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In this prospective cohort of 1,012 Swiss hospital employees, 3 different assays were used to screen serum for SARS-CoV-2 antibodies. Seropositivity was 1%; the positive predictive values of the lateral-flow immunoassay were 64% (IgG) and 13% (IgM). History of fever and myalgia most effectively differentiated seropositive and seronegative participants.
The analysis of the geographical distribution of hospital cases is obviously important for the purpose of planning hospital services, but it is of even greater significance in the planning of psychiatric services. This concern motivated our seven-year-long study, which examined hospitalization risks among various categories of psychiatric disorders in the major German city of Hamburg. Our database encompassed 77% (n = 64,000) of all psychiatric admissions in a total of 41 hospitals, most of which are general hospitals. In order to carry out the geographical analysis we employed a new statistical method based on a mixture distribution model. According to our findings, the strongest indications of an increased frequency were among male cases of schizophrenia, drug abuse and organic psychoses, and female cases of neurotic disorders, personality disorders, drug abuse and schizophrenia. We found that some areas are exposed to a risk of hospitalization for these diagnostic categories which is more than 50% above the reference. Contrary to other authors we did not identify an increased frequency of admission concentrated in the inner-city area for any of the diagnostic groups. The risk of hospitalization for schizophrenics was almost entirely associated with the close proximity of psychiatric units, while the risks for neuroses and personality disorders, as well as alcohol and drug abuse, appeared to be concentrated in areas of low social status. However, a statistically relevant correlation between an increased risk of hospitalization and low social status could be determined only for drug abuse and alcoholism. In the end, we did identify two areas in which there was an increased risk of hospitalization for several diagnostic groups, and this information will undoubtedly facilitate the planning of hospital and psychiatric services. The fact that our findings deviate to some extent from other authors – especially with respect to neuroses and personality disorders, but also to addiction – can be attributed to the inclusion of psychiatric cases from general hospitals in our geographic analysis.
Adolescence is a critical period for suicidal risk. Suicide currently ranks as the second or third leading cause of mortality among adolescents in developped countries. It has been shown that a history of suicidal act, of depressive disorder and of a substance use disorder (SUD), alcohol and drugs, are the most prominent risk factors for suicidal behaviour among adolescents.
Data on alcohol and drug use disorders and suicide consisted primarily of reports on alcohol use disorders and, to a lesser extent, opioid use disorder. The magnitude of the association with other drugs is still unclear.
The relationships between substance use disorder and suicidal behaviour are multiple: In the long term, SUD may be associated with increases in stress and co-occuring psychopathology (poor self esteem, feeling of worthlessness, isolation).These elements may reach a level where a suicide attempt is viewed as a means to cope with perceived unsolvable difficulties. During life crises, SUD can also be responsible for inhibiting adaptative coping and desinhibiting suicidal behaviour. Finally, SUD and suicidal behaviour share common vulnerability factors: history of childhood abuse, genetically determined dimensions such as impulsivity or psychiatric disorders, particularly unipolar depressive and bipolar disorder.
Given the comorbidity between SUD and suicide, it is essential for treatment and prevention that all suicidal adolescents be screened for SUD and vice versa. Ideally, adolescents who receive diagnosis of SUD and co-occuring suicidality should follow an integrated treatment protocol that addresses both conditions.
Cariprazine is a potent D3/D2 partial agonist with preferential binding to D3 receptors.
To evaluate the efficacy and safety of cariprazine versus placebo in acute exacerbation of schizophrenia.
A multinational, multicenter, double-blind, randomized, placebo- and active-controlled, fixed-dose trial in patients aged 18–60 years with DSM-IV-TR-defined schizophrenia, current psychotic episode < 2 weeks, and PANSS total score between 80 and 120. After 1-week washout, patients received 6-weeks treatment (cariprazine 1.5, 3.0, or 4.5 mg/d, risperidone 4.0 mg/d, or placebo) and 2-week safety follow-up. Risperidone was used to assess assay sensitivity. Primary and secondary efficacy: baseline to Week 6 change (LOCF) in PANSS total and CGI-S scores, respectively. Safety: adverse events (AEs), vital signs, laboratory measures, extrapyramidal symptom (EPS) scales.
