Explore the vast range of titles available.

لا شك في أن الرئيس الرابع والأربعين للولايات المتحدة الأميركية سيجد في انتظاره سلسلة من التحديات الحاسمة، المعقدة والمتشابكة في الشرق الأوسط، التي تتطلب إيلاءها اهتماما عاجلا. ذلك أن النموذج الذي اعتمده جورج بدليو بوش القائم على تغيير أنظمة الحكم ونشر الديمقراطية بالقوة لم يعد يتلاءم والظروف المتغيرة التي ستواجه الإدارة الجديدة على الأرجح الحاجة ماسة إذن لأفكار جديدة، وتحليلات غير حزبية، وتوصيات حصيفة. والكتاب الذي بين أيديكم يفي بتلك الحاجة على أفضل وجه. في اتسعادة التوازن، تتضافر جهود الخبراء والمختصين بشؤون الشرق الأوسط من مجلس العلاقات الخارجية ومركز صبان لسياسة الشرق الأوسط بمعهد بروكنغز، لتطرح استراتيجية أميركية جديدة لمنظمة حيوية لكن متفجرة كالشرق الأوسط فبناء على أبحاث ميدانية معنقة، قام هؤلاء الخبراء ببلورة مجموعة من التوصيات السياسية برسم الرئيس الأميركي الجديد وقد قامت بفحصها وتمحيصها ونقدها هيئة من المختصين من كلا الحزبين يتمتعون بخبرة سياسية واسعة ومعرفة غنية بالمنطقة، هذا التمرين في تخطيط السياسات الذي استغرق سنة كاملة هو الأول من نوعه على الإطلاق، الذي يوحد جهود وقدرات العاملين في هاتين المؤسستين المحترمتين بالسياسة الخارجية لتنصب على درس وتحليل واحدة من أخطر وأهم مناطق العالم. وكل فصل من هذا الكتاب يستضيف اثنين أو أكثر من الباحثين في مجلس العلاقات الخارجية ومعهد بروكنغز لمعاينة واستعراض التحديات التي ستواجه الرئيس المقبل.

Suicidal ideation and trauma exposure are significant health challenges worldwide, and their interaction increases their burden on individuals and communities. However, limited research has been devoted to these conditions in low- and middle-income countries, where the majority of the burden of these disorders exists. Additionally, unique cultural factors that may contribute to differential relationships in these symptoms and disorders make this an important area to explore. This study examines relationships between the number and types of adverse exposures, PTSD symptoms and severity, depression and suicidal ideation in a sample of Cambodian women with experiences of trauma using logistic and linear regressions. Overall, PTSD severity significantly contributes to suicidal ideation, with hyperarousal symptoms playing a particularly influential role in this association. Further, adverse experiences, including physical abuse and parental mental health problems, contributed significantly to increased suicidal ideation. Lastly, depression severity partially mediates the relationship between PTSD severity and suicidal ideation. These results illustrate the significant role of PTSD in the experience of suicidal ideation, particularly within regions like Cambodia with high trauma loads. These findings point to psychological constructs that may be especially important to include in suicidality screening tools and to target within prevention and intervention efforts.

Forms of cognitive and behavioral therapies (CBTs), including prolonged exposure and cognitive processing therapy, have been empirically validated as efficacious treatments for posttraumatic stress disorder (PTSD). However, the assumption that PTSD develops from dysregulated fear circuitry possesses limitations that detract from the potential efficacy of CBT approaches. An analysis of these limitations may provide insight into improvements to the CBT approach to PTSD, beginning with an examination of negative affect as an essential component to the conceptualization of PTSD and a barrier to the implementation of CBT for PTSD. As such, the literature regarding the impact of negative affect on aspects of cognition (i.e., attention, processing, memory, and emotion regulation) necessary for the successful application of CBT was systematically reviewed. Several literature databases were explored (e.g., PsychINFO and PubMed), resulting in 25 articles that met criteria for inclusion. Results of the review indicated that high negative affect generally disrupts cognitive processes, resulting in a narrowed focus on stimuli of a negative valence, increased rumination of negative autobiographical memories, inflexible preservation of initial information, difficulty considering counterfactuals, reliance on emotional reasoning, and misinterpretation of neutral or ambiguous events as negative, among others. With the aim to improve treatment efficacy of CBT for PTSD, suggestions to incorporate negative affect into research and clinical contexts are discussed.

