A Selection Index for Fat Production in Dairy Cattle Utilizing the Fat Yields of the Cow and Her Close Relatives

Kin selection promotes the evolution of social behaviour that increases the survival and reproductive success of close relatives. One prerequisite for kin selection is that individuals have the ability to discriminate between kin and nonkin. Studies incorporating data on paternal kinship are still rare, but in species with a high male reproductive skew, many adult females will be paternal half siblings. Using both microsatellites and DNA-fingerprinting, we here analyse data on paternal relatedness in order to compare the influence of maternal and paternal kinship on rates of affiliative and aggressive interactions among semi free-ranging adult female rhesus macaques (Macaca mulatta). Because paternal half siblings tend to be peers whereas maternal half siblings are almost always nonpeers, we also examine the interactions between age proximity and genetic relatedness on social behaviour. Genetic analyses show that male reproductive success is strongly skewed with 75% of infants within the troop having a paternal half sibling in the same age cohort. The highest rates of both affiliation and aggression occur among maternal half sisters. Adult females are significantly more affiliative, but not more aggressive, with paternal half sisters than with nonkin. Affiliative relationships declined in conjunction with increasing age difference among paternal half sisters, but the reverse effect was found for affiliative relationships among maternal half siblings. No association emerged among nonkin. Among both maternal and paternal kin, rates of affiliative and aggressive interactions increase as the degree of relatedness increased, thereby questioning the concept of a relatedness threshold as a mediator of social interactions in rhesus macaques. The asymmetry in affiliation and aggression between maternal and paternal half siblings, and the effect of age proximity on partitioning social interactions suggests that context-dependent kin discrimination characterises rhesus macaques. Paternal kin discrimination probably results from an interaction between phenotype matching and familiarity, rather than from one process or the other.

Many animals rely on facial traits to recognize their kin; however, whether these traits have been selected specifically for this function remains unknown. Using deep learning for face recognition, we present the first evidence that interindividual facial resemblance has been selected to signal paternal kinship. Mandrills (Mandrillus sphinx) live in matrilineal societies, in which females spend their entire lives not only with maternal half-sisters (MHS) but also with paternal half-sisters (PHS). We show that PHS have more differentiated social relationships compared to nonkin, suggesting the existence of kin recognition mechanisms. We further demonstrate that facial resemblance increases with genetic relatedness. However, PHS resemble each other visually more than MHS do, despite both kin categories sharing similar degrees of genetic relatedness. This paternally derived facial resemblance among PHS indicates selection to facilitate kin recognition. This study also highlights the potential of artificial intelligence to study phenotypic evolution.

Kin-biased social behaviour in wild adult female white-faced capuchins, Cebus capucinus

Honey bee kin recognition: learning self and nestmate phenotypes

Informatividad a posteriori en casos de paternidad estándar con el kit Investigator Argus X-12 y hallazgos mutacionales

Weights for the Maternal Relatives of Sires

Analysis of X-chromosome short tandem repeats (STRs) is very helpful in deficiency paternity testing. Here, we reported a case of kinship analysis that showed a potentially erroneous inclusion of paternal sisters between two women. The two women shared alleles at 18 X-chromosomal STR loci spanned from 14.76cM (DXS6807) to 184.19cM (DXS7423). When their relatives were not available for testing, biostatistical analysis for the 18 X-chromosomal STR loci and 24 autosomal STR loci revealed the most possible relationship between the two women was paternal sisters. However, when the father of one woman was available, the other father-daughter possibility was excluded. In the end, the likelihood ratio of STR marker and mitochondrial DNA (mtDNA) sequences confirmed the two women were maternal sisters. This case emphasizes a cautionary interpretation of X chromosomal marker in deficiency paternity cases with female offspring. Even though large parts of the X-chromosome haplotypes shared by two females, additional relatives and extended DNA typing (such as mtDNA) may be needed further to ascertain whether they are paternal or maternal sisters.

To determine the importance of genetic effects in the aetiology of pre-eclampsia and gestational hypertension and to investigate whether pre-eclampsia and gestational hypertension share genetic aetiology. Individual record linkage between the population-based Swedish Multi-Generation and the Medical Birth Registers. Sweden. 1,188,207 births between 1987 and 1997 and their parents. Similarities in relatives were measured by the number of pairs concordant and discordant for disease, the odds ratio (OR) and tetrachoric correlations. Estimates of genetic and environmental effect for gestational hypertension, pre-eclampsia and pregnancy-induced hypertension were calculated from structural equation model fitting. Pre-eclampsia and gestational hypertension. Full sisters and mother-daughters were more similar for pre-eclampsia (OR 3.3, 95% confidence interval [CI] 3.0-3.6 and OR 2.6, 95% CI 1.6-4.3, respectively) than half-sisters (maternal half-sisters OR 1.4, 95% CI 0.9-2.2 and paternal half-sisters OR 1.0, 95% CI 0.6-1.6). Full sisters and mother-daughters were also more similar for gestational hypertension than half-sisters. A full sister to a woman with pre-eclampsia also had a significantly increased risk of gestational hypertension (OR 2.5, 95% CI 2.2-2.8). In contrast, the risk for half-sisters was not increased. Model fitting suggested heritability estimates for pre-eclampsia of 31%, for gestational hypertension 20% and for pregnancy-induced hypertension 28%. There is a genetic component in the development of pre-eclampsia and gestational hypertension and the pattern of co-morbidity suggests that they may share part of their genetic aetiology. This could be important for studies of potential susceptibility genes for these diseases.

