MS Abstracts 04c-2g6

  1. Increased IL-23p19 expression in Multiple Sclerosis lesions and its induction in Microglia
    Brain 2007 Feb;130(Pt 2):490-501

  2. IL-23 is increased in Dendritic Cells in Multiple Sclerosis and down-regulation of IL-23 by antisense oligos increases Dendritic Cell IL-10 production
    J Immunol 2006 Jun 15;176(12):7768-74

  3. Soluble Nogo-A, an inhibitor of Axonal regeneration, as a biomarker for Multiple Sclerosis
    Neurology 2007 Jan 23;68(4):283-7

  4. Lack of association between AntiMyelin AntiBodies and progression to Multiple Sclerosis
    N Engl J Med 2007 Jan 25;356(4):371-8

  5. A second Major Histocompatibility Complex susceptibility locus for Multiple Sclerosis
    Ann Neurol 2007 Jan 24

  6. Acute and chronic NeuroEndocrine effects of Interferon-ß-1a in Multiple Sclerosis
    Clin Endocrinol (Oxf) 2007 Feb;66(2):295-303

  7. Evidence for Synaptic stripping by Cortical Microglia
    Glia 2007 Mar;55(4):360-8

  8. A new focal EAE model of Cortical DeMyelination: Multiple Sclerosis-like lesions with rapid resolution of inflammation and extensive ReMyelination
    Brain 2006 Aug;129(Pt 8):1972-83

  9. Neuronal injury in Multiple Sclerosis
    Medicina (B Aires) 2006;66(5):472-85

  10. Glatiramer Acetate in Primary/Progressive Multiple Sclerosis: Results of a multinational, multicenter, double-blind, placebo-controlled trial
    Ann Neurol 2007 Jan;61(1):14-24

  11. Distinct roles of protein kinase R and toll-like receptor 3 in the activation of Astrocytes by Viral stimuli
    Glia 2007 Feb;55(3):239-52

  12. Familial effects on the clinical course of Multiple Sclerosis
    Neurology 2007 Jan 30;68(5):376-83


Increased IL-23p19 Expression In Multiple Sclerosis Lesions And Its Induction In Microglia

Li Y, Chu N, Hu A, Gran B, Rostami A, Zhang GX
Brain 2007 Feb;130(Pt 2):490-501
Thomas Jefferson University, Department of Neurology, Philadelphia, PA, USA
PMID# 17003070

IL-12 has long been considered important in the pathogenesis of Multiple Sclerosis.

However, evidence from recent studies strongly supports the critical role of IL-12-related ProInflammatory Cytokine IL-23, but not IL-12, in the development of Experimental Autoimmune Encephalomyelitis (EAE), an animal model of this disease.

The role of IL-23 in the CNS immunity of Multiple Sclerosis patients has not been elucidated; nor is it known whether human Microglia produce this Cytokine.

In this study we investigated the expression of IL-23p19 and p40, with its key subunit p19 as the focus, in Histologically characterized CNS specimens from Multiple Sclerosis and control cases using in situ hybridization and ImmunoHistoChemistry.

A significant increase in mRNA expression and protein production of both subunits of IL-23 was found in lesion tissues compared with non-lesion tissues.

Double staining showed that activated Macrophages/Microglia were an important source of IL-23p19 in active and chronic active Multiple Sclerosis lesions.

We also detected IL-23p19 expression in mature Dendritic Cells which were preferentially located in the PeriVascular cuff of active lesions.

The finding that human Microglia produce IL-23 was further confirmed by the inducible production of IL-23p19 and p40 in cultured human Microglia in vitro upon different Toll-like receptor stimulations.

Taken together, these findings on the expression of IL-23p19 in Multiple Sclerosis lesions may lead to a better understanding of the events culminating in human Multiple Sclerosis.


IL-23 Is Increased In Dendritic Cells In Multiple Sclerosis And Down-Regulation Of Il-23 By Antisense Oligos Increases Dendritic Cell Il-10 Production

Vaknin-Dembinsky A, Balashov K, Weiner HL
J Immunol 2006 Jun 15;176(12):7768-74
Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, MA 02115, USA
PMID# 16751425

IL-23 is a heterodimeric Cytokine comprising a p19 subunit associated with the IL-12/23p40 subunit.

