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1.
The Ca2+-mobilizing metabolite cyclic ADP-ribose (cADPR) has been shown to release Ca2+ from ryanodine-sensitive stores in many cells. We show that this metabolite at a concentration of 17μM, but not its precursor β-NAD+ nor non-cyclic ADPR at the same concentration, is active in releasing Ca2+ from rabbit skeletal muscle sarcoplasmic reticulum. The release was not sensitive to Ruthenium red (1μM) nor to the ryanodine receptor-specific scorpion toxin Buthotus1-1 (10 μM). In planar bilayer single channel recordings, concentrations up to 50μM cADPR did not increase the open probability of Ruthenium red and toxin-sensitive Ca2+ release channels. Thus Ca2+ release induced by cADPR in skeletal muscle sarcoplasmic reticulum may not involve opening of ryanodine receptors.  相似文献   

2.
The study of Ca2+ sparks has led to extensive new information regarding the gating of the Ca2+ release channels underlying these events in skeletal, cardiac and smooth muscle cells, as well as the possible roles of these local Ca2+ release events in muscle function. Here we review basic procedures for studying Ca2+sparks in skeletal muscle, primarily from frog, as well as the basic results concerning the properties of these events, their pattern and frequency of occurrence during fiber depolarization and the mechanisms underlying their termination. Finally, we also consider the contribution of different ryanodine receptor (RyR) isoforms to Ca2+ sparks and the number of RyR Ca2+ release channels that may contribute to the generation of a Ca2+ spark. Over the decade since their discovery, Ca2+ sparks have provided a wealth of information concerning the function of Ca2+ release channels within their intracellular environment.  相似文献   

3.
In this study we investigated the release of Ca2+ in brain microsomes after Ca2+ loading by the Ca2+-ATPase or by the Na+/Ca2+ exchanger. The results show that in microsomes loaded with Ca2+ by the Ca2+-ATPase, Ins(1,4,5)P3 (5 μM) release 21±2% of the total Ca2+ accumulated, and that in the microsomes loaded with Ca2+ by the Na2+/Ca2+ exchanger, Ins(1,4,5)P3 released 28±3% of the total Ca2+ accumulated. These results suggest that receptors of Ins(1,4,5)P3 may be co-localized with the Na2+/Ca2+ exchanger in the endoplasmic reticulum membrane or that there are Ins(1,4,5)P3 receptors in the plasma membrane where the Na2+/Ca2+ exchanger is normally present, or both. We also found that Ins(1,4,5)P3 inhibited the Ca2+-ATPase by 33.7%, but that it had no significant effect on the Na2+/Ca2+ exchanger.  相似文献   

4.
By mediating the Ca2+ influx that triggers exocytotic fusion, Ca2+ channels play a central role in a wide range of secretory processes. Ca2+ channels consist of a complex of protein subunits, including an 1 subunit that constitutes the voltage-dependent Ca2+-selective membrane pore, and a group of auxiliary subunits, including β, γ, and 2–δ subunits, which modulate channel properties such as inactivation and channel targeting. Subtypes of Ca2+ channels are constituted by different combinations of 1 subunits (of which 10 have been identified) and auxiliary subunits, particularly β (of which 4 have been identified). Activity-secretion coupling is determined not only by the biophysical properties of the channels involved, but also by the relationship between channels and the exocytotic apparatus, which may differ between fast and slow types of secretion. Colocalization of Ca2+ channels at sites of fast release may depend on biochemical interactions between channels and exocytotic proteins. The aim of this article is to review recent work on Ca2+ channel structure and function in exocytotic secretion. We discuss Ca2+ channel involvement in selected types of secretion, including central neurotransmission, endocrine and neuroendocrine secretion, and transmission at graded potential synapses. Several different Ca2+ channel subtypes are involved in these types of secretion, and their function is likely to involve a variety of relationships with the exocytotic apparatus. Elucidating the relationship between Ca2+ channel structure and function is central to our understanding of the fundamental process of exocytotic secretion.  相似文献   

