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 91 records · Page 5Linked to original sources

The influence of gender on the susceptibility to multiple sclerosis in sibships.

A population-based study of pairs of relatives (siblings, second- and third-degree) concordant for multiple sclerosis did not show an excess of like-sexed pairs. In addition, data on human lymphocyte antigen typing for sibling pairs concordant for multiple sclerosis did not find an increase in haplotype sharing for like-sexed pairs. These data do not support the notion that sex-related factors influence multiple-sclerosis susceptibility in families.

Disease Susceptibility↗

[The assessment of social relations in 6 to 12-year-old children in a child and adolescent population in psychiatric consultation].

Starting from Schmiedeck's "personal sphere model" we tried to develop a similar procedure for children (age range 6 to 12 years). It should enable us to analyze the social relationships of a patient from his/her point of view. We examined 85 children of child/adolescent-psychiatric population with the presented method. It focuses upon drawings of the children and assessment of their relationships. The number of closely related persons and the frequency of interpersonal/social contacts allow to estimate the degree of embeddedness of the child into his/her social context. Importance and significance of indicated partners of interaction can be determined by the attachment the child expresses and receives. These assessments give information about the likes and dislikes for the related persons. The range of social experience extends equally for boys and girls as they grow older. At all age levels girls have more social contacts than boys. The sibling relations of the girls show more inconsistencies than those of the boys. Younger children have the tendency to name only the mother as family member. Neurotic and emotionally disturbed children express fewer wishes. Children with social behaviour disorders suffer less from the loss of a closely related person than children with emotional disturbances.

Affective Symptoms↗

Emotion regulation in context: the jealousy complex between young siblings and its relations with child and family characteristics.

Jealousy is a social emotion that has received little attention by developmental researchers. The current study examined sibling jealousy and its relations to child and family characteristics in 60 families with a 16-month-old toddler and an older preschool-age sibling. Sibling jealousy was elicited in social triads consisting of a parent (mother or father) and the two siblings. Positive marital relationship quality (i.e., love and relationship maintenance) was a particularly strong predictor of the older siblings' abilities to regulate jealousy reactions in the mother sessions. Younger siblings' jealous affect with mothers was linked to the child's temperament, whereas older siblings' jealous affect with mothers was related to the child's emotional understanding. Younger siblings displayed more behavioral dysregulation in the mother-sibling triads if there was greater sibling rivalry reported by mothers. Session order (i.e., which sibling was challenged first in the jealousy paradigm) had a strong effect on both the affect and behavioral dysregulation displayed by the older and younger siblings. Results are discussed with respect to the need for future research to consider social relationships as developmental contexts for young children's emotion regulation.

Child, Preschool↗

Prevalence of inflammatory bowel disease in family members of Jewish Crohn's disease patients in Israel.

A familial study of 189 Jewish Crohn's disease patients was conducted in order to evaluate the risk for inflammatory bowel disease (IBD) in relatives of the patients and to try to understand better the genetic component in the etiology of the disease among Jews. One hundred fifty-seven patients filled out questionnaires that were verified by personal interviews. In 10 families (6.6%), a first-degree relative of the propositus was found to have IBD, seven Crohn's disease and three ulcerative colitis. Among first-degree relatives, siblings were more frequently affected: of 400, five had Crohn's disease and one ulcerative colitis. Among 304 parents, two had Crohn's disease and two ulcerative colitis, while none of the propositi's children had IBD. The prevalence of first-degree relatives with Crohn's disease was similar in the 98 and 45 families of Ashkenazi and non-Ashkenazi origin: 5.1% and 4.4%, respectively. The risk for siblings of the probands to be affected were also similar in the two groups: 1.5% and 1.8%; while parents of the probands were affected only in the group of Ashkenazi Jews.

Adolescent↗

Cloned murine non-malignant, spontaneously transformed and chemical tumour-derived cell lines related to the type 2 pneumocyte.

NAL1A is a murine type 2 pneumocyte-related cell line cultured from normal BALB/c adult mouse lung. In vitro spontaneous transformation of 3 out of 7 clones of NAL1A has led to the isolation and establishment in continuous cell culture of sibling-related non-neoplastic (NAL1A) and spontaneously arising neoplastic (NAL1As) cell strains. NAL1As cells exhibited a similar phenotype to cloned NUL1 cells cultured from urethane-induced mouse lung adenomas. All NAL1As and NUL1 clones grew vigorously in 0.3% agar and formed invasive, poorly differentiated carcinomas following subcutaneous inoculation into immunesuppressed mice. Several subcutaneous nodules metastasised preferentially to the lung. All spontaneous and chemically-derived malignant clones were less differentiated than the non-malignant clones as assessed by staining with a type 2 pneumocyte-specific polyclonal antiserum. The clones described in this report form a useful model in the study of spontaneous and chemically-induced neoplastic transformation in mouse epithelial lung cells.

