The effects of twinning on mother—Offspring behavior in range beef cattle

Methods to increase the productivity of beef cattle include induced twinning and multiple fostering of calves on nurse cows, but little is known about the capacity of cows to rear more than one calf in a rangeland environment.Eight single and 14 twin calves and their mothers were studied in a 30.4-ha enclosure in a California rangeland environment from 2 to 20 weeks following parturition. Data were obtained on ingestive, grooming, agonistic, play and sexual behaviors, as well as spatial proximity of calves to mothers and peers.Initially, twins spent more time suckling their mothers than did single calves (presumably due to insufficient milk intake), but later adapted by utilizing natural forage and obtaining milk from alien cows. By 15–20 weeks of age, twins were suckling their dams for less than one-quarter of the time spent at 3–6 weeks, whereas the suckling time of single calves did not decline. Thus, twins may experience a natural early weaning from mother's milk.The hypothesis that mother—Offspring bonds are weaker with twins than with singles was supported by the fact that mothers bearing twins groomed their offspring less than mothers with singles, and twins were normally found at greater distances from their mothers than singles.Most long-distance cow—Calf separations resulted from the cow moving to feed or to obtain water. Reunion of mother and young depended on auditory communication; the calf normally traversed most of the intervening distance.     

Birth order,gestational age,and risk of delivery related perinatal death in twins: retrospective cohort study

ObjectiveTo determine whether twins born second are at increased risk of perinatal death because of complications during labour and delivery.DesignRetrospective cohort study.SettingScotland, 1992 and 1997.ParticipantsAll twin births at or after 24 weeks'' gestation, excluding twin pairs in which either twin died before labour or delivery or died during or after labour and delivery because of congenital abnormality, non-immune hydrops, or twin to twin transfusion syndrome.ResultsOverall, delivery related perinatal deaths were recorded for 23 first twins only and 23 second twins only of 1438 twin pairs born before 36 weeks (preterm) by means other than planned caesarean section (P>0.99). No deaths of first twins and nine deaths of second twins (P=0.004) were recorded among the 2436 twin pairs born at or after 36 weeks (term). Discordance between first and second twins differed significantly in preterm and term births (P=0.007). Seven of nine deaths of second twins at term were due to anoxia during the birth (2.9 (95% confidence interval 1.2 to 5.9) per 1000); five of these deaths were associated with mechanical problems with the second delivery following vaginal delivery of the first twin. No deaths were recorded among 454 second twins delivered at term by planned caesarean section.ConclusionsSecond twins born at term are at higher risk than first twins of death due to complications of delivery. Previous studies may not have shown an increased risk because of inadequate categorisation of deaths, lack of statistical power, inappropriate analyses, and pooling of data about preterm births and term births.

What is already known on this topic

It is difficult to assess the wellbeing of second twins during labourDeliveries of second twins are at increased risk of mechanical problems, such as cord prolapse and malpresentation, after vaginal delivery of first twinsIncreased risks of perinatal death in second twins have not been shown, but the methods of these studies were flawed

What this study adds

Second twins delivered at term are at increased risk of delivery related perinatal deathsIntrapartum anoxia caused 75% of these deaths in second twins, and most of these resulted from mechanical problems after vaginal delivery of first twinsPlanned caesarean section of twins at term may prevent perinatal deaths     

Time trends in twin perinatal mortality in northern England, 1982-94. Northern Region Perinatal Mortality Survey Steering Group.

