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1 w the classic and contemporary literature of genetic load.
2 how a species' unique demography affects its genetic load.
3  to young neurons and a further decline with genetic load.
4 on, complicating breeder's efforts to reduce genetic load.
5 esponses to ongoing selection, and levels of genetic load.
6 ptation but comes at the cost of significant genetic load.
7 itive trait intercorrelations exist, such as genetic load.
8  10 tissues being particularly vulnerable to genetic load.
9 ression as a source of local adaptation, and genetic load.
10 40-60%, with a corresponding decrease in the genetic load.
11 ighly addictive and their abuse has a strong genetic load.
12 ons are vulnerable to extinction due to high genetic load.
13 ffect both individual fitness and population genetic load.
14 ne the molecular events that can instigate a genetic load.
15 ognized as a force that can lower population genetic load.
16 e, high levels of heterozygosity and a large genetic load.
17 f feedback mechanisms to control exposure of genetic load.
18 uce low fitness diploid males, CSD creates a genetic load.
19 pecifically designed to assay locus-specific genetic load.
20 f the phenotype to mutations-and thus reduce genetic load.
21 ixation of beneficial alleles and purging of genetic load.
22  change, but mutation accumulation increases genetic load.
23 on the co-occurrence of childhood trauma and genetic loading.
24 f adverse social determinants of health, and genetic loading.
25  than simplex families suggests an effect of genetic loading.
26 ses of (high environmental exposure+moderate genetic loading), (2) one environmental agent is intraut
27 on, displaying a significant contribution of genetic loading, an overrepresentation of risk genes for
28 w environmental and geographic factors shape genetic load and adaptation, highlighting the need to in
29    We investigated the evolutionary history, genetic load and adaptive potential of the Cat Ba langur
30 ons in populations leads to the buildup of a genetic load and can cause the extinction of populations
31 to small, isolated populations can alleviate genetic load and decrease extinction risk (i.e., genetic
32            Complete homozygosity exposes the genetic load and explains the high rate of congenital ma
33 ng to long-term accumulation and fixation of genetic load and have a higher risk of extinction.
34 N(e)) affects heterozygosity and deleterious genetic load and how these factors may contribute to ext
35 captive breeding program, would mitigate the genetic load and increase the odds of species survival.
36 fusion remains around the definitions of the genetic load and its dynamics, and how they impact indiv
37 ational input and impact the accumulation of genetic load and molecular evolution rates of the integr
38 duction along with mixed mating in models of genetic load and mutation-selection balance.
39 haracterized, as is the relationship between genetic load and putatively adaptive genetic variation.
40 ing selection to prevent the accumulation of genetic load and repeats within the inversions.
41             The negative association between genetic load and selfing rate suggests that purgable par
42 ormed selfing lineages may express recessive genetic load and suffer inbreeding depression.
43 pathological conditions related, in part, to genetic load and, in part, to environmentally induced ep
44 isorder in children with ADHD indexes higher genetic loading and clinical severity.
45 s, yet the exact mutational underpinnings of genetic loads and their fitness consequences remain poor
46    It has a highly heterozygous genome, high genetic load, and genotype-dependent asynchronous flower
47 show how this impacts the composition of the genetic load, and how this affects the extinction risk a
48 ns epistasis, is not affected by problems of genetic load, and is robust to differences in parameters
49 hol consumption is age-dependent, has a high genetic load, and results from an interaction of the str
50  has prevented increases in homozygosity and genetic load, and through forward simulations, we illust
51 t can persist into adult life; the same ADHD genetic loading appears to contribute across the life co
52 pulations therefore experience a substantial genetic load associated with selection against deleterio
53                 While introgressions reduced genetic load at protein-coding sequences, they mostly ha
54  homozygous at the sex locus and represent a genetic load because they are inviable or sterile.
55                          If the evolutionary genetic load can be exposed and removed, the apomixis ge
56 gests that patterns of genetic diversity and genetic load can correspond to genomic signatures of ser
57                                              Genetic load can reduce fitness and hinder adaptation.
58                                        Thus, genetic load causes substantial mortality in inbred Paci
59 red with other reptiles, and harbor a higher genetic load compared with green turtles, reinforcing co
60 tangle the relative contribution of S-linked genetic load compared with overall inbreeding depression
61                         Overall, the role of genetic load depended on both the drug and the tissue ty
62 her than the overall magnitude of the linked genetic load differs between dominant and recessive S-al
63 ve analyzed the effect of segregation on the genetic load due to recurrent deleterious mutations, but
64 have experienced accelerated accumulation of genetic load during the past ~ 120 years of captivity.
65           For phage populations with minimal genetic load, engineering mutation rate increases beyond
66                       The risk allele count (genetic load) exhibits an accelerating pattern of SLE ri
67 ug combinations were remarkably strong, with genetic load explaining up to 83% of the variance in the
68 at this female protective effect arises from genetic load for autism spectrum disorder differentially
69 ificantly modulated by participant sex, with genetic load for autism spectrum disorder influencing fu
70 ntal conditions affect the expression of the genetic load for lifespan and adult mortality rates, or
71                        We tested whether the genetic load for MDD, bipolar disorder, and schizophreni
72  in a stepwise fashion with each increase in genetic load for schizophrenia.