Of 732 randomized patients, 64% completed the study. Mean baseline PANSS (98) and CGI-S scores (4.8) were similar across groups. PANSS total score improvement at Week 6 was statistically significant versus placebo for cariprazine 1.5 mg/d, 3.0 mg/d, and 4.5 mg/d (placebo-adjusted improvements: −7.5, −8.9, −10.4, respectively; P < .001; LOCF) and risperidone (−15.0, P < .001, LOCF); significant improvement on CGI-S was demonstrated for all active treatments (P < .05). The most common cariprazine AEs were insomnia, EPS, akathisia, sedation, nausea, dizziness, and constipation. AE discontinuation rates were 15% for placebo, 10%, 5% and 8% for cariprazine 1.5, 3.0, and 4.5 mg/d, respectively, and 9% for risperidone 4.0 mg/d.
Cariprazine significantly improved PANSS and CGI-S scores versus placebo in acute exacerbation of schizophrenia and was generally well tolerated.
Clinically significant depressive symptoms are common in schizophrenia, and are associated with greater functional impairment and worse outcomes.
To evaluate the effect of lurasidone in patients with a DSM-IV-TR diagnosis of schizophrenia who presented with significant depressive symptoms.
Pooled data were analyzed from 4, six-week, double-blind, placebo-controlled schizophrenia trials, with available MADRS data. Patients with an acute exacerbation of schizophrenia were randomized to fixed, 40–160 mg (n=902) once-daily doses of lurasidone, or placebo (n=439). LOCF-endpoint data were analyzed using ANCOVA. MADRS remission was defined as an endpoint score <10.
At baseline, 45.0% and 24.5% of subjects had a MADRS score of ≥12, and ≥16 respectively. Treatment with lurasidone was associated with significantly greater improvement in the MADRS at LOCF-endpoint compared with placebo in the total sample (-2.8 vs. -1.4; p<0.001), and in each baseline depression severity subgroup: MADRS ≥12 (-6.7 vs. -4.8; p<0.005), and MADRS ≥16 (-9.3 vs. -6.3; p<0.005). Overall, the largest effect size was observed for the 160 mg dose of lurasidone (0.43). For the subgroup with MADRS≥16 at baseline, higher depression remission rates were observed for lurasidone 160 mg (47.8%) compared with lurasidone 80 mg (38.6%) and lurasidone 40 mg (28.6%).
In this pooled, post-hoc analysis, 40-160 mg once-daily doses of lurasidone significantly reduced the severity of depressive symptoms in patients with schizophrenia. Daily doses of 160 mg demonstrated the largest effect size. These results warrant further evaluation of lurasidone in patients with schizophrenia and co-morbid depression.
Effectiveness studies of therapeutic switching of antipsychotics provide valuable clinical information.
Assess effectiveness of switching patients to lurasidone.
To evaluate 3 dosing strategies when switching patients to lurasidone.
Patients were randomized to three open-label lurasidone dosing strategies: 40mg/day for 14 days (n=74); 40mg/day for 7 days then 80mg/day for 7 days (n=88); and 80mg/day for 14 days (n=82) and stratified by their previous treatment (sedating vs non-sedating). Prior antipsychotic was tapered (50% step-down, day 8, discontinued day 14), followed by 4 weeks of flexible dose treatment (40-120 mg/day). Primary outcome was time to treatment failure (TTF). Of the 198 subjects completing core 6-week study, 149 (75.3%) enrolled in a 6-month extension study.
Switching to lurasidone was well tolerated; 198 (81.1%) of subjects completed core study, 19 (7.9%) subjects experienced treatment failure of which 16 (6.7%) discontinued due to an AE. No clinically relevant differences were noted among the 3 dosing strategies. TTF was earlier in patients previously receiving sedating antipsychotics vs. non-sedating (log rank p=0.101). Core study yielded LS mean (SE) within-group improvement on PANSS total score -5.3 (±0.7), LOCF with further improvement of -1.5 (±0.9), LOCF, at Month 6 from extension baseline. Ninety-eight subjects (65.8%) completed extension phase. Premature discontinuation causes included consent withdrawal (12.1%) and AEs (11.4%). Weight and lipid changes at 6 months were minimal.
Switching to lurasidone was safe and well tolerated regardless of initial dosing strategy. Switched patients maintained or improved symptom control during core and extension treatment.
Long-term head-to-head studies comparing atypical antipsychotics are important for clinical decision making.
