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At least 631 records · Page 35Linked to original sources
PubMed2000

Multiple paternity in side-neck turtles Podocnemis expansa: evidence from microsatellite DNA data.

Multiple paternity was found in two clutches of Podocnemis expansa using eight microsatellite loci. When loci were analysed separately a minimum of two males was estimated for nest N23, and three for nest C17. When all loci were combined, three patrilines were detected in N23, and six in C17. The distribution of full-sib cluster sizes indicated a disproportionate contribution of one male to clutch C17, consistent with possible sperm competition, or the mixing of leftover and newly acquired sperm. High mutation rates were detected at several loci. Multiple paternity has positive implications for this endangered species as it may slow the loss of genetic variability caused by drift. This is the first report of multiple paternity in the suborder Pleurodira.

Alleles↗
PubMed2001

High levels of extra-pair paternity in an isolated, low-density, island population of tree swallows (Tachycineta bicolor).

Molecular genetic studies have suggested that apparently nonbreeding males ('floaters') may account for a significant proportion of extra-pair paternity (EPP) in avian populations. Attempts to determine the influence of breeding density on EPP are therefore confounded by the presence of a subpopulation of floaters whose numbers are difficult to estimate. To study EPP in a tree swallow (Tachycineta bicolor) population with few floaters, we chose a nestbox grid on an island with an excess of available breeding sites and very few floaters. We obtained DNA samples from 13 complete families and performed DNA profiling on them using four microsatellite loci. For comparison, we also obtained a sample of 58 extra-pair young (EPY) from a mainland population typed at five microsatellite loci. Paternity assignments among resident males in both populations were made using the microsatellite profiles and a likelihood-based statistical method. Of the 67 island nestlings typed, we found 37 (55%) nestlings from 11 (85%) different nests that were EPY. The proportion of nestlings that were EPY and the proportion of broods containing EPY did not differ significantly between island and mainland populations studied previously. There was no significant difference between island and mainland populations in the proportion of extra-pair paternities assigned among neighbouring resident males. Male breeding density does not appear to affect the ability of female tree swallows to obtain extra-pair fertilizations, at least over the range of densities studied so far. The rate of EPP has remained remarkably consistent over many years, studies and populations implying an important role of active female choice in determining EPP.

Animals↗
PubMed2002

Maternal, paternal and environmental tobacco smoking and breast feeding.

The effects of environmental tobacco smoke (ETS) on breast-feeding patterns are poorly understood, while those of parental smoking on breast-feeding initiation vs. duration have not been clearly delineated. We conducted a prospective, population-based birth cohort study to examine the independent effects of maternal, paternal and ETS on breast-feeding initiation and duration. A total of 6747 Hong Kong Chinese infants were recruited and followed up in 1997-8. We obtained detailed household smoking history and recorded breast-feeding patterns in three follow-up interviews over 9 months. We found that both maternal and paternal smoking were associated with not initiating breast feeding (odds ratio [OR] for ever maternal smoking = 2.51, 95% confidence interval [CI] = 1.63, 3.86; OR for ever paternal smoking = 1.22, 95% CI = 1.08, 1.39). Exposure to ETS in utero and post partum were also related to not starting breast feeding (OR(ETS in utero) = 1.10, 95% CI = 0.99,1.24; OR(ETS post partum) = 1.21, 95% CI = 1.08, 1.36). These effects, however, did not persist for breast-feeding duration of < or = 4 months. Cox proportional hazards modelling confirmed the lack of association between any form of smoking and breast-feeding duration. Our findings suggest that smoking of any kind, during or after pregnancy, is a strong risk indicator for not initiating breast feeding. Smoking as a risk indicator for underlying socio-economic, demographic and psychosocial factors is probably responsible for most of the observed adverse effects, although we cannot rule out direct contributions from pathophysiological mechanisms. Public health strategies directed at these underlying factors should be vigorously pursued to reduce the adverse effects of tobacco on breast feeding and infant health in general.

Adult↗
PubMed2004

Proof of paternity: historical reflections on an andrological-forensic challenge.

