Report on the 1st scientific meeting of the "Verein zur Förderung des Wissenschaftlichen Nachwuchses in der Neurologie" (NEUROWIND e.V.) held in Mittenwalde/Motzen, Germany, Oct. 30th - Nov. 1st, 2009.

MEETING REPORT Open Access
Report on the 1st scientific meeting of the
“Verein zur Förderung des Wissenschaftlichen
Nachwuchses in der Neurologie” (NEUROWIND
e.V.) held in Mittenwalde/Motzen, Germany,
Oct. 30th - Nov. 1st, 2009
Tim Magnus1*, Ralf Linker2*, Sven G Meuth3*, Christoph Kleinschnitz3*, Thomas Korn4*
Abstract
Report on the 1st scientific meeting of the “Verein zur Forderung des Wissenschaftlichen Nachwuchses in der Neu-
rologie” (NEUROWIND e.V.) held in Mittenwalde/Motzen, Germany, Oct. 30th - Nov. 1st, 2009
A scientific meeting report
Introduction
It is with great pleasure and enthusiasm that we intro-
duce the new non-profit “Association for Supporting
Young Scientists in the Field of Neurology in Germany”
("Verein zur Förderung des Wissenschaftlichen Nach-
wuchses in der Neurologie”, NEUROWIND e.V.) http://
www.neurowind.de. As its name suggests, the association
is intended to promote the work of young neurologists
and neuroscientists in German-speaking European coun-
tries. Founded by the neurologists Ralf Linker, Bochum,
Thomas Korn, Munich, Tim Magnus, Hamburg, Sven
G. Meuth, and Christoph Kleinschnitz, Würzburg,
Germany, NEUROWIND e. V. aims to provide an inter-
disciplinary and interactive platform for young researchers
in order to gather and disseminate new knowledge in the
fields of clinical and basic neurosciences. NEUROWIND
e. V. focuses on three main topics: [1] cerebrovascular dis-
eases, [2] neuroinflammation, and [3] neurodegeneration.
Tremendous progress has been made in recent years
in understanding the pathophysiology of individual
disease conditions such as multiple sclerosis (MS),
stroke, or Alzheimer’s disease (AD). In spite of this suc-
cess in unravelling disease mechanisms, the translation
of novel experimental therapies into effective treatment
for patients has so far been unsatisfying for a number of
reasons, with one central problem certainly emanating
from insufficient stringency of the translational process
from bench to bedside and vice versa. One clear aim of
NEUROWIND e. V. is therefore to bring together basic
pathological and therapeutic concepts from different
neurological disease models which at first glance might
appear largely unrelated. However, numerous studies
meanwhile have taught us that pathophysiological path-
ways and effector mechanisms appear to be common to
a variety of different diseases. Good examples are the
only recently recognized role of inflammation in stroke,
M. Parkinson and AD or degenerative processes during
the course of MS. Our ultimate goal is to overcome
out-dated model barriers and raise the efficacy and qual-
ity of translational neurological research by fostering
exchange of information and providing an interactive
platform that favors fruitful discussions necessary to
identify and solve distinct problems.
To reach these ambitious goals, the first scientific
meeting of NEUROWIND e.V. was recently held from
Oct. 30’th - Nov. 1’st, 2009 in Mittenwalde/Motzen,
* Correspondence: t.magnus@uke.uni-hamburg.de; ralf.linker@ruhr-uni-
bochum.de; meuth_s@klinik.uni-wuerzburg.de; christoph.kleinschnitz@mail.
uni-wuerzburg.de; korn@lrz.tu-muenchen.de
1Department of Neurology, University Clinic Hamburg-Eppendorf, Martinistr.
52, D-20246 Hamburg, Germany
2Department of Neurology, St. Josef-Hospital, Ruhr-University,
Universitätsstraße 150, D-44801 Bochum, Germany
Magnus et al. Experimental & Translational Stroke Medicine 2010, 2:7
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© 2010 Magnus et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons
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Germany. Approximately 60 participants mainly on the
level of doctoral students and young postdocs joined the
meeting and presented their scientific work in the beau-
tiful and stimulating environment of the Prussian scen-
ery. A brief summary of the most interesting findings
from the five sessions is given below and the full pro-
gram as well as further information is available at http://
www.neurowind.de.
