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M Traver

Publications and source records attributed to M Traver.

5 recordsLinked to original sources

DNA analysis in a paternity case involving a triploid fetus.

BACKGROUND: A parentage testing laboratory was asked to perform testing in a case of sexual assault that resulted in the conception of a child. Samples submitted to the laboratory included blood from the mother, the alleged father, and the fetus. CASE REPORT: DNA typing was used to determine if the suspect in this sexual assault was the father of the expected child. DNA extracted from these samples was subjected to both restriction fragment length polymorphism and polymerase chain reaction/short-tandem repeat analysis at a total of 13 genetic loci. Examination of DNA profiles for selected markers suggested that the fetus was triploid. Triploidy was confirmed through the use of fluorescent in situ hybridization of chromosomes, employing three chromosome-specific alpha satellite probes and fetal trophoblast nuclei. Statistical interpretation of the test results required identifying a method for calculation that would consider two transmitted paternal genes. Attempts to modify the standard method of calculating a paternity index were unsuccessful, because it was not possible to distinguish between dispermy and diandry as the mechanism of conception. Therefore, the likelihood ratio was calculated as the reciprocal of the random men not excluded value or the proportion of the population that possesses all of the paternal markers observed in the triploid fetus. CONCLUSION: Calculation of a likelihood ratio employing the exclusionary power of a collection of DNA markers appears to be the only method suitable for assigning weight to the significance of DNA matches between an alleged father and a child who is triploid.

Alleles↗

Determination of sibship in any two persons.

BACKGROUND: Parentage testing laboratories may be asked to provide genetic evidence that two persons are or are not related, when no other relatives are available for study. Simple methods using autosomal, codominant, unlinked genetic systems can determine if two people are blood relatives (e.g., siblings). STUDY DESIGN AND METHODS: The odds ratios (full sibship index) of true sibling pairs were determined from two-child paternity cases and compared with regionally and racially matched control pairs of unrelated children. The sharing of two, one, or no alleles was observed in pairs of children at three independent, polymorphic VNTR (variable number of tandem repeat) sequences loci. The sibship index was calculated as (the chance that an observation would occur if two children were siblings) divided by (the chance that it would occur if the two were unrelated). Sibship indices and the frequencies of shared alleles were determined for 20 sibling pairs and 20 control pairs. RESULTS: Sibship index values were less than 1 in all 20 pairs of unrelated children. Sibship index values were greater than 100 in nine pairs of siblings (45%), between 10 and 100 in five pairs (25%), between 1 and 10 in four pairs (20%), and less than 1 in two pairs (10%). Siblings shared two alleles in 17 of 60 observations (28.3%); controls shared two alleles in 0 of 60 observations (0%). CONCLUSION: The sharing of one allele and the sharing of no alleles at a polymorphic locus of high heterozygosity provide limited information for and against sibship, respectively. The sharing of two alleles produces strong evidence favoring sibship. In a given case, the study of more than three polymorphic loci of high heterozygosity may be needed to develop the evidence that two people are siblings. The general logic and methods used for siblings apply to kinship analyses of other two-person pedigrees.

Alleles↗

Interrelationships among human chorionic gonadotropin (hCG), 17 beta-estradiol, progesterone, and estriol in maternal serum: evidence for an inhibitory effect of the fetal adrenal on secretion of hCG.

In normal pregnancy, maternal serum hCG reaches a maximum concentration about 8-10 weeks after the last menstrual period and then decreases. To investigate the possibility that this decrease in hCG is produced by an inhibitory effect of steroids originating in the feto-placental unit, hCG, progesterone, 17 beta-estradiol, and estriol were determined by specific RIAs in 341 serum specimens obtained from 229 different pregnancies. Expressions for predicted hCG as a function of estimated trophoblastic mass and percent predicted hCG were determined to correct for the increase in hCG with increasing trophoblastic mass. The relationships between hCG and progesterone, 17 beta-estradiol, estriol, or estimated trophoblastic mass were not linear. Expression of the hCG data as percent predicted hCG produced linear relationships between hCG and each of the above steroids. Both hCG itself and percent predicted hCG were shown to have a negative regression on estriol (P less than 0.001) and a positive regression on progesterone (P less than 0.001), but not on 17 beta-estradiol (P greater than 0.05), in a multiple linear regression on all three steroids. These data suggest that hCG production is inhibited by a steroid originating in the fetal adrenal. This inhibitory effect plateaus in late pregnancy, allowing a minor late increase in hCG due to increasing trophoblastic mass.

Adrenal Glands↗

Transfusions today.

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Blood Coagulation Factors↗