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PubMed1989

The usefulness of various polymorphisms in paternity testing. Experience with three southern African populations.

Genetic studies have been carried out on 1,059 cases (involving 3,177 blood samples) of disputed paternity. Seventeen polymorphic systems, representing 21 loci, have been used on all the cases and an additional 11 system (12 loci) were used when an exclusion on only one of the system was obtained. The overall rate of exclusion was 34.0% and the data were analysed according to the population from which the case came (white, 'coloured' or black). HLA is the most informative system in all three populations, followed by PGM1, with the rhesus blood group the next most useful in the whites and 'coloured's, whereas ABO is the next most useful in the blacks. The probability of excluding a man falsely accused of paternity was 99.1% in the black, 99.4% in the white and 99.7% in the 'coloured' populations. The data were also used to calculate the probability of paternity in the cases in which an exclusion could not be demonstrated; values of over 98% were found in 98.5% of whites, 98.8% of 'coloureds' and 90% of blacks; a further 9.1% of blacks gave values of 95.1 - 98.0%. The range of genetic markers, representing red cell antigen, red cell enzyme, serum protein and HLA polymorphisms used in this study, meets the requirements of an efficient paternity testing service.

Black People↗
PubMedDate not supplied

Genetic marker analysis in cases of disputed paternity when the alleged father is deceased.

Data are presented to demonstrate the utility of genetic marker analysis in cases of disputed paternity in which the alleged father is deceased prior to testing. The first case involves the histocompatibility (HLA) typing of the alleged father's parents and presumed mother and child, in which the deceased alleged father (AF) was not excluded from paternity. The second case involves a similar situation. However, the deceased AF was not clearly excluded from paternity in the HLA system owing to the inability to rule out gene suppression or deletion, but the deceased AF was excluded following red blood cell antigen typing of the man's parents. These two cases demonstrate the utility of genetic marker analysis in cases of disputed paternity in which the AF is deceased. This same type of analysis can be applied to cases in which the presumed mother is either deceased or missing and custody of the child is being sought by the alleged father.

Erythrocytes↗
PubMed1988

HLA and the probability of paternity.

In cases of disputed paternity, blood tests are often used to obtain an estimate of the probability that the accused male is the true father. The interpretation of the genetic data is usually based upon a statistic called the paternity index. This paper shows that the paternity index method cannot be applied to data from compound loci in the absence of information on linkage phase. Since phenotypic data from compound loci, such as HLA, MNSs, and Rh, are often useful in disputed paternity proceedings, they should be analyzed with available alternative statistics.

Female↗
PubMed1988

An expository review of two methods of calculating the paternity probability.

There are two methods for calculating the posttests probability of paternity, viz., the nonexclusion probability method (E method) and the paternity index method (lambda method). This report reviews these two methods and explains the reasons behind them, in the hope that it might alleviate the current controversy between the advocates of these two methods. The emphasis throughout the paper is on exposition, using simple examples to illustrate certain principles or properties. A discussion follows the presentation of the two methods. The calculation of the paternity index is based on the genotype (or phenotype) of the accused man; and the value of the paternity index remains the same whether the accusation itself is true or false.

Biometry↗
PubMed1986

Empirical validation of the Essen-Möller probability of paternity.

The validity of the Essen-Möller formulation probability of paternity is supported by demonstrating its correctness in a model genetic system--the ABO system. An analysis was made of 1,393 paternity cases typed uniformly for HLA-A and -B, ABO, Rh, and MNSs, in which the mother named one man only as the child's father and in which both mother and putative father identified themselves as Caucasian. For purposes of analysis, putative fathers not excluded from paternity by the four systems tested were regarded as actual fathers. The joint distribution of observed triplets of ABO phenotypes is shown to be statistically consistent with expected values, and the fractions of "true" fathers for a given triplet closely approximated the probability of paternity calculated using a realistic prior probability. Recent allegations of fallaciousness of the method by Li and Chakravarty and Aickin are discussed in terms of the results presented.

