ME Association Index of Published ME/CFS Research
The Index of Published ME/CFS Research has now been updated to take account of the research that has been published during the month of December 2018.
The Index is a useful way to locate and then read all relevant research on ME/CFS. It’s free to download and comes with an interactive contents table.
This is an A-Z list of all the most important ME/CFS research studies (and selected key documents and articles), listed by subject matter and author, with links to PubMed or to the Journal it was published in.
You can also find the index in the Research section of our website.
ME/CFS research abstracts from studies published in December 2018
1. Du Preez S, et al. (2018)
A systematic review of enteric dysbiosis in chronic fatigue syndrome/myalgic encephalomyelitis.
Systematic Reviews 7 (1): 241.
Background: Chronic fatigue syndrome or myalgic encephalomyelitis (CFS/ME) is an illness characterised by profound and pervasive fatigue in addition to a heterogeneous constellation of symptoms. The aetiology of this condition remains unknown; however, it has been previously suggested that enteric dysbiosis is implicated in the pathogenesis of CFS/ME. This review examines the evidence currently available for the presence of abnormal microbial ecology in CFS/ME in comparison to healthy controls, with one exception being probiotic-supplemented CFS/ME patients, and whether the composition of the microbiome plays a role in symptom causation.
Methods: EMBASE, Medline (via EBSCOhost), Pubmed and Scopus were systematically searched from 1994 to March 2018. All studies that investigated the gut microbiome composition of CFS/ME patients were initially included prior to the application of specific exclusion criteria. The association between these findings and patient-centred outcomes (fatigue, quality of life, gastrointestinal symptoms, psychological wellbeing) are also reported.
Results: Seven studies that met the inclusion criteria were included in the review. The microbiome composition of CFS/ME patients was compared with healthy controls, with the exception of one study that compared to probiotic-supplemented CFS/ME patients. Differences were reported in each study; however, only three were considered statistically significant, and the findings across all studies were inconsistent. The quality of the studies included in this review scored between poor (< 54%), fair (54-72%) and good (94-100%) using the Downs and Black checklist.
Conclusions: There is currently insufficient evidence for enteric dysbiosis playing a significant role in the pathomechanism of CFS/ME. Recommendations for future research in this field include the use of consistent criteria for the diagnosis of CFS/ME, reduction of confounding variables by controlling factors that influence microbiome composition prior to sample collection and including more severe cases of CFS/ME.
2. Franklin JD, et al. (2018)
Peak Oxygen Uptake in Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis: A Meta-Analysis
International Journal of Sports Medicine [Epub ahead of print].
To evaluate the magnitude of the difference in VO2peak between patients with Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis (CFS/ME) and apparently healthy controls, 7 databases (Cochrane, PubMed, PsycINFO, Web of Knowledge, Embase, Scopus, Medline) were searched for articles published up to March 2018.
Search terms included “chronic fatiguesyndrom*”AND (“peak” OR “maxim*” OR “max”) AND (“oxygen uptake” OR “oxygen consumption” OR “VO2peak” or “VO2max”. Eligibility criteria were adults>18 y with clinically diagnosed CFS/ME, with VO2peak measured in a maximal test and compared against an apparently healthy control group.
The methodological quality of included studies was assessed using a modified Systematic Appraisal of Quality for Observational Research critical appraisal framework. A random effects meta-analysis was conducted on 32 cross-sectional studies (effects).
Pooled mean VO2peak was 5.2 (95% CI: 3.8-6.6) ml.kg-1min-1 lower in CFS/ME patients vs. healthy controls. Between-study variability (Tau) was 3.4 (1.5-4.5) ml.kg-1min-1 indicating substantial heterogeneity. The 95% prediction interval was -1.9 to 12.2 ml.kg-1min-1. The probability that the effect in a future study would be>the minimum clinically important difference of 1.1 ml.kg-1min-1 (in favour of controls) was 0.88 – likely to be clinically relevant.
Synthesis of the available evidence indicates that CFS/ME patients have a substantially reduced VO2peak compared to controls.
3. Germain A, et al. (2018)
Prospective Biomarkers from Plasma Metabolomics of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Implicate Redox Imbalance in Disease Symptomatology
Metabolites 8 (4).
