Article

Minor Physical Anomalies and Family Adversity

as Risk Factors for Violent Delinquency in Adolescence
Louise Arseneault, Ph.D.
Richard E. Tremblay, Ph.D.
Bernard Boulerice, Ph.D.
Jean R. Sguin, Ph.D.
Jean-Franois Saucier, M.D.
MINOR PHYSICAL ANOMALIES
ARSENEAULT, TREMBLAY, BOULERICE, ET AL.

Objective: Minor physical anomalies are

considered indicators of disruption in fetal development. They have been found
to predict behavioral problems and psychiatric disorders. This study examined
the extent to which minor physical anomalies, family adversity, and their interaction predict violent and nonviolent delinquency in adolescence.
Method: Minor physical anomalies were
assessed in a group of 170 adolescent boys
from low socioeconomic status neighborhoods of Montral. The boys had been enrolled in a longitudinal study since their
kindergarten year, when an assessment of
family adversity had been made on the
basis of familial status and the parents occupational prestige, age at the birth of the
first child, and educational level. Adolescent delinquency was measured by using
self-reported questionnaires and a search
of official crime records.

Results: Results from logistic regression

analyses indicated that both the total
count of minor physical anomalies and
the total count of minor physical anomalies of the mouth were significantly associated with an increased risk of violent delinquency in adolescence, beyond the
effects of childhood physical aggression
and family adversity. Similar findings were
not found for nonviolent delinquency.
Conclusions: Ch ildre n with a h ighe r
count of minor physical anomalies, and
especially a higher count of anomalies of
the mouth, could be more difficult to socialize for different and additive reasons:
they may have neurological deficits, and
they may have feeding problems in the
first months after birth. Longitudinal
studies of infants with minor physical
anomalies of the mouth are needed to
understand the process by which they fail
to learn to inhibit physical aggression.
(Am J Psychiatry 2000; 157:917923)

erious violent delinquency is at its peak during late

adolescence and early adulthood (1). However, violent behaviors do not appear suddenly during the teen years.
Longitudinal studies have shown that childhood disruptive behaviors are among the best predictors of delinquency and adult antisocial personality (2, 3). These findings suggest that violent delinquency has precursors early
in life (4). Therefore, etiological factors early in life should
logically be studied. Precursors such as family context and
perinatal complications are among the earliest factors
that could influence behavioral development (5, 6).
In their elaboration of a theoretical framework for the
study of violence, Raine et al. (7) suggested that biological
factors predispose individuals to psychopathology specifically in adverse environments. Poor environmental conditions are expected to exacerbate physiological predispositions toward psychopathology, whereas favorable
environmental conditions are expected to compensate for
them. Few studies have simultaneously considered environmental conditions and perinatal risk factors. One of
those rare studies (8) showed that individuals who had
neuromotor deficits at age 1 year and grew up in unstable
family environments were more at risk of becoming crim-

Am J Psychiatry 157:6, June 2000

inals than those with only one of these risk factors. Another study (9) showed that violent crimes were predicted
by the interaction between maternal rejection at age 1 and
birth complications. Taken together, these studies suggest
that the development of violent behavior may be influenced by a biosocial process that takes place during the
very first years of life.
Birth complications are not the earliest biological risk
factors for behavioral disorder. During pregnancy, the fetus is exposed to various influences that could negatively
affect its development. These influences are partly responsible for the development of minor physical anomalies, trivial aberrations that can be found on many parts of
the body. Minor physical anomalies are considered indicators of fetal developmental disruption. The specific origin of these anomalies is not yet fully understood, but the
interaction between environmental factors and genetic
determinants is their most likely cause (10, 11). The central nervous system (CNS) may also be affected by factors
responsible for minor physical anomalies because the development of the CNS is concurrent with the development
of the organs that show the minor anomalies. Because
neurological impairments are known to be associated