Like IL-12, IL-23 is expressed predominantly by activated Dendritic Cells (DCs) and Phagocytic Cells, and both Cytokines induce IFN-γ secretion by T-Cells.

The induction of Experimental Autoimmune Encephalitis, the animal model of Multiple Sclerosis (MS), occurs in mice lacking IL-12, but not in mice with targeted disruption of IL-23 or both IL-12 and IL-23.

Thus, IL-23 expression in DCs may play an important role in the pathogenesis of human Autoimmune Diseases such as MS.

We quantified the expression of IL-23 in Monocyte-derived DCs in MS patients and healthy donors and found that DCs from MS patients secrete elevated amounts of IL-23 and express increased levels of IL-23p19 mRNA.

Consistent with this abnormality, we found increased IL-17 production by T-Cells from MS patients.

We then transfected Monocyte-derived DCs from healthy donors with antisense oligonucleotides specific for the IL-23p19 and IL-12p35 genes and found potent suppression of gene expression and blockade of bioactive IL-23 and IL-12 production without affecting cellular viability or DCs maturation.

Inhibition of IL-23 and IL-12 was associated with increased IL-10 and decreased TNF-alpha production. Furthermore, transfected DCs were poor AlloStimulators in the MLR.

Our results demonstrate that an abnormal Th1 bias in DCs from MS patients related to IL-23 exists, and that antisense oligonucleotides specific to IL-23 can be used for Immune modulation by targeting DC gene expression.


Soluble Nogo-A, An Inhibitor Of Axonal Regeneration, As A Biomarker For Multiple Sclerosis

Jurewicz A, Matysiak M, Raine CS, Selmaj K
Neurology 2007 Jan 23;68(4):283-7
Medical University of Lodz, Department of Neurology, 22, Kopcinskiego Street, 90-153 Lodz, Poland
PMID# 17242333

CNS Axons display a poor regenerative response to injury. In Multiple Sclerosis (MS), failure of damaged Axons to regenerate may be a major factor underlying non-reversible Neurologic dysfunction.

Nogo is a development-related molecule inhibiting Axonal regeneration and is a major component of CNS Myelin.

CSF from 114 patients with Remitting/Relapsing MS (RR-MS) and Secondary/Progressive MS (SP-MS) and 153 controls, as well as CNS tissue from 3 patients with MS and 2 controls, were used for this study.

We found soluble 20 kDa Nogo-A product in 96% (110/114) of CSF samples from patients with MS compared with 0/18 from Meningo-Encephalomyelitis, 0/125 from control subjects with Other Neurologic Diseases, and 0/10 from CNS Autoimmune Diseases.

Nogo-A products were present both in RR-MS and SP-MS, as well as in early cases of the disease, but not in NeuroMyelitis Optica. The same Nogo A product was detected in CNS tissue from all patients with MS but not in control CNS tissue.

Soluble Nogo-A may be specific for the CSF of patients with Multiple Sclerosis and its presence may predict failure of Axonal regeneration within the CNS.


Lack Of Association Between AntiMyelin AntiBodies And Progression To Multiple Sclerosis

Kuhle J, Pohl C, Mehling M, Edan G, Freedman MS, Hartung HP, Polman CH, Miller DH, Montalban X, Barkhof F, Bauer L, Dahms S, Lindberg R, Kappos L, Sandbrink R
N Engl J Med 2007 Jan 25;356(4):371-8
University Hospital, Department of Research, Basel, Switzerland
PMID# 17251533

Patients with a single episode of Neurologic dysfunction and Brain Magnetic Resonance Imaging (MRI) scans suggestive of Multiple Sclerosis are at high risk for clinically definite Multiple Sclerosis, but the outcome for individual patients is unpredictable.

An increased risk of progression to clinically definite Multiple Sclerosis in patients with serum AntiBodies against Myelin Oligodendrocyte Glycoprotein (MOG) and Myelin Basic Protein (MBP) has been reported.

We measured serum anti-MOG and anti-MBP IgG and IgM antibodies in 462 patients with a first clinical event suggestive of Multiple Sclerosis and at least two clinically silent lesions on Brain MRI.

The patients were participating in a multicenter trial of treatment with Interferon-ß-1b.

