Nanolesions induced by heavy ions in
human tissues: Experimental and theoretical studies
Marcus Bleicher1,2, Lucas Burigo1,2, Marco Durante*1,3,4, Maren Herrlitz1,3,4,
Michael Krämer3, Igor Mishustin1,5, Iris Müller3, Francesco Natale1,3,
Igor Pshenichnov1,6, Stefan Schramm1,7, Gisela Taucher-Scholz3
and Cathrin Wälzlein1,3,4
Full Research Paper
1Frankfurt Institute for Advanced Studies (FIAS), Ruth-Moufang-Str. 1,
60438 Frankfurt am Main, Germany, 2Institut für Theoretische Physik,
Johann Wolfgang Goethe-Universität, Max-von-Laue-Str. 1, 60438
Frankfurt am Main, Germany, 3GSI Helmholtzzentrum für
Schwerionenforschung GmbH, Planckstr. 1, 64291 Darmstadt,
Germany, 4Technische Universität Darmstadt, Institut für
Festkörperphysik, Hochschulstr. 8, 64289 Darmstadt, Germany,
5National Research Center "Kurchatov Institute", 1, Akademika
Kurchatova pl., Moscow, 123182, Russia, 6Institute for Nuclear
Research, Russian Academy of Sciences, 7a, 60th October
Anniversary prospect, Moscow 117312, Russia and 7Center for
Scientific Computing, Johann Wolfgang Goethe-Universität,
Max-von-Laue-Str. 1, 60438 Frankfurt am Main, Germany
Marco Durante* - M.Durante@gsi.de
* Corresponding author
DNA repair; heavy ions; microdosimetry; Monte Carlo simulations;
nanolesions; radiation-induced nanostructures
Beilstein J. Nanotechnol. 2012, 3, 556–563.
Received: 30 March 2012
Accepted: 24 May 2012
Published: 25 July 2012
This article is part of the Thematic Series "Radiation-induced
nanostructures: Formation processes and applications ".
Guest Editor: M. Huth
© 2012 Bleicher et al; licensee Beilstein-Institut.
License and terms: see end of document.
The biological effects of energetic heavy ions are attracting increasing interest for their applications in cancer therapy and protec-
tion against space radiation. The cascade of events leading to cell death or late effects starts from stochastic energy deposition on
the nanometer scale and the corresponding lesions in biological molecules, primarily DNA. We have developed experimental tech-
niques to visualize DNA nanolesions induced by heavy ions. Nanolesions appear in cells as “streaks” which can be visualized by
using different DNA repair markers. We have studied the kinetics of repair of these “streaks” also with respect to the chromatin
conformation. Initial steps in the modeling of the energy deposition patterns at the micrometer and nanometer scale were made with
MCHIT and TRAX models, respectively.
Beilstein J. Nanotechnol. 2012, 3, 556–563.
In a low-dose field of γ-rays, such as that normally experienced
on Earth due to background radiation, each human cell is
traversed by very few electrons, which hence produce little
damage. However, for energetic heavy ions, the situation is
different. A low dose, such as the one experienced in a manned
mission to the International Space Station or the Moon ,
corresponds to only a few tracks, but each track can affect a
whole tissue or organ, and each cell that is found in the path of
the ion. The central part of the track, where most of the energy
is deposited, has a radial extension of only a few nanometers,
while a lower energy is deposited at a larger distance by ener-
getic δ-rays. Thus, each heavy ion will produce a nanochannel
in neighboring cells in a tissue or organ, a situation that makes
the concept of low dose itself flawed. Although the concept of a
“microlesion” induced by heavy ions in space was already
acknowledged long ago , there is a lack of experimental
models for testing the hypothesis that they represent a distinct,
unique type of damage at the tissue level. Moreover, Monte
Carlo codes should be able to simulate the damage at the
micrometer and even nanometer level, basing on the stochastic
energy deposition pattern. One problem associated with the for-
mation of nanolesions is the nonuniform structure of the target,
i.e., of the cell nucleus . In fact, the compact heterochro-
matin provides a different environment compared to the tran-
scriptionally competent euchromatin, and it had been proposed
that heterochromatin was “refractory” to repair proteins . We
have investigated in detail the structure of nanolesions, their
formation and movement in the cell nucleus, using live cell
microscopy and immunohistochemistry. Stimulated by the
differences in repair kinetics and movement of the tracks in eu-
and heterochromatin, we have further analyzed the histone
modifications (particularly acetylation) along heavy-ion nano-
lesions. We have also started a full-genome deep-sequencing