To evaluate long-term treatment of schizophrenia with lurasidone (LUR) vs. quetiapine XR (QXR; Study 234), or risperidone (RIS; Study 237).
To assess efficacy and safety of lurasidone relative to other antipsychotics.
In study 234(efficacy and safety), subjects received 12 months double-blind, flexible-dose lurasidone(40-160 mg/day) or QXR(200-800 mg/day) after completing a 6 week, randomized, double-blind, placebo-controlled trial with LUR or QXR. In Study 237 (safety) clinically stable adult outpatients received 12-months double-blind treatment with flexible-dose LUR 40-120 mg/day or RIS 2-6 mg/day.
Study 234: continued treatment of LUR responders (n=139) reduced relapse risk by 27.2% vs. continued QXR treatment of QXR responders (n=79). Hospitalization risk was 56.7% lower with LUR vs. QXR. More LUR subjects achieved sustained remission vs. QXR (61.9% vs. 46.3%; p=0.043; 12 months, LOCF), and lower all-cause discontinuation (48% vs 61%). Triglycerides were reduced with LUR; total and LDL cholesterol were unchanged or reduced. Median prolactin change was +0.6 for LUR vs. -0.7 ng/mL for QXR. Study 237: clinically significant weight gain was observed with LUR 13%) vs. RIS (19%) with median change in prolactin 0.4 vs. 14.8 ng/mL, respectively. Comparable efficacy was observed for LUR and RIS (change from baseline in PANSS total score:-4.7 vs. -6.5, and CGI-Severity score:-0.4 vs. -0.4, respectively).
The results of these two 12-month trials suggest that lurasidone is safe and well-tolerated with efficacy comparable to quetiapine XR and risperidone for long-term treatment of schizophrenia.
Lurasidone has demonstrated efficacy treating adults with schizophrenia, the majority of them with chronic, multi-episode schizophrenia.
To assess baseline characteristics and evaluate efficacy of lurasidone in patients with early-stage schizophrenia (ESS).
Evaluate efficacy of lurasidone in patients with ESS.
A pooled analysis of patients with ESS (defined as onset of illness within 3 years of study entry) from three, 6-week, randomized, placebo-controlled, phase 3 trials was performed. Additional analysis was conducted for patients with onset within 5 years. Efficacy was evaluated using a mixed-model repeated-measures analysis of change in PANSS total score and CGISeverity score. Treatment response was defined as ≥20% improvement in PANSS total score from baseline.
857 subjects were randomized to lurasidone and 366 to placebo of which 102(11.9%) lurasidone and 44(12.0%) placebo subjects had ESS (onset within 3 years). Among 146 ESS subjects, 70.5% were male, mean age was 28.6 years. Baseline PANSS total and CGI-S scores were 96.8 and 5.0 respectively. Lurasidone treatment of early-stage schizophrenia subjects showed significant improvement vs placebo in PANSS total score (-25.9 vs -17.3; p< 0.05, effect size=0.42), PANSS positive (-9.6 vs 6.0; p< 0.01) and negative (-5.6 vs -3.2; p=0.014) subscale scores, and improvement in CGI-S score (-1.7 vs -1.3; p=0.089, effect size=0.36). Responder rates were 69% for lurasidone vs 48% for placebo (NNT=5). Similar results were observed in subjects with within 5 years of onset of illness.
In this subgroup analysis, lurasidone was effective in the treatment of patients with early-stage schizophrenia.
Agitation is a common presentation among patients hospitalized for an acute exacerbation of schizophrenia. Rapid and effective control of agitation is an important early treatment goal.
The aim of this post-hoc analysis was to evaluate the efficacy of lurasidone in reducing agitation in patients with an acute exacerbation of schizophrenia.
The analysis was performed on pooled data from 5 six-week, placebo-controlled trials in the subgroup of patients with an acute exacerbation of schizophrenia who met (n=773), or did not meet (n=754), criteria) for agitation (PANSS-Excited Component [EC] score ≥14 at baseline, Citrome, J Clin Psych 2007;68:1876-1885). Patients were randomized to fixed once-daily doses of lurasidone (40-160 mg).
