REVIEW doi:10.1111/j.1360-0443.2008.02157.

Social cognition in alcoholism: a link to

prefrontal cortex dysfunction?
Jennifer Uekermann & Irene Daum
Institute of Cognitive Neuroscience, Ruhr-University of Bochum, Bochum, Germany

ABSTRACT

Aims Alcoholism is associated with a range of cognitive deficits. These deficits might be explained by the ‘frontal lobe
hypothesis’ which suggests a specific vulnerability of the prefrontal cortex (PFC) to the neurotoxic effects of alcohol.
Social cognition is thought to be processed in the PFC, but so far only few studies have addressed the issue of social
cognition deficits in alcoholism. This review aims to evaluate the deficits in social cognition in alcoholic patients. In
addition an outline for future perspectives is given. Methods Medline and Psyclit searches were performed for a 30-year
period (1977–2007). Results Alcoholism is associated clearly with social cognition impairments which include emotional
face and prosody perception problems, theory of mind deficits and humour processing difficulties. Conclusions In
summary, the social cognition impairments are consistent with the frontal lobe hypothesis of alco-holism. Future studies
should focus on (i) the delineation of the basic cognitive processes which underlie social cognition deficits; and (ii) their
relevance as predictors of treatment outcome in alcoholism.

Keywords Alcoholism, frontal lobe, prefrontal cortex, social cognition.

Correspondence to: Jennifer Uekermann, Faculty of Psychology, Institute of Cognitive Neuroscience GAFO 05/607, Ruhr-University of Bochum, Bochum
44780, Germany. E-mail: jennifer.uekermann@ruhr-uni-bochum.de
Submitted 12 July 2007; initial review completed 4 October 2007; final version accepted 11 January 2008

INTRODUCTION person’s emotional stage or intentions. Social cognition is

Alcoholism is associated with a range of cognitive impair-
ments such as attention, memory and executive deficits.
Different neuropsychological models have been postu-
lated to explain the cognitive profile of alcoholics [1].
Empirical support for the ‘right hemisphere hypothesis’ or
the ‘premature aging hypothesis’ is sparse [2]. The ‘mild
generalized dysfunction hypothesis’ of alcoholism
suggests a variable pattern of impairments [3]. The ‘frontal
lobe hypothesis’, on the other hand, is based on the idea of
a specific vulnerability of the prefrontal cortex (PFC) to
the neurotoxic effects of alcohol. This leads to pronounced
executive function impairments in people who suffer from
alcoholism. The latter hypothesis has received strong
support from clinical and neuroimaging studies to account
for social cognition disorders in alco-holics [4].
Skilled social interaction is critically dependent upon
our capacity to understand other people’s minds. Humans
are excellent in drawing conclusions from a per-son’s
facial expression, prosody or body posture upon the
severely disrupted in disorders such as autism [5], schizo-
phrenia [6], dementia [7] and in patients with PFC injury
[8]. Given the link between alcoholism, executive control
impairments and PFC dysfunction, on one hand, and
social cognition and PFC function on the other hand, only
little is known about social cognition in alcoholism.
The present review aims (i) to evaluate the available
evidence of social cognition problems in alcoholism in the
context of the frontal lobe hypothesis; (ii) to discuss the
clinical implications of such deficits; and (iii) to outline
suggestions for future research in this area. First, brain
changes during the course of alcoholism are sum-marized;
then, deficits in facial affect perception and impaired
perception of emotional prosody in alcoholism are focused
upon, following which deficits of theory of mind abilities,
empathy and humour processing will be discussed. In the
concluding section, the clinical implica-tions of social
cognition problems will be discussed with respect to
interpersonal problem solving and relapse prevention.
Furthermore, different strategies for future investigations
will be outlined.

