Associations of delay discounting and drinking trajectories from ages 14 to 22

Background

While drinking alcohol, one must choose between the immediate rewarding effects and the delayed reward of a healthier lifestyle. Individuals differ in their devaluation of a delayed reward based on the time required to receive it, i.e., delay discounting (DD). Previous studies have shown that adolescents discount more steeply than adults and that steeper DD is associated with heavier alcohol use in both groups.

Methods

In a large-scale longitudinal study, we investigated whether higher rates of DD are an antecedent or a consequence of alcohol use during adolescent development. As part of the IMAGEN project, 2220 adolescents completed the Monetary Choice Questionnaire as a DD measure, the Alcohol Use Disorders Identification Test, and the Timeline Follow Back interview at ages 14, 16, 18, and 22. Bivariate latent growth curve models were applied to investigate the relationship between DD and drinking. To explore the consequences of drinking, we computed the cumulative alcohol consumption and correlated it with the development of discounting. A subsample of 221 participants completed an intertemporal choice task (iTeCh) during functional magnetic resonance imaging at ages 14, 16, and 18. Repeated-measures ANOVA was used to differentiate between high-risk and low-risk drinkers on the development of neural processing during intertemporal choices.

Results

Overall, high rates of DD at age 14 predicted a greater increase in drinking over 8 years. In contrast, on average, moderate alcohol use did not affect DD from ages 14 to 22. Of note, we found indicators for less brain activity in top-down control areas during intertemporal choices in the participants who drank more.

Conclusions

Steep DD was shown to be a predictor rather than a consequence of alcohol use in low-level drinking adolescents. Important considerations for future longitudinal studies are the sampling strategies to be used and the reliability of the assessments.

     

Disparities in trauma: the impact of socioeconomic factors on outcomes following traumatic hollow viscus injury

Background

This piece aims to examine the relationships between hollow viscus injury (HVI) and socioeconomic factors in determining outcomes. HVI has well-defined injury patterns with complex postoperative convalescence and morbidity, representing an ideal focus for identifying potential disparities among a homogeneous injury population.

Materials and methods

A retrospective review included patients admitted to a level I trauma center with HVI from 2000–2009, as identified in the Trauma Registry of the American College of Surgeons. Patients with concomitant significant solid organ or vasculature injury were excluded. US Census (2000) median household income by zip code was used as socioeconomic proxy. Demographic and injury-related variables were also included. Endpoints were mortality and outcomes associated with HVI morbidity.

Results

A total of 933 patients with HVI were identified and 256 met inclusion criteria. There were 23 deaths (9.0%), and mortality was not associated with race, gender, income, or payer source. However, lower median household income was significantly associated with longer intervals to ostomy takedown (P = 0.032). Additionally, private payers had significantly lower rates of anastomotic leak (0% [0/73] versus 7.1% [13/183], P = 0.019) and fascial dehiscence (5.5% [4/73] versus 16.9% [31/183], P = 0.016), while self-payers had significantly higher rates of abscess formation, both overall (24% [24/100] versus 10.2% [16/156], P = 0.004) and among penetrating injuries (27.4% [23/84] versus 13.6% [12/88], P = 0.036).

Conclusions

Socioeconomic status may not impact overall mortality among trauma patients with hollow viscus injuries, but private insurance appears to be protective of morbidity related to anastomotic leak, fascial dehiscence, and abscess formation. This supports that socioeconomic disparity may exist within long-term outcomes, particularly regarding payer source.     

Systemic Arterial Endothelial Function in Children and Young Adults with Idiopathic Pulmonary Arterial Hypertension: Is there a Relation to Pulmonary Endothelium-Dependent Relaxation?

