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The Egyptian Journal of Neurology, Psychiatry and Neurosurgery
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Clinical and prognostic significance of baseline microRNA 223 in acute ischemic stroke

The Egyptian Journal of Neurology, Psychiatry and Neurosurgery volume 60, Article number: 46 (2024) Cite this article

Abstract

Background

Acute ischemic stroke (AIS) is the second leading cause of disability and death worldwide. Micro-RNA (miRNA)-223 was first identified as a regulator of hematopoietic lineage differentiation. Later, its diverse roles were discovered in a wide spectrum of pathological conditions. The present study aimed to assess the clinical and prognostic significance of miR-223 in patients with acute ischemic stroke (AIS). The study included 93 patients with AIS diagnosed on the basis of clinical and radiological findings. In addition, there were 50 healthy subjects who served as controls. Patients were classified into two categories: Those with favorable functional outcome (modified Rankin Scale (mRS): 0–2) and others with unfavorable functional outcome (mRS: 3–6) at 6 months post-stroke.

Results

The present prospective longitudinal study included 93 patients with AIS. They included 60 males (64.5%) and 33 females (35.5%) with an age of 64.5 ± 12.4 years. At the end of 6-month follow up, 44 patients (47.3%) had favorable outcome while the remainder 49 patients (52.7%) had unfavorable outcome. Patients with favorable outcome had significantly lower baseline miR-223 levels [median (IQR): 4.4 (2.0–6.3) versus 8.4 (4.5–14.9), p < 0.001], lower HbA1c levels (5.6 ± 1.0 versus 6.2 ± 1.2, p = 0.006) and lower C-reactive protein (CRP) levels [median (IQR): 8.9 (5.1–26.7) versus 15.2 (6.2–39.3) mg/dL, p = 0.02]. Multivariate binary logistic regression analysis recognized high baseline miR-223 [OR (95% CI) 1.13 (1.06–1.24), p = 0.011], infarct size [OR (95% CI) 2.58 (1.66–4.77), p = 0.001] and National Institutes of Health Stroke Scale (NIHSS) [OR (95% CI) 2.11 (1.74–3.09), p = 0.004] as significant predictors of unfavorable outcome in the studied patients.

Conclusions

Elevated baseline miR-223 levels are associated with high NIHSS and larger infarct size at baseline and can effectively predict patients’ outcome at 6-months post-stroke.

Introduction

Acute ischemic stroke (AIS) is the second leading cause of disability and death worldwide with the maximal disease burden noted in low and middle-income countries. Unfortunately, less than 5.0% of patients receive intravenous thrombolysis therapy within the effective therapeutic window [1].

Conventionally, AIS is diagnosed on the basis of imaging data derived from a variety of CT or MRI techniques. However, these modalities have many logistic and diagnostic restrictions particularly in the low-resource setting. Identification of readily available diagnostic tools is expected to improve clinical outcome [2]. In this context, many blood-based biomarkers were suggested to have diagnostic and prognostic value in AIS. The most frequently studied markers are brain natriuretic peptide, S100 calcium-binding protein B [3] and copeptin [4].

MicroRNAs (miRNAs) are small (18–22 nucleotides) non-coding RNAs. The discovery of microRNAs in 1990s revolutionary changed the paradigm of post-transcriptional gene regulation in almost all pathological conditions [5]. In AIS, microRNAs were reported to play diverse pathogenic roles. These include dysregulated lipid hemostasis, inflammatory cells recruitment within the vascular wall, control of endothelial cells behavior, proliferation and migration of vascular smooth muscle cells and regulation of atherosclerotic plaque stability [6, 7]. Moreover, microRNAs are involved in the pathogenesis of multiple AIS risk factors including diabetes mellitus, hypertension and dyslipidemia through disruption of multiple metabolic, immunologic and apoptotic pathways [8].

miRNA-223 was first identified as a regulator of hematopoietic lineage differentiation. Later, its diverse roles were discovered in a wide spectrum of pathological conditions including infectious diseases [9], cardiovascular disorders [10], inflammatory disorders [11, 12], liver and kidney diseases [13, 14], respiratory diseases [15] and miscellaneous malignant conditions [16, 17]. In the central nervous system, miRNA-223 has been linked to ischemic neural injury through targeting type 1 insulin-like growth factor receptor (IGF1R) [18]. The present study aimed to assess the clinical and prognostic significance of miR-223 in patients with AIS.