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 Social cognition in alcoholism 727

BRAIN CHANGES IN ALCOHOLISM responsive cells [48]. Facial expression of emotions is

mediated by the orbitofrontal cortex which is activated,
According to Mann et al. [9], approximately 50–70% of
for example, when a change of facial expression acts as a
alcoholics show signs of brain dysfunction (see also [4]).
social signal for a change in behaviour [49]. This is con-
Volume loss was observed in the cerebellum [10], the
sistent with human lesion evidence of impairments in the
corpus callosum [11,12], the mammillary bodies [13], the
identification of facial emotional expressions in patients
hippocampus [14], the nucleus accumbens [15], the
with ventral PFC damage who showed inappropriate
thalamus, the putamen and the caudate [16]. Cortical
social behaviour [50]. Apart from orbitofrontal lesions,
changes include volume loss of grey and white matter in
anterior cingulate lesions and lesions to Brodman area
the frontal, parietal and temporal cortex, with more pro-
(BA) 9 were also associated with deficits in emotional
nounced white matter changes [17,18]. Electrophysi-
face processing and changes in social behaviour [51].
ological investigations yielded reduced alpha power,
increased beta and theta power [19], a reduced sensory
gating effect [20], a smaller P300 amplitude [21,22], pro- Facial affect perception in alcoholism
longed latencies of auditory-evoked potentials [23] and a
There is a relatively broad database on facial affect per-
larger mismatch negativity [24].
ception in alcoholism. Earlier studies did not report sig-
The frontal lobes appear to be affected disproportion-
nificant group differences between alcoholics and control
ately [4,25,26]. Neuronal loss or reduced regional cere-
subjects in affect perception [52]. Nevertheless, alcohol-
bral blood flow ratio (rCBF) have been found consistently
ics tended to overestimate the intensity of the shown
[27–29]. Recent studies reported reduced activations in the
emotions [53]. In these investigations the facial expres-
cingulate, medial and superior frontal regions in alcoholic
sions displayed full-blown emotions, which does not nec-
subjects [30]. Grey matter reduction in the dorsolateral
essarily reflect ecological conditions. Philippot et al. [54]
PFC is correlated with executive function impairments
presented emotional face expressions using four intensity
[31]. Taken together, these findings clearly support the
levels (0%, 30%, 70% and 100%), and the subjects rated
frontal lobe hypothesis of alcoholism.
each expression on a seven-point scale. Alcoholics
showed significant impairments in the decoding of emo-
tional expressions, overestimating the intensity of emo-
FACIAL AFFECT PERCEPTION
tions even for neutral faces. Deficits in the perception of
Definition of relevant terms emotional faces were also found in a recent investigation
by Clark et al. [55]. Confirming a clear emotional bias,
Faces are multi-dimensional stimuli, which convey simul-
alcoholics showed a tendency to mislabel sad expressions
taneously signals of social and motivational significance
as being hostile (angry/disgusted) [56], as well as
[32]. Faces involve information about identity, gender
enhanced fear responses and a different response pattern
and age, but they also include information about emotion,
to anger and disgust [57]. In addition, they were more
gaze direction and intentions. Faces are thus associated
likely to judge a happy face as a face reflecting a negative
with important social and biologically mean-ingful
mood state [54]. Impaired perception of negative facial
incentives [33]. The ability to identify emotions from
emotions in alcoholism has been related recently to ante-
facial expressions is acquired during childhood and levels
rior cingulate cortex dysfunction [58]. Alcoholics have
off during adolescence [34]. Faces code six basic emotions
also been shown to take longer in decoding emotional
[35] which are identified consistently at levels above
facial expressions than controls [59].
chance [36].
Problems in the identification of facial affect are of
The ability to correctly identify emotions from facial
considerable clinical relevance, as inappropriate responses
expressions is an important social skill [37]. Disruption of
may lead to a potential escalation of interper-sonal
this ability may lead to misunderstandings and signifi-cant
conflicts.
impairments of interpersonal communication. Not
An important issue is to clarify whether the observed
surprisingly, the reduced ability to decode facial expres-
problems contribute to the development or the mainte-
sions of emotions was found to be related to low social
nance of alcoholism and thus are linked to a predisposi-
competence and low popularity in peer groups [38–40].
tion or whether they are the result of alcoholism. This
issue can be resolved partially by investigating the persis-
Brain mechanisms of facial affect perception
tence of the deficits during abstinence. Konreich et al.
In primates, face recognition has been linked to areas in [60] presented the faces used by Philippot et al. [54] to
the temporal cortex [41–45] which project to areas of the recently detoxified alcoholics (RA) and to alcoholic
orbitofrontal cortex [42–44,46,47]. An indirect pro-jection patients who had been abstinent for at least 2 months
involves the amygdala, which also has face- (AA). The AA group performed better than the RA group