approach to correlate the microscopy data with the cellular
response. In principle, the nanolesion structure can be predicted
by accurate Monte Carlo simulations of the energy deposition
by the projectile and of the target structure. We used the Monte
Carlo model for heavy-ion therapy (MCHIT) code  to simu-
late the energy deposition to micrometer-sized objects, e.g., cell
nuclei, and compared the results to microdosimetric spectra
previously measured . To further describe the nanometer
region, the GSI track structure Monte Carlo code TRAX ,
whose purpose is to properly describe the creation and trans-
port of low energy electrons, has been extended to describe
Results and Discussion
Nanolesions in different regions of the chromatin
Physics obviously predicts that streaks produced by heavy ions
in the DNA should be linear. However, using a double-strand
Figure 1: Bending of linear ion-induced γH2AX streaks indicates chro-
matin density-dependent damage relocation. Three types of γH2AX
patterns, each shown in a mouse embryo fibroblast nucleus and as a
schematic drawing, were observed at ion-hit chromo centers: bent
streaks (upper panel), interrupted streaks (middle panel) and internal
signals (lower panel). Modified from .
break (DSB)-specific marker (phosphorylated histone γH2AX),
we found “bending” of the streaks when cells were fixed for
30 min or more after irradiation  (Figure 1). Reconstruction
of the track dynamics by using live-cell imaging (Supporting
Information File 1) and the heavy-ion microbeam (Figure 2)
Beilstein J. Nanotechnol. 2012, 3, 556–563.
Figure 3: Accumulation of H4K16ac in mouse embryonic fibroblasts. Cells were irradiated with Au ions (energy: 8 MeV/n, linear energy transfer
(LET): 13000 keV/μm; fluence: 3·106 ions/cm2) at a low angle and fixed after 1 h. H4K16ac (green) is increased at damage sites. DNA damage is
shown by γH2AX staining (red). DNA is counterstained with ToPro3 (blue). From  – Copyright: GSI Helmholtzzentrum für Schwerionenforschung
Figure 2: Relocation dynamics of damage sites centrally induced
within heterochromatic chromo centers. (a) The mouse embryo fibrob-
last (MEF) nucleus was irradiated with single sulfur ions and immunos-
tained 5 min after irradiation. H2AX is phosphorylated and the repair
protein XRCC1 accumulates at heterochromatic DSBs directly after
single-ion irradiation. The left-hand image shows the aimed targeting
of chromo centers (red crosses) for single-ion irradiation by using
Hoechst 33342 (grey scale) as a marker in the nuclei of living MEF
cells. The right-hand image shows the same nucleus after fixation at
5 min after irradiation. DNA-damage-induced foci of the repair factor
XRCC1 (green) and γH2AX (red) are clearly visualized at the sites of
ion traversal. Both proteins colocalize within each of the targeted
chromo centers (blue: DAPI DNA staining). (b) Analysis of the time-
dependent localization of XRCC1 and γH2AX radiation-induced foci.
Relative frequencies of each position are given for the indicated post-
irradiation intervals and (n), the total number of ion-hit chromo centers
from three independent experiments, is indicated. Error bars represent
the SEM. Figure adapted from .
showed that DNA-DSBs are indeed formed within heterochro-
matin, but they are relocated to euchromatin and the repair
kinetics are slower than for euchromatic lesions . These
results in mammalian cells have also been observed at the
Lawrence Berkeley Laboratory in Drosophila , thus
suggesting that the lesion relocation from hetero- to euchro-
matin is a universal phenomenon.
Conformational changes in chromatin
The results described above point to a large-scale chromatin
decondensation at sites of nanometric DNA lesions. This obser-
vation shifted our attention from the analysis of “DNA nano-
lesions” to a more general concept of “chromatin nanolesions”.
Histone modifications, especially histone acetylation at defined
lysine residues, play a major role in changing the density of
chromatin. To explain the local decompaction of heterochro-
matic regions that takes place at sites of DNA damage , we
investigated the acetylation of different histone residues that
may be involved in this process. We investigated the histone
residues H4K16 as well as H3K56. It is known that these
residues play a role in the DNA damage response after irradi-
ation by X-rays and UV-lasers [10,11]. In a limited fraction of
cells, we measured H4K16ac streaks after exposure to heavy
ions (white arrow in Figure 3) that are clearly distinguishable
from the H4K16ac signal in the whole nucleus .
