ActiveGuard: An Active DNN IP Protection Technique via Adversarial Examples

The training of Deep Neural Networks (DNN) is costly, thus DNN can be considered as the intellectual properties (IP) of model owners. To date, most of the existing protection works focus on verifying the ownership after the DNN model is stolen, which cannot resist piracy in advance. To this end, we propose an active DNN IP protection method based on adversarial examples against DNN piracy, named ActiveGuard. ActiveGuard aims to achieve authorization control and users' fingerprints management through adversarial examples, and can provide ownership verification. Specifically, ActiveGuard exploits the elaborate adversarial examples as users' fingerprints to distinguish authorized users from unauthorized users. Legitimate users can enter fingerprints into DNN for identity authentication and authorized usage, while unauthorized users will obtain poor model performance due to an additional control layer. In addition, ActiveGuard enables the model owner to embed a watermark into the weights of DNN. When the DNN is illegally pirated, the model owner can extract the embedded watermark and perform ownership verification. Experimental results show that, for authorized users, the test accuracy of LeNet-5 and Wide Residual Network (WRN) models are 99.15% and 91.46%, respectively, while for unauthorized users, the test accuracy of the two DNNs are only 8.92% (LeNet-5) and 10% (WRN), respectively. Besides, each authorized user can pass the fingerprint authentication with a high success rate (up to 100%). For ownership verification, the embedded watermark can be successfully extracted, while the normal performance of the DNN model will not be affected. Further, ActiveGuard is demonstrated to be robust against fingerprint forgery attack, model fine-tuning attack and pruning attack

Use the Spear as a Shield: A Novel Adversarial Example based Privacy-Preserving Technique against Membership Inference Attacks

Recently, the membership inference attack poses a serious threat to the privacy of confidential training data of machine learning models. This paper proposes a novel adversarial example based privacy-preserving technique (AEPPT), which adds the crafted adversarial perturbations to the prediction of the target model to mislead the adversary's membership inference model. The added adversarial perturbations do not affect the accuracy of target model, but can prevent the adversary from inferring whether a specific data is in the training set of the target model. Since AEPPT only modifies the original output of the target model, the proposed method is general and does not require modifying or retraining the target model. Experimental results show that the proposed method can reduce the inference accuracy and precision of the membership inference model to 50%, which is close to a random guess. Further, for those adaptive attacks where the adversary knows the defense mechanism, the proposed AEPPT is also demonstrated to be effective. Compared with the state-of-the-art defense methods, the proposed defense can significantly degrade the accuracy and precision of membership inference attacks to 50% (i.e., the same as a random guess) while the performance and utility of the target model will not be affected

Circadian clock disruption in autoimmune thyroiditis

Objective: A vicious cycle between circadian disruption and escalating immune responses has been described in diverse inflammatory disease. The current study aimed to explore the role of circadian clock disruption in autoimmune thyroiditi s (AIT). Methods: Thirty AIT patients and 30 controls were enrolled and biopsied for thyroid tissues. Alterations of core clock genes expression in AIT thyr oid tissues, and its association with serum and tissue inflammatory biomarkers were a ssessed. For animal studies, C57BL/6J mice administered with porcine thyroglobulin or PBS (as control) combined with adjuvants were sacrificed at four time points to i nvestigate the circadian characteristic of experimental autoimmune thyroiditis (EAT). Light shift (LS) conditions were used to explore the influence of external circadian disturb ance on EAT. Results: The expression of clock genes BMAL1 and PER2 was significantly reduced in thyroid tissues from AIT patients and was negatively correlated to levels of thyroid peroxidase antibodies. In mouse models, diurnal fluctuations of proinflammatory cytokines were demonstrated, and further exposing mice to LS le d to overproduction of TNF-α, IFN-γ, and anti-thyroglobulin antibodies. Circadian analysis revealed significant oscillations of Bmal1, Clock, Per2, Cry1, Ror, and Rev-erb, which was broadly disturbed in EAT, LS, and EAT + LS groups. Conclusions: This study demonstrates that expression pattern of clock genes was disrupted in AIT thyroid, and chronic circadian disruption may aggravate the inflammatory responses in AIT. Whether maintaining a regular cir cadian rhythm can alleviate autoimmune thyroid diseases warrants further research

A review of compressive sensing in information security field

The applications of compressive sensing (CS) in the fi eld of information security have captured a great deal of researchers\u27 attention in the past decade. To supply guidance for researchers from a comprehensive perspective, this paper, for the fi rst time, reviews CS in information security field from two aspects: theoretical security and application security. Moreover, the CS applied in image cipher is one of the most widespread applications, as its characteristics of dimensional reduction and random projection can be utilized and integrated into image cryptosystems, which can achieve simultaneous compression and encryption of an image or multiple images. With respect to this application, the basic framework designs and the corresponding analyses are investigated. Speci fically, the investigation proceeds from three aspects, namely, image ciphers based on chaos and CS, image ciphers based on optics and CS, and image ciphers based on chaos, optics, and CS. A total of six frameworks are put forward. Meanwhile, their analyses in terms of security, advantages, disadvantages, and so on are presented. At last, we attempt to indicate some other possible application research topics in future

