Relevant bibliographies by topics / Fura-2

Academic literature on the topic 'Fura-2'

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Published: 4 June 2021
Last updated: 25 April 2022

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Journal articles on the topic "Fura-2"

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Tran, N. N. P., P. Leroy, L. Bellucci, A. Robert, A. Nicolas, J. Atkinson, and C. Capdeville-Atkinson. "Intracellular concentrations of Fura-2 and Fura-2/AM in vascular smooth muscle cells following perfusion loading of Fura-2/AM." Pharmacological Research 31 (January 1995): 206. http://dx.doi.org/10.1016/1043-6618(95)87082-2.

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2

Hurley, T. W., M. P. Ryan, and R. W. Brinck. "Changes of cytosolic Ca2+ interfere with measurements of cytosolic Mg2+ using mag-fura-2." American Journal of Physiology-Cell Physiology 263, no. 2 (August 1, 1992): C300—C307. http://dx.doi.org/10.1152/ajpcell.1992.263.2.c300.

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In rat pancreatic and submandibular gland acini during exposure to carbachol, changes in the fluorescence emission intensity ratio (R) of acini loaded with mag-fura-2 resemble changes in cytosolic Ca2+ concentration (Ca2+i) in acini loaded with fura-2. Furthermore, changes of R depend on the presence of extracellular Ca2+ (Ca2+o) but are much less influenced by changes in extracellular Mg2+ (Mg2+o). To evaluate interference with measurement of cytosolic Mg2+ (Mg2+i) by changes in Ca2+i, we determined the dissociation constant (Kd) and Hill coefficient (NH) of the Ca(2+)-mag-fura-2 and Mg(2+)-mag-fura-2 complexes in standard solutions, in intact acini after loading with the acetoxymethyl ester of mag-fura-2 (mag-fura-2/AM), and in lysates derived from acini loaded with mag-fura-2/AM. The Kd of the Ca(2+)-mag-fura-2 complex in acini (determined with ionomycin) was 20.49 +/- 5.20 microM, and NH was 1.44 +/- 0.16 (n = 24). Kd of the Mg(2+)-mag-fura-2 complex in acini was 2.25 +/- 0.98 mM, and NH was 1.20 +/- 0.20 (n = 25). Mean Kd values were slightly lower in acinar lysates and in solutions of standard mag-fura-2. In acini from either gland, 1,2-bis(2-aminophenoxy)ethan-N,N,N',N'-tetraacetic acid (BAPTA) suppressed carbachol-induced Ca2+i transients. The R value in stimulated acini loaded with BAPTA and mag-fura-2 increased slightly when Mg2+o was increased from less than 10 nM to 1.2 mM, suggesting that Mg2+ influx contributes to the maintenance of Mg2+i during exposure to carbachol. Under these conditions, pancreatic acinar Mg2+i is 0.53 +/- 0.14 mM (n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)
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Kass, G. E., D. L. Webb, S. C. Chow, J. Llopis, and P. O. Berggren. "Receptor-mediated Mn2+ influx in rat hepatocytes: comparison of cells loaded with Fura-2 ester and cells microinjected with Fura-2 salt." Biochemical Journal 302, no. 1 (August 15, 1994): 5–9. http://dx.doi.org/10.1042/bj3020005.

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In single Fura-2 ester-loaded hepatocytes, stimulation by vasopressin, but not emptying of the agonist-sensitive Ca2+ store by 2,5-di-(t-butyl)hydroquinone, resulted in an increase in the rate of Fura-2 fluorescence-quenching by Mn2+. Similarly, in cells microinjected with Fura-2 salt, vasopressin stimulated Mn2+ entry while 2,5-di-(t-butyl)hydroquinone or thapsigargin did not. The pattern of Fura-2 quenching by Mn2+ only correlated with the movement of Mn2+ across the plasma membrane.
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Owen, C. S. "Spectra of intracellular Fura-2." Cell Calcium 12, no. 6 (June 1991): 385–93. http://dx.doi.org/10.1016/0143-4160(91)90064-l.

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Becker, P. L., and F. S. Fay. "Photobleaching of fura-2 and its effect on determination of calcium concentrations." American Journal of Physiology-Cell Physiology 253, no. 4 (October 1, 1987): C613—C618. http://dx.doi.org/10.1152/ajpcell.1987.253.4.c613.

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This study was performed to determine the effect of photobleaching on the spectral properties of the calcium-sensitive fluorescent dye fura-2. Fura-2, whether in cells or in calibrating solutions, was found to be bleached when exposed to excitation light. In contrast to the widely held belief, photobleaching altered the spectral properties of the dye. Decomposition of the excitation spectra of partially bleached fura-2 solutions revealed an intermediate that is still fluorescent and is not sensitive to calcium over the same range as fura-2, but which can bind calcium in the millimolar range. The presence of this intermediate violates one of the assumptions on which the ratio method of calibration is based; that is, that the only fluorescent species present are the calcium-bound and the free anion forms of fura-2. Thus, if photobleaching occurs, the ratio method will not give accurate calcium concentration values. We calculate that as little as an 8% loss of total fluorescence intensity is sufficient to produce a large error. Photobleaching of fura-2-loaded cells and fura-2 containing calibrating solutions can be minimized by reducing the oxygen concentration and by reducing the excitation light intensity. Strategies are presented to help maintain a high signal-to-noise ratio in fura-2 fluorescence detection systems, despite a lower excitation intensity so that photobleaching, and the resulting inaccuracies in calculated [Ca2+], can be largely avoided.
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Jensen, P. E., M. J. Mulvany, C. Aalkjaer, H. Nilsson, and H. Yamaguchi. "Free cytosolic Ca2+ measured with Ca(2+)-selective electrodes and fura 2 in rat mesenteric resistance arteries." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 2 (August 1, 1993): H741—H746. http://dx.doi.org/10.1152/ajpheart.1993.265.2.h741.

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Free cytosolic Ca2+ was measured with sub-micrometer-tip, double-barrelled, Ca(2+)-selective electrodes and fura 2 in rat mesenteric resistance arteries. The purpose was to establish intracellular free Ca2+ concentration ([Ca2+]i) values in resting and stimulated vessels. Isolated vessels were mounted for isometric force measurements. Measured with electrodes, mean [Ca2+]i was 115 and 708 nM under resting and norepinephrine-activated conditions, respectively. Fura 2 was calibrated intracellularly including determination of the intracellular dissociation constant (Kd) of the fura 2:Ca2+ complex. The intracellular Kd was 342 nM. With this value of Kd, fura 2 measurements of mean [Ca2+]i were 129 and 537 nM under resting and norepinephrine-activated conditions, respectively. The values measured with the two techniques were thus in good accordance.
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Scaduto, Russell C., and Lee W. Grotyohann. "Hydrolysis of Ca2+-sensitive fluorescent probes by perfused rat heart." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 5 (November 2003): H2118—H2124. http://dx.doi.org/10.1152/ajpheart.00881.2001.