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a disease of enigmatic origin with no established cure. Its constellation of symptoms has silently ruined the lives of millions of people around the world. A plethora of hypotheses have been vainly investigated over the past few decades, so that the biological basis of this debilitating condition remains a mystery.
In this study, we investigate whether there is a disturbance in homeostasis of metabolic networks in the plasma of a female 32-patient cohort compared to 19 healthy female controls. Extensive analysis of the 832-metabolite dataset generated by Metabolon®, covering eight biological classes, generated important insight into metabolic disruptions that occur in ME/CFS.
We report on 14 metabolites with differences in abundance, allowing us to develop a theory of broad redox imbalance in ME/CFS patients, which is consistent with findings of prior work in the ME/CFS field. Moreover, exploration of enrichment analysis using www.MetaboAnalyst.ca provides information concerning similarities between metabolite disruptions in ME/CFS and those that occur in other diseases, while its biomarker analysis unit yielded prospective plasma biomarkers for ME/CFS.
This work contributes key elements to the development of ME/CFS diagnostics, a crucial step required for discovering a therapy for any disease of unknown origin.
4. Haig-Ferguson A, et al. (2018)
“It’s not one size fits all”; the use of videoconferencing for delivering therapy in a Specialist Paediatric Chronic Fatigue Service
Internet Interventions [Epub ahead of print].
Background: There are few specialist paediatric Chronic Fatigue Syndrome (CFS/ME) services in the UK. Therefore, the distance some families have to travel to reach these services can be a barrier to accessing evidence-based treatment. Videoconferencing technology such as Skype provides a means of delivering sessions remotely. This study aimed to explore the views of children and young people, their parents, and healthcare professionals of treatment delivered by videoconferencing in a specialist paediatric CFS/ME team.
Methods: To explore the experiences of the participants, a qualitative design was selected. Twelve young people (age 9–18), and 6 parents were interviewed about their experience of treatment sessions delivered via videoconferencing within a specialist CFS/ME service. A focus group explored the views of healthcare professionals (N = 9) from the service. Thematic analysis was used.
Results: Three themes were identified from the data: “Challenges and concerns”, “Benefits” and “Treatment provision”. Challenges and concerns that participants identified were; difficulties experienced with technology; a sense of a part of communication being lost with virtual connections; privacy issues with communicating online and feeling anxious on a screen.
Participants felt that benefits of videoconferencing were; improving access to the chronic fatigue service; convenience and flexibility of treatment provision; a sense of being more open online and being in the comfort of their own home. In terms of treatment provision participants talked about videoconferencing as a part of a hierarchy of communication; the function of videoconferencing within the context of the chronic fatigue service; additional preparation needed to utilise videoconferencing and an assumption that videoconferencing is “part of young people’s lives”.
Conclusions: Although the experience of sessions provided by videoconferencing was different to sessions attended in person, participants tended to be positive about videoconferencing as an alternative means of accessing treatment, despite some barriers. Videoconferencing could be an additional option within an individualised care plan, but should not be an alternative to face to face support.
5. Herrera S, et al. (2018)
Genome-epigenome interactions associated with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
Epigenetics 5: 1-17.
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex disease of unknown etiology. Multiple studies point to disruptions in immune functioning in ME/CFS patients as well as specific genetic polymorphisms and alterations of the DNA methylome in lymphocytes. However, potential interactions between DNA methylation and genetic background in relation to ME/CFS have not been examined.
In this study we explored this association by characterizing the epigenetic (~480 thousand CpG loci) and genetic (~4.3 million SNPs) variation between cohorts of ME/CFS patients and healthy controls. We found significant associations of DNA methylation states in T-lymphocytes at several CpG loci and regions with ME/CFS phenotype. These methylation anomalies are in close proximity to genes involved with immune function and cellular metabolism. Finally, we found significant correlations of genotypes with methylation modifications associated with ME/CFS.
The findings from this study highlight the role of epigenetic and genetic interactions in complex diseases and suggest several genetic and epigenetic elements potentially involved in the mechanisms of disease in ME/CFS.
6. Hulens M, et al. (2018)
The link between idiopathic intracranial hypertension, fibromyalgia, and chronic fatigue syndrome: exploration of a shared pathophysiology
Journal of Pain Research 11: 3129-3140.