Throughout the history of medicine, there have been difficulties in forensic proving of unsolved paternities, making this a major andrological-forensic challenge. In the Roman empire, children procreated by incest, called 'incestuosi', had no rights at all and other illegitimates, e.g. children born of prostitutes or as a result of adultery, could not assert rights towards the father. Only through the 'corpus iuris civilis' of the Roman Emperor Justinian I (6th century ad) could claims of alimony be made in some cases. In later times, evidence of presumable impotence of a potential father was determined by the congressus, where defined juristical 'sexual fights' had to be held before official matrons, surgeons and priests. Men had to demonstrate their erectile and ejaculatory function. A special significance must be attributed to the microscopical discovery of spermatozoa by the medical student Johann Ham in 1677 and the further investigation by Antoni van Leeuwenhoek. After centuries of personally biased and scientifically incorrect concepts of paternity determination, the discovery of the blood grouping system by Karl Landsteiner at the beginning of the 20th century paved the way for sophisticated techniques to prove or rather to disprove paternity. In 1921, Reuben Ottenberg from New York was the first to suggest the application of the system to medico-legal questions, but it was not before the 1950s that legal courts accepted this method. A famous example of disregarding clear blood grouping results was the case of the movie star Charles Chaplin in California in 1946. Modern DNA techniques, today the golden standard in forensic medicine, have also been applied recently for historical investigations. One of the very illustrious examples is the dispute about Thomas Jefferson, third President of the US, fathering a child of one of his slaves.

Andrology↗
PubMed2000

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↗
PubMed2005

Epigenetic programming in the preimplantation rat embryo is disrupted by chronic paternal cyclophosphamide exposure.

Preconceptional paternal exposure to cyclophosphamide, a widely used anticancer agent, leads to increases in embryo loss, malformations, and behavioral deficits in offspring; these abnormalities are transmissible to subsequent generations [Auroux, M., Dulioust, E., Selva, J. & Rince, P. (1990) Mutat. Res. 229, 189-200]. Little information exists on the mechanisms underlying this male-mediated developmental toxicity. We assessed the impact of paternal cyclophosphamide exposure on the dynamic regulation of histone H4 acetylation at lysine 5 and DNA methylation in preimplantation rat embryos. Zygotes sired by drug-treated males displayed advanced developmental progression, increased pronuclear areas, and disruption of the epigenetic programming of both parental genomes. Early postfertilization zygotic pronuclei were hyperacetylated; by mid-zygotic development, male pronuclei were dramatically hypomethylated, whereas female pronuclei were hypermethylated. Micronuclei were substantially elevated, and histone H4 acetylation at lysine 5 localization to the nuclear periphery was disrupted in two-cell embryos fertilized by cyclophosphamide-exposed spermatozoa. This finding demonstrates that paternal exposure to this drug induces aberrant epigenetic programming in early embryos. We hypothesize that disturbances in epigenetic programming contribute to heritable instabilities later in development, emphasizing the importance of epigenetic risk assessment after chemotherapy.

Acetylation↗
PubMed1980

Caring for the dying: advocacy or paternalism.

Moral dilemmas in the care of a dying person ideally should be decided in the context of that person's own freely determined understanding of death. At the philosophical, the clinical, and the personal levels, the primal question of how to understand death must be addressed before decisions are made concerning much ethical problems as euthanasia. Philosophers and practitioners who fail to do this are guilty of an a priori paternalism toward the dying, on whom their conclusions will be imposed. Until we have determined, together with the person involved, the way in which that person wants to view his or her death, any prior ethical judgment not only is presumptuous but infringes on the most basic freedom, that of determining the meaning that one's own experience shall have. The role of advocacy is an alternative to the traditional paternalism toward the dying. The essay attempts to (a) develop the distinctions among paternalism, consumerism, and advocacy; (b) propose a concept of advocacy as the assistance to the dying in freely determining how to understand their dying and death; (c) describe three of the views of death (naturalistic, religious, and existentialist) that need to be understood by those who assist the dying in exercising their freedom of self-determination.

Attitude to Death↗
PubMed1998

Mutations in fibroblast growth-factor receptor 3 in sporadic cases of achondroplasia occur exclusively on the paternally derived chromosome.

More than 97% of achondroplasia cases are caused by one of two mutations (G1138A and G1138C) in the fibroblast growth factor receptor 3 (FGFR3) gene, which results in a specific amino acid substitution, G380R. Sporadic cases of achondroplasia have been associated with advanced paternal age, suggesting that these mutations occur preferentially during spermatogenesis. We have determined the parental origin of the achondroplasia mutation in 40 sporadic cases. Three distinct 1-bp polymorphisms were identified in the FGFR3 gene, within close proximity to the achondroplasia mutation site. Ninety-nine families, each with a sporadic case of achondroplasia in a child, were analyzed in this study. In this population, the achondroplasia mutation occurred on the paternal chromosome in all 40 cases in which parental origin was unambiguous. This observation is consistent with the clinical observation of advanced paternal age resulting in new cases of achondroplasia and suggests that factors influencing DNA replication or repair during spermatogenesis, but not during oogenesis, may predispose to the occurrence of the G1138 FGFR3 mutations.

