Sexual Risk for HIV Among Gay Male Couples: A Longitudinal Study of the Impact of Relationship Dynamics

While the relationship context itself is increasingly being examined to understand sexual risk behavior among gay male couples, few studies have examined relationship dynamics and HIV risk longitudinally. We aimed to investigate relationship dynamics and psychosocial predictors of unprotected anal intercourse (UAI) with outside partners of serodiscordant or unknown HIV serostatus (UAIOUT) over time as well as UAI with primary partner in serodiscordant couples (UAIPP). We recruited a sample of 566 ethnically diverse, seroconcordant and serodiscordant couples and interviewed them six times over the course of 3 years. The surveys encompassed relationship dynamics between the partners and sexual behavior with primary and outside partners. We fit generalized linear mixed models for both the UAI outcomes with time and relationship dynamics as predictors while controlling for relationship length. Analyses of the longitudinal data revealed that, in both categories of couples, those with higher levels of positive relationship dynamics (e.g., commitment, satisfaction) were less likely to engage in UAIOUT. Higher investment in sexual agreement and communication were among the factors that significantly predicted less UAIOUT for seroconcordant couples, but not for the serodiscordant couples. For serodiscordant couples, greater levels of attachment and intimacy were associated with greater odds of UAIPP while increased HIV-specific social support was associated with lower odds of UAIPP. These results underscore the importance of creating and tailoring interventions for gay couples that help maintain and strengthen positive relationship dynamics as they have the potential to produce significant changes in HIV risk behavior and thereby in HIV transmission.     

Social Branding to Decrease Smoking Among Young Adults in Bars

Objectives. We evaluated a Social Branding antitobacco intervention for “hipster” young adults that was implemented between 2008 and 2011 in San Diego, California.Methods. We conducted repeated cross-sectional surveys of random samples of young adults going to bars at baseline and over a 3-year follow-up. We used multinomial logistic regression to evaluate changes in daily smoking, nondaily smoking, and binge drinking, controlling for demographic characteristics, alcohol use, advertising receptivity, trend sensitivity, and tobacco-related attitudes.Results. During the intervention, current (past 30 day) smoking decreased from 57% (baseline) to 48% (at follow-up 3; P = .002), and daily smoking decreased from 22% to 15% (P < .001). There were significant interactions between hipster affiliation and alcohol use on smoking. Among hipster binge drinkers, the odds of daily smoking (odds ratio [OR] = 0.44; 95% confidence interval [CI] = 0.30, 0.63) and nondaily smoking (OR = 0.57; 95% CI = 0.42, 0.77) decreased significantly at follow-up 3. Binge drinking also decreased significantly at follow-up 3 (OR = 0.64; 95% CI = 0.53, 0.78).Conclusions. Social Branding campaigns are a promising strategy to decrease smoking in young adult bar patrons.Tobacco companies1 and public health authorities2–5 recognize young adulthood as a critical time when experimenters either quit or transition to regular tobacco use. Young adults are also aspirational role models for youths.1,6,7 Tobacco companies devote considerable resources to reaching young adults to encourage tobacco use,1,8–11 and young adults have a high prevalence of smoking.12 In California in 2011, young adults had the highest smoking prevalence of any age group, and the Department of Health estimated that 32% of California smokers started smoking between the ages of 18 and 26 years.13 Although they are more likely to intend to quit and successfully quit than older adults,14–17 young adults are less likely to receive assistance with smoking cessation.18,19 Although there are few proven interventions to discourage young adult smoking,20 cessation before age 30 years avoids virtually all of the long-term adverse health effects of smoking.21Tobacco companies have a long history of using bars and nightclubs to reach young adults and to encourage smoking.1,6,9–11,22–24 Bar attendance and exposure to tobacco bar marketing is strongly associated with smoking.25 The 1998 Master Settlement Agreement and Food and Drug Administration regulations that limit tobacco advertising to youths, explicitly permit tobacco marketing in “adult only” venues, including bars and nightclubs.26,27Aggressive tobacco marketing may actually be more intensive in smoke-free bars: a 2010 study of college students attending bars found that students in the community with a smoke-free bar law were more likely to be approached by tobacco marketers, offered free gifts, and to take free gifts for themselves than in communities without a smoke-free bar law.28 Bars and nightclubs also attract young adults who are more likely to exhibit personality traits such as sensation seeking,29 increasing their risk30 independently of receptivity to tobacco advertising; tobacco promotional messages resonate with these personality traits.8,31 Tobacco marketing campaigns are tailored to specific segments of the population defined by psychographics (e.g., values, attitudes, shared interests, such as tastes in music and fashion, and friend groups) and demographic criteria, and they aim to create positive smoker images, identities, and social norms for smoking.1,8 Tobacco marketing campaigns also focus on young adult trendsetters to leverage peer influence to promote smoking.6,10In contrast to the tobacco companies’ efforts, most young adult health interventions take place in colleges or health centers rather than social environments.32–39 Bars and nightclub venues represent an opportunity to reach those at highest risk for long-term smoking morbidity and mortality.40 We evaluated the effectiveness of an intervention to decrease cigarette smoking by countering tobacco industry marketing strategies targeting young adults attending bars and nightclubs in the San Diego, California, “hipster” scene. Because tobacco and alcohol use are strongly linked,41,42 we also examined the effects of the intervention on alcohol use and among binge drinkers. We found a significant decrease in smoking in the community where the intervention took place, including significant decreases among nondaily smokers and binge drinkers, as well as a significant decrease in binge drinking.     