Methods

The present prospective longitudinal study protocol was approved by the local ethical committee and all patients and/or their legal guardians provided informed consent before participating in the study. The study included 93 patients with AIS diagnosed on the basis of clinical and radiological findings. Patients were excluded if they had previous episodes of AIS, associated neoplasms, active infections or immunological disorders. In addition, there were 50 age and sex-matched healthy controls.

All patients were submitted to careful history taking, sophisticated general and neurological examination, standard laboratory assessment and radiological examination using computed tomography and/or magnetic resonance imaging. At presentation, patients were assessed using the National Institutes of Health Stroke Scale (NIHSS) [19]. Functional outcome was assessed using the modified Rankin Scale (mRS) at stroke unit discharge and at 6 months after stroke. Patients were classified into two categories: Those with favorable functional outcome (modified Rankin Scale (mRS): 0–2) and others with unfavorable functional outcome (mRS: 3–6) [20]. Stroke etiology was classified using the Trial of Org 10,172 in Acute Stroke Treatment (TOAST) criteria as large-artery atherosclerosis, cardioembolism, small-vessel occlusion, stroke of other determined cause and stroke of undetermined cause [21]. Lesions sizes were ranked into (1) small lesion with a volume < 10 ml; (2) medium lesion of 10–100 ml; and (3) large lesion with a volume > 100 ml [22].

RNAs were extracted from serum using Qiagen (Valencia, CA) kits. For real-time qPCR, a MiScript SYBR Green PCR kit (Qiagen, USA) and primer sets for miR223 and mir U6 as an internal control were used (Qiagen, USA). The expression levels of microRNA-223 were identified using the Ct method.

Data obtained from the present study were expressed as mean and standard deviation (SD), median and interquartile range (IQR) or number and percent. Variables were compared using t test, Mann–Whitney U test or chi-square test as appropriate. Binary logistic regression analysis was used to identify predictors of unfavorable outcome. Receptor operator characteristic (ROC) curve analysis was used to assess the diagnostic performance of the investigated marker. All statistical operations were processed using SPSS 27 with p value less than 0.05 considered statistically significant.

Results

The present study included 93 patients with AIS. They included 60 males (64.5%) and 33 females (35.5%) with an age of 64.5 ± 12.4 years. In addition, there were 50 age and sex-matched healthy controls. Patients had significantly higher circulating miR-223 levels as compared to controls [median (IQR):5.99 [3.02–15.82] versus 1.15 (0.97–1.38) p < 0.001]. At the end of 6-month follow up, 44 patients (47.3%) had favorable outcome while the remainder 49 patients (52.7%) had unfavorable outcome. Comparison between patients with favorable and unfavorable outcomes revealed that the former group are significantly younger (61.7 ± 11.0 versus 70.5 ± 13.3 years, p < 0.001) with significantly higher frequency of females (47.7% versus 24.5%, p = 0.019). Also, it was found that patients with favorable outcome had significantly lower frequency of large-sized infarcts (9.1% versus 34.7%, p = 0.002). In addition, it was found that patients with favorable outcome had significantly lower HbA1c levels (5.6 ± 1.0% versus 6.2 ± 1.2, p = 0.006), lower CRP levels [median (IQR): 8.9 mg/dL (5.1–26.7) versus 15.2 (6.2–39.3), p = 0.02] and lower miR-223 levels [median (IQR): 4.4 (2.0–6.3) versus 8.4 (4.5–14.9), p < 0.001] (Table 1).

