lāhaur : Māvrā, 2009.

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Bebeji, Dahiru. Shangai (furar dawa). Kano [Nigeria] : Distributor, Bebeji Merchandise Co., 1990.

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Vasiliev, Boris. Stalin mi-a furat copilăria. Chișinău : Baștina-Radog, 2010.

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Yāsīn, al-Sayyid. al- ʻAwlamah : Furaṣ-- wa-makhāṭir. [Cairo] : Mīrīt, 1999.

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Chapitres de livres sur le sujet "Fura2"

Hoek, Jan B., Kathleen E. Coll, Thomas A. Rooney et Andrew P. Thomas. « Synchronized Ca2+ Transients Induced by Glucagon in Fura2 Loaded Hepatocytes ». Dans Biology of Cellular Transducing Signals, 323–32. Boston, MA : Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0559-0_33.

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Gooch, Jan W. « Furan ». Dans Encyclopedic Dictionary of Polymers, 330. New York, NY : Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_5360.

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Mogol, Burçe Ataç, et Vural Gökmen. « Furan ». Dans Chemical Hazards in Thermally-Processed Foods, 87–105. Singapore : Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8118-8_4.

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Gooch, Jan W. « Furan Resin ». Dans Encyclopedic Dictionary of Polymers, 330–31. New York, NY : Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_5361.

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Gooch, Jan W. « Furan Prepreg ». Dans Encyclopedic Dictionary of Polymers, 331. New York, NY : Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_5362.

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Demaison, J. « 413 C4H4O Furan ». Dans Asymmetric Top Molecules. Part 2, 293. Berlin, Heidelberg : Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-10400-8_161.

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Guenther, Helmut. « Furan in Coffee ». Dans Coffee, 307–18. Oxford, UK : Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781119949893.ch18.

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Li, Jie Jack. « Paal-Knorr furan synthesis ». Dans Name Reactions, 265. Berlin, Heidelberg : Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04835-1_208.

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Li, Jie Jack. « Feist-Bénary furan synthesis ». Dans Name Reactions, 118. Berlin, Heidelberg : Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04835-1_96.

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McKillip, William J. « Chemistry of Furan Polymers ». Dans ACS Symposium Series, 408–23. Washington, DC : American Chemical Society, 1989. http://dx.doi.org/10.1021/bk-1989-0385.ch029.

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Actes de conférences sur le sujet "Fura2"

Nakajima, Kosuke, Yuichi Itoh, Takayuki Tsukitani, Kazuyuki Fujita, Kazuki Takashima, Yoshifumi Kitamura et Fumio Kishino. « FuSA2 touch display ». Dans the ACM International Conference. New York, New York, USA : ACM Press, 2011. http://dx.doi.org/10.1145/2076354.2076421.

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HENRIQUE FREIRE ARAUJO, LUIZ, José Augusto Rosário Rodrigues, FABIO NASARIO et Paulo José Samenho Moran. « Biotransformation of Biomass Furan Derivatives ». Dans XXIV Congresso de Iniciação Científica da UNICAMP - 2016. Campinas - SP, Brazil : Galoa, 2016. http://dx.doi.org/10.19146/pibic-2016-51633.

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Poll, C. T., et J. Westwick. « THE ROLE OF IONISED INTRACELLULAR FREE CALCIUM ([Ca++]i) IN THROMBIN-INDUCED DENSE GRANULE SECRETION ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644475.

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Fura 2 is one of a recently-introduced family of Ca++ indicators with improved fluorescent properties compared to quin 2 (Grynkiewicz et al 1985). This study has examined the role of [Ca++]i in thrombin-induced dense granule release using prostacyclin-washed human platelets loaded with either thedense granule marker 14C-5HT (5HT) alone or with 5HT together with quin 2 ([quin2]i = 0.8mM) or fura 2 ([fura 2]i 20-30µM). In the presence of ImM extracellular calcium concentration ([Ca++]i) the [Ca++]e in quin 2 and fura 2 loaded platelets was 93±2 (n=10 experiments) and 133±0.3nM (n=12 experiments) respectively. In either quin 2 or fura 2 loaded platelets suspended in the presence of ImM [Ca++]e, thrombin (0.23-23.InM) promoted a rapid (in secs)concentration-dependent elevation of [Ca++]i from basal values to levels l-2µM, together with a parallel release of dense granules almost identical to that obtained with thrombin in non dye loaded platelets. In fura 2 loaded cells, removal of [Ca++]e inhibited the elevation of [Ca++]i induced by a sub-maximal concentration of thrombin (0.77nM) by 43+5% (n=4) but interestingly had no significant effect (p<0.05) on the rise in [Ca++]i elicited by low thrombin doses (0.231nM). Neither did lowering [Ca++]e inhibit the release of 5HT evoked by thrombin ( 0.231-23.InM) from either fura 2 loaded or non dye loaded platelets. In contrast, in quin 2 loaded platelets, removal of [Ca++]e inhibited the thrombin (0.231-23.InM) stimulated rise in [Ca++]i-by 90% and the 5HT release response to either low (0.231nM), sub-maximal (0.77nM) or maximal (23.InM) thrombin by 100% (n=4), 87+2°/o (n=6)and 2+l°/o (n=4) respectively. Fura 2 but not quin 2 loaded cells suspended in ImM [Ca++]e exhibited a Ca++ response to thrombin concentrations >2.31nM which could be separated into a rapid phasic component and a more sustained 'tonic' like component inhibitable by removal of [Ca++]e or by addition of ImM Ni++ . These data suggest the use of fura 2 rather than quin 2 for investigating stimulus response coupling in platelets, particularly when [Ca++]e is less than physiological. We thank the British Heart Foundation and Ciba-Geigy USA for financial support.