917

MINOR PHYSICAL ANOMALIES

with behavioral problems (12), minor physical anomalies

may well reflect CNS risk factors for the development of
behavioral disorders.
Studies have shown that a higher count of minor physical anomalies is found in groups of individuals with psychiatric diagnoses such as schizophrenia (13), autism (14),
and hyperactivity (15, 16) and among individuals with aggressive behaviors (17). Waldrop and Halverson (18) argued that it is the total number, and not any specific minor
physical anomaly, that predicts behavior problems. An approach that associates the location of minor physical
anomalies with behavioral disorders may also be informative. For example, a higher incidence of anomalies of the
mouth has been linked with psychosis in three studies
(1921). Studies that have focused on the association between minor physical anomalies and aggressive behavior
have not examined specific links with parts of the body
where minor physical anomalies occur. Further, minor
physical anomalies alone may not be sufficient to adequately predict violent delinquency. Current biosocial
models of psychopathological development suggest that
clear prediction of risk may be found when looking at minor physical anomalies in conjunction with environmental factors (7).
In support of this view, three studies have reported that
deprived psychosocial environments influence the link
between the total count of minor physical anomalies and
behavioral disorders (2224). In these studies of biosocial
interactions, characteristics of the social environment
were measured during adolescence or concurrently with
outcome. In her developmental theory of antisocial behaviors, Moffitt (25) suggested that the interaction between early environmental characteristics and neuropsychological deficits engenders chronic violent antisocial
behavior. Because antisocial behaviors tend to emerge
from a childhood pattern of chronic disruptive behaviors,
one would expect that the positive or negative impact of
the environment on the development of violent behavior
in individuals with CNS malformations could be traced
back to childhood. Further, Moffitt suggested that this interaction could be a specific etiological mechanism for violent offenses as opposed to nonviolent offenses. Evidence supporting this assumption has been reported in
empirical studies (9, 22).
The first aim of the study reported here was to test the
hypothesis that the cumulative incidence of minor physical anomalies, family adversity during the preschool years
as an index of family disadvantage, and their interaction
predict violent delinquency at the end of adolescence in a
study group of inner-city boys. The second aim was to
identify the specific anomalies involved in violent delinquency. The third aim was to test the hypothesis that those
predictions are specific to violent delinquency as opposed
to nonviolent delinquency.

918

Method
Sample
Participants were involved in an ongoing longitudinal study of
boys from lower socioeconomic status areas in Montral (26).
Fifty-three schools were selected because of the students low
score on a socioeconomic index that was based on family earnings, occupational prestige, and parents schooling (27). Kindergarten teachers were asked to rate the behaviors of the boys in
their classes. Only white, French-speaking boys whose mother
and father were born in Canada were included in the sample (N=
1,037) in order to have a culturally homogeneous group.
Data on minor physical anomalies were collected during a laboratory visit of a study group of 177 boys when they were 14 years
of age. The boys were selected on the basis of teacher ratings of
physical aggression and anxiety from age 6 to 12 (see reference
28) by using the Social Behavior Questionnaire (29). Physical aggression was measured with three items: fights with other children; kicks, bites, hits other children; and bullies other children.
The anxiety scale comprised five items: fearful, distressed, worried, solitary, and cries. Each item was scored on a frequency scale
ranging from 0 to 2. The Cronbach value for internal consistency
for the anxiety scale was 0.76 when the boys were ages 6, 10, 11,
and 12. For the physical aggression scale, the mean Cronbach
value when the boys were between ages 6 and 12 was 0.84 and
ranged from 0.78 to 0.87. The boys had to meet at least one of the
following four overlapping criteria to be selected for the study
group: 1) high aggressive or anxious behavioral pattern indicated
by scores above the 70th percentile at age 6 and at least 2 other
years, 2) low aggressive or anxious behavioral pattern indicated
by scores below the 70th percentile at all assessments, 3) pattern
of late-onset physical aggressiveness or anxiety indicated by
scores above the 70th percentile only at age 12, and 4) prior visits
to the laboratory. Compared to the rest of the sample (N=860), the
study group was more aggressive, hyperactive, inattentive, and
anxious in kindergarten, but was similar in socioeconomic characteristics and in prosociality. The behavioral differences were
due to an overrepresentation of aggressive and anxious boys in
the study group as a result of the selection criteria. Because all
boys were recruited in regular schools, none of them had mental
retardation, severe intellectual deficits, or significant physical
handicaps. Data on minor physical anomalies and delinquent behaviors were available for 170 boys, 96% of the study group. Written informed consent was obtained from both the boys and their
parents.

