Displacement, Polygyny, Romantic Jealousy, and Intimate Partner Violence: A Qualitative Study among Somali Refugees in Ethiopia.

Romantic jealousy is a well-known relational driver of intimate partner violence (IPV), but is under-studied among displaced and polygynous populations. This study aimed to explore factors that elicit jealousy among Somali refugees in the Bokolmayo Refugee camp in Ethiopia, and the pathways leading from jealousy to IPV against women and men, to inform interventions. We conducted an exploratory, thematic analysis of 30 in-depth interviews with both women and men who were Somali refugees, as well as elders and religious leaders, organizational and service providers, policy makers, and host community members. We found that jealousy experienced by women was elicited by an unequal distribution of money and affection between co-wives, which was exacerbated by displacement-related economic hardship, and women in monogamous partnerships suspecting their husband of having other relationships. The jealousy experienced by men was elicited by their wives' increased financial independence and interactions with other men when working outside of the home, which became more common because of displacement-related economic hardship and relaxed patriarchal gender norms. IPV interventions should address jealousy and controlling behaviors in all relationship types. Addressing conflict and relationship dynamics in polygynous households and in humanitarian settings may require specialized content, acknowledging the complex interactions and resource allocation between co-wives. Gender-transformative interventions that move away from masculinities that are built on the provider role and the introduction of alternative masculinities could also be effective in reducing IPV in this and other similar contexts.

Changes in Pain and Psychosocial Functioning and Transition to Chronic Pain in Pediatric Sickle Cell Disease: A Cohort Follow-up Study.

OBJECTIVES: This study aimed to: (1) examine changes in pain, psychosocial functioning, and health care utilization among children and adolescents with sickle cell disease (SCD) over a 2-year period and (2) identify baseline biopsychosocial variables associated with the development and maintenance of chronic SCD pain at follow-up. MATERIALS AND METHODS: Forty-two youth (8 to 18 y old) with SCD completed a battery of self-report measures at baseline and 2-year follow-up. Analgesic, Anesthetic, and Addiction Clinical Trial Translational Innovations Opportunities and Networks and American Pain Society Pain Taxonomy (AAPT) diagnostic criteria were used to categorize patients into pain frequency groups at both timepoints: chronic (pain on most [≥15] d/mo for the past 6 mo, per AAPT diagnostic criteria), episodic (pain on 1 to 14 d/mo), or asymptomatic (0 d/mo). RESULTS: At baseline, 31% (n=13) had chronic pain, 50% (n=21) episodic pain, and 19% (n=8) were asymptomatic. At follow-up, 40.5% (n=17) had chronic pain, 52.4% (n=22) episodic pain, and 7.1% (n=3) were asymptomatic. Between baseline and 2-year follow-up, 12% (n=5) developed chronic SCD pain. Depressive symptoms and admissions for pain significantly increased over time for youth with chronic pain (Ps<0.05). An interaction effect revealed that baseline pain groups differed in their change in pain intensity over time (P<0.01). Baseline psychosocial factors (ie, higher functional disability, greater depressive symptoms, higher pain catastrophizing, and lower quality of life) were significantly associated with chronic pain at follow-up. DISCUSSION: Biopsychosocial factors may be associated with the development and maintenance of chronic SCD pain and their relative contributions warrant further study.

Systems Analysis of the 22q11.2 Microdeletion Syndrome Converges on a Mitochondrial Interactome Necessary for Synapse Function and Behavior.

Neurodevelopmental disorders offer insight into synaptic mechanisms. To unbiasedly uncover these mechanisms, we studied the 22q11.2 syndrome, a recurrent copy number variant, which is the highest schizophrenia genetic risk factor. We quantified the proteomes of 22q11.2 mutant human fibroblasts from both sexes and mouse brains carrying a 22q11.2-like defect, Df(16)A+/- Molecular ontologies defined mitochondrial compartments and pathways as some of top ranked categories. In particular, we identified perturbations in the SLC25A1-SLC25A4 mitochondrial transporter interactome as associated with the 22q11.2 genetic defect. Expression of SLC25A1-SLC25A4 interactome components was affected in neuronal cells from schizophrenia patients. Furthermore, hemideficiency of the Drosophila SLC25A1 or SLC25A4 orthologues, dSLC25A1-sea and dSLC25A4-sesB, affected synapse morphology, neurotransmission, plasticity, and sleep patterns. Our findings indicate that synapses are sensitive to partial loss of function of mitochondrial solute transporters. We propose that mitoproteomes regulate synapse development and function in normal and pathological conditions in a cell-specific manner.SIGNIFICANCE STATEMENT We address the central question of how to comprehensively define molecular mechanisms of the most prevalent and penetrant microdeletion associated with neurodevelopmental disorders, the 22q11.2 microdeletion syndrome. This complex mutation reduces gene dosage of ∼63 genes in humans. We describe a disruption of the mitoproteome in 22q11.2 patients and brains of a 22q11.2 mouse model. In particular, we identify a network of inner mitochondrial membrane transporters as a hub required for synapse function. Our findings suggest that mitochondrial composition and function modulate the risk of neurodevelopmental disorders, such as schizophrenia.