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Rat hearts were loaded with the fluorescent calcium indicators fura 2, indo 1, rhod 2, or fluo 3 to determine cytosolic calcium levels in the perfused rat heart. With fura 2, however, basal tissue fluorescence increased above anticipated levels, suggesting accumulation of intermediates of fura 2-AM deesterification. To examine this process, we separated the intermediates of the deesterification process using HPLC after incubation of fura 2-AM with tissue homogenates and after loading in the rat heart. Loading of hearts with fura 2-AM resulted in tissue levels of fura 2 free acid that were only 5% of the total heart dye content of all fura 2 species. The parent fura 2-AM form accumulated without accumulation of intermediate products. Similar results were obtained with indo 1-AM. Fluo 3 loaded very poorly in perfused hearts. Unlike other indictors, rhod 2 rapidly loaded in perfused hearts and was completely converted to the free acid form. To determine the subcellular localization of the free acid form of these indictors, mitochondria from indicator-loaded hearts were assayed for the free acid form. Approximately 75% of the total amount of rhod 2 in hearts could be recovered in isolated mitochondria. Subcellular localization of indo 1 and fura 2 was more evenly distributed between mitochondria and nonmitochondrial compartments. We conclude that measurement of calcium in the perfused rat heart using surface fluorescence with either indo 1 or fura 2 is complicated by an inconsistent accumulation of the parent ester and that the resulting signal cannot be easily calibrated using “in situ” methods using the free acid form. Rhod 2 does not display this shortcoming, but like other indicators, it also loads into the mitochondrial matrix.
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Carroll, S. L., M. G. Klein, and M. F. Schneider. "Calcium transients in intact rat skeletal muscle fibers in agarose gel." American Journal of Physiology-Cell Physiology 269, no. 1 (July 1, 1995): C28—C34. http://dx.doi.org/10.1152/ajpcell.1995.269.1.c28.

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Intact single fibers enzymatically dissociated from rat flexor digitorum brevis muscle were suspended in 0.5% low-melting-temperature agarose gel to minimize fiber movement during action potentials or trains of action potentials. Resting Ca2+ concentration ([Ca2+]) and changes in [Ca2+] were monitored using the fluorescent calcium indicator fura 2. The time course and waveform of [Ca2+] transients during an action potential or trains of action potentials in fibers in agarose were calculated using kinetic parameters previously determined to correct for the calcium-fura 2 kinetic delay. Half times of the calculated calcium transients for single action potentials were 30-fold briefer than the original fura 2 signals. To confirm the time course and waveform of the calculated calcium transients, changes in [Ca2+] were monitored using the more rapidly equilibrating calcium indicator mag-fura 2. [Ca2+] transients for fibers containing fura 2 had very similar time courses and waveforms as mag-fura 2 signals from other fibers, indicating that the corrections for the calcium-fura 2 kinetic delay were accurate. The advantages of the agarose gel suspension are discussed.
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Steinberg, S. F., J. P. Bilezikian, and Q. Al-Awqati. "Fura-2 fluorescence is localized to mitochondria in endothelial cells." American Journal of Physiology-Cell Physiology 253, no. 5 (November 1, 1987): C744—C747. http://dx.doi.org/10.1152/ajpcell.1987.253.5.c744.

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The new, highly fluorescent, calcium-sensitive dye, fura-2, can be loaded nondisruptively into intact cells by means of its permeant ester and used to measure the free calcium ion concentration in individual cells. For fura-2 to signal cytosolic calcium, it must be distributed homogeneously and exclusively throughout the cytoplasmic space. However, microscopic examination of bovine aortic endothelial cells loaded with fura-2 by exposure to its permeant ester reveals fluorescence associated with discrete intracellular structures rather than the homogeneous distribution expected for a cytosolic stain. Simultaneous labeling of bovine aortic endothelial cells with fura-2 and rhodamine 123 (a mitochondrial fluorescent vital stain) identifies these structures as mitochondria. Subcellular dye localizations are not observed when the cells are loaded with other putative cytosolic stains that gain access to the cytosol by means of a membrane permeant ester. Both carboxyfluorescein and indo-1 (another member of the family of second generation calcium indicators) stain the cytoplasm diffusely. It is suggested that fura-2 fluorescence accumulates in certain cells in association with mitochondria. It is important to assess the intracellular distribution of fura-2 when this indicator is used to measure the free cytosolic calcium ion concentration.
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Tram, N. N. P., P. Leroy, L. Bellucci, A. Robert, A. Nicolas, J. Atkinson, and C. Capdeville-Atkinson. "Intracellular concentrations of Fura-2 and Fura-2/AM in vascular smooth muscle cells following perfusion loading of Fura-2/AM in arterial segments." Cell Calcium 18, no. 5 (November 1995): 420–28. http://dx.doi.org/10.1016/0143-4160(95)90057-8.

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Dissertations / Theses on the topic "Fura-2"

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Silva, Orivaldo Lopes da. "Incorporação de cálcio iônico em células ósseas induzida por campo elétrico." Universidade de São Paulo, 1995. http://www.teses.usp.br/teses/disponiveis/76/76132/tde-10062014-163725/.

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Acredita-se que sinais elétricos endógenos afetem remodelamento, metabolismo, reparo e crescimento ósseos. Existe uma ampla literatura que trata do efeito de sinais elétricos externos sobre as respostas de síntese, mitogênese e proliferação em osteoblastos e células ósseas in vitro. Acredita-se que as respostas fisiológicas ao estimulo elétrico sejam devidas a mecanismos celulares que envolvem variações na concentração citosólica de cálcio. No presente estudo esse efeito celular foi observado através da estimulação direta, por campo elétrico de intensidade fisiologicamente significativa de 10mV/cm e frequência 1,5 MHz, de células ósseas em cultura primária obtidas a partir da calota calvária de ratos da raça Sprague-Dawley. Os mecanismos de transdução do campo elétrico são investigados pela mensuração em tempo real do efeito do campo elétrico na concentração citosólica de Ca2+ utilizando-se técnica de fluorescência de Fura-2, em um sistema que permite a medida em células individuais. As estimulações elétricas resultaram em variações significativas na concentração de cálcio citosólico. Mais especificamente, observou-se um aumento na amplitude e na duração das oscilações de cálcio iônico, com tempos de latência variáveis para as células estudadas.
Endogenous electrical signals have been thought to affect bone remodeling, metabolism, healing and growth. Much literature exists concerning the effect of external electrical signals on synthetic, mitogenic, and proliferative responses of osteoblasts or osteoblast-like cells in vitro. Physiological responses to electrical stimulation are thought to be due to cellular mechanisms involving cytosolic calcium concentration changes. In this study this cellular effect was observed by directly stimulating primary culture bone cells from Sprague-Dawley rat calvaria at physiological significant field strength of 10 mV/cm and frequency 1,5 MHz. Electric field transduction mechanisms are investigated by measuring the real-time electric field effect on cytosolic Ca+2 concentrations using Fura-2 fluorescence technology in a system capable of measurement on a cell-by-cell basis. The electrical stimulations resulted in significant changes in cytosolic calcium concentration. More specifically, an increase was noted in calcium oscillation amplitude and duration, and a variable response latency period for the cells studied.
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Hadrovic, Banina. "A study of TRPV1 and TRPV4 ion channels in the beta cells by using fura-2 based microfluorometry." Thesis, Mälardalen University, School of Sustainable Development of Society and Technology, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-7350.

