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Altered dopamine (DA) transporter densities have been implicated in mechanisms of vulnerability and relapse in human alcoholics. The regional distribution and density of the DA transporter was studied in alcohol-preferring vervet monkeys to investigate baseline status and regulation of the DA transporter at different stages of chronic alcohol drinking. Combined ligand binding and in vitro autoradiography of the cocaine congener [125I]RTI-55 (beta-CIT) demonstrated a significant increase in DA transporter densities in abstinent alcohol-preferring monkeys over those in alcohol-avoiding monkeys. Chronic alcohol consumption down-regulated DA transporter densities, and this effect was reversed by acute withdrawal. These results demonstrate that the DA transporter is regulated by alcohol exposure and suggest that increased DA transporter densities may be a phenotypic marker of alcohol preference in vulnerable monkeys.

Both genetic and environmental factors, such as stress, are important in determining alcohol consumption. Furthermore, both stress and alcohol influence the activity of the hypothalamic-pituitary-adrenal (HPA)-axis. Thus, the present studies investigated the response of the HPA axis to stress and the effect of ethanol on the stress response, in subjects at high (HR) and low (LR) risk of alcoholism as determined from their family history. Twenty HR and 20 LR subjects performed a stress-inducing task 30 min following the ingestion of either a placebo drink or a low dose of ethanol. The levels of plasma adrenal corticotropic hormone (ACTH) and cortisol were measured prior to and for four hours following initiation of the treatment. Changes with time in the plasma hormone levels following ingestion of either a placebo or an ethanol drink, without the performance of the stress task, served as controls to compare the stress-induced changes. Neither the placebo nor the ethanol drink altered the plasma ACTH and cortisol concentrations. High risk subjects presented lower basal ACTH, but not cortisol, levels and a lower stress-induced increase in plasma ACTH concentration than LR subjects. Furthermore, the HR subjects presented a delayed post-stress recovery of the plasma ACTH and cortisol levels. Ethanol consumption prior to the stress task attenuated (ACTH) or abolished (cortisol) the stress-induced increase in the plasma hormone concentrations of both LR and HR subjects. Thus, there are quantitative differences on the response of the HPA-axis to stress between HR and LR subjects, while ingestion of low amounts of ethanol prior to the performance of the stress task had a similar effect on HR and LR individuals.

This study estimated the daily energy intake (EI) and energy expenditure (TDEE) in female varsity rugby union players during a weekly training/game cycle. Fifteen (nine forwards, six backs) players (20.5 ± 0.4 y, 167.1 ± 1.8 cm, 74.9 ± 2.9 kg) were monitored for a 7-day period (one fitness, two heavy training, one light training, one game, and two recovery days) during their regular season. The average EI throughout the week for all 15 players was 2158 ± 87 kcal. There were no significant differences between days, but the lowest EI (1921 ± 227 kcal) occurred on the mid-week recovery day and the highest on game day (2336 ± 231 kcal). The average TDEE was 2286 ± 168 kcal (~6% > EI). The mean energy availability (EA) over the 7-day period was 31.1 ± 3.6 kcal/kg FFM/day for the group. Of the players, 14% were in the optimal EA range (>45 kcal/kg FFM/day); 34% were in the moderate range (≥30–45 kcal/kg FFM/day); and 52% had a poor EA of <30 kcal/kg FFM/day. Carbohydrate (3.38 ± 0.36 g/kg/day, 45% of EI); fat (1.27 ± 0.12 g/kg/day, 37% of EI); and protein (1.38 ± 0.12 g/kg/day, 18% of EI) consumption remained similar throughout the week (p > 0.05). The players consumed 6% less energy than they expended, providing poor to moderate EA; therefore, daily carbohydrate intake recommendations were not met.

Preformed gas bubbles can increase energy absorption from an ultrasound beam and therefore they have been proposed for an enhancer of ultrasound treatments. Although tissue temperature measurements performed in vivo using invasive thermocouple probes and MRI thermometry have demonstrated increased tissue temperature, the microscopic temperature distribution has not been investigated so far. In this study the transfer of heat between bubbles and tissue during focused ultrasound was simulated. Microbubble oscillations were simulated within a rat cortical microvascular network reconstructed from in vivo dual-photon microscopy images and the power density of these oscillations was used as an input term in the Pennes bioheat transfer equation. The temperature solution from the bioheat transfer equation was mapped onto vascular data to produce a three-dimensional temperature map. The results showed high temperatures near the bubbles and slow temperature rise in the tissue. Heating was shown to increase with increasing bubble frequency and insonation pressure, and showed a frequency-dependent peak. The goal of this research is to characterize the effect of various parameters on bubble-enhanced therapeutic ultrasound to allow better treatment planning. These results show that the induced temperature elevations have nonuniformities which may have a significant impact on the bio-effects of the exposure.