Table 1 Clinical and laboratory findings in the studied patients in relation to discharge outcome (n = 93)
Full size table

Spearman’s correlation analysis identified significant correlation between miR-223 levels and infarct size (r = 0.35, p < 0.001), NIHSS (r = 0.29, p = 0.004), cholesterol levels (r = 0.23, p = 0.03), HDL (r = -0.33, p = 0.001) and CRP levels (r = 0.27, p = 0.001) in all patients (Table 2). Multivariate binary logistic regression analysis recognized infarct size [OR (95% CI): 2.58 (1.66–4.77), p = 0.001], NIHSS [OR (95% CI): 2.11 (1.74–3.09), p = 0.004] and miR-223 [OR (95% CI): 1.13 (1.06–1.24), p = 0.011] as significant predictors of unfavorable outcome in the studied patients (Table 3). ROC curve analysis showed good performance of miR-223 in distinguishing patients with favorable outcome from their counterparts with unfavorable outcome [Cut-off: 6.56, AUC: 0.713, sensitivity: 71.4%, specificity: 79.5%] (Fig. 1).

Table 2 Correlation between baseline mir-223 levels and clinical and laboratory data
Full size table
Table 3 Predictors of unfavorable outcome at 6 months in the studied patients
Full size table
Fig. 1
figure 1

ROC curve for miR-223 and outcome

Full size image

Discussion

The present study found that circulating baseline miR-223 levels are significantly increased in AIS patients as compared to healthy controls. Moreover, the study identified a relation between elevated miR-223 levels and NIHSS scores, stroke volume and unfavorable outcome at 6 months. These findings with consistent with the study of Wang and colleagues [23] who noted that miR-223 levels within 72 h after stroke are elevated in AIS patients in comparison to controls. The study of Chen and colleagues [24] additionally identified an association between elevated miR-223 levels and poor short-term outcomes. Likewise, it was found that diabetic patients with AIS had significantly higher miR-223 levels in plasma [25] and peripheral blood mononuclear cells [26] when compared with their counterparts without stroke. Results of the present study are also supported by the experimental work of Voelz and colleagues [27] who noted increased cortical and serum expression of miR-223-3p after transient middle cerebral artery occlusion in rats. In contradiction with these results, the experimental work of Harraz and colleagues [28] suggested that miR-223 may play a neuroprotective role in ischemic brain injury through downregulation of glutamate receptor subunits (GluR2) with subsequent inhibition of N-methyl-d-aspartate (NMDA)-induced calcium influx into hippocampal neurons which aggravates neuronal death after ischemia.

The effects exerted by overexpression of miR-223 in AIS patients can be explained by multiple mechanisms. It was noted that platelets-induced miR-223 is responsible for enhancement of vascular endothelial cell apoptosis in stroke patients through targeting insulin-like growth factor 1 receptor [29]. In another experimental study on ischemic brain extract, it was reported that miR-223 overexpression resulted in suppression of IκB kinase alpha which enhances cellular response to inflammation [30]. Moreover, it was found that miR-223 inhibited proliferation of cortical neurons by inhibition of type 1 insulin-like growth factor receptor expression [18].

Results of the present study may have useful therapeutic implications. In one study, it was shown that use of anti-miR-223-5p was associated with better expression the K + -dependent Na + /Ca2 + exchanger and NCKX2 known for its neuroprotective functions [31]. It was also demonstrated that electropuncture could reduce experimental ischemic brain injury through inhibition of the miR-223/Nod-like receptor Pyrin Domain Containing 3 (NLRP3) pathway [32].

In another experimental work using in-vitro cell model and middle cerebral artery occlusion in-vivo rat model, it was found that reduced ribosomal protein L34-antisense RNA1 (RPL34-AS1) was associated with more brain damage in IS model. Its neuroprotective effects are reversed by miR-223-3p and it is thought it can be used as a therapeutic target in ischemic stroke via regulation of the 223-3p/insulin-like growth factor 1 receptor axis [33].

Conclusions

In conclusion, higher miR-223 levels are associated with high NIHSS and infarct size at baseline and can effectively predict patients’ outcome at 6-months post-stroke. However, these conclusions may be limited by the relatively small sample size and the short duration of follow up.