Accelerated aging of selective brain structures in human immunodeficiency virus infection: a controlled,longitudinal magnetic resonance imaging study

Advances in treatment have transformed human immunodeficiency virus (HIV) infection from an inexorable march to severe morbidity and premature death to a manageable chronic condition, often marked by good health. Thus, infected individuals are living long enough that there is a potential for interaction with normal senescence effects on various organ systems, including the brain. To examine this interaction, the brains of 51 individuals with HIV infection and 65 uninfected controls were studied using 351 magnetic resonance imaging and a battery of neuropsychological tests collected 2 or more times over follow-up periods ranging from 6 months to 8 years. Brain tissue regions of interest showed expected age-related decrease in volume; cerebrospinal fluid-filled spaces showed increase in volume for both groups. Although HIV-infected individuals were in good general health, and free of clinically-detectable dementia, several brain regions supporting higher-order cognition and integration of functions showed acceleration of the normal aging trajectory, including neocortex, which extended from the frontal and temporal poles to the parietal lobe, and the thalamus. Beyond an anticipated increase in lateral ventricle and Sylvian fissure volumes and decrease in tissue volumes (specifically, the frontal and sensorimotor neocortices, thalamus, and hippocampus) with longer duration of illness, most regions also showed accelerated disease progression. This accelerated loss of cortical tissue may represent a risk factor for premature cognitive and motor compromise if not dementia. On a more promising note, HIV-infected patients with increasing CD4 counts exhibited slower expansion of Sylvian fissure volume and slower declines of frontal and temporoparietal cortices, insula, and hippocampus tissue volumes. Thus, attenuated shrinkage of these brain regions, likely with adequate pharmacologic treatment and control of further infection, has the potential of abating decline in associated higher-order functions, notably, explicit memory, executive functions, self-regulation, and visuospatial abilities.     

Downregulation of P-cadherin expression in hepatocellular carcinoma induces tumorigenicity

P-cadherin is a major contributor to cell-cell adhesion in epithelial tissues, playing pivotal roles in important morphogenetic and differentiation processes and in maintaining tissue integrity and homeostasis. Alterations of P-cadherin expression have been observed during the progression of several carcinomas where it appears to act as tumor suppressive or oncogenic in a context-dependent manner. Here, we found a significant downregulation of P-cadherin in hepatocellular carcinoma (HCC) cell lines and tissues compared to primary human hepatocytes and non-malignant liver tissues. Combined immunohistochemical analysis of a tissue microarray containing matched pairs of HCC tissue and corresponding non-tumorous liver tissue of 69 patients confirmed reduced P-cadherin expression in more than half of the cases. In 35 human HCC tissues, the P-cadherin immunosignal was completely lost which correlated with tumor staging and proliferation. Also in vitro, P-cadherin suppression in HCC cells via siRNA induced proliferation compared to cells transfected with control-siRNA. In summary, downregulation of P-cadherin expression appears to induce tumorigenicity in HCC. Therefore, P-cadherin expression may serve as a prognostic marker and therapeutic target of this highly aggressive tumor.     