Climate change is increasingly recognized as one of the greatest threats to human health of the 21st century, with consequences that mental health professionals are also likely to face. While physical health impacts have been increasingly emphasized in literature and practice, recent scholarly literature indicates that climate change and related weather events and environmental changes can profoundly impact psychological well-being and mental health through both direct and indirect pathways, particularly among those with pre-existing vulnerabilities or those living in ecologically sensitive areas. Although knowledge is still limited about the connections between climate change and mental health, evidence is indicating that impacts may be felt at both the individual and community levels, with mental health outcomes ranging from psychological distress, depression and anxiety, to increased addictions and suicide rates. Drawing on examples from diverse geographical areas, this article highlights some climate-sensitive impacts that may be encountered by mental health professionals. We then suggest potential avenues for public mental health in light of current and projected changes, in order to stimulate thought, debate, and action.

Abstract Background There is concern in the international community regarding the influence of climate change on weather variables and seasonality that, in part, determine the rates of malaria. This study examined the role of sociodemographic variables in modifying the association between temperature and malaria in Kanungu District (Southwest Uganda). Methods Hospital admissions data from Bwindi Community Hospital were combined with meteorological satellite data from 2011 to 2014. Descriptive statistics were used to describe the distribution of malaria admissions by age, sex, and ethnicity (i.e. Bakiga and Indigenous Batwa). To examine how sociodemographic variables modified the association between temperature and malaria admissions, this study used negative binomial regression stratified by age, sex, and ethnicity, and negative binomial regression models that examined interactions between temperature and age, sex, and ethnicity. Results Malaria admission incidence was 1.99 times greater among Batwa than Bakiga in hot temperature quartiles compared to cooler temperature quartiles, and that 6–12 year old children had a higher magnitude of association of malaria admissions with temperature compared to the reference category of 0–5 years old (IRR = 2.07 (1.40, 3.07)). Discussion Results indicate that socio-demographic variables may modify the association between temperature and malaria. In some cases, such as age, the weather-malaria association in sub-populations with the highest incidence of malaria in standard models differed from those most sensitive to temperature as found in these stratified models. Conclusion The effect modification approach used herein can be used to improve understanding of how changes in weather resulting from climate change might shift social gradients in health.

Compared with other health areas, the mental health impacts of climate change have received less research attention. The literature on climate change and mental health is growing rapidly but is characterised by several limitations and research gaps. In a field where the need for designing evidence-based adaptation strategies is urgent, and research gaps are vast, implementing a broad, all-encompassing research agenda will require some strategic focus.We followed a structured approach to prioritise future climate change and mental health research. We consulted with experts working across mental health and climate change, both within and outside of research and working in high, middle, and low-income countries, to garner consensus about the future research priorities for mental health and climate change. Experts were identified based on whether they had published work on climate change and mental health, worked in governmental and non-governmental organisations on climate change and mental health, and from the professional networks of the authors who have been active in the mental health and climate change space.Twenty-two experts participated from across low- and middle-income countries (n = 4) and high-income countries (n = 18). Our process identified ten key priorities for progressing research on mental health and climate change.While climate change is considered the biggest threat to global mental health in the coming century, tackling this threat could be the most significant opportunity to shape our mental health for centuries to come because of health co-benefits of transitioning to more sustainable ways of living. Research on the impacts of climate change on mental health and mental health-related systems will assist decision-makers to develop robust evidence-based mitigation and adaptation policies and plans with the potential for broad benefits to society and the environment.

Normal males received amino acid mixtures designed to raise or lower tryptophan availability, and thus to raise or lower brain serotonin synthesis. They also received alcoholic or non-alcoholic drinks. The subjects were tested in the Taylor Competitive Reaction Time Task in which they competed against a (non-existent) partner in a reaction time task. The magnitude of electric shocks that the subjects were willing to give to their bogus partner was used as a measure of aggression. Lowered tryptophan levels and ingestion of alcohol were associated with increased aggression. Our data support the idea that low serotonin levels may be involved in the etiology of aggression. They suggest that subjects with low brain serotonin levels may be particularly susceptible to alcohol-induced violence.

Several studies have documented the retrograde facilitation of memory by alcohol, but the mechanisms responsible for this curious effect are unknown. In an experiment designed to complement previous studies on incidental learning, social drinkers (men aged 18 to 30; n= 44) took part in an experiment examining the effects of alcohol on intentional learning of emotionally salient verbal stimuli. Learning occurred when participants were sober. Alcohol or placebo (1.0 vs. 0.1 ml/kg) was consumed after learning, and memory was tested, sober, 24 hr later. Compared with placebo, alcohol modestly enhanced recall of positive but not negative stimuli. Furthermore, results suggest that the reinforcing effects on memory for positive (relative to negative) stimuli occurred in association with acute psychomotor stimulant effects during the ascending limb of the blood alcohol curve. The present finding that alcohol appeared to enhance intentional learning in association with its incentive effects contrasts results from previous studies, demonstrating that alcohol appears to enhance incidental learning by memory mechanisms independent of its incentive effects. These findings support a theory of alcoholism that is based on motivational systems.