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The calcium ion (Ca2+) is an important ion that regulates many cellular functions including exocytosis, contraction of muscles, neural functions, fertilization and cell division. In the plasma membrane of cells there are different Ca2+ channels, including the transient receptor potential (TRP) family of cation channels. The TRP channels are activated by physical stimuli like temperature, stretch, osmolality, and also various ligands. These channels are divided into seven subfamilies, namely TRPC, TRPV, TRPM, TRPML, TRPA, TRPP, and TRPN.

 

TRP channels can regulate the cytoplasmic free Ca2+ concentration ([Ca2+]i)  and are therefore important for research of insulin secretion from beta (β) cells. With TRP research new and more effective treatment methods for people with diabetes can be developed. People with type 2 diabetes have a decreased insulin secretion from beta (β) cells, in response to glucose. Cytoplasmic free Ca2+ concentration ([Ca2+]i)  is important for insulin secretion. It is therefore desirable to find compounds that can increase [Ca2+]i in pancreatic β cells and thereby increase insulin secretion.

 

 

The aim of this project was to investigate whether pancreatic β cells express TRPV1 and TRPV4 ion channels. If the channels are expressed in β cells the [Ca2+]i can be increased by identifying substances that stimulate TRPV1 and TRPV4 channels. The results can then be used for providing better treatment for patients with diabetes type 2. Insulinoma cells from rat (S5 cells) were used as a model for β cells. [Ca2+]i was measured from single fura-2 loaded S5 cells by ratiometric microfluorometry. To test whether TRPV1 is expressed,

N-(4-hydroxyphenyl)-Arachidonoylamide (AM404) and [5-hydroxyl-1-(4-hydroxy-3-methoxyphenyl)decan-3-one] ([6]-gingerol) were used. To test whether TRPV4 was expressed, a TRPV4-selective agonist 4alpha-Phorbol 12,13-Didecanoate namely 4α–PDD was used.

 

The two agonist of TRPV1, AM404 and [6]-gingerol increased [Ca2+]i . Capsaicin a classical activator of TRPV1 used as a control also increased [Ca2+]i . These increases were inhibited by capsazepine, a specific blocker of TRPV1. 4α–PDD, a specific agonist of TRPV4 also increased [Ca2+]i. These results suggest that S5 cells express both TRPV1 and TRPV4 channels and that AM404, [6]-gingerol and 4α–PDD are potential substances for increasing the insulin secretion from β cells.


Kalciumjonen (Ca2+) är en viktig jon och förmedlar signaler i processer som cellutsöndring, muskelkontraktion, nervfunktion, fertilisering och celldelning. I cellers plasmamembran finns det olika sorters Ca2+ -kanaler, inklusive transient receptor potential (TRP) jonkanalerna. TRP kanalerna aktiveras av fysisk stimulans, så som temperatur, utsträckning, osmolalitet men också av olika ligander. TRP kanalerna är indelade i sju underfamiljer, TRPC, TRPV, TRPM, TRPML, TRPA, TRPP,och TRPN.

 

TRP kanalerna reglerar den fria Ca2+ koncentrationen ([Ca2+]i)  i cytoplasman och är därmed viktiga för forskning inom insulinutsöndringen från beta (β) celler. Med denna forskning kan nya och effektivare behandlingsmetoder för personer med diabetes utvecklas. Personer med typ 2 diabetes har bl.a. en minskad insulinfrisättning i beta (β) celler som orsakar en glukosökning i blodet. Den fria Ca2+ -koncentrationen ([Ca2+]i) i cytoplasman är viktig för insulinfrisättningen. Det är därför önskvärt att hitta kemiska föreningar som kan bidra till en ökning av [Ca2+]i i bukspottkörtelns β celler och därmed också ge en ökad insulinfrisättning.

 

Målet med detta projekt har varit att undersöka om β celler från bukspottkörtel uttrycker jonkanalerna TRPV1 och TRPV4. Om β celler uttrycker dessa kanaler kan [Ca2+]i i cytoplasman ökas genom att identifiera substanser som stimulerar just TRPV1 och TRPV4 kanaler. Resultaten kan användas för att bidra med bättre behandling till diabetespatienter med typ 2 diabetes. Tumoriserade celler från råtta (S5) användes som modell för β celler. [Ca2+]i mättes från enskilda fura-2 laddade S5 celler med hjälp av ett ratiometriskt mikrofluorometriskt system. För att undersöka om TRPV1 finns testades ämnena N-(4-hydroxyphenyl)-Arachidonoylamide (AM404) och [5-hydroxyl-1-(4-hydroxy-3-methoxyphenyl)decan-3-one] ([6]-gingerol). För att undersöka om TRPV4 finns användes det TRPV4-specifika ämnet (4alpha-Phorbol 12,13-Didecanoate)

4α–PDD.

 

De båda TRPV1 agonisterna AM404 och [6]-gingerol inducerade en ökning i [Ca2+]i. Capsaicin som är en klassisk TRPV1 agonist ökade också [Ca2+]i och användes som kontroll. Alla dessa koncentrationsökningar inhiberades av capsazepine, som är en TRPV1- antagonist. 4α–PDD som är en specifik TRPV4 agonist ökade också [Ca2+]i.

 

Resultaten tyder på att S5 cellerna uttrycker både TRPV1 och TRPV4 kanaler samt att AM404, [6]-gingerol och 4α–PDD är alla substanser med potential att öka insulinfrisättningen från bukspottkörtelns β celler.

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Beurg, Maryline. "Couplage excitation-contraction des cellules musculaires striées : étude des variations transitoires de calcium par imagerie de fura-2." Bordeaux 1, 1995. http://www.theses.fr/1995BOR10530.

