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1 ptions that DIPGs are molecularly similar to adult disease.
2 during pregnancy affect fetal programming of adult disease.
3 how early life events in childhood influence adult disease.
4 ty and mortality and is also associated with adult disease.
5 concept termed the developmental origins of adult disease.
6 the well documented developmental origins of adult disease.
7 iovascular postnatal outcomes, indicative of adult disease.
8 harmful when re-expressed in the context of adult disease.
9 t clarifying fetal determinants of infant or adult disease.
10 th weight and fetal/developmental origins of adult disease.
11 size at birth and childhood risk factors for adult disease.
12 tory factor to the reported fetal origins of adult disease.
13 upport for the "fetal origins" hypothesis of adult disease.
14 reported associations between birth size and adult disease.
15 urvival and predispose to the development of adult disease.
16 ssociations between childhood overweight and adult disease.
17 to systemic alterations, which may encourage adult disease.
18 is epidemiologically associated with various adult diseases.
19 id in the identification of fetal origins of adult diseases.
20 omplications and the in utero programming of adult diseases.
21 common variants that confer risk for common adult diseases.
22 tcomes, including a role as an antecedent to adult diseases.
23 ation between birth weight and these chronic adult diseases.
25 at the observations on early life effects on adult diseases and the persistence of methylation change
27 ic consensus is emerging that the origins of adult disease are often found among developmental and bi
31 ltidrug resistant phenotype and, at least in adult disease, demonstrated that the presence of this pa
32 of neurodegeneration and disability in young adults, disease discordance in monozygotic twins has bee
36 gs support the growing realization that many adult diseases have their origins in early life by empha
40 tal animals addressing the 'Fetal Origins of Adult Disease' hypothesis have established a relationshi
41 care providers 1) recognize risk factors for adult disease in children and 2) institute effective int
42 -cell tumours differ from the adolescent and adult disease in many ways, leading to complexities in a
45 ternal outcomes and very long-term outcomes (adult diseases) is too scarce to draw any conclusions.
47 etal development might influence the risk of adult disease may be relevant to many age-related diseas
50 tically explain the developmental origins of adult disease, namely the hypothesis that many complex a
51 traditional view that COPD is exclusively an adult disease occurring after years of inhalational insu
53 lthood, remain fertile, and, as in the human adult disease, older mice accumulate glycogen in the dia
61 pediatric (e.g., asthma, allergy) as well as adult disease risk (e.g., chronic obstructive pulmonary
64 ualties, we investigated the extent to which adult-disease risk factors vary systematically according
65 tion, distinctions between the pediatric and adult diseases seem more quantitative than absolute.
66 are associated with common birth defects and adult diseases, several of which can be suppressed with
68 lized in newborn screening in common complex adult diseases such as cardiovascular disease, insulin r
71 growing burden of non-communicable, chronic, adult diseases that have their origins in early life, to
72 een implicated in numerous developmental and adult diseases, their specific impact on biological path
73 with increased susceptibility to a range of adult diseases through an unknown mechanism of cellular
74 ept of fetal and early infant programming of adult diseases to the immune system and suggest that ear
75 ns (EC), and activated interstitial cells of adult diseased valves share characteristics of embryonic
76 ese findings may have implications regarding adult diseases whose risks are associated with adolescen
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