Antibodies were assessed by Western blot analysis at baseline, and the results compared with the time and rate of progression to clinically definite Multiple Sclerosis or a diagnosis of Multiple Sclerosis as defined by an international panel (the McDonald Criteria).

Regular visits were scheduled for the assessment of Neurologic impairment and for MRI before treatment and at months 3, 6, 9, 12, 18, and 24.

No associations were found between the presence of Anti-MOG and Anti-MBP IgM and IgG AntiBodies and progression to clinically definite Multiple Sclerosis.

Or, a diagnosis of Multiple Sclerosis according to the McDonald Criteria, either in the entire cohort or in any subgroups of the study population.

Serum AntiBodies against MOG and MBP, as detected by Western blot analysis, are not associated with an increased risk of progression to clinically definite Multiple Sclerosis in patients who have had a Clinically Isolated Syndrome suggestive of Multiple Sclerosis.

Copyright 2007 Massachusetts Medical Society.


A Second Major Histocompatibility Complex Susceptibility Locus For Multiple Sclerosis

Yeo TW, De Jager PL, Gregory SG, Barcellos LF, Walton A, Goris A, Fenoglio C, Ban M, Taylor CJ, Goodman RS, Walsh E, Wolfish CS, Horton R, Traherne J, Beck S, Trowsdale J, Caillier SJ, Ivinson AJ, Green T, Pobywajlo S, Lander ES, Pericak-Vance MA, Haines JL, Daly MJ, Oksenberg JR, Hauser SL, Compston A, Hafler DA, Rioux JD, Sawcer S
Ann Neurol 2007 Jan 24
University of Cambridge, Department of Clinical NeuroSciences, Addenbrooke's Hospital, Cambridge, United Kingdom
PMID# 17252545

Variation in the Major Histocompatibility Complex (MHC) on Chromosome 6p21 is known to influence susceptibility to Multiple Sclerosis with the strongest effect originating from the HLA-DRB1 gene in the Class II region.

The possibility that other genes in the MHC independently influence susceptibility to Multiple Sclerosis has been suggested but remains unconfirmed.

Using a combination of microsatellite, single nucleotide polymorphism, and Human Leukocyte Antigen (HLA) typing.

We screened the MHC in trio families looking for evidence of residual association above and beyond that attributable to the established DRB1*1501 risk haplotype.

We then refined this analysis by extending the genotyping of classical HLA loci into independent cases and control subjects.

Screening confirmed the presence of residual association and suggested that this was maximal in the region of the HLA-C gene.

Extending analysis of the classical loci confirmed that this residual association is partly due to allelic heterogeneity at the HLA-DRB1 locus, but also reflects an independent effect from the HLA-C gene.

Specifically, the HLA-C*05 allele, or a variant in tight linkage disequilibrium with it, appears to exert a protective effect (p = 3.3 x 10(-5)).

Variation in the HLA-C gene influences susceptibility to Multiple Sclerosis independently of any effect attributable to the nearby HLA-DRB1 gene.

Ann Neurol 2007.


Acute And Chronic NeuroEndocrine Effects Of Interferon-ß-1a In Multiple Sclerosis

Then Bergh F, Kumpfel T, Yassouridis A, Lechner C, Holsboer F, Trenkwalder C
Clin Endocrinol (Oxf) 2007 Feb;66(2):295-303
Max Planck Institute of Psychiatry, Section of Neurology, Kraepelinstrasse 10, 80804 Munchen, Germany
PMID# 17224002

Treatment of Multiple Sclerosis with Interferon-beta (IFN-ß) results in variable responses interindividually. Cytokine-hormone interactions may modulate the therapeutic effects of IFN-ß.

Since hyperactivity of the Hypothalamo-Pituitary-Adrenal (HPA Axis) and other NeuroEndorine disturbances occur in Multiple Sclerosis, we determined the detailed NeuroEndocrine response of patients with Multiple Sclerosis to IFN-ß.

Design & Patients
Longitudinal open-label study. Eight patients with Relapsing/Remitting Multiple Sclerosis (four women, age 31.9 +/- 1.5 years, EDSS 1.5-2.5).

Plasma ACTH, Cortisol, Prolactin, GH, TSH, LH and FSH were determined in 30-min intervals during 8 h on four occasions: after intramuscular injection of saline; after the first dose of IFN-ß-1a; after the second IFN-ß dose with oral Indomethacin pretreatment; and after 3 months of IFN-ß therapy.