5.
Ca2+ efflux from the sarcoplasmic reticulum (SR) is routed primarily through SR Ca2+ release channels (ryanodine receptors, RyRs). When clusters of RyRs are activated by trigger Ca2+ influx through L-type Ca2+ channels (dihydropyridine receptors, DHPR), Ca2+ sparks are observed. Close spatial coupling between DHPRs and RyR clusters and the relative insensitivity of RyRs to be triggered by Ca2+ together ensure the stability of this positive-feedback system of Ca2+ amplification. Despite evidence from single channel RyR gating experiments that phosphorylation of RyRs by protein kinase A (PKA) or calcium-calmodulin dependent protein kinase II (CAMK II) causes an increase in the sensitivity of the RyR to be triggered by [Ca2+]i there is little clear evidence to date showing an increase in Ca2+ spark rate. Indeed, there is some evidence that the SR Ca2+ content may be decreased in hyperadrenergic disease states. The question is whether or not these observations are compatible with each other and with the development of arrhythmogenic extrasystoles that can occur under these conditions. Furthermore, the appearance of an increase in the SR Ca2+ “leak” under these conditions is perplexing. These and related complexities are analyzed and discussed in this report. Using simple mathematical modeling discussed in the context of recent experimental findings, a possible resolution to this paradox is proposed. The resolution depends upon two features of SR function that have not been confirmed directly but are broadly consistent with several lines of indirect evidence: (1) the existence of unclustered or “rogue” RyRs that may respond differently to local [Ca2+]i in diastole and during the [Ca2+]i transient; and (2) a decrease in cooperative or coupled gating between clustered RyRs in response to physiologic phosphorylation or hyper-phosphorylation of RyRs in disease states such as heart failure. Taken together, these two features may provide a framework that allows for an improved understanding of cardiac Ca2+ signaling.  相似文献   

6.
Cyclic ADP-ribose (cADPR) is a novel Ca2+ mobilizing second messenger, which is capable of inducing Ca2+ release from the sarcoplasmic reticulum (SR) via activation of ryanodine receptors (RyR) in vascular cells. This signaling nucleotide has also been reported to participate in generation or modulation of intracellular Ca2+ sparks 2+waves or oscillations, Ca2+-induced Ca2+ release (CICR) and spontaneous transient outward currents (STOCs) in vascular smooth muscle cells (VSMCs). With respect to the role of cADPR-mediated signaling in mediation of vascular responses to different stimuli, there is accumulating evidence showing that cADPR is importantly involved in the Ca2+ response of vascular endothelial cells (ECs) and VSMCs to various chemical factors such as vasoactive agonists acetylcholine, oxotemorine, endothelin, and physical stimuli such as stretch, electrical depolarization and sheer stress. This cADPR-RyR-mediated Ca2+ signaling is now recognized as a fundamental mechanism regulating vascular function. Here we reviewed the literature regarding this cADPR signaling pathway in vascular cells with a major focus on the production of cADPR and its physiological roles in the control of vascular tone and vasomotor response. We also summarized some publish results that unveil the underlying mechanisms mediating the actions of cADPR in vascular cells. Given the importance of Ca2+ in the regulation of vascular function, the results summarized in this brief review will provide new insights into vascular physiology and circulatory regulation.  相似文献   

7.
In permeabilized lacrimal acinar cells, cyclic ADP-ribose (cADP-ribose) and inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) release Ca2+ in a dose dependent manner from distinct thapsigargin-sensitive Ca2+ pools. Ryanodine specifically blocks the Ca2+ response to cADP-ribose, whereas heparin strongly reduces the response to Ins(1,4,5)P3 application. GTP causes a rapid Ca2+ release by a ryanodine- and heparin-insensitive mechanism and potentiates Ins(1,4,5)P3 but not cADP-ribose evoked Ca2+ release. It is estimated that cADP-ribose can release 16 μmol Ca2+/I cells, whereas Ins(1,4,5)P3 can mobilize 55 μmol Ca2+/I cells. The results suggest that cADP-ribose and Ins(1,4,5)P3 release Ca2+ from distinct internal stores and that a third Ca2+ pool exists which can selectively interact with the Ins(1,4,5)P3-sensitive Ca2+ store by a GTP-mediated process.  相似文献   

