Enhancing the Hodgkin-Huxley Equations: Simulations Based on the First Publication in the Biophysical Journal.

The experiments in the Cole and Moore article in the first issue of the Biophysical Journal provided the first independent experimental confirmation of the Hodgkin-Huxley (HH) equations. A log-log plot of the K current versus time showed that raising the HH variable n to the sixth power provided the best fit to the data. Subsequent simulations using n(6) and setting the resting potential at the in vivo value simplifies the HH equations by eliminating the leakage term. Our article also reported that the K current in response to a depolarizing step to ENa was delayed if the step was preceded by a hyperpolarization. While the interpretation of this phenomenon in the article was flawed, subsequent simulations show that the effect completely arises from the original HH equations.

A whole-cell and single-channel study of the voltage-dependent outward potassium current in avian hepatocytes.

Voltage-dependent membrane currents were studied in dissociated hepatocytes from chick, using the patch-clamp technique. All cells had voltage-dependent outward K+ currents; in 10% of the cells, a fast, transient, tetrodotoxin-sensitive Na+ current was identified. None of the cells had voltage-dependent inward Ca2+ currents. The K+ current activated at a membrane potential of about -10 mV, had a sigmoidal time course, and did not inactivate in 500 ms. The maximum outward conductance was 6.6 +/- 2.4 nS in 18 cells. The reversal potential, estimated from tail current measurements, shifted by 50 mV per 10-fold increase in the external K+ concentration. The current traces were fitted by n2 kinetics with voltage-dependent time constants. Omitting Ca2+ from the external bath or buffering the internal Ca2+ with EGTA did not alter the outward current, which shows that Ca2+-activated K+ currents were not present. 1-5 mM 4-aminopyridine, 0.5-2 mM BaCl2, and 0.1-1 mM CdCl2 reversibly inhibited the current. The block caused by Ba was voltage dependent. Single-channel currents were recorded in cell-attached and outside-out patches. The mean unitary conductance was 7 pS, and the channels displayed bursting kinetics. Thus, avian hepatocytes have a single type of K+ channel belonging to the delayed rectifier class of K+ channels.

Piezopotential gated nanowire--nanotube hybrid field-effect transistor.

We report the first piezoelectric potential gated hybrid field-effect transistors based on nanotubes and nanowires. The device consists of single-walled carbon nanotubes (SWNTs) on the bottom and crossed ZnO piezoelectric fine wire (PFW) on the top with an insulating layer between. Here, SWNTs serve as a carrier transport channel, and a single-crystal ZnO PFW acts as the power-free, contact-free gate or even an energy-harvesting component later on. The piezopotential created by an external force in the ZnO PFW is demonstrated to control the charge transport in the SWNT channel located underneath. The magnitude of the piezopotential in the PFW at a tensile strain of 0.05% is measured to be 0.4-0.6 V. The device is a unique coupling between the piezoelectric property of the ZnO PFW and the semiconductor performance of the SWNT with a full utilization of its mobility. The newly demonstrated device has potential applications as a strain sensor, force/pressure monitor, security trigger, and analog-signal touch screen.

The kinase Grk2 regulates Nedd4/Nedd4-2-dependent control of epithelial Na+ channels.

Epithelial Na(+) channels mediate the transport of Na across epithelia in the kidney, gut, and lungs and are required for blood pressure regulation. They are inhibited by ubiquitin protein ligases, such as Nedd4 and Nedd4-2, with loss of this inhibition leading to hypertension. Here, we report that these channels are maintained in the active state by the G protein-coupled receptor kinase, Grk2, which has been previously implicated in the development of essential hypertension. We also show that Grk2 phosphorylates the C terminus of the channel beta subunit and renders the channels insensitive to inhibition by Nedd4-2. This mechanism has not been previously reported to regulate epithelial Na(+) channels and provides a potential explanation for the observed association of Grk2 overactivity with hypertension. Here, we report a G protein-coupled receptor kinase regulating a membrane protein other than a receptor and provide a paradigm for understanding how the interaction between membrane proteins and ubiquitin protein ligases is controlled.

Opportunistic Control Over Shared Wireless Channels

© 2015 IEEE.We consider a wireless control architecture with multiple control loops over a shared wireless medium. A scheduler observes the random channel conditions that each control system experiences over the shared medium and opportunistically selects systems to transmit at a set of non-overlapping frequencies. The transmit power of each system also adapts to channel conditions and determines the probability of successfully receiving and closing the loop. We formulate the optimal design of channel-aware scheduling and power allocation that minimize the total power consumption while meeting control performance requirements for all systems. In particular, it is required that for each control system a given Lyapunov function decreases at a specified rate in expectation over the random channel conditions. We develop an offline algorithm to find the optimal communication design, as well as an online protocol which selects scheduling and power variables based on a random observed channel sequence and converges almost surely to the optimal operating point. Simulations illustrate the power savings of our approach compared to other non-channel-aware schemes.