scholarly journals Cardioprotection against Ischemia/Reperfusion by Licochalcone B in Isolated Rat Hearts

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Jichun Han ◽  
Dong Wang ◽  
Bacui Yu ◽  
Yanming Wang ◽  
Huanhuan Ren ◽  
...  
Keyword(s):  
Infarct Size ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Left Ventricular Pressure ◽  
Treated Group ◽  
Left Ventricular ◽  
Control Group ◽  
Myocardial Infarct Size ◽  
Triphenyltetrazolium Chloride

The generation of reactive oxygen species (ROS) is a major cause of heart injury induced by ischemia-reperfusion. The left ventricular developed pressure (LVDP) and the maximum up/down rate of left ventricular pressure (±dp/dtmax⁡) were documented by a physiological recorder. Myocardial infarct size was estimated macroscopically using 2,3,5-triphenyltetrazolium chloride staining. Coronary effluent was analyzed for lactate dehydrogenase (LDH) and creatine kinase (CK) release to assess the degree of cardiac injury. The levels of C-reactive protein (CRP), interleukin-8 (IL-8), tumor necrosis factor-α(TNF-α), and interleukin-6 (IL-6) were analyzed to determine the inflammation status of the myocardial tissue. Cardiomyocyte apoptosis analysis was performed using the In Situ Cell Death Detection Kit, POD. Accordingly, licochalcone B pretreatment improved the heart rate (HR), increased LVDP, and decreased CK and LDH levels in coronary flow. SOD level and GSH/GSSG ratio increased, whereas the levels of MDA, TNF-α, and CRP and activities of IL-8 and IL-6 decreased in licochalcone B-treated groups. The infarct size and cell apoptosis in hearts from licochalcone B-treated group were lower than those in hearts from the I/R control group. Therefore, the cardioprotective effects of licochalcone B may be attributed to its antioxidant, antiapoptotic, and anti-inflammatory activities.

Abstract 102: Acute Mechanical Unloading of the Left Ventricle Promotes Cardioprotective Signaling and Limits Myocardial Infarct Size

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Navin K Kapur ◽  
Vikram Paruchuri ◽  
Xiaoying Qiao ◽  
Kevin Morine ◽  
Wajih Syed ◽  
...  
Keyword(s):  
Infarct Size ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Stroke Work ◽  
Coronary Reperfusion ◽  
Group 2 ◽  
The Impact ◽  
Group 1

Management of an acute myocardial infarction (AMI) focuses on restoring oxygen supply to limit myocardial damage, however ischemia-reperfusion injury (IRI) remains a major determinant of mortality in AMI. No studies have targeted initially reducing left ventricular stroke work (LVSW) to limit IRI in AMI. The Impella CP axial-flow pump reduces LVSW. We tested the hypothesis that first reducing myocardial work and delaying coronary reperfusion reduces infarct size by activating cardioprotective signaling pathways. Methods: AMI was induced by occlusion of the left anterior descending artery (LAD) via angioplasty for 90 minutes in 50kg male Yorkshire swine (n=5/group). In Group 1, the LAD was reperfused for 120 minutes. In Group 2, after 90 minutes of ischemia the Impella CP device was activated and the LAD left occluded for an additional 60 minutes (150 minutes of LAD occlusion total), followed by 120 minutes of reperfusion. The Impella CP was active throughout reperfusion. Western blot analysis quantified myocardial kinase activity. Results: Compared to Group 1, Group 2 had a reduced LVSW, LV end-diastolic volume and end-diastolic pressure after reperfusion [Fig A]. Group 2 showed increased myocardial phosphorylation of cardioprotective kinases: AKT, ERK, GSK3β and STAT-3 [Fig B]. Compared to Group 1, the percent myocardial infarct size normalized to the area at risk (AAR) was reduced in Group 2 (73+13% vs 42+15%, p=0.02). Conclusion: We report the potential benefit of primarily unloading the heart and delaying coronary reperfusion to salvage myocardium in AMI. This is the first report to examine the impact of the Impella CP on cardioprotective signaling in the heart.