Availability of data and materials

The datasets used and analyzed during the current study are available from the corresponding author upon reasonable request.

Abbreviations

AF:

Atrial fibrillation

AIS:

Acute ischemic stroke

BMI:

Body mass index

CRP:

C-reactive protein

FBG:

Fasting blood glucose

Hb:

Hemoglobin

HDL:

High-density lipoprotein

IGF1R:

Insulin-like growth factor receptor

IQR:

Interquartile range

LDL:

Low-density lipoprotein

mRS:

Modified Rankin Scale

miRNAs:

MicroRNAs

NIHSS:

National Institutes of Health Stroke Scale

TIA:

Transient ischemic attack

TOAST:

Trial Org 10,172 classification in Acute Stroke Treatment

WBCs:

White blood cells

References

  1. Saini V, Guada L, Yavagal DR. Global epidemiology of stroke and access to acute ischemic stroke interventions. Neurology. 2021;97(20 Suppl 2):S6–16.

    PubMed  Google Scholar 

  2. Patil S, Rossi R, Jabrah D, Doyle K. Detection, diagnosis and treatment of acute ischemic stroke: current and future perspectives. Front Med Technol. 2022;24(4): 748949.

    Article  Google Scholar 

  3. Monbailliu T, Goossens J, Hachimi-Idrissi S. Blood protein biomarkers as diagnostic tool for ischemic stroke: a systematic review. Biomark Med. 2017;11(6):503–12.

    Article  CAS  PubMed  Google Scholar 

  4. Blek N, Szwed P, Putowska P, Nowicka A, Drela WL, Gasecka A, et al. The diagnostic and prognostic value of copeptin in patients with acute ischemic stroke and transient ischemic attack: a systematic review and meta-analysis. Cardiol J. 2022;29(4):610–8.

    Article  PubMed  PubMed Central  Google Scholar 

  5. Aziz F, Chakraborty A, Khan I, Monts J. Relevance of miR-223 as potential diagnostic and prognostic markers in cancer. Biology (Basel). 2022;11(2):249.

    CAS  PubMed  Google Scholar 

  6. Jiang Q, Li Y, Wu Q, Huang L, Xu J, Zeng Q. Pathogenic role of microRNAs in atherosclerotic ischemic stroke: implications for diagnosis and therapy. Genes Dis. 2021;9(3):682–96.

    Article  PubMed  PubMed Central  Google Scholar 

  7. Fullerton JL, Thomas JM, Gonzalez-Trueba L, Trivett C, van Kralingen JC, Allan SM, et al. Systematic review: association between circulating microRNA expression and stroke. J Cereb Blood Flow Metab. 2022;42(6):935–51.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Qian Y, Chopp M, Chen J. Emerging role of microRNAs in ischemic stroke with comorbidities. Exp Neurol. 2020;331: 113382. https://doi.org/10.1016/j.expneurol.2020.113382.

    Article  CAS  PubMed  Google Scholar 

  9. Haneklaus M, Gerlic M, O’Neill LA, Masters SL. miR-223: infection, inflammation and cancer. J Intern Med. 2013;274(3):215–26.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Taïbi F, Metzinger-Le Meuth V, Massy ZA, Metzinger L. miR-223: an inflammatory oncomiR enters the cardiovascular field. Biochim Biophys Acta. 2014;1842(7):1001–9.

    Article  PubMed  Google Scholar 

  11. Aziz F. The emerging role of miR-223 as novel potential diagnostic and therapeutic target for inflammatory disorders. Cell Immunol. 2016;303:1–6.

    Article  CAS  PubMed  Google Scholar 

  12. Yuan X, Berg N, Lee JW, Le TT, Neudecker V, Jing N. MicroRNA miR-223 as regulator of innate immunity. J Leukoc Biol. 2018;104(3):515–24.

