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The world, society and education are constantly evolving, and to respond to these changes, the main governmental institutions have been proposing different global strategies to focus efforts in the same direction. Currently, the United Nations and its 17 Sustainable Development Goals (SDG) have presented a series of indicators that could help to minimise the environmental, economic and social instability we are experiencing. In this sense, Education for Sustainable Development (ESD) has been described as a fundamental factor. Specifically, in previous work, we argued that physical education (PE) could be a good tool to contribute to SDGs. Based on this, no research analysing the voices of Physical Education Teachers (PET) on how this contribution could be made has been identified in previous literature. Therefore, the objectives of this research are: (1) to analyse the voices and opinions of active PETs in terms of the knowledge they have about Sustainable Development (SD); (2) to determine their opinions about the contribution that PE could make to SDGs; and finally, (3) to identify the challenges and limitations of pedagogical action of SD in PE. For this purpose, a qualitative analysis through a semi-structured interview with 41 active PETs was carried out. The main findings will be presented and discussed around four themes: (a) agreement on the concept of sustainability; (b) PE can contribute to the achievement of SDGs; (c) ambiguity in applying SDGs to PE lessons; and (d) teachers’ constraints on how to implement SDGs in PE. It seems to indicate that PETs do not have a multidimensional vision of sustainable development. While they recognise the potential of PE to contribute to SDGs through awareness raising and student learning, they point to its pedagogical and formative constraints as the main barriers to being able to contribute. They pointed to a lack of knowledge on how to do so, guidelines on how to integrate ESD, lack of involvement, shortage of time or resources in school physical education.

While the harmful effects of alcohol abuse are well documented, experimental and clinical data support a potential benefit of light to moderate alcohol consumption. Cross-sectional studies have suggested an association between alcohol consumption and multiple sclerosis (MS) disability. In the absence of prospective, longitudinal studies, the causal nature of this relationship cannot be established. It remains possible that patients with increased disability progression reduce their alcohol intake. Even though there is substantial evidence for anti-inflammatory effects of low-to-moderate doses of alcohol, the associations need to be interpreted very cautiously. This study discusses the current state of knowledge about MS and alcohol consumption, and the limitations in conducting research with retrospective data in patients with MS.

Lysophosphatidic acid species (LPA) are lipid bioactive signaling molecules that have been recently implicated in the modulation of emotional and motivational behaviors. The present study investigates the consequences of either genetic deletion or pharmacological blockade of lysophosphatidic acid receptor-1 (LPA1) in alcohol consumption.The experiments were performed in alcohol-drinking animals by using LPA1-null mice and administering the LPA1 receptor antagonist Ki16425 in both mice and rats.In the two-bottle free choice paradigm, the LPA1-null mice preferred the alcohol more than their wild-type counterparts. Whereas the male LPA1-null mice displayed this higher preference at all doses tested, the female LPA1-null mice only consumed more alcohol at 6% concentration. The male LPA1-null mice were then further characterized, showing a notably increased ethanol drinking after a deprivation period and a reduced sleep time after acute ethanol administration. In addition, LPA1-null mice were more anxious than the wild-type mice in the elevated plus maze test. For the pharmacological experiments, the acute administration of the antagonist Ki16425 consistently increased ethanol consumption in both wild-type mice and rats; while it did not modulate alcohol drinking in the LPA1-null mice and lacked intrinsic rewarding properties and locomotor effects in a conditioned place preference paradigm. In addition, LPA1-null mice exhibited a marked reduction on the expression of glutamate-transmission-related genes in the prefrontal cortex similar to those described in alcohol-exposed rodents.Results suggest a relevant role for the LPA/LPA1 signaling system in alcoholism. In addition, the LPA1-null mice emerge as a new model for genetic vulnerability to excessive alcohol drinking. The pharmacological manipulation of LPA1 receptor arises as a new target for the study and treatment of alcoholism.

Activity pacing (AP) is a concept that is central to many chronic pain theories and treatments, yet there remains confusion regarding its definition and effects.To review the current knowledge concerning AP and integrate this knowledge in a manner that allows for a clear definition and useful directions for future research.A narrative review of the major theoretical approaches to AP and of the empirical evidence regarding the effects of AP interventions, followed by an integrative discussion.The concept of AP is derived from 2 main traditions: operant and energy conservation. Although there are common elements across these traditions, significant conceptual and practical differences exist, which has led to confusion. Little empirical evidence exists concerning the efficacy of AP as a treatment for chronic pain.Future research on AP should be based on a clear theoretical foundation, consider the context in which the AP behavior occurs and the type of pacing problem ("underactivity" vs. "overactivity"), and should examine the impact of AP treatment on multiple clinical outcomes. We provide a provisional definition of AP and specific recommendations that we believe will move the field forward.