Assessment of Minor Physical Anomalies

Minor physical anomalies were assessed as part of an extensive
evaluation of body characteristics when the boys came to the laboratory. The 18 minor physical anomalies from the Waldrop scale
were measured (30). A frequency scale was used in the analyses
because it involved less judgment bias and was highly correlated
with weighted scores for the anomalies (15, 18, 30). The anomalies were located in six different areas of the body: the mouth,
ears, eyes, head, hands, and feet. The total count of these anomalies has been reported to be stable from birth to adolescence (31).
The frequency for one of the anomalies (a big gap between the
first and the second toes) was exceptionally elevated (Table 1).
The feet were the only anatomical region for which the cumulative count of minor physical anomalies was not correlated to the
total count of anomalies and was negatively associated with
anomalies of the eyes (pairwise r=0.16, N=175) and with anomalies of the hands (pairwise r=0.15, N=176). Our study group was
drawn from a culturally homogeneous population that is known
to have a relatively homogeneous gene pool (32). Thus, the toe
gap may be characteristic of that population. We therefore decided to exclude this anomaly from the total count of minor physAm J Psychiatry 157:6, June 2000

ARSENEAULT, TREMBLAY, BOULERICE, ET AL.

TABLE 1. Minor Physical Anomalies in 44 Violent Delinquent Adolescent Boys and 42 Nonviolent Delinquent Adolescent
Boys
Total Study Group
(N=170)a
Location and Nature of Minor Physical Anomaly
Mouth
High steepled palate
Furrowed tongue
Smooth-rough spots
Ears
Malformed
Asymmetrical
Low seated
Soft and pliable
Adherent lobes
Eyes
Epicanthus
Hypertelorism
Head
Electric fine hair
Two or more hair whorls
Large circumference
Hands
Fifth finger curved
Single palmar crease
Feet
Third toe length
Partial syndactyly
Big gap between toes

Violent Delinquents
(N=44)b

Nonviolent
Delinquents (N=42)b

37
31
67

21.8
18.2
39.4

12
10
23

27.3
22.7
52.3

10
7
20

23.8
16.7
47.6

18
57
47
57
64

10.6
33.5
27.6
33.5
37.6

1
19
10
17
15

2.3
43.2
22.7
38.6
34.1

2
15
9
13
15

4.8
35.7
21.4
31.0
35.7

80
15

47.3
8.8

21
6

47.7
13.6

23
4

54.8
9.5

12
61
25

7.2
35.9
15.1

5
20
6

11.4
45.5
14.0

3
10
7

7.1
23.8
17.1

43
7

25.3
4.1

14

31.8

12
1

28.6
2.4

6
113

3.5
66.5

1
22

2.3
50.0

28

66.7

Data missing on epicanthus for one participant, on electric fine hair for three participants, and on large circumference of the head for four
participants.
b Data missing on large circumference of the head for one participant.
ical anomalies. A similar decision was made in a previous study
when anomalies were found to be the norm rather than an exception (33). Because of this exclusion, we did not examine minor
physical anomalies of the feet in analyses of separate anatomical
regions.

Family Adversity
Seven socioeconomic indices were used to create an index of
family adversity (29). These indices were mothers and fathers occupational prestige, mothers and fathers age at birth of their first
child, mothers and fathers education level, and familial status.
The accumulation of these different variables has been shown to
increase the risk of behavioral disorders by creating stressful rearing conditions (34). Occupational prestige reflected a socioeconomic index of jobs in Canada (35), and familial status referred to
whether both biological parents were living with the boy. Information on these indices was collected during a telephone interview with the mother at the end of the boys kindergarten year.
Because we hypothesized that environmental conditions have an
impact on behaviors early in life, only the measure of adversity
when the boy was age 6 was used, as it represented the earliest index of the socioeconomic conditions in which the boy grew up.
Except for familial status, all indices were given a score of 1 if they
were below the 30th percentile in the present sample and a score
of 0 if they were above the 30th percentile. For familial status, a
score of 1 was given if the boy was not living with his two biological parents during his kindergarten year. The maximum family
adversity score was 7 for a boy living with one biological parent
and a stepparent and was 4 for a boy living with one parent only.
Therefore, the total family adversity score was divided by 7 if the
boy was living with two parents and by 4 if he was living with one
parent. The study group scores ranged from 0 to 1 (mean=0.34,
SD=0.23), with higher scores representing more adversity. Study
group members did not differ from the rest of the sample on each
family adversity index. This composite measure of the degree of
Am J Psychiatry 157:6, June 2000

adversity in families when the boy was age 6 was shown to be predictive of a stable level of childhood physical aggression in the
large sample and was highly correlated with family adversity
scores when the boy was age 12 (r=0.85) (5). In addition, this index
was related to verbal learning difficulties within this study group
(28) and was associated with childhood externalizing disorders in
a sample of more than 3,000 French-speaking children (36). The
scores were standardized for easier interpretation of the results.