Low-dose dobutamine cardiovascular magnetic resonance segmental strain study of early phase of intramyocardial hemorrhage rats

BACKGROUND: This study investigates the segmental myocardial strain of the early phase of intramyocardial hemorrhage (IMH) caused by reperfused myocardial infarction (MI) in rats by low-dose dobutamine (LDD) cardiovascular magnetic resonance (CMR) feature-tracking. METHODS: Nine sham rats and nine rats with 60-min myocardial ischemia followed by 48-h reperfusion were investigated using CMR, including T2*-mapping sequence and fast imaging with steady-state precession (FISP)-cine sequence. Another FISP-cine sequence was acquired after 2 min of dobutamine injection; the MI, IMH, and Non-MI (NMI) areas were identified. The values of peak radial strains (PRS) and peak circumferential strains (PCS) of the MI, IMH and NMI segments were acquired. The efficiency of PRS and PCS (EPRS and EPCS, respectively) were calculated on the basis of the time of every single heartbeat. RESULTS: The PRS, PCS, EPRS, and EPCS of the sham group increased after LDD injection. However, the PRS, PCS, EPRS, and EPCS of the IMH segment did not increase. Moreover, the PRS and PCS of the MI and NMI segments did not increase, but the EPRS and EPCS of these segments increased. The PRS, PCS, EPRS, and EPCS of the IMH segment were lower than those of the MI and NMI segments before and after LDD injection, but without a significant difference between MI segment and NMI segment before and after LDD injection. CONCLUSIONS: LDD could help assess dysfunctions in segments with IMH, especially using the efficiency of strain. IMH was a crucial factor that decreased segmental movement and reserved function

Myocardial infarction size as an independent predictor of intramyocardial haemorrhage in acute reperfused myocardial ischaemic rats

BACKGROUND: In previous studies, haemorrhage occurred only with large infarct sizes, and studies found a moderate correlation between the extent of necrosis and haemorrhage, but the extent of infarction size in these studies was limited. This study aimed to find the correlations between intramyocardial haemorrhage (IMH), myocardial infarction (MI), and myocardial oedema (ME) from small to large sizes of MI in a 7.0-T MR scanner. METHODS: Different sizes of myocardial infarction were induced by occluding different sections of the proximal left anterior descending coronary artery (1-3 mm under the left auricle). T2*-mapping, T2-mapping and late gadolinium enhancement (LGE) sequences were performed on a 7.0 T MR system at Days 2 and 7. T2*- and T2-maps were calculated using custom-made software. All areas were expressed as a percentage of the entire myocardial tissue of the left ventricle. The rats were divided into two groups based on the T2* results and pathological findings; MI with IMH was referred to as the + IMH group, while MI without IMH was referred to as the -IMH group. RESULTS: The final experimental sample consisted of 25 rats in the + IMH group and 10 rats in the -IMH group. For the + IMH group on Day 2, there was a significant positive correlation between IMH size and MI size (r = 0.677, P \u3c 0.01) and a positive correlation between IMH size and ME size (r = 0.552, P \u3c 0.01). On Day 7, there was a significant positive correlation between IMH size and MI size (r = 0.711, P \u3c 0.01), while no correlation was found between IMH size and ME size (r = 0.429, P = 0.097). The MI sizes of the + IMH group were larger than those of the -IMH group (P \u3c 0.01). CONCLUSIONS: Infarction size prior to reperfusion is a critical factor in determining IMH size in rats

Mechanism-based target therapy in primary biliary cholangitis: opportunities before liver cirrhosis?

Primary biliary cholangitis (PBC) is an immune-mediated liver disease characterized by cholestasis, biliary injuries, liver fibrosis, and chronic non-suppurative cholangitis. The pathogenesis of PBC is multifactorial and involves immune dysregulation, abnormal bile metabolism, and progressive fibrosis, ultimately leading to cirrhosis and liver failure. Ursodeoxycholic acid (UDCA) and obeticholic acid (OCA) are currently used as first- and second-line treatments, respectively. However, many patients do not respond adequately to UDCA, and the long-term effects of these drugs are limited. Recent research has advanced our understanding the mechanisms of pathogenesis in PBC and greatly facilitated development of novel drugs to target mechanistic checkpoints. Animal studies and clinical trials of pipeline drugs have yielded promising results in slowing disease progression. Targeting immune mediated pathogenesis and anti-inflammatory therapies are focused on the early stage, while anti-cholestatic and anti-fibrotic therapies are emphasized in the late stage of disease, which is characterized by fibrosis and cirrhosis development. Nonetheless, it is worth noting that currently, there exists a dearth of therapeutic options that can effectively impede the progression of the disease to its terminal stages. Hence, there is an urgent need for further research aimed at investigating the underlying pathophysiology mechanisms with potential therapeutic effects. This review highlights our current knowledge of the underlying immunological and cellular mechanisms of pathogenesis in PBC. Further, we also address current mechanism-based target therapies for PBC and potential therapeutic strategies to improve the efficacy of existing treatments

