Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Sibling Relations”

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 73 records · Page 4Linked to original sources

[Finding the way in a new family--ressources and conflicts in patchwork and successive families].

A new family follows the separation of a former nuclear family. At least one of the new partners and its children had to do mourning work to overcome the former separation. Children and adolescents need a reliable network of familiar relations. The following article discusses the communalities and differences and the chances and difficulties in new families (patchwork families, successive families and step families). The resources of all the members, adults and children, are a key issue. Flexibility and dynamics are special resources of new families which can be learned in a therapeutic process. A special focus lies on the strengths of the sibling relations. A high capacity to communicate and to handle the actual problems is needed to succeed as a new family. A new family means the ongoing bargaining of the former and actual relationships as parents and as children.

Adaptation, Psychological↗

Interaction of older brothers and sex-typing in the prediction of sexual orientation in men.

Numerous studies indicate that homosexual men have, on average, more older brothers than do heterosexual men. One explanation of the "older brother" effect comes from D. J. Bem (1996), who argued that an increased number of older brothers in homosexual men can result if older brothers enhance a feminine boy's sense of being different from (and hence his attraction to) other males. Thus, he argued that an interaction between older brothers and sex-typing will occur, such that when a boy is high in femininity, number of older brothers may strongly predict a homosexual orientation; and when a boy is low in femininity, number of older brothers may not or may only weakly predict a homosexual orientation. In this study, the relations among sibling characteristics (e.g., older brothers), childhood sex-typing, and sexual orientation were examined using a database of a large sample of homosexual and heterosexual men (N > 1,000) archived at the Kinsey Institute (A. P. Bell, M. S. Weinberg, & S. K. Hammersmith, 1981a). No significant Older Brother x Sex-Typing interaction effect was observed. These results join other recent evidence that postnatal (e.g., learning/environmental) mechanisms probably do not underlie the older brother effect in men.

Adult↗

Correcting for ascertainment bias of relative-risk estimates obtained using affected-sib-pair linkage data.

Locus-specific sibling relative risk is often estimated using affected-sib-pair lod score analysis of affected sibships and may be used to decide whether to continue or discontinue the search for additional susceptibility genes. We showed that relative-risk estimates obtained using affected-sib-pair data are asymptotically unbiased when each pair is given a weight inversely proportional to the sibship ascertainment probability. Here we show by simulation that the extent of the bias of relative risks estimated using the incorrect ascertainment weights is small for dominant models, but large for single-locus recessive models and some two-locus heterogeneity models. Since in practice the ascertainment scheme is often unknown, we investigate methods for jointly estimating ascertainment and relative risks from affected-sibship data. Given a sufficient sample size, a reasonable estimate of relative risk may always be obtained using only affected pairs from sibships with two affected and no unaffected siblings. This estimate, which has a large variance, may then be used in a three-stage procedure (which we call the alpha method) to estimate consistently both the ascertainment probabilities and the relative risks with greater precision. We additionally propose correction factors to eliminate small-sample bias of relative risks and investigate the bias due to error in the estimate of disease locus location.

Bias↗

Effects of residential instability on Head Start children and their relationships with older siblings: influences of child emotionality and conflict between family caregivers.

This study examined the influence that residential dislocations have on child behavior problems, depression, peer competence, cognitive competence, and the quality of sibling relations in a sample of 70 Head Start children, aged 32 to 67 months, and their older brothers and sisters, aged 48 to 155 months. This was the first study to investigate the sibling relationship in the context of high residential mobility. Information on child characteristics was obtained from mothers and teachers. Sibling data (warmth/harmony and conflict) were obtained from coding videotaped interactions. Child emotionality was found to be an important moderator of the effects of residential mobility on young, poor children and their siblings; caregiver conflict was a less powerful moderator of these effects. Residential instability seemed to compromise the warmth/harmony of the sibling relationship. It was concluded that the effects of residential instability are complex and cannot be understood without considering child characteristics, such as temperament, and the family context in which the child lives.

Caregivers↗

Perceptions of parenting as predictors of boys' sibling and peer relations.

This study included 71 target boys (8 to 10 years), their siblings, and mothers to examine the relations among mothering, fathering, sibling aggression, and peer outcomes. Siblings whose mothers were known to be more rejecting were observed and reported to be more aggressive with one another than siblings whose mothers were less rejecting. Moreover, boys who experienced more aggressive sibling interactions were more likely to be nominated by their peers as being aggressive and were less accepted by their peers. Although fathering failed to evince a direct influence on sibling aggression, an indirect effect was evidenced in that less accepting fathering related to more rejecting mothering. It appeared that boys' aggressive experiences with their siblings mediated, in part, the association between maternal rejection and their peer aggression and that peer aggression was a mediating link between sibling aggression and boys' acceptance by their peers.