The mean baseline PANSS-EC scores were similar for lurasidone vs. placebo in the high (16.7 vs. 16.8) and low (10.9 vs. 10.7) agitation subgroups. In the high agitation subgroup, treatment with lurasidone (vs. placebo) was associated with significantly greater improvement in PANSS-EC scores at days 3/4 (-2.0 vs. -1.3; p<0.001) and day 7 (-2.6 vs. -1.8; p<0.001). At week 6 endpoint, improvement on lurasidone vs. placebo was greater in the high vs. low agitation groups on the PANSS-EC score (effect size, 0.43 vs. 0.31), and comparable on the PANSS total score (effect size, 0.57 vs. 0.58).
In this pooled post-hoc analysis, treatment with lurasidone significantly reduced agitation by day 3/4 in patients hospitalized with an acute exacerbation of schizophrenia. The magnitude of improvement at week 6 was similar in both the high and low agitation groups.
Atypical antipsychotics bind to multiple receptor types and subtypes. Improved outcomes in schizophrenia are linked to activity at D2 and serotonin receptors 5-HT7, 5-HT2A and 5-HT1A.
To characterize the receptor-binding profile of lurasidone and other antipsychotics.
To compare receptor-binding profiles of antipsychotics.
Replicated, side-by-side receptor-binding assays used human recombinant receptors (for 5-HT7, α2A, and α2C) or membrane-fractions of animal CNS tissue. Affinities were determined via Hill plot analysis for IC50values; Ki values were determined using Ki=IC50/(1+ S/Kd) (S=concentration of competing radioligand, Kd=dissociation constant).
Lurasidone displayed potent binding and full antagonism at dopamine D2(Ki, 1.68nM) and serotonin 5-HT2A(Ki, 2.03nM) receptors (the highest D2affinity of all tested agents). Lurasidone's dopamine binding was selective for D2receptors. Unlike other antipsychotics tested, lurasidone had very high affinity and full antagonism at serotonin 5-HT7(Ki, 0.49nM), and nanomolar affinity (Ki=6.75nM) with weak-moderate partial agonism at serotonin 5-HT1Areceptors., Lurasidone showed higher affinity for 5-HT7, 5-HT2A, and 5-HT1Areceptors relative to D2receptor-binding than other agents. Lurasidone displayed moderate affinity for α2C adrenoceptors (Ki, 10.8nM); moderate-weak affinity for α1adrenoceptors (Ki, 48nM); and minimal or unappreciable affinity for receptors associated with undesirable effects (5-HT2C [Ki, 415nM], histamine H1[IC50>1000nM] and muscarinic [cholinergic] M1[IC50>1000nM] receptors).
The unique pharmacological profile of lurasidone is consistent with observed antipsychotic efficacy, low-tomoderate likelihood of EPS, low weight-gain potential, and possible mood, anxiety, and cognitive benefits.
Recent studies of subaerial volcano carbon flux have challenged previous assumptions about carbon recycling in the mantle and the ratio of ingassing to outgassing. This chapter reviews the current state of knowledge of the flux of carbon from subaerial volcanoes at subduction zones and intraplate locations, as well as through diffuse degassing away from volcanic vents. It also reviews the importance of crustal carbonate assimilation and carbonate platforms on these fluxes. The chapter presents an overview of how these fluxes are estimated – including descriptions of new technologies and recent field campaigns – and the timescales of flux measurements. It also summarizes what is currently known about the flux of carbon versus other volatile elements in these various settings. Supplemental online material is available for this chapter at www.cambridge.org/9781108477499#resources.
Maternal perinatal depression exerts pervasive effects on the developing brain, as evidenced by electroencephalographic (EEG) patterns that differ between children of women who do and do not meet DSM or ICD diagnostic criteria. However, little research has examined if the same EEG pattern of right-frontal alpha asymmetry exists in newborns and thus originates in utero independent of postnatal influences, and if depressive symptoms are associated with this neural signature. Utilizing 125-lead EEG (n=18), this study considered clinician-rated maternal prenatal depressive symptoms in relation to newborn EEG. Maternal depressive symptomatology was associated with greater relative right-frontal alpha asymmetry during quiet sleep. These results suggest that even subclinical levels of maternal depression may influence infant brain development, and further support the role of the prenatal environment in shaping children’s future neurobehavioral trajectories.
To assess the burden of bloodstream infections (BSIs) among pediatric hematology-oncology (PHO) inpatients, to propose a comprehensive, all-BSI tracking approach, and to discuss how such an approach helps better inform within-center and across-center differences in CLABSI rate
Prospective cohort study
US multicenter, quality-improvement, BSI prevention network
PHO centers across the United States who agreed to follow a standardized central-line–maintenance care bundle and track all BSI events and central-line days every month.