8.
The ability of neurotensin (NT) to elevate cytosolic Ca2+ in small cell lung cancer (SCLC) cells was investigated using the fluorescent Ca2+ indicator Fura 2-AM. Using SCLC cell line NCI-H345, NT elevated cytosolic Ca2+ levels in a concentration-dependent manner. Using a 10 nM dose, NT and C-terminal fragments such as NT(8–13) but not N-terminal fragments such as NT(1–8) elevated the cytosolic Ca2+ levels. Because EGTA (5 mM) did not affect the NT response, NT may cause release of Ca2+ from intracellular stores. These data indicate that SCLC NT receptors may use Ca2+ as a second messenger.  相似文献   

9.
Fluoxetine, a selective 5-HT uptake inhibitor, inhibited 15 mM K+-induced [3H] 5-HT release from rat spinal cord and cortical synaptosomes at concentrations > 0.5 uM. This effect reflected a property shared by another selective 5-HT uptake inhibitor paroxetine but not by less selective uptake inhibitors such as amitriptyline, desipramine, imipramine or nortriptyline. Inhibition of release by fluoxetine was inversely related to both the concentration of K+ used to depolarize the synaptosomes and the concentration of external Ca2+. Experiments aimed at determining a mechanism of action revealed that fluoxetine did not inhibit voltage-independent release of [3H] 5-HT release induced by the Ca2+-ionophore A 23187 or Ca2+-independent release induced by fenfluramine. Moreover the 5-HT autoreceptor antagonist methiothepin did not reverse the inhibitory actions of fluoxetine on K+-induced release. Further studies examined the effects of fluoxetine on voltage-dependent Ca2+ channels and Ca2+ entry. Whereas fluoxetine and paroxetine inhibited binding of [3H] nitrendipine to the dihydropyridine-sensitive L-type Ca2+ channel, the less selective uptake inhibitors did not alter binding. The dihydropyridine antagonist nimodipine partially blocked fluoxetine-induced inhibition of release. Moreover enhanced K+-stimulated release due to the dihydropyridine agonist Bay K 8644 was reversed by fluoxetine. Fluoxetine also inhibited the K+-induced increase in intracellular free Ca2+ in fura-2 loaded synaptosomes. These data are consistent with the suggestion that fluoxetine inhibits K+-induced [3H] 5-HT release by antagonizing voltage-dependent Ca2+ entry into nerve terminals.  相似文献   

10.
We previously demonstrated that oxysterols added to the culture medium of NRK 49F cells labelled with [14C] arachidonic acid potentiated arachidonic acid (AA) release and prostaglandin (PG) E2 biosynthesis induced by the activation of these cells with fetal calf serum (FCS). In the absence of FCS, oxysterols had no effect on AA release. As phospholipase (Plase) A2 activity is Ca2+-dependent, we investigated whether oxysterol potentiating effect on AA release was related to an effect of these compounds on cell Ca2+ concentration. In this paper, we show that the intensity of potentiation by oxysterol varies with the external cell Ca2+ concentration; when external Ca2+ is chelated by EGTA, the oxysterol effect persists, though it is decreased. The Ca2+ channel inhibitor nifedipine does not decrease the potentiating effect of 25-OH cholesterol, indicating that, if oxysterol favours Ca2+ entry into the cell, the nifedipine inhibited channel is not involved. At the usual concentration (5 μm/ml), oxysterols are not able to increase, mimmediately or after a short time of contact (90 min) the concentration of intracellular free Ca2+ ([Ca2+])i measured by fluorescence of Quinn-2; at very high concentration of oxysterol (25 μm/ml), [Ca2+]i only slightly increases (+30%). The liberation of AA induced by cell activation with the Ca2+ ionophore ionomycin is also potentiated by 25-OH cholesterol. All these observations are not in favour of a proper effect o oxysterols on cell Ca2+ level.  相似文献   

11.
We have studied the effects of cholinegic agonists on the rates of insulin release and the concentrations of diacylglycerol (DAG) and intracellular free Ca2+ ([Ca2+]i) in the β-cell line MIN6. Insulin secretion was stimulated by glucose, by glibenclamide and by bombesin. In the presence of glucose, both acetylcholine (ACh) and carbachol (CCh) produced a sustained increase in the rate of insulin release which was blocked by EGTA or verapamil. The DAG content of MIN6 β-cells was not affected by glucose. Both CCh and ACh evoked an increase in DAG which was maximal after 5 min and returned to basal after 30 min; EGTA abolished the cholinergic-induced increased in DAG. ACh caused a transient rise in [Ca2+]i which was abolished by omission of Ca2+ or by addition of devapamil. Thus, cholinergic stimulation of β-cell insulin release is associated with changes in both [Ca2+]i and DAG. The latter change persists longer than the former and activation of protein kinase C and sensitization of the secretory process to Ca2+ may underlie the prolonged effects of cholinergic agonists on insulin release. However, a secretory response to CCh was still evident after both [Ca2+]i and DAG had returned to control values suggesting that additional mechanisms may be involved.  相似文献   

