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Abstract Winter Arctic sea-ice concentration (SIC) decline plays an important role in Arctic amplification which, in turn, influences Arctic ecosystems, midlatitude weather and climate. SIC over the Barents-Kara Seas (BKS) shows large interannual variations, whose origin is still unclear. Here we find that interannual variations in winter BKS SIC have significantly strengthened in recent decades likely due to increased amplitudes of the El Niño-Southern Oscillation (ENSO) in a warming climate. La Niña leads to enhanced Atlantic Hadley cell and a positive phase North Atlantic Oscillation-like anomaly pattern, together with concurring Ural blocking, that transports Atlantic ocean heat and atmospheric moisture toward the BKS and promotes sea-ice melting via intensified surface warming. The reverse is seen during El Niño which leads to weakened Atlantic poleward transport and an increase in the BKS SIC. Thus, interannual variability of the BKS SIC partly originates from ENSO via the Atlantic pathway. 

Flexible and stretchable bioelectronics provides a biocompatible interface between electronics and biological systems and has received tremendous attention for in situ monitoring of various biological systems. Considerable progress in organic electronics has made organic semiconductors, as well as other organic electronic materials, ideal candidates for developing wearable, implantable, and biocompatible electronic circuits due to their potential mechanical compliance and biocompatibility. Organic electrochemical transistors (OECTs), as an emerging class of organic electronic building blocks, exhibit significant advantages in biological sensing due to the ionic nature at the basis of the switching behavior, low driving voltage (<1 V), and high transconductance (in millisiemens range). During the past few years, significant progress in constructing flexible/stretchable OECTs (FSOECTs) for both biochemical and bioelectrical sensors has been reported. In this regard, to summarize major research accomplishments in this emerging field, this review first discusses structure and critical features of FSOECTs, including working principles, materials, and architectural engineering. Next, a wide spectrum of relevant physiological sensing applications, where FSOECTs are the key components, are summarized. Last, major challenges and opportunities for further advancing FSOECT physiological sensors are discussed.

 

We give sharp conditions for the large time asymptotic simplification of aggregation-diffusion equations with linear diffusion. As soon as the interaction potential is bounded and its first and second derivatives decay fast enough at infinity, then the linear diffusion overcomes its effect, either attractive or repulsive, for large times independently of the initial data, and solutions behave like the fundamental solution of the heat equation with some rate. The potential$$W(x) \sim \log |x|$$$W\left(x\right)\sim log\left|x\right|$for$$|x| \gg 1$$$\left|x\right|\gg 1$appears as the natural limiting case when the intermediate asymptotics change. In order to obtain such a result, we produce uniform-in-time estimates in a suitable rescaled change of variables for the entropy, the second moment, Sobolev norms and the$$C^\alpha $$$C^{\alpha }$regularity with a novel approach for this family of equations using modulus of continuity techniques.

 

Plants can regenerate new organs from damaged or detached tissues. In the process of de novo root regeneration (DNRR), adventitious roots are frequently formed from the wound site on a detached leaf. Salicylic acid (SA) is a key phytohormone regulating plant defenses and stress responses. The role of SA and its acting mechanisms during de novo organogenesis is still unclear. Here, we found that endogenous SA inhibited the adventitious root formation after cutting. Free SA rapidly accumulated at the wound site, which was accompanied by an activation of SA response. SA receptors NPR3 and NPR4, but not NPR1, were required for DNRR. Wounding-elevated SA compromised the expression of AUX1, and subsequent transport of auxin to the wound site. A mutation in AUX1 abolished the enhanced DNRR in low SA mutants. Our work elucidates a role of SA in regulating DNRR and suggests a potential link between biotic stress and tissue regeneration.