Summary of the scientific contributions to the
NEUROWIND meeting 2009
Contributions in the fields of neuroimmunology and
neurodegeneration
Experimental autoimmune encephalomyelitis (EAE) is
widely used to investigate the biology of autoreactive T
cells in vivo. While EAE is considered an animal model
to simulate inflammatory aspects of MS, similar aspects
can be studied in the peripheral nervous system in the
model of experimental autoimmune neuritis (EAN; work
on new therapeutics in EAN presented by Gerd Meyer
zu Hörste from the group of Bernd Kieseier, Dept. of
Neurology, University of Düsseldorf). A series of myelin
antigens have been identified as potential targets of
autoreactive T cells and the most frequently used epi-
tope to induce EAE in C57Bl/6 mice is the myelin oligo-
dendrocyte glycoprotein (MOG) peptide 35-55. T cell
receptor (TCR) transgenic mice with specificity for
MOG35-55 have been generated and are used as a
spontaneous model of MS since up to 10 percent of
MOG35-55 TCR transgenic mice develop EAE without
active immunization. As has recently been found by the
group of Hartmut Wekerle and Florian Kurschus (Max
Planck Institute for Neurobiology, Munich and Institute
of Molecular Medicine, University Medical Center of
the Johannes Gutenberg-University Mainz), MOG35-55
specific T cells from TCR transgenic mice also recognize
another autoantigen, i. e. neurofilament-M (NF-M) pep-
tide 18-30 [1]. Although NF-M and MOG belong to
completely distinct protein families, the NF-M epitope
shares essential TCR-contacting residues with MOG35-
55 that allow for it to be recognized by MOG35-55 spe-
cific T cells when bound to the C57Bl/6 MHC class II
complex (I-Ab). From these studies arises the concept
of ‘cumulative’ autoimmunity with a degenerate TCR
receptor recognizing several autoantigens that may not
be related, thus surpassing the threshold to clinically
manifest organ specific autoimmune inflammation. In a
variety of EAE models using knockout animals, factors
that enhance the pathogenicity of autoreactive T cells
were characterized.
In the past, IFN-g production by autoreactive T cells
has been regarded as pathogenic hallmark of autoanti-
gen specific T cells, which prompted the idea that organ
specific autoimmunity might be a “Th1 disease” [2].
More recently, another phenotype of CD4+ T helper
cells, so-called Th17 cells have been implicated in the
development of EAE and other autoimmune disorders
[3]. However, the plasticity of Th17 cells, which have
been named after their signature cytokine IL-17, appears
to be greater than that of Th1 cells. Whereas the combi-
nation of TGF-b and IL-6 in mouse (and TGF-b plus
IL-21/or IL-1 in man) are the differentiation factors for
Th17 cells [4-7], IL-23 has a major role in the stabiliza-
tion of IL-17 production by Th17 cells and thus in sta-
bilization of the functional phenotype of these cells.
Very recent work performed in the group of Thomas
Korn (presented by Malte Christian Claussen, Dept. of
Neurology, Technical University of Munich) points to
functions of IL-23 that are extrinsic to classical ab T
cells since non-classical T cells and perhaps even non-T
cells express the IL-23R and respond to IL-23 by pro-
duction of cytokines. Usage of IL-23R reporter mice will
provide us with important information on the role of
IL-23 activated non-classical T cells in tissue inflamma-
tion and autoimmunity. The population dynamics and
migration events of both T cells and non-T cells into
the CNS during EAE are still under intense investiga-
tion, and meticulous flow cytometric analysis has been
applied by Karin Steinbach from the groups of Manuel
Friese and Eva Tolosa (Center for Molecular Neurobiol-
ogy, Hamburg) to reveal the temporal pattern of
immune cell infiltration into the CNS during EAE. At
the onset of disease, Th1 cells and Th17 cells accumu-
late in the CNS almost simultaneously. However, IL-17
production by T cells in the CNS appears to be sus-
tained in actively induced MOG35-55 EAE. As far as
the T cell/target interaction in the CNS is concerned,
still little is known about the relative impact of Th1 vs
Th17 cells. Indeed, the exact pathogenic role of Th17
cells in vivo is not yet understood. Besides secreting
cytokines and chemokines to attract other immune cells
like neutrophils, Th17 cells may also directly interact
with target structures in the CNS like naked axons that
have been stripped off their myelin sheaths. Here, excit-
ing in vivo imaging studies using the two photon techni-
que [8] have been presented by Volker Siffrin from the
group of Frauke Zipp (Dept. of Neurology, University
Clinic of Mainz). These investigations revealed that
Th17 cells indeed were able to induce axonal damage in
an MHC class II independent manner. Although the
mechanism of lesion generation remains to be deter-
mined, perforin degranulation may be involved in indu-
cing axonal damage.