Pulmonary arterial endothelial function is known to be affected in patients with idiopathic pulmonary arterial hypertension (IPAH). Current reports also detected peripheral systemic arterial dysfunction in IPAH patients. The purpose of this study was to assess whether there is a relation between pulmonary arterial and systemic arterial endothelial function. Pulmonary arterial endothelium-dependent relaxation was assessed by changes in pulmonary blood flow in response to acetylcholine which were determined using intravascular Doppler flow measurements. Pulmonary flow reserve (PFR) was calculated as the ratio of pulmonary blood flow velocity in response to acetylcholine relative to baseline values. Systemic arterial endothelial function was assessed by the vascular response to reactive hyperemia, and was recorded non-invasively by peripheral arterial finger tonometry under standardized conditions. Thirteen children and young adults [mean age 16.7 (±5.6) years] with IPAH and 13 age-/gender-matched controls were included in the study. Digital reactive hyperemic index (RHI) of the IPAH patients was 1.54 (±0.69), and of the controls was 1.67 (±0.66) [p = 0.64]. The mean baseline flow velocity in the segmental pulmonary artery of all patients was 18.5 (±5.5) cm/s, increasing to 27.4 (±12.3) cm/s (p = 0.003) during acetylcholine infusion. The calculated mean PFR was 1.48 (±0.4). There was no significant correlation between the PFR and RHI (r = 0.19; p = 0.54). According to our results, systemic arterial endothelial function assessed by peripheral arterial finger tonometry was not significantly impaired in children and young adults with IPAH compared with age-/gender-matched controls. There was no correlation between systemic arterial and pulmonary arterial endothelial function, suggesting that different mechanisms may contribute to their pathogenesis and progression.     

Adiposity and estrogen receptor-positive,postmenopausal breast cancer risk: Quantification of the mediating effects of fasting insulin and free estradiol

Adiposity increases estrogen receptor (ER)-positive postmenopausal breast cancer risk. While mechanisms underlying this relationship are uncertain, dysregulated sex-steroid hormone production and insulin signaling are likely pathways. Our aim was to quantify mediating effects of fasting insulin and free estradiol in the adiposity and ER-positive postmenopausal breast cancer association. We used data from a case–cohort study of sex hormones and insulin signaling nested within the Melbourne Collaborative Cohort Study. Eligible women, at baseline, were not diagnosed with cancer, were postmenopausal, did not use hormone therapy and had no history of diabetes or diabetes medication use. Women with ER-negative disease or breast cancer diagnosis within the first follow-up year were excluded. We analyzed the study as a cumulative sampling case–control study with 149 cases and 1,029 controls. Missing values for insulin and free estradiol were multiply imputed with chained equations. Interventional direct (IDE) and indirect (IIE) effects were estimated using regression-based multiple-mediator approach. For women with body mass index (BMI) >30 kg/m² compared to women with BMI 18.5–25 kg/m², the risk ratio (RR) of breast cancer was 1.75 (95% confidence interval [CI] 1.05–2.91). The estimated IDE (RR) not through the mediators was 1.03 (95% CI 0.43–2.48). Percentage mediated effect through free estradiol was 72% (IIE-RR 1.56; 95% CI 1.11–2.19). There was no evidence for an indirect effect through insulin (IIE-RR 1.12; 95% CI 0.68–1.84; 28% mediated). Our results suggest that circulating free estradiol plays an important mediating role in the adiposity–breast cancer relationship but does not explain all of the association.     

Theoretical potential for endometrial cancer prevention through primary risk factor modification: Estimates from the EPIC cohort

Endometrial cancer (EC) incidence rates vary ~10-fold worldwide, in part due to variation in EC risk factor profiles. Using an EC risk model previously developed in the European EPIC cohort, we evaluated the prevention potential of modified EC risk factor patterns and whether differences in EC incidence between a European population and low-risk countries can be explained by differences in these patterns. Predicted EC incidence rates were estimated over 10 years of follow-up for the cohort before and after modifying risk factor profiles. Risk factors considered were: body mass index (BMI, kg/m²), use of postmenopausal hormone therapy (HT) and oral contraceptives (OC) (potentially modifiable); and, parity, ages at first birth, menarche and menopause (environmentally conditioned, but not readily modifiable). Modeled alterations in BMI (to all ≤23 kg/m²) and HT use (to all non-HT users) profiles resulted in a 30% reduction in predicted EC incidence rates; individually, longer duration of OC use (to all ≥10 years) resulted in a 42.5% reduction. Modeled changes in not readily modifiable exposures (i.e., those not contributing to prevention potential) resulted in ≤24.6% reduction in predicted EC incidence. Women in the lowest decile of a risk score based on the evaluated exposures had risk similar to a low risk countries; however, this was driven by relatively long use of OCs (median = 23 years). Our findings support avoidance of overweight BMI and of HT use as prevention strategies for EC in a European population; OC use must be considered in the context of benefits and risks.     

