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Dim light melatonin onset (DLMO) is considered the most reliable marker of the circadian rhythm phase in humans. DLMO may moderately correlate with sleep onset and sleep offset time. There are no sufficient data about the correlations between DLMO and clinical scales assessing sleep quality and daytime symptoms of poor night sleep. The aim of the study was to determine the association between DLMO and basic sleep parameters from actigraphy and sleep diaries, as well as the association between DLMO and the following insomnia clinical scales: the Athens Insomnia Scale (AIS), Insomnia Severity Index (ISI), Epworth Sleepiness Scale (ESS), and chronotype questionnaires: Morningness–Eveningness Questionnaire (MEQ) and Composite Scale of Morningness (CSM). Participants of the study were healthy volunteers. Sleep parameters were measured by sleep diaries and actigraphy, and the following clinical scales: the AIS, ISI, and ESS, and chronotype questionnaires: MEQ and CSM. DLMO was calculated based on plasma melatonin concentration. The blood samples were collected hourly at five time points between 20:00 and 00:00 during the session in dim red light (<50 lux). Melatonin concertation was determined by LC-MS/MS. Twenty-one volunteers participated in the study. DLMO was calculated in 12 participants. There was a significant correlation between DLMO and ISI (r = 0.60, p = 0.038) and ESS (r = 0.61, p = 0.034). The correlation coefficient between the DLMO and the AIS was also high, however insignificant (r = 0.57, p = 0.054). There were no significant correlations between DLMO and chronotype scales MEQ and CSM. DLMO did not correlate with sleep onset and sleep offset; however, DLMO correlated with the Sleep Fragmentation Index (SFI) (r = 0.67, p = 0.017). DLMO is associated with poorer sleep maintenance, a stronger feeling of insomnia, and sleepiness during the day. Simultaneously, chronotype pattern and circadian rhythm parameters do not correlate with DLMO. Biological circadian rhythm does not reflect the real-life sleep–wake rhythm, indicating that the lifestyle is more often disconnected from the biological clock. [ABSTRACT FROM AUTHOR]

The effects of celecoxib on a broad spectrum of mood disorders and on inflammatory parameters have not yet been comprehensively evaluated. The aim of this study was to systematically summarize the available knowledge on this topic. Data from both preclinical and clinical studies were analyzed, considering the efficacy and safety of celecoxib in the treatment of mood disorders, as well as the correlation of inflammatory parameters with the effect of celecoxib treatment. Forty-four studies were included. We found evidence supporting the antidepressant efficacy of celecoxib in a dose of 400 mg/day used for 6 weeks as an add-on treatment in major depression (SMD = −1.12 [95%Cl: −1.71,−0.52], p = 0.0002) and mania (SMD = −0.82 [95% CI:−1.62,−0.01], p = 0.05). The antidepressant efficacy of celecoxib in the above dosage used as sole treatment was also confirmed in depressed patients with somatic comorbidity (SMD = −1.35 [95% CI:−1.95,−0.75], p < 0.0001). We found no conclusive evidence for the effectiveness of celecoxib in bipolar depression. Celecoxib at a dose of 400 mg/d used for up to 12 weeks appeared to be a safe treatment in patients with mood disorders. Although an association between celecoxib response and inflammatory parameters has been found in preclinical studies, this has not been confirmed in clinical trials. Further studies are needed to evaluate the efficacy of celecoxib in bipolar depression, as well as long-term studies evaluating the safety and efficacy of celecoxib in recurrent mood disorders, studies involving treatment-resistant populations, and assessing the association of celecoxib treatment with inflammatory markers. [ABSTRACT FROM AUTHOR]

The effects of acetylsalicylic acid (ASA) on mood disorders (MD) and on inflammatory parameters in preclinical and clinical studies have not yet been comprehensively evaluated. The aim of this study was to systematically summarize the available knowledge on this topic according to PRISMA guidelines. Data from preclinical and clinical studies were analyzed, considering the safety and efficacy of ASA in the treatment of MD and the correlation of inflammatory parameters with the effect of ASA treatment. Twenty-one studies were included. Both preclinical and clinical studies found evidence indicating the safety and efficacy of low-dose ASA in the treatment of all types of affective episodes in MD. Observational studies have indicated a reduced risk of all types of affective episodes in chronic low-dose ASA users (HR 0.92, 95% CI: 0.88, 0.95, p < 0.0001). An association between ASA response and inflammatory parameters was found in preclinical studies, but this was not confirmed in clinical trials. Further long-term clinical trials evaluating the safety and efficacy of ASA in recurrent MD, as well as assessing the linkage of ASA treatment with inflammatory phenotype and cytokines, are required. There is also a need for preclinical studies to understand the exact mechanism of action of ASA in MD. [ABSTRACT FROM AUTHOR]

Schizophrenia is a chronic mental illness, which remains difficult to treat. A high resistance to the available therapies, their insufficient efficacy, and numerous side effects are the reasons why there is an urgent need to develop new antipsychotics. This study aimed to assess the antipsychotic-like effects of JJGW08, a novel arylpiperazine alkyl derivative of salicylamide, in rodents. First, considering the JJGW08 receptor profile, we investigated the compound's intrinsic activity towards dopamine D2 and serotonin 5-HT1A, 5-HT2A, and 5-HT7 receptors using functional assays. Next, we assessed the effect of JJGW08 on MK-801- and amphetamine-induced hyperlocomotion, its risk of inducing catalepsy and impairing motor coordination, as well as the anxiolytic-like effects in the four-plate and marble burying tests in mice. Finally, we investigated the antipsychotic-like properties of JJGW08 in rats using MK-801-induced hyperlocomotion and prepulse inhibition tests. We found that JJGW08 showed antagonistic properties at dopamine D2 and serotonin 5-HT1A, 5-HT2A, and 5-HT7 receptors. However, the effect on the 5-HT2A and 5-HT7 receptors was very weak. Moreover, the tested compound showed an antipsychotic-like effect in MK-801- and amphetamine-induced hyperlocomotion but not in a prepulse inhibition test in rats. Notably, JJGW08 demonstrated anxiolytic-like properties in both behavioral tests. Importantly, the compound did not induce catalepsy or motor coordination impairment in mice at antipsychotic-like doses. Our study suggests it is worth searching for new potential antipsychotics among arylpiperazine alkyl derivatives of salicylamide. [ABSTRACT FROM AUTHOR]