ABO Blood-Group System↗
PubMed1986

No fallacies in the formulation of the paternity index.

In a recent publication, Li and Chakravarti claim to have shown that the paternity index is not a likelihood ratio. They present a method of estimating the prior probability of paternity from a sample of previous court cases on the basis of exclusions and nonexclusions. They propose calculating the posterior probability on the basis of this estimated prior and the test result expressed as exclusion/nonexclusion. Their claim is wrong--the paternity index is a likelihood-ratio, that is, the ratio of the likelihood of the observation conditional on the two mutually exclusive hypotheses. Their proposed method of estimating the prior has been long known, has been applied to several samples, and is inferior (in terms of variance of the estimate) to maximum likelihood estimation based on all the phenotypic information available. Their proposed "new method" of calculating a posterior probability is based on the use of a less informative likelihood ratio 1/(1-PE) instead of Gürtler's fully informative paternity index X/Y (Acta Med Leg Soc Liege 9:83-93, 1956), but is otherwise identical to the Bayesian approach originally introduced by Essen-Möller in 1938.

Humans↗
PubMed1986

Paternal age and the occurrence of birth defects.

The association between paternal age and the occurrence of birth defects was studied using data collected in Metropolitan Atlanta. Paternal-age information for babies born with defects was obtained from birth certificates, hospital records, and interviews with mothers; for babies born without defects, the information was obtained from birth certificates. Several statistical techniques were used to evaluate the paternal-age-birth-defects associations for 86 groups of defects. Logistic regression analysis that controlled for maternal age and race indicated that older fathers had a somewhat higher risk for having babies with defects, when all types of defects were combined; an equivalent association for older mothers was not found. Logistic regression analyses also indicated modestly higher risks for older fathers for having babies with ventricular septal defects and atrial septal defects and substantially higher risks for having babies with defects classified in the category chondrodystrophy (largely sporadic achondroplasia) and babies with situs inversus. An association between elevated paternal age and situs inversus has not been reported before; the magnitude of the estimated increased risk for situs inversus was about the same as that found in this study for chondrodystrophy.

Congenital Abnormalities↗
PubMed1985

Paternal-age and birth-order effect on the human secondary sex ratio.

Because of conflicting results in previous analyses of possible maternal and paternal effects on the variation in sex ratio at birth, records of United States live births in 1975 were sorted by offspring sex, live birth order (based on maternal parity), parental races, and, unlike prior studies, ungrouped parental ages. Linear regression and logistic analysis showed significant effects of birth order and paternal age on sex ratio in the white race data (1.67 million births; 10,219 different combinations of independent variables). Contrary to previous reported results, the paternal-age effect cannot be ascribed wholly to the high correlation between paternal age and birth order as maternal age, even more highly correlated with birth order, does not account for a significant additional reduction in sex-ratio variation over that accounted for by birth order alone.

Adolescent↗
PubMed1985

The effect of differences in gene frequency on probability of paternity.

Knowledge of gene frequencies in populations is required for the calculation of probability of paternity. The question remains open as to the degree of accuracy of gene frequency estimates required to give accurate probability of paternity figures. This is of special concern in the HLA system, which has haplotype frequencies known to vary in populations. This paper presents computer simulation data comparing probability of paternity calculations using HLA data from California and North Carolina. Comparisons were made between geographic regions, and between blacks and whites within a geographic region. It was found that when the absolute probability of paternity is high, the average differences induced were small, but at lower probabilities the changes can be large. Differences were most pronounced between black and white populations. Examples of individual cases are given to illustrate the huge differences that can be induced in some cases by changing gene frequency.

Child↗
PubMed1984

Some fallacies in the computation of paternity probabilities.

