Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PATERNITY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources
PubMed1990

Wilms' tumor and paternal occupation.

A case-control study was conducted to examine the relationship between Wilms' tumor and paternal occupational exposures. The case group consisted of 200 children diagnosed as having Wilms' tumor who were registered at selected National Wilms' Tumor Study institutions during the period June 1, 1984, to May 31, 1986. Disease-free controls were matched to each case using a random digit dialing procedure. The parents of cases and controls completed a self-administered questionnaire. There was no consistent pattern of increased risk for paternal occupational exposure to hydrocarbons or lead found in this study. However, certain paternal occupations were found to have an elevated odds ratio (OR) of Wilms' tumor, including vehicle mechanics, auto body repairmen, and welders. Offspring of fathers who were auto mechanics had a 4- to 7-fold increased risk of Wilms' tumor for all 3 time periods. The largest increased odds ratio for auto mechanics was in the preconception period [OR = 7.58; 95% confidence interval (CI) = 0.90-63.9]. Welders had a 4- to 8-fold increased odds ratio, with the strongest association during pregnancy (OR = 8.22; CI = 0.95-71.3). Although chance cannot be excluded as a possible explanation, association of Wilms' tumor with these occupations has been reported in previous studies. Further study is needed to provide data on the specific occupational exposures involved.

Boron↗
PubMed1990

Families, murder, and insanity: a psychiatric review of paternal neonaticide.

Neonaticide is the killing of a newborn within the first 24 h of life. Although relatively uncommon, numerous cases of maternal neonaticide have been reported. To date, only two cases of paternal neonaticide have appeared in the literature. The authors review neonaticide and present two new case reports of paternal neonaticide. A psychodynamic explanation of paternal neonaticide is formulated. A new definition for neonaticide, more consistent with biological and psychological determinants, is suggested.

Acute Disease↗
PubMed1989

Paternal occupational exposures and the risk of Down syndrome.

An exploratory case-control study of paternal occupation as a risk factor for Down syndrome was conducted. With the use of the British Columbia Health Surveillance Registry, 1,008 cases of live-born Down syndrome were identified for the period 1952-73. Two controls were matched to each case by using the birth files of British Columbia. Paternal occupation was obtained from the birth notice. Elevated maternal age-adjusted relative risks of Down syndrome were found for fathers employed as janitors (odds ratio [OR] = 3.26; 95% confidence interval [C.I.] = 1.02-10.44); mechanics (OR = 3.27; C.I. = 1.57-6.80); farm managers/workers (OR = 2.03; C.I. = 1.25-3.03); material-moving equipment operators (OR = 1.88; C.I. = 0.93-3.82); food processors (OR = 1.79; C.I. = 0.96-3.31); sheet-metal workers, iron workers, and other metalworkers (OR = 1.57; C.I. = 0.92-2.69); and sawmill workers (OR = 1.43; C.I. = 0.90-2.66). This large study provides new leads for further evaluation of the role of paternal exposures in the etiology of Down syndrome.

British Columbia↗
PubMed1989

Paternal behavioral mutagenesis.

Cocaine hydrochloride (0 to 30 mg/kg, s.c.) was administered daily for a minimum of 72 days to Long Evans rats. Animals receiving the lower doses were pair fed to animals receiving the higher dose. Males were bred to untreated females. Paternal cocaine administration did not affect litter size, birth weight, or weight at weaning, but did result in offspring hyperactivity. A similar study was conducted for paternal alcohol consumption in Long Evans rats. Males consumed alcohol (35%, 17.5% or 0% ethanol derived calories) for 8 to 9 weeks and were then bred to untreated females. Males consuming the lower concentrations were pair fed to 35% EDC animals. Paternal alcohol consumption did not affect birth weight or weight at weaning but resulted in offspring hypoactivity. Mice sired by alcohol-consuming males were also hypoactive.

Animals↗
PubMedDate not supplied

Coordinated maternal imprinting and paternal genotype determined the ultimate level of hepatic cytochrome P-450 and associated monooxygenase activities.