Dexamethasone-Corticotropin-Releasing Hormone test was performed before and at 3 months on IFN-ß.

Compared to saline, IFN injection resulted in marked rise in plasma ACTH (mean, 370% of baseline), Cortisol (214%), Prolactin (253%) and GH (756%), between 2 and 6 h after injection. With Indomethacin, Hormone secretion occurred with reduced peak values.

Endocrine response adapted partially after 3 months of treatment. HPA axis activity decreased in most patients, but increased in one patient with frequent relapses.

Marked NeuroEndocrine effects occur in response to IFN-ß in Multiple Sclerosis.

Upon prolonged treatment, these effects partially adapt, and HPA Axis hyperactivity is reduced. Prospective studies to determine the relation to individual treatment response can be based on these findings.


Evidence for Synaptic stripping by Cortical Microglia

Trapp BD, Wujek JR, Criste GA, Jalabi W, Yin X, Kidd GJ, Stohlman S, Ransohoff R
Glia 2007 Mar;55(4):360-8
Lerner Research Institute, The Cleveland Clinic, Department of NeuroSciences, Cleveland, OH 44195, USA
PMID# 17136771

Recent studies have described significant DeMyelination and Microglial activation in the Cerebral Cortex of Brains from Multiple Sclerosis patients.

To date, however, experimental models of Cortical DeMyelination or Cortical inflammation have not been extensively studied.

In this report we describe focal Cortical inflammation induced by stereotaxic injection of killed bacteria (BCG), followed 1 month later by subcutaneous injection of the same Antigen, a protocol that overcomes the Immune privilege of the Cortex.

IntraCerebral BCG injection produced focal Microglial activation at the injection site (termed acute lesion).

Ten days after peripheral challenge (termed Immune-mediated lesion), larger areas and higher densities of activated Microglia were found near the injection site.

In both paradigms, activated Microglia and/or their processes closely apposed Neuronal Perikarya and Apical Dendrites.

In the Immune-mediated lesions, approximately 45% of the AxoSomatic Synapses was displaced by activated Microglia.

Upon activation, therefore, Cortical Microglial migrate to and strip Synapses from Neuronal Perikarya.

Since Neuronal pathology was not a feature of either the acute or Immune-mediated lesion, Synaptic stripping by activated Microglia may have NeuroProtective consequences.


A New Focal EAE Model Of Cortical DeMyelination: Multiple Sclerosis-Like Lesions With Rapid Resolution Of Inflammation And Extensive ReMyelination

Merkler D, Ernsting T, Kerschensteiner M, Bruck W, Stadelmann C
Brain 2006 Aug;129(Pt 8):1972-83
Georg August University Gottingen, Department of NeuroPathology, Gottingen, Germany
PMID# 16714315

Recent studies have revealed widespread DeMyelination in the Cortex of patients with Chronic Multiple Sclerosis. In contrast to White Matter lesions, Cortical Multiple Sclerosis lesions are accompanied by only minor inflammation.

Research into the pathogenesis of Cortical lesion formation has been hampered by the fact that the conventional rodent model of Multiple Sclerosis, Experimental Autoimmune Encephalomyelitis (EAE), does not regularly affect the Cortex.

To overcome this limitation we developed a new rat model of Cortical Multiple Sclerosis.

Lesions were stereotactically targeted to the Cerebral Cortex by injection of pro-inflammatory mediators in animals that were immunized subclinically with Myelin Oligodendrocyte Glycoprotein (MOG).

We thus generated highly reproducible DeMyelinated lesions in the NeoCortex with remarkable histological similarities to Cortical Multiple Sclerosis lesions.

The focal Cortical EAE model led to the typical pattern of IntraCortical and SubPial DeMyelination, infiltration with inflammatory cells, Complement deposition, acute Axonal damage and Neuronal cell death.

Surprisingly, extensive Cortical Inflammation largely resolved within 2 weeks. Furthermore, Cortical DeMyelination was readily compensated by rapid ReMyelination.

Our data thus suggest that Cortical inflammation is a transient phenomenon, and that ReMyelination of Cortical inflammatory-DeMyelinating lesions may occur rapidly.