Infections were categorized as CLABSI (stratified by mucosal barrier injury–related, laboratory-confirmed BSI [MBI-LCBI] versus non–MBI-LCBI) and secondary BSI, using National Healthcare Safety Network (NHSN) definitions. Single positive blood cultures (SPBCs) with NHSN defined common commensals were also tracked.
Between 2013 and 2015, 34 PHO centers reported 1,110 BSIs. Among them, 708 (63.8%) were CLABSIs, 170 (15.3%) were secondary BSIs, and 232 (20.9%) were SPBCs. Most SPBCs (75%) occurred in patients with profound neutropenia; 22% of SPBCs were viridans group streptococci. Among the CLABSIs, 51% were MBI-LCBI. Excluding SPBCs, CLABSI rates were higher (88% vs 77%) and secondary BSI rates were lower (12% vs 23%) after the NHSN updated the definition of secondary BSI (P<.001). Preliminary analyses showed across-center differences in CLABSI versus secondary BSI and between SPBC and CLABSI versus non-CLABSI rates.
Tracking all BSIs, not just CLABSIs in PHO patients, is a patient-centered, clinically relevant approach that could help better assess across-center and within-center differences in infection rates, including CLABSI. This approach enables informed decision making by healthcare providers, payors, and the public.
Lithium sulfur (Li–S) batteries have the potential to provide higher energy storage density at lower cost than conventional lithium ion batteries. A key challenge for Li–S batteries is the loss of sulfur to the electrolyte during cycling. This loss can be mitigated by sequestering the sulfur in nanostructured carbon–sulfur composites. The nanoscale characterization of the sulfur distribution within these complex nanostructured electrodes is normally performed by electron microscopy, but sulfur sublimates and redistributes in the high-vacuum conditions of conventional electron microscopes. The resulting sublimation artifacts render characterization of sulfur in conventional electron microscopes problematic and unreliable. Here, we demonstrate two techniques, cryogenic transmission electron microscopy (cryo-TEM) and scanning electron microscopy in air (airSEM), that enable the reliable characterization of sulfur across multiple length scales by suppressing sulfur sublimation. We use cryo-TEM and airSEM to examine carbon–sulfur composites synthesized for use as Li–S battery cathodes, noting several cases where the commonly employed sulfur melt infusion method is highly inefficient at infiltrating sulfur into porous carbon hosts.
Parasites can influence host population dynamics, community composition and evolution. Prediction of these effects, however, requires an understanding of the influence of ecological context on parasite distributions and the consequences of infection for host fitness. We address these issues with an amphibian – trematode (Digenea: Echinostomatidae) host–parasite system. We initially performed a field survey of trematode infection in first (snail) and second (larval green frog, Rana clamitans) intermediate hosts over 5 years across a landscape of 23 ponds in southeastern Michigan. We then combined this study with a tadpole enclosure experiment in eight ponds. We found echinostomes in all ponds during the survey, although infection levels in both snails and amphibians differed across ponds and years. Echinostome prevalence (proportion of hosts infected) in snails also changed seasonally depending on host species, and abundance (parasites per host) in tadpoles depended on host size and prevalence in snails. The enclosure experiment demonstrated that infection varied at sites within ponds, and tadpole survival was lower in enclosures with higher echinostome abundance. The observed effects enhance our ability to predict when and where host–parasite interactions will occur and the potential fitness consequences of infection, with implications for population and community dynamics, evolution and conservation.
