Background: Endothelial dysfunction (ED) is one of the earliest subclinical indicators of impaired cardiovascular health and several non-invasive tools have been developed to evaluate vascular function, including strain gauge plethysmography (SGP), brachial artery flow-mediated dilation (FMD) via ultrasound, and peripheral artery tonometry (PAT). While these tools have extensively been studied during a resting condition, the responses following acute exercise are not as well characterized. Purpose: The purpose of this study was to compare the pre- and post-exercise vascular function values obtained with SGP, FMD, and PAT. Relationships among the primary outcome variables obtained with each assessment tool were also evaluated. Methods: Vascular function was assessed in 17 sedentary, apparently healthy male subjects (24±4 yrs; 24.5±3.2 kg/m2) at rest and following an acute submaximal exercise bout with SGP, FMD, and PAT. Results: During rest, post-occlusion reactive hyperemia resulted in significant (p<0.05) increases in forearm blood flow (FBF; 2.13±1.03 vs 6.35 ± 2.90 mL/min/100 mL tissue) and area under the curve (AUC; 226.77 ± 111.20 vs 588.22 ±283.33 mL/min/100 mL) as determined by SGP. Brachial artery diameter (BAD) as assessed with FMD was increased by 5.3% (p<0.05). Resting reactive hyperemia index (RHI) as assessed by PAT was observed to be 1.73±0.34. Significant exercise-induced increases (p<0.05) were observed in baseline and post-occlusion FBF and baseline AUC values utilizing SGP. Additionally, FMD baseline blood velocity was significantly increased (91.8±11.1 vs 108.0±17.1 cm/sec, p<0.05) and the PAT augmentation index (AI) was significantly more negative (-8.8 ±9.4 vs -18.9±8.4%, p<0.05) after exercise. There were no significant correlations observed among the primary outcome measures obtained from each assessment technique. There was, however, a moderate correlation between pre-exercise vascular reactivity as assessed by SGP and change in blood velocity as assessed by FMD (r= 0.566, p= 0.035). Conclusions: The addition of an exercise stress to vascular function assessment may offer greater insight into the health of the vasculature. This initial study was undertaken to further evaluate the pre- to post-exercise responses obtained using three commonly employed vascular function assessment techniques in healthy individuals. Additional research as to the value of the addition of an exercise stress to vascular function assessment in individuals with traditional cardiovascular disease risk factors or known cardiovascular disease is warranted.