Adenoma↗

Antinuclear antibodies in patients with scleroderma (systemic sclerosis) and in their blood relatives and spouses.

OBJECTIVE: To test the postulate that there is a higher prevalence of antinuclear antibodies (ANAs) in serum samples from blood relatives and from spouses of patients with scleroderma than in control samples, and that this provides evidence for both genetic and environmental factors influencing autoimmunity in scleroderma. METHOD: Testing for ANAs was performed on 58 patients with scleroderma, 30 of their spouses, 74 first degree relatives, and 66 control subjects broadly age matched to the patients, their spouses, and about half of the relatives (siblings and parents). RESULTS: On the basis of an ANA titre of > 40 as positive, 12 (18%) of the controls, 55 (95%) of the patients, one (3%) of the spouses and five (7%) of the relatives would be classified as positive. Thirty seven (64%) of the patients had defined specificities (ACA, Scl 70, U1 (RNP)) but none of the controls, spouses, or relatives had antibodies of these specificities. CONCLUSION: These findings give no support to the postulate that environmental or genetic factors contribute to the ANAs in scleroderma.

Adult↗

Familial association between coeliac disease and ulcerative colitis: preliminary communication.

One hundred and twenty patients who were members of the Nottinghamshire Coeliac Group completed a questionnaire about the occurrence of coeliac disease, ulcerative colitis and Crohn's disease amongst first-degree relatives. Siblings were at a 20-fold risk of developing coeliac disease and a 15-fold risk of developing ulcerative colitis, and significantly increased risks for these two conditions were also seen in other family members. The relatives of patients with coeliac disease are at increased risk not only of developing coeliac disease but also ulcerative colitis. This provides further support for a possible role of a dietary allergen in the development of ulcerative colitis.

Adolescent↗

Search for intracranial aneurysm susceptibility gene(s) using Finnish families.

BACKGROUND: Cerebrovascular disease is the third leading cause of death in the United States, and about one-fourth of cerebrovascular deaths are attributed to ruptured intracranial aneurysms (IA). Epidemiological evidence suggests that IAs cluster in families, and are therefore probably genetic. Identification of individuals at risk for developing IAs by genetic tests will allow concentration of diagnostic imaging on high-risk individuals. We used model-free linkage analysis based on allele sharing with a two-stage design for a genome-wide scan to identify chromosomal regions that may harbor IA loci. METHODS: We previously estimated sibling relative risk in the Finnish population at between 9 and 16, and proceeded with a genome-wide scan for loci predisposing to IA. In 85 Finnish families with two or more affected members, 48 affected sibling pairs (ASPs) were available for our genetic study. Power calculations indicated that 48 ASPs were adequate to identify chromosomal regions likely to harbor predisposing genes and that a liberal stage I lod score threshold of 0.8 provided a reasonable balance between detection of false positive regions and failure to detect real loci with moderate effect. RESULTS: Seven chromosomal regions exceeded the stage I lod score threshold of 0.8 and five exceeded 1.0. The most significant region, on chromosome 19q, had a maximum multipoint lod score (MLS) of 2.6. CONCLUSIONS: Our study provides evidence for the locations of genes predisposing to IA. Further studies are necessary to elucidate the genes and their role in the pathophysiology of IA, and to design genetic tests.

Journal Article↗

The relative contribution of sibling deviance and peer deviance in the prediction of substance use across middle childhood.

This study investigated the quality of sibling relationships and sibling deviancy in a sample of children at-risk for substance use and antisocial behavior. Based on a history of empirical and theoretical models suggesting strong associations between children's development in the context of relationships and the emergence of delinquency and drug use, this research extends previous efforts by including sibling relationships in this developmental model, linking siblings with later substance use. Sibling relationship quality as well as peer deviance were examined using a multirater, multimethod assessment procedure. We tested 3 constructs (deviancy, warmth, and conflict) related to sibling behavior. Only sibling deviance and peer deviance directly predicted substance use. When both sibling deviance and peer deviance were examined as predictors of changes in substance use over time, only sibling deviance was significant. Implications for the development of substance use behavior in middle childhood are discussed.