Adolescent↗

Heterogeneity of insulin response in relatives of type-I and type-II diabetics.

In 30 first-degree relatives (siblings or children) of type-I diabetics and 17 relatives (children) of type-II diabetics as well as in 19 healthy subjects a two-hour glucose infusion test (GIT, 12 mg/kg b.w./min) primed by a starting bolus of 0.33 g/kg b.w. was performed to evaluate carbohydrate tolerance (CHT) and insulin secretion pattern. After 4 to 5 years the test was repeated and the results were compared with those of the initial GIT. The glucose-stimulated insulin response of the early secretion phase (0--5 min) decreased during the follow-up study in relatives of type-II diabetics with normal CHT (in tendency) and with glucose intolerance (p less than 0.05) but not in relatives of type-I diabetics. A rightward shift of the glucose-insulin response curve was seen in the former group. Relatives of type-II diabetics with impaired CHT showed a striking abnormality in B-cell responsiveness. In relatives of type-I diabetics a disturbed glucose-insulin response curve could not be observed. The insulin response during the late phase of insulin secretion did not differ significantly among the groups. The conclusion drawn from our findings is that responsiveness of pancreatic B-cells seems to be directly affected genetically in first-degree relatives of type-II but not of type-I diabetics. Thus, diabetes mellitus cannot be regarded as one disorder with a similar genetic background.

Adult↗

[HL-A system and diabetes mellitus].

In 19 families of juvenile diabetes patients intravenous glucose tolerance was tested and HLA antigens were determined. A total of 68 first degree blood relations (siblings, parents, children) was studied. Taking the age dependent variabilities of the glucose assimilation coefficient (k-value) into consideration, glucose intolerance was found in 35.5% of the blood relations. Particularly in blood relations (above all in siblings) aged under 35 and with glucose intolerance, a trend to increased frequencies of those HLA antigens (B8, BW15, CW3) associated with juvenile diabetes was found, but it is not yet clear whether this association will be of practical significance.

Adult↗

Familial aggregation of environmental risk factors and familial aggregation of disease.

Almost all human diseases have been shown to aggregate familially to some degree. This familiality is generally taken as evidence for the existence of a genetic etiologic mechanism or environmental factors common to family members, or a combination of both. It has been argued that for a disease with strong familial aggregation, environmental risk factors alone are unlikely to account for such strong aggregation, unless the presumed environmental risk factors are associated with enormous risk. This paper revisits this issue through the use of a novel statistical model. Ascertainment bias aside, the author demonstrates that familial aggregation could be explained by multiple interactive risk factors, each of which may confer a low disease risk and thus contribute only a minuscule portion to disease familiality. For example, two correlated risk factors (r=0.5), each with a relative risk of 5 and acting multiplicatively, could give rise to a sibling relative risk of 1.96. Therefore, it may not be sufficient to argue for a genetic component for a disease based solely on the notion that no high risk environmental factors have been found. In view of this, there is a need to examine carefully the roles of multiple environmental risk factors in disease familiality.

Bias↗

Screening of family members of patients with premature coronary heart disease; results from the EUROASPIRE II family survey.

AIMS: To determine whether the Joint European Societies' recommendations that first degree blood relatives of patients with premature coronary heart disease (CHD) should be screened for coronary risk factors is being followed and, if so, how effectively these relatives are being managed. METHODS AND RESULTS: Using a postal questionnaire, 3322 relatives (siblings and children >/=18 years of age) of 1289 index patients in the EUROASPIRE II survey who had suffered from premature CHD (men under 55 years and women under 65 years) were asked whether screening for coronary risk factors had occurred and, if so, how they were being managed in terms of lifestyle advice and drug therapies. Overall, screening for coronary risk factors because of CHD in the family was only performed in 11.1% of siblings and 5.6% of children. However, prevalences of different cardiac risk factors were high both in relatives and offspring and a clear familial clustering could be documented. Less than 50% of siblings and 25% of children were given some general lifestyle advice regarding cardiac risk factors. Moreover, active interventions such as starting antihypertensive or lipid lowering drugs were rarely carried out, particularly in children of patients with premature CHD. CONCLUSIONS: European physicians rarely screen family members of patients with premature CHD for cardiac risk factors. General lifestyle style advice or active treatment for these risk factors are also rarely given. However, since these family members have a high prevalence and familial clustering of cardiac risk factors, they form an ideal target population for primary prevention of CHD in high-risk patients.

Adult↗

Children's selective coping after a bus disaster: confronting behavior and perceived support.