Abstract 17348: Necrostatin 7 Limits Myocardial Infarct Size and Reduces Cardiac Remodeling After Permanent Coronary Occlusion in Rats

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yuri Dmitriev ◽  
Sarkis Minasian ◽  
Anna Dracheva ◽  
Andrey Karpov ◽  
Svetlana Chefu ◽  
...  
Keyword(s):  
Infarct Size ◽  
Rat Model ◽  
Coronary Occlusion ◽  
Ventricular Remodeling ◽  
Ischemia Reperfusion Injury ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Morphological Characteristics ◽  
Left Ventricular ◽  
Myocardial Infarct Size

Background: Reduction of irreversible myocardial ischemia-reperfusion injury (IRI) remains important. One of the promising strategies aimed at myocardial IRI alleviation is modulation of programmed cell death (PCD) pathways. PCD mode displaying morphological characteristics of necrosis, and amenable to pharmacological manipulation is referred to as necroptosis. Necroptosis inhibitor necrostatin-1 has been shown to exert cardio- and neuroprotective effects. In the present work, the effect of necrostatin-7 (Nec-7) on myocardial injury in the rat model of permanent coronary occlusion was studied. Methods: Male Wistar rats (n = 19) were anesthetized with pentobarbital. The animals were subjected to permanent coronary occlusion (PCO) and intraperitoneal (i.p.) Nec-7 administration 1 h prior to PCO at a dose of 14.5 mg/kg in dimethyl sulfoxide (DMSO) or DMSO alone at a dose of 3.1 g/kg. Control rats were treated with saline. Three weeks after PCO, serum levels of NT-proBNP were measured, and histological outcomes were assessed. The infarct size (IS, %) and infarct length (IL, mm) were analyzed morphometrically. Results: DMSO caused significant reduction in serum NT-proBNP level vs. Control (0.3 ± 0.19 vs. 0.5 ± 0.22 ng/ml, p = 0.001), while Nec-7 further decreased NT-proBNP level in comparison with DMSO (0.2 ± 0.14 ng/ml, p = 0.008 vs. DMSO). Compared with Control, DMSO reduced adverse left ventricular remodeling, as evidenced by reduction in IS (16.0 ± 2.92 and 12.9 ± 1.72%, p = 0.015) and IL (6.2 ± 0.89 and 3.8 ± 0.35 mm, p = 0.008). Nec-7 treatment resulted in additional reduction of both IS and IL vs. DMSO group (9.0 ± 4.91 % and 2.9 ± 1.62 mm, respectively; p = 0.013 and p = 0.011 vs. DMSO, respectively). Conclusion: Nec-7 has cardioprotective properties, reducing myocardial wall stress and myocardial remodeling in the rat model of myocardial infarction.

Remote preconditioning reduces ischemic injury in the explanted heart by a KATP channel-dependent mechanism

2005 ◽  
Vol 288 (3) ◽  
pp. H1252-H1256 ◽  
Author(s):  
Steen B. Kristiansen ◽  
Ole Henning ◽  
Rajesh K. Kharbanda ◽  
Jens Erik Nielsen-Kudsk ◽  
Michael Rahbek Schmidt ◽  
...  
Keyword(s):  
Infarct Size ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Limb Ischemia ◽  
Underlying Mechanism ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Remote Preconditioning ◽  
Langendorff Preparation ◽  
Explanted Heart

