Effect of Sensory Attenuation on Cortical Movement-Related Oscillations

This study examined the impact of induced sensory deficits on cortical, movement-related oscillations measured using electroencephalography (EEG). We hypothesized that EEG patterns in healthy subjects with induced sensory reduction would be comparable to EEG found after chronic loss of sensory feedback. EEG signals from 64 scalp locations were measured from 10 healthy subjects. Participants dorsiflexed their ankle after prolonged vibration of the tibialis anterior (TA). Beta band time frequency decompositions were calculated using wavelets and compared across conditions. Changes in patterns of movement-related brain activity were observed following attenuation of sensory feedback. A significant decrease in beta power of event-related synchronization was associated with simple ankle dorsiflexion after prolonged vibration of the TA. Attenuation of sensory feedback in young, healthy subjects led to a corresponding decrease in beta band synchronization. This temporary change in beta oscillations suggests that these modulations are a mechanism for sensorimotor integration. The loss of sensory feedback found in spinal cord injury patients contributes to changes in EEG signals underlying motor commands. Similar alterations in cortical signals in healthy subjects with reduced sensory feedback implies these changes reflect normal sensorimotor integration after reduced sensory input rather than brain plasticity

Spark Ignition Measurements in Jet A: part II

An improved system for measuring the ignition energy of liquid fuel was built to perform experiments on aviation kerosene (Jet A). Compared to a previously used system (Shepherd et al. 1998), the present vessel has a more uniform temperature which can be held constant for long periods of time. This ensures thermal equilibrium of the liquid fuel and the vapor inside the vessel. A capacitive spark discharge circuit was used to generate damped sparks and an arrangement of resistors and measurement probes recorded the voltage and current histories during the discharge. This permitted measurement of the energy dissipated in the spark, providing a more reliable, quantitative measure of the ignition spark strength. With this improved system, the ignition energy of Jet A was measured at temperatures from 35C to 50C pressures from 0.300 bar (ambient pressure at 30 kft) to 0.986 bar (ambient pressure near sea level), mass-volume ratios down to 3 kg/m^3, with sparks ranging from 10 mJ to 0.3 J. Special fuel blends with flash points (Tfp) from 29C to 73.5C were also tested. The statistical properties of the ignition threshold energy were investigated using techniques developed for high-explosive testing. Ignition energy measurements at 0.585 bar with high mass-volume ratios (also referred to as mass loadings) showed that the trend of the dependence of ignition energy on temperature was similar for tests using the stored capacitive energy and the measured spark energy. The ignition energy was generally lower with the measured spark energy than with the stored spark energy. The present ignition energy system was capable of clearly resolving the difference in ignition energy between low and high mass-volume ratios. The ignition energy vs. temperature curve for 3 kg/m^3 was shifted approximately 5C higher than the curve for high mass-volume ratios of 35 kg/m^3 or 200 kg/m^3. The ignition energy was subsequently found to depend primarily on the fuel-air mass ratio of the mixture, although systematic effects of the vapor composition are also evident. As expected, the ignition energy increased when the initial pressure was raised from 0.585 bar to 0.986 bar, and decreased when the pressure was decreased to 0.3 bar. Finally, tests on special fuels having flash points different from that of commercial Jet A showed that the minimum ignition temperature at a spark energy of about 0.3 J and a pressure of 0.986 bar depends linearly on the flash point of the fuel

A systems-biology approach to understanding the ciliopathy disorders.

'Ciliopathies' are an emerging class of genetic multisystemic human disorders that are caused by a multitude of largely unrelated genes that affect ciliary structure/function. They are unified by shared clinical features, such as mental retardation, cystic kidney, retinal defects and polydactyly, and by the common localization of the protein products of these genes at or near the primary cilium of cells. With the realization that many previously disparate conditions are a part of this spectrum of disorders, there has been tremendous interest in the function of cilia in developmental signaling and homeostasis. Ciliopathies are mostly inherited as simple recessive traits, but phenotypic expressivity is under the control of numerous genetic modifiers, putting these conditions at the interface of simple and complex genetics. In this review, we discuss the ever-expanding ciliopathy field, which has three interrelated goals: developing a comprehensive understanding of genes mutated in the ciliopathies and required for ciliogenesis; understanding how the encoded proteins work together in complexes and networks to modulate activity and structure-function relationships; and uncovering signaling pathways and modifier relationships