Purpose: Idiopathic intracranial hypertension (IICH) is a condition characterized by raised intracranial pressure (ICP), and its diagnosis is established when the opening pressure measured during a lumbar puncture is elevated >20 cm H2O in nonobese patients or >25 cm H2O in obese patients.
Papilledema is caused by forced filling of the optic nerve sheath with cerebrospinal fluid (CSF). Other common but underappreciated symptoms of IICH are neck pain, back pain, and radicular pain in the arms and legs resulting from associated increased spinal pressure and forced filling of the spinal nerves with CSF.
Widespread pain and also several other characteristics of IICH share notable similarities with characteristics of fibromyalgia (FM) and chronic fatigue syndrome (CFS), two overlapping chronic pain conditions. The aim of this review was to compare literature data regarding the characteristics of IICH, FM, and CFS and to link the shared data to an apparent underlying physiopathology, that is, increased ICP.
Methods: Data in the literature regarding these three conditions were compared and linked to the hypothesis of the shared underlying physiopathology of increased cerebrospinal pressure.
Results: The shared characteristics of IICH, FM, and CFS that can be caused by increased ICP include headaches, fatigue, cognitive impairment, loss of gray matter, involvement of cranial nerves, and overload of the lymphatic olfactory pathway.
Increased pressure in the spinal canal and in peripheral nerve root sheaths causes widespread pain, weakness in the arms and legs, walking difficulties (ataxia), and bladder, bowel, and sphincter symptoms.
Additionally, IICH, FM, and CFS are frequently associated with sympathetic overactivity symptoms and obesity. These conditions share a strong female predominance and are frequently associated with Ehlers-Danlos syndrome.
Conclusion: IICH, FM, and CFS share a large variety of symptoms that might all be explained by the same pathophysiology of increased cerebrospinal pressure.
7. Joustra ML, et al. (2018)
Physical Activity and Sleep in Chronic Fatigue Syndrome and Fibromyalgia Syndrome: Associations with Symptom Severity in the General Population Cohort LifeLines.
Pain Research and Management 2018: 8.
Objective: The aim of the current study was to compare physical activity and sleep duration between patients with chronic fatigue syndrome (CFS), patients with fibromyalgia syndrome (FMS), and controls and to examine the association between physical activity level and sleep duration with symptom severity within these patient groups.
Methods: This study used data of LifeLines, a general population cohort in which 1.0% (, 63.7% female, age 44.9 (SD 11.6) years) reported CFS, 3.0% (; 91.6% female; age 48.4 (SD 10.7) years) reported FMS, and 95.7% (; 57.9% female; age 44.3 (SD 12.4) years) reported neither CFS nor FMS. Physical activity, sleep duration, and symptom severity were assessed by questionnaires and analysed using ANCOVA and regression analyses, adjusted for age, sex, body mass index, smoking, and educational level.
Results: Patients with CFS and FMS had significantly lower physical activity scores (8834 ± 5967 and 8813 ± 5549 MET ∗ minutes) than controls (9541 ± 5533; ). Patients with CFS had the longest sleep duration (466 ± 86 minutes) compared to patients with FMS and controls (450 ± 67 and 446 ± 56; ).
A linear association between physical activity, sleep duration, and symptom severity was only found in controls, in whom higher physical total activity scores and longer sleep duration were associated with a lower symptom severity.
In contrast, quadratic associations were found in all groups: both relatively low and high physical activity scores and relatively short and long sleep duration were associated with higher symptom severity in CFS, FMS, and controls.
Conclusion: This study indicates that patients with CFS or FMS sleep longer and are less physically active than controls on average. Both low and high levels of physical activity and short and long sleep duration are associated with higher symptom severity, suggesting the importance of patient-tailored treatment.
8. Mackay A and Tate WP (2018)
A compromised paraventricular nucleus within a dysfunctional hypothalamus: A novel neuroinflammatory paradigm for ME/CFS.
International Journal of Immunopathology and Pharmacology.
