Metabolic Effects of Mental Stress during Over- and Underfeeding in Healthy Women

Objective: To assess the short-term consequences of carbohydrate or fat overfeeding or of food restriction on the metabolic effects of mental stress in healthy lean women. Research Methods and Procedures: The effects of a sympathetic activation elicited by mental stress were evaluated in a group of healthy women after standardized isocaloric feeding (ISO) or after a 3-day overfeeding with 40% excess calories as either carbohydrate overfeeding (CHO OF) or fat overfeeding (FAT OF). Oxygen consumption rate (VO ₂) was measured as an index of energy expenditure, and subcutaneous glycerol concentrations were monitored with microdialysis. The same measurements were performed in another group of healthy women after ISO and after a 3-day period of underfeeding with a protein sparing modified fast (UF). Results: In all conditions, mental stress significantly increased heart rate, blood pressure, plasma norepinephrine and epinephrine concentrations, and VO ₂, and produced a nonsignificant increase in subcutaneous glycerol concentrations. CHO OF and FAT OF did not alter the effects of mental stress on VO ₂ and subcutaneous glycerol concentrations. In contrast, UF increased basal VO ₂ but significantly reduced its stimulation by mental stress. UF also enhanced the increase in subcutaneous glycerol concentrations during mental stress. Discussion: UF reduces the stimulation of energy expenditure and enhances lipolysis during sympathetic activation. These adaptations may be involved in mobilization of endogenous fat while limiting weight loss. In contrast, short-term overfeeding fails to alter the sympathetic control of energy expenditure and lipolysis.     

Is EEG-biofeedback an Effective Treatment in Autism Spectrum Disorders? A Randomized Controlled Trial

EEG-biofeedback has been reported to reduce symptoms of autism spectrum disorders (ASD) in several studies. However, these studies did not control for nonspecific effects of EEG-biofeedback and did not distinguish between participants who succeeded in influencing their own EEG activity and participants who did not. To overcome these methodological shortcomings, this study evaluated the effects of EEG-biofeedback in ASD in a randomized pretest–posttest control group design with blinded active comparator and six months follow-up. Thirty-eight participants were randomly allocated to the EEG-biofeedback, skin conductance (SC)-biofeedback or waiting list group. EEG- and SC-biofeedback sessions were similar and participants were blinded to the type of feedback they received. Assessments pre-treatment, post-treatment, and after 6 months included parent ratings of symptoms of ASD, executive function tasks, and 19-channel EEG recordings. Fifty-four percent of the participants significantly reduced delta and/or theta power during EEG-biofeedback sessions and were identified as EEG-regulators. In these EEG-regulators, no statistically significant reductions of symptoms of ASD were observed, but they showed significant improvement in cognitive flexibility as compared to participants who managed to regulate SC. EEG-biofeedback seems to be an applicable tool to regulate EEG activity and has specific effects on cognitive flexibility, but it did not result in significant reductions in symptoms of ASD. An important finding was that no nonspecific effects of EEG-biofeedback were demonstrated.     

Soluble Ecto-5′-nucleotidase (5′-NT), Alkaline Phosphatase,and Adenosine Deaminase (ADA1) Activities in Neonatal Blood Favor Elevated Extracellular Adenosine

Extracellular adenosine, a key regulator of physiology and immune cell function that is found at elevated levels in neonatal blood, is generated by phosphohydrolysis of adenine nucleotides released from cells and catabolized by deamination to inosine. Generation of adenosine monophosphate (AMP) in blood is driven by cell-associated enzymes, whereas conversion of AMP to adenosine is largely mediated by soluble enzymes. The identities of the enzymes responsible for these activities in whole blood of neonates have been defined in this study and contrasted to adult blood. We demonstrate that soluble 5′-nucleotidase (5′-NT) and alkaline phosphatase (AP) mediate conversion of AMP to adenosine, whereas soluble adenosine deaminase (ADA) catabolizes adenosine to inosine. Newborn blood plasma demonstrates substantially higher adenosine-generating 5′-NT and AP activity and lower adenosine-metabolizing ADA activity than adult plasma. In addition to a role in soluble purine metabolism, abundant AP expressed on the surface of circulating neonatal neutrophils is the dominant AMPase on these cells. Plasma samples from infant observational cohorts reveal a relative plasma ADA deficiency at birth, followed by a gradual maturation of plasma ADA through infancy. The robust adenosine-generating capacity of neonates appears functionally relevant because supplementation with AMP inhibited whereas selective pharmacologic inhibition of 5′-NT enhanced Toll-like receptor-mediated TNF-α production in neonatal whole blood. Overall, we have characterized previously unrecognized age-dependent expression patterns of plasma purine-metabolizing enzymes that result in elevated plasma concentrations of anti-inflammatory adenosine in newborns. Targeted manipulation of purine-metabolizing enzymes may benefit this vulnerable population.     

Energy Metabolism in Rhizomes of Acorus calamus (L.) and in Tubers of Solanum tuberosum (L.) With Regard to their Anoxia Tolerance

Rhizomes of the marsh plant Acorus calamus (L.) and tubers of the flooding-intolerant Solanum tuberosum (L.) var. Bintje, both kept under strict anoxia, differ markedly in their fermentation properties. The fermentation capacities as measured by ADH and LDH activities and their respective product concentrations were estimated. While rhizomes of Acorus calamus, having high ADH and low LDH activities, accumulate mainly ethanol, tubers of Solanum tuberosum tend towards lactic acid fermentation. The total amount of adenine nucleotides is quite stable in Acorus calamus, whereas they show a sharp decline in S. tuberosum during the first 6h of anoxia. The adenylate energy charge of A. calamus recovers after a short initial drop (AEC > 0.8). AEC values of S. tuberosum decrease rapidly and remain at very low values (AEC ～ 0.3). Tuber tissues became soft and lost viability after about 48–72 h of anoxia at 25 °C. This might be due to tissue acidification and impaired energy metabolism, but not to the lack of energy reserves. Energy metabolism of A. calamus is well adapted to anoxia.     

Seasonal variation and an “outbreak” of frog predation by tamarins

We report temporal variation and an “outbreak” of frog predation by moustached tamarins, Saguinus mystax, in north-eastern Peruvian Amazonia. Frog predation rates were generally very low, but strongly increased in October 2015. Other high rates, identified by outlier analyses, were also observed in September–November of other years. Over all study years, predation rates in this 3-month period were significantly higher than those in the remainder of the year, suggesting a seasonal pattern of frog predation by tamarins. Reduced fruit availability or increased frog abundance or a combination of both may be responsible for both the seasonal pattern and the specific “outbreak” of frog predation.     

Identification of an intracellular domain of the EGF receptor required for high-affinity binding of EGF

Although all EGF receptors in EGF receptor-expressing cells are molecularly identical, they can be subdivided in two different classes that have either a high or a low affinity for EGF. Specifically the high-affinity class is associated with filamentous actin. To determine whether the interaction of the EGF receptor with actin induces its high-affinity state, we studied EGF-binding properties of an EGF receptor mutant that lacks the actin-binding site. Interestingly, we found that cells expressing this mutant receptor still display both high- and low-affinity classes of EGF receptors, indicating that the actin-binding domain does not determine the high-affinity binding state. By further mutational analysis we identified a receptor domain, within the tyrosine kinase domain, that regulates the affinity for EGF.