1 AP-PCR analysis was consistent with
intrafamilial A. actinomycetemcomitans transmission.
2 g every week, a repeated and harmful form of
intrafamilial aggression.
3 However, there is high
intrafamilial and interfamilial phenotypic variability.
4 There was wide
intrafamilial and interfamilial variability in clinical
5 Intrafamilial and interfamilial variation in retinal sev
6 Phenotypes were comparable, but some
intrafamilial and interfamilial variations were noted.
7 a in the nasopharynx serve as reservoirs for
intrafamilial and nosocomial transmission.
8 tion in a large family characterized by high
intrafamilial clinical phenotype variability.
9 There was no evidence of
intrafamilial clustering of particular phenotypes.
10 gh horizontal transmission in childhood from
intrafamilial contacts and that transmission continues i
11 ared 270 duplication carriers with their 102
intrafamilial control individuals, 390 reciprocal deleti
12 suggest that duplication carriers outperform
intrafamilial control subjects with the same IQ level.
13 on carriers, 44 duplication carriers, and 71
intrafamilial control subjects.
14 Intrafamilial correlation analysis showed that other fac
15 The heritability and
intrafamilial correlation coefficients were assessed for
16 The high
intrafamilial correlation of HPV multiplicity is already
17 There was no
intrafamilial correlation regarding CFA levels.
18 The
intrafamilial dynamics of endemic infection with human h
19 From a model of
intrafamilial evolution, a prediction could be made that
20 Parenting quality and behaviour are the
intrafamilial factors most strongly associated with bull
21 ver, these risks are small and likely due to
intrafamilial factors or disease activity.
22 Conclusion: When
intrafamilial factors were taken into consideration, H1N
23 To consider
intrafamilial factors, we compared pregnancies within th
24 (FSHD) is characterized by marked inter- and
intrafamilial heterogeneity in its clinical expression.
25 rated the validity and applicability of this
intrafamilial model for the prediction of intraspecies S
26 However, application of a PLATO-derived
intrafamilial model with the intraspecies-derived model
27 e the odds of being HHV-8 seropositive among
intrafamilial pairs.
28 d the relative risk of colonization in these
intrafamilial pairs.
29 ally complex disease characterized by marked
intrafamilial phenotype diversity.
30 with phenotypes in Finnish patients with NS,
intrafamilial phenotype variations, and the type of immu
31 However, the discordant
intrafamilial phenotypes of 16p11.2 deletion carriers su
32 Nevertheless, we observed highly variable
intrafamilial phenotypes, suggesting the strong influenc
33 H2 mutation associated with a high degree of
intrafamilial phenotypic heterogeneity: Y141C.
34 The extensive interfamilial and
intrafamilial phenotypic variability observed suggests t
35 Marked inter- and
intrafamilial phenotypic variability of the disease was
36 Intrafamilial phenotypic variability was also observed i
37 ction system defects, suggest mechanisms for
intrafamilial phenotypic variability, and account for re
38 It is characterized by considerable
intrafamilial phenotypic variation and focal cyst format
39 spinal muscular atrophy exhibiting dramatic
intrafamilial phenotypic variation.
40 Intrafamilial recombinations placed MEFV in the approxim
41 Higher levels of
intrafamilial sociopolitical conflict was associated wit
42 used whole-genome sequencing to investigate
intrafamilial spread among 4 siblings of infection due t
43 oposed and relationships within at least 126
intrafamilial taxa also have been inferred.
44 The distribution, clonality, and
intrafamilial transmission of highly leukotoxic A. actin
45 However, significant inter- and
intrafamilial variability and apparent incomplete penetr
46 Inter- and
intrafamilial variability exists and we observed one pat
47 plaining an important part of the inter- and
intrafamilial variability in ADPKD.
48 he clinical spectrum of the disorder and the
intrafamilial variability in disease presentation.
49 Both interfamilial and
intrafamilial variability in expression is well recogniz
50 The inter- and
intrafamilial variability in expression of FGFR2 mutatio
51 ion are at the genic and allelic levels, but
intrafamilial variability indicates that genetic backgro
52 Such
intrafamilial variability may arise from environmental f
53 nd a genetic mechanism that may underlie the
intrafamilial variability of ADPKD progression.
54 Considerable
intrafamilial variability was observed, reflecting the i
55 There is extensive interfamilial as well as
intrafamilial variability with respect to the manifestat
56 characterized by BEM with little inter- and
intrafamilial variability, and retinal dystrophy with va
57 genetic disorder with substantial inter- and
intrafamilial variability, that also exhibits remarkable
58 t is associated with large interfamilial and
intrafamilial variability, which can be explained to a l
59 ure and two were associated with significant
intrafamilial variable expressivity, including isolated
60 Interfamilial and
intrafamilial variation in disease severity was observed
61 However, the large
intrafamilial variation in the progression rate of ADPKD
62 Intrafamilial variations of the malformations strongly s
63 busers had more frequently witnessed serious
intrafamilial violence (3.1, 1.0-10.0).