A Plug-and-Play Defensive Perturbation for Copyright Protection of DNN-based Applications

Wide deployment of deep neural networks (DNNs) based applications (e.g., style transfer, cartoonish), stimulating the requirement of copyright protection of such application's production. Although some traditional visible copyright techniques are available, they would introduce undesired traces and result in a poor user experience. In this paper, we propose a novel plug-and-play invisible copyright protection method based on defensive perturbation for DNN-based applications (i.e., style transfer). Rather than apply the perturbation to attack the DNNs model, we explore the potential utilization of perturbation in copyright protection. Specifically, we project the copyright information to the defensive perturbation with the designed copyright encoder, which is added to the image to be protected. Then, we extract the copyright information from the encoded copyrighted image with the devised copyright decoder. Furthermore, we use a robustness module to strengthen the decoding capability of the decoder toward images with various distortions (e.g., JPEG compression), which may be occurred when the user posts the image on social media. To ensure the image quality of encoded images and decoded copyright images, a loss function was elaborately devised. Objective and subjective experiment results demonstrate the effectiveness of the proposed method. We have also conducted physical world tests on social media (i.e., Wechat and Twitter) by posting encoded copyright images. The results show that the copyright information in the encoded image saved from social media can still be correctly extracted.Comment: 9 pages, 7 figure

Neuronal intermediate filament inclusion disease may be incorrectly classified as a subtype of FTLD-FUS

Background: The majority of cases of frontotemporal lobar degeneration (FTLD) are characterized by focal cortical atrophy with an underlying tau or TDP-43 proteinopathy. A subset of FTLD cases, however, lack tau and TDP-43 immunoreactivity, but have neuronal inclusions positive for ubiquitin, referred to as atypical FTLD (aFTLD-U). Studies have demonstrated that ubiquitin-positive inclusions in aFTLD-U are immunoreactive for fused in sarcoma (FUS). As such, the current nosology for this entity is FTLD-FUS, which is thought to include not only aFTLD-U but also neuronal intermediate filament inclusion disease (NIFID) and basophilic inclusion body disease. Objective: To compare pathological features of cases of aFTLD-U and NIFID. Methods: We reviewed the neuropathology of 15 patients (10 males and 5 females; average age at death 54 years (range 41-69 years)) with an antemortem clinical diagnosis of a frontotemporal dementia and pathological diagnosis of aFTLD-U (n=8) or NIFID (n=7). Sections were processed for immunohistochemistry and immunoelectron microscopy with FUS, TDP-43, and α-internexin (αINX) antibodies. Results: Eight cases had pathologic features consistent with FTLD-FUS, with severe striatal atrophy (7/8 cases), as well as FUS-positive neuronal cytoplasmic and vermiform intranuclear inclusions, but no αINX immunoreactivity. Five cases had features consistent with NIFID, with neuronal inclusions positive for both FUS and αINX. Striatal atrophy was present in only two of the NIFID cases. Two cases had αINX-positive neuronal inclusions consistent with NIFID, but both lacked striatal atrophy and FUS immunoreactivity. Surprisingly, one of these two NIFID cases had lesions immunoreactive for TDP-43. Discussion: While FUS pathology remains a prominent feature of aFTLD-U, there is pathologic heterogeneity, including rare cases of NIFID with TDP-43- rather than FUS-positive inclusions

Magnon-induced non-Markovian friction of a domain wall in a ferromagnet

Motivated by the recent study on the quasiparticle-induced friction of solitons in superfluids, we theoretically study magnon-induced intrinsic friction of a domain wall in a one-dimensional ferromagnet. To this end, we start by obtaining the hitherto overlooked dissipative interaction of a domain wall and its quantum magnon bath to linear order in the domain-wall velocity and to quadratic order in magnon fields. An exact expression for the pertinent scattering matrix is obtained with the aid of supersymmetric quantum mechanics. We then derive the magnon-induced frictional force on a domain wall in two different frameworks: time-dependent perturbation theory in quantum mechanics and the Keldysh formalism, which yield identical results. The latter, in particular, allows us to verify the fluctuation-dissipation theorem explicitly by providing both the frictional force and the correlator of the associated stochastic Langevin force. The potential for magnons induced by a domain wall is reflectionless, and thus the resultant frictional force is non-Markovian similarly to the case of solitons in superfluids. They share an intriguing connection to the Abraham-Lorentz force that is well-known for its causality paradox. The dynamical responses of a domain wall are studied under a few simple circumstances, where the non-Markovian nature of the frictional force can be probed experimentally. Our work, in conjunction with the previous study on solitons in superfluids, shows that the macroscopic frictional force on solitons can serve as an effective probe of the microscopic degrees of freedom of the system.Comment: 13 pages, 2 figure

