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Fraternal twins

Studies conducted in twins show a threefold increased risk of psoriasis in monozygotic twins versus fraternal twins.7 In addition, based on a study in 3,095 families with psoriasis, the calculated lifetime risk of developing psoriasis if no parent, one parent, or both parents have psoriasis was found to be 0.04, 0.28, and 0.65, respectively. If there was already one affected child in the family, the risks were increased to 0.24, 0.51, and 0.83, respectively.7,9 As many as 71% of patients with psoriasis during childhood have some positive family history.1 Similarly, psoriatic arthritis is heritable, with a prevalence 19 times higher in first-degree relatives of patients with psoriatic arthritis than in the general population.7... [Pg.950]

The influence of genetics in leukemia is supported by several observations. For example, among identical twins, the occurrence of ALL is associated with a 20% to 25% chance of the disease developing in the other twin within 1 year. In fraternal twins, there is a fourfold increase in the risk of leukemia compared with the normal population. Additionally, leukemia is known to be increased in several chromosomally abnormal populations. Patients with Down s syndrome have a 20 times increased risk of developing leukemia compared with the rest of the population. Patients with Klinefelter s syndrome and Bloom s syndrome also have an increased incidence of leukemias.7... [Pg.1399]

Genetics clearly play a role in obesity. It has been noted that an adopted child s body weight is usually more similar to the body weight of his or her biological parents than that of his or her adopted parents. Identical twins usually have similar occurrences of obesity. Studies have also shown that fraternal twins do not show this same likelihood of obesity when one twin is overweight, the other is very often not. These examples help demonstrate that genetics play a significant role in obesity. [Pg.22]

Concordance rates are compared in monozygotic (identical) and dizygotic (fraternal) twins to assess the contribution of genes to a trait These rates can be used to estimate heritability, the proportion of variation in a trait caused by genes. [Pg.337]

Odor thresholds in humans appear to be more influenced by the environment than genetics. The detection thresholds for acetic acid, isobutyric acid, and cyclohexanone varied as much in monozygotic twins as in fraternal twins. Instead, smoking and diabetes were related to lower olfactory sensitivity, and body fatness and alcohol consumption to greater sensitivity to the latter two compounds (Hubert eta/., 1980). [Pg.119]

As with most other anxiety disorders, the cause of OCD remains far from certain. There seems to be a genetic factor that makes people more likely to develop OCD because first-degree relatives (that is, people like siblings and parents) of patients who have OCD show a statistically increased rate of OCD-type symptoms even if they do not experience the full-blown version of the disorder. Also, studies of identical and fraternal twins show that where one twin has OCD, the other twin has a 67% chance... [Pg.35]

It has been long-recognized that heredity is a major factor in diabetes. Identical twins who share all the same genes have a much greater risk of diabetes than fraternal twins who may... [Pg.353]

The answer is d. (Murray, pp 812—828. Scriver, pp 3-45. Sack, pp 57-84. Wilson, pp 123—148.) The case described represents one of the more common chromosomal causes of reproductive failure. Turner mosaicism. Turner s syndrome represents a pattern of anomalies including short stature, heart defects, and infertility. Turner s syndrome is often associated with a 45,X karyotype (monosomy X) in females, but mosaicism (i.e., two or more cell lines with different karyotypes in the same individual) is common. However, chimerism (i.e., two cell lines in an individual arising from different zygotes, such as fraternal twins who do not separate) is extremely rare. Trisomy refers to three copies of one chromosome, euploidy to a normal chromosome number, and monoploidy to one set of chromosomes (haploidy in humans). [Pg.327]

Identical twins most of the time will both have autism. The rate of a fraternal twin having autism is zero to 10 percent,... [Pg.193]

Not quite. Autism in identical twins can be caused by a shared fetal environmental impact rather than by direct genetic transmission. The reality is that like mental retardation, autism is a behaviorally defined syndrome with a possibly wide variety of both genetic and nongenetic causes. The often-quoted concordance rate of 90 percent among identical twins is accurate for broad autism but not for severe (narrow) autism, for which twin concordance is only about 60 percent. Also in contrast to the ABC News report, the concordance among fraternal twins can be as high as 23 percent for broad autism.55... [Pg.194]

Definitely not. The similar environments in these studies is the postnatal environment. The prenatal environment is never considered in the analysis. For twins reared in similar postnatal environments, we don t know if the higher twin-pair IQ correlations for MZ twins are due to identity of genes or similarity of fetal environments. It is certainly possible that the fetal environments (including reactions to impacts) of identical twins are always more similar than the fetal environments of fraternal twins. We don t know enough yet about human twin biology to discount that possibility. [Pg.249]

The discovery of polymorphic N-acetylation was linked to observations on the safety, metabolism, and pharmacokinetics of the antitubercular drug, isoniazid. When urinary excretion of isoniazid was evaluated in identical twins, fraternal twins, and unrelated subjects, the variability in its excretion depended upon genetic similarity. Ultimately, in a classic experiment by Evans and colleagues that measured the plasma isoniazid concentration in subjects who had taken a single 10 mg/kg dose of isoniazid, a clear polymorphic frequency distribution was revealed with an antimode of 2.5 ug/mL. Thus, two acetylator phenotypes were identified, and the slow acetylator phenotype had a frequency of 52%, and was an autosomal recessive trait. The slow acetylator phenotype, if treated with isoniazid (INH) is at increased risk of INH-induced arthralgias, neuropathy, and hepatotoxicity. [Pg.161]

Grimley, P.M., F. Dong, and H. Rui (1999). StatSa and Stat5b Fraternal twins of signal transduction and transcriptional activation. Cytokine Growth Factor Rev. 10, 131-57. [Pg.372]

Two individuals that develop from a single fertilized egg cell by its division into two genetically identical parts. Each part eventually gives rise to a separate individual and these twins have identical DNA sequences. However, differences in patterns of methylation and acetylation of their DNA can result in differences in gene expression, which may explain observed differences in looks, etc. Compare fraternal twins. [Pg.413]

It is now well accepted that genetic variants affect responses to drugs and chemicals (Kalow, 1965 Bums, 1968). One of the earliest studies in this field compared plasma dmg half-lives in identical and fraternal twin pairs and demonstrated that greater differences existed between the fraternal twins (Vesell and Page, 1968). In recent years, several more monogenic pharmacogenetic traits have been reported (Nebert et al., 2008). One example... [Pg.314]


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See also in sourсe #XX -- [ Pg.194 , Pg.243 , Pg.244 , Pg.247 , Pg.248 , Pg.249 ]




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