To understand the pre- and postnatal maternal influence on hepatic drug metabolism later in adult life, we have chosen to study the mouse hybrid (129/sv x LS) offspring derived from contrasting parental lines in a designated maternal environment. Results of these studies revealed that the following: 1) sex of the offspring was the major determinant for cytochrome P-450-specific content and for the activity of aryl hydrocarbon hydroxylase, testosterone 16 alpha-hydroxylase, acetanilide hydroxylase, and NADPH-cytochrome c reductase; 2) maternal factor(s) affected cytochrome P-450-specific content and the activities of acetanilide hydroxylase and aryl hydrocarbon hydroxylase but not of testosterone 15 alpha- and 16 alpha-hydroxylases or NADPH-cytochrome c reductase; 3) superimposed upon sex and maternal determination, paternal genotype significantly contributed to adult hepatic cytochrome P-450-specific content; 4) interactions between sex of the offspring and maternal factor(s) accounted for the development of testosterone 15 alpha- and 16 alpha-hydroxylase activities later in adult life; and 5) with the exception of testosterone 16 alpha-hydroxylase activity, other yet undefined factors, including the paternal genotype, contributed to most of the measured hepatic monooxygenase activities. The mechanism of coordinated maternal imprinting and paternal genotype in determining the levels of hepatic cytochrome P-450 and its associated monooxygenase activities is discussed.

Animals↗
PubMed1978

Maternal alloimmunisation in pregnancy. In vitro studies of T cell-dependent immunity to paternal alloantigens.

A secondary in vitro allograft reaction was used to demonstrate that spleen cells derived from allogeneically mated inbred mice were immunised against paternal alloantigens. In addition to the heightened alloantigen-specific in vitro response of these spleen cells, it was also found that spleen cells froma a wide variety of syngeneically and allogeneically mated mice were nonspecifically more reactive in the in vitro allograft reaction than spleen cells from virgin mice. However, when spleen cells freshly harvested from allogeneically mated mice were tested in a direct 51Cr release assay, lysis of target cells bearing the paternal alloantigens was demonstrable in only one-third of the experiments. It is proposed that T cell immunisation to paternal alloantigens occurs in pregnancy, but that cell-mediated cytotoxicity is inhibited.

Animals↗
PubMed1986

Effect of paternal alcohol ingestion on fetal growth in rats.

To determine the effect of paternal alcohol consumption on fetal growth, male rats were given ethanol in drinking water and rat chow ad libitum (alcohol group), or water and the same amount of rat chow as that consumed by the alcohol group, but the ethanol was substituted isocalorically with corn starch (pair-fed group), or water and rat chow ad libitum (ad libitum control group). The ethanol concentration in the drinking water was 10% (v/v) for the first week, 20% the second week, and 30% during the next four weeks. After six weeks on this regimen the male rats were mated with females of the same strain not treated with alcohol. The rate of fertile matings was not significantly affected by the paternal alcohol intake. On day 21 of gestation no significant differences were seen with respect to fetal and placental weights, litter size or male to female sex ratio of the fetuses among the alcohol, pair-fed and ad libitum control groups. The results indicate that rat fetal growth is not sensitive to the effects of paternal alcohol consumption.

Animals↗
PubMed1987

Transfer of antibodies directed to paternal major histocompatibility class I antigens from pregnant mice to the developing fetus.

The placental transmission of antibodies directed toward paternal MHC Class I antigens to the developing fetus was studied to assess their effect on the expression of MHC antigens during fetal development and on the development of immune function. 125I-monoclonal anti-paternal MHC antibodies injected i.v. into pregnant mice on day 15 of gestation were efficiently transferred to the fetus within 24 hr in a dose-dependent manner. Biochemical studies on the transferred radioactivity showed that intact antibodies accumulated in the fetus for up to 3 days after antibody injection. During the same period, antibodies were eliminated from the maternal system. The transfer and accumulation of anti-MHC antibodies were independent of the MHC haplotype of the fetus. The pathway of antibody transfer and the localization of transmitted antibodies in the fetus were studied by autoradiographic analysis of the entire fetoplacental unit 24 hr after the injection of anti-paternal MHC antibodies. Our results indicate that antibodies are transferred by way of the placenta and yolk sac, and reach the fetus predominantly via the circulation. Within the embryo proper, the highest levels of antibody were found in the order of blood greater than thymus greater than fetal liver. Most other fetal organs, with the exception of brain and cartilage, showed antibody accumulation, but to a lesser extent. This pattern of antibody distribution over different tissues was similar for allogeneic and syngeneic fetuses. These findings demonstrate that various fetal tissues, including developing lymphoid cells can be directly exposed to the maternally transmitted anti-MHC antibodies, with possible functional consequences on the development of the fetal immune system.