Adolescent↗

Celiac disease: strongly heritable, oligogenic, but genetically complex.

Celiac disease, or gluten-sensitive enteropathy, is a small intestinal disorder which affects up to 1:250 people in the United States. Disease development has a strong genetic component, with a sibling relative risk (lambda(s)) of 30. One susceptibility locus is the MHC region, with a particular association with the HLA-DQ alleles DQA1*0501 and DQB1*0201. However, haplotype sharing studies suggest that genes within the MHC complex contribute no more than 40% to the sibling familial risk of disease. This means that the stronger genetic risk is likely to be conferred by a small number of non-HLA-linked genes. Genome-wide linkage studies, plus linkage and association studies of candidate loci have been used to try to identify these genes. However, these studies have either failed to detect loci, or produced inconsistent results. Such difficulties in identifying susceptibility genes are encountered when investigating any complex genetic disorder. Information from the Human Genome Project, coupled with new technology for high throughput single nucleotide polymorphism typing may help to identify the non-HLA determinants of celiac disease in the future.

Celiac Disease↗

ApoE gene and familial risk of Alzheimer's disease as predictors of odour identification in older adults.

The study examined odour identification ability in healthy older adults at increased risk for developing Alzheimer's disease (AD). We recruited a sample (n = 24) of siblings related to probable AD cases and an age-matched control sample (n = 47). All participants were genotyped for the presence of the ApoE epsilon4 allele. Performance on a simple olfactory task of odour identification was compared according to positive family history of AD and ApoE epsilon4 status. The sibling group showed an odour identification deficit compared to the control group. Whilst there was no independent influence of ApoE epsilon4 status on odour identification, there was a significant interaction between positive family history and ApoE epsilon4 status. Sibling epsilon4 carriers showed the greatest odour identification deficit and their performance was significantly poorer than both the sibling non-epsilon4 carrier and control epsilon4 carrier groups. Odour identification deficits like those reported here are considered to be early cognitive markers of incipient AD. In this respect, these findings support the need to both monitor individuals at increased risk of the disease and introduce olfactory-mediated cognitive tasks into the diagnostic setting.

Age Factors↗

Insulin-like growth factor type-1 receptor down-regulation associated with dwarfism in Holstein calves.

Perturbations in endocrine functions can impact normal growth. Endocrine traits were studied in three dwarf calves exhibiting retarded but proportionate growth and four phenotypically normal half-siblings, sired by the same bull, and four unrelated control calves. Plasma 3,5,3'-triiodothyronine and thyroxine concentrations in dwarfs and half-siblings were in the physiological range and responded normally to injected thyroid-releasing hormone. Plasma glucagon concentrations were different (dwarfs, controls>half-siblings; P<0.05). Plasma growth hormone (GH), insulin-like growth factor-1 (IGF-1) and insulin concentrations in the three groups during an 8-h period were similar, but integrated GH concentrations (areas under concentration curves) were different (dwarfs>controls, P<0.02; half-siblings>controls, P=0.08). Responses of GH to xylazine and to a GH-releasing-factor analogue were similar in dwarfs and half-siblings. Relative gene expression of IGF-1, IGF-2, GH receptor (GHR), insulin receptor, IGF-1 type-1 and -2 receptors (IGF-1R, IGF-2R), and IGF binding proteins were measured in liver and anconeus muscle. GHR mRNA levels were different in liver (dwarfs<controls, P<0.002; dwarfs<half-siblings, P=0.06; half-siblings<controls, P=0.08) but not in muscle. IGF-1R mRNA abundance in liver in half-siblings and controls was 2.4- and 2.5-fold higher (P=0.003 and P=0.001, respectively) and in muscle tissue was 2.3- and 1.8-fold higher (P=0.01 and P=0.08, respectively) than in dwarfs. Hepatic IGF-1R protein levels (Western blots) in muscle were 2.5-fold higher (P<0.05) and in liver and muscle (quantitative immunohistochemistry) were higher (P<0.02 and P<0.07, respectively) in half-siblings than in dwarfs. The reduced presence of IGF-1R may have been the underlying cause of dwarfism in studied calves.

Animals↗

Genetic analysis of plasma amine oxidase activity in schizophrenia.