Local and remote ischemic preconditioning (IPC) reduce ischemia-reperfusion (I/R) injury and preserve cardiac function. In this study, we tested the hypothesis that remote preconditioning is memorized by the explanted heart and yields protection from subsequent I/R injury and that the underlying mechanism involves sarcolemmal and mitochondrial ATP-sensitive K+ (KATP) channels. Male Wistar rats (300–350 g) were randomized to a control ( n = 10), a remote IPC ( n = 10), and a local IPC group ( n = 10). Remote IPC was induced by four cycles of 5 min of limb ischemia, followed by 5 min of reperfusion. Local IPC was induced by four cycles of 2 min of regional myocardial ischemia, followed by 3 min of reperfusion. The heart was excised within 5 min after the final cycle of preconditioning, mounted in a perfused Langendorff preparation for 40 min of stabilization, and subjected to 45 min of sustained ischemia by occluding the left coronary artery and 120 min of reperfusion. I/R injury was assessed as infarct size by triphenyltetrazolium staining. The influence of sarcolemmal and mitochondrial KATP channels on remote preconditioning was assessed by the addition of glibenclamide (10 μM, a nonselective KATP blocker), 5-hydroxydecanoic acid (5-HD; 100 μM, a mitochondrial KATP blocker), and HMR-1098 (30 μM, a sarcolemmal KATP blocker) to the Langendorff preparation before I/R. The role of mitochondrial KATP channels as an effector mechanism for memorizing remote preconditioning was further studied by the effect of the specific mitochondrial KATP activator diaxozide (10 mg/kg) on myocardial infarct size. Remote preconditioning reduced I/R injury in the explanted heart (0.17 ± 0.03 vs. 0.39 ± 0.05, P < 0.05) and improved left ventricular function during reperfusion compared with control ( P < 0.05). Similar effects were obtained with diazoxide. Remote preconditioning was abolished by the addition of 5-HD and glibenclamide but not by HMR-1098. In conclusion, the protective effect of remote preconditioning is memorized in the explanted heart by a mechanism that involves mitochondrial KATP channels.

Isoflurane Preconditions Myocardium Against Infarction via  Activation of Inhibitory Guanine Nucleotide Binding Proteins

2000 ◽  
Vol 92 (5) ◽  
pp. 1400-1407 ◽  
Author(s):  
Wolfgang G. Toller ◽  
Judy R. Kersten ◽  
Eric R. Gross ◽  
Paul S. Pagel ◽  
David C. Warltier
Keyword(s):  
Infarct Size ◽  
Pertussis Toxin ◽  
Myocardial Infarct ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Area At Risk ◽  
Rate Of Increase ◽  
Gi Protein

Background Isoflurane-induced myocardial protection during ischemia is mediated by adenosine triphosphate-regulated potassium (KATP) channels; however, the intracellular signal transduction cascade responsible for this process has been incompletely evaluated. The authors tested the hypothesis that isoflurane reduces myocardial infarct size through a Gi protein-mediated process. Methods Forty-eight hours after pretreatment with vehicle (0.9% saline) or the Gi protein inhibitor pertussis toxin (10 microg/kg intravenously), barbiturate-anesthetized dogs (n = 43) were instrumented for measurement of aortic and left ventricular pressures and maximum rate of increase of left ventricular pressure. All dogs were subjected to a 60-min left anterior descending coronary artery occlusion followed by 3-h reperfusion. In four separate groups, vehicle- or pertussis toxin-pretreated dogs were studied with or without administration of 1 minimum alveolar concentration isoflurane. In two additional groups, dogs received the direct KATP channel agonist nicorandil (100 microg/kg bolus and 10 microg x kg-1 x min-1 intravenous infusion) in the presence or absence of pertussis toxin pretreatment. Myocardial perfusion and infarct size were measured with radioactive microspheres and triphenyltetrazolium staining, respectively. Results Isoflurane significantly (P &lt; 0.05) decreased infarct size to 7 +/- 2% of the area at risk compared with control experiments (26 +/- 2%). Pertussis toxin pretreatment alone had no effects on myocardial infarct size (31 +/- 4%) but blocked the beneficial effects of isoflurane (21 +/- 3%). Nicorandil decreased infarct size (11 +/- 2%), but, in contrast to isoflurane, this effect was independent of pertussis toxin pretreatment (11 +/- 1%). Conclusion Isoflurane reduces myocardial infarct size by a Gi protein-mediated mechanism in vivo.