The dynamics of perinatal mortality rates (PNMR) and causes of death in twin pregnancies over 13 years in the Northern Region of the National Health Service in England is described. All twin perinatal deaths occurring between 1982-1994 were identified from the Northern Region Perinatal Mortality Survey. The twinning rate increased from 9.9 per 1000 maternities in 1982 to 12.0 in 1994. There was a total of 10,734 twin pregnancies and of these 421 resulted in 530 perinatal deaths. The perinatal mortality rate in twins significantly decreased over time (1982-87, 55.4 per 1000; 1988-94, 44.4 per 1000; P = 0.01). The PNMR was significantly higher for twins from like-sexed than from unlike-sexed pairs (53.5 and 34.4 per 1000 respectively, P < 0.001). Despite no improvement in birthweight distribution in the twin population, birthweight-specific perinatal mortality rates for both like and unlike-sexed twins decreased for each birthweight category in 1988-94 compared with 1982-87. Twins with very low birthweight (< 1500 g) comprised 69%, and preterm twins (< 37 completed weeks of gestation) 74.9% of all twin perinatal deaths. The major immediate cause of early neonatal death was pulmonary immaturity (63%); antepartum anoxia caused 76.9% of antenatal deaths. Unexplained preterm labour and intrauterine death were the leading obstetric factors underlying death in twins. Despite a decrease over the 13 years, the perinatal mortality rate in twins in the Northern Region remains high. Continued monitoring of trends in twinning and mortality rates is needed to inform health care planning.     

The Developmental Genetics of Hybrid Inviability: A Mitotic Defect in Drosophila Hybrids

We report studies of the developmental basis of hybrid inviability in the Drosophila melanogaster complex. The pathology of these hybrids closely resembles that of mitotic mutants in D. melanogaster. We use mosaic and cytological analyses to show that hybrid male inviability is associated with, and probably caused by, a defect in mitotic cell division. In the mosaic study, we find that male clones produced in otherwise female hybrids are not cell lethal but are very small, probably reflecting defects in mitotic proliferation. Cytological inspection of larval neuroblasts reveals a profound mitotic defect in hybrids: chromosomes show a near-complete failure to condense even after 2 hr of incubation in colchicine. Both the defect in clonal proliferation and in chromatin condensation are rescued by mutations known to rescue normally inviable hybrid males. We present a simple model in which hybrid inviability is partly or entirely caused by a mitotic defect; this defect is, in turn, caused by an interaction between the Hybrid male rescue (Hmr) locus of D. melanogaster and autosomal gene(s) from D. melanogaster's sister species.     

Inviability of dam recA and dam recB cells of Escherichia coli is correlated with their inability to repair DNA double-strand breaks produced by mismatch repair.

The molecular basis for the inviability of dam-3 recA200(Ts) and dam-3 recB270(Ts) cells was studied. The dam-3 recA200(Ts) cells were inviable in yeast extract-nutrient broth or in minimal medium at 42 degrees C. Although the dam-3 recB270(Ts) cells were inviable in yeast extract-nutrient broth at 42 degrees C, they were viable at 42 degrees C in minimal medium, in which the high salt content suppresses the mutant phenotype caused by the recB270(Ts) mutation at 42 degrees C. Under the growth conditions rendering dam rec cells inviable, the cells accumulated double-strand breaks in their DNA. Introduction of a mutL or mutS mutation restored the viability of dam-3 recB270(Ts) cells grown in yeast extract-nutrient broth at 42 degrees C and eliminated the formation of DNA double-strand breaks in these cells. We conclude that the inability to repair DNA double-strand breaks produced by the mismatch repair process accounts for the inviability of the dam recA and dam recB cells.     

