Depression and anxiety symptoms during the transition to early adulthood for people with intellectual disabilities.

BACKGROUND: The transition to adulthood is a major developmental milestone; a time of self-discovery and increased independence. For young adults (YA) with intellectual disabilities (ID), however, this period is especially challenging. The increased incidence of mental health disorders in this population, such as depression and anxiety, make this transition even more difficult, increasing caregiver burden at a time when the young adult would traditionally be gaining independence. It is not clear, however, why YA with ID are more susceptible and what factors may predict mental health symptoms. METHOD: Potential risk and protective factors (demographic variables, coping styles, sense of hopelessness, unmet achievement of adulthood milestones, self-reflection and insight) of anxiety and depression symptoms were assessed in 55 YA with ID and a sample of age-matched controls. RESULTS: Insight was the strongest predictor of anxiety (with gender in the controls) for YA with and without ID, with increased insight predicting fewer anxiety symptoms. However, YA with ID had significantly less insight than their aged-matched counterparts and significantly higher levels of anxiety. They were also less likely to have achieved traditional adulthood milestones. Maladaptive coping was the strongest predictor of depression for YA with ID. In comparison, both maladaptive coping and insight predicted depression in controls. More maladaptive coping predicted increased depressive symptoms in both populations, whilst increased insight predicted fewer depressive symptoms in controls. CONCLUSIONS: Insight and maladaptive coping are potential targets in the treatment of anxiety and depression among YA with ID. Longitudinal intervention studies exploring the efficacy of such targeted programmes in reducing mental health symptoms and improving the transition to adulthood for these young people are recommended.

'At the end of the day, it is more important that he stays happy': an interpretative phenomenological analysis of people who have a sibling with 22q11.2 deletion syndrome.

BACKGROUND: 22q11.2 deletion syndrome (22q11.2DS) is the most common microdeletion syndrome. However, there is little research examining the effect of this multisystem disorder on the family, particularly siblings. The current study was a phenomenological exploration of sense-making in siblings of a person with 22q11.2DS. METHOD: Interpretative phenomenological analysis informed a detailed and open examination of being a sibling of a person with 22q11.2DS. Using in-depth semistructured interviews, five typically developing siblings (two men, three women) of people with 22q11.2DS were individually interviewed, providing the data set for transcription and thematic analysis. RESULTS: The theme 'They are the priority' overarched two subordinate themes that emerged from participants' descriptions of the struggle with acceptance and finding positive meaning. Participants oscillated between conflicting feelings about their sibling with 22q11.2DS always taking centre stage. For example, they felt anger, guilt and resentment; yet, they also embraced patience, empathy and gratitude. CONCLUSIONS: This phenomenological study provides a foundation for future research relating to 22q11.2DS and fostering family wellbeing, particularly around acceptance and psychological growth. The siblings in this study actively withdrew from their family to allow prioritisation of their affected sibling. However, this does not mean that their needs should be overlooked. There are easily accessible resources to support siblings of individuals with disabilities, and it is important for health professionals and parents to consider these options.

A tale worth telling: the impact of the diagnosis experience on disclosure of genetic disorders.

BACKGROUND: Research suggests children with genetic disorders exhibit greater coping skills when they are aware of their condition and its heritability. While the experiences parents have at diagnosis may influence their decision to disclose the diagnosis to their children, there is little research into this communication. The aim of the current study was to examine the relationship between the diagnosis experience and the disclosure experience for parents of children with developmental disorders of a known genetic aetiology: parents of children with 22q11.2 deletion syndrome (22q11DS) were compared with a group of parents with children affected with other genetic diagnoses, with a similar age of diagnosis (e.g. fragile X syndrome) and a group where diagnosis generally occurs early (i.e. Down syndrome). METHOD: The sample comprised 559 parents and caregivers of children with genetic developmental disorders, and an online survey was utilised. Items from the questionnaire were combined to create variables for diagnosis experience, parental disclosure experience, child's disclosure experience, and parental coping and self-efficacy. RESULTS: Across all groups parents reported that the diagnosis experience was negative and often accompanied by a lack of support and appropriate information. Sixty-eight per cent of those in the 22q11DS and 58.3% in the Similar Conditions groups had disclosed the diagnosis to their child, whereas only 32.7% of the Down syndrome group had. Eighty-six per cent of the Down syndrome group felt they had sufficient information to talk to their child compared with 44.1% of the Similar Conditions group and 32.6% of the 22q11DS group. Parents reported disclosing the diagnosis to their child because they did not want to create secrets; and that they considered the child's age when disclosing. In the 22q11DS and Similar Conditions groups, a poor diagnosis experience was significantly associated with negative parental disclosure experiences. In the Similar Conditions group, a poor diagnosis experience was also significantly associated with a more negative child disclosure experience. CONCLUSIONS: As expected this study highlights how difficult most parents find the diagnosis experience. Importantly, the data indicate that the personal experiences the parents have can have a long-term impact on how well they cope with telling their child about the diagnosis. It is important for clinicians to consider the long-term ramifications of the diagnosis experience and give the parents opportunities; through, for instance, psychoeducation to prepare for telling their child about the diagnosis. Further research is warranted to explore what type of information would be useful for parents to receive.