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Le couplage excitation-variation transitoire de ca2+ (e-vt) constitue l'etape cle du couplage e-c des muscles squelettiques. A l'aide de la technique d'imagerie du fura-2, nous avons suivi la dynamique et la distribution spatiale de la concentration de calcium intracellulaire pendant le developpement des myotubes de rat, de souris dysgeniques et humains en culture. Les myotubes de rat in vitro presentent temporairement un stade dit quiescent durant lequel ces cellules sont incapables de se contracter alors qu'elles possedent un couplage e-vt de ca2+ fonctionnel. Lors du couplage e-vt, la liberation de calcium du rs semble se faire en deux etapes successives: la premiere serait regulee par le potentiel et la deuxieme semble etre controlee par le calcium (cicr). Au cours du developpement, les myotubes de rat presentent un couplage e-vt de type cardiaque. Ce couplage apparaissant precocement et de facon fugace reste localise aux extremites des cellules. Les myotubes de souris mdg/mdg bien que depourvus de la sous-unite alphal du r-dhp presentent un couplage e-vt de ca2+ de type cardiaque, localise aux extremites des cellules jeunes. Le support moleculaire d'un tel couplage, faisant office de detecteur de potentiel et de canal calcium, n'a pu etre defini, l'entree de calcium n'etant sensible a aucun des inhibiteurs traditionnels des canaux calciques. De par sa localisation ce couplage pourrait avoir un role dans le processus de fusion cellulaire. En culture, les myotubes humains non innerves ne se contractent pas mais possedent toutefois un couplage e-vt de ca2+ fonctionnel de type squelettique. Dans ces cellules, le noyau presente une vt de ca2+ induite par le potentiel plus lente que celle du cytoplasme, ce qui laisse suggerer des mecanismes de controle du calcium different au niveau du noyau. Le calcium possederait non seulement un role primordial dans la contraction mais aussi peut-etre dans la differenciation du muscle
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Lascombe, Marie-Laure. "Le couplage excitation-contraction dans les cellules musculaires striées normales et dysgéniques : étude par imagerie de fluorescence de fura-2." Bordeaux 1, 1992. http://www.theses.fr/1992BOR10519.

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Pour etudier les mecanismes du couplage excitation-contraction dans les cellules musculaires striees normales et dysgeniques (mdg/mdg) nous avons suivi la dynamique et la distributionspatiale des variations de la ca#2#+#i par videomicroscopie de fluorescence et traitement des images. Dans les myotubes normaux, nous avons trouve: a) l'existence, dans une etape de la myogenese, d'un couplage excitation-augmentation de la ca#2#+#i n'induisant pas de contraction; b) sous l'action de l'acetylcholine, la variation calcique est biphasique avec d'abord la liberation de calcium apparemment module par un second messager ou une proteine g. Dans les myotubes de souris mdg/mdg, nous avons constate la presence d'un couplage excitation-augmentation de la ca#2#+#i localise aux extremites des cellules. Le detecteur de voltage semble etre different de celui actuellement connu, le recepteur des dihydropyridines
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Castro, Kraftchenko Joel, and kraf0005@flinders edu au. "STORE OPERATED Ca2+ CHANNELS IN LIVER CELLS: REGULATION BY BILE ACIDS AND A SUB-REGION OF THE ENDOPLASMIC RETICULUM." Flinders University. Medicine, 2008. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20080826.135311.

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Cholestasis is an important liver pathology. During cholestasis bile acids accumulate in the bile canaliculus affecting hepatocyte viability. The actions of bile acids require changes in the release of Ca2+ from intracellular stores and in Ca2+ entry. The target(s) of the Ca2+ entry pathway affected by bile acids is, however, not known. The overall objective of the work described in this thesis was to elucidate the target(s) and mechanism(s) of bile acids-induced modulation of hepatocytes calcium homeostasis. First, it was shown that a 12 h pre-incubation with cholestatic bile acids (to mimic cholestasis conditions) induced the inhibition of Ca2+ entry through store-operated Ca2+ channels (SOCs), while the addition of choleretic bile acids to the incubation medium caused the reversible activation of Ca2+ entry through SOCs. Moreover, it was shown that incubation of liver cells with choleretic bile acids counteracts the inhibition of Ca2+ entry caused by pre-incubation with cholestatic bile acids. Thus, it was concluded that SOCs are the target of bile acids action in liver cells. Surprisingly, despite the effect of choleretic bile acids in activating SOCs, the Ca2+ dye fura-2 failed to detect choleretic bile acid-induced Ca2+ release from intracellular stores in the absence of extracellular Ca2+. However, under the same conditions, when the sub-plasma membrane Ca2+ levels were measured using FFP-18 Ca2+ dye, choleretic bile acid induced a transient increase in FFP-18 fluorescence. This evidence suggested that choleretic bile acids-induced activation of Ca2+ entry through SOCs, involving the release of Ca2+ from a region of the endoplasmic reticulum (ER) located in the vicinity of the plasma membrane.
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Scanlon, Mary. "Cellular mechanism of neutrophil chemotaxis: the role of CA+2, as viewed with the fluorescent dye, FURA-2, in the polarization of human polymorphonuclear leukocytes following stimulation with the chemoattractant, F-Methionyl-Leucyl-Phenylalanine: a thesis." eScholarship@UMMS, 1987. https://escholarship.umassmed.edu/gsbs_diss/320.

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The mechanism by which a cell translates a spatially oriented, extracellular signal into a change in morphology and behavior is the key to understanding many biological processes. In order to investigate this general phenomenon, I have studied the chemotactic response of human polymorphonuclear leukocytes (PMN's) to f-methionyl-leucyl-phenylalanine (fMLP). Stimulation of PMN's with fMLP produces a plethora of intracellular events, including increases in cytosolic Ca+2. PMN's are also morphologically and behaviorally polarized by stimulation with chemoattractant; the membrane components and cytosolic organelles of polarized PMN's become asymmetrically distributed. Polarization and subsequent orientation of PMN's in the direction of fMLP are steps which precede and are necessary for chemotaxis. I have chosen to examine the role of Ca+2, a ubiquitous second messenger, in the polarization of PMN's to fMLP. To accomplish this goal, Ca+2 has been measured in resting and polarized PMN's, utilizing the intracellular fluorescence of the Ca+2-sensitive dye, fura-2. Initial experiments have revealed a Ca+2-insensitive form of fura-2 associated with PMN's which, if uncorrected, would lead to erroneous measurements of [Ca+2]. I have suggested putative sources for the Ca+2-insensitive fluorescence in PMN's and have presented two methods for accurate calculation of [Ca+2] in spite of the additional component of fluorescence. As measured from the cell-associated fluorescence of fura-2, [Ca+2] increases without a detectable lag upon addition of fMLP to PMN's in suspension. The rise in [Ca+2] is associated with an increase in the percentage of cells which polarize to fMLP. The increases in [Ca+2] and in polarization are both directly related to increases in the concentration of chemoattractant. Inhibition of the rise in [Ca+2], by exposure of the human donor to aspirin or addition of EGTA to isolated cells, results in a concommitant reduction in the percentage of cells which polarize to fMLP. These findings are consistent with the hypothesis that Ca+2 acts as a second messenger in the pathway of transduction of the extracellular signal which results in polarization. However, addition of ionomycin, the Ca+2-selective ionophore, to PMN's did not induce polarization either in the presence or in the absence of fMLP. This result suggests that increases Ca+2, which appear to be necessary for polarization, are locally distributed within the fMLP-stimulated PMN. Examination of the subcellular distribution of Ca+2 using the digital imaging microscope reveals that Ca+2 is not uniformly distributed in the polarized PMN. Cells polarized by stimulation with fMLP often exhibit regional differences in [Ca+2] from front to tail. The magnitude and direction of the intracellular gradient varies among cells and suggests that within individual cells, the heterogeneity of [Ca+2] varies temporally and spatially as the cell chemotaxes. The results of the experiments conducted in this dissertation suggest that Ca+2 plays an important role as second messenger in fMLP-stimulated PMN's. I suggest that the morphological polarity of the chemotactic PMN is dependent upon the establishment and maintenance of an intracellular Ca+2 gradient.
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Westerlund, Johanna. "Pulsatile insulin release from single islets of Langerhans." Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-494.