Familial factors in early deaths: Twins followed 30 years to ages 51–61 in 1978

Summary Subjects in the National Academy of Sciences-National Research Council Twin Registry of 31,848 male twin veterans were followed for mortality from 1 January 1946, or from the date of entry into military service if that was later, to 31 December 1978. During this time 3,573 deaths occurred among them, 837 due to trauma and 2,712 due to disease.Mortality from all causes for the entire follow-up period was 10.2% among 11,350 monozygotic (MZ) twins and 11.4% among 14,450 dizygotic (DZ) twins. Mortality of veterans is known to be favorable compared to U.S. males. Among U.S. males of the same ages as the two respective twin zygosity groups, a mortality of 13.9% would have been expected during this time period. Observed mortality from trauma was 2.3% for MZ twins and 2.5% for DZ twins, with 3.0% expected in either group. Observed mortality from all disease was 7.9% for MZ twins and 8.8% for DZ twins, with 10.9% expected in either group.For total mortality, the case twin concordance rates, based on individual deaths, were 28.2% among MZ twins and 17.7% among DZ twins. For trauma, respectively by zygosity, these concordance rates were 6.9% and 3.9%. In this sample, familial factors appear to be of little consequence in trauma deaths. For all disease the concordance rates were 30.1% and 17.4%. Estimating heritability of liability to death from disease, as proposed by Edwards (1969), provides values of h ²=r=0.51 for MZ twins, h ²=2r=0.48 for DZ twins, and h ₂=2(r _MZ–r _DZ=0.54 using data for the two zygosity groups combined.Presented in abbreviated form at The Third International Congress of Twin Studies, Jerusalem, Israel, 19 June 1980     

Iron stocks and risk of anemia in twins

This study aims to compare the risk of anemia by iron deficiency in mothers and infants of twin and single pregnancy. It concerned 33 couples of twins and 31 control, all 97 being term newborns. At birth, ferritinemia is significantly lower in twins, and reticulocytes count is significantly higher; their mothers have a significantly lower hemoglobin level and higher reticulocytes percentage and count. At 3 and 6 months, hemoglobin level and mean corpuscular hemoglobin are significantly lower in twins, as at 6 months ferritinemia is significantly lower in twins. Iron stocks constituted in utero are significantly lower in twin pregnancy, and this study support the early preventive iron treatment in twins.     

The outcome of twin pregnancies complicated by single fetal death after 20 weeks of gestation.

A retrospective study involving 972 twin births was conducted to evaluate the maternal and fetal outcomes of twin pregnancies complicated by single fetal death. The incidence of single fetal death in twin pregnancies after 20 weeks was 3.3%. Preterm birth rates for 37 and 32 gestational weeks were 81.3% and 41.6% respectively. The median interval between the diagnosis of fetal death and the delivery was 11 days (range 1-27 days). Eighteen (56%) infants were delivered by cesarean and 14 (43%) vaginally. Twin-twin transfusion syndrome (TTTS) was the cause of single fetal death in 8 of 32 twin pregnancies (25%). Ten of the surviving co-twins were lost in the neonatal period (31.3%) and half of those neonatal deaths were due to TTTS. TTTS is the major contributor for perinatal mortality in same-sex twins complicated by single fetal death. The death of one twin in utero should not be the only indication for preterm delivery, and in case of severe prematurity with a stable intrauterine environment; expectant management may be advisable until fetal lung maturation ensues.     

Yeast Mer1 Mutants Display Reduced Levels of Meiotic Recombination

Mutations at the MER1 locus were identified in a search for meiotic mutants defective in chromosome segregation. mer1 strains show decreased levels of inter- and intrachromosomal meiotic recombination and produce inviable spores. The MER1 gene was cloned by complementation of the spore inviability phenotype. Strains carrying disruptions of the MER1 gene are mitotically viable. The epistatic relationships between MER1 and previously characterized meiotic genes are described.     

DNA synthesis during meiosis of eight-spored strains ofChlamydomonas reinhardi

Summary In strain 137F ofChlamydomonas reinhardi, the zygospores undergo one round of nuclear DNA replication followed by three divisions to produce octospores. The third division without replication has been interpreted by Sueoka et al. (1967, 1969) to mean that the gametes and vegetative cells have at least binemic chromosomes. We have repeated their experiments using the same strain. However, the meiotic products were inviable — unable to undergo postmeiotic vegetative growth, DNA replication or division. On the other hand, using a variant of strain 137C which also has three divisions during germination we have shown that meiosis is normal. Zygospores from this strain undergo two rounds of nuclear DNA replication prior to the formation of octospores. These meiotic products are viable and capable of postmeiotic vegetative growth, replication and division. Since the third division without DNA replication subsequent to the two meiotic divisions leads to inviable products, and the strain which has viable products after three divisions does not lack the additional replication, meiosis inChlamydomonas reinhardi provides no evidence of a bineme chromosome structure.     