A neuroinflammatory paradigm is presented to help explain the pathophysiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). The hypothalamic paraventricular nucleus (PVN) is responsible for absorbing and processing multiple, incoming and convergent ‘stress’ signals, and if this cluster of neurons were affected (by neuroinflammation), the ongoing hypersensitivity of ME/CFS patients to a wide range of ‘stressors’ could be explained.
Neuroinflammation that was chronic and fluctuating, as ‘inflammatory-marker’ studies support, could reflect a dynamic change in the hypothalamic PVN’s threshold for managing incoming ‘stress’ signals. This may not only be a mechanism underpinning the characteristic feature of ME/CFS, post-exertional malaise, and its associated debilitating relapses, but could also be responsible for mediating the long-term perpetuation of the disease.
Triggers (sustained physiological ‘stressors’) of ME/CFS, such as a particular viral infection, toxin exposure, or a traumatic event, could also target the hypothalamic PVN, a potentially vulnerable site in the brains of ME/CFS susceptible people, and disruption of its complex neural circuitry could account for the onset of ME/CFS. In common with the different ‘endogenous factors’ identified in the early ‘neuroinflammatory’ stages of the ‘neurodegenerative’ diseases, an as yet, unidentified factor within the brains and central nervous system (CNS) of ME/CFS patients might induce both an initial and then sustained ‘neuroinflammatory’ response by its ‘innate immune system’.
Positron emission tomography/magnetic resonance imaging has reinforced evidence of glial cell activation centred on the brain’s limbic system of ME/CFS patients. Neuroinflammation causing dysfunction of the limbic system and its hypothalamus together with a consequently disrupted autonomic nervous system could account for the diverse range of symptoms in ME/CFS relating, in particular to fatigue, mood, cognitive function, sleep, thermostatic control, gastrointestinal disturbance, and hypotension.
9. Ottman A, Warner CB and Brown JN (2018)
The role of mirtazapine in patients with fibromyalgia: a systematic review.
Rheumatology International 28 (12): 2217-2224.
Mirtazapine is commonly used to treat major depressive disorder. Due to its effects on multiple neurotransmitters, it has been investigated for possible benefits in patients with fibromyalgia. The objective of this systematic review is to assess the efficacy and safety of mirtazapine in the treatment of patients with fibromyalgia.
Pubmed (1946-May 2018), Embase (1947-May 2018), CENTRAL, and ClinicalTrials.gov were queried using the search term combination: fibromyalgia, pain, chronic pain, neuralgia, neuropathic pain, chronic widespread pain, or chronic pain syndrome and mirtazapine. Studies appropriate to the objective were evaluated, including three randomized, placebo-controlled trials and one open-label trial, investigating the effect of mirtazapine in patients with fibromyalgia.
In patients with fibromyalgia, treatment with mirtazapine resulted in improvements in pain, sleep, and quality of life. Study durations ranged from 6 to 13 weeks and studies used varying dosing strategies for mirtazapine. Minor occurrences of somnolence, weight gain, nasopharyngitis, dry mouth, and increased appetite were reported with mirtazapine use.
Based on the reviewed literature, mirtazapine appears to be a promising therapy to improve pain, sleep, and quality of life in patients with fibromyalgia. These benefits were demonstrated in patients that were treatment naïve and those that had failed previous therapies. Additional clinical evidence through larger and longer length trials would be of benefit to further define the role of mirtazapine for patients with fibromyalgia.
10. Russell A, et al. (2018)
Persistent fatigue induced by interferon-alpha: a novel, inflammation-based, proxy model of chronic fatigue syndrome
Psychoneuroendocrinology [Epub ahead of print].
The role of immune or infective triggers in the pathogenesis of Chronic Fatigue Syndrome (CFS) is not yet fully understood. Barriers to obtaining immune measures at baseline (i.e., before the trigger) in CFS and post-infective fatigue model cohorts have prevented the study of pre-existing immune dysfunction and subsequent immune changes in response to the trigger.
This study presents interferon-alpha (IFN-α)-induced persistent fatigue as a model of CFS. IFN-α, which is used in the treatment of chronic Hepatitis C Virus (HCV) infection, induces a persistent fatigue in some individuals, which does not abate post-treatment, that is, once there is no longer immune activation. This model allows for the assessment of patients before and during exposure to the immune trigger, and afterwards when the original trigger is no longer present.