scholarly journals Cardioprotective Effect of the Aqueous Extract of Lavender Flower against Myocardial Ischemia/Reperfusion Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Dong Wang ◽  
Xin Guo ◽  
Mingjie Zhou ◽  
Jichun Han ◽  
Bo Han ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Aqueous Extract ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Myocardial Oxidative Stress ◽  
Myocardial Ischemia Reperfusion

This study was conducted to evaluate the cardioprotective property of the aqueous extract of lavender flower (LFAE). The myocardial ischemia/reperfusion (I/R) injury of rat was prepared by Langendorff retrograde perfusion technology. The heart was preperfused with K-H solution containing LFAE for 10 min before 20 minutes global ischemia, and then the reperfusion with K-H solution was conducted for 45 min. The left ventricular developed pressure (LVDP) and the maximum up/downrate of left ventricular pressure (±dp/dtmax) were recorded by physiological recorder as the myocardial function and the myocardial infarct size was detected by TTC staining. Lactate dehydrogenase (LDH) and creatine kinase (CK) activities in the effluent were measured to determine the myocardial injury degree. The superoxide anion dismutase (SOD) and malondialdehyde (MDA) in myocardial tissue were detected to determine the oxidative stress degree. The results showed that the pretreatment with LFAE significantly decreased the myocardial infarct size and also decreased the LDH, CK activities, and MDA level, while it increased the LVDP, ±dp/dtmax, SOD activities, and the coronary artery flow. Our findings indicated that LFAE could provide protection for heart against the I/R injury which may be related to the improvement of myocardial oxidative stress states.

Mediating δ-opioid-initiated heart protection via the β2-adrenergic receptor: role of the intrinsic cardiac adrenergic cell

2007 ◽  
Vol 293 (1) ◽  
pp. H376-H384 ◽  
Author(s):  
Ming-He Huang ◽  
Hui-Qun Wang ◽  
William R. Roeske ◽  
Yochai Birnbaum ◽  
Yewen Wu ◽  
...  
Keyword(s):  
Infarct Size ◽  
Adrenergic Receptor ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Similar Degree ◽  
Myocardial Infarct Size ◽  
Dependent Manner ◽  
Opioid Agonist

Stimulation of cardiac β2-adrenergic receptor (β2-AR) or δ-opioid receptor (DOR) exerts a similar degree of cardioprotection against myocardial ischemia in experimental models. We hypothesized that δ-opioid-initiated cardioprotection is mediated by the intrinsic cardiac adrenergic (ICA) cell via enhanced epinephrine release. Using immunohistochemical and in situ hybridization methods, we detected in situ tyrosine hydroxylase (TH) mRNA and TH immunoreactivity that was colocalized with DOR immunoreactivity in ICA cells in human and rat hearts. Western blot analysis detected DOR protein in ICA cells isolated from rat ventricular myocytes. The physiology of DOR expression was examined by determining changes of cytosolic Ca2+ concentration ([Ca2+]i) transients in isolated rat ICA cells using fluorescence spectrophotometry. Exposing the selective δ-opioid agonist d-[Pen2,5]enkephalin (DPDPE) to ICA cells increased [Ca2+]i transients in a concentration-dependent manner. Such an effect was abolished by the Ca2+ channel blocker nifedipine. HPLC-electrochemical detection demonstrated a 2.4-fold increase in epinephrine release from ICA cells following DPDPE application. The significance of the ICA cell and its epinephrine release in δ-opioid-initiated cardioprotection was demonstrated in the rat myocardial infarction model and ICA cell-ventricular myocyte coculture. DPDPE administered before coronary artery occlusion or simulated ischemia-reperfusion reduced left ventricular infarct size by 54 ± 15% or myocyte death by 26 ± 4%, respectively. β2-AR blockade markedly attenuated δ-opioid-initiated infarct size-limiting effect and abolished δ-opioid-initiated myocyte survival protection in rat ICA cell-myocyte coculture. Furthermore, δ-opioid agonist exerted no myocyte survival protection in the absence of cocultured ICA cells during ischemia-reperfusion. We conclude that δ-opioid-initiated myocardial infarct size reduction is primarily mediated via endogenous epinephrine/β2-AR signaling pathway as a result of ICA cell activation.