Membrane-Located Expression of Thioesterase From Acinetobacter baylyi Enhances Free Fatty Acid Production With Decreased Toxicity in Synechocystis sp. PCC6803

It has been previously reported that photosynthetic production of extracellular free fatty acids (FFAs) in cyanobacteria was realized by thioesterases (TesA) mediated hydrolysis of fatty acyl-ACP in cytosol and excretion of the FFA outside of the cell. However, two major issues related to the genetically modified strains need to be addressed before the scale-up commercial application becomes possible: namely, the toxicity of FFAs, and the diversity of carbon lengths of fatty acids that could mimic the fossil fuel. To address those issues, we hypothesized that generating FFAs near membrane could facilitate rapid excretion of the FFA outside of the cell and thus decrease toxicity caused by intracellular FFAs in the cytosolic expression of thioesterase. To realize this, we localized a leaderless thioesterase (AcTesA) from Acinetobacter baylyi on the cytosolic side of the inner membrane of Synechocystis sp. PCC6803 using a membrane scaffolding system. The engineered strain with AcTesA on its membrane (mAcT) produced extracellular FFAs up to 171.9 ± 13.22 mg⋅L-1 compared with 40.24 ± 10.94 and 1.904 ± 0.158 mg⋅L-1 in the cytosol-expressed AcTesA (AcT) and wild-type (WT) strains, respectively. Moreover, the mAcT strain generated around 1.5 and 1.9 times less reactive oxygen species than AcT and WT, respectively. Approximately 78% of total FFAs were secreted with an average rate of 1 mg⋅L-1⋅h-1, which was higher than 0.44 mg⋅L-1⋅h-1 reported previously. In the case of mAcT strain, 60% of total secreted FFAs was monounsaturated (C18:1) which is the preferable biodiesel component. Therefore, the engineered mAcT strain shows enhanced FFAs production with less toxicity which is highly desirable for biodiesel production

Note on Light-like Tachyon Condensation

In this paper closed string emission and open string pair production from the light-like rolling tachyon solution are calculated in subcritical string theory in the background of a linear dilaton. The rolling light-like tachyon represents the inhomogeneous decay of unstable D-brane. The decay rate is given by the imaginary part of annulus diagram which can be calculated using the boundary state/sigma-model method. It is found that the decay rate is finite in the open string ultraviolet region and depends on tachyon profile in the open string infrared region.Comment: 15 pages, no figures,discussion added, published versio

A Randomly-Controlled Study on the Cardiac Function at the Early Stage of Return to the Plains after Short-Term Exposure to High Altitude

High altitude acclimatization and adaptation mechanisms have been well clarified, however, high altitude de-adaptation mechanism remains unclear. In this study, we conducted a controlled study on cardiac functions in 96 healthy young male who rapidly entered the high altitude (3700 m) and returned to the plains (1500 m) after 50 days. Ninety eight healthy male who remained at low altitude were recruited as control group. The mean pulmonary arterial pressure (mPAP), left ventricular ejection fraction (LVEF), left ventricular fraction shortening (LVFS), cardiac function index (Tei index) were tested. Levels of serum creatine kinase isoform MB (CK-MB), lactate dehydrogenase isoenzyme-1 (LDH-1), endothelin-1 (ET-1), nitrogen oxide (NO), serum hypoxia-inducible factor-1α (HIF-1α), 8-iso-prostaglandin F2α (8-iso PGF2α), superoxide dismutase (SOD) and malonaldehyde (MDA) were measured at an altitude of 3700 m and 1500 m respectively. The results showed that after short-term exposure to high altitude mPAP and Tei index increased significantly, while LVEF and LVFS decreased significantly. These changes were positively correlated with altitude. On the 15th day after the subjects returned to low altitude, mPAP, LVEF and LVFS levels returned to the same level as those of the control subjects, but the Tei index in the returned subjects was still significantly higher than that in the control subjects (P<0.01). We also found that changes in Tei index was positively correlated with mPAP, ET-1, HIF-1α and 8-iso PGF2α levels, and negatively correlated with the level of NO, LVEF, LVFS, CK-MB and LDH-1. These findings suggest that cardiac function de-adapts when returning to the plains after short-term exposure to high altitude and the function recovery takes a relatively long time