Social anxiety disorder (SAD) is one of the most frequent mental disorders. Exposure to virtual reality can be a solution complementing standard CBT (cognitive-behavioral therapy) or can be used as an independent therapeutic tool. The study's objective was to assess the safety and efficacy of using self-administered virtual reality exposure vs. CBT and CBT with virtual exposure. We assessed the efficacy of the applied intervention with the Leibowitz Social Anxiety Scale (LSAS). We compared three groups: CBT (n = 25), CBT + VR (n = 29), and self-administered therapy without aid of a therapist (n = 19). The results indicated that all three groups showed changes on the LSAS. The simple effect analysis showed that there were no differences between experimental conditions at T0 (session 1) and T1 (session 9) and that the only significant difference occurred at T2 (session 14). The pairwise comparisons showed that the participants in the VR condition scored higher on the LSAS score during the measurement at T2 than participants in CBT condition. Our study has several limitations. The presented initial study shows that the methods of CBT for social anxiety used so far are also effective, while the VR tool for self-therapy requires further research. [ABSTRACT FROM AUTHOR]

Introduction and hypothesis: A link between psychiatric comorbidities and overactive bladder symptomatology has been suggested by preclinical and clinical studies. Given this, we hypothesized that a psychiatric history and current treatment with psychotropic medications could be related to the severity of overactive bladder and incontinence symptoms in patients referred to a tertiary care urogynecological center. Methods: One hundred and twenty-seven female patients diagnosed with an overactive bladder were screened for a lifetime history of psychiatric disorders and the type and number of psychotropic medications currently taken. The overall severity of overactive bladder symptoms was assessed using the Indevus Urgency Severity Scale. The severity and impact of urinary incontinence on the quality of life were quantified with the International Consultation on Incontinence Questionnaire-Urinary Incontinence Short Form. Urinary incontinence was further quantified with the aid of the Urinary Distress Inventory-6. The patients were screened for stress urinary incontinence using the Stamey Incontinence Score. Results: A psychiatric history, as well as current use of at least two psychotropic medications, was associated with increased severity of overactive bladder symptoms. A history of depression and current treatment with any selective serotonin reuptake inhibitor was associated with increased severity of stress urinary incontinence symptoms. Current treatment with other psychotropic medications, including sedative-hypnotics and drugs with anticholinergic properties was not related to the severity of overactive bladder and incontinence symptoms. [ABSTRACT FROM AUTHOR]

Electroconvulsive therapy (ECT) remains the most effective therapy in treatment-resistant depression. However, the safety of ECT has been consistently questioned, particularly among elderly patients. We assessed the efficacy and safety of ECT in patients before and after 65 years old. The study was conducted between 2015 and 2018 and included 91 patients (61 under and 29 over 65 years old) with major depression undergoing ECT. The Hamilton Depression Rating Scale was used to evaluate efficacy. Cognitive functions were assessed using: MMSE, RAVLT, Trail Making Test, Stroop Test and Autobiographical Memory Interview-Short Form. ECT was more effective in older patients as compared to younger (p < 0.001). No serious adverse events were observed in either group. Increased blood pressure and arrhythmias were more common in the older compared to the younger group (p = 0.044 and p = 0.047, respectively), while disturbances of consciousness did not differ between groups (p = 0.820). Most of the cognitive functions remained unchanged compared to baseline, whereas the outcomes of MMSE, RAVLT and Stroop tests showed greater improvements in the older compared to the younger group (all p < 0.05). The decline in the retrieval consistency of autobiographical memory was more pronounced in the younger group (p = 0.024). ECT is a highly effective, safe and well-tolerated method of treating depression regardless of age. [ABSTRACT FROM AUTHOR]

The effects of acetylsalicylic acid (ASA) on mood disorders (MD) and on inflammatory parameters in preclinical and clinical studies have not yet been comprehensively evaluated. The aim of this study was to systematically summarize the available knowledge on this topic according to PRISMA guidelines. Data from preclinical and clinical studies were analyzed, considering the safety and efficacy of ASA in the treatment of MD and the correlation of inflammatory parameters with the effect of ASA treatment. Twenty-one studies were included. Both preclinical and clinical studies found evidence indicating the safety and efficacy of low-dose ASA in the treatment of all types of affective episodes in MD. Observational studies have indicated a reduced risk of all types of affective episodes in chronic low-dose ASA users (HR 0.92, 95% CI: 0.88, 0.95, p < 0.0001). An association between ASA response and inflammatory parameters was found in preclinical studies, but this was not confirmed in clinical trials. Further long-term clinical trials evaluating the safety and efficacy of ASA in recurrent MD, as well as assessing the linkage of ASA treatment with inflammatory phenotype and cytokines, are required. There is also a need for preclinical studies to understand the exact mechanism of action of ASA in MD.