scholarly journals Phosphatidylserine Supplementation as a Novel Strategy for Reducing Myocardial Infarct Size and Preventing Adverse Left Ventricular Remodeling

2021 ◽  
Vol 22 (9) ◽  
pp. 4401
Author(s):  
David Schumacher ◽  
Adelina Curaj ◽  
Mareike Staudt ◽  
Franziska Cordes ◽  
Andreea R. Dumitraşcu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Ventricular Remodeling ◽  
Heart Function ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Novel Strategy

Phosphatidylserines are known to sustain skeletal muscle activity during intense activity or hypoxic conditions, as well as preserve neurocognitive function in older patients. Our previous studies pointed out a potential cardioprotective role of phosphatidylserine in heart ischemia. Therefore, we investigated the effects of phosphatidylserine oral supplementation in a mouse model of acute myocardial infarction (AMI). We found out that phosphatidylserine increases, significantly, the cardiomyocyte survival by 50% in an acute model of myocardial ischemia-reperfusion. Similar, phosphatidylserine reduced significantly the infarcted size by 30% and improved heart function by 25% in a chronic model of AMI. The main responsible mechanism seems to be up-regulation of protein kinase C epsilon (PKC-ε), the main player of cardio-protection during pre-conditioning. Interestingly, if the phosphatidylserine supplementation is started before induction of AMI, but not after, it selectively inhibits neutrophil’s activation, such as Interleukin 1 beta (IL-1β) expression, without affecting the healing and fibrosis. Thus, phosphatidylserine supplementation may represent a simple way to activate a pre-conditioning mechanism and may be a promising novel strategy to reduce infarct size following AMI and to prevent myocardial injury during myocardial infarction or cardiac surgery. Due to the minimal adverse effects, further investigation in large animals or in human are soon possible to establish the exact role of phosphatidylserine in cardiac diseases.

scholarly journals ω-3 Polyunsaturated Fatty Acid Postconditioning Protects the Isolated Perfused Rat Heart from Ischemia-Reperfusion Injury

2018 ◽  
Vol 8 (3) ◽  
pp. 173-182 ◽  
Author(s):  
Fu-wei Zhang ◽  
Jian Tong ◽  
Yu-sheng Yan ◽  
Qun-qing Chen ◽  
Xiao-ping Zhao
Keyword(s):  
Infarct Size ◽  
Rat Heart ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Mitochondrial Damage ◽  
Myocardial Infarct Size ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart ◽  
Cardioprotective Effects

Aims: This study aimed to evaluate the cardioprotective effects of ω-3 polyunsaturated fatty acids (PUFAs) postconditioning against ischemia-reperfusion (I/R) injury. Methods: Sixty Sprague-Dawley rats were randomly divided into 4 groups (n = 15 for each) and used to generate the Langendorff isolated perfused rat heart model. The sham group received a continuous perfusion of 150 min. The remaining three I/R-treated groups sequentially received a 30-min perfusion, a 30-min cardioplegia, and a 90-min reperfusion. The I/R-ischemic preconditioning (IP) group additionally received three cycles of 20-s reperfusion and 20-s coronary reocclusion preceded the 90 min of reperfusion. The I/R-ω group were perfused with ω-3 PUFAs for 15 min before the 90 min of reperfusion. The myocardial infarct size, the degree of mitochondrial damage, the antioxidant capacity of the myocardium, and the cardiac functions during reperfusion were compared among groups. Results: Compared with the I/R group, the I/R-ω group had significantly reduced myocardial infarct size, reduced levels of lactate dehydrogenase and malondialdehyde, elevated superoxide dismutase level, and elevated rising (+dp/dtmax) and descending (–dp/dtmax) rate of left ventricular pressure. The I/R-ω group had a significantly lower rate of mitochondrial damage in myocardial tissue compared with the I/R and I/R-IP groups. Conclusion: ω-3 PUFA postconditioning possesses good cardioprotective effects and may be developed into a therapeutic strategy for myocardial I/R injury.

