SimSwap: An Efficient Framework For High Fidelity Face Swapping

We propose an efficient framework, called Simple Swap (SimSwap), aiming for generalized and high fidelity face swapping. In contrast to previous approaches that either lack the ability to generalize to arbitrary identity or fail to preserve attributes like facial expression and gaze direction, our framework is capable of transferring the identity of an arbitrary source face into an arbitrary target face while preserving the attributes of the target face. We overcome the above defects in the following two ways. First, we present the ID Injection Module (IIM) which transfers the identity information of the source face into the target face at feature level. By using this module, we extend the architecture of an identity-specific face swapping algorithm to a framework for arbitrary face swapping. Second, we propose the Weak Feature Matching Loss which efficiently helps our framework to preserve the facial attributes in an implicit way. Extensive experiments on wild faces demonstrate that our SimSwap is able to achieve competitive identity performance while preserving attributes better than previous state-of-the-art methods. The code is already available on github: https://github.com/neuralchen/SimSwap.Comment: Accepted by ACMMM 202

Liposome clusters with shear stress-induced membrane permeability

In the present work experimental investigations of the flow characteristic and heat transport of wavy silicone oil films were accomplished with different angles of inclination (13°, 30°, 60° and 90°) and Kapitza numbers, which allow a deeper view into the structure and the heat transport phenomena. From the experimental results of laminar-wavy and turbulent films dimensionless approximation equations for different parameters were determined for the description of the film flow like the film thickness, wave frequency and the wave velocity. Furthermore new boundaries for the different film regimes could be discriminated from the results. A substantial part of the work was the development of more suitable temporally and locally high resolving measurement techniques. Thus a measurement technique on the basis of the fluorescence intensity method was developed, which is able to determine simultaneously the film thickness and the wave velocity. A further component of the work was the measurement of the film velocity of periodically excited two-dimensional-wavy films with the Particle Image Velocimetry PIV. The velocity field of a complete length of a two-dimensional wave could be reconstructed by simultaneous film thickness measurements. By measurements of the wall temperature distribution with a developed measuring system on the basis of the infrared thermography the influence of the wavy surface on the heat transfer within the laminar-wavy flow range could be examined. The results of the flow characteristic investigations of wavy film flow are valuable contributions to understand the influence of the waves on hydrodynamics and heat-transport

Stratifin regulates stabilization of receptor tyrosine kinases via interaction with ubiquitin-specific protease 8 in lung adenocarcinoma

Previously we have reported that stratifin (SFN, 14-3-3 sigma) acts as a novel oncogene, accelerating the tumor initiation and progression of lung adenocarcinoma. Here, pull-down assay and LC-MS/MS analysis revealed that ubiquitin-specific protease 8 (USP8) specifically bound to SFN in lung adenocarcinoma cells. Both USP8 and SFN showed higher expression in human lung adenocarcinoma than in normal lung tissue, and USP8 expression was significantly correlated with SFN expression. Expression of SFN, but not of USP8, was associated with histological subtype, pathological stage, and poor prognosis. USP8 stabilizes receptor tyrosine kinases (RTKs) such as EGFR and MET by deubiquitination, contributing to the proliferative activity of many human cancers including non-small cell lung cancer. In vitro, USP8 binds to SFN and they co-localize at the early endosomes in lung adenocarcinoma cells. Moreover, USP8 or SFN knockdown leads to downregulation of tumor cellular proliferation and upregulation of apoptosis, p-EGFR or p-MET, which are related to the degradation pathway, and accumulation of ubiquitinated RTKs, leading to lysosomal degradation. Additionally, mutant USP8, which is unable to bind to SFN, reduces the expression of RTKs and p-STAT3. We also found that interaction with SFN is critical for USP8 to exert its auto-deubiquitination function and avoid dephosphorylation by PP1. Our findings demonstrate that SFN enhances RTK stabilization through abnormal USP8 regulation in lung adenocarcinoma, suggesting that SFN could be a more suitable therapeutic target for lung adenocarcinoma than USP8