Delinquent Behavior
At age 17, the boys were asked to respond to 27 items measuring delinquent behaviors that took place at home, at school, and
with their friends (26). Four scales were created on the basis of
items measuring physical aggression, theft, vandalism, and substance use. The Cronbach values for internal consistency of the
four scales measured at age 17 were 0.78, 0.87, 0.73, and 0.82, respectively. Scores on the four scales at ages 16 and 17 were significantly correlated (r=0.62 [N=767], 0.67 [N=767], 0.45 [N=764],
and 0.72 [N=766], respectively). Self-reported delinquency scales
virtually identical to the one used in this study have been reported to have both concurrent and predictive validity (37). The
score on the first scale (physical aggression) was considered a
measure of self-reported violent delinquency, and the scores on
the last three scales (theft, vandalism, and substance use) were
summed to represent self-reported nonviolent delinquency. Data
at age 16 were used for five participants whose data at age 17 were
missing. Thirty-eight violent delinquents and 40 nonviolent delinquents were identified by using a 75th percentile cutoff point,
given the skewed distributions of the two self-reported delinquency scales.
Criminal status was determined by a search of the criminal
records for all boys in the sample as of age 19. Crimes were classified as violent or nonviolent according to the Canadian criminal
code. Violent crimes such as illegal possession of a weapon, animal cruelty, and violent threats were found in 67 boys of the larger

919

MINOR PHYSICAL ANOMALIES

TABLE 2. Prediction of Violent and Nonviolent Deliquency in Adolescent Boys According to Logistic Regression Analyses of
Physical Anomalies, Childhood Physical Aggression and Anxiety, and Familiy Adversity
Violent Delinquency (N=44)
Regression Analysis and Constituent Covariables
Regression 1: total anomalies
Childhood physical aggression
Childhood anxiety
Family adversity at age 6
Total minor physical anomalies
Regression 2: anomalies of the moutha
Family adversity at age 6
Minor physical anomalies of the mouth
Regression 3: anomalies of the earsa
Family adversity at age 6
Minor physical anomalies of the ears
Regression 4: anomalies of the eyesa
Family adversity at age 6
Minor physical anomalies of the eyes
Regression 5: anomalies of the heada
Family adversity at age 6
Minor physical anomalies of the head
Regression 6: anomalies of the handsa
Family adversity at age 6
Minor physical anomalies of the hands

Nonviolent Delinquency (N=42)

SE

Odds

SE

Odds

0.28
0.13
0.36
0.20

0.15
0.10
0.19
0.10

1.3*
0.9
1.4*
1.2*

0.05
0.21
0.03
0.03

0.15
0.11
0.19
0.10

1.1
0.8*
1.0
1.0

0.31
0.52

0.19
0.24

1.4
1.7*

0.03
0.23

0.19
0.24

1.0
1.3

0.38
0.07

0.18
0.16

1.5*
1.1

0.06
0.18

0.19
0.17

1.1
0.8

0.37
0.15

0.18
0.31

1.4*
1.2

0.06
0.22

0.19
0.30

1.1
1.2

0.37
0.34

0.19
0.28

1.4*
1.4

0.03
0.34

0.19
0.30

1.0
0.7

0.38
0.19

0.18
0.37

1.5*
1.2

0.08
0.21

0.19
0.37

1.1
1.2

B, SE, and odds values for the covariables childhood physical aggression and anxiety were similar to those in regression 1.
* p<0.05.

sample and in 11 of the 170 boys in the study group (6.5%). Nonviolent crimes such as robbery, breaking and entering, and prostitution were found in 44 boys of the large sample and in five
members of the study group (2.9%). Given the overlap between
self-reports and official records of delinquency (2=36.3, df=1,
p<0.001, for violent delinquency; and 2=19.4, df=1, p<0.001, for
nonviolent delinquency), we identified a violent delinquent
group of 44 boys, or 25.9% of the study group, who had been arrested for a violent crime or had reported committing a violent offense, and a nonviolent delinquent group of 42 boys, or 24.7% of
the study group, who had been arrested for a nonviolent crime or
had reported committing a nonviolent offense. The violent and
nonviolent groups were not mutually exclusive; 21 participants
committed both violent and nonviolent offenses, 23 committed
only violent offenses, and 21 committed only nonviolent offenses.