AIMS: Substance use and dependence is very common among people living with HIV-infection. Since substances like alcohol and marijuana as well as the HIV virus itself are believed to have negative effects on cognition and the brain, our aim was to test the hypothesis that current and lifetime marijuana and heavy alcohol use are associated with cognitive dysfunction in people with HIV-infection. METHODS: Boston ARCH cohort participants consisted of 215 HIV-infected adults with substance dependence or current or past injection drug use. In cross-sectional, regression analyses we tested the association between current marijuana use (number of days marijuana was used in the past 30 days), current heavy alcohol use (number of heavy drinking days in the past 30 days defined as ≥4 drinks for women and ≥ 5 for men in 24 hours), lifetime marijuana use (number of years marijuana was used ≥ 3 times per week), lifetime alcohol use (total Kg), duration of heavy alcohol use (# of years alcohol was use > 84 grams or > 6 drinks per day), and three measures of cognitive dysfunction: i) memory and ii) attention domains of the Montreal Cognitive Assessment (MoCA), and iii) 4-item cognitive function scale (CF4) from the Medical Outcomes Study HIV Health Survey (MOS-HIV, range 0-100). Eight multivariable models were fit comparing: 1. current marijuana use by each cognitive outcome, 2. current heavy alcohol use by each cognitive outcome, 3. lifetime marijuana use by each cognitive outcome, 4. lifetime alcohol use (Kg) by each cognitive outcome, 5. lifetime marijuana use, duration of heavy alcohol use, current heavy alcohol use, and current marijuana use by each cognitive outcome, 6. lifetime marijuana use, lifetime alcohol use (Kg), current heavy alcohol use, and current marijuana use by each cognitive outcome, 7. the interaction between current marijuana and heavy alcohol use by each cognitive outcome, and 8. the interaction between lifetime marijuana and lifetime alcohol use (Kg) by each cognitive outcome. Analyses were adjusted for demographics, primary language, comorbidities, depressive symptoms, anxiety, antiretroviral therapy, HIV-viral load, CD4 count, lifetime cocaine use, cocaine use in the past 30 days, illicit opioid use in the past 30 days, and any prescribed opioids. RESULTS: Participant characteristics were as follows: Mean age 49 yrs., 35% female, 20% white, 66% ≥ 12 years of education, 86% English as primary language, 82% unemployed, mean Charlson comorbidity score 2.9, 28% scored ≥ 3 on the PHQ-2 indicating depressive symptoms, 44% scored ≥ 8 on OASIS indicating symptoms of anxiety, 58% had Hepatitis C infection at some point in their life, 86% were on HAART, 72% had an HIV-viral load < 200 copies/mL, CD4 cell count/mm3 was 10% <200 and 33% 200 - <500, mean HIV duration was 16 years, lifetime cocaine use was 9 years, 30% used cocaine in the past 30 days, 25% used illicit opioids in the past 30 days, and 61% were prescribed opioids. Current marijuana use was significantly associated with a lower MOS-HIV CF4 score in three of the fully adjusted models (1,5, and 6) listed previously with a decrease in 0.30 points for every day of use, but neither MoCA score. Current heavy alcohol use was also associated with a higher MOS-HIV CF4 score in model 5, increasing 0.36 points for every day of use. This finding did not confirm our hypothesis and in fact was opposite our projections. Lifetime marijuana use and lifetime alcohol use were not associated with any measure of cognitive dysfunction, and there was no interaction between lifetime marijuana use and lifetime alcohol use with cognitive dysfunction, and no interaction between current marijuana use and current alcohol use with cognitive dysfunction. CONCLUSION: Current marijuana use may be associated with cognitive dysfunction. We also detected an unexpected association between current heavy alcohol use and better cognitive function, but it is not biologically plausible. However, we did not detect associations between lifetime alcohol or marijuana use and cognitive dysfunction among people with substance dependence and HIV-infection. Further research, particularly on long-term exposure to substances, should include subtler measures of cognitive dysfunction and consider whether or not cognitive dysfunction that may be the consequence of marijuana and alcohol use is detectable among those who have many other factors effecting cognition. These results suggest that marijuana use should not be considered benign for individuals with substance dependence and HIV-infection.