A new technique for tricuspid valve repair addressing the subvalvular apparatus in functional tricuspid regurgitation

Annular dilatation is the main mechanism for tricuspid regurgitation, but right ventricular dilatation often adds a restrictive mechanism, which may limit durability. We describe a subvalvular technique anchoring the chordal origins to the annuloplasty, with the aim to stabilize valve geometry and increase durability. A Goretex suture is attached to the anterior papillary muscle. One arm of the suture is stitched through the septal muscle and both arms are atrialized underneath the septal leaflet and tied to the annuloplasty band. In 12 patients (75 ± 6 years, EuroSCORE II 10 ± 9%), severe-torrential tricuspid regurgitation was successfully reduced to mild. Results were stable in all but one patient during follow-up (1–15 months). NYHA class and general health status was improved. This subvalvular technique is safe with the potential to generate a durable repair.     

Loss of heterozygosity at locus F13B on chromosome 1q in human medulloblastoma

Medulloblastoma is a primitive neuroectodermal tumor of the cerebellum with poorly understood pathogenesis. Previous studies have reported loss of heterozygosity (LOH) on chromosome arms 17p, 11p and 9q and cytogenetic abnormalities of chromosome 1 in medulloblastoma. We have used the polymerase chain reaction to amplify 10 microsatellites on the short arm and B microsatellites on the long arm of chromosome 1 to assess allelic loss in 22 medulloblastomas. Loss of heterozygosity (LOH) on chromosome 1 was found in 9 cases. Eight medulloblastomas (36%) showed an interstitial LOH on chromosome 1q. The common region of overlap was mapped between DISI604 and DIS237 and included the locus F13B in the chromosomal region 1q31–q32.1. An additional tumor had LOH in a proximal region of 1p, but did not exhibit LOH on 1q. None of the medulloblastomas exhibited LOH of the telomeric portion of chromosome 1p, which has been associated with several other human malignancies. Our data suggest the presence of a putative tumor suppressor gene located near the locus F13B on chromosome arm 1q that appears to be involved in the pathogenesis of medulloblastoma. © 1996 Wiley-Liss, Inc.     

Platelet Aggregation Inhibiting and Anticoagulant Effects of Oligoamines,XXVIII: Oligoamines with Fluorescent Properties. Part C: Fluorescent Oligoamines with Enhanced Hydrophilic Properties

Fifteen fluorescent oligoamines with one or two fluorescent groups and two or three basic N-functions were prepared and tested for antiplatelet activity (Born-test). Five compounds involving three different fluorophores, i.e. 2-fluorenyl, 1-pyrenyl, and 9-phenanthryl, show an IC₅₀ of 7–11 μmol/L. They are suitable to serve as probes in the field of oligoamine-biopolymere interactions.     

Prognostic impact of distinct genetic entities in pediatric diffuse glioma WHO-grade II—Report from the German/Swiss SIOP-LGG 2004 cohort

Reports on pediatric low-grade diffuse glioma WHO-grade II (DG2) suggest an impaired survival rate, but lack conclusive results for genetically defined DG2-entities. We analyzed the natural history, treatment and prognosis of DG2 and investigated which genetically defined sub-entities proved unfavorable for survival. Within the prospectively registered, population-based German/Swiss SIOP-LGG 2004 cohort 100 patients (age 0.8-17.8 years, 4% neurofibromatosis [NF1]) were diagnosed with a DG2. Following biopsy (41%) or variable extent of resection (59%), 65 patients received no adjuvant treatment. Radiologic progression or severe neurologic symptoms prompted chemotherapy (n = 18) or radiotherapy (n = 17). Multiple lines of salvage treatment were necessary for 19/35 patients. Five years event-free survival dropped to 0.44, while 5 years overall survival was 0.90 (median observation time 8.3 years). Extensive genetic profiling of 65/100 DG2 identified Histone3-K27M-mutation in 4, IDH1-mutation in 11, BRAF-V600-mutation in 12, KIAA1549-BRAF-fusions in 6 patients, while the remaining 32 tumor tissues did not show alterations of these genes. Progression to malignant glioma occurred in 12 cases of all genetically defined subgroups within a range of 0.5 to 10.8 years, except for tumors carrying KIAA1549-BRAF-fusions. Histone3-K27M-mutant tumors proved uniformly fatal within 0.6 to 2.4 years. The current LGG treatment strategy seems appropriate for all DG2-entities, with the exemption of Histone3-K27M-mutant tumors that require a HGG-related treatment strategy. Our data confirm the importance to genetically define pediatric low-grade diffuse gliomas for proper treatment decisions and risk assessment.