Dual-Shutter Optical Vibration Sensing.

Visual vibrometry is a highly useful tool for remote capture of audio, as well as the physical properties of materials, human heart rate, and more. While visually-observable vibrations can be captured directly with a high-speed camera, minute imperceptible object vibrations can be optically amplified by imaging the displacement of a speckle pattern created by shining a laser beam on the vibrating surface. In this paper, we propose a novel method for sensing vibrations at high speeds (up to 63 kHz), for multiple scene sources at once, using sensors rated for only 130 Hz operation.

Confocal non-line-of-sight imaging based on the light-cone transform.

How to image objects that are hidden from a camera's view is a problem of fundamental importance to many fields of research, with applications in robotic vision, defence, remote sensing, medical imaging and autonomous vehicles. Non-line-of-sight (NLOS) imaging at macroscopic scales has been demonstrated by scanning a visible surface with a pulsed laser and a time-resolved detector. Whereas light detection and ranging (LIDAR) systems use such measurements to recover the shape of visible objects from direct reflections, NLOS imaging reconstructs the shape and albedo of hidden objects from multiply scattered light.

Measurement of subcellular force generation in neurons.

Forces are important for neuronal outgrowth during the initial wiring of the nervous system and after trauma, yet subcellular force generation over the microtubule-rich region at the rear of the growth cone and along the axon has never, to our knowledge, been directly measured. Because previous studies have indicated microtubule polymerization and the microtubule-associated proteins Kinesin-1 and dynein all generate forces that push microtubules forward, a major question is whether the net forces in these regions are contractile or expansive. A challenge in addressing this is that measuring local subcellular force generation is difficult.

Ultrastructural and cellular basis for the development of abnormal myocardial mechanics during the transition from hypertension to heart failure.

Although the development of abnormal myocardial mechanics represents a key step during the transition from hypertension to overt heart failure (HF), the underlying ultrastructural and cellular basis of abnormal myocardial mechanics remains unclear. We therefore investigated how changes in transverse (T)-tubule organization and the resulting altered intracellular Ca(2+) cycling in large cell populations underlie the development of abnormal myocardial mechanics in a model of chronic hypertension. Hearts from spontaneously hypertensive rats (SHRs; n = 72) were studied at different ages and stages of hypertensive heart disease and early HF and were compared with age-matched control (Wistar-Kyoto) rats (n = 34).

Inhibition of the late sodium current slows t-tubule disruption during the progression of hypertensive heart disease in the rat.

The treatment of heart failure (HF) is challenging and morbidity and mortality are high. The goal of this study was to determine if inhibition of the late Na(+) current with ranolazine during early hypertensive heart disease might slow or stop disease progression. Spontaneously hypertensive rats (aged 7 mo) were subjected to echocardiographic study and then fed either control chow (CON) or chow containing 0.

Can triggered arrhythmias arise from propagation of calcium waves between cardiac myocytes?

Intracellular Ca2+ overload can induce regenerative Ca2+ waves that activate inward current in cardiac myocytes, allowing the cell membrane to achieve threshold. The result is a triggered extrasystole that can, under the right conditions, lead to sustained triggered arrhythmias. In this review, we consider the issue of whether or not Ca2+ waves can travel between neighboring myocytes and if this intercellular Ca2+ diffusion can involve enough cells over a short enough period of time to actually induce triggered activity in the heart.

The role of stretching in slow axonal transport.

Axonal stretching is linked to rapid rates of axonal elongation. Yet the impact of stretching on elongation and slow axonal transport is unclear. Here, we develop a mathematical model of slow axonal transport that incorporates the rate of axonal elongation, protein half-life, protein density, adhesion strength, and axonal viscosity to quantify the effects of axonal stretching.

Slowing of axonal regeneration is correlated with increased axonal viscosity during aging.

Background: As we age, the speed of axonal regeneration declines. At the biophysical level, why this occurs is not well understood.

Results: To investigate we first measured the rate of axonal elongation of sensory neurons cultured from neonatal and adult rats.

Variability in timing of spontaneous calcium release in the intact rat heart is determined by the time course of sarcoplasmic reticulum calcium load.

Background: Abnormalities in intracellular calcium (Ca) cycling during Ca overload can cause triggered activity because spontaneous calcium release (SCR) activates sufficient Ca-sensitive inward currents to induce delayed afterdepolarizations (DADs). However, little is known about the mechanisms relating SCR and triggered activity on the tissue scale.

Methods And Results: Laser scanning confocal microscopy was used to measure the spatiotemporal properties of SCR within large myocyte populations in intact rat heart.

Ranolazine antagonizes the effects of increased late sodium current on intracellular calcium cycling in rat isolated intact heart.

Pathological conditions, including ischemia and heart failure, are associated with altered sodium channel function and increased late sodium current (I(Na,L)), leading to prolonged action potential duration, increased intracellular sodium and calcium concentrations, and arrhythmias. We used anemone toxin (ATX)-II to study the effects of increasing I(Na,L) on intracellular calcium cycling in rat isolated hearts. Cardiac contraction was abolished using paralytic agents.

Modeling mitochondrial dynamics during in vivo axonal elongation.

Many models of axonal elongation are based on the assumption that the rate of lengthening is driven by the production of cellular materials in the soma. These models make specific predictions about transport and concentration gradients of proteins both over time and along the length of the axon. In vivo, it is well accepted that for a particular neuron the length and rate of growth are controlled by the body size and rate of growth of the animal.

A physical model of axonal elongation: force, viscosity, and adhesions govern the mode of outgrowth.

Whether the axonal framework is stationary or moves is a central debate in cell biology. To better understand this problem, we developed a mathematical model that incorporates force generation at the growth cone, the viscoelastic properties of the axon, and adhesions between the axon and substrate. Using force-calibrated needles to apply and measure forces at the growth cone, we used docked mitochondria as markers to monitor movement of the axonal framework.