© 2008 The Authors. Journal compilation © 2008 Society for the Study of Addiction Addiction, 103, 726–735
728 Jennifer Uekermann & Irene Daum
and did not overestimate intensity of affect. This suggests
that the decoding of facial expressions improves during
abstinence, similar to the course of other cognitive func-
tions [61]. The results imply further that affect perception
impairments are due at least partially to the deleterious
effects of alcohol consumption and do not reflect a pre-
disposition for the development of alcoholism. This inter-
pretation has also been supported by Townshend & Duka
[57], who reported that enhanced fear recognition in faces
was related to the number of detoxifications. However, it
should be noted that the two groups in the study by
Philippot [54] differed in duration of illness, consumption
and/or family history of alcoholism. In a longitudinal
design, Foisy et al. [62] did not observe an improvement
of emotional face perception after
3 months of abstinence. This study yielded complex inter-
action patterns with family history of alcoholism which
were difficult to interpret. This issue therefore needs to be
re-addressed in more detail. It should also be taken into
account that alcoholic patients, who later dropped from
treatment, showed the most pronounced impairments at
baseline. Interpersonal conflicts resulting from deficits in
the perception of emotional facial expressions might be a
relevant mediator variable in this regard (see above).
Indeed, Kornreich et al. [63] reported an association
between such impairments and interpersonal problems,
which in turn may lead to relapse [64].
EMOTIONAL PROSODY PERCEPTION
Definition of relevant terms
As outlined above, the ability to interpret the affective
state of other people is an important social skill. Prosody,
which is a non-linguistic aspect of language, involves
acoustic features such as stress, timing, intonation pat-
terns, pitch, rhythm and differential pausing. Prosody
enables the transfer of information beyond the informa-
tion which is expressed by word choice or grammar [65–
69]. Prosody can be subdivided into linguistic prosody,
which supports the comprehension of semantics and
syntax, dialectical prosody, which refers to regional
differences in prosody, idiosyncratic prosody, which
reflects individual differences and affective prosody,
which conveys the emotional tone of language [69,70]. If
the language content is not consistent with the emotional
tone, the affective prosodic content usually takes prece-
dence [71–73].
Neural mechanisms of emotional prosody perception
In a neuroanatomical model, Ross [74] postulated that
prosodic information is processed in right-sided peri-
sylvian regions which are organized in analogy to lan-
guage areas of the left hemisphere. According to this
© 2008 The Authors. Journal compilation © 2008 Society for the Study of Addiction
model, expression of emotional prosody is processed in
the homologue of Broca’s area in the right inferior frontal
cortex, whereas comprehension is believed to depend
upon the homologue of Wenicke’s area in the right supe-
rior temporal region. More recent studies have suggested
an additional involvement of a range of other brain areas
in the PFC and the basal ganglia [75–77]. Wildgruber et
al. [77] described three successive stages of emotional
prosody perception. The first stage is characterized by the
extraction of suprasegmental acoustic information, and the
second stage by the representation of meaningful
suprasegmental acoustic sequences. The first stage recruits
mainly primary and higher-order acoustic regions of the
right hemisphere, and the second stage posterior regions
of the right superior temporal sulcus. The third stage
involves the explicit evaluation of the emotional prosody
which is linked to bilateral processing in the inferior
frontal cortex.
Perception of emotional prosody in alcoholism
Studies on emotional prosody perception in alcoholism are
sparse. An early study by Oscar-Berman et al. [53], which
presented sentences expressing happy, sad, angry and
neutral prosody, did not find differences between
alcoholics and control subjects. In a more recent investi-
gation by Monnot et al. [78] the Aprosodia Battery [79]
was administered to alcoholics. In the first subtest, the
sentence ‘I am going to the other movies’ is presented in a
happy, angry, sad, surprised, disinterested, bored and
neutral voice. In addition, two stress patterns are used
(emphasis on ‘am’ or emphasis on ‘other’) to assess the
ability to suppress attention to linguistic prosody cues.
Subjects are instructed to indicate the emotional tone of
the sentence. The second subtest includes 24 monosyl-
labic (‘ba ba ba ba ba’) and the third subtest 24 asyllabic
(‘aaaaahhhhh’) utterances with the same emotional and
stress patterns. In another subtest, 24 pairs of the first
subtest are presented and subjects are instructed to indi-
cate whether the two sentences are spoken with the same
or a different emotional tone. Alcoholics were found to be
impaired on all but the fourth subtest. Performance was
unrelated to demographic variables, but was correlated
significantly with variables reflecting alcoholism biogra-
phy (e.g. age at first drunken episode, alcohol abuse
chronicity, abuse onset age, alcohol use of mother). In a
further study, the most severe deficits were observed in
alcoholic patients with a history of fetal alcohol exposure
[80].
The question of whether emotional prosody percep-
tion was affected disproportionately if semantic content
differed from emotional prosody was investigated by
Uekermann et al. [81], who administered the Tübingen
Affect Battery [82], a German adaptation of the Florida
Addiction, 103, 726–735

