Relationship dissatisfaction and other risk factors for future relationship dissolution: a population-based study of 18,523 couples

Purpose

There has been a marked increase in divorce rates in most Western societies over the last 50 years. Relationship dissolution is associated with negative consequences both for adults and children, so it is important to understand the factors that help retain marital stability. The first aim of this prospective study was to identify risk factors for relationship dissolution in 18,523 couples in Norway, with a particular focus on individual dissatisfaction with the relationship. The second aim was to assess interaction effects between relationship dissatisfaction and other predictors of relationship dissolution.

Methods

Pregnant women and their partners enrolled in the Norwegian Mother and Child Cohort study completed questionnaires during the pregnancy that asked about relationship dissatisfaction, strain, demographics, and other risk factors. The main outcome variable was relationship dissolution in the 39-month period from gestational week 30–36 months postpartum. Associations between the risk factors and relationship dissolution were estimated by logistic regression analysis.

Results

Except for younger female age, relationship dissatisfaction in women and lower education in men, were the strongest predictors of relationship dissolution. Another strong factor was women’s persistent strain. No significant interaction effects were found between relationship dissatisfaction and the other variables in the analyses.

Conclusions

Dissatisfaction with the relationship, in particular in women, and low male education are important predictors of relationship dissolution, although other factors are also related to dissolution. There are only few studies on relationship predictors of dissolution conducted in Europe, and the current study adds to this body of knowledge.     

ADHD and the externalizing spectrum: direct comparison of categorical,continuous, and hybrid models of liability in a nationally representative sample

Purpose

Alcohol use disorders, substance use disorders, and antisocial personality disorder share a common externalizing liability, which may also include attention-deficit hyperactivity disorder (ADHD). However, few studies have compared formal quantitative models of externalizing liability, with the aim of delineating the categorical and/or continuous nature of this liability in the community. This study compares categorical, continuous, and hybrid models of externalizing liability.

Method

Data were derived from the 2004–2005 National Epidemiologic Survey on Alcohol and Related Conditions (N = 34,653). Seven disorders were modeled: childhood ADHD and lifetime diagnoses of antisocial personality disorder (ASPD), nicotine dependence, alcohol dependence, marijuana dependence, cocaine dependence, and other substance dependence.

Results

The continuous latent trait model provided the best fit to the data. Measurement invariance analyses supported the fit of the model across genders, with females displaying a significantly lower probability of experiencing externalizing disorders. Cocaine dependence, marijuana dependence, other substance dependence, alcohol dependence, ASPD, nicotine dependence, and ADHD provided the greatest information, respectively, about the underlying externalizing continuum.

Conclusions

Liability to externalizing disorders is continuous and dimensional in severity. The findings have important implications for the organizational structure of externalizing psychopathology in psychiatric nomenclatures.     

Personality disorders are important risk factors for disability pensioning

Purpose

To determine whether personality disorders (PDs) are associated with increased risk of disability pensioning in young adults, independent of other common mental disorders.

Methods

2,770 young adults from the general population were assessed for PDs by the Structured Interview for DSM-IV Personality, and for common mental disorders by the Composite of International Diagnostic Interview. These data were linked to the Norwegian National Insurance Administration’s recordings of disability benefits for a 10-year period. Logistic regression analyses were applied to investigate the association between PDs and disability pensioning. The analyses were conducted for three types of PD measures: categorical diagnoses (any PD), dimensional scores of individual PDs and higher order components retrieved by principal component analyses.

Results

Having any PD was strongly associated with disability pensioning, regardless of disability diagnosis. The estimated odds ratio (OR) was substantially higher for PDs [OR 4.69 (95 % confidence interval (CI) 2.6–8.5)] than for mood disorders [OR 1.3 (CI 0.7–2.3)] and anxiety disorders [OR 2.3 (CI 1.3–4.3)]. Measured dimensionally, all PD traits except antisocial traits were significantly associated with disability pensioning. After adjusting for co-occurring traits of other PDs, only schizoid, dependent and borderline PD traits showed a significant positive association with disability pension, while antisocial traits showed a significant negative association. The principal component analyses showed that negative affectivity, psychoticism, and detachment was associated with an increased risk of disability pensioning, while antagonism/disinhibition and obsessivity were not.

Conclusions

PDs are strongly associated with disability pensioning in young adults, and might be more important predictors of work disability than anxiety and depressive disorders. Certain aspects of pathologic personalities are particularly important predictors of disability.     