    Article  CAS  PubMed  Google Scholar 

  13. Ye D, Zhang T, Lou G, Liu Y. Role of miR-223 in the pathophysiology of liver diseases. Exp Mol Med. 2018;50(9):1–12.

    Article  CAS  PubMed  Google Scholar 

  14. Metzinger-Le Meuth V, Metzinger L. miR-223 and other miRNA’s evaluation in chronic kidney disease: innovative biomarkers and therapeutic tools. Noncoding RNA Res. 2019;4(1):30–5.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Roffel MP, Bracke KR, Heijink IH, Maes T. miR-223: a key regulator in the innate immune response in asthma and COPD. Front Med (Lausanne). 2020;19(7):196.

    Article  Google Scholar 

  16. Zhou K, Feng X, Wang Y, Liu Y, Tian L, Zuo W, et al. miR-223 is repressed and correlates with inferior clinical features in mantle cell lymphoma through targeting SOX11. Exp Hematol. 2018;58:27-34.e1.

    Article  CAS  PubMed  Google Scholar 

  17. Favero A, Segatto I, Perin T, Belletti B. The many facets of miR-223 in cancer: oncosuppressor, oncogenic driver, therapeutic target, and biomarker of response. Wiley Interdiscip Rev RNA. 2021;12(6): e1659.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Feng SJ, Zhang XQ, Li JT, Dai XM, Zhao F. miRNA-223 regulates ischemic neuronal injury by targeting the type 1 insulin-like growth factor receptor (IGF1R). Folia Neuropathol. 2018;56(1):49–57.

    Article  PubMed  Google Scholar 

  19. NIH stroke scale. https://www.ninds.nih.gov/health-information/public-education/know-stroke/health-professionals/nih-stroke-scale. Accessed June 2022

  20. Isaksson E, Wester P, Laska AC, Näsman P, Lundström E. Validation of the simplified modified rankin scale questionnaire. Eur Neurol. 2020;83(5):493–9.

    Article  PubMed  Google Scholar 

  21. Adams HP Jr, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, et al. Classification of subtype of acute ischemic stroke definitions for use in a multicenter clinical trial. Stroke. 1993;24(1):35–41.

    Article  PubMed  Google Scholar 

  22. Katan M, Fluri F, Morgenthaler NG, Schuetz P, Zweifel C, Bingisser R, et al. Copeptin: a novel, independent prognostic marker in patients with ischemic stroke. Ann Neurol. 2009;66(6):799–808.

    Article  CAS  PubMed  Google Scholar 

  23. Wang Y, Zhang Y, Huang J, Chen X, Gu X, Wang Y, et al. Increase of circulating miR-223 and insulin-like growth factor-1 is associated with the pathogenesis of acute ischemic stroke in patients. BMC Neurol. 2014;8(14):77.

    Article  Google Scholar 

  24. Chen Y, Song Y, Huang J, Qu M, Zhang Y, Geng J, et al. Increased circulating exosomal miRNA-223 is associated with acute ischemic stroke. Front Neurol. 2017;27(8):57.

    Google Scholar 

  25. Yang S, Zhao J, Chen Y, Lei M. Biomarkers associated with ischemic stroke in diabetes mellitus patients. Cardiovasc Toxicol. 2016;16(3):213–22.

    Article  CAS  PubMed  Google Scholar 

  26. Long Y, Zhan Q, Yuan M, Duan X, Zhou J, Lu J, et al. The expression of microRNA-223 and FAM5C in cerebral infarction patients with diabetes mellitus. Cardiovasc Toxicol. 2017;17(1):42–8.

    Article  CAS  PubMed  Google Scholar 

  27. Voelz C, Ebrahimy N, Zhao W, Habib P, Zendedel A, Pufe T, Beyer C, Slowik A. Transient focal cerebral ischemia leads to miRNA alterations in different brain regions, blood serum, liver, and spleen. Int J Mol Sci. 2021;23(1):161. https://doi.org/10.3390/ijms23010161.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  28. Harraz MM, Eacker SM, Wang X, Dawson TM, Dawson VL. MicroRNA-223 is neuroprotective by targeting glutamate receptors. Proc Natl Acad Sci USA. 2012;109(46):18962–7.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  29. Pan Y, Liang H, Liu H, Li D, Chen X, Li L, et al. Platelet-secreted microRNA-223 promotes endothelial cell apoptosis induced by advanced glycation end products via targeting the insulin-like growth factor 1 receptor. J Immunol. 2014;192(1):437–46.