Animals↗
PubMed1985

Quantitative and spectrotypic analysis of paternal IgG2a expression in normal and allotype-suppressed mice.

The synthesis and clonal diversity of IgG2a molecules bearing the paternally inherited immunoglobulin allotype have been examined in the offspring of matings between BALB/c mothers (Igh-1a) and SJL or C57BL/10 males (both Igh-1b) using a sensitive quantitative single radial immunodiffusion in gel assay and isoelectric focusing with autoradiography. In normal litters, the first detectable paternally-marked IgG2a is extensively polyclonal in both F1 crosses (i.e. diversity precedes expression); however, there is a delay of 2-3 weeks in the first appearance of the clonally diverse set of molecules when these are coded by the SJL genome, compared with the C57BL/10. Delayed maturation of allelically-excluded Igh-1b-expressing B cells in the (BALB/c X SJL)F1 may explain the unique susceptibility of these offspring to chronic allotype suppression when exposed to maternal anti-Igh-1b antibodies in early life. We find that, although such suppressed mice may begin life with a (delayed) synthesis of polyclonal IgG2a of paternal allele (Igh-1b), the condition of chronic suppression later imposed in the majority of mice is associated with spectrotype (clonal) simplicity.

Animals↗
PubMed1985

Dictyate oocytes of a kangaroo (Macropus robustus) show paternal inactivation at the X-linked Gpd locus.

Purified samples of large numbers of dictyate oocytes from 13 M. robustus pouch young heterozygous for glucose-6-phosphate dehydrogenase type and six homozygous controls were examined electrophoretically to determine activity states at the Gpd locus. Like somatic cortical and medullary cells, oocytes expressed only the maternal phenotype irrespective of the direction of the cross. No evidence was found of reactivation of the inactive (paternal) allele or inactivation of both maternal and paternal alleles. It was therefore concluded that unlike eutherian dictyate oocytes, only a single (maternal) allele is active in each dictyate oocyte in M. robustus. The stage of reactivation of the paternal allele remains to be determined.

Animals↗
PubMed1983

[Comparison of the size of paternal and maternal homologous chromosomes during the first 2 cleavage divisions in mouse embryos].

The mouse metaphase chromosomes of the 1st and 2nd cleavage divisions were prepared without colchicine and stained with trypsin-Giemsa. Both the homologues had the same pattern of differential staining (position and number of bands and interbands) in all pairs of chromosomes. The measurements of homologues of the 1st, 2nd, 3rd, 4th and 5th pairs of autosomes have shown that at the first cleavage division metaphase the paternal chromosomes are 1.2 times, on the average longer than the maternal ones, whereas at the second division metaphase no reliable differences in the length of homologues were found. In mice, thus, the heterocyclic pattern of the paternal and maternal sets of chromosomes manifested itself during the 1st cleavage division only and disappeared fully beginning from the 2nd division. This appears to be due to the early functional activity of chromosomes, i.e. to the fact that already in the 2-cell embryos both the maternal and paternal genes are expressed.

Animals↗
PubMed1984

Paternal effects on the human sex ratio at birth: evidence from interracial crosses.

The effects of interracial crossing on the human sex ratio at birth were investigated using United States birth-certificate data for 1972-1979. The sex ratio was 1.059 for approximately 14 million singleton infants born to white couples, 1.033 for 2 million born to black couples, and 1.024 for 64,000 born to American Indian couples. Paternal and maternal race influences on the observed racial differences in sex ratio were analyzed using additional data on approximately 97,000 singleton infants born to white-black couples and 60,000 born to white-Indian couples. After adjustment for mother's race, white fathers had significantly more male offspring than did black fathers (ratio of sex ratios [RSR] = 1.027) and Indian fathers (RSR = 1.022). On the other hand, after adjustment for father's race, white mothers did not have more male offspring than did black mothers (RSR = 0.998) or Indian mothers (RSR = 1.009). The paternal-race effect persisted after adjustment for parental ages, education, birth order, and maternal marital status. The study shows that the observed racial differences in the sex ratio at birth are due to the effects of father's race and not the mother's. The study points to paternal determinants of the human sex ratio at fertilization and/or of the prenatal differential sex survival.