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Insulin release from single islets of Langerhans is pulsatile. The secretory activities of the islets in the pancreas are coordinated resulting in plasma insulin oscillations. Nutrients amplitude-regulate the insulin pulses without influencing their frequency. Diabetic patients show an abnormal plasma insulin pattern, but the cause of the disturbance remains to be elucidated. Ithe present thesis the influence of the cytoplasmic calcium concentratio([Ca2+]i) and cell metabolism on pulsatile insulin release was examined in single islets of Langerhans from ob/ob-mice. Glucose stimulation of insulin release involves closure of ATP-sensitive K+ channels (KATP channels), depolarization, and Ca2+ influx in β-cells. In the presence of 11 mM glucose, pulsatile insulin secretion occurs in synchrony with oscillations i[Ca2+]i. When [Ca2+]i is low and stable, e.g. under basal conditions, low amplitude insulin pulses are still observed. When [Ca2+]i is elevated and non-oscillating, e.g. when the β-cells are depolarized by potassium, high amplitude insulin pulses are observed. The frequency of the insulin pulses under these conditions is similar to that observed when [Ca2+]i oscillations are present. By permanently opening or closing the KATP channels with diazoxide or tolbutamide, respectively, it was investigated if glucose can modulate pulsatile insulin secretion when it does not influence the channel activity. Under these conditions, [Ca2+]i remained stable whereas the amplitude of the insulin pulses increased with sugar stimulation without change in the frequency. Metabolic inhibition blunted but did not prevent the insulin pulses. The results indicate that oscillations in metabolism can generate pulsatile insulin release when [Ca2+]i is stable. However, under physiological conditions, pulsatile secretion is driven by oscillations in metabolism and [Ca2+]i, acting in synergy.

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Egunlusi, Ayodeji Olatunde. "Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection." Thesis, University of the Western Cape, 2014. http://hdl.handle.net/11394/3904.

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>Magister Scientiae - MSc
This study focused on the synthesis of a series of novel tricycloundecane derivatives and evaluation of these compounds for neuroprotection using the fluorescent ratiometric calcium assay that indicates the ability of the test compounds to inhibit NMDA receptors and VGCC. The cycloaddition reaction between p-benzoquinone and monomerised dicyclopentadiene yielded tricycloundeca- 4,9-diene-3,6-dione which was used as the base structure and further derivatised. These derivatives were conjugated with benzylamine to form a series of imines and amines. A total of 10 compounds were synthesised for evaluation of inhibition of calcium influx through NMDA receptor channels and voltage-gated calcium channels. The structures were confirmed using NMR, IR and MS. On the proton NMR, the characteristic AB-quartet system was observed in the region of 1-2 ppm for all the compounds and the aromatic moiety was observed between 6.5-7.5 ppm for the novel polycyclic amines. These, with other functional groups, were used to confirm the individual structures
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9

Liu, Li. "Roles of PMCA Isoforms in Ca2+-Homeostasis and Contractility of Bladder Smooth Muscle: Evidence from PMCA Gene-Ablated Mice." Cincinnati, Ohio : University of Cincinnati, 2007. http://rave.ohiolink.edu/etdc/view.cgi?acc_num=ucin1178307168.

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Thesis (Ph.D.)--University of Cincinnati, 2007.
Advisor: Richard J. Paul. Title from electronic thesis title page (viewed Apr. 4, 2009). Keywords: PMCA (human gene symbols; ATP2B); SERCA2 (human gene symbols; ATP2A2); NCX; bladder smooth muscle; Ca²⁺ homeostasis; gene-altered mice. Ca²⁺ waves; Ca²⁺ sparks; Fura-PE3; Fluo-4; Indo-1; multi-photon microscopy. Includes abstract. Includes bibliographical references.
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Ahmed, Meftun. "Oscillatory Ca2+ signaling in glucose-stimulated murine pancreatic β-cells : Modulation by amino acids, glucagon, caffeine and ryanodine." Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1408.

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Oscillations in cytoplasmic Ca2+ concentration ([Ca2+]i) is the key signal in glucose-stimulated β-cells governing pulsatile insulin release. The glucose response of mouse β-cells is often manifested as slow oscillations and rapid transients of [Ca2+] i. In the present study, microfluorometric technique was used to evaluate the role of amino acids, glucagon, ryanodine and caffeine on the generation and maintenance of [Ca2+] i oscillations and transients in individual murine β-cells and isolated mouse pancreatic islets. The amino acids glycine, alanine and arginine, at around their physiological concentrations, transformed the glucose-induced slow oscillations of [Ca2+] i in isolated mouse β-cells into sustained elevation. Increased Ca2+ entry promoted the reappearance of the slow [Ca2+] i oscillations. The [Ca2+] i oscillations were more resistant to amino acid transformation in intact islets, supporting the idea that cellular interactions are important for maintaining the oscillatory activity. Individual rat β-cells responded to glucose stimulation with slow [Ca2+] i oscillations due to periodic entry of Ca2+ as well as with transients evoked by mobilization of intracellular stores. The [Ca2+] i oscillations in rat β-cells had a slightly lower frequency than those in mouse β-cells and were more easily transformed into sustained elevation in the presence of glucagon or caffeine. The transients of [Ca2+] i were more common in rat than in mouse β-cells and often appeared in synchrony also in cells lacking physical contact. Depolarization enhanced the generation of [Ca2+] i transients. In accordance with the idea that β-cells have functionally active ryanodine receptors, it was found that ryanodine sometimes restored oscillatory activity abolished by caffeine. However, the IP3 receptors are the major Ca2+ release channels both in β-cells from rats and mice. Single β-cells from ob/ob mice did not differ from those of lean controls with regard to frequency, amplitudes and half-widths of the slow [Ca2+] i oscillations. Nevertheless, there was an excessive firing of [Ca2+] i transients in the β-cells from the ob/ob mice, which was suppressed by leptin at close to physiological concentrations. The enhanced firing of [Ca2+] i transients in ob/ob mouse β-cells may be due to the absence of leptin and mediated by activation of the phospholipase C signaling pathway.