Clock-Gating-Aware Low Launch WSA Test Pattern Generation for At-Speed Testing

Capture power management has become a necessity to avoid at-speed scan testing yield loss, especially for modern complex and low power designs. This paper proposes a test pattern generation methodology that utilizes the available clock-gating mechanism, a popular low power design technique, to reduce the launch cycle weighted switching activity (WSA) for at-speed scan testing. Compared to previous techniques that consider clock-gating, a significant launch cycle WSA reduction is achieved without severe test pattern inflation.2011 IEEE International Test Conference, 20-22 September 2011, Anaheim, CA, US

ER stress response plays an important role in aggregation of α-synuclein

<p>Abstract</p> <p>Background</p> <p>Accumulation of filamentous α-synuclein as Lewy bodies is a hallmark of Parkinson's disease. To identify the mechanisms involved in α-synuclein assembly and determine whether the assemblies are cytotoxic, we developed a cell model (3D5) that inducibly expresses wild-type human α-synuclein and forms inclusions that reproduce many morphological and biochemical characteristics of Lewy bodies. In the present study, we evaluated the effects of several histone deacetylase inhibitors on α-synuclein aggregation in 3D5 cells and primary neuronal cultures. These drugs have been demonstrated to protect cells transiently overexpressing α-synuclein from its toxicity.</p> <p>Results</p> <p>Contrary to transient transfectants, the drug treatment did not benefit 3D5 cells and primary cultures. The treated were less viable and contained more α-synuclein oligomers, active caspases 3 and 9, as well as ER stress markers than non-treated counterparts. The drug-treated, induced-3D5 cells, or primary cultures from transgenic mice overexpressing (<2 fold) α-synuclein, displayed more α-synuclein oligomers and ER stress markers than non-induced or non-transgenic counterparts. Similar effects were demonstrated in cultures treated with tunicamycin, an ER stressor. These effects were blocked by co-treatment with salubrinal, an ER stress inhibitor. In comparison, co-treatment with a pan caspase inhibitor protected cells from demise but did not reduce α-synuclein oligomer accumulation.</p> <p>Conclusions</p> <p>Our results indicate that an increase of wild-type α-synuclein can elicit ER stress response and sensitize cells to further insults. Most importantly, an increase of ER stress response can promote the aggregation of wild type α-synuclein.</p

Tangential Flow Filtration for Highly Efficient Concentration of Extracellular Vesicles from Large Volumes of Fluid

Concentration of extracellular vesicles (EVs) from biological fluids in a scalable and reproducible manner represents a major challenge. This study reports the use of tangential flow filtration (TFF) for the highly efficient isolation of EVs from large volumes of samples. When compared to ultracentrifugation (UC), which is the most widely used method to concentrate EVs, TFF is a more efficient, scalable, and gentler method. Comparative assessment of TFF and UC of conditioned cell culture media revealed that the former concentrates EVs of comparable physicochemical characteristics, but with higher yield, less single macromolecules and aggregates (<15 nm in size), and improved batch-to-batch consistency in half the processing time (1 h). The TFF protocol was then successfully implemented on fluids derived from patient lipoaspirate. EVs from adipose tissue are of high clinical relevance, as they are expected to mirror the regenerative properties of the parent cells

Detection of sebaceous gland hyperplasia with dermoscopy and reflectance confocal microscopy

BackgroundSebaceous gland hyperplasia (SGH) is a benign cutaneous proliferation of the sebaceous glands that are mostly present on the face or the neck of older adults. They typically appear as single or multiple soft umbilicated papules; however, in challenging cases, it can be difficult to distinguish them from trichoepitheliomas, base cell carcinomas, or other tumors. Although pathological results have diagnostic value, the significance of non-invasive examinations in diagnosis and differential diagnosis is also worth exploring.ObjectivesThis study aimed to describe the dermoscopic and reflectance confocal microscopy (RCM) features of SGH.MethodsA total of 31 patients diagnosed with SGH, according to clinical and histopathological standards, were examined using dermoscopy and RCM between March 2018 and January 2022.ResultsDermoscopically, lesions revealed a yellowish-red background and a faint-yellow background in 25 (80.65%) and six cases (19.35%), respectively. White-yellowish lobulated structures in the center of the lesion were present in 31 patients (100%) and umbilications in 19 patients (61.29%). Crown vessels at the periphery of the lesions were observed in 11 patients (35.48%), whereas irregular linear vessels were observed on the surface of the lesions in 18 patients (58.06%). Under RCM, all lesions presented a honeycomb pattern in the epidermis and the typical morulae-shaped sebaceous lobules in the dermis. A dilated follicular infundibulum was observed in 15 patients (48.39%) and dilated vessels in 26 patients (83.87%).ConclusionDermoscopy and RCM enabled us to describe the imaging features of SGH. Combining these two useful tools provides a non-invasive basis for accurate clinical diagnosis