Black People↗
PubMed1981

Tetratological evaluation of mouse fetuses after paternal alcohol ingestion.

Numerous studies have appeared in the literature which suggest that paternal alcohol consumption may have adverse effects on subsequent offspring. However, to date, no teratologic examination has been performed on fetuses conceived subsequent to paternal alcohol consumption. The present study has examined fetuses conceived by alcohol-treated male Swiss webster mice for gross anatomical congenital defects in an attempt to evaluate a possible mechanism for decreased viability of offspring sired by alcoholic males. Sexually mature males were maintained for 28 days on a total liquid nutriment diet in which alcohol (6.3%, v/v, U.S.P. ethanol) comprised 32% of the caloric content. Subsequently, the animals were mated with nulliparous females. On day 18 of gestation, the gravid females were sacrificed and the fetuses were examined for congenital defects. Only 14% of the matings which occurred 3--5 days after alcohol treatment resulted in pregnancy, as compared to a pregnancy rate of 100% for matings from pair-fed controls during the same period. Fetuses sired by alcohol-treated males during this time had reduced birth weights (0.85 +/- 0.04 g vs 0.92 +/- 0.11 g;p = 0.059) and crown-rump lengths (1.83 +/- 0.06 cm vs 1.99 +/- 0.11 cm;p less than 0.001) as compared to control fetuses. The frequency of congenital defects did not differ significantly between the experimental and control groups. No significant differences were noted between experimental and control progeny conceived more than 5 days after alcohol treatment. These results suggest that although some changes may be seen in progeny sired by alcohol treated males, the specific anomalies associated with the Fetal Alcohol Syndrome are most probably not due to paternal alcoholism.

Abnormalities, Drug-Induced↗
PubMed1994

[The relation between birth weight and paternal occupation].

The relationship between paternal occupation and infant birth weight stratified by sex and parity was analyzed based on 1985 vital statistics. The following results were obtained: 1) There were some differences with high statistical significance detected in Mean Birth Weight (MBW) according to 11 different categories of paternal occupation. The lowest MBW was observed in the unemployed and the highest was in protective service workers. 2) The MBW was significantly decreased and the frequency of low birth weight was significantly increased in infants of unemployed father, compared with those of employed. 3) In infants where the father was unemployed, intrauterine growth rate and mean gestational period, which are considered to be two major processes governing birth weight, were delayed and shortened respectively. Based on these results, it is suggested that paternal unemployment may somehow interfere with fetal growth. Further study is needed to clarify the mechanism of this observed relationship. 1) Professional and technical workers. 2) Managers and officials. 3) Clerical and related workers. 4) Sales workers. 5) Agricultural, forestry and fisheries workers. 6) Mining workers. 7) Workers in transport and communications occupation. 8) Craftsmen, production process workers and labours. 9) Protective service workers. 10) Service workers. 11) Unemployed.

Adult↗
PubMed1994

Preferential amplification of the paternal allele in neuroblastomas with N-myc amplification.

There is increasing evidence that imprinting plays an important role in influencing the parental origin of genes involved in cancer-specific rearrangements. In advanced stage neuroblastomas, both allelic loss of the short arm of chromosome 1 (1p) and amplification of the proto-oncogene N-myc are often seen. Therefore, we analyzed 22 human neuroblastomas with N-myc amplification to determine the parental origin of the N-myc allele that is amplified and the 1p allele that is deleted. We used at least three polymorphisms for both the 1p and the N-myc locus to analyze blood and tumor samples from neuroblastoma patients, as well as blood samples from their parents. We determined that the paternal allele of N-myc was amplified in 12 of 15 informative cases (P = 0.02), and the paternal allele on 1p was lost in 6 of 11 informative cases (P > 0.2). These results suggest that parental imprinting does not appear to affect the 1p allele that is deleted, at least in the cases that we have examined. However, imprinting has an important influence on determining the N-myc allele that is amplified in these tumors, suggesting that the paternal allele is either more highly expressed or more likely to undergo amplification.

Alleles↗
PubMed1994

Detection of new paternal dystrophin gene mutations in isolated cases of dystrophinopathy in females.