Association of sleep apnea with clinically silent microvascular brain tissue changes in acute cerebral ischemia

The aim of this study was to determine the importance of sleep apnea in relation to clinically silent microvascular brain tissue changes in patients with acute cerebral ischemia. Patients with acute cerebral ischemia prospectively underwent nocturnal respiratory polygraphy within 5 days from symptom-onset. Sleep apnea was defined as apnea–hypopnea-index (AHI) ≥5/h. Experienced readers blinded to clinical and sleep-related data reviewed brain computed tomography and magnetic resonance imaging scans for leukoaraiosis and chronic lacunar infarctions. Ischemic lesions were considered clinically silent when patients did not recall associated stroke-like symptoms. Functional outcome was assessed with modified Rankin Scale at discharge, 6 and 12 months. Fifty-one of 56 (91 %) patients had sleep apnea of any degree. Patients with moderate-to-severe leukoaraiosis (Wahlund score ≥5) were found to have higher mean AHI than those with none or mild leukoaraiosis (34.4 vs. 12.8/h, p < 0.001). Moderate-to-severe sleep apnea (AHI ≥15/h) was found to be an independent predictor of moderate-to-severe leukoaraiosis (adjusted OR 6.03, 95 % CI 1.76–20.6, p = 0.0042) and of moderate-to-severe leukoaraiosis associated with clinically silent chronic lacunar infarctions (adjusted OR 10.5, 95 % CI 2.19–50.6, p = 0.003). The higher the Wahlund score and the AHI, the more likely unfavorable functional outcome resulted over time (p = 0.0373). In acute cerebral ischemia, sleep apnea is associated with clinically silent microvascular brain tissue changes and may negatively influence functional outcome. Routine sleep apnea screening and further investigation of possible long-term effects of non-invasive ventilatory treatment of sleep apnea appear warranted in this at-risk population.     

cIMPACT‐NOW update 7: advancing the molecular classification of ependymal tumors

Advances in our understanding of the biological basis and molecular characteristics of ependymal tumors since the latest iteration of the World Health Organization (WHO) classification of CNS tumors (2016) have prompted the cIMPACT‐NOW group to recommend a new classification. Separation of ependymal tumors by anatomic site is an important principle of the new classification and was prompted by methylome profiling data to indicate that molecular groups of ependymal tumors in the posterior fossa and supratentorial and spinal compartments are distinct. Common recurrent genetic or epigenetic alterations found in tumors belonging to the main molecular groups have been used to define tumor types at intracranial sites; C11orf95 and YAP1 fusion genes for supratentorial tumors and two types of posterior fossa ependymoma defined by methylation group, PFA and PFB. A recently described type of aggressive spinal ependymoma with MYCN amplification has also been included. Myxopapillary ependymoma and subependymoma have been retained as histopathologically defined tumor types, but the classification has dropped the distinction between classic and anaplastic ependymoma. While the cIMPACT‐NOW group considered that data to inform assignment of grade to molecularly defined ependymomas are insufficiently mature, it recommends assigning WHO grade 2 to myxopapillary ependymoma and allows grade 2 or grade 3 to be assigned to ependymomas not defined by molecular status.     

Recent achievements in developing selective Gq inhibitors

G proteins are key mediators of G protein-coupled receptor (GPCR) signaling, facilitating a plethora of important physiological processes. The role of G proteins is much less understood than other aspects of GPCR function, which is largely due to the shortage of potent and selective G protein inhibitors. The natural cyclic depsipeptides YM-254890 and FR900359 are two of the very few known selective inhibitors of the G_q subfamily, and are used as unique pharmacological tools in the study of G _q-mediated signaling. Moreover, a peptide-based G protein antagonist-2A (GP-2A), a 27-residue peptide (27mer(I860A)) derived from phospholipase C-β3 (PLC-β3), and the small molecule BIM-46187 have also been characterized as selective G _q inhibitors within the past 5 years. In this review, we highlight the recent development in chemical syntheses, characterization, and mechanism of action of these selective G _q inhibitors. The development and application of G _q-selective inhibitors will expand our knowledge of the structure and function of G protein-mediated signaling, shed light on the development of inhibitors for other G protein classes, and feed in to drug discovery for diseases where G proteins are implicated, including various forms of cancer.