Legal identification of fathers by means of a "paternity probability" has been used in European courts for decades, and has recently been introduced into American courts and accepted by some of them. The voluminous literature on this topic contains virtually no fundamental criticism of the logical basis for the probabilistic computations. Here I suggest that the "paternity probability" suffers from three basic fallacies: (1) contrary to claims, the figure is not, in fact, the probability that the alleged father is the true father, (2) the denominator of the likelihood ratio used in the computation is driven by (sometimes self-contradictory) assumptions and is not based on facts, and (3) post-inclusionary computations are based on speculation about genotypes that does not constitute scientific evidence. It is recommended that pending the resolution of these difficulties "paternity probabilities" should not be computed or introduced as positive evidence of paternity.

Bayes Theorem↗
PubMed1983

[The importance of HLA typing in cases of disputed paternity].

In dispute paternity, the biologists must reply to two questions: 1. Is the paternity excluded or possible? 2. If it is possible, what is its probability? Valid answers can be given, using several genetic markers, among which HLA genes are specially interesting. Looking at HLA-A, B, C, DR typing of child, mother and presumed father, we propose a method which allows a direct calculation of paternity probability. Crossing over between HLA genes in presumed father and in mother are also considered in this method. In our experience, adding the date provided by the HLA genes and other genetic markers, we obtained, either formal exclusions, or possible paternities with a probability almost always higher than 90%.

Female↗
PubMed1980

Exclusions and attributions of paternity: practical experiences of forensic genetics and statistics.

The Swedish State Institute for Blood Group Serology is a central government laboratory handling all blood typing in paternity cases in Sweden, each year testing 1,500-2,000 cases using about 13 polymorphisms. Of the accused men, 35%-40% are nonfathers, but in one-man cases (about 78% of all cases), approximately 75% are the true fathers. Exclusions appear to be distributed as expected from allele frequencies, and the paternity probability of nonexcluded men is assessed with a Bayesian approach. Some cases are retested in extended investigations which raise theoretical exclusion capability from about 87% to about 99%. Both the results of extended investigations and the theoretical consideration of the distribution of paternity probabilities support the use of such positive statistical evidence for the attribution of paternity.

Adult↗
PubMedDate not supplied

Paternal involvement after perinatal death.

This study describes paternal involvement after perinatal death in a large, mostly minority, lower socioeconomic status sample. Paternal presence at birth, holding the baby, and presence at a follow-up appointment were the indicators of paternal involvement. Perinatal death was defined as miscarriage, stillbirth, or neonatal death within 12 hours of birth. Data were collected from a retrospective chart review under the auspices of the Perinatal Mortality Counseling Program at Shands Hospital at the University of Florida, a tertiary care referral center in north central Florida. The sample included 722 cases of perinatal death between July 1978 and April 1991. The results indicated that many fathers experienced perinatal grief. More than half attended the birth, a quarter chose to hold their baby, and one fifth returned with the mother to follow-up appointments. Paternal-maternal cohabitation was the variable most predictive of the fathers' involvement after perinatal death. Race was predictive of the father being present at birth and at the follow-up visit, with white fathers more likely to be present than black fathers. Married fathers and those employed in a professional or manual labor occupation were more likely to be present at the birth than fathers who were unemployed, students, incarcerated, or in the military. Gestational age was predictive of the father holding the baby, with the likelihood increasing 1.04 times for each week of increase in gestational age. This study supports the need to include fathers in grief counseling, and the further investigation of the involvement of fathers when a perinatal death occurs.

Adult↗
PubMed1994

Association of paternal diagnostic X-ray exposure with risk of infant leukemia. Investigators of the Childrens Cancer Group.