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Books on the topic "Fura-2"

1

Furī na 2-ri. Tōkyō: Sonī Magajinzu, 2006.

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Spells of fury: Building Windows 95 games using DirectX 2. Corte Madera, CA: Waite Group Press, 1996.

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Nara-ken Tenri-shi Furu iseki Jōmon jidai sōki no chōsa: 1984 12--1985 2 chōsa. [Tenri-shi]: Maizō Bunkazai Tenrikyō Chōsadan, 1988.

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Operation Urgent Fury: The planning and execution of joint operations in Grenada, 12 October-2 November 1983. Washington, DC: Joint History Office, Office of the Chairman of the Joint Chiefs of Staff, 1997.

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Perry, Philip J. Synthesis and biological evaluation of novel cytotoxic heterocyclic compounds: Furo (2,3-b) naphthoquinones and 2-aryl-4H-3,1-benzoxazin-4-ones. Leicester: De Montfort University, 1996.

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Moore, URS Dames &. Inventory of dioxin and furan emissions to air, land and water in Ireland for 2000 and 2010 (2000-DS-2-M1): Synthesis report. Johnstown Castle, Co. Wexford: Environmental Protection Agency, 2002.

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Markaz Dirāsāt al-Khalīj wa-al-Jazīrah al-ʻArabīyah, ed. Nadwat Duwal Majlis al-Taʻāwun al-Khalījī wa-Juhūd Taḥqīq al-Amn wa-al-Istiqrār khilāla al-ʻAqd al-Qādim, al-Furaṣ wa-al-Quyūd: 1-2 Māyū 2001, al-Kuwayt. [Kuwait]: Markaz Dirāsāt al-Khalīj wa-al-Jazīrah al-ʻArabīyah, Jāmiʻat al-Kuwayt, 2001.

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Suzuki, Hidetaku. Jugyō-zukuri o chūshin ni kamaeta kyōdō kenkyū no soshikika: Kyōshoku daigakuin de mananda koto o furu ni ikashi, kenkyū kadai "manabiyasui kankyō no sōzō, yorokobi ga kanjirareru jugyō o mezashite" no moto kenkyū o susumeta, kenkyū shunin to shite no 2-nenkan o furikaette. Fukui-shi: Fukui Daigaku Daigakuin Kyōikugaku Kenkyūka Kyōshoku Kaihatsu Senkō, 2009.

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Arnold, J. Douglas, and Zach Meston. Awesome Sega Genesis Secrets 3. Lahaina, HI: Sandwich Islands Publishing, 1993.

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Prima. Official Sega Genesis: Power Tips Book, Volume 3. Rocklin, CA: Prima Publishing, 1994.

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Book chapters on the topic "Fura-2"

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Grouselle, M., and D. Georgescauld. "Fura-2 Imaging of Intracellular Free Calcium Dynamics in Excitable Cells." In Water and Ions in Biomolecular Systems, 229–40. Basel: Birkhäuser Basel, 1990. http://dx.doi.org/10.1007/978-3-0348-7253-9_23.

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Patel, Anish, Robert A. Hirst, Charlotte Harrison, Kazuyoshi Hirota, and David G. Lambert. "Measurement of [Ca2+]i in Whole Cell Suspensions Using Fura-2." In Methods in Molecular Biology, 37–47. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-086-1_2.

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Xu, Yan-Jun, Qiming Shao, and Naranjan S. Dhalla. "Fura-2 fluorescent technique for the assessment of Ca2+ homeostasis in cardiomyocytes." In Novel Methods in Molecular and Cellular Biochemistry of Muscle, 149–57. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6353-2_16.

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Smith, Stephen J., Luis R. Osses, and George J. Augustine. "Fura-2 Imaging of Localized Calcium Accumulation Within Squid ‘Giant’ Presynaptic Terminal." In Calcium and Ion Channel Modulation, 147–55. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0975-8_12.

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Johnson, Martin. "Calcium Imaging of Store-Operated Calcium (Ca2+) Entry (SOCE) in HEK293 Cells Using Fura-2." In Calcium Signalling, 163–72. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9018-4_15.

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Wiltink, Anneke, Arnoud van der Laarse, Nel P. M. Herrmann-Erlee, Joke M. van der Meer, and Dirk L. Ypey. "The Use of the Fluorescent Probe Fura-2 For Intracellular Free Calcium Measurements: Some Methodological Aspects." In Biotechnology Applications of Microinjection, Microscopic Imaging, and Fluorescence, 133–42. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2828-9_16.

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Hayes, Brendan A., P. V. Avdonin, and U. S. Ryan. "MAG-FURA-2 Elicited Fluorescent Response of Subcellular Magnesium in Endothelial Cells: A Sharp Contrast with Calcium." In Vascular Endothelium, 256–57. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_35.

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De Nadai, Andrea, Nicola Vajente, Diana Pendin, and Andrea Mattarei. "Mt-fura-2, a Ratiometric Mitochondria-Targeted Ca2+ Sensor. Determination of Spectroscopic Properties and Ca2+ Imaging Assays." In Methods in Molecular Biology, 187–215. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1262-0_12.

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Hayashi, H., N. Noda, H. Miyata, S. Suzuki, A. Kobayashi, M. Hirano, T. Kawai, T. Hayashi, and N. Yamazaki. "Changes in Cell Morphology, [Ca2+]i and pHi During Metabolic Inhibition in Isolated Myocytes of Diabetic Rats Using Dual-Loading of Fura-2 and BCECF." In Developments in Cardiovascular Medicine, 183–98. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3512-6_18.

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Winkelmann, J. "Diffusion of air (1); 2-methyl-furan (2)." In Gases in Gases, Liquids and their Mixtures, 1816. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-49718-9_1374.

