4,270 research outputs found
Laplacian-Steered Neural Style Transfer
Neural Style Transfer based on Convolutional Neural Networks (CNN) aims to
synthesize a new image that retains the high-level structure of a content
image, rendered in the low-level texture of a style image. This is achieved by
constraining the new image to have high-level CNN features similar to the
content image, and lower-level CNN features similar to the style image. However
in the traditional optimization objective, low-level features of the content
image are absent, and the low-level features of the style image dominate the
low-level detail structures of the new image. Hence in the synthesized image,
many details of the content image are lost, and a lot of inconsistent and
unpleasing artifacts appear. As a remedy, we propose to steer image synthesis
with a novel loss function: the Laplacian loss. The Laplacian matrix
("Laplacian" in short), produced by a Laplacian operator, is widely used in
computer vision to detect edges and contours. The Laplacian loss measures the
difference of the Laplacians, and correspondingly the difference of the detail
structures, between the content image and a new image. It is flexible and
compatible with the traditional style transfer constraints. By incorporating
the Laplacian loss, we obtain a new optimization objective for neural style
transfer named Lapstyle. Minimizing this objective will produce a stylized
image that better preserves the detail structures of the content image and
eliminates the artifacts. Experiments show that Lapstyle produces more
appealing stylized images with less artifacts, without compromising their
"stylishness".Comment: Accepted by the ACM Multimedia Conference (MM) 2017. 9 pages, 65
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Mobile Protons Limit the Stability of Salt Bridges in the Gas Phase: Implications for the Structures of Electrosprayed Protein Ions.
Electrosprayed protein ions can retain native-like conformations. The intramolecular contacts that stabilize these compact gas-phase structures remain poorly understood. Recent work has uncovered abundant salt bridges in electrosprayed proteins. Salt bridges are zwitterionic BH+/A- contacts. The low dielectric constant in the vacuum strengthens electrostatic interactions, suggesting that salt bridges could be a key contributor to the retention of compact protein structures. A problem with this assertion is that H+ are mobile, such that H+ transfer can convert salt bridges into neutral B0/HA0 contacts. This possible salt bridge annihilation puts into question the role of zwitterionic motifs in the gas phase, and it calls for a detailed analysis of BH+/A- versus B0/HA0 interactions. Here, we investigate this issue using molecular dynamics (MD) simulations and electrospray experiments. MD data for short model peptides revealed that salt bridges with static H+ have dissociation energies around 700 kJ mol-1. The corresponding B0/HA0 contacts are 1 order of magnitude weaker. When considering the effects of mobile H+, BH+/A- bond energies were found to be between these two extremes, confirming that H+ migration can significantly weaken salt bridges. Next, we examined the protein ubiquitin under collision-induced unfolding (CIU) conditions. CIU simulations were conducted using three different MD models: (i) Positive-only runs with static H+ did not allow for salt bridge formation and produced highly expanded CIU structures. (ii) Zwitterionic runs with static H+ resulted in abundant salt bridges, culminating in much more compact CIU structures. (iii) Mobile H+ simulations allowed for the dynamic formation/annihilation of salt bridges, generating CIU structures intermediate between scenarios (i) and (ii). Our results uncover that mobile H+ limit the stabilizing effects of salt bridges in the gas phase. Failure to consider the effects of mobile H+ in MD simulations will result in unrealistic outcomes under CIU conditions
Testing the Robustness of Solution Force Fields for MD Simulations on Gaseous Protein Ions.
