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Sexually victimized women may make sexual decisions differently than nonvictimized women. This study used an eroticized scenario and laboratory alcohol administration to investigate the roles of victimization history, intoxication, and relationship context in women's perceptions of a male partner and their subsequent intentions for unprotected sex. A community sample of 436 women completed childhood sexual abuse (CSA) and adolescent/adult sexual assault (ASA) measures. After random assignment to an alcohol or control condition, participants read and projected themselves into a sexual scenario that depicted the male partner as having high or low potential for a lasting relationship. Participants rated their perceptions of his intoxication, sexually transmitted infection (STI) risk level, and anticipated reactions to insistence on condom use. They then indicated their likelihood of allowing the partner to decide how far to go sexually (abdication) and of engaging in unprotected sex. Structural equation modeling (SEM) analyses revealed that intoxication predicted greater unprotected sex likelihood indirectly via abdication. CSA and ASA predicted partner perceptions, which in turn predicted unprotected sex likelihood. These findings indicate that, compared to their nonvictimized counterparts, sexually victimized women may respond differently in sexual encounters partly as a function of their perceptions of partners' STI risk and anticipated reactions to condom insistence.

This study used an experimental paradigm to investigate the roles of sexual victimization history and alcohol intoxication in young women’s sexual-emotional responding and sexual risk taking. A nonclinical community sample of 436 young women, with both an instance of heavy episodic drinking and some HIV/STI risk exposure in the past year, completed childhood sexual abuse (CSA) and adolescent/adult sexual assault (ASA) measures. A majority of them reported CSA and/or ASA, including rape and attempted rape. After random assignment to a high alcohol dose (.10 %) or control condition, participants read and projected themselves into an eroticized scenario of a sexual encounter involving a new partner. As the story protagonist, each participant rated her positive mood and her sexual arousal, sensation, and desire, and then indicated her likelihood of engaging in unprotected sex. Structural equation modeling analyses revealed that ASA and alcohol were directly associated with heightened risk taking, and alcohol’s effects were partially mediated by positive mood and sexual desire. ASA was associated with attenuated sexual-emotional responding and resulted in diminished risk taking via this suppression. These are the first findings indicating that, compared to non-victimized counterparts, sexually victimized women respond differently in alcohol-involved sexual encounters in terms of sexual-emotional responding and risk-taking intentions. Implications include assessing victimization history and drinking among women seeking treatment for either concern, particularly women at risk for HIV, and alerting them to ways their histories and behavior may combine to exacerbate their sexual risks.

Tobacco use is associated with variation at the 15q25 gene cluster and the cytochrome P450 (CYP) genes CYP2A6 and CYP2B6. Despite the variety of outcomes associated with these genes, few studies have adopted a data-driven approach to defining tobacco use phenotypes for genetic association analyses. We used factor analysis to generate a tobacco use measure, explored its incremental validity over a simple indicator of tobacco involvement: cigarettes per day (CPD), and tested both phenotypes in a genetic association study. Data were from the University of California, San Francisco Family Alcoholism Study (n = 1942) and a Native American sample (n = 255). Factor analyses employed a broad array of tobacco use variables to establish the candidate phenotype. Subsequently, we conducted tests for association with variants in the nicotinic acetylcholine receptor and CYP genes. We explored associations with CPD and our measure. We then examined whether the variants most strongly associated with our measure remained associated after controlling for CPD. Analyses identified one factor that captured tobacco-related problems. Variants at 15q25 were significantly associated with CPD after multiple testing correction (rs938682: p = .00002, rs1051730: p = .0003, rs16969968: p = .0003). No significant associations were obtained with the tobacco use phenotype; however, suggestive associations were observed for variants in CYP2B6 near CYP2A6 (rs45482602: ps = .0082, .0075) and CYP4Z2P (rs10749865: ps = .0098, .0079). CPD captures variation at 15q25. Although strong conclusions cannot be drawn, these finding suggest measuring additional dimensions of problems may detect genetic variation not accounted for by smoking quantity. Replication in independent samples will help further refine phenotype definition efforts. Different facets of tobacco-related problems may index unique genetic risk. CPD, a simple measure of tobacco consumption, is associated with variants at the 15q25 gene cluster. Additional dimensions of tobacco problems may help to capture variation at 19q13. Results demonstrate the utility of adopting a data-driven approach to defining phenotypes for genetic association studies of tobacco involvement and provide results that can inform replication efforts.