An accumulation of H3K56ac was not observed. These find-
ings suggest that H4K16ac may also play a role in the damage
response after irradiation with heavy ions. Since it is known that
acetylation of H4K16 changes chromatin to a more open con-
formation it has to be elucidated whether H4K16 acetylation is
involved in decompaction of DNA at damage sites. However,
not all of the cells presented visible H4K16ac streaks, and the
effect was observed only with very heavy Au ions. At the
fluence used in our experiments (3·106 Au-ions/cm2) we
measured an average of three streaks/cell by using DNA repair
Beilstein J. Nanotechnol. 2012, 3, 556–563.
markers, and therefore less than 5% of the cells should have no
streaks according to Poisson statistics. Moreover, experiments
with lighter ions did not produce clear signals. Further experi-
ments are underway to clarify these issues.
Genome-wide screening of the chromatin nano-
Alternatively to observation by microscope, the distribution of
DNA nanolesions can be investigated with the novel ChIP-Seq
technology , which allows the mapping of DNA-protein
interactions sequence-wise and genome-wide. We used
ChIPSeq to provide a genome-scale sequence-based map of the
γH2AX signature induced by ionizing radiation. Compaction
state of chromatin domains was characterized by multipara-
metric analysis (e.g., GC content), and the distribution of radia-
tion-induced γH2AX along such chromatin domains was
investigated. This complex study is still underway, but prelimi-
nary results (Figure 4) suggest that γH2AX is positively corre-
lated to the GC content. Such a feature would indicate that a
less compact state (high GC content) could be a more favorable
environment for γH2AX spreading than highly compact hete-
Figure 4: The phosphorylated H2AX distribution after radiation is
correlated with the GC base content (a genomic feature associated
with high gene content) of the transcriptionally competent and relaxed
chromatin (euchromatin). The chromosome 1 profile is shown in the
cartoon, with dark bands corresponding to heterochromatin and light
bands to euchromatin (from chromosome G-banding). Preliminary
ChIP-Seq data show that the γH2AX signature (orange) is enriched in
high-GC-content DNA sequences (black line, below) and dark chromo-
somal bands (e.g., p31.1, q41), corresponding to a very low GC
content are underrepresented. From  – Copyright: GSI
Helmholtzzentrum für Schwerionenforschung GmbH.
MCHIT simulations of microdosimetry distributions
The Monte Carlo method is a convenient technique to account
for the interactions of beam nuclei and all secondary particles
with tissues. The MCHIT  based on the Geant4 toolkit was
created in the Frankfurt Institute for Advanced Studies (FIAS)
to study the propagation of therapeutic beams in extended
media. MCHIT calculates the spatial distribution of energy
deposited in a tissue-like phantom, taking into account the frag-
mentation of beam nuclei.
A practical way to investigate energy deposition to objects
equivalent to living cells consists of measurements with detec-
tors called tissue-equivalent proportional counters (TEPC).
Typically a TEPC is designed as a low-pressure gas chamber a
few millimeters in size. The energy ε delivered to the small
sensitive volume in a single event fluctuates due to the
stochastic nature of particle propagation in media. Micro-
dosimetry measurements provide the probability distributions
for lineal energy defined as y = ε/<l>, where <l> is the mean
chord length of the sensitive volume of the detector. The distri-
butions of lineal energy (microdosimetric spectra) are directly
related to the biological effects of radiation.
The MCHIT model was used to simulate microdosimetry
measurements at GSI . In this experiment the micro-
dosimetry yd(y) spectra (see  for their definition) were
collected on the beam axis, as well as off-axis, inside a water
phantom, irradiated by a narrow 300 A MeV 12C beam. Simula-
tion results for four TEPC positions inside the phantom are
shown in Figure 5. Two of the four measurements (marked as
“0 cm”) were performed on the beam axis and the other two at
10 cm radius at the beam entrance to the water phantom
(“plateau”) and at the depth of the Bragg peak (“peak”).
