Sleep disturbances are a core feature of Post-traumatic Stress Disorder (PTSD), especially in children and adolescents. The existing literature suggests a potential relationship between sleep quality and cognitive function in this population, but empirical studies are limited. This study aimed to investigate the association between sleep quality and cognition in children and adolescents with PTSD attending a public school in Medellín, Colombia.

Using a quantitative, cross-sectional exploratory design, we examined a sample of 130 students (106 females and 24 males) aged 11 to 16 years (mean age = 12.9, SD = 1.35), from sixth to eighth grade. Seventy-one participants met the criteria for PTSD, while 59 served as the control group. Data were collected using the Pittsburgh Sleep Quality Index (PSQI) and the DSM-5 TR+COG Questionnaire of Symptoms Associated with Traumatic Experiences in Childhood or Adolescence and Neurocognitive Symptoms.

Comparative analysis between the PTSD and control groups was conducted using the Student's t-test. Pearson correlation was employed to assess the relationship between sleep quality and neurocognitive function. Significant differences were found between the groups across various sleep dimensions: total score (t(128)=4.85, p<0.001, d=0.85), sleep latency (t(128)=4.11, p<0.001, d=0.72), sleep disturbances (t(128)=3.91, p<0.001, d=0.69), and daytime dysfunction (t(128)=4.36, p<0.001, d=0.76). Additionally, a positive correlation was identified between sleep quality and cognition (r=0.49, p<0.001, 95% CI 0.74 to 0.86).

These findings underscore the significant impact of PTSD on sleep quality and its subsequent effect on cognitive function. Potential clinical implications include the need for interventions targeting sleep disturbances as part of PTSD treatment. This study highlights the intricate relationship between traumatic experiences, cognitive alterations, and sleep quality, calling for further research in this area.

Objectives: The association between anti-Ro/SSA antibodies and the appearance of cardiac rhythm disorders in adults is discussed. We aim to study this relationship, together with active treatments and comorbidities, and its impact on daily clinical practice in adults with systemic autoimmune diseases (SADs).

Methods: This cross-sectional single-center study was conducted in a tertiary hospital between January 2021 and March 2022. A sample of adult patients followed up in the SAD Unit with a diagnosis of an SAD and previously tested for anti-Ro/SSA and anti-La/SSB were recruited. All of them underwent a 12-lead electrocardiogram.

Results: In total, 167 patients were included. In total, 90 (53.9%) were positive for anti-Ro60, 101 (60.5%) for anti-Ro52, and 45 (26.9%) for anti-La/SSB; 52 (31.3%) were triple-negative. In total, 84% were women, and the mean age was 59 years (standard deviation 12.8). The most common SAD was primary Sjögren’s syndrome (34.8%), followed by systemic lupus erythematosus (24.6%) and rheumatoid arthritis (22.8%). A statistically significant relationship was found between anti-Ro52 positivity and cardiac rhythm disorders (relative risk = 2.007 [1.197–3.366]), specifically QTc prolongation (relative risk = 4.248 [1.553–11.615]). Multivariate regressions showed a significant association, with diabetes mellitus being the most related comorbidity. The association between anti-Ro52 antibodies and atrioventricular conduction disorders was not significant.

Conclusions: The presence of anti-Ro52 antibodies in adult patients with SADs is associated with an increased risk of QTc prolongation. The electrocardiographic screening of patients with SAD, anti-Ro52 antibodies, and other risk factors, like diabetes mellitus or QT-prolonging drugs, seems advisable. Those with baseline electrocardiogram abnormalities or additional risk factors should undergo electrocardiographic monitoring.

Annona muricata, also known as soursop, is a member of the Annonaceae family and has a long history of traditional uses. It is an evergreen plant that grows in tropical and subtropical regions of the world, primarily in Africa, South America, and Southeast Asia. The A. muricata plant's miraculous nature is a boon to mankind, and it has been widely used in folk medicine. A. muricata preparations on the market include candies, syrups, beverages, ice creams, and shakes. Several studies have concluded that the plant contains over 212 chemical constituents, such as acetogenins, alkaloids, and phenols. The plant has antibacterial, antiviral, antifungal, antitumor, anthelminthic, analgesic, antiarthritic, hypotensive, anti-inflammatory, and immune-enhancing effects, as well as anti-diabetic activity. Although some toxicities have been reported, the extract of A. muricata is effective and safe. This study aims to formulate and evaluate a herbal antilice cream containing the ethanolic extract of Annona muricata (leaves). Soursop leaves were blended and the extract was obtained by a maceration process. Then, a cream was obtained using the slab technique or an extemporaneous method. The antilice cream was optimized by preparing three formulations (F1, F2, F3) using different concentrations of the extract and ingredients. The formulation wasevaluated for various parameters, like physical appearance, irritancy, pH, viscosity, spreadability, washability, greasiness, and antilice activity .