Studies on the family aggregation of postpartum hemorrhage (PPH) are scarce and with inconsistent results, and to what extent current birthweight influences recurrence between relatives remains to be studied. Further, family aggregation of PPH has been studied from an individual, but not from a public heath perspective. We aimed to investigate family aggregation of PPH in Norway, how birthweight influences these effects, and to estimate the proportion of PPH cases attributable to a family history of PPH and current birthweight. Using data from the Medical Birth Registry of Norway, Statistics Norway, and Central Population Registry of Norway we identified individuals as newborns, parents, grandparents, and full and half-siblings, and studied 1002687mother-offspring, 841164 father-offspring, and 761011 both-parents-offspring pairs. We used multilevel logistic regression to calculate odds ratios (OR) with 95% CI. If the birth of the mother but not of the father involved PPH, then the OR of PPH (>500mL) in the next generation was 1.44 (95% CI 1.39-1.49). If the birth of the father but not of the mother involved PPH, then OR was 1.12 (95% CI 1.08-1.16). These effects were stronger in severe PPH. Recurrence between siblings was highest between full sisters (OR 1.47, 95% CI 1.41-1.52), followed by maternal half-sisters, paternal half-sisters, and partners of full brothers. A family history of PPH or birthweight of 4000g or more accounted for ≤5% and 15% of the total number of PPH cases, respectively. A history of PPH in relatives influenced the recurrence risk of PPH in a dose-response pattern consistent with the anticipated proportion of shared genes. The recurrence was highest through the maternal line.

Components of Genetic Variation for Descriptive Type Traits of Holsteins1,2

A simple method for calculating the likelihood ratio in a kinship test using X-chromosomal markers incorporating linkage, linkage disequilibrium, and mutation.

Preterm delivery (PTD) is a complex trait with a significant familial component. However, no specific inheritance patterns have been established. The authors examined the contribution of PTDs in both the woman's family and her partner's family to her risk of PTD. The authors linked birth information from Danish national registers with pedigree information from the Danish Family Relations Database for 1,107,124 live singleton deliveries occurring from 1978 to 2004. Risk ratios were estimated comparing women with and without various PTD histories. Women with previous PTDs were at greatly increased risk of recurrent PTD (risk ratio = 5.6, 95% confidence interval: 5.5, 5.8); however, their PTD risk was unaffected by a partner's history of preterm children with other women. PTDs to a woman's mother, full sisters, or maternal half-sisters also increased her PTD risk (risk ratio = 1.6, 95% confidence interval: 1.5, 1.6), whereas PTDs in her paternal half-sisters, the female partners of her male relatives, or members of her partner's family did not affect her PTD risk. Inheritance patterns were similar for all gestational ages from very early through late PTD. The substantial portion of PTD risk explained by effects passed through the female line suggests a role for either imprinting or mitochondrial inheritance.

Patient: 37-year-old Hispanic female. History of Present Illness: The patient is a known carrier of the TP53 mutation. Her surgical history includes a total abdominal hysterectomy, bilateral salpingo-oophorectomy, ovarian cystectomy, tonsillectomy, left upper chest port replacement, and fourth left toe amputation due to an Aspergillus infection. She has been diagnosed with gastroesophageal reflux disease, hypertension, and herpes simplex virus. The patient has frequent episodes of neutropenic fever along with other bacterial and viral infections secondary to stage I triple-positive breast cancer. She is on many medications to treat her numerous conditions. In summer 2011, she underwent a bilateral mastectomy, which presented with 1.3 cm infiltrating ductal carcinoma with high-grade ductal carcinoma in situ (DCIS) and negative sentinel lymph nodes. No malignancy was found in the left breast, only intraductal papilloma. Prior to the initiation of chemotherapy, she presented with new onset thrombocytopenia. Family History: Both the patient’s father and half brother have been diagnosed with brain tumors; her father subsequently expired. Several paternal aunts, first cousins, and a half sister were diagnosed with breast cancer prior to age 50. A paternal half sister has stage IV breast cancer with metastasis to the bone. Social History: Married, no children; denies any use of tobacco, alcohol, or illicit drugs. 1. Which of the patient’s laboratory findings are abnormal? 2. What does the patient’s peripheral smear reveal? Based on these findings, what is the differential diagnosis? Based on the principal laboratory results and peripheral blood smear findings, what additional test(s) is/are required to aid in the diagnosis? 3. What is the patient’s most likely diagnosis and what additional test(s) is/are appropriate to confirm diagnosis? 4. What is the significance of being a carrier for the TP-53 mutation? 5. What is the patient’s …

When agonistic interventions are nepotistic, individuals are expected to side more often with kin but less often against kin in comparison with non-kin. As yet, however, few mammal studies have been in a position to test the validity of this assertion with respect to paternal relatedness. We therefore used molecular genetic kinship testing to assess whether adult female rhesus macaques (Macaca mulatta) from the free-ranging colony of Cayo Santiago (Puerto Rico) bias their interventions in ongoing dyadic aggressive interactions towards maternal and paternal half-sisters compared with unrelated females. It turned out that females supported maternal half-sisters significantly more often than paternal half-sisters or non-kin regardless of the costs associated with such interventions. Similarly, females targeted maternal half-sisters significantly less often than non-kin when this was associated with high costs. Unrelated females provided significantly higher mean rates of both high- and low-cost support to each other than did paternal half-sisters. However, females targeted paternal half-sisters significantly less often than non-kin when targeting was at low cost, suggesting that females refrain from intervening against paternal half-sisters. Our data confirm the general view that coalition formation in female mammals is a function of both the level of maternal relatedness and of the costs of intervention. The patterns of coalition formation among paternal kin were found to be more complex, and may also differ across species, but clear evidence for paternal kin discrimination was observed in female rhesus as predicted by kin selection theory.

A genetic analysis of litter traits in Bauscat and Giza White rabbits