See: Complement Abstract Index


Neuronal Injury In Multiple Sclerosis

Correale J, Meli F, Ysrraelit C
Medicina (B Aires) 2006;66(5):472-85
Instituto de Investigaciones Neurologicas Dr. Raul Carrea (FLENI), Departamento de Neurologia, Facultad de Ciencias Biomedicas Universidad Austral, Buenos Aires, Argentina
PMID# 17137182

The concept of Multiple Sclerosis (MS) as a DeMyelinating Disease is deeply ingrained. Although the existence of a NeuroDegenerative component has always been apparent, it has only recently become emphasized.

Thus, in recent years several studies have identified Axonal degeneration as the major determinant of irreversible Neurological disability in patients with MS.

Axonal injury begins at disease onset and remains clinically silent for many years; irreversible Neurological disability develops when a threshold of Axonal Loss is reached and CNS compensatory mechanisms are exhausted.

    The precise mechanisms of Axonal loss are poorly understood, and three hypotheses have been proposed:
  1. The damage is caused by an inflammatory process
  2. There is an excessive accumulation of Intra-Axonal Ca2+
  3. DeMyelinated Axons undergo degeneration due to lack of Trophic Support by Myelin, or Myelin forming cells

Although MS has traditionally been regarded as a disease of White Matter, DeMyelination can also occur in the Cerebral Cortex. Cortical Lesions exhibit Neuronal injury represented by Dendritic and Axonal transection as well as Neuronal Apoptosis.

Because conventional Nuclear Magnetic Resonance (NMR) is limited in its ability to provide specific information about Axonal pathology in MS, new techniques such as, Diffusion-weighted MRI, Proton Magnetic Resonance Spectroscopy, Functional MRI.

As well as novel techniques designed to measure Atrophy have been developed to monitor MS evolution.

Recognition that MS is in part a NeuroDegenerative Disease should trigger critical rethinking on the pathogenic mechanisms of this disease and provides new targets for a rational treatment.


Glatiramer Acetate In Primary/Progressive Multiple Sclerosis: Results Of A Multinational, Multicenter, Double-Blind, Placebo-Controlled Trial

PROMiSe Trial Study Group
Wolinsky JS, Narayana PA, O'connor P, Coyle PK, Ford C, Johnson K, Miller A, Pardo L, Kadosh S, Ladkani D
Ann Neurol 2007 Jan;61(1):14-24
The University of Texas Health Science Center at Houston, Department of Neurology, Houston, TX
PMID# 17262850

To determine whether Glatiramer Acetate (GA) slows accumulation of disability in Primary/Progressive Multiple Sclerosis.

A total of 943 patients with Primary/Progressive Multiple Sclerosis were randomized to GA or placebo (PBO) in this 3-year, double-blind trial.

The primary end point was an intention-to-treat analysis of time to 1- (entry Expanded Disability Status Scale, 3.0-5.0) or 0.5-point Expanded Disability Status Scale change (entry Expanded Disability Status Scale, 5.5-6.5) sustained for 3 months.

The trial was stopped after an interim analysis by an independent data safety monitoring board indicated no discernible treatment effect on the primary outcome. Intention-to-treat analyses of disability and Magnetic Resonance Imaging end points were performed.

There was a nonsignificant delay in time to sustained accumulated disability in GA- versus PBO-treated patients (hazard ratio, 0.87 [95% confidence interval, 0.71-1.07]; p = 0.1753), with significant decreases in enhancing lesions in year 1 and smaller increases in T2 lesion volumes in years 2 and 3 versus PBO.

Post hoc analysis showed that survival curves for GA-treated male patients diverged early from PBO-treated male subjects (hazard ratio, 0.71 [95% confidence interval, 0.53-0.95]; p = 0.0193).

The trial failed to demonstrate a treatment effect of GA on Primary/Progressive Multiple Sclerosis.

Both the unanticipated low event rate and premature discontinuation of study medication decreased the power to detect a treatment effect.

Post hoc analysis suggests GA may have slowed clinical progression in male patients who showed more rapid progression when untreated.

Ann Neurol 2007;61:14-24.