Acute myocardial infarction is the commonest cause of death in firefighters, accounting for 45% of all deaths on duty. Compared with an average life expectancy of 77 years in the general population, the average age of cardiovascular death in firefighters is 50 years suggesting that occupational hazards are responsible for premature disease. The risk of acute myocardial infarction is increased 12- to 136-fold during rescue and firefighting duties, and is likely to reflect a combination of factors including strenuous physical exertion, mental stress, heat and pollutant exposure. Previous studies have established that the duties of a firefighter, in particular fire suppression, put inordinate strain on the cardiovascular system yet the exact mechanisms underlying the increased risk of myocardial infarction remain poorly defined. In a series of studies, I assessed the effect of occupation-specific risk factors on cardiovascular health in a combination of controlled and real-life studies in order to better define these mechanisms, hypothesising that exposure to high temperatures, strenuous physical exertion, psychological stress and air pollution either alone or in combination caused vascular dysfunction and thrombosis. In order to assess if firefighters had a greater cumulative risk of cardiovascular disease due to their occupation at baseline, I assessed the cardiovascular function of group of healthy, off-duty firefighters and compared this to a group of healthy age- and sex-matched off-duty police officers; an occupational group with similar responsibilities but a much lower risk of on-duty cardiovascular events. I was able to demonstrate that traditional cardiovascular risk factors, vascular endothelial function and thrombogenicity were similar in the two groups concluding that the excess of cardiovascular events and deaths in on-duty firefighters are due to the acute and transient effects of strenuous physical exertion, psychological stress, heat and exposure to air pollutants. Having established that off-duty firefighters had no apparent increased risk of cardiovascular events, I then went on to clarify the effects of combustion derived air pollution in the form of wood smoke on the cardiovascular system. The suppression of wildland or forest fires is globally the single most important duty of the fire service. Previous work within our institution has demonstrated the adverse effects of combustion derived air pollution, in the form of diesel exhaust, on the cardiovascular system. In a similar fashion, I assessed the effect of a wood smoke inhalation in a group of healthy off-duty firefighters by performing controlled exposures to wood smoke utilising a unique and well characterised facility. Interestingly, unlike diesel-exhaust, the exposure to wood smoke had no adverse effect on vascular endothelial function or thrombogenicity in this group concluding that cardiovascular events during wildland fire suppression may not be directly related to wood smoke inhalation but instead precipitated by other mechanisms such as strenuous physical exertion or dehydration. Latterly, I proceeded to evaluate the effects of strenuous physical exertion and heat exposure by comprehensively assessing a number of cardiovascular end points following controlled exposure to a fire simulation activity in a group of healthy, off-duty firefighters. I was able to demonstrate that exposure to extreme heat and physical exertion impaired vasomotor function and increased thrombus formation. Moreover, I demonstrated cardiac troponin concentrations increased suggesting that fire suppression activity may cause myocardial injury. These important findings suggest pathogenic mechanisms to explain the association between fire suppression activity and acute myocardial infarction. In the final phase of work, I endeavoured to assess the effects of real-life firefighter activities on the cardiovascular system. In an ambitious study, I attempted to undertake a comprehensive assessment of cardiovascular function in healthy firefighters following three periods of duty: fire suppression, alarm response and non-emergency activity. I was unable to complete enough studies to adequately power an analysis and draw any firm conclusions about the effect of these duties on cardiovascular health. Further work is required in a real-world setting to more clearly define the occupational risk factors underlying the increased risk of cardiovascular events associated with specific firefighter duties Understanding the biological mechanisms and environmental factors that predispose firefighters to cardiovascular events is essential if we are to develop effective methods for the prevention of acute myocardial infarction on-duty. This body of work has greatly improved the understanding of the mechanisms underlying the increased risk of cardiovascular events on duty and calls for the immediate evaluation of current practice in order to minimise risk to firefighters in the future. Examples of where improvements should be made include strategies to ensure adequate hydration and cooling following exposure to heat and physical exertion, change to working patterns to limit the duration of extreme exposures, and education, training and screening programmes to reduce the impact of traditional and occupational cardiovascular risk factors.

Thesis (MSc (Clinical Psychology)) -- University of Limpopo, 2010.

No description available.

In this thesis, the link between substance abuse and family dysfunction is examined, and an argument is made for the assessment of family dysfunction when treating clients with substance abuse issues. Family dysfunction has been associated with a broad range of problems in children (e.g., low self esteem, increased risk of child abuse) through to adolescence and adulthood (e.g., increased risk of mental disorders such as depressive disorders, substance abuse disorders, and personality disorders) (Kaplan & Sadock, 1998). It is not the purpose of this thesis to suggest that family dysfunction causes substance abuse but rather to highlight that family dysfunction can in some cases place the individual at greater risk of substance abuse. Therefore, in order to understand the reasons why substance abuse developed and how it is maintained in the present requires the assessment of family dysfunction. Further, the importance of assessing the role and impact that family dysfunction may have had on the client, may help to better understand the nature and extent of substance abuse so that relevant and appropriate treatment goals for change may be set, progress monitored, and risk of relapse reduced. Chapter 1 provides a brief introduction to this thesis, and Chapter 2 is a review of the literature on the impact of family dysfunction including poor parental attachment and supervision, neglect, physical and sexual abuse, in adolescence and adulthood. Four case studies are presented to illustrate how family dysfunction and substance abuse may be related, thus highlighting the importance of assessing family dysfunction when treating substance abuse clients. All of the case studies include an individual with a substance abuse disorder (namely heroin) but they are diverse in terms of the types and extent of family dysfunction. The final chapter discusses the case studies in relation to the literature reviewed. Lastly, it gives consideration to the implication of a history of family dysfunction, and how it may impact negatively on treatment and therefore prognosis.

No description available.

No description available.

