Family-based psychological interventions for domestically adoptive families: a systematic review.

Adopted children are often at a risk of experiencing several neurobiological and psychosocial difficulties. Adoptive parents must support these difficulties whilst managing their own idiosyncratic challenges. Family-based psychotherapeutic interventions which promote adoptive family functioning, environments and relationships can mediate these difficulties for adopted families. This review synthesises evidence exploring family-based psychological interventions for adoptive families, appraises the literature's strengths and weaknesses, and reports characteristics of promising interventions. Included studies recruited domestically adoptive families receiving psychotherapeutic interventions delivered to at least one adoptive parent and child. The authors searched seven electronic information databases, four grey literature databases, two journals and five relevant websites up to 12.12.2022. The quantitative Risk of Bias in Non-Randomised Studies of Interventions tool and the qualitative Critical Skills Appraisal Programme checklist assessed risk of bias. The narrative synthesis presents 20 papers detailing 18 studies involving at least 729 adopted children and 829 adoptive parents. Findings provide preliminary support for integrative interventions which include aspects of sensory activities, attachment-based play, Dyadic Developmental Psychotherapy and Eye Movement Desensitisation and Reprocessing with Therapeutic Input provided to adopted children and adoptive parents separately, alongside the adoptive family. However, risk of bias was high, limiting the conclusions. Future research should examine the feasibility, acceptability and efficacy of integrative therapeutic approaches for adoptive families to further direct clinical practice.

Sex-specific responses to slow progressive pressure overload in a large animal model of HFpEF.

Approximately 50% of all heart failure (HF) diagnoses can be classified as HF with preserved ejection fraction (HFpEF). HFpEF is more prevalent in females compared with males, but the underlying mechanisms are unknown. We previously showed that pressure overload (PO) in male felines induces a cardiopulmonary phenotype with essential features of human HFpEF. The goal of this study was to determine if slow progressive PO induces distinct cardiopulmonary phenotypes in females and males in the absence of other pathological stressors. Female and male felines underwent aortic constriction (banding) or sham surgery after baseline echocardiography, pulmonary function testing, and blood sampling. These assessments were repeated at 2 and 4 mo postsurgery to document the effects of slow progressive pressure overload. At 4 mo, invasive hemodynamic studies were also performed. Left ventricle (LV) tissue was collected for histology, myofibril mechanics, extracellular matrix (ECM) mass spectrometry, and single-nucleus RNA sequencing (snRNAseq). The induced pressure overload (PO) was not different between sexes. PO also induced comparable changes in LV wall thickness and myocyte cross-sectional area in both sexes. Both sexes had preserved ejection fraction, but males had a slightly more robust phenotype in hemodynamic and pulmonary parameters. There was no difference in LV fibrosis and ECM composition between banded male and female animals. LV snRNAseq revealed changes in gene programs of individual cell types unique to males and females after PO. Based on these results, both sexes develop cardiopulmonary dysfunction but the phenotype is somewhat less advanced in females.NEW & NOTEWORTHY We performed a comprehensive assessment to evaluate the effects of slow progressive pressure overload on cardiopulmonary function in a large animal model of heart failure with preserved ejection fraction (HFpEF) in males and females. Functional and structural assessments were performed at the organ, tissue, cellular, protein, and transcriptional levels. This is the first study to compare snRNAseq and ECM mass spectrometry of HFpEF myocardium from males and females. The results broaden our understanding of the pathophysiological response of both sexes to pressure overload. Both sexes developed a robust cardiopulmonary phenotype, but the phenotype was equal or a bit less robust in females.

Chaplaincy in the outpatient setting-getting from here to there.

One of the most evident trends in US health care and health care generally in the developed world is that more and more care is shifting to outpatient settings. This change opens up substantial opportunities, and in many cases, expectations for chaplains to extend the breadth of the care they provide in any health system. However, it also brings many challenges. This paper describes the journey of four very different inpatient chaplaincy services into the outpatient setting. These four examples focus on settings that would historically be thought of as outpatient-those that see patients within the brick and mortar of the health system.

Ventromedial hypothalamus-specific Ptpn1 deletion exacerbates diet-induced obesity in female mice.

Protein-tyrosine phosphatase 1B (PTP1B) regulates food intake (FI) and energy expenditure (EE) by inhibiting leptin signaling in the hypothalamus. In peripheral tissues, PTP1B regulates insulin signaling, but its effects on CNS insulin action are largely unknown. Mice harboring a whole-brain deletion of the gene encoding PTP1B (Ptpn1) are lean, leptin-hypersensitive, and resistant to high fat diet-induced (HFD-induced) obesity. Arcuate proopiomelanocortin (POMC) neuron-specific deletion of Ptpn1 causes a similar, but much milder, phenotype, suggesting that PTP1B also acts in other neurons to regulate metabolism. Steroidogenic factor-1-expressing (SF-1-expressing) neurons in the ventromedial hypothalamus (VMH) play an important role in regulating body weight, FI, and EE. Surprisingly, Ptpn1 deletion in SF-1 neurons caused an age-dependent increase in adiposity in HFD-fed female mice. Although leptin sensitivity was increased and FI was reduced in these mice, they had impaired sympathetic output and decreased EE. Immunohistochemical analysis showed enhanced leptin and insulin signaling in VMH neurons from mice lacking PTP1B in SF-1 neurons. Thus, in the VMH, leptin negatively regulates FI, promoting weight loss, whereas insulin suppresses EE, leading to weight gain. Our results establish a novel role for PTP1B in regulating insulin action in the VMH and suggest that increased insulin responsiveness in SF-1 neurons can overcome leptin hypersensitivity and enhance adiposity.