戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 how early life events in childhood influence adult disease.
2 the well documented developmental origins of adult disease.
3 to systemic alterations, which may encourage adult disease.
4 haracteristics during pregnancy, and risk of adult disease.
5 ptions that DIPGs are molecularly similar to adult disease.
6 during pregnancy affect fetal programming of adult disease.
7 ty and mortality and is also associated with adult disease.
8  concept termed the developmental origins of adult disease.
9  factors and presentation largely similar to adult disease.
10 contributing to the developmental origins of adult disease.
11 iovascular postnatal outcomes, indicative of adult disease.
12  harmful when re-expressed in the context of adult disease.
13 t clarifying fetal determinants of infant or adult disease.
14 th weight and fetal/developmental origins of adult disease.
15 size at birth and childhood risk factors for adult disease.
16 tory factor to the reported fetal origins of adult disease.
17 upport for the "fetal origins" hypothesis of adult disease.
18 and mortality and the risk for childhood and adult disease.
19 reported associations between birth size and adult disease.
20 urvival and predispose to the development of adult disease.
21 ssociations between childhood overweight and adult disease.
22 ith PCV21 also targeting sizeable burdens of adult disease.
23 avior when compared with pediatric and young adult disease.
24 iour when compared with paediatric and young adult disease.
25 genetic subtypes of pediatric B-ALL and also adult disease.
26  in childhood cardiomyopathies compared with adult disease.
27 id in the identification of fetal origins of adult diseases.
28 omplications and the in utero programming of adult diseases.
29  common variants that confer risk for common adult diseases.
30 tcomes, including a role as an antecedent to adult diseases.
31 ation between birth weight and these chronic adult diseases.
32  may profoundly impact fetal risk for future adult diseases.
33 is epidemiologically associated with various adult diseases.
34 rogenitor cells is a predisposing factor for adult disease and dysregulated stress responses.
35 at the observations on early life effects on adult diseases and the persistence of methylation change
36  III alleles) locus has been associated with adult diseases and with birth size.
37 ic consensus is emerging that the origins of adult disease are often found among developmental and bi
38 ertain degree of continued plasticity in the adult diseased brain.
39 ion may underpin the intrauterine origins of adult disease, but longitudinal studies linking placenta
40 ould participate in the transmission of some adult disease-causing genotypes.
41 Hypothesis" or the "developmental origins of adult disease" concept.
42 ese findings support the thesis that the LTL-adult disease connection is principally determined befor
43 ltidrug resistant phenotype and, at least in adult disease, demonstrated that the presence of this pa
44 rtilization embryos for genetic liability to adult diseases, despite a lack of comprehensive modeling
45 of neurodegeneration and disability in young adults, disease discordance in monozygotic twins has bee
46                                              Adult disease-driven drug development will continue to d
47                           The fetal basis of adult disease (FeBAD) hypothesis states that many adult
48 e expression colocalize with birthweight and adult disease genetic associations, facilitating mechani
49  disease (FeBAD) hypothesis states that many adult diseases have a fetal origin.
50 gs support the growing realization that many adult diseases have their origins in early life by empha
51 iscuss the relevance of the fetal origins of adult disease hypothesis to the dementias.
52 is described by the developmental origins of adult disease hypothesis.
53              Although the 'foetal origins of adult disease' hypothesis has significant relevance to p
54 tal animals addressing the 'Fetal Origins of Adult Disease' hypothesis have established a relationshi
55 care providers 1) recognize risk factors for adult disease in children and 2) institute effective int
56 -cell tumours differ from the adolescent and adult disease in many ways, leading to complexities in a
57 ed by postnatal overweight, confers risk for adult disease including diabetes.
58                                      Whether adult disease is caused by intrauterine beta-cell-specif
59 ternal outcomes and very long-term outcomes (adult diseases) is too scarce to draw any conclusions.
60                Most epidemiologic studies of adult diseases lack exposure data from the distant past.
61 etal development might influence the risk of adult disease may be relevant to many age-related diseas
62 ates suggest the prevalence of pediatric and adult disease may be similar.
63          Live imaging of spinal MNs from the adult disease mice demonstrates impaired dynein-driven r
64 have been challenging in vivo, especially in adult disease models such as cancer, which include mixtu
65 tically explain the developmental origins of adult disease, namely the hypothesis that many complex a
66 traditional view that COPD is exclusively an adult disease occurring after years of inhalational insu
67 c lymphocytic leukemia (CLL) is an incurable adult disease of unknown etiology.
68 lthood, remain fertile, and, as in the human adult disease, older mice accumulate glycogen in the dia
69 mation, limiting respiratory compensation to adult disease or injury.
70                  Furthermore, in contrast to adult disease, patients with childhood-onset disease had
71 gnalling, which is potentially linked to the adult disease phenotype.
72 vely immature iPSC-CMs to fully recapitulate adult disease phenotypes.
73           The hypothesis of fetal origins of adult disease posits that early developmental exposures
74 equencing technology open a new strategy for adult disease prevention by genetic screening.
75  conditions and may help predict the risk of adult disease programmed in utero.
76                                           In adults, disease rates decline following intermittent col
77        With the advent of genetic testing in adults, disease-related, structural brain changes can be
78 pediatric (e.g., asthma, allergy) as well as adult disease risk (e.g., chronic obstructive pulmonary
79 y life exposures are important predictors of adult disease risk.
80 eractions at the genetic level in predicting adult disease risk.
81                             Social trends in adult-disease risk factors do not emerge exclusively in
82 ualties, we investigated the extent to which adult-disease risk factors vary systematically according
83 tion, distinctions between the pediatric and adult diseases seem more quantitative than absolute.
84 are associated with common birth defects and adult diseases, several of which can be suppressed with
85 ns between early childhood poverty and these adult disease states may be immune-mediated.
86 lized in newborn screening in common complex adult diseases such as cardiovascular disease, insulin r
87 ions like anemia and helps to prevent future adult diseases such as osteoporosis.
88 ons, such as DNA methylation, that influence adult disease susceptibility.
89 growing burden of non-communicable, chronic, adult diseases that have their origins in early life, to
90 een implicated in numerous developmental and adult diseases, their specific impact on biological path
91  with increased susceptibility to a range of adult diseases through an unknown mechanism of cellular
92 ept of fetal and early infant programming of adult diseases to the immune system and suggest that ear
93 ns (EC), and activated interstitial cells of adult diseased valves share characteristics of embryonic
94 ese findings may have implications regarding adult diseases whose risks are associated with adolescen
95 dition such as OSA can be linked to specific adult diseases will be presented.