Robust Identity Perceptual Watermark Against Deepfake Face Swapping

Notwithstanding offering convenience and entertainment to society, Deepfake face swapping has caused critical privacy issues with the rapid development of deep generative models. Due to imperceptible artifacts in high-quality synthetic images, passive detection models against face swapping in recent years usually suffer performance damping regarding the generalizability issue. Therefore, several studies have been attempted to proactively protect the original images against malicious manipulations by inserting invisible signals in advance. However, the existing proactive defense approaches demonstrate unsatisfactory results with respect to visual quality, detection accuracy, and source tracing ability. In this study, we propose the first robust identity perceptual watermarking framework that concurrently performs detection and source tracing against Deepfake face swapping proactively. We assign identity semantics regarding the image contents to the watermarks and devise an unpredictable and unreversible chaotic encryption system to ensure watermark confidentiality. The watermarks are encoded and recovered by jointly training an encoder-decoder framework along with adversarial image manipulations. Extensive experiments demonstrate state-of-the-art performance against Deepfake face swapping under both cross-dataset and cross-manipulation settings.Comment: Submitted for revie

Loss of TMEM106B Ameliorates Lysosomal and Frontotemporal Dementia-Related Phenotypes in Progranulin-Deficient Mice.

Progranulin (GRN) and TMEM106B are associated with several common neurodegenerative disorders including frontotemporal lobar degeneration (FTLD). A TMEM106B variant modifies GRN-associated FTLD risk. However, their functional relationship in vivo and the mechanisms underlying the risk modification remain unclear. Here, using transcriptomic and proteomic analyses with Grn−/− and Tmem106b−/− mice, we show that, while multiple lysosomal enzymes are increased in Grn−/− brain at both transcriptional and protein levels, TMEM106B deficiency causes reduction in several lysosomal enzymes. Remarkably, Tmem106b deletion from Grn−/− mice normalizes lysosomal protein levels and rescues FTLD-related behavioral abnormalities and retinal degeneration without improving lipofuscin, C1q, and microglial accumulation. Mechanistically, TMEM106B binds vacuolar-ATPase accessory protein 1 (AP1). TMEM106B deficiency reduces vacuolar-ATPase AP1 and V0 subunits, impairing lysosomal acidification and normalizing lysosomal protein levels in Grn−/− neurons. Thus, Grn and Tmem106b genes have opposite effects on lysosomal enzyme levels, and their interaction determines the extent of neurodegeneration

High endemicity of alveolar echinococcosis in Yili Prefecture, Xinjiang Autonomous Region, the People’s Republic of China: infection status in different ethnic communities and in small mammals

Alveolar echinococcosis (AE) is a neglected zoonosis caused by the larval stage of the fox/dog tapeworm Echinococcus multilocularis. In this study, we collected data on 286 AE cases reported from Yili Prefecture, Xinjiang Autonomous Region, the People’s Republic of China from 1989 to 2015 with an annual incidence (AI) of 0.41/100,000. Among the patients, 73.08% were diagnosed in the last 11 years. The incidence (0.51–1.22 cases/100,000 residents) was higher in the high-altitude mountainous areas than those in low level areas (0.19–0.29/100,000 residents). In term of ethnic group, the AI of AE in Mongolian (2.06/100,000 residents) and Kazak (0.93/100,000) groups had higher incidence than the other ethnic groups, indicating sheep-farming activity is a risk for infection given that sheep farming is mainly practiced by these two groups in the prefecture. A total of 1411 small mammals were captured with 9.14% infected with E. multilocularis metacestodes. Microtus obscurus was the dominant species captured in the mountainous pasture areas with 15.01% infection rate, whereas Mus musculus and Apodemus sylvaticus were the dominant small mammals in the low altitude areas. Only 0.40% of A. sylvaticus were infected with E. multilocularis. These findings show that Yili Prefecture is a highly endemic area for AE and that the high-altitude pasture areas favorable for M. obscurus may play an important role in its transmission in this region

ERAD Substrate Recognition by the HRD1 Transmembrane Domain : : A Molecular Genetic Analysis