Data were obtained from 675 seventh graders grieving the death of 19 and injury of 14 fellow students in a traffic accident. Frequency of confronting behaviors was inversely related to their intensity. Perceived helpfulness of the various support person categories (oneself, parents, siblings, relatives, friends, classmates, classroom teachers, guidance counselors, psychologists) was related to current stress levels, context of the disaster, and prior helping relationships. Personal loss and situational variables affected confronting behavior and stress reaction levels. Specific helpful support persons affected interest in individual and/or group treatment. Findings were consistent with a model of search and selection of helpful support persons in community-wide stressful situations.

Accidents, Traffic↗

Conservation of locus-specific microsatellite variability across species: a comparison of two Drosophila sibling species, D. melanogaster and D. simulans.

Fifteen microsatellite loci were studied in Drosophila melanogaster and Drosophila simulans, two closely related sibling species which split 2-3.5 MYA. Within-species variances in repeat number were found to differ up to 1,000-fold among individual microsatellite loci. A significant correlation of log variances between both species indicated a locus-specific mutation rate of microsatellites. Hence, locus-specific effects are apparently among the major forces influencing microsatellite variation and deserve more consideration in microsatellite analysis.

Africa↗

An extended genome scan in 442 Canadian multiple sclerosis-affected sibships: a report from the Canadian Collaborative Study Group.

Multiple sclerosis (MS) is a complex trait with a sibling relative risk (lambda(sibs)) between 18 and 36. We report a multistage genome scan of 552 sibling pairs from 442 families, the largest MS family sample assessed for linkage. The first stage consisted of a genome scan for linkage with 498 microsatellite markers at an average spacing of 7 cM in 219 sibling pairs. The second stage involved further genotyping of markers from positive regions in an independent sample of 333 affected sibling pairs. The global distribution of allele sharing for all markers showed a shift towards greater sharing within the affected sibling pair group but not in the discordant sibling pair group. This shift indicates that the number of contributing genetic factors is likely to be moderate to large. Only markers at chromosome 6p showed significant evidence for linkage (MLOD=4.40), while other regions were only suggestive (1p, 2q, 5p, 9q, 11p, 12q, 18p, 18q and 21q) with MLODs greater than 1.0. The replication analysis involving all 552 affected sibling pairs confirmed suggestive evidence for five locations, namely, 2q27 (MLOD=2.27), 5p15 (MLOD=2.09), 18p11 (MLOD=1.68), 9q21 (MLOD=1.58) and 1p31 (MLOD=1.33). Suggestive linkage evidence for a previously reported location on chromosome 17q (MLOD=1.67) and a prior association with marker D17S789 was replicated. We showed that the overall excess allele sharing we observed for the entire sample was due to increased allele sharing within the DRB1*15 negative subgroup alone. This observation is most consistent with a model of genetic heterogeneity between HLA and other genetic loci. These findings offer guidance for future genetic studies including dense SNP linkage disequilibrium analysis.

Canada↗

Genetic counseling: a comparison of counselee's genetic knowledge before and after (Part III).

Forty-seven mothers of children with Down syndrome were evaluated on their knowledge of genetic facts pertaining to Down syndrome. We found that more knowledge of this disorder was acquired by counselees before counseling than from counseling. The data show that counseling is most effective in enhancing counselees' knowledge of general genetics, ie, the origin of the extra chromosome in a child with Down syndrome. In contrast, counselees had the most difficulty in learning the recurrence risks for others, including the risks for relatives, siblings, and the population in general. A finding of practical importance is that formal education is inversely related to the amount of information counselees learned from counseling. Mothers with less than a high school education acquired most of their genetic knowledge from counseling, while those with more than a high school education acquired most of this information before counseling.

Down Syndrome↗

beta2-adrenergic receptor activation and genetic polymorphisms in autism: data from dizygotic twins.

Gestational and genetic factors can contribute to autism during infancy and early childhood through their effects on fetal brain development. Previous twin studies have shown strong genetic components for the development of autism, a disorder that can have multiple causes. We investigated the effects of prenatal overstimulation of the beta2-adrenergic receptor in dizygotic twins who were exposed to terbutaline, a selective beta2-adrenergic receptor agonist used to treat premature labor, as a gestational factor. As a possible genetic mechanism, we studied two beta2-adrenergic receptor polymorphisms in twins from whom DNA was available: glycine substitution at codon 16 (16G) and glutamic acid substitution at codon 27 (27E), which show diminished desensitization in vivo compared with the wild-type receptor. Continuous terbutaline exposure for 2 weeks or longer was associated with increased concordance for autism spectrum disorders in dizygotic twins (relative risk = 2.0), with a further increase in the risk for male twins with no other affected siblings (relative risk = 4.4). A significant association was found between the presence of 16G and 27E polymorphisms in autistic patients compared with population controls (P = .006). Prenatal overstimulation of the beta2-adrenergic receptor by terbutaline or by increased signaling of genetic polymorphisms of the beta2-adrenergic receptor that have diminished desensitization can affect cellular responses and developmental programs in the fetal brain, leading to autism.

