242 research outputs found
Finite-size scaling of out-of-time-ordered correlators at late times
Chaotic dynamics in quantum many-body systems scrambles local information so
that at late times it can no longer be accessed locally. This is reflected
quantitatively in the out-of-time-ordered correlator of local operators, which
is expected to decay to zero with time. However, for systems of finite size,
out-of-time-ordered correlators do not decay exactly to zero and in this paper
we show that the residual value can provide useful insights into the chaotic
dynamics. When energy is conserved, the late-time saturation value of the
out-of-time-ordered correlator of generic traceless local operators scales as
an inverse polynomial in the system size. This is in contrast to the inverse
exponential scaling expected for chaotic dynamics without energy conservation.
We provide both analytical arguments and numerical simulations to support this
conclusion.Comment: improved presentatio
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Interplay of Staphylococcal and Host Proteases Promotes Skin Barrier Disruption in Netherton Syndrome.
Netherton syndrome (NS) is a monogenic skin disease resulting from loss of function of lymphoepithelial Kazal-type-related protease inhibitor (LEKTI-1). In this study we examine if bacteria residing on the skin are influenced by the loss of LEKTI-1 and if interaction between this human gene and resident bacteria contributes to skin disease. Shotgun sequencing of the skin microbiome demonstrates that lesional skin of NS subjects is dominated by Staphylococcus aureus (S. aureus) and Staphylococcus epidermidis (S. epidermidis). Isolates of either species from NS subjects are able to induce skin inflammation and barrier damage on mice. These microbes promote skin inflammation in the setting of LEKTI-1 deficiency due to excess proteolytic activity promoted by S. aureus phenol-soluble modulin α as well as increased bacterial proteases staphopain A and B from S. aureus or EcpA from S. epidermidis. These findings demonstrate the critical need for maintaining homeostasis of host and microbial proteases to prevent a human skin disease
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