Duchenne muscular dystrophy is one of the most common lethal monogenic disorders and is caused by dystrophin deficiency. The disease is transmitted as an X-linked recessive trait; however, recent biochemical and clinical studies have shown that many girls and women with a primary myopathy have an underlying dystrophinopathy, despite a negative family history for Duchenne dystrophy. These isolated female dystrophinopathy patients carried ambiguous diagnoses with presumed autosomal recessive inheritance (limb-girdle muscular dystrophy) prior to biochemical detection of dystrophin abnormalities in their muscle biopsy. It has been assumed that these female dystrophinopathy patients are heterozygous carriers who show preferential inactivation of the X chromosome harboring the normal dystrophin gene, although this has been shown for only a few X:autosome translocations and for two cases of discordant monozygotic twin female carriers. Here we study X-inactivation patterns of 13 female dystrophinopathy patients--10 isolated cases and 3 cases with a positive family history for Duchenne dystrophy in males. We show that all cases have skewed X-inactivation patterns in peripheral blood DNA. Of the nine isolated cases informative in our assay, eight showed inheritance of the dystrophin gene mutation from the paternal germ line. Only a single case showed maternal inheritance. The 10-fold higher incidence of paternal transmission of dystrophin gene mutations in these cases is at 30-fold variance with Bayesian predictions and gene mutation rates. Thus, our results suggest some mechanistic interaction between new dystrophin gene mutations, paternal inheritance, and skewed X inactivation. Our results provide both empirical risk data and a molecular diagnostic test method, which permit genetic counseling and prenatal diagnosis of this new category of patients.

Adolescent↗
PubMed1996

Decrease in the CGGn trinucleotide repeat mutation of the fragile X syndrome to normal size range during paternal transmission.

The fragile X syndrome, the most common inherited form of mental retardation, is caused by the expansion of a CGGn trinucleotide repeat in the FMR-1 gene. Although the repeat number usually increases during transmission, few cases with reduction of an expanded CGGn repeat back to the normal size range have been reported. We describe for the first time a family in which such reduction has occurred in the paternal transmission. The paternal premutation (delta = 300 bp) was not detected in one of the five daughters or in the son of this daughter, although he had the grandpaternal RFLP haplotype. Instead, fragments indicating the normal CGGn repeat size were seen on a Southern blot probed with StB12.3. PCR analysis of the CGGn repeat confirmed this; in addition to a maternal allele of 30 repeats, an allele of 34 repeats was detected in the daughter and, further, in her son. Sequencing of this new allele revealed a pure CGGn repeat configuration without AGG interruptions. No evidence for a somatic mosaicism of a premutation allele in the daughter or a normal allele in her father was detected when investigating DNA derived from blood lymphocytes and skin fibroblasts. Another unusual finding in this family was lack of the PCR product of the microsatellite marker RS46 (DXS548) in one of the grandmaternal X chromosomes, detected as incompatible inheritance of RS46 alleles. The results suggest an intergenerational reduction in the CGGn repeat from premutation size to the normal size range and stable transmission of the contracted repeat to the next generation. However, paternal germ-line mosaicism could not be excluded as an alternative explanation for the reverse mutation.

Base Sequence↗
PubMed1996

Complete paternal isodisomy for chromosome 8 unmasked by lipoprotein lipase deficiency.

Uniparental disomy (UPD)-the inheritance of two homologous chromosomes from a single parent-may be unmasked in humans by the unexpected appearance of developmental abnormalities, genetic disorders resulting from genomic imprinting, or recessive traits. Here we report a female patient with familial chylomicronemia resulting from complete lipoprotein-lipase (LPL) deficiency due to homozygosity for a frameshift mutation in exon 2 of the LPL gene. She was the normal term product of an unremarkable pregnancy and had shown normal development until her current age of 5.5 years. The father (age 33 years) and the mother (age 24 years) were unrelated and healthy, with no family history of stillbirths or malformations. The father was a heterozygous carrier of the mutation, whereas no mutation in the LPL gene was detected in the mother. Southern blotting did not reveal any LPL gene rearrangement in the proband or her parents. The proband was homozygous for 17 informative markers spanning both arms of chromosome 8 and specifically for the haplotype containing the paternally derived LPL gene. This shows that homozygosity for the defective mutation in the LPL gene resulted from a complete paternal isodisomy for chromosome 8. This is the first report of UPD for chromosome 8 unmasked by LPL deficiency and suggests that normal development can occur with two paternally derived copies of human chromosome 8.

Adult↗