889 resultados para Twin coronet porphyrins
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Includes index.
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Includes index.
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Includes index.
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"Published by direction of the House of Representatives."
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Saline Valley Farms was an experiment in cooperative farming and living begun in 1932 by Harold S. Gray.
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Saline Valley Farms was an experiment in cooperative farming and living begun in 1932 by Harold S. Gray.
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Description based on: 1898; title from cover.
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Bibliography: p. 41-43.
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We have rated eye color on a 3-point scale (1=blue/grey, 2=hazel/green, 3=brown) in 502 twin families and carried out a 5-10 cM genome scan (400-757 markers). We analyzed eye color as a threshold trait and performed multipoint sib pair linkage analysis using variance components analysis in Mx. A lod of 19.2 was found at the marker D15S1002, less than 1 cM from OCA2, which has been previously implicated in eye color variation. We estimate that 74% of variance in eye color liability is due to this QTL and a further 18% due to polygenic effects. However, a large shoulder on this peak suggests that other loci affecting eye color may be telomeric of OCA2 and inflating the QTL estimate. No other peaks reached genome-wide significance, although lods >2 were seen on 5p and 14q and lods >1 were additionally seen on chromosomes 2, 3, 6, 7, 8, 9, 17 and 18. Most of these secondary peaks were reduced or eliminated when we repeated the scan as a two locus analysis with the 15q linkage included, although this does not necessarily exclude them as false positives. We also estimated the interaction between the 15q QTL and the other marker locus but there was only minor evidence for additive x additive epistasis. Elaborating the analysis to the full two-locus model including non-additive main effects and interactions did not strengthen the evidence for epistasis. We conclude that most variation in eye color in Europeans is due to polymorphism in OCA2 but that there may be modifiers at several other loci.
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We examined whether there are crosscultural differences in the magnitude of genetic and environmental contributions to risk of becoming a regular smoker and of persistence in smoking in men and women. Standard methods of epidemiologic and genetic analysis were applied to questionnaire data on history of cigarette use obtained from large samples of male and female like-sex twins from three different countries: Australia (N = 2284 pairs), Sweden (N = 8651 pairs), and Finland (N = 10,948 pairs). Samples were subdivided into three age groups (AG), 18-25 years, 26-35 years, and 36-46 years of age. The magnitude of genetic influence for lifetime smoking was found to be consistent across country and AG for women (46%) and men (57%), and estimates of the contribution from environmental influences shared by twin and co-twin could be equated across all countries by AG for the women (from youngest to oldest AG: 45%, 35%, and 26%), but not for men, with separate estimates obtained for the Scandinavian (33%, 29%, and 19%) and the Australian men (26%, 9%, and 11 %). There was no evidence for an important role for shared environmental influences on persistent smoking, and the genetic contribution was found to be consistent in magnitude in men and women, and the same across country and AG (52%). There are strong genetic influences on smoking behavior, and that risk of becoming a smoker (but not persistence in smoking) may be modified by experiences shared by twins that differ by AG and, at least for men, cultural background.
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The negative effects of very low birthweight on intellectual development have been well documented, and more recently this effect has been shown to generalise to birthweights within the normal range. In this study we investigate the etiology of this relationship by using a classical twin design to disentangle the contributions of genes and environment. A previous Dutch study (Boomsma et al., 2001) examining these effects indicated that genes were important in mediating the association of birthweight to full IQ measured at ages 7 and 10, but not at ages 5 and 12. Here the association between birthweight and IQ at age 16 is considered (N = 523 twin pairs). Using variance components modeling we found that the genetic variance in birthweight (4%) completely overlapped with that in verbal IQ but not performance or full IQ. Results further showed the importance of shared environmental effects on birthweight (similar to 60%) but not on IQ (with genes explaining up to 72% of IQ variance). Models incorporating a direction of causation parameter between birthweight and IQ provided adequate fit to the data in either causal direction for performance and full IQ, but the model with verbal 10 causing birthweight was preferred to one in which birthweight influenced verbal IQ. As the measurement of birthweight precedes the measurement of twins' IQ at age 16, the influence of verbal IQ might be better considered as a proxy for parents' 10 or education, and it is possible that brighter mothers provide better prenatal environments for their children.
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Arsenic has been classified as a human carcinogen based on epidemiological data however the mechanism of its carcinogenicity is still unclear. Urinary biomarkers for chronic arsenic exposure would be valuable as an early warning indicator for timely interventions. In this study, young female C57BI/6J mice were given drinking water containing 0, 100, 250 and 500 mug As-v/L as sodium arsenate ad libitum for 12 months. Urine was collected bimonthly for urinary arsenic methylation assay and porphyrin analysis. All detectable arsenic species showed strong linear correlation with administered dosage and the arsenic methylation patterns were similar in all three treatment groups. No significant changes of methylation patterns were observed over time for either the control or test groups. Urinary coproporphyrin III was significantly increased in the 8th month in 250 and 500 mug/L groups and remained significantly dose-related after 10 and 12 months. Coproporphyrin I also showed a significant dose-response relationship after 12 months. Our results confirm that urinary arsenic is a useful biomarker for internal dose. The alteration of porphyrin profile suggests that arsenic can affect the heme metabolism and this may occur prior to the onset of arsenic induced carcinogenesis. (C) 2004 Elsevier Ireland Ltd. All rights reserved.