While the role of CD4+ T cells for the induction of
immunopathology is a proven fact in EAE, it has been
difficult to assess the mechanism of how CD8+ cyto-
toxic T cells contribute to lesion formation in this
model. Interestingly, CD8+ T cells are present in human
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MS lesions and have been shown to be clonally
expanded suggesting a pathogenic role of these cells [9].
However, only recently new tools have become available
to study the role of CD8+ T cells in an experimental
setting [10]. Furthermore, double transgenic mice have
been generated that express OVA as a neo-autoantigen
in a cell type specific manner in oligodendrocytes under
the MBP promoter and at the same time bear a trans-
genic TCR for a specific OVA-peptide on their CD8+ T
cells (OT-I) [11]. In a highly interesting study by Kerstin
Göbel and Nico Melzer from the group of Heinz Wiendl
(Dept. of Neurology, University Clinic of Würzburg),
brain slices from MBP-OVA transgenic mice have been
used to investigate the interaction of OT-I cells with oli-
godendrocytes presenting OVA-peptide [12]. While OT-
I cells induced apoptosis in oligodendrocytes via direct
attack, neighboring neurons were also affected, revealing
the possibility of perforin-driven collateral damage in
neurons. Besides immunohistochemical and optical
methods to characterize lesion formation on a molecular
level in vivo, electrophysiological methods like patch
clamp approaches are also being used to further charac-
terize the impact of cytotoxic T lymphocytes (CTLs) on
neurons. In vitro, it is possible to measure the break-
down of the neuronal membrane potential when these
neurons, that have been induced to express MHC class I
and have been loaded with OVA peptide, are attacked
by OVA-peptide specific CD8+ OT-I T cells. Again it
appears that this process of CTL-dependent damage to
neurons is perforin mediated since perforin deficient
OT-I cells fail to short-circuit axons. In order to
approach questions of CTL/target interaction on the
molecular level in vivo, viral models of neuroinflamma-
tion are helpful tools. Recently, a model of LCMV infec-
tion is being explored in which the infecting agent (an
RNA virus) can be manipulated by reverse genetics and
specific T cell responses against infected neurons can be
monitored [13,14].
In this model which is being established by Mario
Kreutzfeldt from the group of Doron Merkler at the
Dept. of Neuropathology, University of Göttingen, the
avidity of the CTL/peptide/MHC class I interaction can
be modified and differential immunopathological
responses can be studied in vivo. Lesion generation in
neuroinflammation is not only dependent on cytotoxic
CD8+ T cells, but monocytes and macrophages are
major players in inducing damage to myelin and neu-
rons. While T cell-derived IFN-g is considered the cano-
nical molecule to activate macrophages, a series of other
stimuli can trigger effector functions in these cells.
Interestingly, adhesion of monocytes to immobilized pla-
telets results in massive TNF production by monocytes.