Sex differences in birth defects: a study of opposite-sex twins

BACKGROUND: Sex differences in structural birth defects are often confounded by environmental risk factors. Opposite-sex twins provide a unique model for detecting sex differences in birth defects while maximally controlling environmental risk factors in a natural setting. METHODS: Population data from the Florida Birth Defects Registry were analyzed. A total of 4,768 pairs of twins who were discordant for sex and born between 1996 and 2001 were analyzed. The McNemar test was used to compare the differences between a male twin and his twin sister for the risk of developing specific defects and organ-system defects. RESULTS: Of 4,768 twin pairs, 225 males (4.72%) and 175 females (3.67%) had birth defects. Among opposite-sex twin pairs, males had a 29% higher risk for birth defects than their twin sisters. Compared to their twin sisters, males had a 5.4 times higher risk for pyloric stenosis and a 2.4 times higher risk for obstructive genitourinary defect, but only one-tenth the risk for congenital hip dislocation. CONCLUSIONS: Sex differences in birth defects exist between opposite-sex twins.     

A three-locus system of interspecific incompatibility underlies male inviability in hybrids between Drosophila buzzatii and D. koepferae

In hybrids between the sibling species D. buzzatii and D. koepferae, both sexes are more or less equally viable in the F₁: However, backcross males to D. buzzatii are frequently inviable, apparently because of interspecific genetic incompatibilities that are cryptic in the F₁. We have performed a genetic dissection of the effects of the X chromosome from D. koepferae. We found only two cytological regions, termed hmi-1 and hmi-2, altogether representing 9% of the whole chromosome, which when introgressed into D. buzzatii cause inviability of hybrid males. Observation of the pattern of asynapsis of polytene chromosomes (incomplete pairing, marking introgressed material) in females and segregation analyses were the technique used to infer the X chromosome regions responsible for this hybrid male inviability. The comparison of these results with those previously obtained with the same technique for hybrid male sterility in this same species pair indicate that in the X chromosome of D. koepferae there are at least seven times more regions that produce hybrid male sterility than hybrid male inviability. We have also found that the inviability brought about by the introgression of hmi-1 is suppressed by the cointrogression of two autosomal sections from D. koepferae. Apparently, these three regions conform to a system of species-specific complementary factors involved in an X-autosome interaction that, when disrupted in backcross hybrids by recombination with the genome of its sibling D. buzzatii, brings about hybrid male inviability.     

Uniparental chromosome elimination in the early embryogenesis of the inviable salmonid hybrids between masu salmon female and rainbow trout male

Chromosome elimination through chromosome loss and partial deletion is known to be one of the causes of embryonic inviability in some salmonid interspecific hybrids. Using fluorescence in situ hybridization and related techniques, including whole chromosome painting and comparative genomic hybridization, parental origin of eliminated chromosomes was identified in the inviable hybrids between masu salmon (Ms, Oncorhynchus masou) female and rainbow trout (Rb, O. mykiss) male at the early embryonic stage prior to death. In these hybrids, the haploid Rb chromosome number decreased to nearly half, whereas the Ms chromosomes were retained as one or occasionally two full haploid complements. The Rb chromosomes were also involved in the frequently observed fragments and micronuclei. Whereas the occurrence of fragments was constant throughout the observed period, chromosome loss occurred mainly from just after fertilization to the blastulae stage. In tissue sections and cell spreads of late blastula, some Rb chromosomes were trapped in the midzone from ana- to telophase, resulting in micronuclei at the subsequent interphase. Micronuclei and mitotic abnormalities were also observed in the androgenetic haploid hybrids. However, such abnormalities were seldom or never observed in the viable reciprocal hybrids. The present findings suggest that the paternal Rb chromosomes in the inviable hybrids are preferentially eliminated through mitotic abnormalities during early embryogenesis, owing to a possible incompatibility between the maternal Ms cytoplasm and paternal Rb genome. Received: 22 August 1996; in revised form: 14 November 1996 / Accepted: 20 November 1996     

Between twins; research summaries; in the real world.