There is increasing interest in health interventions that incorporate genetic risk information. Although genetic feedback has been evaluated as an adjunct to smoking cessation interventions, its efficacy for reducing alcohol-related risks is unknown. The purpose of this study was to evaluate the feasibility, acceptability, and efficacy of a web-based alcohol intervention incorporating genetic feedback and risk information specific to ALDH2 genotype. The ALDH2*2 variant is associated with partial protection against alcohol dependence but confers significantly increased risk for alcohol-related cancers as a function of alcohol exposure. Two hundred Asian-American young adults were randomly assigned to receive web-based personalized genetic feedback or attention-control feedback. Genetic feedback included health risk information specific to alcohol-related cancer or alcohol dependence, depending on genotype. Outcomes included postintervention drinking behavior and theoretical correlates of behavior change. Genetic feedback and risk information resulted in significant reductions in 30-day drinking frequency and quantity among participants with the ALDH2*1/*2 genotype. Genetic feedback was rated highly by participants and also showed some effects on theoretical correlates of behavior change. Results provide initial evidence of the feasibility, acceptability, and brief efficacy of web-based genetic feedback for reducing alcohol-related health risks associated with ALDH2 genotype.

Rates of sexually transmitted infections, including HIV, vary across ethnic minority groups, yet few studies have evaluated sexual risk behaviors and their psychological correlates to determine if risk and protective factors vary by ethnicity. The purpose of the current study was to assess sexual sensation seeking (SSS), sexual inhibition (SIS1 and SIS2), and sexual excitation (SES) as correlates of risky sexual behaviors in 106 (55 male and 51 female) Asian Americans, African Americans, and Caucasian Americans. Results revealed that higher SSS was associated with more vaginal and anal sex partners. Further, the association between SSS and the number of anal sex partners was positive among Asian Americans and Caucasians, but non-significant among African Americans. SIS1 was positively associated with unprotected sex on the first date among Asian Americans and African Americans. However, the association was not significant for Caucasians. SIS2 was negatively associated with general unprotected sex, and SES was positively associated with the number of vaginal sex partners. Findings suggest that ethnicity plays an important moderating role in the relationship between sexual traits and risky sexual behaviors.

Scenarios simulating real-world risk situations have proven effective for substance use intervention methods and could potentially prove useful as an HIV-prevention method. This study explored qualitatively the development and use of such “in-the-moment” methods. We interviewed 97 moderate-drinking women (50 % Caucasian) after participation in an experiment requiring that they project themselves into a risky-sex scenario. Most participants (58 %) reported experiencing the scenario as a reflective tool characterized by two primary themes: (1) increased awareness of risk and (2) contemplation of behavior change. Findings suggest that “in-the-moment” methods depicting real-world risk situations and providing opportunities to reflect about behavioral choices and subsequent outcomes could prove a useful adjunct to HIV/AIDS-prevention interventions. Such methods could potentially augment existing prevention protocols.

Automatic cognitive processes have been shown to be unique predictors of drinking behavior and can be assessed using implicit measures. Drinking motives (e.g., enhancement and coping motives), which are also predictive of alcohol use, have not been studied using implicit measures. Moreover, in the US, implicit measures have been studied in samples largely consisting of Caucasian or White Americans. This study adapted the Implicit Association Test (IAT) to examine automatic analogues of enhancement and coping drinking motives and approach/avoid tendencies in 56 Asian American undergraduates. Enhancement and coping IATs were correlated with self-reported drinking motives and predicted unique variance in drinking frequency and heavy drinking when controlling for self-reported motives. Approach IAT scores were neither associated with self-reported approach/avoid tendencies nor predictive of drinking behaviors. These findings provide initial support for the unique predictive utility of drinking motives in Asian Americans, an understudied population.