    Article  CAS  PubMed  Google Scholar 

  30. Shin JH, Park YM, Kim DH, Moon GJ, Bang OY, Ohn T, et al. Ischemic brain extract increases SDF-1 expression in astrocytes through the CXCR2/miR-223/miR-27b pathway. Biochim Biophys Acta. 2014;1839(9):826–36.

    Article  CAS  PubMed  Google Scholar 

  31. Cuomo O, Cepparulo P, Anzilotti S, Serani A, Sirabella R, Brancaccio P, et al. Anti-miR-223-5p ameliorates ischemic damage and improves neurological function by preventing NCKX2 downregulation after ischemia in rats. Mol Ther Nucleic Acids. 2019;6(18):1063–71.

    Article  Google Scholar 

  32. Sha R, Zhang B, Han X, Peng J, Zheng C, Zhang F, et al. Electroacupuncture alleviates ischemic brain injury by inhibiting the miR-223/NLRP3 pathway. Med Sci Monit. 2019;25(25):4723–33.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  33. Wei XY, Zhang TQ, Suo R, Qu YY, Chen Y, Zhu YL. Long non-coding RNA RPL34-AS1 ameliorates oxygen-glucose deprivation-induced neuronal injury via modulating miR-223-3p/IGF1R axis. Hum Cell. 2022;35(6):1785–96.

    Article  CAS  PubMed  Google Scholar 

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Acknowledgements

We thank all patients and their family members.

Funding

No funding was received for this study.

Author information

Authors and Affiliations

  1. Biochemistry Department, Faculty of Medicine (for Girls), Al-Azhar University, Cairo, Egypt

    Rasha Elsayed Mohamed Abd El Aziz, Wafaa Abdelaziz Emam & Amena Rezk Mohammed

  2. Internal Medicine Department, Faculty of Medicine (for Girls), Al-Azhar University, Cairo, Egypt

    Fatma M. El-senosy & Sammar Ahmed Kasim

  3. Clinical Pathology Department, Faculty of Medicine (for Girls), Al-Azhar University, Cairo, Egypt

    Marwa A. A. Ramadan & Fatima G. Yehia

  4. Medical Microbiology and Immunology, Faculty of Medicine (for Girls), Al-Azhar University, Cairo, Egypt

    Sabah M. Alkhawagah

  5. Neurology Department, Faculty of Medicine (for Girls), Al-Azhar University, Cairo, Egypt

    Rasha Sobhy ElAttar

  6. Neurology Department, Military Medical Academy, Cairo, Egypt

    Ahmed Elsaid Elsayed

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  1. Rasha Elsayed Mohamed Abd El Aziz
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  2. Wafaa Abdelaziz Emam
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Contributions

Conceived and designed the experiments: REMA, WAE, FME, SAK, RSA, AEE enrolled the patients: FGY, MAAR Performed the experiments: SMA, ARM data management and analysis, FGY, MAAR: reagents/materials/analysis tools: FGY, MAAR:, prepared the manuscript: SMA, ARM, read and approve the manuscripts: REMA, WAE, FME, SAK, RSA, AEE. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Rasha Elsayed Mohamed Abd El Aziz.

Ethics declarations

Ethics approval and consent to participate

The study protocol was approved by the ethical committee of Al-Azhar University Faculty of Medicine on 29/8/2023. Informed written consent was obtained from all the patients enrolled in this study.

Informed consent

Written informed consent was obtained from all patients or their legal guardians before enrollment in the study.

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Not applicable.

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The authors declare that they have no competing interests.

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Aziz, R.E.M.A.E., Emam, W.A., El-senosy, F.M. et al. Clinical and prognostic significance of baseline microRNA 223 in acute ischemic stroke. Egypt J Neurol Psychiatry Neurosurg 60, 46 (2024). https://doi.org/10.1186/s41983-024-00823-x

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