12.
In order to examine intracellular modulation of CNS catecholamine release, cerebrocortical synaptosomes were prelabeled with [3H]noradrenaline and permeabilized with streptolysin-O in the absence or presence of Ca2+. Plasma membrane permeabilization allowed efflux of cytosol and left a compartmentalized pool of [3H]noradrenaline intact, approximately 10% of which was released by addition of 10−5 M Ca2+. Addition of activators or inhibitors of protein kinase C, as well as inhibitors of Ca2+-calmodulin kinase II or calcineurin, failed to change Ca2+-induced noradrenaline release. Evoked release from permeabilized synaptosomes deficient in the vesicle-associated phosphoprotein synapsin I was also unchanged. In contrast, addition of a synthetic ‘active domain’ peptide from the myristoylated, alanine-rich C-kinase substrate (MARCKS) protein increased, while addition of calmodulin decreased Ca2+-induced release from the permeabilized synaptosomes, the latter effect being reversed by a peptide inhibitor of calcineurin. Moreover, addition of the actin-destabilizing agent DNase I, as well as antibodies to MARCKS, appeared to increase spontaneous, Ca2+-independent release from noradrenergic vesicles. These results indicate that the MARCKS protein may modulate release from permeabilized noradrenergic synaptosomes, possibly by modulating calmodulin levels and/or the actin cytoskeleton.  相似文献   

13.
Isolated hepatocytes and the isolated perfused rat liver have been used to study the alterations of cytosolic free Ca2+ concentration ([Ca2+]i) produced by 2,5-di(tert-butyl)-l.4-benzohydroquinone (tBuBHQ), a potent inhibitor of hepatic microsomal Ca2+ sequestration (Moore. G.A., McConkey. D.J., Kass, G.E.N., OBrien, P.J. and Orrenius, S. FEBS Lett.,224, 331-336). (1987). Addition of tBuBHQ to isolated hepatocytes caused a rapid increase in [Ca2+]i which was similar in magnitude to the [Ca2+]i elevation induced by the Ca2+ mobilizing hormone, vasopressin. In contrast with vasopressin which caused a Ca2+ transient, tBuBHQ elevated [Ca2+]i to a new steady state that was maintained for up to 15-20min. When vasopressin was administered during the tBuBHQ-induced period of elevated [Ca2+]i. [Ca2+]i, rapidly returned to basal levels. Similarly, if vasopressin was administered just prior to tBuBHQ, the resultant tBuBHQ-dependent change in [Ca2+]i was transient. and not sustained. The hydroquinone mobilized the same intracellular Ca2+ pool as inositol 1,4,5-trisphosphate. but tBuBHQ did not produce any detectable inositol polyphosphate accumulation. IBuBHQ stimulated glucose release from perifused hepatocytes. mimicking the effect of vasopressin. In the perfused liver, tBuBHQ infusion produced a single, slow and prolonged release of Ca2+ into the perfusate and inhibition of subsequent vasopressin-induced Ca2+ effluxes. Inhibition of the response to vasopressin was reversed over time, and closely correlated with the extent of inhibition of both Ca2+ sequestration and (Ca2+-Mg2+)-ATPase activity in microsomes isolated from the isolated perfused liver. The present results are consistent with tBuBHQ inhibiting ATP-dependent Ca2+ sequestration by a direct effect on the endoplasmic reticular Ca2+ pump, which results in net Ca2+ release and elevation of [Ca2+]i. Furthermore. vasopressin appears to stimulate active removal of increased [Ca2+] from the hepatocyte cytosol by a mechanism which does not depend on reuptake of Ca2+ into the endoplasmic reticulum

2,5-Di(tert-butyl) -l,4-benmhydroquinone. calcium. hepatocytes. perfused liver, endoplasmic reticulum  相似文献   