Social cognition dysfunction in adolescents with 22q11.2 deletion syndrome (velo-cardio-facial syndrome): relationship with executive functioning and social competence/functioning.

BACKGROUND: Social difficulties are often noted among people with intellectual disabilities. Children and adults with 22q.11.2 deletion syndrome (22q11DS) often have poorer social competence as well as poorer performance on measures of executive and social-cognitive skills compared with typically developing young people. However, the relationship between social functioning and more basic processes of social cognition and executive functioning are not well understood in 22q11DS. The present study examined the relationship between social-cognitive measures of emotion attribution and theory of mind with executive functioning and their contribution to social competence in 22q11DS. METHOD: The present cross-sectional study measured social cognition and executive performance of 24 adolescents with 22q11DS compared with 27 age-matched typically developing controls. Social cognition was tested using the emotion attribution task (EAT) and a picture sequencing task (PST), which tested mentalising (false-belief), sequencing, cause and effect, and inhibition. Executive functioning was assessed using computerised versions of the Tower of London task and working memory measures of spatial and non-spatial ability. Social competence was also assessed using the parent-reported Strengths and Difficulties Questionnaire. RESULTS: Adolescents with 22q11DS showed impaired false-belief, emotion attribution and executive functioning compared with typically developing control participants. Poorer performance was reported on all story types in the PST, although, patterns of errors and response times across story types were similar in both groups. General sequencing ability was the strongest predictor of false-belief, and performance on the false-belief task predicted emotion attribution accuracy. Intellectual functioning, rather than theory of mind or executive functioning, predicted social competence in 22q11DS. CONCLUSIONS: Performance on social-cognitive tasks of theory of mind indicate evidence of a general underlying dysfunction in 22q11DS that includes executive ability to understand cause and effect, to logically reason about social scenarios and also to inhibit responses to salient, but misleading cues. However, general intellectual ability is closely related to actual social competence suggesting that a generalised intellectual deficit coupled with more specific executive impairments may best explain poor social cognition in 22q11DS.

Impact of atopic dermatitis and loss-of-function mutations in the filaggrin gene on the development of occupational irritant contact dermatitis.

BACKGROUND: Atopic dermatitis (AD) and loss-of-function mutations in the filaggrin gene (FLG) are both associated with chronic irritant contact dermatitis (ICD). As FLG mutations also are a major risk factor for AD, it is not clear whether FLG mutations are an independent risk factor for ICD or whether the risk is mediated by AD. OBJECTIVES: To investigate the relative contribution and interaction of FLG mutations and AD in German patients with occupational ICD and controls (vocational school apprentices). METHODS: A total of 634 patients and 393 controls were genotyped for R501X, 2282del4, R2447X and S3247X. Current or past flexural eczema was used as an indicator of AD. RESULTS: FLG mutations were found in 15·9% of the patients with ICD and 8·3% of the controls, with a crude odds ratio (OR) of 2·09 [95% confidence interval (CI) 1·33-3·28] for the combined genotype. The adjusted OR for FLG mutations, corrected for AD, was 1·62 (95% CI 1·01-2·58). Subjects with AD were at approximately three times higher risk of developing ICD than controls (OR 2·89; 95% CI 2·09-3·99). There was no evidence of an interaction between these two risk factors. CONCLUSIONS: Our results indicate that both FLG mutations and AD increase the risk of ICD. Individuals with concurrent FLG mutations and AD are at the highest risk of developing ICD.

The Importance of Understanding Individual Differences of Emotion Regulation Abilities in 22q11.2 Deletion Syndrome.