Distinct Roles Of Protein Kinase R And Toll-Like Receptor 3 In The Activation Of Astrocytes By Viral Stimuli

Carpentier PA, Williams BR, Miller SD
Glia 2007 Feb;55(3):239-52
Northwestern University Institute for NeuroScience, Feinberg School of Medicine, Department of MicroBiology-Immunology, InterDepartmental ImmunoBiology Center, Chicago, Illinois 60611, USA
PMID# 17091495

Impaired Immune surveillance and constitutive ImmunoSuppressive properties make the Central Nervous System (CNS) a particular challenge to Immune defense, and require that CNS-resident cells be capable of rapidly recognizing and responding to infection.

We have previously shown that Astrocytes respond to treatment with a TLR3 ligand, poly I:C, with the upregulation of Innate Immune functions.

In the current study, we examine the activation of Innate Immune functions of Astrocytes by Theiler's Murine Encephalomyelitis Virus (TMEV), a PicornaVirus, which establishes a persistent infection in the CNS of susceptible strains of mice.

And leads to the development of an Autoimmune DeMyelinating Disease that resembles human Multiple Sclerosis.

Astrocytes infected with TMEV are activated to produce type I Interferons, the Cytokine IL-6, and Chemokines CCL2 and CXCL10.

We further examined the mechanisms that are responsible for the activation of Astrocytes in response to direct Viral infection and treatment with poly I:C.

We found that the cytoplasmic dsRNA-activated kinase PKR is important for Innate Immune Responses to TMEV infection, but has no role in their induction by poly I:C delivered extracellularly.

In contrast, we found that TLR3 has only a minor role in responses to TMEV infection, but is important for responses to poly I:C.

These results highlight the differences between responses induced by direct, NonLytic Virus infection and extracellular poly I:C.

The activation of Astrocytes through these different pathways has implications for the initiation and progression of Viral Encephalitis and DeMyelinating Diseases such as Multiple Sclerosis.

Copyright 2006 Wiley-Liss, Inc.


Familial Effects On The Clinical Course Of Multiple Sclerosis

Hensiek AE, Seaman SR, Barcellos LF, Oturai A, Eraksoi M, Cocco E, Vecsei L, Stewart G, Dubois B, Bellman-Strobl J, Leone M, Andersen O, Bencsik K, Booth D, Celius EG, Harbo HF, Hauser SL, Heard R, Hillert J, Myhr KM, Marrosu MG, Oksenberg JR, Rajda C, Sawcer SJ, Sorensen PS, Zipp F, Compston DA
Neurology 2007 Jan 30;68(5):376-83
University of Cambridge Clinical School, Addenbrooke's Hospital, Department of Clinical NeuroScience, Box 165, Cambridge CB2 2QQ, UK
PMID# 17261686

Familial factors influence susceptibility to Multiple Sclerosis (MS) but it is unknown whether there are additional effects on the natural history of the disease.

We evaluated 1,083 families with > or =2 first-degree relatives with MS for concordance of age at onset, clinical course, and disease severity.

And investigated transmission patterns of these clinical features in affected parent-child pairs.

There is concordance for age at onset for all families (correlation coefficient 0.14; p < 0.001), as well as for affected siblings (correlation coefficient 0.15; p < 0.001).

And affected parent-child pairs (correlation coefficient 0.12; p = 0.03) when each is evaluated separately.

Concordance for year of onset is present among affected siblings (correlation coefficient 0.18; p < 0.001) but not the parent-child group (correlation coefficient 0.08; p = 0.15).

The clinical course is similar between siblings (kappa 0.12; p < 0.001) but not affected parents and their children (kappa -0.04; p = 0.09).

This influence on the natural history is present in all clinical subgroups of Relapsing/Remitting, and Primary and Secondary/Progressive MS, reflecting a familial effect on episodic and Progressive phases of the disease.

There is no concordance for disease severity within any of the considered family groups (correlation coefficients: all families analyzed together, 0.02, p = 0.53; affected sibling group, 0.02, p = 0.61; affected parent-child group, 0.02, p = 0.69).

Furthermore, there are no apparent transmission patterns of any of the investigated clinical features in affected parent-child pairs and no evidence for anticipation or effects of genetic loading.

Familial factors do not significantly affect eventual disease severity.

However, they increase the probability of a Progressive clinical course, either from onset or after a phase of Relapsing/Remitting disease. The familial effect is more likely to reflect genetic than environmental conditions.

The results are relevant for counseling patients and have implications for the design of studies seeking to identify factors that influence the natural history of the disease.

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