Achondroplasia↗
PubMed2003

Preferential paternal origin of microdeletions caused by prezygotic chromosome or chromatid rearrangements in Sotos syndrome.

Sotos syndrome (SoS) is characterized by pre- and postnatal overgrowth with advanced bone age; a dysmorphic face with macrocephaly and pointed chin; large hands and feet; mental retardation; and possible susceptibility to tumors. It has been shown that the major cause of SoS is haploinsufficiency of the NSD1 gene at 5q35, because the majority of patients had either a common microdeletion including NSD1 or a truncated type of point mutation in NSD1. In the present study, we traced the parental origin of the microdeletions in 26 patients with SoS by the use of 16 microsatellite markers at or flanking the commonly deleted region. Deletions in 18 of the 20 informative cases occurred in the paternally derived chromosome 5, whereas those in the maternally derived chromosome were found in only two cases. Haplotyping analysis of the marker loci revealed that the paternal deletion in five of seven informative cases and the maternal deletion in one case arose through an intrachromosomal rearrangement, and two other cases of the paternal deletion involved an interchromosomal event, suggesting that the common microdeletion observed in SoS did not occur through a uniform mechanism but preferentially arose prezygotically.

Abnormalities, Multiple↗
PubMed1982

Paternity testing: analysis of six blood groups and HLA markers, with particular reference to comparison of races.

Blood groups (ABO, Rh, MNSs, Kell, Duffy, and Kidd) and HLA markers were tested in cases involving 563 children of disputed parentage. In 149 (26.5%) cases, the accused men were excluded as the biologic fathers of the children in question. One hundred forty of the 149 exclusions were direct exclusions. Five exclusions were based on red blood cell data alone, i.e., HLA was non-exclusionary. Of the remaining 414 cases in which the alleged father could not be excluded as the biologic father, in 361 (87.2%) instances, the plausibility of paternity ws 95% or greater, and in 385 (93.0%) instances the comparison of men value was 20 or greater. Caucasians, blacks, and men of other races were involved in 367 (65.1%), 185 (33%), and 11 (1.9%) cases, respectively. No significant difference among races was observed in the rate of exclusion of accused men. However, of the non-excluded men, in a significantly greater proportion of black men than white men, the plausibility of paternity was below 95%. The difference was probably due to lower polymorphism of the markers tested in blacks than in whites. It is suggested that tests for additional polymorphic genes be directed towards the 12-15% of the nonexclusionary cases with plausibility of paternity values below 95%.

ABO Blood-Group System↗
PubMed1999

Low birthweight and prematurity in relation to paternal factors: a study of recurrence.

BACKGROUND: The importance of paternal determinants in the occurrence of low birthweight and prematurity is not well known. We investigated these outcomes in siblings and paternal half siblings as a function of changes in putative external determinants between two births in fathers who had experienced the birth of a premature and/or low birthweight (PTB/LBW) infant. METHODS: All fathers who, between 1980 and 1992, had an infant born before 37 completed weeks' gestation or weighing <2500 g and a following child were studied. We identified 14 147 pairs of siblings from Danish national registers. The recurrence risk was studied in three sub-cohorts defined by the outcome in the index child (PTB only, PTB/LBW, LBW only). We estimated the recurrence risk in the younger sibling according to changes of female partner, municipality type, occupation, and father's social status. RESULTS: The overall recurrence risk was 16.7% for preterm delivery and 16.8% for LBW. Changing female partner was, as expected, associated with a reduction in the recurrence risk for both outcomes (RR = 0.40; 95% CI: 0.27-0.60 for preterm delivery and RR = 0.38; 95% CI : 0.26-0.56 for LBW). None of the other studied factors was associated with changes in the recurrence risk. Fathers who changed partner had offspring with similar birthweight and gestational length between the three sub-cohorts, while a difference was evident in offspring to fathers whose female partner was unchanged. CONCLUSIONS: We did not identify any paternal factor of importance in the occurrence of LBW and preterm delivery.

Adult↗
PubMed2000

Changing paternity and the risk of preeclampsia/eclampsia in the subsequent pregnancy.