Plasma amine oxidase (PAO) activity has been implicated in the biology of schizophrenia. PAO activity is, in part, under genetic control, but its mode of inheritance has not been determined. To assess the genetic pattern of PAO activity and its relation to the transmission of schizophrenia, we studied 73 chronic schizophrenic probands and 217 first-degree relatives (siblings and parents). Single-major-locus hypotheses were tested by pedigree analysis methods for quantitative traits. The distribution of PAO activity indicated significant admixture. When the transmission probability model was used, the familial pattern of PAO activity was consistent with mendelian transmission; the environmental hypothesis was rejected. PAO activity was lower in schizophrenic patients than in unaffected relatives, but the mean reduction in enzyme activity was small (10.7%) and the two groups of subjects overlapped greatly in their PAO values. The difference between ill and well relatives was not statistically significant. However, schizophrenia spectrum disorders segregated with low PAO activity in families of low-activity probands, and a greater proportion of ill than well subjects clustered in the low PAO activity mode. The results are interpreted as follows: (1) The transmission of PAO activity may be determined in part by a single major autosomal gene. (2) Low PAO activity does not qualify as a major risk factor in the schizophrenic population at large; however, a relationship may exist between low PAO activity and the transmission of schizophrenia in families of patients with extremely low enzyme activity.

Adolescent↗

A genomewide linkage study of 1,933 families affected by premature coronary artery disease: The British Heart Foundation (BHF) Family Heart Study.

Coronary artery disease (CAD) and its most important complication, myocardial infarction (MI), are the leading cause of premature death in the Western world. CAD has a substantial genetic basis, especially when it occurs early. We investigated the genetic determinants of premature CAD by performing a genomewide linkage analysis of 4,175 affected subjects from 1,933 families recruited throughout the United Kingdom. Each family had at least two available siblings with CAD, with validated onset before age 66 years. Linkage analysis was performed using 416 microsatellite markers. We observed suggestive linkage, for both CAD and MI, to a region on chromosome 2. For CAD, a LOD score of 1.86 was observed at marker D2S2271, which, in an ordered subset analysis, increased to 2.70 in families (n=1,698) with a minimum age at diagnosis of 56 years or younger. For MI, an overlapping peak with a LOD score of 1.15 was observed at marker D2S2216, which increased to 2.1 in families (n=801) with a minimum age at diagnosis of 59 years or younger. Exclusion mapping showed that 100% of the autosomal genome could be excluded for locus-specific sibling relative risks of 1.5 and 1.6 for CAD and MI, respectively. The region identified on chromosome 2 overlaps linked regions observed in two other smaller genome scans for CAD. Together, these findings strongly suggest that there is a locus on chromosome 2 that influences coronary atherosclerosis risk. The exclusion of a common locus that increases risk of CAD to siblings by >50% has important implications for strategies for further defining the genetic basis of CAD.

Age of Onset↗

Low frequency of HLA DRB1*03 - DQB1*02 and DQB1*0302 haplotypes in Romania is consistent with the country's low incidence of Type I diabetes.

AIMS/HYPOTHESIS: Our study aimed to determine the association of HLA class II HLA-DQB1 alleles with Type I (insulin-dependent) diabetes mellitus and the frequencies of these alleles in the Romanian population, which has one of the lowest incidences of Type I diabetes in children aged 0-14 years in Europe at 3-4 cases per 100,000 person-years. METHODS: We used the sequence specific primer-polymerase chain reaction (PCR-SSP) technique to type HLA-DQB1 alleles, the HLA-DRB1alleles DRB1*03 and one single nucleotide polymorphism (SNP) in the insulin gene (INS). We studied 204 Type I diabetic Romanian families, 196 of which were simplex with 70.3 % of subjects diagnosed under 14 years of age. Data was analysed using a modified version of the Transmission Disequilibrium Test, the Transmission Disequilibrium Test itself, and the affected family-based control method. RESULTS: We found, as expected, the strong positive DQB1*02-DRB1*03 and DQB1*0302, and negative DQB1*0602, HLA class II allele associations with Type I diabetes in these Romanian families. However, using the affected family-based control method, we found relatively low population frequencies of DQB1*02-DRB1*03 and DQB1*0302 alleles in Romania (15.8%) compared with Sardinia (31.3%), a high incidence European region (35 cases per 100,000 person-years in children aged 0-14years). The INS locus had a strong effect in this data set with 80.5 % transmission of the susceptible INS allele from parents to affected siblings (relative risk = 4.1). CONCLUSION/INTERPRETATION: Part of the explanation for the low incidence of Type I diabetes in Romania could be the lower frequency of the DRB1*03 DQB1*02 and DQBI*0302 susceptibility haplotypes in this country.