This phenomenon is now being characterized by Harald
Langer in the group of Triantafyllos Chavakis (NIH,
Bethesda, USA). The molecular basis for the interaction
of platelets and monocytes appears to be a ligand/recep-
tor interaction between GPIb on platelets and Mac-1
(CD11b/CD18) on monocytes. Blockade of this interac-
tion results in diminished secretion of TNF by macro-
phages, and GPIb deficient mice develop attenuated
EAE suggesting that platelet-mediated activation of
macrophages might be an important effector mechanism
in this disease. Besides immune cell/neuron interactions,
several further pathways may play an important role in
inflammation-mediated neurodegeneration. Among
others, neurotrophic factors and ion channels have
recently been in the focus of interest. Neurotrophic fac-
tors comprise neutrophins and neurotrophic cytokines
which are mainly produced in the nervous system, but
also by immune cells. As a prototype mediator, the role
of brain derived neurotrophic factor (BDNF) and its
receptors trkB and p75NTR have been characterized in
MS lesions and more recently also in EAE models
[15-17]. Using an experimental approach with bone mar-
row chimera, Tobias Dallenga from the groups of Stefan
Nessler and Christine Stadelmann (Dept. of Neuropathol-
ogy, University of Göttingen) has studied p75NTR-
mediated signaling in immune cells and non-immune
cells during EAE. These data suggest an important role
of immune cell-derived BDNF and p75NTR-mediated
signaling pathways for axon protection. In autoimmune
inflammation, Nav and Kv channels as well as acid sen-
sing ion channels were all shown to play a role for axon
or glial cell function but in part also for regulation of the
immune cell response [18,19]. More recently, a new
family of genes encoding two-pore domain potassium
channels that generate “leak” potassium currents were
characterized. The TASK subfamily of channels, notably
TASK-1 (KCNK3) and TASK-3 (KCNK9), have now been
shown to modulate inflammation and neurodegeneration
in EAE and probably also ischemic stroke, thus identifying
new potential molecular targets for the therapy of inflam-
matory and degenerative CNS disorders. These data were
presented by Petra Ehling from the group of Thomas
Budde, Dept. of Physiology, University of Münster.
Investigation of immune cell/target cell interactions is
certainly a major domain of animal studies. Yet, studies
with human immune cells are required to test the rele-
vance of hypotheses that have been raised in animal
models. We are now witnessing the first reports on
Th17 cells in human MS on a larger scale. Notably, the
frequency of Th17 cell clones but not Th1 clones in the
peripheral blood and the CSF appears to be correlated
with disease activity in relapsing remitting MS [20,21].
In ex vivo analyses performed by Verena Brucklacher-
Waldert from the group of Eva Tolosa (Center for
Molecular Neurobiology, Hamburg), Th17 cells had
a strongly activated phenotype and were relatively
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resistant to regulatory T cell (Treg)-mediated suppres-
sion in comparison with Th1 cells. In contrast to EAE
which is clearly dependent on CD4+ T helper cells,
human MS is more complex and a plethora of other
immune cells are directly or indirectly involved in the
generation of MS lesions. NK cells have been of particu-
lar interest in this regard since their modulation appears
to be the basis of the efficacy of a monoclonal antibody
to the IL-2R (daclizumab) that has recently been tested
in clinical trials [22]. Brady Messmer from Jan Luene-
mann’s group at the Institute for Experimental Immu-
nology, University of Zuerich, Switzerland studied the
role of NK cells in MS patients in more detail. NK have
been identified in MS lesions. CD56dim NK cells are
equipped with the molecular machinery to kill their tar-
get cells and are more prominent in PBMCs as com-
pared with lymph nodes. In contrast, CD56bright NK
cells produce cytokines like IFN-g, TNF, and GM-CSF
and are more abundant in lymph nodes than in PBMCs
[23]. CD56bright NK cells are divided into CD16- and
CD16+ populations. In order to evaluate the role of NK
cells in the pathogenesis of MS in more detail, NK cells
of MS patients were studied and compared with those
of healthy control subjects. In MS patients,
CD56brightCD16- NK cells show impaired expansion and
produce less IFN-g in response to IL-12 whereas the
lytic function of NK cells (CD56dim) appears to be
unchanged. These data suggest that subsets of NK cells
in MS patients display a functionally different phenotype
and may be implicated in the disease process.