Whether short-term, low-potency opioid prescriptions for acute pain lead to future at-risk opioid use remains controversial and inadequately characterized. Our objective was to measure the association between emergency department (ED) opioid analgesic exposure after a physical, trauma-related event and subsequent opioid use. We hypothesized ED opioid analgesic exposure is associated with subsequent at-risk opioid use. Of 1441 subjects completing 3-month follow-up, 872 participants were included for analysis. At-risk opioid use occurred within 3 months in 33/620 (5.3%, CI: 3.7,7.4) participants without ED opioid analgesic exposure; 4/16 (25.0%, CI: 8.3, 52.6) with ED opioid prescription only; 17/146 (11.6%, CI: 7.1, 18.3) with ED opioid administration only; 12/90 (13.3%, CI: 7.4, 22.5) with both. Controlling for clinical factors, adjusted odds ratios (aORs) for at-risk opioid use after ED opioid exposure were: ED prescription only: 4.9 (95% CI 1.4, 17.4); ED administration for analgesia only: 2.0 (CI 1.0, 3.8); both: 2.8 (CI 1.2, 6.5). ED opioids were associated with subsequent at-risk opioid use within three months in a geographically diverse cohort of adult trauma patients. This supports need for prospective studies focused on the long-term consequences of ED opioid analgesic exposure to estimate individual risk and guide therapeutic decision-making.

Adverse posttraumatic neuropsychiatric sequelae are common after trauma. Early identification of individuals at risk for these outcomes could enable the deployment of preventive interventions to survivors at greatest risk. Smartphone keystroke biomarkers show promise in identifying individuals with neuropsychiatric symptoms; however, to our knowledge, no research has examined whether they can be used to identify symptoms in the aftermath of trauma. This study evaluates whether passively collected keystroke data from smartphone use in daily life could identify individuals with high symptom levels, as well as worsening or recovery of symptoms, after trauma exposure. Data from a diverse cohort of individuals presenting to 27 emergency departments after trauma were analyzed. Inclusion criteria were presenting to the emergency department within 72 hours of trauma, age 18-75, and the ability to speak and read English. Exclusion criteria were solid organ injury, significant hemorrhage, operative intervention, or likely admission for over 72 hours. Participants installed an app that passively collected keystroke data during use of any app on their smartphone, beginning in the emergency department. Participants also completed serial symptom assessments over 8 weeks after trauma exposure. A total of 3445 patients met study criteria, provided informed consent, and completed assessments in the emergency department. Of these, 1072 (mean age 40, SD 13; 616/1072, 57.46%, women; 565/1072, 52.71% non-Hispanic Black) installed the app on their Android smartphone and completed the 8-week assessment and were therefore included in analyses. Keystroke biomarkers related to typing speed, identified using bivariate linear mixed models controlling for false discovery rates, were associated with elevated pain, reexperiencing, and mental fatigue (absolute values of rs=0.22-0.25, Ps=.02). Separate change-of-operation and scrolling keystroke biomarkers were associated with increased reexperiencing symptoms (r=0.18, P=.047) and mental fatigue (rs=0.18-0.19, Ps=.031-.047). Further, changes in specific keystroke biomarkers were associated with worsening or recovery of pain (rs=0.07-0.10, Ps=.02), somatic symptoms (rs=0.02, Ps=.02), mental fatigue (rs=0.02-0.04, Ps=.02), sleep disturbance (absolute rs=0.07-0.09, Ps=.02), reexperiencing (rs=0.02-0.04, Ps=.02), and hyperarousal (rs=0.02-0.04, Ps=.02). In general, slower typing and scrolling speeds were associated with higher symptom levels, with small to medium effect sizes. Keystroke data passively collected via smartphone use may help identify individuals with significant or changing posttraumatic symptoms. Future research should continue to explore these keystroke biomarkers and whether they can be leveraged to connect vulnerable trauma survivors to appropriate services. Overall, these results add to the literature, indicating that passively collected keystroke data may help identify individuals with neuropsychiatric symptoms or changes and are, to our knowledge, the first to test whether keystroke biomarkers are useful in the aftermath of trauma. This represents a critical period during which preventive interventions could be deployed to reduce the long-term burden of trauma-related sequelae.