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Conference papers on the topic "Fura-2"

1

Poll, C. T., and J. Westwick. "THE ROLE OF IONISED INTRACELLULAR FREE CALCIUM ([Ca++]i) IN THROMBIN-INDUCED DENSE GRANULE SECRETION." In 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, and T. Miyazaki. "THROMBIN-INDUCED BIPHASIC Ca2+TRANSIENT DETECTED BY FURA-2 FLUORESCENCE WAS COUPLED WITH BIPHASIC Ca2+ UPTAKE IN PLATELETS." In 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, and J.-P. Cazenave. "INCREASED AGGREGATION AND SECRETION RESPONSES OF HUMAN PLATELETS WHEN LOADED WITH THE CALCIUM FLUORESCENT PROBES QUIN2 AND FURA-2." In 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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Van den Bergh, Viviane, Katrien Meuwis, Noel Boens, Frans C. De Schryver, Michel Vincent, Jacques Gallay, and Marcel Ameloot. "Photophysical study of the Ca2+ indicator Fura-2 and the K+ indicator PBFI." In OE/LASE '94, edited by Joseph R. Lakowicz. SPIE, 1994. http://dx.doi.org/10.1117/12.182705.

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Rao, Gundu H. R., and James G. White. "INFLUENCE OF CALCIUM FLUX ON STABILITY OF PLATELET MICROTUBULE COILS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643904.

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Resting human platelets have a characteristic discoid form supported by a circumferential microtubule (MT). Ultrastructural, immunocytochemical and immunofluorescence studies have shown that the circumferential MT is a stable structure which undergoes constriction following exposure of platelets to aggregating agents. However, some biochemical and morphological studies suggested that MT coils dissolved almost completely within seconds after exposure to aggregating agents, then reassembled 1-4 minutes later. One investigation suggested that disappearance of the MT coils was associated with calcium flux caused by agonist stimulation or exposure to the ionophore, A23187. The present study has examined the latter hypothesis directly. Fura 2, a calcium sensitive fluorophore, was loaded into washed platelets at a concentration of 1 μM, the cells washed once and resuspended in HEPES buffer. Fluorescence changes were monitored in a Fluorolog spectrofluorometer.Thrombin stimulation of Fura 2 loaded platelets resulted in an immediate eight fold increase in the level of cytoplasmic calcium. The calcium ionophore, ionomycin, stimulated a 15 fold rise in the cytoplasmic calcium of Fura 2 loaded cells.Samples of thrombin and ionomycin stimulated platelets were fixed in glutaraldehyde and osmic acid at the peak of calcium flux indicated by the rise in fluorescence. Examination of activated platelets in the electron microscope revealed shape change and internal transformation. MT coils were constricted, but did not disappear from platelets fixed during the maximum elevation of cytoplasmic calcium. The findings do not support the concept that the calcium rise produced in platelets following exposure to potent agonists causes disappearance of the circumferential MT.
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Watts, I. S., R. J. Keery, and P. Lumlev. "EFFECT OF EXTRACELLULAR Ca2+ UPON AGONIST-INDUCED Ca2+ TRANSIENTS IN HUMAN PLATELETS: COMPARISON OF QUIN 2 AND FURA 2." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644525.

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In human platelets loaded with the Ca2+ indicator Quin 2 (Q2), elevated cytosolic Ca2+ ([Ca2+]i) induced by platelet agonists is greatly attenuated in the absence of extracellular Ca2+ ([Ca2+]o), suggesting the majority of [Ca2+]i is derived via transmembrane influx. However, the relatively weak fluorescent properties of Q2 require that high intraplatelet concentrations be used which may influence [Ca2+]i homeostasis and platelet function. This is less of a problem with the more intensely fluorescent Ca2+-indicator Fura 2 (F2). We have compared the rise in [Ca2+]i and aggregation induced by a range of agonists at different [Ca2+]o concentrations, in Q2-and F2-loaded platelets. Platelets in citrated PRP were loaded with the acetoxymethyl esters of Q2 (20 μM) or F2 (4 μM) (30 min at 37°C) and then gel-filtered using a low Ca2+ (≃50 μM) buffer (Ca2+L). Platelet count was 1.5×l08 ml-1. Fluorescence was measured at Ex 339 Em 500 nM in aliquots of platelet suspension at 37°C. Aggregation was determined at 37°C by turbidometric and platelet counting techniques. In Q2- and F2-loaded platelets in 1 mM [Ca2+]o, ADP (0.1 to 10 μM), U46619 (0.01 to 1 μM), PAF (0.001 to 1 μM) and thrombin (0.001 to 0.3 Uml-1) caused concentration-related increases in [Ca2+]i and aggregation. In Q2-loaded platelets, the rise in [Ca2+]i to thrombin, ADP, U46619 and PAF was reduced > 90% in both Ca2+L medium and in the absence of [Ca2+]o (4 mM EGTA). In contrast, in F2-loaded platelets, attenuation of the rise in [Ca2+]i to each agonist in Ca2+L and EGTA was much less than in Q2-loaded platelets (e.g. with U46619 (1 μM) only 20% and 40% reduction in Ca2+L and EGTA respectively). With Q2, aggregation was abolished in the presence of EGTA and markedly inhibited in the Ca2+L medium. In contrast with F2 whilst the presence of EGTA abolished aggregation, no inhibition was seen in the Ca2+L medium. In conclusion, agonist stimulation of platelets is associated with an influx of Ca2+, which is greater in Q2- than F2-loaded platelets. In low [Ca2+]o Q2 renders platelets more reliant on Ca2+ influx for aggregation to occur than does F2. Caution should therefore be exercised when correlating [Ca2+]i with aggregation in Q2-loaded platelets.
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Aswani, Kavita. "LED illumination for fluorescence from Fura-2 to Cy7.5 and beyond: A true lamp replacement." In Light-Emitting Devices, Materials, and Applications XXV, edited by Martin Strassburg, Jong Kyu Kim, and Michael R. Krames. SPIE, 2021. http://dx.doi.org/10.1117/12.2576651.

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Matsuno, K., F. Katabami, M. Koyama, K. Abe, K. Sakurada, T. Miyazaki, S. Ozasa, H. Saitoh, I. Maekawa, and H. Matsumiya. "PLATELET-ACTIVATING FACTOR (PAF)-INDUCED INTRACELLULAR Ca MOBILIZATION IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643483.

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PAF-induced intracellular Ca2+ mobilization and platelet aggregation were investigated in human platelets. Cytosolic free Ca2+ concentration ([Ca2+]cyt) was measured by using fluorescent 45Ca2+ probe quin2 and fura-2, and photoprotein aequorin. Ca2+ uptake was measured after stimulation by PAF. Platelet aggregation was studied by recording the change in light transmission with platelet rich plasma (PRP) or washed platelet suspension (WPS).These three Ca2+ -indicators could determine the elevation of [Ca2+ ]cyt that was stimulated by PAF in the presence of extra- cellular Ca2+ (quin2 method: 98.2nM to 289.7nM; fura-2 method: 102.OnM to 351.4nM; aequorin method: 4.1μM to 8.2μM). In the absence of extracellular Ca2+ , however, little elevation of [Ca2+ ]cyt was detected after stimulation by PAF. PAF could evoke the transient Ca2+ uptake.New PAF specific antagonist, ONO-6240 inhibited PAF-induced platelet aggregation at a concentration from lμM dose-dependently, whereas it didn’t inhibit collagen- and thrombin-induced platelet aggregation at a concentration of lOOyM. ONO-6240 inhibited PAF- induced increase in [Ca2+ ]cyt in a dose-dependent manner as deter mined by these Ca2+ -indicators, as well as platelet aggregation.These results suggest the increase in [Ca2+ ]cyt is responsible for platelet aggregation induced by PAF, and the increased Ca2+ is derived from external Ca2+ influx chiefly.
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Lascombe, M. L., M. Grouselle, J. P. Desmazès, D. Georgescauld, J. Koenig, and J. Chapron. "FURA-2 imaging of intracellular free Ca2+ dynamics and distribution induced by acetylcholine and caffeine in embryonic skeletal muscle cells." In The living cell in four dimensions. AIP, 1991. http://dx.doi.org/10.1063/1.40602.

