The research indicated that patients and partners alike struggle with the tremendous impact of bipolar disorder on their lives and on their relationships. Given the high rates of divorce and volatility in these relationships, healthcare professionals can provide (or refer to) emotional and practical support both to patients and spouses on their own, and as a couple in their clinics.

Study Objectives Sleep disturbances and insomnia are highly prevalent in children with Autism Spectrum Disorder (ASD). Sleep homeostasis, a fundamental mechanism of sleep regulation that generates pressure to sleep as a function of wakefulness, has not been studied in children with ASD so far, and its potential contribution to their sleep disturbances remains unknown. Here, we examined whether slow-wave activity (SWA), a measure that is indicative of sleep pressure, differs in children with ASD. Methods In this case-control study, we compared overnight electroencephalogram (EEG) recordings that were performed during Polysomnography (PSG) evaluations of 29 children with ASD and 23 typically developing children. Results Children with ASD exhibited significantly weaker SWA power, shallower SWA slopes, and a decreased proportion of slow-wave sleep in comparison to controls. This difference was largest during the first 2 hours following sleep onset and decreased gradually thereafter. Furthermore, SWA power of children with ASD was significantly negatively correlated with the time of their sleep onset in the lab and at home, as reported by parents. Conclusions These results suggest that children with ASD may have a dysregulation of sleep homeostasis that is manifested in reduced sleep pressure. The extent of this dysregulation in individual children was apparent in the amplitude of their SWA power, which was indicative of the severity of their individual sleep disturbances. We, therefore, suggest that disrupted homeostatic sleep regulation may contribute to sleep disturbances in children with ASD.

Atrial fibrillation (AF) is a progressive arrhythmia with underlying mechanisms that are not fully elucidated, partially due to lack of reliable and affordable animal models. Here, we introduce a system for long-term assessment of AF susceptibility (substrate) in ambulatory rats implanted with miniature electrodes on the atrium. Rats were subjected to excessive aldosterone (Aldo) or solvent only (Sham). An additional group was exposed to myocardial infarction (MI). AF substrate was tested two-and four-weeks post implantation and was also compared with implanted rats early post-implantation (Base). Aldo and MI increased the AF substrate and atrial fibrosis. In the MI group only, AF duration was correlated with the level of atrial fibrosis and was inversely correlated with systolic function. Unexpectedly, Shams also developed progressive AF substrate relative to Base individuals. Further studies indicated that serum inflammatory markers (IL-6, TNF-alpha) were not elevated in the shams. In addition, we excluded anxiety\depression due to social-isolation as an AF promoting factor. Finally, enhanced biocompatibility of the atrial electrode did not inhibit the gradual development of AF substrate over a testing period of up to 8 weeks. Overall, we successfully validated the first system for long-term AF substrate testing in ambulatory rats.Atrial fibrillation (AF) is a growing epidemic, entailing substantial economic costs, morbidity and mortality 1,2 . The pathophysiology of AF is multi-factorial in nature. It involves sources of sustained rapid electrical activity that can trigger arrhythmic episodes as well as pathological mechanisms which alter the electrical and structural substrate for AF in the atrial tissue 3-7 . A full understanding of the molecular mechanisms by which various underlying conditions and factors converge to progressively promote AF substrate is still lacking [8][9][10] . Drugs aimed to target the atrial remodeling (upstream therapies) are attractive new options to prevent AF perpetuation. However, early pre-clinical testing of such drugs is currently difficult due to the absence of reliable and affordable animal models.Traditionally, AF-related models have relied solely on large animals exposed to atrial tachypacing or heart failure 11 . However, over the last two decades, rodents have been increasingly used to study various mechanistic aspects in the pathophysiology of AF 12-18 , and the possibility of using rodents to test new therapies seems attractive. However, several technical limitations constrain the widespread utility of rodents in AF research. Particularly, the small and delicate rodent atria render the implantation of chronic pacing and recording

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Previously, we found that basal corticosterone pulsatility significantly impacts the vulnerability for developing post-traumatic stress disorder (PTSD). Rats that exhibited PTSD-phenotype were characterized by blunted basal corticosterone pulsatility amplitude and a blunted corticosterone response to a stressor. This study sought to identify the mechanisms underlining both the loss of pulsatility and differences in downstream responses. Serial blood samples were collected manually via jugular vein cannula at 10-min intervals to evaluate suppression of corticosterone following methylprednisolone administration. The rats were exposed to predator scent stress (PSS) after 24 h, and behavioral responses were assessed 7 days post-exposure for retrospective classification into behavioral response groups. Brains were harvested for measurements of the glucocorticoid receptor, mineralocorticoid receptor, FK506-binding protein-51 and arginine vasopressin in specific brain regions to assess changes in hypothalamus–pituitary–adrenal axis (HPA) regulating factors. Methylprednisolone produced greater suppression of corticosterone in the PTSD-phenotype group. During the suppression, the PTSD-phenotype rats showed a significantly more pronounced pulsatile activity. In addition, the PTSD-phenotype group showed distinct changes in the ventral and dorsal CA1, dentate gyrus as well as in the paraventricular nucleus and supra-optic nucleus. These results demonstrate a pre-trauma vulnerability state that is characterized by an over-reactivity of the HPA and changes in its regulating factors.

