MHD coal-fired flow facility. Annual technical progress report, October 1979-September 1980

The University of Tennessee Space Institute (UTSI) reports on significant activity, task status, planned research, testing, development, and conclusions for the Magnetohydrodynamics (MHD) Coal-Fired Flow Faclity (CFFF) and the Energy Conversion Facility (ECF)

Human-Robot Adaptive Control of Object-Oriented Action

International audienceThis chapter is concerned with how implicit, nonverbal cues support coordinated action between two partners. Recently, neuroscientists have started uncovering the brain mechanisms involved in how people make predictions about other people's behavioural goals and intentions through action observation. To date, however, only a small number of studies have addressed how the involvement of a task partner influences the planning and control of one's own purposeful action. Here, we review three studies of cooperative action between human and robot partners that address the nature of predictive and reactive motor control in cooperative action. We conclude with a model which achieves motor coordination by task partners each adjusting their actions on the basis of previous trial outcome

Loss-of-function mutations in <em>SLC30A8</em> protect against type 2 diabetes.

Loss-of-function mutations protective against human disease provide in vivo validation of therapeutic targets, but none have yet been described for type 2 diabetes (T2D). Through sequencing or genotyping of ~150,000 individuals across 5 ancestry groups, we identified 12 rare protein-truncating variants in SLC30A8, which encodes an islet zinc transporter (ZnT8) and harbors a common variant (p.Trp325Arg) associated with T2D risk and glucose and proinsulin levels. Collectively, carriers of protein-truncating variants had 65% reduced T2D risk (P = 1.7 &times; 10(-6)), and non-diabetic Icelandic carriers of a frameshift variant (p.Lys34Serfs*50) demonstrated reduced glucose levels (-0.17 s.d., P = 4.6 &times; 10(-4)). The two most common protein-truncating variants (p.Arg138* and p.Lys34Serfs*50) individually associate with T2D protection and encode unstable ZnT8 proteins. Previous functional study of SLC30A8 suggested that reduced zinc transport increases T2D risk, and phenotypic heterogeneity was observed in mouse Slc30a8 knockouts. In contrast, loss-of-function mutations in humans provide strong evidence that SLC30A8 haploinsufficiency protects against T2D, suggesting ZnT8 inhibition as a therapeutic strategy in T2D prevention