73 s aged 18-87 years in 26 families with heavy genetic loading for bipolar disorder.
74 in the polygenic score analysis was from the genetic loading for depressive symptoms (p = 0.001, stan
75 pothesis was that these families have a high genetic loading for impairments in language ability, thu
76  similar trend of association between a high genetic loading for MD and lower response to lithium.
77 o have experienced childhood abuse may carry genetic loading for mental illness has never been tested
78 er, was successful in offsetting unfavorable genetic loading for most lipid traits.
79 Variance component analysis suggested a high genetic loading for predictive pursuit (heritability = 0
80 re approach to test for associations between genetic loading for psychiatric conditions, symptom prof
81  uniquely to the discrimination of degree of genetic loading for schizophrenia and, when combined, we
82                 GCD founding queens suffer a genetic load from mating randomly and produce fewer broo
83 dmixed mice with low heterozygosity and high genetic load had even lower fitness, pointing to a great
84                      Haldane's principle for genetic load has an exact but unfamiliar generalization.
85                                        This 'genetic load' has been estimated in a wide range of anim
86 w demographic history, local adaptation, and genetic load have affected their long-term survival and
87                    Inbreeding depression and genetic load have been widely observed, but their geneti
88 data represent a comprehensive evaluation of genetic load in a multilocus disease.
89 24 drugs showed significant association with genetic load in a pan-cancer analysis.
90    We investigated inbreeding depression and genetic load in a small (N(e) approximately 100) populat
91                               Estimating the genetic load in benign laboratory environments may be in
92 stry, shows incomplete penetrance but a high genetic load in familial clusters of CKD, and is associa
93 ize of Neanderthals resulted in an increased genetic load in Neanderthals relative to modern humans.
94                         We estimate that the genetic load in our populations incurred by residual TM
95 nal techniques now enable us to estimate the genetic load in populations and individuals without dire
96          However, the inclusion of increased genetic load in the form of foreign genes limits the spe
97       We describe approaches to quantify the genetic load in whole-genome sequence data based on evol
98 on is larger than any advantage conferred by genetic loading in unaffected individuals.
99 , and mutational load - a genomic measure of genetic load - in Vitis arizonica, a wild grape native t
100                        Our results show that genetic load is an important component of tumor fitness
101                                         This genetic load is in line with the "cost of domestication"
102  the influence of environmental variation on genetic load is less well characterized, as is the relat
103  low-density lipoprotein cholesterol and IHD genetic load is more than multiplicative, supporting the
104 lity rates, and large sex differences in the genetic load, is highly dependent on environmental condi
105             The PT population exhibited high genetic load (L = 1 - W(PT)/W(AL)) in a range of fitness
106 cluding reduced heterozygosity and increased genetic load, likely due to strong directed breeding.
107 chanisms such as recombination to ameliorate genetic loads may have been in place early in the histor
108                    Beyond being a biomarker, genetic load might be a new, unexplored vulnerability of
109  cases of autism may be the product of (high genetic loading+moderate environmental exposure) and mal
110 eneficial variants, it also contributes to a genetic load of deleterious mutations.
111 chanism mediating disease phenotypes and the genetic load of natural populations.
112 made by one gene in particular, GJB2, to the genetic load of SNHL has strongly affected the assessmen
113 this cohort study revealed a high multitrait genetic loading of persistent symptom trajectories, cons
114       In a large family sample, we show that genetic loads of rare and polygenic risk are inversely c
115 vides a model for considering the effects of genetic load on neurobehavioral responses to drugs.
116 m the Y was permitted by an unexpectedly low genetic load on the Y and this indicates that the origin
117 ed by the cost of selection, measured as the genetic load or the relative fitness variance, both of w
118 iciency in adults is probably due to a lower genetic load overall combined with subtle variation in t
119 = 5.0-7.5) that will have purged much of the genetic load, potentially leading to the lack of observe
120 to regulate multiple genes and decreases the genetic load required for carboxysome assembly in hetero
121                                           No genetic load resulting from the integrated transgenes im
122                                  Analyses of genetic load reveal the purging of potentially high-effe
123 l-induced blackouts including a component of genetic loading shared with frequency of intoxication ma
124                   Given its negative effect, genetic load should make tumors more sensitive to antica
125                     This evidence for a high genetic load strongly supports the dominance theory of h
126 olves and, on average, dogs have 2-3% higher genetic load than gray wolves.
127  genes and the X is expected to harbour less genetic load than the Y.
128 transcription factors will contribute to the genetic load that predisposes certain individuals to dis
129 seases are classic polygenic disorders, with genetic loads that reflect immunopathological processes
130  and the higher the autism spectrum disorder genetic load, the less the depressive symptoms decreased
131  that SVs, particularly inversions, increase genetic load through the accumulation of deleterious nuc
132 ur ability to assess the threat posed by the genetic load to small and declining populations has been
133                                          The genetic load underlying lifespan and adult mortality rat
134 in gene expression associated with increased genetic load, which included cell-cycle checkpoints, DNA
135   Here we investigate whether a "three-hit" (genetic load x environmental factor x sex) theory of aut
136                          Saolas carry a high genetic load, yet their gradual decline resulted in the

 
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