To determine whether changing paternity affects the risk of preeclampsia or eclampsia in the subsequent pregnancy and whether the effect depends on a woman's history of preeclampsia/eclampsia with her previous partner, a cohort study was conducted based on 140,147 women with two consecutive births during 1989-1991 identified through linking of annual California birth certificate data. Among women without preeclampsia/eclampsia in the first birth, changing partners resulted in a 30% increase in the risk of preeclampsia/eclampsia in the subsequent pregnancy compared with those who did not change partners (95% confidence interval: 1.1, 1.6). On the other hand, among women with preeclampsia/eclampsia in the first birth, changing partners resulted in a 30% reduction in the risk of preeclampsia/eclampsia in the subsequent pregnancy (95% confidence interval: 0.4, 1.2). The difference of the effect of changing paternity on the risk of preeclampsia/eclampsia between women with and those without a history of this condition was significant (p < 0.05 for the interaction term). The above estimates were adjusted for potential confounders. These findings suggest that the effect of changing paternity depends on the history of preeclampsia/eclampsia with the previous partner and support the hypothesis that parental human leukocyte antigen sharing may play a role in the etiology of preeclampsia/eclampsia.

Adult↗
PubMed2000

Paternal exposure to cyclophosphamide alters cell-cell contacts and activation of embryonic transcription in the preimplantation rat embryo.

Paternal exposure to chronic low doses of cyclophosphamide, an anticancer agent, results in aberrant embryonic development of the progeny. We hypothesized that paternal exposure to cyclophosphamide disturbs zygotic gene activity regulating proper progression through preimplantation development and that this disturbance results in improper cell-cell interactions. To test this hypothesis, we analyzed cell-cell interactions and the expression of cytoskeletal elements in preimplantation embryos sired by male rats gavaged with saline or 6 mg kg(-1) day(-1) cyclophosphamide for 5 wk. Embryos from control litters had 4-12 cells on Day 2 of gestation; cell-cell contacts were observed consistently. Embryos from litters sired by cyclophosphamide-treated males were frequently abnormal and had lower cell numbers and decreased cell-cell contacts. Steady state concentrations of the mRNAs for cell adhesion molecules (cadherins and connexin 43) and structural proteins (beta-actin, collagen, and vimentin) were low in two- and four-cell control embryos; expression increased dramatically by the eight-cell stage. In contrast, embryos sired by cyclophosphamide-treated males displayed the highest expression of most trancripts at the two-cell stage. In parallel with the mRNA profiles, E-cadherin immmunoreactivity was nearly absent in two-cell control embryos and was strong by the eight-cell stage; immunoreactivity in embryos sired by drug-treated fathers was strong at the two-cell stage but absent at later stages. Thus, drug exposure of the paternal genome led to dysregulated expression of structural elements and decreased cell interactions during preimplantation embryonic development.

Animals↗
PubMed1995

Paternal age and the risk of birth defects in offspring.

Previous studies have shown that advanced paternal age is associated with an increase in new dominant mutations that may result in some rare congenital anomalies or syndromes in the offspring. Nevertheless, few epidemiologic studies have evaluated the effect of paternal age on the risk of more common birth defects. We examined data from the British Columbia Health Surveillance Registry, which included a total of 9,660 cases of birth defects (22 specific defect groups). We chose matched controls from the birth files of British Columbia (1952-1973). With the exception of an unusual change in direction in the 45-49 years age category, we found a general pattern of increasing relative risk estimates (adjusted for maternal age and other factors) with increasing paternal age for neural tube defects, congenital cataracts, reduction defects of the upper limb, and Down syndrome. For example, the adjusted relative risk estimates for neural tube defects in the offspring were 1.2 (for fathers age 30-34 years relative to 25-29 years); 1.3 (35-39); 1.6 (40-44); 0.6 (45-49); and 2.3 (men 50 years and older). Men under 20 years of age were also at increased risk for fathering children with birth defects such as neural tube defects, hypospadias, cystic kidney, and Down syndrome. We hypothesize that among certain commonly observed birth defects a subgroup of cases may be due to new, unrecognized dominant mutations.

Adult↗
PubMed1996

Change in paternity: a risk factor for preeclampsia in multiparas.

Preeclampsia, a hypertensive disorder of pregnancy, is hypothesized to be a maternal immunologic response to foreign fetal antigen derived from the father's sperm. This response may be reduced by prolonged exposure to father's antigen, such as through a prior pregnancy, which may explain why multiparas are typically at lower risk for preeclampsia than nulliparas. Since multiparas with new partners are presented with a new set of paternal antigen, we hypothesize that they would have the same elevated risk for preeclampsia and gestational hypertension as nulliparas, compared with multiparas with no change in partner. We studied 5,068 nulliparas and 5,800 multiparas, 573 of whom had new partners, selected from the Child Health and Development Studies cohort (Oakland, CA, 1959-1967). Preeclampsia was diagnosed in 3.2% of nulliparas, 3.0% of multiparas with changed paternity, and 1.9% of multiparas with no change. Compared with multiparas with no change, the adjusted odds ratio for preeclampsia among nulliparas was 2.5 [95% confidence interval (CI) = 1.8-3.5]; among multiparas with new partners, the adjusted odds ratio for preeclampsia was 1.4 (95% CI = 0.8-2.4). There was a similar pattern of results for gestational hypertension. The adjusted attributable risk of preeclampsia in multiparas associated with a change in paternity was 29%. Although these findings in part support the immunologic theory of preeclampsia, they also suggest that a subsequent pregnancy with any partner is associated with a reduced risk for preeclampsia.