Chromosome 22q11.2 deletion syndrome (22q11DS) is characterised by a complex behavioural phenotype including anxiety, attention-deficit/hyperactivity disorder and psychosis. In the current study, we aimed at improving our understanding of the heterogeneity of behavioural characteristics in a group of 129 young people (aged 4-22) with a confirmed 22q11.2 microdeletion and 116 age and gender matched typically developing controls. Half the participants with 22q11DS had behaviour characterised by emotion dysregulation. A cluster analyses, of the participants with 22q11DS, revealed four groups characterised by intact emotion regulation; predominantly internalizing problems; both internalizing and externalizing problems; and predominantly externalizing difficulties. Importantly, it was found that young people with 22q11DS whose emotion dysregulation was characterised by externalizing problems had the poorest levels of functioning. As our understanding of 22q11DS improves, it is becoming increasingly clear that we need a better understanding of how individual differences and psychosocial factors contribute to, and interact with one another, to result in the observable individual differences in the 22q11DS behavioural phenotype.

Parent-infant interaction quality is related to preterm status and sensory processing.

BACKGROUND: Parent-infant interactions provide the foundation for the development of infant socioemotional wellbeing. Preterm birth can have a substantial, and often detrimental, impact on the quality of early parent-infant interactions. Sensory processing difficulties, common in preterm infants, are further associated with poorer interaction quality. There is a paucity of research, however, examining the links between the quality of parent-infant interaction, preterm birth, and sensory processing difficulties. This study aimed to characterise the quality of interactions of parent-infant dyads involving preterm infants who may display sensory processing differences and examine the associations between parent-infant interaction quality, preterm status and infant sensory processing. METHOD: 67 parent-infant dyads (12-months infant age, 22 preterm, 45 full-term) participated in a recorded, semi-structured 15-minute play interaction. Parents also filled out questionnaires on demographics, and infant sensory processing (Infant and Toddler Sensory Profile-2; ITSP-2). Interaction quality was rated using the Parenting Interactions with Children: Checklist of Observations Linked to Outcomes (PICCOLO). RESULTS: Preterm and full-term infants differed in sensory processing and parent-infant interaction. Infant prematurity was associated with the sensory domains of; visual (r = - 0.37, p = .005), touch (r = - 0.39, p = .002), and movement (rs = - .32, p = .01), as well as the interaction domains of; responsivity (rs;= - .43, p = .001), teaching (rs = - .31, p = .02), and interaction total score (r = - 0.34, p = .01). Interaction quality was related to sensory registration (rs = - .38, p = .008), auditory (rs = - .34, p = .02), seeking (rs = .29, p = .05) and sensory behavioural scores (rs = - .52, p < .001). Overall, interaction quality was best predicted by infant prematurity and auditory scores, R2 = .15, F(1, 47) = 4.01, p = .02. DISCUSSION: Preterm infants differed from their full-term peers in both their sensory processing and in their dyadic interactions with parents. Preterm status was associated with less responsivity and teaching and was found to predict overall interaction quality. Poorer infant sensory processing was associated with less parental teaching, affection and responsivity during interactions. Our results suggest that preterm birth is related to sensory processing difficulties, and that prematurity and sensory processing are differentially associated with aspects of interaction quality. These findings support the further examination of the interplay between preterm birth, sensory processing, and parent-infant interaction quality.

Levels of filaggrin degradation products are influenced by both filaggrin genotype and atopic dermatitis severity.

BACKGROUND: Filaggrin, coded by FLG, is the main source of several major components of natural moisturizing factor (NMF) in the stratum corneum (SC), including pyrrolidone carboxylic acid (PCA) and urocanic acid (UCA). Loss-offunction mutations in FLG lead to reduced levels of filaggrin degradation products in the SC. It has recently been suggested that expression of filaggrin may additionally be influenced by the atopic inflammatory response. In this study, we investigated the levels of several breakdown products of filaggrin in the SC in healthy controls (CTRL) and patients with atopic dermatitis (AD) in relation to FLG null allele status. We examined the relationship between NMF (defined here as the sum of PCA and UCA) and AD severity. METHODS: The SC levels of filaggrin degradation products including PCA, UCA, histidine (HIS) and tyrosine were determined in 24 CTRL and 96 patients with moderate-to-severe AD. All subjects were screened for 11 FLG mutations relevant for the study population. RESULTS: The levels of PCA, UCA and HIS correlated with FLG genotype. Furthermore, these levels were higher in the CTRL when compared to AD patients with no FLG mutations. Multiple regression analysis showed that NMF levels were independently associated with FLG genotype and severity of disease. CONCLUSION: Decreased NMF is a global feature of moderate-to-severe AD; within AD, FLG genotype is the major determinant of NMF, with disease severity as a secondary modifier. NMF components are reliably determined by a noninvasive and relatively inexpensive tape stripping technique.