Patients exposed to trauma often experience high rates of adverse post-traumatic neuropsychiatric sequelae (APNS). The biological mechanisms promoting APNS are currently unknown, but the microbiota-gut-brain axis offers an avenue to understanding mechanisms as well as possibilities for intervention. Microbiome composition after trauma exposure has been poorly examined regarding neuropsychiatric outcomes. We aimed to determine whether the gut microbiomes of trauma-exposed emergency department patients who develop APNS have dysfunctional gut microbiome profiles and discover potential associated mechanisms. We performed metagenomic analysis on stool samples (n = 51) from a subset of adults enrolled in the Advancing Understanding of RecOvery afteR traumA (AURORA) study. Two-, eight- and twelve-week post-trauma outcomes for post-traumatic stress disorder (PTSD) (PTSD checklist for DSM-5), normalized depression scores (PROMIS Depression Short Form 8b) and somatic symptom counts were collected. Generalized linear models were created for each outcome using microbial abundances and relevant demographics. Mixed-effect random forest machine learning models were used to identify associations between APNS outcomes and microbial features and encoded metabolic pathways from stool metagenomics. Microbial species, including Flavonifractor plautii, Ruminococcus gnavus and, Bifidobacterium species, which are prevalent commensal gut microbes, were found to be important in predicting worse APNS outcomes from microbial abundance data. Notably, through APNS outcome modeling using microbial metabolic pathways, worse APNS outcomes were highly predicted by decreased L-arginine related pathway genes and increased citrulline and ornithine pathways. Common commensal microbial species are enriched in individuals who develop APNS. More notably, we identified a biological mechanism through which the gut microbiome reduces global arginine bioavailability, a metabolic change that has also been demonstrated in the plasma of patients with PTSD.

Purpose Post-traumatic stress (PTS) symptoms are highly comorbid with substance use (i.e., alcohol, tobacco, and cannabis). Few studies have investigated potential individual-, household-, and neighborhood-level socioeconomic effect modifiers of this comorbidity in longitudinal analyses. We aim to examine interactions between this multi-level environment and PTS symptoms on future substance use behaviors. Methods Data were drawn from the Advancing Understanding of RecOvery afteR traumA (AURORA) study, including 2943 individuals who presented to the emergency department (ED) within 72 h of a traumatic event. Frequency of tobacco, alcohol, cannabis use, and PTS symptoms were reported at 6 timepoints. Mixed effect Poisson models, clustered by state, were used to generate incidence rate ratios (IRRs) substance use, both cross-sectionally and prospectively. Moderation analysis of PTS and substance use, stratified by household income and area deprivation index (ADI), was conducted using mixed effect models and parallel process growth curves. Results Significant associations were observed between PTS with tobacco, alcohol, and cannabis use frequency cross-sectionally, and for tobacco and alcohol and PTS exposure prospectively. Lower income (P < 0.001) and higher deprivation (P < 0.001) were associated with tobacco use, while higher income (P < 0.001) and less deprivation (P = 0.01) were associated with increased alcohol use. We found modest modification by household income for alcohol and tobacco, and little evidence of modification by neighborhood ADI. Conclusions Household income had greater evidence of effect modification for substance use, compared to neighborhood-level ADI. Our findings demonstrate that household indicators of socioeconomic status likely modify the relationship between PTS and substance use.

Residential segregation is associated with differential exposure to air pollution. Hippocampus structure and function are highly susceptible to pollutants and associated with posttraumatic stress disorder (PTSD) development. Therefore, we investigated associations between residential segregation, air pollutants, hippocampal neurobiology, and PTSD in recent trauma survivors. Participants ( N  = 278; 34% non-Hispanic white, 46% Non-Hispanic Black, 16% Hispanic) completed multimodal neuroimaging two weeks after trauma. Yearly averages of air pollutants (PM 2.5 and NO 2 ) and racial/economic segregation (Index of Concentration at the Extremes) were derived from each participant’s address. Linear models assessed if air pollutants mediated associations between segregation and hippocampal volume, threat reactivity, or parahippocampal cingulum fractional anisotropy (FA) after covarying for age, sex, income, and 2-week PTSD symptoms. Further models evaluated if pollutants or segregation prospectively predicted PTSD symptoms six months post-trauma. We found that non-Hispanic Black participants lived in neighborhoods with significantly greater segregation and air pollution compared to Hispanic and non-Hispanic white participants ( ps  < 0.001). PM 2.5 concentration was positively correlated with threat reactivity ( r (276) = 0.16, p  < 0.006), while NO 2 concentration was positively correlated with hippocampus volume ( r (276) = 0.17, p  < 0.005) and negatively correlated with white matter tract FA ( r (276) = −0.18, p  < 0.003). There was a significant indirect effect of NO 2 between segregation and FA values (β = 0.08, 95% CI[0.01, 0.15]), and an indirect effect of PM 2.5 between segregation and threat reactivity (β = −0.08, 95% CI[−0.14, −0.01]). There was no direct effect of segregation on hippocampal features. Pollutants and segregation were not associated with PTSD symptoms. In conclusion, residential segregation is associated with greater air pollution exposure, which is in turn associated with variability in hippocampal features among recent trauma survivors. Further research is needed to assess relationships between other environmental factors and trauma and stress-related disorders.