Adult↗
PubMed2000

Paternal exposure to lead and infertility.

To assess whether paternal exposure to lead is associated with infertility, we performed a register-based study among married men biologically monitored for exposure to inorganic lead. We obtained information about the marriages and the wives of the men from the Finnish Central Population Register. Data on pregnancies were obtained from medical records. Paternal exposure to lead was assessed on the basis of blood lead measurements. We estimated the risk of infertility, defined as nonoccurrence of a marital pregnancy, by applying binomial regression. For the blood lead categories of 0.5-0.9, 1.0-1.4, 1.5-1.9, 2.0-2.4, and > or =2.5 micromol/L the relative risk of infertility, compared with the risk in the lowest exposure category (<0.5 micromol/L), was 1.27 (95% confidence interval 1.08-1.51), 1.35 (1.12-1.63), 1.37 (1.08-1.72), 1.50 (1.08-2.02), and 1.90 (1.30-2.59), respectively. The findings support the hypothesis that paternal exposure to lead increases the risk of infertility at low occupational exposure levels. We applied proportional hazards regression to the analysis of pregnancy delay. A delay was observed among the wives of men exposed to lead. Exposure to lead was not clearly associated with delayed pregnancy, however, when the analysis was restricted to couples with at least one pregnancy. This finding suggests that the restriction of the study on time to pregnancy to fertile couples may introduce a bias toward no association.

Adult↗
PubMed1993

Oestrogen receptor occurrence in the male mouse brain: modulation by paternal experience.

Paternal behaviour (pup-searching and retrieving of pups) was studied in male house mice with different experience in pup care and oestrogen receptor immunoreactive (ER-IR) cells were localized and quantified in their brains. Experience with pups induced paternal behaviour and correlated with (a) the occurrence of ER-IR cells in the bed nucleus of the stria terminalis, hippocampus, subiculum, lateral septal nuclei, entorhinal and piriform cortex, (b) increased numbers of ER-IR cells in the medial preoptic area and arcuate nucleus of the hypothalamus, and (c) decreased presence of ER-IR cells in the periventricular grey of the midbrain. The data indicate oestrogen receptor modulation in the male brain and suggest that oestrogen binding in distinct brain areas is involved in the regulation of paternal behaviour.

Animals↗
PubMed1994

Paternity by cardiac transplant recipients.

To assess whether children fathered by cardiac transplant recipients are at high risk of teratogenicity, cardiac transplant centers listed with the International Society for Heart and Lung Transplantation were surveyed. Paternities after transplantation by heart (n = 35) and heart-lung (n = 1) allograft recipients have resulted in 42 pregnancies (children's age 3.3 +/- 0.3 years). The fathers' age at conception was < 45 years in 40 (95%) and > 45 years in 2 (5%). Most fathers (86%) were enjoying an active and healthy lifestyle at the time of conception; one (2%) was on dialysis and listed for kidney transplantation due to nephrotic syndrome, 1 (2%) had asthma, 4 (10%) had allograft coronary disease (1 died while waiting for second heart transplant when the child was 2 months old), and 2 (5%) were retransplanted after the pregnancies. Immunosuppressive regimens were reported for 37 paternities; drug protocols at the time of conception were as follows: 25 (60%) CsA/prednisone/AZA, 6 (14%) CsA/prednisone, 4 (10%) CsA/AZA, and 2 (5%) AZA/prednisone. Twenty-six (62%) had received treatment for rejection episodes before conception; seven (17%) had received treatment for rejections since conception. Of the 42 children fathered by these recipients, 3 (7%) were preterm, 1 (2%) had a cleft palate and lip that have subsequently been corrected, 1 (2%) died from interruption of umbilical cord circulation at 24 weeks, and 1 (2%) whose father had familial cardiomyopathy was born with a cardiomyopathy that improved with time. Although the numbers are small, the available data suggest that paternity by cardiac transplant recipients may be safe.

Adult↗