Wide spectrum of filaggrin-null mutations in atopic dermatitis highlights differences between Singaporean Chinese and European populations.

BACKGROUND: Null mutations in the filaggrin gene (FLG) cause ichthyosis vulgaris (IV) and predispose to atopic dermatitis (AD). Cohort studies in Europe and Japan have reported an FLG mutation carrier frequency of between 14% and 56%, but the prevalent European FLG mutations are rare or absent in Chinese patients with IV and AD. OBJECTIVES: To investigate further the spectrum of FLG-null mutations in Chinese patients and to compare it with that in other populations. METHODS: We conducted comprehensive FLG genetic analysis in a discovery cohort of 92 Singaporean Chinese individuals with IV and/or moderate-to-severe AD. All detected FLG mutations were then screened in a cohort of 425 patients with AD and 440 normal controls. Results In total, 22 FLG-null mutations, of which 14 are novel, were identified in this study; the combined null FLG genotype of 17 mutations detected in cases and controls showed strong association with AD [Fisher's exact test; P = 5·3 × 10⁻9; odds ratio (OR) 3·3], palmar hyperlinearity (Fisher's exact test; P = 9·0 × 10⁻¹5; OR 5·8), keratosis pilaris (Fisher's exact test; P = 0·001; OR 4·7) and with increased severity of AD (permutation test; P = 0·0063). CONCLUSIONS: This study emphasizes the wider genetic landscape of FLG-null mutations in Asia that is slowly emerging.

Eukaryotic translation initiation factor 5 (eIF5) acts as a classical GTPase-activator protein.

GTP hydrolysis occurs at several specific stages during the initiation, elongation, and termination stages of mRNA translation. However, it is unclear how GTP hydrolysis occurs; it has previously been suggested to involve a GTPase active center in the ribosome, although proof for this is lacking. Alternatively, it could involve the translation factors themselves, e.g., be similar to the situation for small G in which the GTPase active site involves arginine residues contributed by a further protein termed a GTPase-activator protein (GAP). During translation initiation in eukaryotes, initiation factor eIF5 is required for hydrolysis of GTP bound to eIF2 (the protein which brings the initiator Met-tRNA(i) to the 40S subunit). Here we show that eIF5 displays the hallmarks of a classical GAP (e.g., RasGAP). Firstly, its interaction with eIF2 is enhanced by AlF(4)(-). Secondly, eIF5 possesses a conserved arginine (Arg15) which, like the "arginine fingers" of classical GAPs, is flanked by hydrophobic residues. Mutation of Arg15 to methionine abolishes the ability of eIF5 either to stimulate GTP hydrolysis or to support mRNA translation in vitro. Mutation studies suggest that a second conserved arginine (Arg48) also contributes to the GTPase active site of the eIF2.eIF5 complex. Our data thus show that eIF5 behaves as a classical GAP and that GTP hydrolysis during translation involves proteins extrinsic to the ribosome. Indeed, inspection of their sequences suggests that other translation factors may also act as GAPs.

IC261, a specific inhibitor of the protein kinases casein kinase 1-delta and -epsilon, triggers the mitotic checkpoint and induces p53-dependent postmitotic effects.

The p53-targeted kinases casein kinase 1delta (CK1delta) and casein kinase 1epsilon (CK1epsilon) have been proposed to be involved in regulating DNA repair and chromosomal segregation. Recently, we showed that CK1delta localizes to the spindle apparatus and the centrosomes in cells with mitotic failure caused by DNA-damage prior to mitotic entry. We provide here evidence that 3-[(2,4,6-trimethoxyphenyl)methylidenyl]-indolin-2-one (IC261), a novel inhibitor of CK1delta and CK1epsilon, triggers the mitotic checkpoint control. At low micromolar concentrations IC261 inhibits cytokinesis causing a transient mitotic arrest. Cells containing active p53 arrest in the postmitotic G1 phase by blockage of entry into the S phase. Cells with non-functional p53 undergo postmitotic replication developing an 8N DNA content. The increase of DNA content is accompanied by a high amount of micronucleated and apoptotic cells. Immunfluorescence images show that at low concentrations IC261 leads to centrosome amplification causing multipolar mitosis. Our data are consistent with a role for CK1delta and CK1epsilon isoforms in regulating key aspects of cell division, possibly through the regulation of centrosome or spindle function during mitosis.

p53 is phosphorylated in vitro and in vivo by the delta and epsilon isoforms of casein kinase 1 and enhances the level of casein kinase 1 delta in response to topoisomerase-directed drugs.