Quantitative behavioral genetics studies provide strong evidence for heritable influences on the development of externalizing spectrum behaviors that cut across traditional diagnostic boundaries, including attention-deficit/hyperactivity disorder, oppositional defiant disorder, conduct disorder, antisocial personality disorder, and substance use and dependence. In contrast, molecular genetic studies have focused largely on individual disorders. This chapter reviews findings from genome-wide linkage studies, candidate gene studies, and genome-wide association studies of externalizing spectrum disorders, highlighting genes and gene categories that show relations with multiple disorders on the spectrum. Although still somewhat limited, these results provide important insights into the genetic architecture of the externalizing spectrum. The authors also note substantial divergence in findings across study designs, provide potential explanations for such findings, and describe how future studies might resolve these discrepancies.

Molecular genetic studies of psychiatric traits, including externalizing behaviors, aim to further our understanding of etiology by identifying specific genetic vulnerabilities that give rise to psychopathology. Recently, molecular geneticists have moved from candidate gene studies focused on small sets of genetic variants in single genes and coarse genome-wide linkage scans to genome-wide association studies and genome sequencing studies that examine millions of such variants in a single study. This has led to significant progress in our understanding of the genetic architecture of vulnerability for externalizing behavior. This chapter reviews methods that are used to study the molecular genetics of externalizing spectrum disorders. It begins with a review of the basic research designs used to study genetic variation, then describes how transdiagnostic approaches to phenotype measurement, combined with advances in analytic approaches and genotyping and sequencing technologies, will allow for more powerful molecular genetic investigations of the externalizing spectrum.

Survival and cure rates for childhood cancers in Europe have greatly improved over the past 40 years and are mostly good, although not in all European countries. The EUROCARE-5 survival study estimates survival of children diagnosed with cancer between 2000 and 2007, assesses whether survival differences among European countries have changed, and investigates changes from 1999 to 2007. We analysed survival data for 157 499 children (age 0–14 years) diagnosed between Jan 1, 1978 and Dec 31, 2007. They came from 74 population-based cancer registries in 29 countries. We calculated observed, country-weighted 1-year, 3-year, and 5-year survival for major cancers and all cancers combined. For comparison between countries, we used the corrected group prognosis method to provide survival probabilities adjusted for multiple confounders (sex, age, period of diagnosis, and, for all cancers combined without CNS cancers, casemix). Age-adjusted survival differences by area and calendar period were calculated with period analysis and were given for all cancers combined and the major cancers. We analysed 59 579 cases. For all cancers combined for children diagnosed in 2000–07, 1-year survival was 90·6% (95% CI 90·2–90·9), 3-year survival was 81·0 % (95% CI 80·5–81·4), and 5-year survival was 77·9% (95% CI 77·4–78·3). For all cancers combined, 5-year survival rose from 76·1% (74·4–77·7) for 1999–2001, to 79·1% (77·3–80·7) for 2005–07 (hazard ratio 0·973, 95% CI 0·965–0·982, p<0·0001). The greatest improvements were in eastern Europe, where 5-year survival rose from 65·2% (95% CI 63·1–67·3) in 1999–2001, to 70·2% (67·9–72·3) in 2005–07. Europe-wide average yearly change in mortality (hazard ratio) was 0·939 (95% CI 0·919–0·960) for acute lymphoid leukaemia, 0·959 (0·933–0·986) for acute myeloid leukaemia, and 0·940 (0·897–0·984) for non-Hodgkin lymphoma. Mortality for all of Europe did not change significantly for Hodgkin's lymphoma, Burkitt's lymphoma, CNS tumours, neuroblastoma, Wilms' tumour, Ewing's sarcoma, osteosarcoma, and rhabdomyosarcoma. Disparities for 5-year survival persisted between countries and regions, ranging from 70% to 82% (for 2005–07). Several reasons might explain persisting inequalities. The lack of health-care resources is probably most important, especially in some eastern European countries with limited drug supply, lack of specialised centres with multidisciplinary teams, delayed diagnosis and treatment, poor management of treatment, and drug toxicity. In the short term, cross-border care and collaborative programmes could help to narrow the survival gaps in Europe. Italian Ministry of Health, European Commission, Compagnia di San Paolo Foundation.