Autistic Disorder↗

Risk for smoking-related cancer among relatives of lung cancer patients.

Studies of familial aggregation of cancer provide indirect evidence for the role of genetic predisposition to cancer. In an ongoing case-control study, we evaluated whether first-degree relatives of lung cancer cases are at increased risk of lung and other cancers. Smoking-related cancers were defined as cancers of the lung, bladder, head and neck, kidney, and pancreas. The 806 probands included in this analysis were patients referred to The University of Texas M. D. Anderson Cancer Center (Houston, TX). We identified 663 controls, matched to the cases on age (+/-5 years), sex, ethnicity, and smoking history, who were recruited from a local multispecialty physician practice in the Houston metropolitan area. Self-reported cancer family history data were available for 6430 first-degree relatives of the cases and 4936 first-degree relatives of the controls. An excess of cancer in relatives was evaluated by comparing the observed cancer cases among relatives of the cases with relatives of the controls. We conducted further analysis after stratifying on age of lung cancer onset (age at study registration for controls) and smoking status (never, former, or current) of the probands. We also conducted Cox regression analysis and compared time to cancer diagnosis among the relatives of the cases and controls adjusted for age and smoking status of proband and family members. Siblings [relative risk (RR) = 1.85; P = 0.003] of cases had a significant excess of lung cancer and an excess of smoking-related cancers (RR = 1.29; P = 0.01). We observed evidence of familial aggregation (RR = 1.71; P < 0.001) of lung cancer among relatives of late-onset lung cancer cases. From the Cox regression, we observed a moderate risk for development of lung (RR = 1.25; P = 0.09) and other smoking-related cancers (RR = 1.23; P = 0.05). After adjustment for smoking behavior of probands and their relatives, the risks of lung cancer (RR = 1.33; P = 0.03) and smoking-related cancers (RR = 1.28; P = 0.02) were statistically significant. We further stratified on age at onset and observed no evidence (P = 0.81) of familial aggregation of lung cancer among young onset (<or=55 years of age) lung cancer cases. We also did not observe evidence of familial aggregation (P = 0.88) of smoking-related cancers in the same group. There was no evidence of increased risk (P = 0.77) of lung cancer among relatives of never-smokers. These findings support the need for additional study in the characterization and identification of genetic factors that influence and modulate cancer susceptibility in humans.

Adult↗

Intrafamilial associations of cholesterol and triglyceride among related and unrelated household members.

The purpose of this report was to assess intrafamilial associations of lipids between related and unrelated household members seen in the course of a population-based survey of lipids in schoolchildren and their parents. Fasting plasma total cholesterol and triglyceride levels were measured in 6,857 and 3,079 adults. Age effects were removed for each sex-race group using a third-degree polynomial regression of lipid on age; the residuals were then used as observations in the analyses. For both cholesterol and triglyceride, significant positive correlations existed between father and son, father and daughter, mother and son, and mother and daughter. For both cholesterol and triglyceride, although the mother-child correlations were stronger than those for father-child, they were not significantly different. There were no significant correlations between step, foster, or adoptive parents and children. For cholesterol in sibships of size two, intrasibship correlations for fully related siblings were 0.333, for half-sibs 0.164, and for unrelated sibs, 0.085. Consistently closer intrafamilial cholesterol and triglyceride associations between related than unrelated family members, and the strong parental effects on cholesterol and triglyceride indicate, in aggregate, that a considerable proportion of the variation of cholesterol and triglyceride can be explained by genetic factors.

Adult↗

Discontinuation of immunosuppression for prevention of kidney graft rejection after receiving a bone marrow transplant from the same HLA identical sibling donor.

Induction of tolerance in solid organ transplant recipients has been a long sought goal so that patients will not need lifelong immunosuppression. In this case report we review a patient who received a kidney transplant from an HLA matched related sibling and developed acute leukemia as a consequence of her immunosuppression. The patient was then treated with an allogeneic bone marrow transplant from her kidney donor. After the bone marrow transplant, all immunosuppression therapy for graft rejection and graft versus host disease was stopped. Six months after the bone marrow transplant, the patient's kidney function had no deterioration as a consequence of stopping immunosuppression. This illustrated that a combined solid organ/bone marrow transplant can help to induce tolerance. In fact, the tolerance to the bone marrow transplant for prevention of graft versus host disease may have been accomplished by the prior kidney transplant.

Bone Marrow Transplantation↗