Tobacco smoking and drinking alcohol are common substance use behaviors influenced by both genetic risk and environmental exposures. Traumatic events are highly prevalent, affecting about 70% of people in their lifetime. After trauma, it is unclear what role post-traumatic stress disorder (PTSD) symptoms play in substance use behaviors when accounting for this genetic risk. We used data from the Advancing Understanding of RecOvery afteR traumA (AURORA), which included 2973 participants recruited at emergency departments (EDs) within 72 h of a traumatic event and followed over time. We measured PTSD symptoms via PTSD Checklist for the DSM-5. Tobacco and alcohol consumption as frequency, quantity, and quantity-frequency in the past 30 days. We generated polygenic risk scores with continuous shrinkage for cross-ancestry estimation (PRS-CSx). We tested for main effects between PRS-CSx scores and interactions with PTSD using quasipoisson regression, with week 8 PTSD symptoms and month 6 substance use behaviors after the traumatic event. Tobacco PRS-CSx score increased the risk of tobacco use by 14% (95% CI: 1.01, 1.29, p = 0.03), and alcohol PRS-CSx score did not demonstrate consistent associations in the whole cohort (IRR: 1.08, 95% CI: 0.97, 1.19, p = 0.16). When stratified by ancestry group, both tobacco (IRR: 1.36, 95% CI: 1.14, 1.61, p < 0.001) and alcohol (IRR: 1.24, 95% CI: 1.07, 1.44, p = 0.005) PRS-CSx scores were associated with their respective outcomes in the European ancestry subcohort. Participants with lower genetic risk had stronger associations between re-experiencing symptoms and tobacco use, while participants with higher genetic risk demonstrated weaker association between re-experiencing symptoms and tobacco use. A similar pattern was observed for negative alterations in cognition/mood (NACM) symptoms—participants with lower PRS-CSx scores had stronger associations between NACM symptoms with tobacco use, compared to participants with higher PRS-CSx scores. These interactions were both statistically significant, suggesting an antagonistic effect between PRS-CSx scores and PTSD symptoms on tobacco use.

Objective Several gaps remain in the understanding of the onset, dynamic transitions, and associated risk factors of adverse posttraumatic neuropsychiatric sequelae (APNS) in the acute post‐trauma window. Based on serial assessments of symptoms from a large cohort study, we identified homogeneous statuses across multiple APNS symptom domains and investigated the dynamic transitions among these statuses during the first 2 months after trauma exposure. Furthermore, we studied how symptom onset and transitions are affected by equity‐relevant characteristics. Methods The analysis was based on 2557 participants enrolled in the Advancing Understanding of RecOvery afteR traumA (AURORA). APNS symptoms comprised pain, depression, sleep discontinuity, nightmares, avoidance, re‐experience, anxiety, hyperarousal, somatic symptoms, and mental fatigue. We identified the homogeneous status of APNS symptoms at baseline, 1 month, and 2 months, and explored transition probabilities among these statuses using latent transition analysis. Equity‐relevant characteristics included gender, race, education, family income, childhood trauma, and area deprivation. Results Three homogeneous statuses–low‐, moderate‐, and severe‐symptom–were identified. While the majority of trauma survivors with severe‐ or moderate‐symptom status maintained the same status over time, some transitioned to a less severe symptom status, particularly within the first month. Specifically, females, non‐whites, and those with higher childhood trauma were associated with a decreased likelihood of transitioning to a less severe symptom status. From one to 2 months, lower income was associated with a decreased likelihood of transitioning from moderate‐to low‐symptom status. Conclusions The findings can inform early intervention strategies for APNS, potentially reducing health disparities among trauma survivors. Highlights We investigated the onset, dynamic transitions, and associated risk factors of adverse posttraumatic neuropsychiatric sequelae (APNS) using latent transition analysis. Three homogeneous APNS symptom statuses (low, moderate, and severe) were identified. While most survivors maintained the same status, some followed the recovery trajectory by transitioning to a lesser symptom status. Females, non‐whites, those with childhood trauma, and those with a lower income were less likely to follow a recovery trajectory. Our findings can guide preventive interventions for APNS among trauma survivors.