It is believed that electrosprayed proteins and protein complexes can retain solution-like conformations in the gas phase. However, the lack of high-resolution structure determination methods for gaseous protein ions implies that their properties remain poorly understood. Many practitioners tackle this difficulty by complementing mass spectrometry-based experiments with molecular dynamics (MD) simulations. It is a potential problem that the standard MD force fields used for this purpose (such as OPLS-AA/L and CHARMM) were optimized for solution conditions. The question whether these force fields produce meaningful gas-phase data has received surprisingly little attention. Standard force fields are overpolarized to account for an aqueous environment, i.e., atomic charges and intramolecular dipole moments are ∼20% larger than predicted by gas-phase ab initio methods. Here, we examined the implications of this overpolarization by conducting a series of MD simulations on electrosprayed proteins. Force fields were modified via a charge scaling factor (CSF), while ensuring that the net protein charge remained unchanged. CSF = 0.8 should roughly eliminate water-associated overpolarization. Gas-phase CHARMM simulations on myoglobin with CSF = 0.8 and with unmodified parameters (CSF = 1) yielded similar results, preserving a compact structure that was consistent with ion mobility experiments. Major structural changes caused by weakened charge-dipole and dipole-dipole contacts occurred only when lowering CSF to physically unreasonable values (0.5 and 0.1). Similar results were obtained in mobile-proton OPLS-AA/L simulations on the collision-induced dissociation of transthyretin. Our data support the view that gas-phase MD simulations with standard (solution) force fields are suitable for modeling gaseous protein ions in a semiquantitative manner. Although this is welcome news for the mass spectrometry community, it is hoped that dedicated gas-phase MD force fields will become available in the near future
Thermal Control of Engineered T-cells
Genetically engineered T-cells are being developed to perform a variety of therapeutic functions. However, no robust mechanisms exist to externally control the activity of T-cells at specific locations within the body. Such spatiotemporal control could help mitigate potential off-target toxicity due to incomplete molecular specificity in applications such as T-cell immunotherapy against solid tumors. Temperature is a versatile external control signal that can be delivered to target tissues in vivo using techniques such as focused ultrasound and magnetic hyperthermia. Here, we test the ability of heat shock promoters to mediate thermal actuation of genetic circuits in primary human T-cells in the well-tolerated temperature range of 37–42 °C, and introduce genetic architectures enabling the tuning of the amplitude and duration of thermal activation. We demonstrate the use of these circuits to control the expression of chimeric antigen receptors and cytokines, and the killing of target tumor cells. This technology provides a critical tool to direct the activity of T-cells after they are deployed inside the body
Theory of a Continuous H Normal-to-Superconducting Transition
I study the transition within the Ginzburg-Landau model, with
-component order parameter . I find a renormalized fixed point free
energy, exact in limit, suggestive of a nd-order
transition in contrast to a general belief of a st-order transition. The
thermal fluctuations for force one to consider an infinite set of
marginally relevant operators for . I find , predicting
that the ODLRO does not survive thermal fluctuations in . The result is
a solution to a critical fixed point that was found to be inaccessible within
-expansion, previously considered in E.Brezin, D.R.Nelson,
A.Thiaville, Phys.Rev.B {\bf 31}, 7124 (1985), and was interpreted as a
st-order transition.Comment: 4 pages, self-unpacking uuencoded compressed postscript file with a
figure already inside text; to appear in Phys. Rev. Lett
Field theoretical representation of the Hohenberg-Kohn free energy for fluids
To go beyond Gaussian approximation to the Hohenberg-Kohn free energy playing
the key role in the density functional theory (DFT), the density functional
\textit{integral} representation would be relevant, because field theoretical
approach to perturbative calculations becomes available. Then the present
letter first derives the associated Hamiltonian of density functional,
explicitly including logarithmic entropy term, from the grand partition
function expressed by configurational integrals. Moreover, two things are done
so that the efficiency of the obtained form may be revealed: to demonstrate
that this representation facilitates the field theoretical treatment of the
perturbative calculation, and further to compare our perturbative formulation
with that of the DFT.Comment: 5 pages, revtex, modified on 13 April 2000 [see eqs. (3), (6), and
(13)
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An ANGPTL4-ceramide-protein kinase Cζ axis mediates chronic glucocorticoid exposure-induced hepatic steatosis and hypertriglyceridemia in mice.
Chronic or excess glucocorticoid exposure causes lipid disorders such as hypertriglyceridemia and hepatic steatosis. Angptl4 (angiopoietin-like 4), a primary target gene of the glucocorticoid receptor in hepatocytes and adipocytes, is required for hypertriglyceridemia and hepatic steatosis induced by the synthetic glucocorticoid dexamethasone. Angptl4 has also been shown to be required for dexamethasone-induced hepatic ceramide production. Here, we further examined the role of ceramide-mediated signaling in hepatic dyslipidemia caused by chronic glucocorticoid exposure. Using a stable isotope-labeling technique, we found that dexamethasone treatment induced the rate of hepatic de novo lipogenesis and triglyceride synthesis. These dexamethasone responses were compromised in Angptl4-null mice (Angptl4-/-). Treating mice with myriocin, an inhibitor of the rate-controlling enzyme of de novo ceramide synthesis, serine palmitoyltransferase long-chain base subunit 1 (SPTLC1)/SPTLC2, decreased dexamethasone-induced plasma and liver triglyceride levels in WT but not Angptl4-/- mice. We noted similar results in mice infected with adeno-associated virus-expressing small hairpin RNAs targeting Sptlc2. Protein phosphatase 2 phosphatase activator (PP2A) and protein kinase Cζ (PKCζ) are two known downstream effectors of ceramides. We found here that mice treated with an inhibitor of PKCζ, 2-acetyl-1,3-cyclopentanedione (ACPD), had lower levels of dexamethasone-induced triglyceride accumulation in plasma and liver. However, small hairpin RNA-mediated targeting of the catalytic PP2A subunit (Ppp2ca) had no effect on dexamethasone responses on plasma and liver triglyceride levels. Overall, our results indicate that chronic dexamethasone treatment induces an ANGPTL4-ceramide-PKCζ axis that activates hepatic de novo lipogenesis and triglyceride synthesis, resulting in lipid disorders
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