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Koyama, M., F. Katabami, K. Matsuno, H. Matsumiya, K. Abe, K. Sakurada, S. Ozasa, I. Maekawa et T. Miyazaki. « THROMBIN-INDUCED BIPHASIC Ca2+TRANSIENT DETECTED BY FURA-2 FLUORESCENCE WAS COUPLED WITH BIPHASIC Ca2+ UPTAKE IN PLATELETS ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644476.

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In the last congress on Thrombosis and Haemostasis in SanDiego we presented the biphasic Ca2+transient in thrombin-stimulated platelets detected by quin2. This time we tried to measure Ca2+ transient in platelets using other Ca2+indicators such as fura-2 and aequorin. In order to evaluate the contribution of increased Ca2+ influx across the plasma-membrane in elevating cytosolic free Ca concentration on platelet activation, 45 Ca2+uptake was measured simultaneouslyby silicon-oil centrifugation method with or without 5 mM EGTA treatment. Such EGTA treatment was intended to remove the entire 45Ca 2+bound to the external surface, and the values obtained accounted for the true amount of 45 Ca2+ uptaked by platelets. RESULTS: (1) When the platelets preincubated in Ca2+ poor medium were exposed to 0.1-1.0 mM external Ca2+ a variety of response of Ca2+ transient were observed in this resting state; a sharp and transient peak appeared in aequorin luminescence, while biphasic increase with an initial burst for 6 to 8 s was demonstrated in fura-2 fluorescence. 45 Ca2+uptake measurement resulted in a biphasic response, the time-course of which was correlated well with that of fura-2 fluorescence. (2) Thrombin-induced Ca2+transient was also observed. A remarkable biphasic increase of fluorescence was recognized in fura-2 assay, which showed a sharp and large response during initial 10 s after activation followed by a wide peak for the next 40 s. (3) Although total Ca2+ uptake in thrombin-stimulated platelets without EGTA treatment resulted in the simple convex-shaped increase in platelet 45Ca 2+content, that observed after EGTA treatment showed a distinct biphasic pattern; an initial small uptake during the first 10 s after activation followed by another uptake for the next 40 s. CONCLUSION: (1) Fura-2 measurement is the most excellent method avairable for monitoring intracellular Ca2+transient since the response of 45Ca 2+uptake treated by 5 mM EGTA reflect that of cytosolic Ca2+ concentration detected by fura-2 both in resting and in thrombin-stimulated platelets. (2) Membrane-lipid metabolism such as polyphosphatidilinositol breakdown or arachi-donate cascade may be involved in the mechanism concerning each phase of these Ca2+ mobilization.

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Lanza, F., A. Beretz, M. Kubina et J.-P. Cazenave. « INCREASED AGGREGATION AND SECRETION RESPONSES OF HUMAN PLATELETS WHEN LOADED WITH THE CALCIUM FLUORESCENT PROBES QUIN2 AND FURA-2 ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643760.