Child↗

Family size and the quality of children.

If couples decide to have fewer children in order to achieve higher "quality" offspring, are they correct in assuming that the quality of children bears an important and inverse relation to family size? If they are correct, how does number of children operate to affect individual quality? This research (using U.S. whites primarily) takes educational attainment (among adults) and college plans (among youngsters) as the principal indicators of quality, but also directs some attention to measures of intelligence. The analysis supports the "dilution model" (on average, the more children the lower the quality of each child) and indicates that only children do not suffer from lack of siblings, and that other last-borns are not handicapped by a "teaching deficit." Number of siblings (relative to other background variables) is found to have an important detrimental impact on child quality--an impact compounded by the fact that, when couples are at a stage in life to make family-size decisions, most background factors (however important to the quality of their children) are no longer readily manipulable. A special path analysis of college plans among boys uses a modification of Sewell's Wisconsin Model as its base. The results show that number of siblings is a negative influence on intervening variables affecting college plans. In general, the research documents the unfavorable consequences for individual siblings of high fertility, even in a country that is (at least for whites) as socially, economically, and politically advantaged as the United States.

Adolescent↗

Patterns of mitochondrial variation within and between African malaria vectors, Anopheles gambiae and An. arabiensis, suggest extensive gene flow.

Anopheles gambiae and An. arabiensis are mosquito species responsible for most malaria transmission in sub-Saharan Africa. They are also closely related sibling species that share chromosomal and molecular polymorphisms as a consequence of incomplete lineage sorting or introgressive hybridization. To help resolve these processes, this study examined the partitioning of mtDNA sequence variation within and between species across Africa, from both population genetic and phylogeographic perspectives. Based on partial gene sequences from the cytochrome b, ND1 and ND5 genes, haplotype diversity was high but sequences were very closely related. Within species, little or no population subdivision was detected, and there was no evidence for isolation by distance. Between species, there were no fixed nucleotide differences, a high proportion of shared polymorphisms, and eight haplotypes in common over distances as great as 6000 km. Only one of 16 shared polymorphisms led to an amino acid difference, and there was no compelling evidence for nonneutral variation. Parsimony networks constructed of haplotypes from both species revealed no correspondence of haplotype with either geography or taxonomy. This trend of low intraspecific genetic divergence is consistent with evidence from allozyme and microsatellite data and is interpreted in terms of both extensive gene flow and recent range expansion from relatively large, stable populations. We argue that retention of ancestral polymorphisms is a plausible but insufficient explanation for low interspecific genetic divergence, and that extensive hybridization is a contributing factor.

Animals↗

Eating Disorders and Parkinson's Disease-2: Genetic Epidemiology and Shared Genomics.

OBJECTIVE: Individuals with anorexia nervosa (AN) share premorbid traits with Parkinson's Disease (PD) (e.g.,&#xa0;anxiety) and exhibit a two-fold relative risk of a reported family history of PD. Published estimates of intra- and inter-disorder genetic architecture were extracted and compared prior to conducting novel analyses to provide evidence for cross-disorder genetic risk. METHODS: National register or meta-analytic familial, twin, and common variant genome-wide studies were searched; estimates and findings were extracted and compared. Novel cross-disorder conditional and conjunctional false discovery rate analyses were performed. RESULTS: Sibling relative risks and additive genetic estimates of the two disorders were similar. AN had greater common variant heritability than PD whether measured via infinitesimal model (linkage disequilibrium score regression, LDSC) or causal mixture model (MiXeR). AN had greater polygenicity than PD (mean (SD) 2.50E-03 (1.64E-04) versus 2.72E-4 (1.47E-05), p&#xa0;<&#xa0;0.001), but lower discoverability than PD (4.20E-05 (2.69E-06) versus 1.40E-04 (6.95E-06), p&#xa0;<&#xa0;0.001). Global genetic correlation was significant (e.g.,&#xa0;bivariate LDSC rg&#xa0;=&#xa0;0.10, p&#xa0;=&#xa0;0.0033). Novel analyses identified cross-disorder enrichment, and cross-disorder risk at chr3p21.31. CONCLUSIONS: Cross-disorder AN and PD research identified shared risk variants at chr3p21.31, genes and mechanisms (e.g.,&#xa0;conditioning, fear, and reward) linked to a shared endophenotype.

Parkinson's disease↗