Expression of mutant TDP-43 induces neuronal dysfunction in transgenic mice

<p>Abstract</p> <p>Background</p> <p>Abnormal distribution, modification and aggregation of transactivation response DNA-binding protein 43 (TDP-43) are the hallmarks of multiple neurodegenerative diseases, especially frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U) and amyotrophic lateral sclerosis (ALS). Researchers have identified 44 mutations in the <it>TARDBP </it>gene that encode TDP-43 as causative for cases of sporadic and familial ALS <url>http://www.molgen.ua.ac.be/FTDMutations/</url>. Certain mutant forms of TDP-43, such as M337V, are associated with increased low molecular weight (LMW) fragments compared to wild-type (WT) TDP-43 and cause neuronal apoptosis and developmental delay in chick embryos. Such findings support a direct link between altered TDP-43 function and neurodegeneration.</p> <p>Results</p> <p>To explore the pathogenic properties of the M337V mutation, we generated and characterized two mouse lines expressing human TDP-43 (hTDP-43_M337V) carrying this mutation. hTDP-43_M337Vwas expressed primarily in the nuclei of neurons in the brain and spinal cord, and intranuclear and cytoplasmic phosphorylated TDP-43 aggregates were frequently detected. The levels of TDP-43 LMW products of ~25 kDa and ~35 kDa species were also increased in the transgenic mice. Moreover, overexpression of hTDP-43_M337Vdramatically down regulated the levels of mouse TDP-43 (mTDP-43) protein and RNA, indicating TDP-43 levels are tightly controlled in mammalian systems. TDP-43_M337Vmice displayed reactive gliosis, widespread ubiquitination, chromatolysis, gait abnormalities, and early lethality. Abnormal cytoplasmic mitochondrial aggregates and abnormal phosphorylated tau were also detected in the mice.</p> <p>Conclusion</p> <p>Our novel TDP-43_M337Vmouse model indicates that overexpression of hTDP-43_M337Valone is toxic <it>in vivo</it>. Because overexpression of hTDP-43 in wild-type TDP-43 and TDP-43_M337Vmouse models produces similar phenotypes, the mechanisms causing pathogenesis in the mutant model remain unknown. However, our results suggest that overexpression of the hTDP-43_M337Vcan cause neuronal dysfunction due to its effect on a number of cell organelles and proteins, such as mitochondria and TDP-43, that are critical for neuronal activity. The mutant model will serve as a valuable tool in the development of future studies designed to uncover pathways associated with TDP-43 neurotoxicity and the precise roles TDP-43 RNA targets play in neurodegeneration.</p

Changes of optic nerve head microcirculation in high myopia

AIM: To analyze the correlation of age, spherical equivalent (SE), and axial length (AL) with the microcirculation of optic nerve head (ONH) in high myopia (HM). METHODS: In this cross-sectional clinical study, 164 right eyes were included. Optical coherence tomography angiography (OCTA) was used to detect ONH vessel density. Eyes were classified based on age, SE, and AL. Groups of Age1, Age2, and Age3 were denoted for age classification (Age10.05) and the SE1, SE2, and SE3 groups (all P>0.05). No significant difference was observed in the intrapapillary vascular density (IVD) among AL1, AL2, AL3, and AL4 groups (P>0.05). However, a significant decrease was found in the peripapillary vascular density (PVD) in the AL1, AL2, AL3, and AL4 groups (F=3.605, P=0.015), especially in the inferotemporal (IT; F=6.25, P0.05). The PVD was correlated with AL (r=-0.236, P0.05). CONCLUSION: With the increase of AL, the IVD remains stable while the PVD decreases, especially in the three directions of temporal (IT, TI, and TS). The main cause of microcirculation reduction may be related to AL elongation rather than an increase in age or SE