Turbulence is the major cause of friction losses in transport processes and it is responsible for a drastic drag increase in flows over bounding surfaces. While much effort is invested into developing ways to control and reduce turbulence intensities [1][2][3] , so far no methods exist to altogether eliminate turbulence if velocities are sufficiently large. We demonstrate for pipe flow that appropriate distortions to the velocity profile lead to a complete collapse of turbulence and subsequently friction losses are reduced by as much as 90%. Counterintuitively, the return to laminar motion is accomplished by initially increasing turbulence intensities or by transiently amplifying wall shear. Since neither the Reynolds number nor the shear stresses decrease (the latter often increase), these measures are not indicative of turbulence collapse. Instead, an amplification mechanism 4,5 measuring the interaction between eddies and the mean shear is found to set a threshold below which turbulence is suppressed beyond recovery.Flows through pipes and hydraulic networks are generally turbulent and the friction losses encountered in these flows are responsible for approximately 10% of the global electric energy consumption. Here turbulence causes a severe drag increase and consequently much larger forces are needed to maintain desired flow rates. In pipes, both laminar and turbulent states are stable (the former is believed to be linearly stable for all Reynolds number (Re) values; the latter is stable if Re > 2, 040 (ref. 6 )), but with increasing speed the laminar state becomes more and more susceptible to small disturbances. Hence, in practice most flows are turbulent at sufficiently large Re. While the stability of laminar flow has been studied in great detail, little attention has been paid to the susceptibility of turbulence, the general assumption being that once turbulence is established it is stable.Many turbulence control strategies have been put forward to reduce the drag encountered in shear flows [7][8][9][10][11][12][13][14][15][16][17] . Recent strategies employ feedback mechanisms to actively counter selected velocity components or vortices. Such methods usually require knowledge of the full turbulent velocity field. In computer simulations 7,8 , it could be demonstrated that under these ideal conditions, flows at a low Re number can even be relaminarized. In experiments, the required detailed manipulation of the time-dependent velocity field is, however, currently impossible to achieve. Other studies employ passive (for example, riblets) or active (oscillations or excitation of travelling waves) methods to interfere with the near-wall turbulence creation. Typically here drag reduction of 10 to 40% has been reported, but often the control cost is substantially higher than the gain, or a net gain can be achieved only in a narrow Re number regime.Instead of attempting to control or counter certain components of the complex fluctuating flow fields, we will show in the following that by appropriately dist...

Pulsating flows through tubular geometries are laminar provided that velocities are moderate. This in particular is also believed to apply to cardiovascular flows where inertial forces are typically too low to sustain turbulence. On the other hand, flow instabilities and fluctuating shear stresses are held responsible for a variety of cardiovascular diseases. Here we report a nonlinear instability mechanism for pulsating pipe flow that gives rise to bursts of turbulence at low flow rates. Geometrical distortions of small, yet finite, amplitude are found to excite a state consisting of helical vortices during flow deceleration. The resulting flow pattern grows rapidly in magnitude, breaks down into turbulence, and eventually returns to laminar when the flow accelerates. This scenario causes shear stress fluctuations and flow reversal during each pulsation cycle. Such unsteady conditions can adversely affect blood vessels and have been shown to promote inflammation and dysfunction of the shear stress-sensitive endothelial cell layer.

Summary When crawling through the body, leukocytes often traverse tissues that are densely packed with extracellular matrix and other cells, and this raises the question: How do leukocytes overcome compressive mechanical loads? Here, we show that the actin cortex of leukocytes is mechanoresponsive and that this responsiveness requires neither force sensing via the nucleus nor adhesive interactions with a substrate. Upon global compression of the cell body as well as local indentation of the plasma membrane, Wiskott-Aldrich syndrome protein (WASp) assembles into dot-like structures, providing activation platforms for Arp2/3 nucleated actin patches. These patches locally push against the external load, which can be obstructing collagen fibers or other cells, and thereby create space to facilitate forward locomotion. We show in vitro and in vivo that this WASp function is rate limiting for ameboid leukocyte migration in dense but not in loose environments and is required for trafficking through diverse tissues such as skin and lymph nodes.

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