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Incubation of human platelets with the fluorescent dye esters quin2-AM (10 μM) or fura-2-AM (1 μM) makes possible the direct measurement of intracellular free calcium ([Ca2+1).Underthese conditions, basal levels of [Ca2+]i of 120 ± 16 nM (n=23) using quin2 and 137 ± 15 nM (n=5) using fura-2 can be measured. Both probes record comparable increases of [Ca2 ]i after stimulation with ADP, thrombin, PAF, or U-46619. Incorporation into human platelets of quin2 or fura-2 at the concentrations used to monitor [Ca2+]i leads to the activation of platelets. This was shown by increased aggregation and secretion responses of quin2or fura-2 loaded platelets after stimulationwith ADP (5 μM), PAF (1 μM) and with low concentrations of thrombin (0.015U/ml), collagen (0.5 μg/ml), the endoperoxide analog U-46619 (0.5 μM) or the calcium ionophore A 23187 (1 μM). Quin2 and fura-2 mediated platelet activation could be due to altered arachidonic acid metabolism, since it was partly inhibited by prior treatment with the cyclooxygenase inhibitor acetylsalicylate (1 μM). In contrast, platelets loaded with higher concentrations of calcium chelators (20 to 100 μM quin2-AM)exhibited diminished aggregation responses to all aggregating agents. Thislatter effectwas accompanied by increased fluidity of theplatelet plasma membrane bilayer and by the exposure of a new pool of membranes at the outer surface of platelets, as monitored withtrimethylammonium-diphenylhexatriene (TMA-DPH) in platelets loaded with thenon-fluorescent calcium probe analog MAPT. Platelet shape change, as measured in the aggregometer, was dose-dependently inhibited after loading of quin2 (10-50 μM quin2-AM), even at concentrations which potentiated aggregation. We conclude that incorporation of intracellular calcium chelators alters platelet responses, including at concentrations used to monitor intracellular calcium changes.

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Weaver, J. D., et J. A. Morgan. « Furan Resin Process Replaces Workovers in Gas Storage Reservoirs ». Dans SPE Gas Technology Symposium. Society of Petroleum Engineers, 1988. http://dx.doi.org/10.2118/17742-ms.

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Stevens, Kristof, Marieke Op de Beeck, Sara Figaroli et Annemieke Madder. « Synthesis and cross-linking of new furan nucleic acids ». Dans XIVth Symposium on Chemistry of Nucleic Acid Components. Prague : Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2008. http://dx.doi.org/10.1135/css200810210.

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Hannis Fadzillah Mohsin, Ibtisam Abdul Wahab et Jean-Frederic Faizal Weber Abdullah. « A derivative of furan-2,3-diol from pandan extract ». Dans 2010 International Conference on Science and Social Research (CSSR). IEEE, 2010. http://dx.doi.org/10.1109/cssr.2010.5773758.

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Aminian, Masoud, Mohd Zainal Abidin Ab Kadir, Wan Fatinhamamah Wan Ahmad et Senan Mahmood. « Investigation of paper aging assessment by furan concentration monitoring ». Dans 2009 IEEE Student Conference on Research and Development (SCOReD). IEEE, 2009. http://dx.doi.org/10.1109/scored.2009.5443001.

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Meissner, Maximilian, Martin Darmann, Sigurd Schober, Martin Mittelbach et Christof Sumereder. « Reliability Study of Furan Level Analysis for Transformer Health Prediction ». Dans 2019 IEEE 20th International Conference on Dielectric Liquids (ICDL). IEEE, 2019. http://dx.doi.org/10.1109/icdl.2019.8796785.

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Rapports d'organisations sur le sujet "Fura2"

Stern, Ariana. FLC Notable Technology Award Oleo-Furan Surfactant. Office of Scientific and Technical Information (OSTI), août 2020. http://dx.doi.org/10.2172/1645079.

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Patel, S., M. D. Kaminski et L. Nunez. Polychlorodibenzo-p-dioxin and polychlorodibenzo-furan removal and destruction. Office of Scientific and Technical Information (OSTI), septembre 2003. http://dx.doi.org/10.2172/816759.

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Cureton, LaShonda T., George Fountzoulas et John J. La Scala. Molecular Weight Measurement of Biobased Furan Polyamides via Non-Aqueous Potentiometric Titration. Fort Belvoir, VA : Defense Technical Information Center, juin 2013. http://dx.doi.org/10.21236/ada586113.

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Allcock, Harry R., Jeffrey A. Dodge, Leon S. Van Dyke et Charles R. Martin. Polyphosphazenes Bearing Polymerizable Pyrrole, Thiophene and Furan Side Groups : Synthesis and Chemical Oxidation. Fort Belvoir, VA : Defense Technical Information Center, avril 1992. http://dx.doi.org/10.21236/ada249747.

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Leung, Man-kit. Dimerization kinetics and products of. alpha. -substituted o-quinodimethanes derived from benzene and furan. Office of Scientific and Technical Information (OSTI), juillet 1992. http://dx.doi.org/10.2172/7047444.

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Immediately dangerous to life or health (IDLH) value profile : furan (CAS no.110-00-9). U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, septembre 2016. http://dx.doi.org/10.26616/nioshpub2016171.

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