The p53 tumour suppressor protein plays a key role in the integration of stress signals. Multi-site phosphorylation of p53 may play an integral part in the transmission of these signals and is catalysed by many different protein kinases including an unidentified p53-N-terminus-targeted protein kinase (p53NK) which phosphorylates a group of sites at the N-terminus of the protein. In this paper, we present evidence that the delta and epsilon isoforms of casein kinase 1 (CK1delta and CK1epsilon) show identical features to p53NK and can phosphorylate p53 both in vitro and in vivo. Recombinant, purified glutathione S-transferase (GST)-CK1delta and GST-CK1epsilon fusion proteins each phosphorylate p53 in vitro at serines 4, 6 and 9, the sites recognised by p53NK. Furthermore, p53NK (i) co-purifies with CK1delta/epsilon, (ii) shares identical kinetic properties to CK1delta/epsilon, and (iii) is inhibited by a CK1delta/epsilon-specific inhibitor (IC261). In addition, CK1delta is also present in purified preparations of p53NK as judged by immunoanalysis using a CK1delta-specific monoclonal antibody. Treatment of murine SV3T3 cells with IC261 specifically blocked phosphorylation in vivo of the CK1delta/epsilon phosphorylation sites in p53, indicating that p53 interacts physiologically with CK1delta and/or CK1epsilon. Similarly, over-expression of a green fluorescent protein (GFP)-CK1delta fusion protein led to hyper-phosphorylation of p53 at its N-terminus. Treatment of MethAp53ts cells with the topoisomerase-directed drugs etoposide or camptothecin led to increases in both CK1delta-mRNA and -protein levels in a manner dependent on the integrity of p53. These data suggest that p53 is phosphorylated by CK1delta and CK1epsilon and additionally that there may be a regulatory feedback loop involving p53 and CK1delta.

Specific volumes of lipids in fully hydrated bilayer dispersions.

The neutral buoyancy method of obtaining absolute specific volumes of lipid in multilamellar dispersions is critically investigated. Control experiments show that there is no preferential partitioning of 2H2O vs. H2O into the liposomes, and several thermodynamic properties of the samples, such as the enthalpy change and the volume change of the main transition, are changed very little with deuteration of the solvent. The assumption that the molecular volume of the solvent in the interlamellar space is essentially the same as in bulk solution is discussed; and it is shown to introduce rather small corrections. Previous procedures have been modified to avoid possible kinetic limitations in phases with low water permeability. It is concluded that the molecular volume of lipid in bilayers can be obtained to an accuracy better than 0.002 nm3 (2A3) which is less than 0.2% of typical molecular volumes of lipids.

Gene expression profiling and association of circulating lactoferrin level with obesity-related phenotypes in Latino youth.

BACKGROUND/OBJECTIVES: Low-grade inflammation is an underlying feature of obesity and identifying inflammatory markers is crucial to understanding this disease. Therefore, the purpose of this study was twofold: (i) to perform a global microarray analysis and (ii) to investigate the role of lactoferrin (LTF), one of the most altered genes, in relation to obesity in Latino youth. METHODS: Non-diabetic Latino youth (71 males/92 females; 15.6 ± 3.2 years) were studied. A subset of 39 participants was randomly selected for global microarray analysis profiling from the whole blood sample. Serum LTF was compared between lean (n = 78) and overweight/obese (n = 85) participants. RESULTS: Microarray analysis revealed that a total of 1870 probes were altered in expression ≥1.2-fold and P < 0.05 in overweight/obese participants compared with lean. KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis revealed significant enrichment for pathways including toll-like receptor (TLR) and B cell receptor signalling pathways. LTF and TLR5 were increased in expression by 2.2 and 1.5 fold, respectively, in the overweight/obese participants. Increased LTF concentrations were significantly associated with high risk of obesity-related phenotypes (all P < 0.05). CONCLUSIONS: Our data suggest that increased LTF is associated with obesity risk among Latino youth. This finding is discordant to what has been shown in adults and suggests that age may modulate the association between LTF and obesity-related health.

Cellular localization and developmental regulation of 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1) gene expression in the ovine placenta.