It is known that secondary particles of various charges and
velocities can eventually contribute with similar lineal energy
values. Therefore, the considered yd(y)-distribution is built as a
sum of contributions from various secondary particles repre-
senting a multicomponent radiation field around the primary
beam. The contributions of various fragments to the spectra are
shown separately in Figure 6 for a TEPC located at the Bragg
peak on the beam axis. The peak in the distribution at y ≈
131 keV/μm is due to the primary carbon nuclei while the
second broad peak at y ≈ 25 keV/μm is caused by projectile
fragments produced in fragmentation reactions. The MCHIT
model reproduces the general shape of yd(y) distributions at all
four TEPC positions in the phantom (Figure 5). However, it
underestimates the spectra for TEPCs located far from the beam
axis. This problem is apparently related to an underestimation
of yields of light fragments produced by primary nuclei in the
phantom. The contributions to yd(y) distributions from second-
Beilstein J. Nanotechnol. 2012, 3, 556–563.
Figure 5: Microdosimetric spectra in a water phantom irradiated by 300 A MeV 12C nuclei. Upper (red) histograms are the total spectra calculated
with MCHIT, the lower (blue) histograms show the neutron contributions. Data points from .
Figure 6: Contribution of various fragments to the microdosimetry
spectra measured on the beam axis in the Bragg peak region in a
water phantom irradiated by 300 A MeV 12C nuclei. Histograms repre-
sent MCHIT calculations. Data points from .
ary neutrons are also shown in Figure 5 for the considered
TEPC positions. The neutron contribution increases with the
distance from the beam axis. At the TEPC positions far from the
beam (at 10 cm radius) the total contribution from neutrons
amounts to ≈50% at the plateau and to ≈25% at the Bragg peak
depth. More details on microdosimetry simulations with the
MCHIT model, in particular on specific physics models used in
calculations, can be found elsewhere .
Extensions of the TRAX code
The elevated radiobiological effectiveness of heavy ions can be
attributed to the largely inhomogeneous damage deposition on
the micro- or even nanometer level when compared to sparsely
ionizing reference radiation with the same macroscopic dose
deposition. Whereas photons or electrons show an almost
uniform distribution of interaction events, even on this small-
scale level, the dose deposition caused by ions is centered on
the track core and falls off as 1/r2. Thus, towards the ion-track
Beilstein J. Nanotechnol. 2012, 3, 556–563.
core, local doses deposited by ions can reach values up to kilo-
or even megagrays for the heaviest ions. On the other hand, bio-
logical endpoints important for radiotherapy, such as tumor cell
killing and healthy tissue damage, follow the well-known and
well-proven linear-quadratic dose dependence. This means that
high doses, as they occur in the ion track core, contribute
disproportionally to the radiobiological effect. Thus this part of
the radial dose distribution will contribute most to the radiation
action. Unfortunately the ion track core is also the least known
region in this scenario. Available models usually cut off and
renormalize the radial dose at distances of the order of ten
nanometers to avoid the mathematical divergence at r = 0,
which is justified by reasonable results, but somewhat unsatis-
fying from the physical point of view. Experimental data are
almost nonexistent in this region, even in gases, let alone in
To improve on this situation, at least from the computational
side, we apply our simulation code TRAX , constantly devel-
oped at GSI over several years. It uses the single interaction
Monte Carlo method, rather than a condensed random walk, to
describe radiation action at the lowest possible level. When
inspecting the nanoscale, however, not only the usual ioniza-
tion and excitation events, but also elastic scattering of the pri-
mary ion, which is often neglected, may play a role. Therefore
we have included this interaction in the simulation to evaluate
its influence on the nanoscale damage distribution. Screened
Rutherford cross sections according to Berger  were used to
account for the elastic scattering of ions. The correct implemen-
tation of this additional interaction in the code was bench-
marked against experimental results. Gottschalk et al.  have
measured the angular distribution of 158.6 MeV protons inci-
dent on several different target materials and thicknesses. The
TRAX simulations including elastic ion scattering showed good
agreement with these experimental results, as can be seen in
Additionally the simulations were compared to Highland's
formula , which is a parameterized approximation of the
Molière theory. The implementation of elastic ion scattering is
an important step towards a complete description of the rele-
vant physical effects that contribute to the energy deposition on
the nanoscale. However, further extensions of the code may be
necessary to account for all important physical effects. Figure 8
shows that the elastic scattering of the primary ions has an
effect on the nanometer scale. Energy deposition events, such as
excitation and ionization, which are caused by the primary ions,
no longer occur only at r = 0. The positions are shifted on the
nanometer scale. This reduces the calculated radial dose at r = 0
(not shown in the figure) and increases the calculated radial
dose at radii within the scattering radius of the primary ions.