Endoplasmic Reticulum Associated Degradation (ERAD) is a conserved pathway that is responsible for the degradation of aberrant proteins in the ER. These proteins are first tagged with ubiquitin through the concerted action of E1, E2, and E3 ubiquitination enzymes and then degraded by the proteasome. Hrd1p is one of the principle E3 ubiquitin ligases involved in ERAD. It is an integral ER membrane protein with six transmembrane spans and a cytosolic RING domain and is responsible for the recognition and degradation of a wide variety of ER-localized misfolded proteins, including lumenal (ERAD-L) and integral membrane (ERAD-M) substrates. Previous studies have suggested that Hrd1p substrate recognition function as an "allosteric" model and that the Hrd1p transmembrane domain is a key site for substrate selectivity. To further explore this idea, we have conducted a screen to isolate Hrd1p mutants that show increased activity toward substrates of the HRD pathway. We have isolated a single point mutation in the transmembrane domain of Hrd1p that imparts more effective degradation of an ERAD-M substrate. Further analysis of this mutation revealed that it causes selective increased activity toward a single substrate and degrades all other substrates normally. This selective increase in activity supports the idea that different regions of the transmembrane domain are responsible for the recognition of different Hrd1p substrate

ERAD Substrate Recognition by the HRD1 Transmembrane Domain : : A Molecular Genetic Analysis

Endoplasmic Reticulum Associated Degradation (ERAD) is a conserved pathway that is responsible for the degradation of aberrant proteins in the ER. These proteins are first tagged with ubiquitin through the concerted action of E1, E2, and E3 ubiquitination enzymes and then degraded by the proteasome. Hrd1p is one of the principle E3 ubiquitin ligases involved in ERAD. It is an integral ER membrane protein with six transmembrane spans and a cytosolic RING domain and is responsible for the recognition and degradation of a wide variety of ER-localized misfolded proteins, including lumenal (ERAD-L) and integral membrane (ERAD-M) substrates. Previous studies have suggested that Hrd1p substrate recognition function as an "allosteric" model and that the Hrd1p transmembrane domain is a key site for substrate selectivity. To further explore this idea, we have conducted a screen to isolate Hrd1p mutants that show increased activity toward substrates of the HRD pathway. We have isolated a single point mutation in the transmembrane domain of Hrd1p that imparts more effective degradation of an ERAD-M substrate. Further analysis of this mutation revealed that it causes selective increased activity toward a single substrate and degrades all other substrates normally. This selective increase in activity supports the idea that different regions of the transmembrane domain are responsible for the recognition of different Hrd1p substrate

The role of platelet to mean platelet volume ratio in the identification of adult-onset still’s disease from sepsis

OBJECTIVES: Inflammatory factors exert a significant role in the development of adult-onset Still’s disease (AOSD) and sepsis. Although platelet counts and platelet parameters have long served as indicators for inflammatory diseases, their role in the differential diagnosis between adult-onset still´s disease and sepsis remains unclear. We designed this retrospective study to explore whether the platelet to mean platelet volume (MPV) ratio (PMR) can help to distinguish AOSD from sepsis. METHODS: A total of 110 AOSD patients and 84 sepsis patients were enrolled in the study. Seventy-three AOSD patients and 56 sepsis patients between January 2010 and June 2017 were enrolled in the test cohort to analyze PMR values, which was then validated in the validation cohort (37 AOSD patients and 28 sepsis patients between June 2017 and December 2019). RESULTS: The values of PMR were significantly higher in AOSD patients than in sepsis patients (test cohort, validation cohort, and entire cohort), In the test cohort, logistic regression analysis showed that PMR was an independent risk factor of AOSD (odds ratios [OR]: 9.22, 95% confidence interval [CI] 2.15-39.46, p=0.003). Further receiver operating characteristic curve (ROC) analysis showed that the area under the ROC curve was 0.735 (95% CI 0.631-0.839, po0.001) for PMR alone and 0.925 (95% CI 0.869-0.980, po0.001) for the combination of PMR and serum ferritin. Consistently, the validation cohort exhibited analogous results. CONCLUSIONS: PMR could be used as a single indicator or a complementary indicator to distinguish AOSD from sepsis

