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Background According to the diathesis-stress model, some individuals may have a certain underlying vulnerability (diathesis) that can be environmental or biological, such as a childhood trauma or a genetic predisposition. Hence, it is important to understand the epigenetic factors and the presence of biomarkers related to mental illness and suicide risk. Objective The present study aimed to evaluate if the presence of rs1800871 (IL- 10), rs2020933 (5-HTT) and rs1800629 (TNF – α) polymorphisms express different outcomes in terms of physical, psychological health and quality of life, considering the relations among them and the social environment, through observation of the psychological, physical, environment domains and the quality of social relations. Method A multivariate analysis (MANOVA) of the data was conducted, in which 481 participants were assessed through the instruments Quality of Life Brief Questionnaire (QOL – brief), Beck's Scale of Suicide Ideation (BSI) and the Mini International Neuropsychiatric Interview (MINI 5.5.0). The participants´ DNA was collected through a saliva sample of the oral mucosa. From the studied sample, 306 participants had mental disorder (MD) with no history of suicide attempt (HSA), 145 showed MD with HSA and 175 participants. Results A statistically significant difference (0.001 and 0.004) was found in the interaction of two factors, namely the social relationships domain and the presence of the IL- 10 polymorphism, leading to increased suicide risk and lower levels of quality of life in the physical domain. The interaction between the rs1800871 (IL-10) polymorphism and lower levels of quality of life in the environment and social environment domains appears to be related to a worse perception of physical health and a higher risk of suicide, which highlights the epigenetic influence for both physical and mental illness.

© Springer-Verlag GmbH Germany, part of Springer Nature 2020., Rationale: The nuclear receptor retinoid X receptor (RXR) belongs to a nuclear receptor superfamily that modulates diverse functions via homodimerization with itself or several other nuclear receptors, including PPARα. While the activation of PPARα by natural or synthetic agonists regulates the sleep-wake cycle, the role of RXR in the sleep modulation is unknown. Objectives: We investigated the effects of bexarotene (Bexa, a RXR agonist) or UVI 3003 (UVI, a RXR antagonist) on sleep, sleep homeostasis, levels of neurochemical related to sleep modulation, and c-Fos and NeuN expression. Methods: The sleep-wake cycle and sleep homeostasis were analyzed after application of Bexa or UVI. Moreover, we also evaluated whether Bexa or UVI could induce effects on dopamine, serotonin, norepinephrine epinephrine, adenosine, and acetylcholine contents, collected from either the nucleus accumbens or basal forebrain. In addition, c-Fos and NeuN expression in the hypothalamus was determined after Bexa or UVI treatments. Results: Systemic application of Bexa (1 mM, i.p.) attenuated slow-wave sleep and rapid eye movement sleep. In addition, Bexa increased the levels of dopamine, serotonin, norepinephrine epinephrine, adenosine, and acetylcholine sampled from either the nucleus accumbens or basal forebrain. Moreover, Bexa blocked the sleep rebound period after total sleep deprivation, increased in the hypothalamus the expression of c-Fos, and decreased NeuN activity. Remarkably, UVI 3003 (1 mM, i.p.) induced opposite effects in sleep, sleep homeostasis, neurochemicals levels, and c-Fos and NeuN activity. Conclusions: The administration of RXR agonist or antagonist significantly impaired the sleep-wake cycle and exerted effects on the levels of neurochemicals related to sleep modulation. Moreover, Bexa or UVI administration significantly affected c-Fos and NeuN expression in the hypothalamus. Our findings highlight the neurobiological role of RXR on sleep modulation., This work was supported by the Escuela de Medicina, Universidad Anáhuac Mayab (PresInvEMR2018), given to E. MR.

The sleep–wake cycle is a neurobiological phenomenon that shows intervals of activity alternating with restfulness that appears with a periodicity approximating the 24-hour day-night cycle. The sleep–wake cycle is under the control of diverse neuroanatomical and neurochemical systems, including monoaminergic, cholinergic, adenosinergic among many other systems. In addition, neuroanatomical centers linked to sleep promotion, such as the hypothalamus, project to the cerebral cortex, subcortical relays, and brainstem. In addition, the sleep–wake cycle has been associated to aberrant features known as sleep disorders. Here, we will discuss the role of specific gene expression on sleep disturbances. Given the expansion of the knowledge in the sleep–wake cycle area, it is indeed ambitious to describe all the genetics involved in the sleep modulation. However, in this chapter we reviewed the current understanding of the sleep disorders and gene expression.

Objective: To investigate the prevalence of psychiatric disorders among women in ambulatory treatment for polycystic ovary syndrome (PCOS) and to correlate its clinical and demographic aspects with mental disorders. Methodology: Seventy-two patients in ambulatory treatment at the Endocrinal and Gynaecological Institute of the Federal University of Rio de Janeiro were evaluated using Diagnostic and Statistical Manual for Mental Disorders, Fourth Edition criteria by means of MINI (Mini International Neuropsychiatric Interview, version 4.4). Polycystic ovary syndrome was confirmed according to the ultrasonographic criteria of Adams and by clinical parameters. Results: Forty-one patients (57%) presented at least one psychiatric diagnosis. Among them, the prevalence of mood disorder reached 78%. The most prevalent diagnostics were major depression (26.4%) and bipolar disorder (11.1%). Conclusion: A high prevalence of mental disorders was observed, especially major depression and bipolar disorder. The data obtained regarding the relationship between PCOS and mood disorders in a Brazilian sample is in accordance with recent research findings in the same area.

Our aim was to describe the clinical features of 35% CO2-induced panic attacks in patients with panic disorder (PD) (Diagnostic and Statistical Manual and Mental Disorders, Fourth Edition) and compare them with the last spontaneous panic attack in patients with PD who had not had a panic attack after the 35% CO2 challenge test. We examined 91 patients with PD submitted to the CO2 challenge test. The test consisted of exhaling as fully as possible, took a fast vital capacity breath, held their breath for 8 seconds, exhaled, and then repeated the fast vital capacity breath, again holding for 8 seconds. The patients inhaled the 35% CO2/65% O2 mixture or atmospheric compressed air, randomly selected in a double-blind design. Scales were applied before and after the test. A total of 68.1% (n = 62) patients with PD had a panic attack (responders) after the CO2 test (chi2(1) = 25.87, P = .031). The last spontaneous panic attack and the symptom profile from the patients with PD who had not had a panic attack after the test (n = 29, 31.9%) were described to compare. The responders had more respiratory symptoms (chi2(1) = 19.21, P.001), fulfilling the criteria for respiratory PD subtype (80.6%); the disorder started earlier (Mann-Whitney, P.001), had a higher familial prevalence of PD (chi2(1) = 20.45, P = .028), and had more previous depressive episodes (chi2(1) = 27.98, P.001). Our data suggest that there is an association between respiratory PD subtype and hyperreactivity to a CO2 respiratory challenge test. The responders may be a subgroup of respiratory PD subtype with future diagnostic and therapeutic implications.