Figure 7: Simulated angular distributions of 158.6 MeV protons inci-
dent on 0.66 cm beryllium (upper picture) and 0.30 cm carbon (lower
picture) with TRAX. The binning of the histogram in the TRAX simula-
tion is 0.03 degrees. In the case of the beryllium target, fitting a
Gaussian distribution to the simulated data resulted in a Gaussian
width of (0.30 ± 0.01)° which is exactly the same result as experimen-
tally determined in . Highland's formula  led to a width of 0.27°.
In the case of carbon, the fit to the TRAX results resulted in a
Gaussian width of (0.28 ± 0.01)°, while Gottschalk et al.  deter-
mined this width to be (0.26 ± 0.01)°. Highland's formula  resulted
in 0.24° for the carbon target.
We have developed experimental techniques to visualize nano-
lesions in human tissues and to analyze these lesions genome-
wide. In our approach, nanolesions are induced by very heavy
ions and studied by the recruitment of repair proteins and the
epigenetic changes in the chromatin surrounding the damaged
DNA molecule. We concluded that the structure of the nano-
lesions depends strongly on the target structure, where the target
is not only DNA, but the protein-nucleic acid complex (chro-
matin). Monte Carlo codes MCHIT and TRAX can elegantly
reproduce the measured [6,17] energy deposition patterns
following the passage of energetic heavy ions. However, further
efforts are required to improve the MCHIT model accuracy in
calculating spectra far from the beam axis and to extend TRAX
to complex inhomogeneous targets. Novel target simulations
will be necessary to simulate the observed formation and
dynamics of nanolesions in tissues. Further extensions of the
MCHIT and TRAX code will be necessary to obtain a satisfac-
tory description of energy deposition and track behavior at the
nanometer scale in realistic targets.
Detailed experimental methods for immunohistochemistry and
live-cell imaging in our laboratories are described elsewhere
[8,12]. We have recently installed a 405 nm laser for photoacti-
Beilstein J. Nanotechnol. 2012, 3, 556–563.
Figure 8: In the upper picture, the tracks of 10 individual oxygen ions
with a primary energy of 2.57 MeV/u, incident on water, are shown
while the elastic scattering of ions is neglected. They all travel straight
through the medium. The blue spots indicate the interaction positions
of the secondary electrons. In the central picture the same plot is
shown including the elastic scattering of ions. The angular deflection
over a travelling length of 1 μm can be seen. On the nanometer scale,
the shift of ionization and excitation events of the primary ions is
noticeable. The resulting radial dose with and without elastic ion scat-
tering is shown in the lower picture. It can be seen that the radial dose
differs in the area that is equal to the radius of the elastic scattering of
ions. The deflection of the primary ions leads to a natural "diffusion" of
the radial dose.
vation studies . The experimental setup is based on a Leica
IRE2 inverted microscope equipped with LED light sources and
a climate chamber for controlling of the temperature, humidity
and CO2 concentration, for long-term live-cell observations.
Image acquisition is done by a Hamamatsu C7190 EB-CCD
camera. Photobleaching of GFP-tagged H2B in living HeLa
cells by the 405 laser is demonstrated in Figure 9. By turning
and panning of the laser circle, the logo of the Beilstein-Institut
was visualized by pseudocoloring of the bleached regions.
Details of the microdosimetry measurements are given in .
We simulated with MCHIT the TEPC model LET-1/2, Far West
Technology at a gas pressure of 120 mbar, equivalent to 2.7 μm
Figure 9: Living HeLa cells expressing histone H2B tagged to GFP
were photobleached. Bleaching within a region of three sectors of a
circle depletes fluorescence from the bleached region. Colors of the
three regions were adjusted with ImageJ and the different channels
were merged. From  – Copyright: GSI Helmholtzzentrum für
Supporting Information File 1
The animation in Supporting Information File 1 shows a
real time observation of the recruitment of GFP-XRCC1 to
two charged particle tracks traversing the nucleus of a
living MEF cell during high energy (1 GeV/n) uranium
irradiation. From these 3-D image stacks, movies were
generated by making maximum projections of the
fluorescence intensity using Image J
(http://rsb.info.nih.gov/ij/). Red color indicates
Cherry-tagged HP1α (marking chromocenters), green color
GFP-XRCC1. Total imaging time: 9.5 min. Shot noise (due
to neutron scattering) indicates the irradiation time points.
