Sex differences in the relationship between brain gray matter volume and psychological resilience in late adolescence.

Psychological resilience reflects an individual's ability to adapt and cope successfully in adverse environments and situations, making it a crucial trait in resisting stress-linked mental disorders and physical diseases. Although prior literature has consistently shown that males are more resilient than females, the sex-linked neuroanatomical correlates of psychological resilience are largely unknown. This study aims to explore the sex-specific relation between psychological resilience and brain gray matter volume (GMV) in adolescents via structural magnetic resonance imaging (s-MRI). A cohort of 231 healthy adolescents (121/110 females/males), aged 16 to 20 completed brain s-MRI scanning and Connor-Davidson Resilience Scale (CD-RISC) and other controlling behavioral tests. With s-MRI data, an optimized voxel-based morphometry method was used to estimate regional GMV, and a whole-brain condition-by-covariate interaction analysis was performed to identify the brain regions showing sex effects on the relation between psychological resilience and GMV. Male adolescents scored significantly higher than females on the CD-RISC. The association of psychological resilience with GMV differed between the two sex groups in the left ventrolateral prefrontal cortex extending to the adjacent anterior insula, with a positive correlation among males and a negative correlation among females. The sex-specific association between psychological resilience and GMV might be linked to sex differences in the hypothalamic-pituitary-adrenal axis and brain maturation during adolescence. This study may be novel in revealing the sex-linked neuroanatomical basis of psychological resilience, highlighting the need for a more thorough investigation of the role of sex in future studies of psychological resilience and stress-related illness.

Immunoglobulin-driven Complement Activation Regulates Proinflammatory Remodeling in Pulmonary Hypertension.

Rationale: Pulmonary hypertension (PH) is a life-threatening cardiopulmonary disorder in which inflammation and immunity have emerged as critical early pathogenic elements. Although proinflammatory processes in PH and pulmonary arterial hypertension (PAH) are the focus of extensive investigation, the initiating mechanisms remain elusive.Objectives: We tested whether activation of the complement cascade is critical in regulating proinflammatory and pro-proliferative processes in the initiation of experimental hypoxic PH and can serve as a prognostic biomarker of outcome in human PAH.Methods: We used immunostaining of lung tissues from experimental PH models and patients with PAH, analyses of genetic murine models lacking specific complement components or circulating immunoglobulins, cultured human pulmonary adventitial fibroblasts, and network medicine analysis of a biomarker risk panel from plasma of patients with PAH.Measurements and Main Results: Pulmonary perivascular-specific activation of the complement cascade was identified as a consistent critical determinant of PH and PAH in experimental animal models and humans. In experimental hypoxic PH, proinflammatory and pro-proliferative responses were dependent on complement (alternative pathway and component 5), and immunoglobulins, particularly IgG, were critical for activation of the complement cascade. We identified Csf2/GM-CSF as a primary complement-dependent inflammatory mediator. Furthermore, using network medicine analysis of a biomarker risk panel from plasma of patients with PAH, we demonstrated that complement signaling can serve as a prognostic factor for clinical outcome in PAH.Conclusions: This study establishes immunoglobulin-driven dysregulated complement activation as a critical pathobiological mechanism regulating proinflammatory and pro-proliferative processes in the initiation of experimental hypoxic PH and demonstrates complement signaling as a critical determinant of clinical outcome in PAH.

Out-of-hospital cardiac arrest in high-rise buildings: delays to patient care and effect on survival.

BACKGROUND: The increasing number of people living in high-rise buildings presents unique challenges to care and may cause delays for 911-initiated first responders (including paramedics and fire department personnel) responding to calls for out-of-hospital cardiac arrest. We examined the relation between floor of patient contact and survival after cardiac arrest in residential buildings. METHODS: We conducted a retrospective observational study using data from the Toronto Regional RescuNet Epistry database for the period January 2007 to December 2012. We included all adult patients (≥ 18 yr) with out-of-hospital cardiac arrest of no obvious cause who were treated in private residences. We excluded cardiac arrests witnessed by 911-initiated first responders and those with an obvious cause. We used multivariable logistic regression to determine the effect on survival of the floor of patient contact, with adjustment for standard Utstein variables. RESULTS: During the study period, 7842 cases of out-of-hospital cardiac arrest met the inclusion criteria, of which 5998 (76.5%) occurred below the third floor and 1844 (23.5%) occurred on the third floor or higher. Survival was greater on the lower floors (4.2% v. 2.6%, p = 0.002). Lower adjusted survival to hospital discharge was independently associated with higher floor of patient contact, older age, male sex and longer 911 response time. In an analysis by floor, survival was 0.9% above floor 16 (i.e., below the 1% threshold for futility), and there were no survivors above the 25th floor. INTERPRETATION: In high-rise buildings, the survival rate after out-of-hospital cardiac arrest was lower for patients residing on higher floors. Interventions aimed at shortening response times to treatment of cardiac arrest in high-rise buildings may increase survival.

Automated Data Abstraction of Cardiopulmonary Resuscitation Process Measures for Complete Episodes of Cardiac Arrest Resuscitation.

BACKGROUND: Cardiopulmonary resuscitation (CPR) process measures research and quality assurance has traditionally been limited to the first 5 minutes of resuscitation due to significant costs in time, resources, and personnel from manual data abstraction. CPR performance may change over time during prolonged resuscitations, which represents a significant knowledge gap. Moreover, currently available commercial software output of CPR process measures are difficult to analyze. OBJECTIVE: The objective was to develop and validate a software program to help automate the abstraction and transfer of CPR process measures data from electronic defibrillators for complete episodes of cardiac arrest resuscitation. METHODS: We developed a software program to facilitate and help automate CPR data abstraction and transfer from electronic defibrillators for entire resuscitation episodes. Using an intermediary Extensible Markup Language export file, the automated software transfers CPR process measures data (electrocardiogram [ECG] number, CPR start time, number of ventilations, number of chest compressions, compression rate per minute, compression depth per minute, compression fraction, and end-tidal CO2 per minute). We performed an internal validation of the software program on 50 randomly selected cardiac arrest cases with resuscitation durations between 15 and 60 minutes. CPR process measures were manually abstracted and transferred independently by two trained data abstractors and by the automated software program, followed by manual interpretation of raw ECG tracings, treatment interventions, and patient events. Error rates and the time needed for data abstraction, transfer, and interpretation were measured for both manual and automated methods, compared to an additional independent reviewer. RESULTS: A total of 9,826 data points were each abstracted by the two abstractors and by the software program. Manual data abstraction resulted in a total of six errors (0.06%) compared to zero errors by the software program. The mean ± SD time measured per case for manual data abstraction was 20.3 ± 2.7 minutes compared to 5.3 ± 1.4 minutes using the software program (p = 0.003). CONCLUSIONS: We developed and validated an automated software program that efficiently abstracts and transfers CPR process measures data from electronic defibrillators for complete cardiac arrest episodes. This software will enable future cardiac arrest studies and quality assurance programs to evaluate the impact of CPR process measures during prolonged resuscitations.