scholarly journals New Interventional Therapies beyond Stenting to Treat ST-Segment Elevation Acute Myocardial Infarction

2021 ◽  
Vol 8 (9) ◽  
pp. 100
Author(s):  
Pablo Vidal-Calés ◽  
Pedro L. Cepas-Guillén ◽  
Salvatore Brugaletta ◽  
Manel Sabaté
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Ischemia Reperfusion Injury ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
St Segment Elevation ◽  
St Segment

Myocardial infarction remains the principal cause of death in Europe. In patients with ST-segment-elevation myocardial infarction (STEMI), a promptly revascularization with primary percutaneous intervention (PCI) has transformed prognosis in the last decades. However, despite increasing successful PCI procedures, mortality has remained unchanged in recent years. Also, due to an unsatisfactory reperfusion, some patients have significant myocardial damage and suffer left ventricular adverse remodeling with reduced function—all that resulting in the onset of heart failure with all its inherent clinical and socioeconomic burden. As a consequence of longer ischemic times, distal thrombotic embolization, ischemia-reperfusion injury and microvascular dysfunction, the resultant myocardial infarct size is the major prognostic determinant in STEMI patients. The improved understanding of all the pathophysiology underlying these events has derived to the development of several novel therapies aiming to reduce infarct size and to improve clinical outcomes in these patients. In this article, based on the mechanisms involved in myocardial infarction prognosis, we review the new interventional strategies beyond stenting that may solve the suboptimal results that STEMI patients still experience.

Endothelin A and B receptor antagonist bosentan reduces postischemic myocardial injury in the rat: critical timing of administration

2005 ◽  
Vol 83 (3) ◽  
pp. 259-266 ◽  
Author(s):  
Zhengyuan Xia ◽  
Kuo-Hsing Kuo ◽  
John H McNeill ◽  
David M Ansley
Keyword(s):  
Myocardial Ischemia ◽  
Myocardial Injury ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Control Treatment ◽  
Control Group ◽  
Myocardial Infarct Size ◽  
Early Reperfusion ◽  
Endothelin 1

The purpose of this study was to investigate the effects of bosentan, a mixed endothelin receptor A and B subtype antagonist, on myocardial ischemia-reperfusion injury and to explore the influence of the timing of bosentan administration on its cardioprotective effects. Adult rat hearts were perfused by the Langendorff technique with Krebs-Henseleit solution (KH) at a constant flow rate at 10 mL/min. Global myocardial ischemia was induced by stopping KH perfusion for 40 min, and this was followed by 60 min of reperfusion. Hearts were randomized to 1 of 3 experimental groups (n = 7 each): untreated control; treatment with bosentan 1 µmol/L 10 min prior to, during 40 min global ischemia, and for 15 min of reperfusion (BOS); or treatment with bosentan 1 µmol/L after 15 min of reperfusion (BOS-R). We observed that BOS-R, but not the BOS treatment regimen, significantly reduced the release of cardiac-specific creatine kinase and postischemic myocardial infarct size (P < 0.05 vs. control) without affecting myocardial contractility. Left ventricular developed pressure in the BOS group was significantly (P < 0.01) lower than that in the control group throughout reperfusion. It is concluded that pharmacologically delayed antagonism of endothelin-1 during reperfusion attenuates postischemic myocardial injury. Endothelin-1 antagonist application during early reperfusion may exacerbate postischemic myocardial dysfunction.Key words: bosentan, ischemia, heart, rat, endothelin-1 antagonist.

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