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Oraevsky, Alexander A., Olga A. Cabello, Qin Shan, Frank K. Tittel, and Philip D. Henry. "Detection of calcium activity in human monocytes by the fura-2 fluorescence method: in vitro differentiation sensitizes cells to dihydropyridine calcium channel modulators." In OE/LASE '94, edited by George S. Abela. SPIE, 1994. http://dx.doi.org/10.1117/12.179909.

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Reports on the topic "Fura-2"

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Philosoph-Hadas, Sonia, Richard Crain, Shimon Meir, Nehemia Aharoni, and Susan Lurie. Calcium-Mediated Signal Transduction during Leaf Senescence. United States Department of Agriculture, November 1995. http://dx.doi.org/10.32747/1995.7604925.bard.

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We have examined the possibility that modulation of [Ca2+]cyt may represent a signal which induces senescence processes in leaves, through triggering of lipid hydrolysis leading to the cascade of detriorative events. Characterization of the signal transduction components operating during leaf senescence was gained by studying various Ca2+-dependent activities of parsley and chrysanthemum leaves, in relation to several senescence functions, and in response to senescence-modulating hormones (ethylene,ABA, BA and IAA). Some innovative findings regarding the control of senescence processes by [Ca2+]cyt were established: Several Ca2+-or CaM-related compounds were shown to modulate [Ca2+]cyt and action, thereby affecting whole leaf senescence. The involvement of [Ca2+]cyt in mediating the effects of senescence-modulating hormones has been demonstrated. Loss of energized Ca2+-transport capability of PM was found to an early event in leaf senescence, which occurs before changes in senescence parameters are observed, and while other PM ATPase enzymes still retain about 50% of their activities. A general pattern of increased phosphorylation of PM proteins with advanced senescence, which could be modified by plant hormones applied in vivo (BA) or in vitro (ABA), sa found. Taken together, all this indirect evidence indicate that [Ca2+]cyt is elevated due to the senescence-induced decrease in the ability to extrude Ca2+, which results particularly from reduced PM Ca2++-transport capability rather than increased operation of Ca2+ channels or elevated Ins(1,4,5)P3 levels. The direct proof for such a senescence-related elevation in [Ca2+]cyt was provided for the first time by the Ca2+ imaging measures with fura-2, showing a rise in [Ca2+]cyt of mesophyll cells upon senescence induction, which preceeded changes in typical senescence characteristics. This research provides strong evidence for regarding the rise in [Ca2+]cyt as a primary event in induction of the senescence syndrome in detached leaves. The findings have also broad implications for postharvest handling of leafy crops and ornamentals, and open new avenues for employing Ca2+-related inhibitors to delay leaf senescence.
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Rouseff, Russell L., and Michael Naim. Characterization of Unidentified Potent Flavor Changes during Processing and Storage of Orange and Grapefruit Juices. United States Department of Agriculture, September 2002. http://dx.doi.org/10.32747/2002.7585191.bard.

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Citrus juice flavor quality traditionally diminishes after thermal processing and continuously during storage. Our prior studies found that four of the five most potent off-aromas formed during orange juice storage had not been identified. The primary emphasis of this project was to characterize and identify those potent flavor degrading aroma volatiles so that methods to control them could be developed and final flavor quality improved. Our original objectives included: 1 Isolate and characterize the most important unidentified aroma impact compounds formed or lost during pasteurization and storage. 2. Determination of thiamine and carotenoid thermal decomposition and Strecker degradation pathways in model solutions as possible precursors for the unidentified off-flavors. 3. Evaluate the effectiveness of an "electronic nose" to differentiate the headspace aromas of from untreated and heat pasteurized orange and grapefruit juices. 4. Use model systems of citrus juices to investigate the three possible precursor pathways (from 2) for flavor impact compounds formed or lost during pasteurization or storage. RESULTS - The components responsible for citrus storage off flavors and their putative precursors have now been identified. Certain carotenoids (b-carotene) can thermally degrade to produce b-ionone and b-damascenone which are floral and tobacco smelling respectively. Our GC-O and sensory experiments indicated that b-damascenone is a potential storage off-flavor in orange juice. Thiamine (Vitamin B1) degradation produces 2-methyl-3-furan thiol, MFT, and its dimer bis(2- methyl-3-furyl) disulfide which both produce meaty, savory aromas. GC-O and sensory studies indicated that MFT is another storage off-flavor. Methional (potato aroma) is another off flavor produced primarily from the reaction of the native amino acid, methionine, and oxidized ascorbic acid (vitamin C). This is a newly discovered pathway for the production of methional and is more dominant in juices than the classic Maillard reaction. These newly identified off flavors diminish the flavor quality of citrus juices as they distort the flavor balance and introduce non-typical aromas to the juice flavor profile. In addition, we have demonstrated that some of the poor flavor quality citrus juice found in the market place is not only from the production of these and other off flavors but also due to the absence of desirable flavor components including several potent aldehydes and a few esters. The absence of these compounds appears to be due to incomplete flavor volatile restoration after the making of juice concentrates. We are the first to demonstrate that not all flavor volatiles are removed along with water in the production of juice concentrate. In the case of grapefruit juice we have documented which flavor volatiles are completely removed, which are partially removed and which actually increase because of the thermal process. Since more that half of all citrus juices is made into concentrate, this information will allow producers to more accurately restore the original flavor components and produce a juice with a more natural flavor. IMPLICATIONS - We have shown that the aroma of citrus juices is controlled by only 1-2% of the total volatiles. The vast majority of other volatiles have little to no direct aroma activity. The critical volatiles have now been identified. The ability to produce high quality citrus juices requires that manufacturers know which chemical components control aroma and flavor. In addition to identifying the critical flavor components (both positive and negative), we have also identified several precursors. The behavior of these key aroma compounds and their precursors during common manufacturing and storage conditions has been documented so manufacturers in Israel and the US can alter production practices to minimize the negative ones and maximize the positive ones.
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