This study was designed to examine the cellular localization and developmental regulation of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) type 1 gene expression in the ovine placenta. Placental tissues were collected at discrete times between days 59 and 143 of pregnancy (term = 145 days). Levels of 11 beta-HSD1 mRNA were determined by Norther blot analysis. The level of both dehydrogenase and reductase activities of 11 beta-HSD1 was assessed by a radiometric conversion assay using cortisol and cortisone as physiological substrates. The cellular localization of 11 beta-HSD1 protein was determined by standard immunohistochemical technique using a polyclonal antibody specific for the ovine protein. High levels of 11 beta-HSD1 mRNA were detected in the placenta by day 59, and there was a trend towards a decrease between days 98-103 and 125-128 (P = 0.06). The level of placental 11 beta-HSD1 mRNA remained unchanged thereafter. Levels of both 11 beta-HSD1 dehydrogenase and reductase activities followed a similar pattern except that in both cases there was a significant decrease between 98-103 and 125-128 (P < 0.05). Moreover, under the present assay conditions, the dehydrogenase activity was always predominant, suggesting that the net effect of placental 11 beta-HSD1 activity would lead to glucocorticoid inactivation. Thus, the decreased 11 beta-HSD1 activity in the placenta at days 125-128 was consistent with, and may help to explain, the apparent increase in the placental transfer of cortisol from mother to fetus during that time. Throughout pregnancy, intense 11 beta-HSD1 immunoreactivity was detected in fetal trophoblastic cells, maternal stromal cells and blood vessels. In contrast, maternal syncytium was immunonegative before day 125, but became immunopositive thereafter. The observed predominant direction of 11 beta-HSD1 activity in vitro and its pattern of localization in the ovine placenta are consistent with the hypothesis that placental 11 beta-HSD protects the fetus from adverse effects of maternal glucocorticoids by inactivating glucocorticoids locally.

Ovine 11 beta-hydroxysteroid dehydrogenase type 2 gene predicts a protein distinct from that deduced by the cloned kidney cDNA at the C-terminus.

The gene encoding ovine 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD2) was cloned and characterized. This gene consists of five exons and is greater than 4 kb in length. It contains an open reading frame of 1215 bp, which encodes a protein of 404 amino acids with a predicted MW of 44 kDa. The deduced ovine 11 beta-HSD2 protein displays over 78% sequence identity to those of the human, rabbit, rat, and mouse. However, this differs from the published sequence of ovine kidney 11 beta-HSD2 cDNA which predicts a protein of 427 amino acids. Sequence alignment indicated that this discrepancy is attributed to two single nucleotide omissions in the published cDNA sequence which resulted in a shift in the open reading frame at the codon for residue 358. Therefore, the present results have provided conclusive evidence that the primary structure of 11 beta-HSD2 protein is well conserved between the sheep and the other four mammals. Moreover, Northern blot analysis of total RNA samples from 15 peripheral tissues and seven brain regions of the mature fetal sheep revealed that the expression of 11 beta-HSD2 gene is highly tissue-specific in that it is only expressed in the kidney and adrenal gland, and at a much lower abundance in the testis, colon and placenta. The cloning of the sheep 11 beta-HSD2 gene should facilitate future studies on the regulation of 11 beta-HSD2 gene expression during fetal development in a mammalian model.

Ongoing postdivorce conflict and child disturbance.

This paper reports on the disturbed behavior of children who are subject to entrenched parental disputes over their custody and care after separation and divorce. The 56 children who varied in racial and socioeconomic origin were 4 to 12 years old at entry into the study. They were assessed at two points: at the time of the custody dispute and 2.5 years later. The extent of the child's involvement in the dispute and the amount of role reversal between parent and child predicted total behavior problems and aggression at the time of the legal dispute. These same factors, together with the rate of verbal and physical aggression between parents, predicted total behavior problems, depression, withdrawn/uncommunicative behavior, somatic complaints, and aggression at the 2-year follows-up. There were no main effects for sex and age. However, at the 2-year mark, girls in high-conflict families were more depressed and withdrawn, and older children in high-conflict situations had more somatic complaints and were more aggressive. The findings are considered in the light of a number of etiological mechanisms by which parental conflict affects children.

A clinical typology of interparental violence in disputed-custody divorces.

From two studies of high-conflict divorcing families in child custody disputes, four characteristic profiles of interparental violence were identified: ongoing or episodic battering by males, female-initiated violence, interactive violence controlled by males, and violence engendered by separation or postdivorce trauma. A fifth profile, culled from a subsample of members of the first two groups, was characterized by psychotic and paranoid reactions.