Negative capacitance (NC) is a promising route towards low-power electronics. Here, a theory clarifying the connection between NC and voltage amplification is presented, and it is predicted that incipient ferroelectric states that do not necessarily maximize NC can result in a tenfold voltage amplification.
Giant voltage amplification from electrostatically induced incipient ferroelectric statesFerroelectrics subject to suitable electric boundary conditions present a steady negative capacitance response. When the ferroelectric is in a heterostructure, this behaviour yields a voltage amplification in the other elements, which experience a potential difference larger than the one applied, holding promise for low-power electronics. So far research has focused on verifying this effect and little is known about how to optimize it. Here, we describe an electrostatic theory of ferroelectric/dielectric superlattices, convenient model systems, and show the relationship between the negative permittivity of the ferroelectric layers and the voltage amplification in the dielectric ones. Then, we run simulations of PbTiO3/SrTiO3 superlattices to reveal the factors most strongly affecting the amplification. In particular, we find that giant effects (up to tenfold increases) can be obtained when PbTiO3 is brought close to the so-called ‘incipient ferroelectric’ state.
Representative ferroelectric states of PbTiO3/SrTiO3 superlattices.
Mónica Graf, Hugo Aramberri, Pavlo Zubko & Jorge Íñiguez
doi: 10.1038/s41563-022-01332-z | |
Reconstituted cytoskeleton networks linked with catch bonds display increased mechanical strength and crack resistance than those containing slip bonds, and simultaneously being more deformable, which allows for better adaptability to new mechanical environments.
Weak catch bonds make strong networksMolecular catch bonds are ubiquitous in biology and essential for processes like leucocyte extravasion and cellular mechanosensing. Unlike normal (slip) bonds, catch bonds strengthen under tension. The current paradigm is that this feature provides ‘strength on demand’, thus enabling cells to increase rigidity under stress. However, catch bonds are often weaker than slip bonds because they have cryptic binding sites that are usually buried. Here we show that catch bonds render reconstituted cytoskeletal actin networks stronger than slip bonds, even though the individual bonds are weaker. Simulations show that slip bonds remain trapped in stress-free areas, whereas weak binding allows catch bonds to mitigate crack initiation by moving to high-tension areas. This ‘dissociation on demand’ explains how cells combine mechanical strength with the adaptability required for shape change, and is relevant to diseases where catch bonding is compromised, including focal segmental glomerulosclerosis caused by the α-actinin-4 mutant studied here. We surmise that catch bonds are the key to create life-like materials.
Single-molecule measurements of actin filament binding reveal catch bonding for WT α-actinin-4 but not the K255E mutant.
Yuval Mulla, Mario J. Avellaneda, Antoine Roland, Lucia Baldauf, Wonyeong Jung, Taeyoon Kim, Sander J. Tans & Gijsje H. Koenderink
doi: 10.1038/s41563-022-01288-0 | |
长按扫描二维码，关注Nature Materials公众号