Whether low level radiation exposure before conception increases the risk of leukemia in offspring has been much debated. No study has specifically evaluated the effect of parental preconception diagnostic X-ray exposure in the development of leukemia among infants. Mothers of 302 infant leukemia cases (diagnosed at < or = 18 months of age) and 558 individually matched regional controls, and fathers of 250 cases and 361 controls, were independently interviewed to obtain information on X-ray exposures. Paternal preconception X-ray exposure was associated with an increased risk of infant leukemia, higher risks being linked to exposures closer to conception. X-ray related leukemia risk varied with exposure site and histopathological type, the highest risk being for acute lymphocytic leukemia related to two or more X-rays of the lower gastrointestinal (GI) tract and lower abdomen (odds ratio, 3.78; 95% confidence interval, 1.49-9.64). A positive association was observed between acute lymphocytic leukemia and number of paternal X-rays of the lower GI and lower abdomen (trend test, P < 0.01), upper GI (P = 0.04), and chest (P = 0.08). Exposures of head and neck and limbs were unrelated to risk. The risk of acute myelogenous leukemia was unrelated to paternal X-ray exposure, except for a marginally significant association (trend test, P = 0.07) for upper GI X-rays. No consistent association between maternal X-ray exposure and infant leukemia was observed. The results of this study suggest that paternal low level radiation exposure before conception is associated with an increased risk of infant leukemia, although the nature of this association needs to be further evaluated.

Adult↗
PubMed1977

[The Duffy blood group system in the determination of paternity].

Authors report in detail recent achievments the investigation of Duffy's blood group system. Genetics of the system is shortly reviewed. Results of their own population-genetical investigation--carried out on 723 non-related persons by the aid of anti-Fy(a) and anti-Fy(b) serum--are also described. According to the author's data frequency of the phenotype Fy(a+b-)=19,63%, of the phenotype Fy(a+b)=50,91%, and of the phenotype Fy(a-b+)=29.46%. Data of the gene-frequency: Fya=0,451; Fyb=0,549. Presence of the gene Fy(-) was not revealed. The Duffy system--among others--was examined in 299 cases of discussed paternity. In 30 cases (10.3%) paternity was excluded on the base of it. In 31 men (8.29%) out of 374 the paternity cystem. Maximal (theoretical) chance of exclusion calculated from the data got in own investigations: 18.625%. Examined and calculated values of the chance of exclusion in cases of opposed homozygotes (12.26%) and in cases of the lack of characteristics (6.36%) were similar to a suitable degree. Technical problems of the investigation are further discussed. Author recommend the use of the examination of Duffy system in cases of discussed paternity.

Blood Group Antigens↗
PubMed1996

[Paternity probability in the cases of incest].

To calculate the paternity probability in the cases of incest where the alleged father was either the father or the brother of the plaintiff's mother, some algebraic expressions applicable to a simple codominant diallelic genetic marker system were derived by modifying the formulas of Essen-Möller and Komatsu (the both formulas gave the same result). The paternity probability in the incest case is generally lower than that in usual case, because in the former case an allele present in the mother is sometimes found in both the alleged father and the child (plaintiff), even if the alleged father is not true father. The paternity probability in the incest case, however, becomes higher than that in usual case when an allele is common to both the alleged father and the child but not to the mother. The mean value of paternity probability becomes lower, as the relationship becomes closer between the alleged father and the mother.

Alleles↗
PubMedDate not supplied

Paternal exposures and the question of birth defects.

Compared to maternal exposures, little attention has been paid to the possibility of paternally induced adverse effects on fetal development. There is increasing concern, however, about the potential for male-mediated developmental toxicity brought about by exposure to teratogenic agents. This is evidenced by the number of calls regarding paternal exposures that are received by teratogen information services. In this paper, we report the experience of the state of Florida's Teratogen Information Services regarding questions asked about paternal exposures, and briefly review what is known about the risk of paternal exposure to the 10 agents which are most frequently queried.

Abnormalities, Drug-Induced↗
PubMed1996

[Paternity determination in cases of incest using multiallelic loci DNA polymorphisms].

The analysis of genetic markers in man allows to efficiently resolve cases of dubious paternity. Lately, the use of genetic markers derived from DNA analysis allows high exclusion probabilities. A particular case are those consultations whom the progenitors are closely related, in which the criteria to attribute paternity are modified. The present report explains the analysis methods and interpretation of results in situations of doubtful paternity in cases of incest between father and daughter, using monolocus DNA polymorphisms. The method is illustrated through the analysis of four cases seen at the Servicio Médico Legal of Santiago. To be able to determine paternity in these cases of incest, at least three multiallelic loci in which mother and son have different genotypes must be examined.

Alleles↗