Based on seven measured sections from Svalbard, the marine strata of the Permian Kapp Starostin Formation are arranged into seven transgressive–regressive sequences (TR1–TR7) of c. 4–5 Ma average duration, each bound by a maximum regressive surface. Facies, including heterozoan-dominated limestones, spiculitic cherts, sandstones, siltstones and shales, record deposition within inner, middle and outer shelf areas. The lowermost sequence, TR1, comprises most of the basal Vøringen Member, which records a transgression across the Gipshuken Formation following a hiatus of unknown duration. Temperate to cold, storm-dominated facies established in inner to middle shelf areas between the latest Artinskian and Kungurian. Prolonged deepening during sequences TR2 and TR3 was succeeded by a long-term shallowing-upward trend that lasted until the latest Permian (TR4–TR7). A major depocentre existed in central and western Spitsbergen while to the north, Dickson Land remained a shallow platform, leading to a shallow homoclinal ramp in NE Spitsbergen and Nordaustlandet. The Middle Permian extinction (late Capitanian) is recorded near the base of TR6 in deeper parts of the basin only; elsewhere this sequence is not recorded. Likewise the youngest sequence, TR7, extending to the upper formational contact of latest Permian age, is found only in the basin depocentre. Comparison with age-equivalent strata in the Sverdrup Basin of Canada reveals a remarkably similar depositional history, with, for example, two (third-order) sea-level cycles recorded in the Late Permian of both regions, in keeping with the global record. Sequence stratigraphy may therefore be a powerful correlative tool for onshore and offshore Permian deposits across NW Pangaea.
Fast computers enable the solution of quantum many-body problems by Monte Carlo methods. As computing power increased dramatically over the years, similarly impressive advances occurred at the level of the algorithms, so that we are now in a position to perform accurate simulations of large systems of interacting quantum spins, Bosons, and (to a lesser extent) Fermions. The purpose of this book is to present and explain the quantum Monte Carlo algorithms being used today to simulate the ground states and thermodynamic equilibrium states of quantum models defined on a lattice. Our intent is not to review all relevant algorithms – there are too many variants to do so comprehensively – but rather to focus on a core set of important algorithms, explaining what they are and how and why they work.
Our focus on lattice models, such as Heisenberg and Hubbard models, has at least two implications. The first is obviously that we are not considering models in the continuum where extensive use of quantum Monte Carlo methods traditionally has focused on producing highly accurate ab initio calculations of the ground states of nuclei, atoms, molecules, and solids. Quantum Monte Carlo algorithms for simulating the ground states of continuum and lattice models, however, are very similar. In fact, the lattice algorithms are in many cases derived from the continuum methods. With fewer degrees of freedom, lattice models are compact and insightful representations of the physics in the continuum.
The second implication is a focus on both zero and finite temperature algorithms. On a lattice, it is natural to study phase transitions. In particular, the recent dramatic advances in quantum Monte Carlo lattice methods for the simulation of quantum spin models were prompted by a need for more efficient and effective ways to study finite-temperature transitions. While quantum Monte Carlo is profitably used to study zero temperature phase transitions (quantum critical phenomena), some ground state algorithms have no finite temperature analogs and vice versa. In many respects, the lattice is where the current algorithmic action is.
The book is divided into four parts. The first part is a self-contained, more advanced than average, discussion of the Monte Carlo method, its use, and its foundations.
We provide exact computations for the drift of random walks in dependent random environments, including k-dependent and moving average environments. We show how the drift can be characterized and evaluated using Perron–Frobenius theory. Comparing random walks in various dependent environments, we demonstrate that their drifts can exhibit interesting behavior that depends significantly on the dependency structure of the random environment.
Childhood maltreatment (CM) has consistently been linked with adverse outcomes including substance use disorders and adult sexual revictimization. Adult sexual victimization itself has been linked with psychopathology but has predominately been studied in women. The current investigation examines the impact of CM and co-occurring psychopathology on adult sexual victimization in men and women, replicating findings in three distinct samples.
We investigated the association between continuous CM factor scores and adult sexual victimization in the Childhood Trauma Study (CTS) sample (N = 2564). We also examined the unique relationship between childhood sexual abuse (CSA) and adult sexual victimization while adjusting for co-occurring substance dependence and psychopathology. We replicated these analyses in two additional samples: the Comorbidity and Trauma Study (CATS; N = 1981) and the Australian Twin-Family Study of Alcohol Use Disorders (OZ-ALC; N = 1537).
Analyses revealed a significant association with CM factor scores and adult sexual victimization for both men and women across all three samples. The CSA factor score was strongly associated with adult sexual victimization after adjusting for substance dependence and psychopathology; higher odds ratios were observed in men (than women) consistently across the three samples.
A continuous measure of CSA is independently associated with adult sexual trauma risk across samples in models that included commonly associated substance dependence and psychopathology as covariates. The strength of the association between this CSA measure and adult sexual victimization is higher in magnitude for men than women, pointing to the need for further investigation of sexual victimization in male community samples.