Statistical Analyses
Logistic regression analyses were used to test the predictive
value of minor physical anomalies and family adversity. To control for the selection criteria, mean scores for physical aggression
and anxiety at ages 6, 10, 11, and 12 were used as covariates and
entered in the first step of the analyses. Minor physical anomalies
and family adversity were then forced in the second and third
steps, and the interaction term was left free to enter in a forward
stepwise selection in the last step of the analyses. These procedures were repeated for the total count of minor physical anomalies and separately for the minor physical anomaly score of each
anatomical region. In the analyses, violent delinquents were
compared to participants who did not commit violent offenses,
and nonviolent delinquents were compared to participants who
did not commit nonviolent offenses.

Results
Table 1 shows the frequency of minor physical anomalies in the study group. High percentages of study group
members had anomalies in the regions of the ears and the
mouth. Inconsistent percentages were found for anomalies observed in other anatomical regions. Compared to

920

the total study group, the violent delinquent boys had a

higher percentage of anomalies of the mouth and, inconsistently, of some anomalies of other anatomical regions.
After excluding the toe-gap anomaly, the mean total count
of minor physical anomalies for 167 participants in the entire study group (data were missing for some anomalies)
was 3.7 (SD=1.89, range=09). This mean is similar to
means reported for other at-risk samples of preadolescents: mean=3.4 (SD=1.84, range=09) (17) and mean=
3.58 (SD=2.4, range=010) (16). The total count of minor
physical anomalies among the participants had the highest association with anomalies of the ears (r=0.70, N=167),
followed by anomalies of the eyes (r=0.52, N=167) and
anomalies of the mouth (r=0.51, N=167). Anomalies of the
mouth were positively correlated with anomalies of the
eyes (pairwise r=0.26, N=175).
We first tested to what extent the total count of minor
physical anomalies, the family adversity score, and their
interaction predicted violent delinquency during adolescence. The results depicted in Table 2 show a significant
effect of the total count of minor physical anomalies, beyond significant effects of childhood physical aggression
and family adversity. This result indicated that each increment of one anomaly augmented by a factor of 1.2 the risk
of violent delinquency during adolescence, and each increment of one standard deviation on the family adversity
index augmented that risk by 1.4. The effect of the interaction between the total minor physical anomaly count and
family adversity in predicting violent delinquency did not
reach statistical significance.
We then examined the relation of minor physical anomalies of each anatomical region and their interaction with
family adversity at age 6 in predicting adolescent violent
delinquency. Results of logistic regressions showed a sigAm J Psychiatry 157:6, June 2000

ARSENEAULT, TREMBLAY, BOULERICE, ET AL.

nificant main effect for anomalies of the mouth, beyond

the effect of childhood physical aggression (Table 2). Each
increment of one anomaly in the area of the mouth augmented by a factor of 1.7 the risk of violent delinquency
during adolescence. Family adversity no longer predicted
violent delinquency, because of its significant association
with minor physical anomalies of the mouth (r=0.16, N=
170). This result indicated that the cumulative count of
minor physical anomalies of the mouth and family adversity shares a part of the variance that explained adolescent
violent delinquency. The interaction between minor physical anomalies of the mouth and family adversity did not
reach statistical significance and did not enter the model.

velopment of anomalies of the palate starts at the ninth

week of gestation, whereas anomalies of the hands develop during the eighth week. It is then plausible that
insults occurring at specific periods during gestation
increase the risks for the development of violent delinquency as a result of atypical brain development. The
identification of specific sites of minor physical anomalies
that are related to specific behavior disorders should help
clarify which part of the CNS may be affected and thus
may be involved in a given behavioral problem. This clarification would be achieved by establishing the correspondence between the period of vulnerability for the affected
organ and the CNS developmental phases.