Research on unusually long birth intervals between twin and triplet deliveries is reviewed. A recent multicentre study reported gestational and survival data for 35 multiple birth sets from 12 centers, and evaluated conservative treatment strategies for mothers delivering one twin fetus. Next, findings from three recent twin studies are reviewed: effects of close inter-twin communication on longevity; case report of dizygous twins with a single chorion; and a case of discordance for hemihypertrophy in an MZ female twin pair. The article concludes with summaries of three interesting and informative anecdotal accounts of twins.     

Me14, a Yeast Gene Required for Meiotic Recombination

Mutants at the MEI4 locus were detected in a search for mutants defective in meiotic gene conversion. mei4 mutants exhibit decreased sporulation and produce inviable spores. The spore inviability phenotype is rescued by a spo13 mutation, which causes cells to bypass the meiosis I division. The MEI4 gene has been cloned from a yeast genomic library by complementation of the recombination defect and has been mapped to chromosome V near gln3. Strains carrying a deletion/insertion mutation of the MEI4 gene display no meiotically induced gene conversion but normal mitotic conversion frequencies. Both meiotic interchromosomal and intrachromosomal crossing over are completely abolished in mei4 strains. The mei4 mutation is able to rescue the spore-inviability phenotype of spo13 and 52 strains (i.e., mei4 spo13 rad52 mutants produce viable spores), indicating that MEI4 acts before RAD52 in the meiotic recombination pathway.     

Twins are more different than commonly believed,but made less different by compensating behaviors

Twin studies are popular, because twins are believed to be the same/similar in genes and environmental exposures. It is well documented, however, that the firstborns are healthier at birth. We use the entire U.S. record of twin births during 1995–2000 to show that the survival duration parameters differ between twins depending on the birth order. We also find that wiser (i.e., older or educated) or married (i.e., resource-richer) mothers take more care of the weaker, which is a “compensating” behavior reducing the twin difference, as opposed to “reinforcing (the twin difference)” behavior. The systematic survival pattern difference and the mother's intervention against nature send cautions to twin studies that regard twins homogeneous to interpret their findings accordingly. Since the survival duration in our data is 97% right-censored in one year, we devise a quantile-based ‘fixed-effect’ semiparametric estimator that can handle heavy censoring, which is our methodological contribution.     

Monozygotic twins discordant for constitutive BRCA1 promoter methylation, childhood cancer and secondary cancer

We describe monozygotic twins discordant for childhood leukemia and secondary thyroid carcinoma. We used bisulfite pyrosequencing to compare the constitutive promoter methylation of BRCA1 and several other tumor suppressor genes in primary fibroblasts. The affected twin displayed an increased BRCA1 methylation (12%), compared with her sister (3%). Subsequent bisulfite plasmid sequencing demonstrated that 13% (6 of 47) BRCA1 alleles were fully methylated in the affected twin, whereas her sister displayed only single CpG errors without functional implications. This between-twin methylation difference was also found in irradiated fibroblasts and untreated saliva cells. The BRCA1 epimutation may have originated by an early somatic event in the affected twin: approximately 25% of her body cells derived from different embryonic cell lineages carry one epigenetically inactivated BRCA1 allele. This epimutation was associated with reduced basal protein levels and a higher induction of BRCA1 after DNA damage. In addition, we performed a genome-wide microarray analysis of both sisters and found several copy number variations, i.e., heterozygous deletion and reduced expression of the RSPO3 gene in the affected twin. This monozygotic twin pair represents an impressive example of epigenetic somatic mosaicism, suggesting a role for constitutive epimutations, maybe along with de novo genetic alterations in recurrent tumor development.     