Fifty-five patients undergoing IFN-α treatment for chronic HCV were assessed at baseline, during the 6–12 months of IFN-α treatment, and at six-months post-treatment. Measures of fatigue, cytokines and kynurenine pathway metabolites were obtained. Fifty-four CFS patients and 57 healthy volunteers completed the same measures at a one-off assessment, which were compared with post-treatment follow-up measures from the HCV patients.
Eighteen patients undergoing IFN-α treatment (33%) were subsequently defined as having ‘persistent fatigue’ (the proposed model for CFS), if their levels of fatigue were higher six-months post-treatment than at baseline; the other 67% were considered ‘resolved fatigue’. Patients who went on to develop persistent fatigue experienced a greater increase in fatigue symptoms over the first four weeks of IFN-α, compared with patients who did not (Δ Treatment Week (TW)-0 vs. TW4; PF: 7.1 ± 1.5 vs. RF: 4.0 ± 0.8, p = 0.046). Moreover, there was a trend towards increased baseline interleukin (IL)-6, and significantly higher baseline IL-10 levels, as well as higher levels of these cytokines in response to IFN-α treatment, alongside concurrent increases in fatigue. Levels increased to more than double those of the other patients by Treatment Week (TW)4 (p = 0.011 for IL-6 and p = 0.001 for IL-10).
There was no evidence of an association between persistent fatigue and peripheral inflammation six-months post-treatment, nor did we observe peripheral inflammation in the CFS cohort. While there were changes in kynurenine metabolites in response to IFN-α, there was no association with persistent fatigue. CFS patients had lower levels of the ratio of kynurenine to tryptophan and 3-hydroxykynurenine than controls.
Future studies are needed to elucidate the mechanisms behind the initial exaggerated response of the immune system in those who go on to experience persistent fatigue even if the immune trigger is no longer present, and the change from acute to chronic fatigue in the absence of continued peripheral immune activation.
11. Strassheim V, et al. (2018)
Managing fatigue in postural tachycardia syndrome (PoTS): The Newcastle approach
Autonomic Neuroscience 215: 56-61.
Fatigue is a significant symptom that is frequently reported by those with postural tachycardia syndrome (PoTS). There are a variety of reasons why those with PoTS might experience fatigue and as a consequence an individualised approach to management is most appropriate.
In this chapter we will examine the prevalence of fatigue in those with PoTS, its overlap with conditions such as chronic fatigue syndrome and describe a clinical approach to the management of fatigue in those with PoTS.
12. Stubhaug B, et al. (2018)
A 4-Day Mindfulness-Based Cognitive Behavioral Intervention Program for CFS/ME. An Open Study, With 1-Year Follow-Up.
Frontiers in Psychiatry 9: 720.
Background: Chronic Fatigue Syndrome/Myalgic Encephalopathy (CFS/ME) is an incapacitating illness in which single treatment interventions seem to have variable effects. Based on an earlier study we have conducted a new study with a concentrated intervention program.
The aims of this study were to: (1) explore the clinical course for patients with CFS/ME who participated in a treatment program delivered during four consecutive days, and (2) evaluate their satisfaction with this program.
Methods: 305 patients diagnosed with CFS/ME (Oxford criteria), recruited from a clinical population referred to a specialist outpatient clinic, participated in an open uncontrolled study of the clinical course through 1 year.
The study group participated in a 4-day group intervention program, comprised by education, cognitive group therapy sessions, mindfulness sessions, physical activity and writing sessions, within a context of cognitive behavioral therapy, mindfulness, acceptance and commitment model.
Assessments were done by self-reports prior to the first consultation, 1 week before and 1 week after the intervention program, and at 3 months and 1 year after the intervention. SPSS 23 and R 3.3 were used for statistical analyses. The associations between case definitions and the outcome measures (Chalder Fatigue Scale (FS), Short Form 36 (SF-36) physical functioning scale) were assessed by a linear mixed effects model (LME).
Results: Results showed statistically significant clinical changes for 80% of the patients after the intervention, changes being sustained through 1 year after the program. For both Fatigue Scale (FS) and the SF-36 there were statistically significant effects of time from baseline to all time points with a statistically significant drop in scores, applying the linear mixed effects model.