Study Objectives: Sleep disturbances and insomnia are highly prevalent in children with Autism Spectrum Disorder (ASD). Sleep homeostasis, a fundamental mechanism of sleep regulation that generates pressure to sleep as a function of wakefulness, has not been studied in children with ASD so far, and its potential contribution to their sleep disturbances remains unknown. Here, we examined whether slow wave activity (SWA), a measure that is indicative of sleep pressure, differs in children with ASD. Methods:In this case-control study, we compared overnight electroencephalogram (EEG) recordings that were performed during Polysomnography (PSG) evaluations of 29 children with ASD and 23 typically developing children.Results: Children with ASD exhibited significantly weaker SWA power, shallower SWA slopes, and a decreased proportion of slow wave sleep in comparison to controls. This difference was largest during the first two hours following sleep onset and decreased gradually thereafter. Furthermore, SWA power of children with ASD was significantly, negatively correlated with the time of their sleep onset in the lab and at home, as reported by parents. Conclusions:These results suggest that children with ASD may have a dysregulation of sleep homeostasis that is manifested in reduced sleep pressure. The extent of this dysregulation in individual children was apparent in the amplitude of their SWA power, which was indicative of the severity of their individual sleep disturbances. We, therefore, suggest that disrupted homeostatic sleep regulation may contribute to sleep disturbances in children with ASD. Statement of significance:Sleep disturbances are apparent in 40-80% of children with autism. Homeostatic sleep regulation, a mechanism that increases the pressure to sleep as a function of prior wakefulness, has not been studied in children with autism. Here, we compared Polysomnography exams of 29 children with autism and 23 matched controls. We found that children with autism exhibited reduced slow-wave-activity power and shallower slopes, particularly during the first two hours of sleep. This suggests that they develop less pressure to sleep. Furthermore, the reduction in slow-wave-activity was associated with the severity of sleep disturbances as observed in the laboratory and as reported by parents. We, therefore, suggest that disrupted homeostatic sleep regulation may contribute to sleep disturbances of children with autism.

Objective To explore coping strategies for persons with bipolar affective disorder and their partners. Background Bipolar disorder poses interpersonal and practical challenges for patients and their partners. Although the divorce rate is high among persons with bipolar disorder, few studies have examined how these people and their partners cope with the condition. Method 11 persons with bipolar affective disorder and 10 partners of people with bipolar affective disorder were interviewed separately about coping. Data were analyzed using the grounded theory method. Results Both patients and partners reported that coping strategies included professional help, social support, and emotional, instrumental, and religious coping strategies. Conclusions Persons with bipolar disorder and their partners draw on similar coping strategies, but the former draw more on social support and instrumental coping strategies, and their partners draw on emotional coping strategies. Both members of the couple are dependent on the use of professional support—psychiatric, psychological, and psychosocial—when it is readily available and easily accessible, and this was a key aspect of coping with the disorder. Implications Clinical interventions should focus on providing support for partners, who are integral to the health and well‐being of persons with bipolar disorder and who experience substantial strain associated with their caregiving duties. Focusing on strategies to strengthen the spousal relationship is an essential aspect of care.

Endocannabinoids play a role in adaptation to stress and regulate the release of glucocorticoids in stressed and unstressed conditions. We recently found that basal corticosterone pulsatility may significantly impact the vulnerability for developing post-traumatic-stress-disorder (PTSD), suggesting that the endocannabinoid system may contribute to its development. To examine this, we exposed rats to predator scent stress (PSS). Behavioral reactions were recorded seven days post-PSS. Cerebrospinal fluid (CSF) was collected from anesthetized rats shortly after PSS exposure to determine the levels of 2-arachidonoyl glycerol (2-AG) and anandamide (AEA). To correlate between endocannabinoids and corticosterone levels, rats were placed in metabolic cages for urine collection. To assess the levels of endocannabinoids in specific brain regions, rats’ brains were harvested one day after behavioral analysis for staining and fluorescence quantification. Moreover, 2-AG was elevated in the CSF of PTSD-phenotype rats as compared with other groups and was inversely correlated with corticosterone urinary secretion. Eight days post-PSS exposure, hippocampal and hypothalamic 2-AG levels and hippocampal AEA levels were significantly more reduced in the PTSD-phenotype group compared to other groups. We posit that maladaptation to stress, which is propagated by an abnormal activation of endocannabinoids, mediates the subsequent stress-induced behavioral disruption, which, later, reduces neuronal the expression of endocannabinoids, contributing to PTSD symptomology.