Systemic delivery of therapeutic agents remains ineffective against diffuse intrinsic pontine glioma (DIPG), possibly due to an intact blood-brain-barrier (BBB) and to dose-limiting toxicity of systemic chemotherapeutic agents. Convection-enhanced delivery (CED) into the brainstem may provide an effective local delivery alternative for DIPG patients.The aim of this study is to develop a method to perform CED into the murine brainstem and to test this method using the chemotherapeutic agent carmustine (BiCNU). To this end, a newly designed murine CED catheter was tested in vitro and in vivo. After determination of safety and distribution, mice bearing VUMC-DIPG-3 and E98FM-DIPG brainstem tumors were treated with carmustine dissolved in DW 5% or carmustine dissolved in 10% ethanol.Our results show that CED into the murine brainstem is feasible and well tolerated by mice with and without brainstem tumors. CED of carmustine dissolved in 5% DW increased median survival of mice with VUMC-DIPG-3 and E98FM-DIPG tumors with 35% and 25% respectively. Dissolving carmustine in 10% ethanol further improved survival to 45% in mice with E98FM-DIPG tumors.Since genetically engineered and primary DIPG models are currently only available in mice, murine CED studies have clear advantages over CED studies in other animals.CED in the murine brainstem can be performed safely, is well tolerated and can be used to study efficacy of chemotherapeutic agents orthotopically. These results set the foundation for more CED studies in murine DIPG models.

There is ongoing debate regarding the validity of the distinction of alcohol abuse and dependence, the distinction between normality and alcohol abuse, and the absence of craving in the DSM-IV classification of alcohol use disorders. In this study, we examine the discriminant validity of the DSM-IV alcohol use disorder diagnoses in three different populations (98 patients from an alcohol treatment service, 68 nontreatment-seeking heavy drinkers, and 75 psychiatric outpatients). We compare the results of the DSM-IV classification with an alternative classification that requires craving and withdrawal for the diagnosis of dependence and at least two DSM-IV abuse-dependence symptoms for the diagnosis of abuse: the Craving Withdrawal Model (CWM). Although the total prevalence of any alcohol use disorder did not differ between DSM-IV and CWM, the distinction between normality and abuse and between abuse and dependence was better for the CWM categories.

The main system of central ethanol oxidation is mediated by the enzyme catalase. By reacting with H2O2, brain catalase forms compound I (the catalase–H2O2 system), which is able to oxidize ethanol to acetaldehyde in the brain. Previous studies have demonstrated that pharmacological manipulations of brain catalase activity modulate the stimulant effects of ethanol in mice. However, the role of H2O2 in the behavioral effects of ethanol has not yet been clearly addressed. In the present study, we investigated the effects of alpha-lipoic acid (LA), a scavenging agent for H2O2, on ethanol-induced locomotor stimulation. CD-1 mice were pretreated with LA [0–100 mg/kg, intraperitoneally (IP)] 0–60 min prior to administration of ethanol (0–3.75 g/kg, IP). In another experiment, animals were pretreated with LA (0, 25, or 50 mg/kg, IP) 30 min before cocaine (10 mg/kg, IP), amphetamine (2 mg/kg, IP), or caffeine (25 mg/kg, IP). After these treatments the animals were placed in an open-field chamber and their locomotor activity was measured for 20 min. LA 25, 50, and 100 mg/kg IP prevented ethanol-induced locomotor stimulation. LA did not affect the locomotor-stimulating effects of cocaine, amphetamine, and caffeine. Additionally, we demonstrated that LA prevents the inactivation of brain catalase by 3-amino-1,2,4-triazole, thus indicating that H2O2 levels are reduced by LA. These data support the idea that a decrease in cerebral H2O2 production by LA administration inhibits ethanol-stimulated locomotion. This study suggests that the brain catalase–H2O2 system, and by implication centrally formed acetaldehyde, plays a key role in the psychopharmacological effects of ethanol.

The hollow-fibre oxygenator is a key component of any extracorporeal circuit used to provide cardiopulmonary bypass (CPB) during open-heart surgery. Since the oxygenator is placed downstream of the pump, the energy losses over it have a direct impact on the quality of pulsatile pressure and flow waveforms. The objective of this study was to describe the effects of hydrodynamic characteristics of the oxygenator on energy transfer during pulsatile, normothermic CPB. Twenty-three adult patients scheduled for coronary bypass surgery were divided randomly into two groups, using either an oxygenator (Group 1) with a relatively high-resistance and low-compliance (2079 ± 148 dyn.s.cm-5 and 0.00348 ± 0.00071 ml.mmHg-1, respectively) or an oxygenator (Group 2) with a relatively low-resistance and high-compliance (884 ± 464 dyn.s.cm-5 and 0.01325 ± 0.00161 ml .mmHg-1, respectively). During perfusion, pre- and post-oxygenator pressures, radial artery pressure, and blood flow were recorded simultaneously. A 32% decline of mean pressure was observed in Group 1 and a 16% decline in Group 2 (p<0.0001). Another decrease by approximately 73% in mean pressure in the rest of the perfusion system was noted in both groups. The mean radial artery pressure did not differ between the groups (74 ± 6 mmHg in Group 1 and 73 ± 6 mmHg in Group 2, p=0.608). Although lower total energy transfer indices were noticed through the low-resistance oxygenator (Group 2), both oxygenators showed a decrease of the generated pump oscillatory energy of approximately 50%. Despite the differences in resistance and compliance of the hollow-fibre oxygenators used, both oxygenators cause a comparable loss of generated oscillatory energy. Exclusion of the oxygenator downstream of the pulsatile pump would improve energy transfer during CPB.