Affect Battery [79]. In addition to subtests which require
the identification of linguistic prosody and same/different
judgments of prosody of spoken sentences, tasks include
the identification of semantically congruent and incon-
gruent affective prosody and cross-modal matching of
affective prosody to facial expression or vice versa. Alco-
holic patients showed severe deficits with respect to
naming incongruent affective prosody, naming affective
prosody of semantically neutral sentences and matching of
affective prosody to facial expressions. The incongru-ent
affective prosody condition is of particular relevance as it
taps the ability to suppress distraction in the face of
conflicting information [83]. Because alcoholic patients
also had problems in identifying emotional prosody for
neutral semantic content, inhibitory control difficulties
alone cannot account for the prosody perception deficits.
In the light of findings of affective prosody impairments
after PFC damage and activation of the inferior frontal
lobe during processing of emotional prosody, the impair-
ments of alcoholic patients are consistent with the frontal
lobe hypothesis of alcoholism.
THEORY OF MIND AND EMPATHY
Definition of relevant terms
The ability to reason about mental states of other people
and to predict and understand other people’s behaviour on
the basis of their mental states has been referred to as
‘theory of mind’ (TOM [84]) and ‘intentional stance’
[85]. The process by which the mind of other people is
represented is referred to as ‘mentalizing’ [86]. A range of
different tasks have been developed for the investigation
of TOM abilities [87]. A popular approach is the false
belief task, which requires the understanding that another
person may have a false belief [88].
Whereas TOM involves the knowledge of thoughts,
beliefs and intentions of others, empathy refers to insight
into the emotional states and feelings of other people.
Empathy can be defined as a complex form of psychologi-
cal inference, in which observation, memory, knowledge
and reasoning are combined to yield insights into the
thoughts and feelings of others [89]. At least three pro-
cesses are thought to underlie empathy: ‘feeling what
another person is feeling, knowing what another person is
feeling, and having the intention to respond compas-
sionately to another person’s distress’ [90].
Neural mechanisms of theory of mind and empathy
Social neuroscience has begun recently to address the
neural underpinnings of TOM and empathy. Activation of
the medial PFC has been observed in association with
TOM tasks [91], together with activations in the temporo-
parietal junction and the temporal poles [92]. Consistent
© 2008 The Authors. Journal compilation © 2008 Society for the Study of Addiction
Social cognition in alcoholism 729
with these findings, mentalizing impairments were
observed in PFC lesion patients [8]. In summary, theory of
mind is believed to be processed in a network involving
the PFC and temporal cortex [91,93–96].
PFC regions are also involved in empathy, as
supported by impairments after PFC lesions [97]. In a
recent inves-tigation by Shamay-Tsoory et al. [98],
stimulus material representing second-order false beliefs,
ironic utterances and situations displaying social faux pas
were adminis-tered. Patients with medial PFC damage
were unimpaired at inferring knowledge of other people,
but showed impairments if cognitive and affective facets
had to be integrated. In a subsequent imaging study [99],
signifi-cant correlations between medial superior frontal
gyrus activations and empathy scores emerged, supporting
the view that this region is important for the integration of
affective and cognitive information.
Theory of mind and empathy in alcoholism
Potential impairments of TOM abilities and empathy have
as yet received little attention in alcoholism research. In a
recent investigation by Uekermann et al. [100], 24 joke
stories were presented. After the presentation of each joke,
mentalizing ability was assessed by questions about the
perspective of the first and second protagonists. The third
question addressed TOM knowledge, which was
necessary for the comprehension of the correct punchline.
The TOM score of alcoholic patients was sig-nificantly
lower when compared to healthy controls. In addition,
reduced mentalizing ability was associated with humour-
processing deficits, both being dependent upon the ability
to take the perspectives of the protagonists in order to
comprehend the correct punchlines. The findings are,
however, limited by the fact that the mentalising task did
not separate theory of mind, i.e. the knowledge about
thoughts, beliefs and intentions of other people and
empathy, i.e. the knowledge regarding the emotional states
and feelings of other people. Further studies are therefore
needed in order to address the issue of a link between
empathy and TOM.
HUMOUR PROCESSING
Definition of relevant terms
Humour enhances social interaction and therefore plays an
important role in human social life. Humour has been
associated with good health and wellbeing. Humour
reduces the impact of stressful events and has a beneficial
effect on immune system activity [101]. In addition to the
physiological effects, a sense of humour was correlated
positively with psychological health and negatively with