Patients admitted with autoimmune thrombocytopenic purpura (ITP) are high-risk due to their susceptibility to bleeding and limitations on medical interventions. Heart failure (HF) is a widespread condition that significantly impairs quality of life, complicating the management of ITP. These patients often use blood thinners, exacerbating their risk profile. This study analyzed the National Inpatient Sample database for 2019-2020 to examine the impact of HF on ITP patients. The cohort included 27,885 patients hospitalized with ITP, of which 1,950 (7%) also had HF. Multivariate regression analysis was used to assess the outcomes. The results showed no significant difference in mortality (OR 1.1, 95% CI 0.52-2.29, P=0.795) and length of stay (+1.14 days, 95% CI 0.32-1.95, P=0.006) between the groups. However, hospitalization costs increased significantly for patients with HF (+17,762 USD, 95% CI 3,439-35,439, P=0.04). HF patients had higher odds of acute respiratory failure (OR 2.44, 95% CI 1.31-4.52, P=0.005), ICU admission (OR 1.86, 95% CI 1.015-3.41, P=0.044), and acute coronary syndrome (OR 6.27, 95% CI 1.05-37.47, P=0.04). No significant differences were found in major (OR 1, 95% CI 0.66-1.51, P=0.983) and minor bleeding (OR 1.36, 95% CI 0.33-5.58, P=0.666), blood transfusions (OR 0.81, 95% CI 0.52-1.25, P=0.352), platelet transfusions (OR 0.98, 95% CI 0.73-1.30, P=0.897), venous thromboembolism (OR 0.93, 95% CI 0.36-2.38, P=0.887), mechanical ventilation (OR 1.79, 95% CI 0.92-3.48, P=0.084), cardiac arrest (OR 3.04, 95% CI 0.65-14.11, P=0.156), acute kidney injury (OR 1.07, 95% CI 0.77-1.47, P=0.661), and sepsis (OR 1.61, 95% CI 0.59-4.39, P=0.346). In summary, HF in ITP patients is associated with higher hospitalization costs, increased acute respiratory failure, ICU admissions, and cardiac events, but not mortality or bleeding. Effective HF management in ITP patients is crucial for mitigating adverse outcomes and optimizing care.

Schizophrenia is a serious and chronic psychiatric disorder that affects approximately 1% of the global population. Characterized by a wide range of symptoms, schizophrenia is multifactorial, with genetic, environmental, and stress factors havinga key role in its development. In this context, cortisol, a stress-related hormone, and microglia, immune cells of the central nervous system, emerge as key players in understanding schizophrenia. In this study, the interconnections between cortisol, microglia, and neuroinflammation in the aetiology of schizophrenia were explored. Recent scientific evidence highlights the importance of these elements in modulating the stress response and their potential impact on neuroinflammation and the development of schizophrenia. Furthermore, the clinical relevance of these interactions and their potential for the development of new therapeutic approaches are highlighted. Through this analysis, we sought to provide a comprehensive view of the complex interactions between cortisol, microglia, and neuroinflammation and their role in schizophrenia, highlighting the need for future investigations and integrated approaches to treating this debilitating mental illness. This review involved an extensive bibliographic search in electronic databases, such as Google Scholar, PubMed, and ScienceDirect, as well as other sources, including books and websites. Descriptors such as "schizophrenia", "glial cells", "cortisol", "oxidative stress", and "neuroinflammation" were used, without systematic search inclusion and exclusion criteria. Relevant studies were selected based on the evaluation of titles and abstracts, prioritizing recent publications in Portuguese, English, and Spanish. The results covered information about schizophrenia, genetic and biochemical aspects, and treatments, presented through narrative texts and figures.

Keywords: psychiatric disorder; hormone; adrenal glands; glial cell; neuronal inflammation

Background and aims: Stanford type A aortic dissection (AD) is a degenerative aortic remodelling disease marked by exceedingly high mortality without effective pharmacologic therapies. Smooth muscle cells (SMCs) lining tunica media adopt a range of states, and their transformation from contractile to synthetic phenotypes fundamentally triggers AD. However, the underlying pathomechanisms governing this population shift, and subsequent AD, particularly at distinct disease temporal stages, remain elusive.

Methods: Ascending aortas from nine patients undergoing ascending aorta replacement and five individuals undergoing heart transplantation were subjected to single-cell RNA sequencing. The pathogenic targets governing the phenotypic switch of SMCs were identified by trajectory inference, functional scoring, single-cell regulatory network inference, and clustering, regulon, and interactome analyses, and confirmed using human ascending aortas, primary SMCs, and a β-aminopropionitrile monofumarate-induced AD model.

Results: The transcriptional profiles of 93 397 cells revealed a dynamic temporal-specific phenotypic transition and marked elevation of the activator protein-1 (AP-1) complex, actively enabling synthetic SMC expansion. Mechanistically, tumour necrosis factor signalling enhanced AP-1 transcriptional activity by dampening mitochondrial oxidative phosphorylation (OXPHOS). Targeting this axis with the OXPHOS enhancer coenzyme Q10 or AP-1-specific inhibitor T-5224 impedes phenotypic transition and aortic degeneration while improving survival by 42.88% (58.3%-83.3% for coenzyme Q10 treatment), 150.15% (33.3%-83.3% for 2-week T-5224), and 175.38% (33.3%-91.7% for 3-week T-5224) in the β-aminopropionitrile monofumarate-induced AD model.

Conclusions: This cross-sectional compendium of cellular atlases of human ascending aortas during AD progression provides previously unappreciated insights into a transcriptional programme permitting aortic degeneration, highlighting a translational proof of concept for an anti-remodelling intervention as an attractive strategy to manage temporal-specific AD by modulating the tumour necrosis factor-OXPHOS-AP-1 axis.