Further analyses were performed to examine whether

the significant effect found for the total count of minor
physical anomalies was attributable to anomalies of the
mouth that were included in the scale. We repeated the
analysis after having removed anomalies of the mouth
from the total count of minor physical anomalies. The results indicated that the total count of anomalies no longer
predicted adolescent violent delinquency, although family
adversity still did. Finally, we examined whether the significant effects found were specific to violent delinquency, as
suggested by Mednick and Kandel (22). Results presented
in Table 2 support the hypothesis by showing no significant association between adolescent nonviolent delinquency and minor physical anomalies or between adolescent nonviolent delinquency and the interaction of minor
physical anomalies and family adversity.

Anomalies of the mouth could also impact childrens

behavior regulation in less direct ways. Orofacial structures are involved from birth onward in many functions
such as communication, emotional expression, mastication, and deglutition, which may have a wide range of consequences on development (41). Anomalies of the mouth
may affect sucking and other feeding behaviors during the
first years of life and thus may affect physical development
as well as the mother-child relationship (42). Infants who
experience feeding problems such as failure to thrive often show neurological problems (43) and are reported to
have more behavior problems during childhood than infants without feeding problems (44). Thus, children with
minor physical anomalies of the mouth could be more difficult to socialize for different and additive reasons: they
may have neurological deficits as well as feeding problems
in the first months after birth.

Discussion
The goal of this study was to assess the contribution of
minor physical anomalies, family adversity, and their interaction to the prediction of delinquency during adolescence. Minor physical anomalies of different anatomical
regions were examined in an attempt to get a more precise
idea of the organic structures and processes involved in
the development of adolescent delinquency. Separate
analyses were used to predict violent delinquency and
nonviolent delinquency because the two types of delinquency could have different etiologies (25).
Adolescent boys with higher counts of anomalies, and
especially with anomalies of the mouth, were found to be
most at risk for violent delinquency. Previous studies of
minor physical anomalies have shown that anomalies of
the mouth are more frequent in children with psychoses
and in adults with schizophrenia (19, 20). Anomalies of the
mouth have been found in individuals with neurological
deficits (38, 39) and could be associated with CNS dysfunctions that increase the risk for violent delinquency.
The CNS develops in a sequential and hierarchical way
(40), and each organ has a specific critical period of vulnerability to teratogens that may result in developmental
disruption (10). For example, the critical period for the deAm J Psychiatry 157:6, June 2000

Unlike Mednick and Kandels study (22), the study reported here found that the interaction between minor
physical anomalies and family adversity did not predict violent delinquency. Mednick and Kandels use of a dichotomized score for minor physical anomalies may explain the
differences in results compared to those reported here. It
is possible that the significant interaction in their study reflected a nonlinear effect of minor physical anomalies, as
their analyses did not control for quadratic effects.
The study reported here was limited to French-speaking, Caucasian males from low socioeconomic status areas in a large city, overrepresenting subjects with stable
childhood physical aggression and anxiety. Replications in
other populations will be needed to confirm the importance of anomalies of the mouth in the prediction of violent delinquency. Longitudinal studies of infants will also
be needed to examine the process by which infants with
these anomalies would fail to learn to inhibit physical aggression. Preventive interventions would be different depending on whether the risk for violent delinquency is
through feeding problems, neurological deficits, or a mixture of these factors, or through other factors, such as parent-child interactions, that were not addressed in this
study.

921

MINOR PHYSICAL ANOMALIES

Received April 2, 1998; revisions received Dec. 3, 1998, and Nov.

12, 1999; accepted Nov. 18, 1999. From the Research Unit on Childrens Psychosocial Maladjustment, University of Montral; the
Fernand Seguin Research Center, University of Montral; the Institute
of Psychiatry, University of London; and the Department of Psychiatry, University of Montral. Address reprint requests to Dr. Tremblay,
Research Unit on Childrens Psychosocial Maladjustment, University
of Montral, 3050 blvd. Edouard-Montpetit, C.P. 6128 succ. centreville, Montral, Qubec, Canada H3C 3J7; gripret@ere.umontreal.ca
(e-mail).
Supported by a fellowship from the Conseil Qubcois pour la Recherche Sociale (Dr. Arseneault) and by grants from the Social Sciences and Humanities Research Council of Canada, the Conseil
Qubcois pour la Recherche Sociale, and Qubecs Fonds pour la
Formation des Chercheurs et lAide la Recherche.
The authors thank the study group members.

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