Further lessons on the relation between immune cells
and CNS tissue can be learned from degenerative dis-
eases and their respective animal models. Here, studies
in mouse models of Alzheimer’s disease (AD) as well as
Huntington’s disease (HD) recently gained much inter-
est. Initially, AD has been characterized by formation of
amyloid plaques, neurofibrillary tangles and subsequent
neurodegeneration. More recently, the role of immune
cells, most notably microglia, in this process has been
characterized. While the exact sequence of events even-
tually leading to neuronal death still remain to be deter-
mined, several mediators involved in regulation of
microglia have been identified. Here, especially chemo-
kines and their receptors were found to play an impor-
tant role, e.g. for cell migration (work presented by
Marius Krauthausen from the group of Markus Müller
and Michael Heneka, Dept. of Neurology, University of
Bonn). The modulation of such factors may critically
regulate microglial function and finally also influence
the process of neurodegeneration. Similar observations
were reported in models of HD which are characterized
by formation of intraneuronal huntingtin aggregates and
neuronal dysfunction. Here, innovative neurobiological
treatment approaches such as anti-sense technologies or
stem-cell based repair strategies can reduce huntingtin
aggregate load and improve functional deficits in mouse
models of HD as presented by Christian Saß from the
Dept. of Neurology, University Clinic of Aachen. In
addition, more established treatment strategies such as
therapy with immunomodulators appear to be effective
as well (Christiane Reick, Dept. of Neurology, St. Josef-
Hospital, Ruhr-University Bochum). These data point to
a role of the immune system in HD, but also to a puta-
tive neuroprotective function of these drugs, thus open-
ing up an exciting new avenue of translational research
linking the fields of neuroimmunology and
neurobiology.
Contributions on stroke and vascular pathology
Ischemic stroke is a devastating disease that represents
the second leading cause of death worldwide. Each year,
575.000 people in Europe fall victim to ischemic stroke,
which is estimated to cost 71.8 billion Euros [European
Stroke Initiative]. It is estimated that the lifetime risk
for stroke is between 8% and 10%. Early restoration of
blood flow remains the treatment of choice for limiting
brain injury following stroke. While reperfusion of the
ischemic brain is desirable in principle, it may also fos-
ter tissue damage under certain conditions. Reperfusion
appears to augment the inflammatory response and
causes additional injury to adjacent brain tissue. Hence,
a rapidly evolving area of stroke research involves defin-
ing the molecular and cellular basis for this secondary
tissue injury and inflammation associated with transient
cerebral ischemia. For this research, primarily the mid-
dle cerebral artery occlusion reperfusion model in mice
is used.
The inflammatory response seen in this model is
initiated by an accumulation of microglia and the secre-
tion of pro-inflammatory cytokines such as IL-1b, IL-6
or MCP-1 (researched by Mathias Gelderblom from the
groupd of Tim Magnus, Dept. of Neurology, University
Clinic Hamburg-Eppendorf, Hamburg). On the cellular
level, infiltration of the ischemic hemisphere by macro-
phages, lymphocytes, and dendritic cells (DCs) within
the first day precedes neutrophilic influx. Up-regulation
of MHC-II and the co-stimulatory molecule CD80
demonstrate activation of these cells arguing for a pro-
inflammatory environment. However, also regulatory
immune cells (NKT cells, CD4-/CD8-T lymphocytes,
Foxp3+ T cells) accumulate in the ischemic brain [24].
The functional relevance of inflammatory cells can be
proven in knockout animals such as Rag deficient mice
that lack B and T cells and are largely protected from
inflammatory damage secondary to ischemic stroke [25].
Conversely, depletion of regulatory T cells (Treg)
induces a significant increase in infarct size pointing to
a relevant part of these cells in regulating post-stroke
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inflammation [26]. Furthermore, inhibition of cell migra-
tion into the lesioned brain might become an interesting
approach to modulate stroke-induced immune pathways.
Arthur Liesz from the group of Roland Veltkamp, Dept.
of Neurology, University of Heidelberg, showed that
blockage of immune cell entry results in smaller infarcts
and an improved neurological outcome. This blockage
was achieved by an antibody preventing the binding of
a 4 integrins, a common therapeutic approach also in
MS. So far, it remains unclear which cell type (if any) is
the key player in ischemic stroke. However, it seems
likely that T cells and their subtypes play an important
role while the function of neutrophils, which also
express a 4 integrins, is not yet clear.
In contrast to the local pro-inflammatory response
within the CNS, changes in the systemic immune com-
partment indicate a more general stroke-associated
immune suppression. The latter can, as Odilio Engel from
Andreas Meisel’s group at the Dept. of Experimental Neu-
rology, Charité Universitätsmedizin Berlin, points out, be
observed in patients as well as in the animal model, where
an increased bacterial load is found in the lungs of stroked
rodents. The immunosuppressive effect may be elicited by
an increase in vagal activation and subsequent secretion of
acetylcholine in lymph nodes and spleen.