Speech‐in‐noise understanding in older age: The role of inhibitory cortical responses

Studies of central auditory processing underlying speech‐in‐noise (SIN) recognition in aging have mainly concerned the degrading neural representation of speech sound in the auditory brainstem and cortex. Less attention has been paid to the aging‐related decline of inhibitory function, which reduces the ability to suppress distraction from irrelevant sensory input. In a response suppression paradigm, young and older adults listened to sequences of three short sounds during MEG recording. The amplitudes of the cortical P30 response and the 40‐Hz transient gamma response were compared with age, hearing loss and SIN performance. Sensory gating, indicated by the P30 amplitude ratio between the last and the first responses, was reduced in older compared to young listeners. Sensory gating was correlated with age in the older adults but not with hearing loss nor with SIN understanding. The transient gamma response expressed less response suppression. However, the gamma amplitude increased with age and SIN loss. Comparisons of linear multi‐variable modeling showed a stronger brain–behavior relationship between the gamma amplitude and SIN performance than between gamma and age or hearing loss. The findings support the hypothesis that aging‐related changes in the balance between inhibitory and excitatory neural mechanisms modify the generation of gamma oscillations, which impacts on perceptual binding and consequently on SIN understanding abilities. In conclusion, SIN recognition in older age is less affected by central auditory processing at the level of sensation, indicated by sensory gating, but is strongly affected at the level of perceptual organization, indicated by the correlation with the gamma responses.     

Regulative mechanisms of chondrocyte adhesion

Interaction between chondrocytes and extracellular matrix is considered a key factor in the generation of grafts for matrix-associated chondrocyte transplantation. Therefore, our objective was to study the influence of differentiation status on cellular attachment. Adhesion of chondrocytes to collagen type II increased after removal from native cartilage up to the third day in monolayer in a dose-dependent manner. Following dedifferentiation after the second passage, adhesion to collagen types I (-84%) and II (-46%) decreased, whereas adhesion to fibrinogen (+59%) and fibronectin (+43%) increased. A cartilage construct was developed based on a clinically established collagen type I scaffold. In this matrix, more than 80% of the cells could be immobilized by mechanisms of adhesion, filtration, and cell entrapment. Confocal laser microscopy revealed focal adhesion sites as points of cell-matrix interaction, as well as collagen type II expression in the cartilage graft after two weeks of in vitro cultivation. Basic fibroblast growth factor (bFGF) treated chondrocytes showed increased adhesion to collagen types I and II, fibronectin, and fibrinogen. Attachment to these investigated proteins significantly enhanced cell proliferation. Matrix design in cartilage engineering must meet the biological demands of amplified cells, because adhesion of chondrocytes depends on their differentiation status and is regulated by bFGF.     

Leben und Sterben in Wohngemeinschaften für Menschen mit Demenz

Community based housing for people with dementia is gaining importance. In co-operation between the people concerned, their relatives, professionals and volunteers, person-centred care, nursing and guidance can be realised within small units. Questions regarding end of life, dying, grief and the role of palliative care form the basis of the exploratory qualitative study presented here. Coping with end of life, ethical decisions and the relevance of hospice and palliative care in the field are highlighted. The results of the study show that “shared flats for people with dementia” are good places for death and dying. Close relationships, good communication with relatives and highly motivated professionals can be regarded as powerful resources. So far only few co-operations between hospice and palliative care exist. Areas of improvement encompass clinical issues and coping with bereavement.     

The role of human papillomavirus in screening for cervical cancer

PURPOSE: To review the options for effectively screening for cervical cancer, including human papilloma virus (HPV) identification, cytologic screening, colposcopy, or a combination approach. Current pathophysiology, diagnostic criteria, treatment approaches, and patient preparation and education related to cervical cancer screening and prevention are also included. DATA SOURCES: Comprehensive review of current literature, including research and review articles. CONCLUSION: Because the Papanicolau (Pap) smear is a screening tool, not a diagnostic tool, further studies must be done to identify the actual nature of discovered abnormalities. Of particular concern is the classification of atypical squamous cells of undetermined significance (ASCUS), which may simply indicate inflammation, or may be the first indicator of serious pathology. Following ASCUS Pap smears with HPV screening will allow for a clarification of the best approach to treatment. A screening algorithm supported by a review of the literature is proposed. IMPLICATIONS FOR PRACTICE: Cervical cancer is a preventable disease caused by certain forms of HPV. Current screening protocols are based on the use of the Pap smear; and in areas where this test is routine and available, morbidity and mortality rates have dropped dramatically. Many women throughout the world and in underserved regions of the U. S. do not have adequate access to routine screening with Pap smear technology. As long as women continue to die needlessly of cervical cancer, more comprehensive and accessible screening methods must be explored. (Cutting the unnecessary worldwide and in the U. S.).