psychological distress such as depression [102–104].
Addiction, 103, 726–735
730 Jennifer Uekermann & Irene Daum
Empirical studies of humour processing were based
mainly on the ‘incongruity resolution theory’ [105].
According to this theory, humour comprehension involves
an initial stage of incongruity detection, fol-lowed by a
second stage of incongruity resolution, i.e. the explanation
in the context of the joke. Processing of slapstick humour
requires only the first stage, the incon-gruity detection.
The cognitive component of humour refers to the
comprehension of humorous stimuli, whereas the affective
component involves appreciation of the joke. It has been
suggested recently that executive functions and TOM
make a differential contribution to the affective and
cognitive components of humour pro-cessing [106].
Neural mechanisms of humour processing
Earlier lesion studies have linked incongruity detection to
the left and incongruity resolution to the right hemispheres
[107–109]. More recent approaches have emphasized the
role of the PFC in humour processing
[110]. Patients with damage involving the PFC tended to
respond less strongly to humorous stimuli [111,112], and
funniness was related to activations in the medial PFC and
in the cerebellum in imaging studies [113].
Humour processing in alcoholism
Despite the proposed PFC vulnerability to the neurotoxic
effects of alcohol and a PFC involvement in humour pro-
cessing, to our knowledge there are only two studies which
addressed humour processing in alcoholism. Cermak et al.
[52] administered a cartoon task to 20 chronic alcoholics
from in-patient clinics. They presented cartoons with
alternative endings: a funny and coherent ending, a
slapstick ending or different neutral or non-humorous
endings. Alcoholics frequently chose endings which were
unrelated to the main topic, and their diffi-culties were
interpreted in terms of impairments in inte-grating
different aspects of a narrative. As funniness ratings were
not included, the error pattern might reflect a general
preference of slapstick humour rather than a humour-
processing deficit per se. The deficit might also be
attributed, at least partly, to deficient TOM abilities or
executive functions [106].
In a further humour-processing study [114], joke stems
were presented and participants had to choose among
different endings reflecting incongruity and/or resolution
(correct funny punchline, a slapstick alterna-tive, logical
and illogical alternatives) and they also had to give
funniness ratings. Each joke stem was then presented with
the correct punchline and three questions assessed
mentalizing abilities. Alcoholics selected a significantly
lower number of correct punchlines and chose more
logical and slapstick endings. Their funniness ratings
© 2008 The Authors. Journal compilation © 2008 Society for the Study of Addiction
were generally lower than those of controls, indicating a
combined impairment of cognitive and affective compo-
nents of humour processing. The deficits in alcoholics
were related to both executive function impairments and
reduced mentalizing ability. This pattern is consistent with
PFC dysfunction in alcoholism.
CONCLUSIONS, CLINICAL IMPLICATIONS AND
SUGGESTIONS FOR FUTURE INVESTIGATIONS
General conclusions
Alcoholism has been shown to be associated with a range
of social cognition impairments in the domains of emo-
tional face and prosody perception, theory of mind and
humour processing. Whereas a relatively broad database
exists with respect to affect perception in faces or prosody,
relatively little is known about more complex aspects of
social cognition. Taken as a whole, the problems of alco-
holic patients are consistent with the hypothesis of a dis-
proportionate vulnerability of the PFC to the neurotoxic
effects of alcohol. Future studies will have to provide
better insight into the functional contribution of other
regions and the neuronal networks involved in social
cognition.
Predictive value of social
cognition problems in alcoholism
Individuals with social cognition deficits will frequently
commit errors during social exchange. If acquired early in
life, such a deficit may impair the development of
adequate communicational, social and occupational skills.
However, the potential prognostic value of social
cognition deficits is as yet largely unknown. Cooper et al.
[115] and Sher & Trull [116] reported that regulation of
affective experience, in particular transient and chronic
negative affect, is an important motive underlying alcohol
use. The social cognition difficulties of alcoholics—affect
perception deficits, a negative bias in affect perception,
significantly higher intensity ratings, theory of mind as
well as humour processing deficits— may lead to
discomfort and stress in social situations, which may result
in turn in alcohol consumption and relapse. This
hypothesis is supported by recent findings indicating a link
between deficits in the perception of emotional facial
expressions and interpersonal problems [63], which
contribute to relapse [64]. Furthermore, severe
impairments in identifying emotional facial expression
were associated with treatment dropout [62]. The
underlying mechanisms, the prognostic value and the
potential mediators of social cognition deficits, however,
remain to be determined in more detail.
Addiction, 103, 726–735