Contribution of twin pregnancy to perinatal mortality and fetal growth retardation; reversal of growth retardation after birth.

A survey of factors associated with perinatal mortality in 511 twins and fetal growth retardation and its reversal in 262 twins is presented. The incidence of stillbirth was almost 50% higher in twins than in singletons and the neonatal mortality was six times as high. Eighty percent of the neonatal deaths occurred in infants born prior to or at 30 weeks of gestation; 93% of the deaths were in infants weighing less than 1500 g and 75% occurred within 48 hours of birth. Fetal malnutrition was the main cause of stillbirth, and respiratory distress syndrome and asphyxia neonatorum were the main causes of neonatal death. One quarter of the twins had fetal growth retardation, a prevalence 10 times that in singletons. In almost all, the growth retardation was reversed by high-energy feedings. Although twins represented only 1% of all pregnancies and 2% of live births, they composed 12% of infants with early neonatal death and 17% of growth-retarded infants. A program is suggested for reduction of twin mortality and morbidity.     

Variable transmission rates of a B-chromosome in Myrmeleotettix maculatus (Thunb.) (Acrididae: Orthoptera)

Karyotype comparisons of both parents and progeny from single pair matings in the grasshopper Myrmeleotettix maculatus have shown that there is an accumulation of the large mitotically stable B-chromosome when transmitted through the female. This is presumed to result from a preferential segregation of univalent B-chromosomes at the first division of female meiosis and occurs irrespective of whether the B's are odd or even in number. In the male there is a loss of B-chromosomes. This loss does not appear to be due simply to the lagging and elimination of B-chromosomes in meiosis but probably involves sperm formation or function. When the balance of the gain and loss after one generation is calculated, it shows large overall accumulation in crosses involving individuals from a population in Wales, and a slight loss in individuals from a population in East Anglia. Such differences in transmission rates may be responsible for differences in B-frequency between populations. Since the B-chromosome frequency of these two populations has remained stable over five years, possible forces in the maintenance of the equilibria are examined. Females with B-chromosomes produce more aneuploid embryos than 0B females, but neither this cause of inviability nor general embryo mortality seem sufficient to produce an equilibrium situation. It is necessary to postulate that progeny with more than 2B chromosomes are inviable in order to approach equilibria. The presence of B-chromosomes in females has also led to the formation of polyploid embryos. The possible involvement of repetitive DNA in the formation of unreduced egg nuclei and preferential segregation is discussed.     

Yeast meiotic mutants proficient for the induction of ectopic recombination.

A screen was designed to identify Saccharomyces cerevisiae mutants that were defective in meiosis yet proficient for meiotic ectopic recombination in the return-to-growth protocol. Seven mutants alleles were isolated; two are important for chromosome synapsis (RED1, MEK1) and five function independently of recombination (SPO14, GSG1, SPOT8/MUM2, 3, 4). Similar to the spoT8-1 mutant, mum2 deletion strains do not undergo premeiotic DNA synthesis, arrest prior to the first meiotic division and fail to sporulate. Surprisingly, although DNA replication does not occur, mum2 mutants are induced for high levels of ectopic recombination. gsg1 diploids are reduced in their ability to complete premeiotic DNA synthesis and the meiotic divisions, and a small percentage of cells produce spores. mum3 mutants sporulate poorly and the spores produced are inviable. Finally, mum4-1 mutants produce inviable spores. The meiotic/sporulation defects of gsg1, mum2, and mum3 are not relieved by spo11 or spo13 mutations, indicating that the mutant defects are not dependent on the initiation of recombination or completion of both meiotic divisions. In contrast, the spore inviability of the mum4-1 mutant is rescued by the spo13 mutation. The mum4-1 spo13 mutant undergoes a single, predominantly equational division, suggesting that MUM4 functions at or prior to the first meiotic division. Although recombination is variably affected in the gsg1 and mum mutants, we hypothesize that these mutants define genes important for aspects of meiosis not directly related to recombination.