Another facet in stroke research is related to the occur-
rence of oxidative stress. Cells and especially neurons
have to deal within minutes with reactive oxygen and
nitrogen species (ROS/RNS). One attractive candidate
source for oxidative stress in acute ischemic stroke are
NADPH oxidases, the only known enzyme family that
has ROS as their sole enzymatic product. These are the
molecules of a specific research interest for Tobias
Schwarz form Christoph Kleinschnitz’s group at the
Dept. of Neurology, University Clinic of Würzburg. In
rodents 4 NOX genes exist, and in the rodent brain NOX
are mainly expressed in neurons and the vasculature with
NOX4 being the most abundant isoform. In an interest-
ing study using NOX1, NOX2 and NOX4 deficient mice
as well as the specific NOX Inhibitor VAS2870, the
pathophysiological role of the different NOX isoforms in
ischemic stroke has now been assessed in terms of infarct
development and blood-brain-barrier damage.
Our current performance in the acute treatment of
stroke patients is moderate at best and, therefore, addi-
tional efforts to enhance tissue repair are badly needed.
As outlined above, inflammatory cascades are active
during cerebral ischemia. However, their effects are not
necessarily detrimental, as Karen Gertz from the group
of Matthias Endres, Dept. of Neurology, Charité Univer-
sitätsmedizin Berlin, reminds us. IL-6, for example,
helps to increase vascular repair and possibly neogenesis
and can improve long term outcome in experimental
stroke. Other strategies involve the use of stem cells
(presented by Jens Minnerup from the group of Wolf-
Rüdiger Schäbitz, Dept. of Neurology, University of
Münster). However, it appears that significant tissue
repair derived from endogenous stem cells is not realis-
tic in ischemic stroke, at least in the near future. The
systemic application has turned out difficult since it is
not easy to derive the perfect cell that is undifferentiated
enough to integrate and survive but develops into a
functional neuron. Although some functional improve-
ment can be seen in stroked rodents after the applica-
tion of neurospheres depending on their differentiation
protocol, the therapeutic effects are still relatively small.
Finally, Jan Klohs from Ulrich Dirnagl’s group at the
Dept. of Experimental Neurology, Charité Universitäts-
medizin Berlin, introduced a new imaging technique in
rodent stroke models [27]. Near-infrared fluorescence
(NIRF) imaging is suitable to visualize distinct molecules
involved in the pathophysiology of ischemic stroke in
rodents in vivo by utilizing specific NIRF probes, e.g.
against matrix metalloproteinases (MMPs). Although its
temporal resolution is still relatively low, this non-inva-
sive method could be useful in monitoring treatment
responses in individual animals over time.
Concluding remarks
Lesion formation and repair are always essential events
in pathological conditions in the CNS. Although distinct
diseases, vascular, inflammatory and neurodegenerative
disorders of the CNS may share pathological sequences
on the cellular and molecular level. Decades of experi-
ence and gathering of knowledge in the formation, traf-
ficking and effector functions of immune cells in
neuroinflammatory conditions may help to better under-
stand the involvement of immune cells in vascular dis-
eases and neurodegenerative disorders. Thus, comparing
cellular reactions in the peripheral immune compart-
ment and the CNS across different disease models may
offer an unconventional but very efficient means to gen-
erate new ideas and promote research. We hope that
our initiative will help young researches to create new
concepts and opportunities to improve the understand-
ing of many neurological diseases and to find new treat-
ment options. We encourage all members of the
neurological community to support our idea and pro-
vide constructive input for the upcoming meeting in
October 2010.
Acknowledgements
The first scientific meeting of NEUROWIND e.V. was kindly supported by
Merck Serono GmbH, Darmstadt, Germany (unrestricted grant to
NEUROWIND e.V.). The authors thank all speakers at the 1’st NEUROWIND e.
V. scientific meeting. We thank Ms. Anke Bauer, Wuerzburg, for editing the
manuscript.
Co-investigators at the 1st scientific meeting of NEUROWIND e.V. (in
alphabetical order)
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