Project TENDR: Targeting environmental neuro-developmental risks. the TENDR consensus statement

Children in America today are at an unacceptably high risk of developing neurodevelopmental disorders that affect the brain and nervous system including autism, attention deficit hyperactivity disorder, intellectual disabilities, and other learning and behavioral disabilities. These are complex disorders with multiple causes—genetic, social, and environmental. The contribution of toxic chemicals to these disorders can be prevented. Approach: Leading scientific and medical experts, along with children’s health advocates, came together in 2015 under the auspices of Project TENDR: Targeting Environmental Neuro-Developmental Risks to issue a call to action to reduce widespread exposures to chemicals that interfere with fetal and children’s brain development. Based on the available scientific evidence, the TENDR authors have identified prime examples of toxic chemicals and pollutants that increase children’s risks for neurodevelopmental disorders. These include chemicals that are used extensively in consumer products and that have become widespread in the environment. Some are chemicals to which children and pregnant women are regularly exposed, and they are detected in the bodies of virtually all Americans in national surveys conducted by the U.S. Centers for Disease Control and Prevention. The vast majority of chemicals in industrial and consumer products undergo almost no testing for developmental neurotoxicity or other health effects. Conclusion: Based on these findings, we assert that the current system in the United States for evaluating scientific evidence and making health-based decisions about environmental chemicals is fundamentally broken. To help reduce the unacceptably high prevalence of neurodevelopmental disorders in our children, we must eliminate or significantly reduce exposures to chemicals that contribute to these conditions. We must adopt a new framework for assessing chemicals that have the potential to disrupt brain development and prevent the use of those that may pose a risk. This consensus statement lays the foundation for developing recommendations to monitor, assess, and reduce exposures to neurotoxic chemicals. These measures are urgently needed if we are to protect healthy brain development so that current and future generations can reach their fullest potential

GRAIN BOUNDARY STRUCTURE IN Ni3Al

The influence of boron segregation and non-stoichiometry on grain boundary structure in Ni3Al was studied by transmission and scanning electron microscopy techniques. Small angle twist and tilt boundaries were produced by hot pressing misoriented single crystals of both doped and undoped material. Dislocation structures were observed in both bicrystal and polycrystal grain boundaries. In most cases the grain boundary dislocations were found to have the expected a Burgers vector, however in one case dislocations with Burgers vector a/2 have been observed. Using a SEM diffraction technique the frequency of occurrence of grain boundary types was examined and found to be unchanged by the addition of boron

DIFFRACTION STUDIES OF THE ATOMIC STRUCTURE OF LARGE ANGLE [001] TWIST BOUNDARIES

Cet article récapitule les résultats de l'application des techniques de diffraction à l'etude de la structure atomique des joints de grains. La détermination de la structure de la projection d'un joint [001] à grand angle de torsion est décrite. L'influence de la nature du métal c.f.c. et de la liaison sur la structure du joint est étudiée. S'appuyant sur les résultats des études de diffraction, les auteurs proposent des généralisations concernant les structures des joints [001] à grands angles de torsion.The results of the application of diffraction techniques to study the atomic structure of grain boundaries are reviewed. The determination of the projected structure of a large angle [001] twist boundary is described. The influence of f.c.c. metal type and bonding type on boundary structure is examined. Generalizations are made concerning the structure of large angle [001] twist boundaries based on the results of the diffraction studies

Endogenous fatty acid synthesis drives brown adipose tissue involution.

Thermoneutral conditions typical for standard human living environments result in brown adipose tissue (BAT) involution, characterized by decreased mitochondrial mass and increased lipid deposition. Low BAT activity is associated with poor metabolic health, and BAT reactivation may confer therapeutic potential. However, the molecular drivers of this BAT adaptive process in response to thermoneutrality remain enigmatic. Using metabolic and lipidomic approaches, we show that endogenous fatty acid synthesis, regulated by carbohydrate-response element-binding protein (ChREBP), is the central regulator of BAT involution. By transcriptional control of lipogenesis-related enzymes, ChREBP determines the abundance and composition of both storage and membrane lipids known to regulate organelle turnover and function. Notably, ChREBP deficiency and pharmacological inhibition of lipogenesis during thermoneutral adaptation preserved mitochondrial mass and thermogenic capacity of BAT independently of mitochondrial biogenesis. In conclusion, we establish lipogenesis as a potential therapeutic target to prevent loss of BAT thermogenic capacity as seen in adult humans