Research on the Formulation Design of Nano-Oil Displacement Agents Suitable for Xinjiang Jimusaer Shale Oil

In order to improve the recovery efficiency of the Jimusaer tight reservoir in Xinjiang, the nanometer oil displacement agent system suitable for the Jimusaer reservoir was used. In view of the low permeability, high formation temperature, and high salinity characteristics of the prepared water in the Jimusaer tight conglomerate reservoir in Xinjiang, the performance of the nanometer oil displacement agent affecting oil recovery was studied; the study considered interfacial tension, temperature resistance, wetting performance, static oil washing efficiency, and long-term stability. Nanometer oil displacement agent No. 4 had the lowest interfacial tension and could reach the order of 10−1 mN∙m−1; it had excellent temperature resistance and the best static oil washing efficiency and stability. Nano-oil displacement agent No. 2 had the best emulsification performance and wettability and also had good stability. By studying the performance and final oil displacement effect of the nano-oil displacement agent, it was found that the key factor affecting the oil displacement effect of this reservoir was the interfacial activity of the nano-oil displacement agent. When the interfacial tension was lower, it produced strong dialysis for oil displacement. The emulsification effect has a negative effect on low-permeability reservoirs, mainly because the fluid produces strong emulsification in low-permeability reservoirs; thus, it can easily block the formation and cause high pressure. An excessive or small contact angle is not conducive to oil displacement. An excessive contact angle means strong hydrophilicity, which can cause a strong Jamin effect in oil-friendly formations. If the contact angle is too small, it has strong lipophilicity and can lead to poor solubility in water. Nano-oil displacement agent No. 4 had the best oil displacement effect, with an oil recovery increase of 7.35%, followed by nanometer oil displacement agent No. 1, with an oil recovery increase of 5.70%. Based on all the performance results, nanometer oil displacement agent No. 4 was more suitable as the oil displacement agent and can be used to enhance oil recovery in the Jimusaer reservoir. This study has laid a foundation for the chemical flooding development of shale oil in the Xinjiang oilfield

MLN4924 Treatment Diminishes Excessive Lipid Storage in High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease (NAFLD) by Stimulating Hepatic Mitochondrial Fatty Acid Oxidation and Lipid Metabolites

MLN4924 is a selective neddylation inhibitor that has shown great potential in treating several cancer and metabolic diseases, including obesity. However, it remains largely unknown whether MLN4924 has similar effect on non-alcoholic liver disease (NAFLD), which is closely associated with metabolic disorders. Here, we investigated the role of MLN4924 in NAFLD treatment and the underlying mechanism of the action using primary hepatocytes stimulated with free fatty acid, as well as high-fat diet (HFD)-induced NAFLD mouse models. We found that MLN4924 can inhibit the accumulation of lipid and reduce the expression of peroxisome proliferator-activated receptor γ (PPARγ), a key player in adipocyte differentiation and function in both in vivo and in vitro models. Moreover, we verified its important role in decreasing the synthesis and accumulation of fat in the liver, thus mitigating the development of NAFLD in the mouse model. The body weight and fat mass in MLN4924-treated animals were significantly reduced compared to the control group, while the metabolic activity, including O2 consumption, CO2 and heat production, also increased in these animals. Importantly, we demonstrated for the first time that MLN4924 can markedly boost mitochondrial fat acid oxidation (FAO) to alter liver lipid metabolism. Finally, we compared the metabolites between MLN4924-treated and untreated Huh7 cells after fatty acid induction using lipidomics methods and techniques. We found induction of several metabolites in the treated cells, including Beta-guanidinopropionic acid (b-GPA) and Fluphenazine, which was in accordance with the increase of FAO and metabolism. Together, our study provided a link between neddylation modification and energy metabolism, as well as evidence for targeting neddylation as an emerging therapeutic approach to tackle NAFLD