Please note the fast GFP-XRCC1 recruitment along tracks,
disappearance of euchromatic foci (green) and the
prolonged retention of heterochromatic GFP-XRCC1
(yellow, overlapping HP1α) in the left radiation track.
Beilstein J. Nanotechnol. 2012, 3, 556–563. Download full-text
Supporting Information File 2
Supporting Information File 2 is a high resolution
animation showing real time GFP-XRCC1 recruitment to
the high energy uranium ion track traversing a single MEF
chromocenter (red, marked by Cherry-HP1α). Note the
billowing motion of the damaged domain (XRCC1, green;
appears yellow due to HP1α overlap in heterochromatin)
and a drift toward the chromocenter periphery.
This work was supported by the Beilstein-Institut, Frankfurt am
Main, Germany (NanoBiC collaboration).
1. Durante, M.; Cucinotta, F. A. Rev. Mod. Phys. 2011, 83, 1245–1281.
2. Todd, P. Adv. Space Res. 1983, 3, 187–194.
3. Jakob, B.; Durante, M. Radiat. Res. 2012, 177, 524–532.
4. Kim, J.-A.; Kruhlak, M.; Dotiwala, F.; Nussenzweig, A.; Haber, J. E.
J. Cell Biol. 2007, 178, 209–218. doi:10.1083/jcb.200612031
5. Pshenichnov, I.; Botvina, A.; Mishustin, I.; Greiner, W.
Nucl. Instrum. Methods Phys. Res., Sect. B 2010, 268, 604–615.
6. Martino, G.; Durante, M.; Schardt, D. Phys. Med. Biol. 2010, 55,
7. Krämer, M.; Durante, M. Eur. Phys. J. D 2010, 60, 195–202.
8. Jakob, B.; Splinter, J.; Conrad, S.; Voss, K.-O.; Zink, D.; Durante, M.;
Löbrich, M.; Taucher-Scholz, G. Nucleic Acids Res. 2011, 39,
9. Chiolo, I.; Minoda, A.; Colmenares, S. U.; Polyzos, A.; Costes, S. V.;
Karpen, G. H. Cell 2011, 144, 732–744. doi:10.1016/j.cell.2011.02.012
10.Miller, K. M.; Tjeertes, J. V.; Coates, J.; Legube, G.; Polo, S. E.;
Britton, S.; Jackson, S. P. Nat. Struct. Mol. Biol. 2010, 17, 1144–1151.
11.Li, X.; Corsa, C. A. S.; Pan, P. W.; Wu, L.; Ferguson, D.; Yu, X.;
Min, J.; Dou, Y. Mol. Cell. Biol. 2010, 30, 5335–5347.
12.Herrlitz, M.; Müller, I.; Liefke, A. L.; Becker, G.; Durante, M.;
Taucher-Scholz, G. GSI Scientific Report 2012, 60, 1448.
13.Iacovoni, J. S.; Caron, P.; Lassadi, I.; Nicolas, E.; Massip, L.;
Trouche, D.; Legube, G. EMBO J. 2010, 29, 1446–1457.
14.Natale, F.; Rapp, A.; Durante, M.; Taucher-Scholz, G.; Cardoso, M. C.
GSI Scientific Report 2012, 84, 1542.
15.Burigo, L.; Pshenichnov, I.; Mishustin, I.; Bleicher, M., Microdosimetry
of radiation fields from therapeutic 12C beams in water: a study with
Geant4 toolkit, in preparation.
16.Berger, M. J. Methods Comput. Phys. 1963, 1, 135.
17.Gottschalk, B.; Koehler, A. M.; Schneider, R. J.; Sisterson, J. M.;
Wagner, M. S. Nucl. Instrum. Methods Phys. Res., Sect. B 1993, 74,
18.Highland, V. L. Nucl. Instrum. Methods 1975, 129, 497–499.
19.Khan, R.; Herrlitz, M.; Jakob, B.; Durante, M.; Taucher-Scholz, G.
GSI Scientific Report 2012, 75, 1490.
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