Cognitive mechanisms underlying social
cognition deficits in alcoholism
Humour processing has been shown to be linked to the
integrity of executive control abilities [106,114], but yet it
remains unclear to what extent TOM abilities are medi-
ated by executive functions [117–119]. Along similar
lines, there is evidence for a relation between the percep-
tion of emotional prosody and executive impairments.
Judging emotional prosody in spoken sentences requires
holding stimuli in working memory, inhibition of the task
irrelevant semantic meaning of the sentences and/or
successful switching between the semantic meaning and
emotional prosody. Significant associations between affect
perception and executive functions have been reported for
patients with focal brain lesions [120], Par-kinson’s
disease [121] and schizophrenia [122]. The relationship
between executive functions and affect perception in
alcoholism is still unclear, as are potential dissociations
between TOM and empathy [96].
Nature of social cognition deficits
The available database does not allow any clear conclu-
sions as to whether social cognition impairments in alco-
holism reflect a predisposition and/or whether they are the
consequence of the neurotoxic effects of alcohol, given the
conflicting findings of the functional recovery during
abstinence [60,62]. High dropout rates and inconclusive
findings concerning the role of family history of
alcoholism limit the interpretation of available data.
Alcoholics with a family history of alcoholism tend to
show more severe impairments [123], and family history
and substance use may be separate risk factors for poorer
cognitive outcome and social cognition impair-ments
[124]. Further studies of high-risk groups are clearly
needed to investigate this issue in more detail.
Implication for treatment of alcoholism
The wide range of social cognition impairments and the
associated interpersonal and communication problems
may be important contributing factors that might result in
relapse [60]. A related deficit concerns interpersonal
problem-solving. Nixon et al. [125] and Patterson et al.
[126] administered the Adaptive Skills Battery [127] to
alcoholic patients. Participants are instructed to respond
with either a typical response (the response he/she would
be most likely to give) or the optimal response to a series
of social situations. While alcoholics did not differ from
con-trols with respect to optimal responses, they clearly
dif-fered on typical responses, suggesting that alcoholics
seem to know what to do in a given interpersonal situa-
tion, but do not implement this knowledge to guide
behaviour. Adaptive skills are related to treatment
© 2008 The Authors. Journal compilation © 2008 Society for the Study of Addiction
Social cognition in alcoholism 731
outcome [127], and social skills training have a beneficial
effect on the course of treatment [128–130]. Social skills
training included modelling, behavioural rehearsal, feed-
back, role-playing and strategies for dealing with four
classes of potential relapse-precipitating events (e.g.
negative mood, interpersonal pressure). Given the avail-
able database it is, however, likely that alcoholics suffer
from basic social cognition deficits, which contribute to
interpersonal problems and may play a role in relapse. The
strategies which are included so far in current social skills
training may thus not be sufficient for the effective
treatment of alcoholism, and the investigation of the
relationship between social cognition deficits and inter-
personal problem-solving would be necessary to arrive at
better treatment approaches. The results of such investi-
gations should make an important contribution to the
design and development of new social skills training
interventions in alcoholism.
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