Addressing climate change with behavioral science: a global intervention tournament in 63 countries

Effectively reducing climate change requires marked, global behavior change. However, it is unclear which strategies are most likely to motivate people to change their climate beliefs and behaviors. Here, we tested 11 expert-crowdsourced interventions on four climate mitigation outcomes: beliefs, policy support, information sharing intention, and an effortful tree-planting behavioral task. Across 59,440 participants from 63 countries, the interventions’ effectiveness was small, largely limited to nonclimate skeptics, and differed across outcomes: Beliefs were strengthened mostly by decreasing psychological distance (by 2.3%), policy support by writing a letter to a future-generation member (2.6%), information sharing by negative emotion induction (12.1%), and no intervention increased the more effortful behavior—several interventions even reduced tree planting. Last, the effects of each intervention differed depending on people’s initial climate beliefs. These findings suggest that the impact of behavioral climate interventions varies across audiences and target behaviors

Medical physiology and experimentation: reconsidering the undergraduate examination structure

No abstract available

Comments to the Editor concerning the cholinergic response to manganese-induced neurotoxicity, based on the paper entitled "The inhibitory effect of manganese on acetylcholinesterase activity enhances oxidative stress and neuroinflammation in the brain" by Santos et al.

No abstract available

Selegiline long-term effects on brain acetylcholinesterase, (Na+,K+)-ATPase activities, antioxidant status and learning performance of aged rats

The aim of this study was to investigate the effects of selegiline ((-)deprenyl), an irreversible inhibitor of monoaminoxidase-B (MAO-B): (a) on brain acetylcholinesterase (AChE), (Na(+),K(+))-ATPase and Mg(2+)-ATPase activities; (b) total antioxidant status (TAS); (c) learning performance and to evaluate possible correlation between biochemical and behavioral findings after long-term drug administration in aged male rats. Selegiline (0.25mgkg(-1) rat) was administered once every other day for 50 days. Learning parameters were tested through a two-way active avoidance procedure taking place in an Ugo-Basile automated shuttle box device. Enzyme activities and TAS were evaluated spectrophotometrically in brain homogenates of decapitated animals. TAS was significantly lower in aged compared to adult rats and this was reversed by selegiline administration. The decrease of free radical production by selegiline resulted in the stimulation of AChE and (Na(+),K(+))-ATPase. Mg(2+)-ATPase activity was not affected by the drug. Selegiline seems to improve the avoidance performance as compared to control groups. It is concluded that: (a) MAO-B inhibition and/or free radical protection on tyrosine hydroxylase by the drug may increase brain catecholamine concentrations resulting possibly in (Na(+),K(+))-ATPase stimulation; (b) AChE and (Na(+),K(+))-ATPase activation by the drug could modulate brain cholinergic, catecholaminergic and serotoninergic systems as well as the neural excitability and metabolic energy production; and (c) selegiline seems to improve the learning performance of aged rats

Effects of fulminant hepatic encephalopathy on the adult rat brain antioxidant status and the activities of acetylcholinesterase, (Na(+),K (+))- and Mg (2+)-ATPase: comparison of the enzymes' response to in vitro treatment with ammonia

Hepatic encephalopathy can be a life-threatening complication of fulminant hepatic failure. By understanding the pathophysiology involved in the induction of this neuropsychiatric disorder, future therapeutic and/or preventive attempts could be considered. In this study, an attempt has been made in order to shed more light on the mechanisms involved in the effects of thioacetamide (TAA)-induced fulminant hepatic encephalopathy on: (a) the adult rat brain total antioxidant status (TAS) and (b) the activities of acetylcholinesterase (AChE), (Na(+),K(+))-ATPase and Mg(2+)-ATPase. Moreover, in vitro experiments were conducted in order to evaluate the possible role of ammonia (incubated as NH(4)Cl, in a toxic concentration of 3mM) in the observed effects of TAA-induced fulminant hepatic encephalopathy on the examined adult rat brain enzyme activities. Fulminant hepatic encephalopathy caused a significant decrease in TAS (-22%, p < 0.001) and the activity of Na(+),K(+)-ATPase (-26%, p < 0.001), but had non-significant effects on the whole brain AChE and Mg(2+)-ATPase activities. The in vitro experiments (conducted through a 3h incubation with ammonia), showed no significant alterations in any of the examined parameters. Our in vitro and in vivo findings suggest that alterations in AChE and Mg(2+)-ATPase activities are not involved in the pathophysiology of the adult-onset fulminant hepatic encephalopathy, while the observed Na(+),K(+)-ATPase inhibition could be a result of the oxidative stress, neurotransmission deregulation, and/or of the presence of other toxic substances (that appear to act as direct or indirect inhibitors of the enzyme) and not due to the excess accumulation of ammonia in the brain

Serotoninergic impairment and aggressive behavior in Alzheimer's disease.

The overall goal of all therapeutic interventions in Alzheimer's disease (AD) is to: (a) optimize the impaired functions and (b) restore an affordable quality of life for both the patient and his surroundings. AD has been characterized by a significant serotoninergic impairment. It is well known that impaired serotoninergic function is related to aggressive behavior. We, herein, review the past and recent evidence that seems to link the serotoninergic system with aggressive manifestations in AD patients. Managing the aggressive behavior of these patients might be of significant medical, social and economical importance. However, there is still a long way to go until we verify the exact pathophysiological mechanism(s) involved in the induction of aggression in AD patients. The current data underlines a complex relationship between the observed serotoninergic impairment in AD patients and the (a) cholinergic system, (b) the endocrine (hormonal) state, (c) the nutritional habits, (d) the genetic background and (e) the caregiving environment

Can acetylcholinesterase activity be considered as a reliable biomarker for the assessment of cadmium-induced neurotoxicity?

Gonçalves et al. (2012) recently reported the findings of a long-awaited study on the effects of long-term dietary-induced exposure to cadmium (Cd) on the acetylcholinesterase (AChE) activity of adult rodents’ brain regions. Their study can be regarded as a significant contribution to the field, as there is paucity of information on the AChE activity in brain regions following exposure to Cd. However, the Cd-induced modulation of AChE activity is an issue surrounded by controversy. We, herein, discuss and summarize the relative in vivo and in vitro experimental data, and set out to answer the straightforward question: can AChE activity be considered as a reliable biomarker for the assessment of Cd-induced neurotoxicity? At this time, we can not answer in the affirmative because of the variation in techniques used and conclusions reached. We make a plea that authors aiming to explore this potential use of brain AChE activity in the future: (a) are aware of the biases that their experimental approach might exert upon this neurochemical parameter, (b) avoid the use of anaesthesia as a mode of sacrifice and clarify its timing, (c) decide upon the use of previously-studied in vivo experimental schemes (so that they can provide comparable results), and finally, (d) identify pharmacological, biochemical and molecular approaches that are appropriate to clarify the implicated mechanism(s) through which Cd modifies AChE activity