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Biomedical subjects

Thomas M Fischer

Publications and source records attributed to Thomas M Fischer.

6 recordsLinked to original sources

Interfacial thermocapillary vortical flow for microfluidic mixing.

We present a method for the mixing of fluids in a quasi two-dimensional system with low Reynolds number by means of generating a vortical flow. A two-dimensional cavitation bubble is induced in liquid-expanded phase by locally heating a Langmuir monolayer at the air/liquid interface with an IR laser. The laser-induced cavitation bubble works as a microfluidic pump and generates a thermocapillary flow around the pump. As a result, the surrounding liquid-expanded phase flows in one direction. Perturbing the thermocapillary flow with solid folds that are created by compression and reexpansion of the monolayer induces the vortical flow behind the folds. Applying the equation of creeping flow, we find a torque halfway from the center causing the vortical flow. The vorticity created in this way stretches the liquid-expanded and gaseous phase in the azimuthal direction and at the same time thins both phases in the radial direction. If the vortical flow could be maintained long enough to reach a radial thinning that would allow the interdiffusion of surfactants at the surface, then this technique would open a route for the effective two-dimensional microfluidic mixing at low Reynolds numbers.

1,2-Dipalmitoylphosphatidylcholine↗

Fold-speed control in collapsing mixed phospholipid monolayers.

Mixed monolayers of dipalmitoylphosphatidylcholine (DPPC) and dipalmitoyl-phosphatidylserine are compressed beyond their collapse pressure. Primary and secondary folds that grow perpendicular to the compression direction are observed using Brewster angle microscopy. The secondary fold velocity is measured with a fast charge-coupled device camera. We observe a reduction in secondary fold speed when increasing the mole fraction of the softer DPPC component in the monolayer. The fracture kinetics follows theoretical predictions for the fold coarsening dynamics of uniaxially stressed three-dimensional systems.

1,2-Dipalmitoylphosphatidylcholine↗

Shape memory of human red blood cells.

The human red cell can be deformed by external forces but returns to the biconcave resting shape after removal of the forces. If after such shape excursions the rim is always formed by the same part of the membrane, the cell is said to have a memory of its biconcave shape. If the rim can form anywhere on the membrane, the cell would have no shape memory. The shape memory was probed by an experiment called go-and-stop. Locations on the membrane were marked by spontaneously adhering latex spheres. Shape excursions were induced by shear flow. In virtually all red cells, a shape memory was found. After stop of flow and during the return of the latex spheres to the original location, the red cell shape was biconcave. The return occurred by a tank-tread motion of the membrane. The memory could not be eliminated by deforming the red cells in shear flow up to 4 h at room temperature as well as at 37 degrees C. It is suggested that 1). the characteristic time of stress relaxation is >80 min and 2). red cells in vivo also have a shape memory.

Biomechanical Phenomena↗

Synaptic augmentation contributes to environment-driven regulation of the aplysia siphon-withdrawal reflex.

This research shows that short-term synaptic plasticity can play a critical role in shaping the behavioral response to environmental change. In Aplysia, exposure to turbulent environments produces a stable reduction in the duration of the siphon-withdrawal reflex (SWR) and the responsiveness of siphon motor neurons. Recovery takes >1 min after a brief (10 sec-5 min) exposure but <1 min after a long (10 min) exposure. Here we demonstrate that (1) in-turbulence and post-turbulence phases of regulation depend on different cellular processes and (2) the post-turbulence phase of regulation is mediated by augmentation (AUG), an activity-dependent form of short-term synaptic plasticity. In reduced preparations (tail, siphon, and CNS), we show that treatment with 100 microm d-tubocurarine has no effect on in-turbulence regulation but blocks up to 90% of post-turbulence regulation, indicating that these phases of regulation are mediated by distinct cellular process. We then show that (1) turbulence induces activity in L30 inhibitory interneurons, (2) this activation produces AUG that lasts 1 min after a brief exposure to turbulence, and (3) manipulations that attenuate L30 AUG also attenuate regulation after brief turbulence. We also found that long (10 min) exposures to turbulence do not produce a post-turbulence phase of regulation because L30 activity declines over the course of a long turbulence exposure, leading to the decay of AUG before turbulence offset. Our results demonstrate a specific behavioral function of AUG and show how interactions between cellular processes can confer temporal sensitivity in the network regulation of behavior.

Animals↗

Temporal and spatial aspects of an environmental stimulus influence the dynamics of behavioral regulation of the Aplysia siphon-withdrawal response.

Exposure to turbulence, an environmental stimulus, produces behavioral adaptation in the Aplysia siphon-withdrawal response (SWR). The authors show that the duration and spatial extent of turbulence influence adaptation recovery. In terms of duration, recovery in whole animals and reduced preparations (tail, siphon, and CNS) was more rapid after longer exposures to turbulence (10 min) than after briefer exposures (10 s-5 min). In terms of spatial extent, recovery in reduced preparations was more rapid after diffuse turbulence (tail and siphon together) compared with focal turbulence (siphon alone). Furthermore, spatial extent and duration interact: Duration regulates recovery only when turbulence is diffuse. Results suggest that SWR adaptation reflects a composite of cellular processes, including short-term synaptic enhancement in L30 inhibitory interneurons.

Animals↗