BioTillion (United States)

In soft materials, a clear relationship between material properties and human sensory perception has long been desired for design of consumer products, but the link has remained evasive. Favorable perception indicates that customers enjoy a product and are likely to continue using it or purchase it again. Perception is frequently measured subjectively by consumer test panels in terms of descriptive sensory words such as softness, smoothness, thickness, etc. that lack established scientific definitions. In this work, we move beyond ambiguous definitions and detail a method to objectively measure and quantify human-material interactions using a representative series of viscoelastic putties. We show that human behaviors have direct rheological meaning with features that are characterized using transient recovery rheology. The rheology scales logarithmically at perception-relevant timescales, akin to Fechner's law. Our work explains variability in user-reported perception and demonstrates a way to construct direct relationships between user behavior and measurable rheology.

There is an increasing requirement to supply Inverter Based Resource (IBR) models compiled using the actual code used in the inverter-controls to support detailed electromagnetic transient (EMT) studies. Similarly, EMT models of Power Plant Controllers (PPC), which are commonly used for managing these utility-scale renewable energy plants, are also required by the utilities. However, validation of these models against the performance of the actual hardware controller is seldom provided. It is generally assumed that the performance of the model, based on the actual controller source code or, identical block-diagram, is the same as the hardware controller performance. However, this may not be acceptable to all end-users since the simulation platform and the hardware are two significantly different computing platforms. Validation via field tests is usually narrow in scope. The hardware-in-loop (HIL) validation using a real-time digital simulator is a well accepted, more flexible, and cost-effective method for a thorough validation. This paper presents the HIL validation of an EMT model of a PPC against its actual hardware controller.

The aims of this study were to 1. define the responses of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), glucagon, and peptide YY (PYY) to an oral meal and to intravenous L-arginine; and 2. examine correlation of enteroendocrine hormones with insulin secretion. We hypothesized a relationship between circulating incretin concentrations and insulin secretion. Subjects with normal glucose tolerance (NGT, n = 23), prediabetes (PDM, n = 17), or with type 2 diabetes (T2DM, n = 22) were studied twice, following a mixed test meal (470 kCal) (mixed meal tolerance test [MMTT]) or intravenous L-arginine (arginine maximal stimulation test [AST], 5 g). GLP-1 (total and active), PYY, GIP, glucagon, and β cell function were measured before and following each stimulus. Baseline enteroendocrine hormones differed across the glucose tolerance (GT) spectrum, T2DM generally >NGT and PDM. In response to MMTT, total and active GLP-1, GIP, glucagon, and PYY increased in all populations. The incremental area-under-the-curve (0-120 min) of analytes like total GLP-1 were often higher in T2DM compared with NGT and PDM (35-51%; P < 0.05). At baseline glucose, L-arginine increased total and active GLP-1 and glucagon concentrations in all GT populations (all P < 0.05). As expected, the MMTT and AST provoked differential glucose, insulin, and C-peptide responses across GT populations. Baseline or stimulated enteroendocrine hormone concentrations did not consistently correlate with either measure of β cell function. Both MMTT and AST resulted in insulin and enteroendocrine hormone responses across GT populations without consistent correlation between release of incretins and insulin, which is in line with other published research. If a defect is in the enteroendocrine/β cell axis, it is probably reduced response to rather than diminished secretion of enteroendocrine hormones.