14.
钙信号是细胞调节各项生命活动的重要机制。神经元通过胞外钙离子(calcium ion, Ca2+)内流、内质网Ca2+释放以及Ca2+释放介导的Ca2+内流等方式产生具有时空特异性的钙信号,用于调控多种生物学过程,例如动作电位的调节、神经递质的释放、轴突的生长以及突触可塑性等。神经元胞内Ca2+浓度因受到细胞精确调控而处于动态平衡之中。若钙信号失调导致平衡被打破,则会造成神经元功能异常甚至死亡。近年来多项研究表明,钙稳态失衡与神经退行性疾病,例如阿尔茨海默病等的产生和发展密切相关,由此发展出关于阿尔茨海默病的钙假说。该假说认为,神经元钙稳态调节机制的持续性改变是神经元功能失常、大脑产生慢性疾病的重要因素。阿尔茨海默病发生发展过程中,神经元胞浆钙水平异常增高,致使多种钙依赖性酶的活性异常,进而影响基因转录。虽然内质网钙稳态的变化目前仍存在一定的争议,但较为确定的是线粒体中存在着钙超载的现象,导致氧化磷酸化反应下调,活性氧的产量增加,进而引发细胞凋亡。本文主要介绍了神经元钙信号系统及其功能,简要梳理了阿尔茨海默病钙假说的相关研究,并对后续研究进行了展望。  相似文献   

15.
Treatment of U937 cells with a sublethal concentration of tert-butylhydroperoxide generates DNA single strand breakage in U937 cells and this response is increased by caffeine, ATP, pyruvate or antimycin A. As we previously reported (Guidarelli, Clementi, Brambilla and Cantoni, (1997) Biochem. J. 328, 801-806), the enhancing effects of antimycin A are mediated by inhibition of complex III and the ensuing formation of superoxides and hydrogen peroxide in a reaction in which ubisemiquinone serves as an electron donor. Active electron transport was required in pyruvate-supplemented cells since the increased genotoxic response occurred as a consequence of enforced mitochondrial Ca2+ accumulation, a process driven by the increased electrochemical gradient. The enhancing effects of caffeine or ATP were also the consequence of mitochondrial Ca2+ accumulation but these responses were independent on electron transport. The increased formation of DNA lesions resulting from exposure to tert-butylhydroperoxide associated with the Ca2+-mobilizing agents or the respiratory substrate was mediated by arachidonic acid generated by Ca2+-dependent activation of phospholipase A2. Melittin, a potent phospholipase A2 activator, and reagent arachidonic acid mimicked the effects of caffeine, ATP or pyruvate on the tert-butylhydroperoxide-induced DNA single strand breakage.  相似文献   

16.
利用化学测定法分析高温、单氰胺和TDZ 3种破眠处理对“曙光”油桃休眠花芽H2O2代谢的主要影响,利用非损伤微测技术检测H2O2对休眠芽Ca2+转运的影响,研究H2O2在芽休眠解除过程中的调控作用.结果表明: 在深休眠时期,高温和单氰胺处理均能诱导芽内H2O2含量升高和过氧化氢酶(CAT)活性降低,并具有显著的破眠作用;TDZ对H2O2含量及CAT、过氧化物酶(POD)活性影响不大,破眠效果较差.休眠花芽原基组织钙通道活跃,对外源Ca2+呈吸收状态.外源H2O2可诱导休眠花芽原基组织Ca2+转运发生变化,低浓度H2O2降低Ca2+吸收速率,高浓度H2O2使组织对Ca2+的转运由吸收转变为释放.这表明休眠芽内H2O2信号和Ca2+信号相关联,通过诱导H2O2积累调控Ca2+信号可能在高温和单氰胺打破休眠的信号转导过程中起重要作用.  相似文献   

17.
The store-mediated Ca2+ entry was detected in single and cluster of rat submandibular acinar cells by measuring the Ca2+ activated ionic membrane currents. In the cells where intracellular Ca2+ was partly depleted by stimulation with submaximal concentration of acetylcholine (ACh) under a Ca2+-free extracellular condition, an employment of external Ca2+ in the absence of ACh caused a sustained increase of the K+ current without affecting the Cl current. A renewed ACh challenge without external Ca2+ caused repetitive spikes of both K+ and Cl currents due to the Ca2+ release. SK & F 96365 inhibited the generation of the sustained K+ current and refilling of the Ca2+ store following the Ca2+ readmission. It is suggested that the Ca2+ enters the cell through the store-mediated pathway near the K+ channels and is taken up by the store. Thus, only Ca2+ released from the store can activate both the K+ and Cl currents.  相似文献   