A subgroup fulfilling the inclusion criteria from the PACE study (Chalder Fatigue Scale >6/11, SF-36 Physical functioning <65/100) showed clinically significant improvement through 1 year, changes in outcome measures were statistically significant (p < 0.001). None of the patients included in the program dropped out, and a great majority of patients expressed high satisfaction with the content, focus and amount of treatment.
Conclusions: Clinical changes observed from pre-treatment to 1 year follow-up could represent effects of the 4-day concentrated intervention program, and should be further explored in a controlled study.
13. Tsai SY, et al. (2018)
Increased risk of chronic fatigue syndrome following burn injuries
Journal of Translational Medicine 16 (1): 342.
Background: The overlapping symptoms and pathophysiological similarities between burn injury and chronic fatigue syndrome (CFS) are noteworthy. Thus, this study explores the possible association between burn injury and the subsequent risk of CFS.
Method: We used data from the Taiwan National Health Insurance system to address the research topic. The exposure cohort comprised of 17,204 patients with new diagnoses of burn injury. Each patient was frequency matched according to age, sex, index year, and comorbidities with four participants from the general population who did not have a history of CFS (control cohort). Cox proportional hazards regression analysis was conducted to estimate the relationship between burn injury and the risk of subsequent CFS.
Result: The incidence of CFS in the exposure and control cohorts was 1.61 and 0.86 per 1000 person-years, respectively. The exposure cohort had a significantly higher overall risk of subsequent CFS than did the control cohort (adjusted hazard ratio [HR] = 1.48, 95% confidence interval [CI] = 1.41-1.56). The risk of CFS in patients with burn injury in whichever stratification (including sex, age, and comorbidity) was also higher than that of the control cohort.
Conclusion: The findings from this population-based retrospective cohort study suggest that thermal injury is associated with an increased risk of subsequent CFS and provided a point of view suggesting burn injuries in sun- exposed areas such as the face and limbs had greater impact on subsequent development of CFS compared with trunk areas. In addition, extensively burned areas and visible scars were predictors of greater physiological and psychosocial that are needed to follow-up in the long run.
14. Twisk F. (2018)
Myalgic Encephalomyelitis or What? The International Consensus Criteria
Diagnostics 9 (1): 1.
Myalgic encephalomyelitis (ME) is a neuromuscular disease with two distinctive types of symptoms (muscle fatigability or prolonged muscle weakness after minor exertion and symptoms related to neurological disturbance, especially of sensory, cognitive, and autonomic functions) and variable involvement of other bodily systems. Chronic fatigue syndrome (CFS), introduced in 1988 and re-specified in 1994, is defined as (unexplained) chronic fatigue accompanied by at least four out of eight listed (ill-defined) symptoms.
Although ME and CFS are two distinct clinical entities (with partial overlap), CFS overshadowed ME for decades. In 2011, a panel of experts recommended abandoning the label CFS and its definition and proposed a new definition of ME: the International Consensus Criteria for ME (ME-ICC). In addition to post-exertional neuroimmune exhaustion (PENE), a mandatory feature, a patient must experience at least three symptoms related to neurological impairments; at least three symptoms related to immune, gastro-intestinal, and genitourinary impairments; and at least one symptom related to energy production or transportation impairments to meet the diagnosis of ME-ICC.
A comparison between the original definition of ME and the ME-ICC shows that there are some crucial differences between ME and ME-ICC. Muscle fatigability, or long-lasting post-exertional muscle weakness, is the hallmark feature of ME, while this symptom is facultative for the diagnosis under the ME-ICC. PENE, an abstract notion that is very different from post-exertional muscle weakness, is the hallmark feature of the ME-ICC but is not required for the diagnosis of ME.
The diagnosis of ME requires only two type of symptoms (post-exertional muscle weakness and neurological dysfunction), but a patient has to experience at least eight symptoms to meet the diagnosis according to the ME-ICC. Autonomic, sensory, and cognitive dysfunction, mandatory for the diagnosis of ME, are not compulsory to meet the ME-ICC subcriteria for ‘neurological impairments’.
In conclusion, the diagnostic criteria for ME and of the ME-ICC define two different patient groups. Thus, the definitions of ME and ME-ICC are not interchangeable.
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