Erectile performance anxiety (EPA) is a subset of sexual anxiety characterized by a fear of erectile failure. EPA has been shown to play a pivotal role in male sexual problems including premature ejaculation and erectile dysfunction (Loudon, 1998; Perelman, 2006). EPA affects approximately 14% to 23% of U.S. men across age groups (Laumann, Paik, & Rosen, 1999), and is the most common proximal cause of psychogenic ED (Hale & Strassberg, 1990; Hedon, 2003; Perelman, 1994; Rosen, 2001). Phosphodiesterase type 5 (PDE5) inhibitors such as sildenafil citrate (brand-name Viagra) are the first line of pharmacological treatment for ED. Recreational use of PDE5 inhibitors -- defined as unprescribed use with the goal of sexual enhancement and prevention of erectile failure among men without clinically significant erectile difficulties. Approximately 13.4% of young men between the ages of 18 - 30 report using PDE5 inhibitors recreationally. The most commonly reported reason for off-prescription use is to enhance one's sexual performance, i.e., longer lasting erections or impress one's sexual partner (Bechara, Casabe, De Bonis, Helien, & Bertolino, 2010; Harte & Meston, 2011; Holt, 2009; Korkes, Costa-Matos, Gasperini, Reginato, & Perez, 2008; Musacchio, Hartrich, & Garofalo, 2006). Reducing anxiety -- specifically EPA is often given as a reason for recreational use, though to a lesser extent (Korkes et al., 2008; Schnetzler, Banks, Kirby, Zou, & Symonds, 2010). However, PDE5 inhibitors do not exert a significant increase in penile tumescence among men without erectile dysfunction (Mondaini et al., 2008). The actual sexual enhancement from recreational use of PDE5 inhibitors among this population would be limited in that blood flow to the healthy erectile tissue is already optimal. The proposed study aimed to examine the effects of an erection-enhancing pill description misattribution on anticipatory anxiety and subsequent subjective and physiological sexual response to an audiovisual erotic stimulus. Participants underwent two assessments of their subjective and physiological arousal response to an erotic film after randomization to one of three conditions (erection-enhancing pill description, memory-enhancing pill description, or a no pill control). It was hypothesized that compared to those in the memory-enhancing pill group and the no pill control group, participants in the erection-enhancing pill group would respond with greater anticipatory anxiety and dampened penile tumescence in response to a subsequent no-pill erotic film presentation. Results of the study provided partial support for the hypothesized negative effects of the pill attribution manipulation. In the subset of subjects with complete pre and post-manipulation physiological data, those led to believe they ingested an erectile-enhancing herb showed a dampening of erectile tumescence to a subsequent erotic film presentation. Also, consistent with prediction, erectile performance anxiety was associated with decreased tumescence after the bogus "average" erectile performance feedback compared to baseline. These findings suggest that pill attribution may influence sexual arousal to some extent, despite methodological issues such as partial physiological data loss and believability of the pill instructional set manipulation. / text

Cigarette smoking represents the most preventable cause of morbidity and mortality in the world today, and is responsible for enormous health-related economic burdens. Among other medical sequelae, erectile impairment has been shown to be associated with chronic tobacco use. The primary aim of the present study was to provide the first empirical investigation of the effects of smoking cessation on physiological and subjective indices of sexual health. Sixty-five long-term, heavy smoking men participated in a smoking cessation program and were assessed at baseline (while smoking regularly), at mid-treatment (while using a high dose nicotine transdermal patch), and at 4-week follow-up. Physiological and subjective sexual arousal indices, as well as self-reported sexual functioning (as measured by the International Index of Erectile Functioning (IIEF)) were assessed during each visit. Intent-to-treat analyses indicated that at followup successful quitters (n = 20), compared to those who relapsed (n = 45), showed significant improvements in physiological and subjective sexual arousal. Specifically, men demonstrated enhanced erectile responses, decreased latencies to reach maximum erectile capacity, and faster onset to reach maximum subjective sexual arousal. Although participants displayed across-session enhancements in self reported sexual function, successful quitters did not show a differential improvement compared to participants who relapsed. The results of the present investigation provide the first empirical evidence that smoking cessation significantly enhances both physiological and self-reported indices of sexual health in long-term male smokers, irrespective of baseline erectile impairment. It is hoped that these results may serve as a novel and enticing means to influence men to quit smoking. Increasing successful smoking cessation in men would significantly enhance quality of life, substantially reduce premature death, and alleviate enormous economic burdens caused by smoking-related diseases. / text