18.
Ca2+ uptake by rat brain mitochondria was studied under different experimental conditions. The most rapid uptake of Ca2+ occurred in the presence of ATP, succinate and Pi. ATP alone also supported Ca2+ uptake. In contrast, no Ca2+ uptake occurred with succinate and Pi when no ATP was added. Oligomycin and atractylate completely inhibited ATP-supported Ca2+ uptake but produced only a partial inhibition of Ca2+ transport in the presence of ATP, succinate and Pi. ATP plays a dual role in its action on brain mitochondria; it can support Ca2+ uptake by itself and it serves a function in allowing respiration-dependent Ca2+ uptake to proceed. The latter role of ATP does not involve transfer of energy from the nucleotide.  相似文献   

19.
Release of γ-aminobutyric acid (GABA) can be elicited by electrical field stimulation even in the absence of external Ca2+. Indeed, the release of GABA under such conditions is even higher than in the presence of Ca2+. To investigate the underlying mechanism of this phenomenon, the release of endogenous GABA from rat striatal slices was measured by high performance liquid chromatography with electro- chemical detection. Electrical stimulation at 2 Hz for 3 min elevated GABA efflux by 4.5-fold. Withdrawing external Ca2+ and adding 1 mM EGTA produced a small, transient increase in the basal efflux of GABA and increased electrically-evoked overflow 3-fold. Tetrodotoxin (5 μM) did not affect basal efflux in either normal or Ca2+-free conditions, but abolished electrically-evoked release. In the presence of normal Ca2+, nipecotic acid (1 mM) enhanced both spontaneous efflux and evoked overflow. Nipecotic acid also increased spontaneous release when external Ca2+ was removed. However, in the absence of Ca2+, nipecotic acid failed to increase electrically evoked GABA overflow. These results suggest that there exists a Ca2+-independent process for GABA release via the same carrier system that is utilized for high affinity GABA uptake.  相似文献   

20.
We investigated the initiation of Ca2+waves underlying triggered propagated contractions (TPCs) occurring in rat cardiac trabeculae under conditions that simulate the functional non-uniformity caused by mechanical or ischemic local damage of the myocardium. A mechanical discontinuity along the trabeculae was created by exposing the preparation to a small constant flow jet of solution with a composition that reduces excitation–contraction coupling in myocytes within that segment. Force was measured and sarcomere length as well as [Ca2+]i were measured regionally. When the jet-contained Caffeine, BDM or Low-[Ca2+], muscle-twitch force decreased and the sarcomeres in the exposed segment were stretched by shortening of the normal regions outside the jet. During relaxation the sarcomeres in the exposed segment shortened rapidly. Short trains of stimulation at 2.5 Hz reproducibly caused Ca2+-waves to rise from the borders exposed to the jet. Ca2+-waves started during force relaxation of the last stimulated twitch and propagated into segments both inside and outside of the jet. Arrhythmias, in the form of non-driven rhythmic activity, were triggered when the amplitude of the Ca2+-wave increased by raising [Ca2+]o. The arrhythmias disappeared when the muscle uniformity was restored by turning the jet off. We have used the four state model of the cardiac cross bridge (Xb) with feedback of force development to Ca2+ binding by Troponin-C (TnC) and observed that the force–Ca2+ relationship as well as the force–sarcomere length relationship and the time course of the force and Ca2+ transients in cardiac muscle can be reproduced faithfully by a single effect of force on deformation of the TnC·Ca complex and thereby on the dissociation rate of Ca2+. Importantly, this feedback predicts that rapid decline of force in the activated sarcomere causes release of Ca2+ from TnC.Ca2+,which is sufficient to initiate arrhythmogenic Ca2+ release from the sarcoplasmic reticulum. These results show that non-uniform contraction can cause Ca2+-waves underlying TPCs, and suggest that Ca2+ dissociated from myofilaments plays an important role in the initiation of arrhythmogenic Ca2+-waves.  相似文献   

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