Shear Capacity of Monolithic Concrete Joints without Transverse Reinforcement.

yesA mechanism analysis based on the upper-bound theorem of concrete plasticity for monolithic concrete joints without transverse reinforcement is presented. Concrete is modelled as a rigid–perfectly plastic material obeying modified Coulomb failure criteria. Existing stress–strain relationships of concrete in compression and tension are comprehensively modified using the crack band theory to allow for concrete type and maximum aggregate size. Simple equations for the effectiveness factor for compression, ratio of effective tensile strength to compressive strength and angle of concrete friction are then mathematically developed using the modified stress–strain relationships of concrete. In addition, 12 push-off specimens made of all-lightweight, sand–lightweight and normal-weight concrete having maximum aggregate size between 4 and 19 mm were physically tested. Test results and mechanism analysis clearly showed that the shear capacity of monolithic concrete joints increased with the increase of the maximum aggregate size and dry density of concrete. The mean and standard deviation of the ratio between experimentally measured and predicted (by the mechanism analysis shear capacities) are 1·01 and 0·16 respectively, showing a closer prediction and less variation than Vecchio and Collins' equation, regardless of concrete type and maximum aggregate size

Relating reflex gain modulation in posture control to underlying neural network properties using a neuromusculoskeletal model

During posture control, reflexive feedback allows humans to efficiently compensate for unpredictable mechanical disturbances. Although reflexes are involuntary, humans can adapt their reflexive settings to the characteristics of the disturbances. Reflex modulation is commonly studied by determining reflex gains: a set of parameters that quantify the contributions of Ia, Ib and II afferents to mechanical joint behavior. Many mechanisms, like presynaptic inhibition and fusimotor drive, can account for reflex gain modulations. The goal of this study was to investigate the effects of underlying neural and sensory mechanisms on mechanical joint behavior. A neuromusculoskeletal model was built, in which a pair of muscles actuated a limb, while being controlled by a model of 2,298 spiking neurons in six pairs of spinal populations. Identical to experiments, the endpoint of the limb was disturbed with force perturbations. System identification was used to quantify the control behavior with reflex gains. A sensitivity analysis was then performed on the neuromusculoskeletal model, determining the influence of the neural, sensory and synaptic parameters on the joint dynamics. The results showed that the lumped reflex gains positively correlate to their most direct neural substrates: the velocity gain with Ia afferent velocity feedback, the positional gain with muscle stretch over II afferents and the force feedback gain with Ib afferent feedback. However, position feedback and force feedback gains show strong interactions with other neural and sensory properties. These results give important insights in the effects of neural properties on joint dynamics and in the identifiability of reflex gains in experiments

Effects of intravenous fructose on gastric emptying and antropyloroduodenal motility in healthy subjects

Gastric emptying (GE) of glucose is regulated closely, not only as a result of inhibitory feedback arising from the small intestine, but also because of the resulting hyperglycemia. Fructose is used widely in the diabetic diet and is known to empty from the stomach slightly faster than glucose but substantially slower than water. The aims of this study were to determine whether intravenous (iv) fructose affects GE and antropyloroduodenal motility and how any effects compare to those induced by iv glucose. Six healthy males (age: 26.7 ± 3.8 yr) underwent concurrent measurements of GE of a solid meal (100 g ground beef labeled with 20 MBq 99mTc-sulfur colloid) and antropyloroduodenal motility on three separate days in randomized order during iv infusion of either fructose (0.5 g/kg), glucose (0.5 g/kg), or isotonic saline for 20 min. GE (scintigraphy), antropyloroduodenal motility (manometry), and blood glucose (glucometer) were measured for 120 min. There was a rise in blood glucose (P < 0.001) after iv glucose (peak 16.4 ± 0.6 mmol/l) but not after fructose or saline. Intravenous glucose and fructose both slowed GE substantially (P < 0.005 for both), without any significant difference between them. Between t = 0 and 30 min, the number of antral pressure waves was less after both glucose and fructose (P < 0.002 for both) than saline, and there were more isolated pyloric pressure waves during iv glucose (P = 0.003) compared with fructose and saline (P = NS for both) infusions. In conclusion, iv fructose slows GE and modulates gastric motility in healthy subjects, and the magnitude of slowing of GE is comparable to that induced by iv glucose.Julie E. Stevens, Selena Doran, Antonietta Russo, Deirdre O'Donovan, Christine Feinle-Bisset, Christopher K. Rayner, Michael Horowitz and Karen L. Jone