Efficient and Provably-secure Certificateless Strong Designated Verifier Signature Scheme without Pairings

Strong designated verifier signature (generally abbreviated to SDVS) allows signers to obtain absolute control over who can verify the signature, while only the designated verifier other than anyone else can verify the validity of a SDVS without being able to transfer the conviction. Certificateless PKC has unique advantages comparing with certificate-based cryptosystems and identity-based PKC, without suffering from key escrow. Motivated by these attractive features, we propose a novel efficient CL-SDVS scheme without bilinear pairings or map-to-point hash operations. The proposed scheme achieves all the required security properties including EUF-CMA, non-transferability, strongness and non-delegatability. We also estimate the computational and communication efficiency. The comparison shows that our scheme outperforms all the previous CL-(S)DVS schemes. Furthermore, the crucial security properties of the CL-SDVS scheme are formally proved based on the intractability of SCDH and ECDL assumptions in random oracle model

efficient identity-based strong designated verifier signature schemes

Strong designated verifier signature (SDVS) makes it possible for a signer to convince a designated verifier that he or she has signed a message in such a way that the designated verifier cannot transfer the signature to any third party and no third party can even verify the validity of the signature. Recently, Kang et al. proposed an identity-based SDVS (IBSDVS) scheme that is claimed to be unforgeable and strong. However, in this paper, we show that their scheme is actually forgeable, delegatable, and not strong. We then propose an improved efficient IBSDVS scheme with short signature size and provide formal security proofs based on the computational Diffie-Hellman assumption in the random oracle model. We also show that the performance of our scheme outperforms all the existing IBSDVS schemes known in the literature. Furthermore, we propose an extension of our scheme achieving the stronger notion of nondelegatability and provide formal security proofs. The extended scheme is also showed to achieve high efficiency and short signature size. © 2012 John Wiley & Sons, Ltd.Strong designated verifier signature (SDVS) makes it possible for a signer to convince a designated verifier that he or she has signed a message in such a way that the designated verifier cannot transfer the signature to any third party and no third party can even verify the validity of the signature. Recently, Kang et al. proposed an identity-based SDVS (IBSDVS) scheme that is claimed to be unforgeable and strong. However, in this paper, we show that their scheme is actually forgeable, delegatable, and not strong. We then propose an improved efficient IBSDVS scheme with short signature size and provide formal security proofs based on the computational Diffie-Hellman assumption in the random oracle model. We also show that the performance of our scheme outperforms all the existing IBSDVS schemes known in the literature. Furthermore, we propose an extension of our scheme achieving the stronger notion of nondelegatability and provide formal security proofs. The extended scheme is also showed to achieve high efficiency and short signature size. © 2012 John Wiley & Sons, Ltd

privacy preserving of trust management credentials based on trusted computing

Korea Communications Commission (KCC)Privacy disclosure of forward direction credentials and backward direction credentials is an important security defect in existing trust management systems. In this paper, a novel distributed privacy preserving scheme for trust management credentials is proposed to solve this problem. Based on the trusted computing technology, the scheme provides the sealed protection for the credentials with privacy sensitive information and guarantees all the Deduced Composite Credential Constructing Units running in participant platforms untampered. In the process of collecting credentials, the deduced composite of multiple credentials replaces the single credential as the irreducible constituent to prevent the uncontrolled disclosure of privacy attributes. By modifying the traditional privacy preserving pattern, our scheme avoids the inadvertent disclosure of credential privacy attributes and provides a reliable solution for many privacy sensitive fields such as medical, business, and so on. © Springer-Verlag Berlin Heidelberg 2010

Improving Topic-Based Data Exchanges among IoT Devices

Data exchange is one of the huge challenges in Internet of Things (IoT) with billions of heterogeneous devices already connected and many more to come in the future. Improving data transfer efficiency, scalability, and survivability in the fragile network environment and constrained resources in IoT systems is always a fundamental issues. In this paper, we present a novel message routing algorithm that optimizes IoT data transfers in a resource constrained and fragile network environment in publish-subscribe model. The proposed algorithm can adapt the dynamical network topology of continuously changing IoT devices with the rerouting method. We also present a rerouting algorithm in Message Queuing Telemetry Transport (MQTT) to take over the topic-based session flows with a controller when a broker crashed down. Data can still be communicated by another broker with rerouting mechanism. Higher availability in IoT can be achieved with our proposed model. Through demonstrated efficiency of our algorithms about message routing and dynamically adapting the continually changing device and network topology, IoT systems can gain scalability and survivability. We have evaluated our algorithms with open source Eclipse Mosquitto. With the extensive experiments and simulations performed in Mosquitto, the results show that our algorithms perform optimally. The proposed algorithms can be widely used in IoT systems with publish-subscribe model. Furthermore, the algorithms can also be adopted in other protocols such as Constrained Application Protocol (CoAP)

CA increased cardiomyocyte viability through repressing ferroptosis.

(A) Relative iron concentration was assessed using commercial kits in H9c2 cells treated with DOX (4 μM) and CA (100 μM) (n = 3). (B) qRT-PCR assay of Gpx4, Ptgs2, and Acsl4 mRNA levels in H9c2 cells treated with DOX (4 μM) and CA (100 μM) (n = 3). Western blot assay (C) and quantification of Gpx4 (D), Acsl4 (E), and Ptgs2 (F) protein levels in H9c2 cells treated with DOX (4 μM) and CA (100 μM) (n = 3). (G) H9c2 cells were treated with 4 μM of DOX in the presence or absence of CA (100 μM), Fer-1 (1 μM), or Erastin (10 μM) for 24 h, and cell viability was measured with CCK8 (n = 3). *p<0.05, **p<0.01.</p

CA activated Nrf2/HO-1 signaling <i>in vitro</i>.

Western blot assay (A) and quantification (C) of cytoplasmic Nrf2 protein levels in H9c2 cells treated with DOX (4 μM) and CA (100 μM) (n = 3). Western blot assay (B) and quantification (C) of nuclear Nrf2 protein levels in H9c2 cells treated with DOX (4 μM) and CA (100 μM) (n = 3). (D) qRT-PCR assay of HO-1 mRNA levels in H9c2 cells treated with DOX (4 μM) and CA (100 μM) (n = 3). Western blot assay (E) and quantification (F) of cytoplasmic HO-1 protein levels in H9c2 cells treated with DOX (4 μM) and CA (100 μM) (n = 3). **p<0.01.</p

Multinomial machine learning identifies independent biomarkers by integrated metabolic analysis of acute coronary syndrome

Abstract A multi-class classification model for acute coronary syndrome (ACS) remains to be constructed based on multi-fluid metabolomics. Major confounders may exert spurious effects on the relationship between metabolism and ACS. The study aims to identify an independent biomarker panel for the multiclassification of HC, UA, and AMI by integrating serum and urinary metabolomics. We performed a liquid chromatography-tandem mass spectrometry (LC–MS/MS)-based metabolomics study on 300 serum and urine samples from 44 patients with unstable angina (UA), 77 with acute myocardial infarction (AMI), and 29 healthy controls (HC). Multinomial machine learning approaches, including multinomial adaptive least absolute shrinkage and selection operator (LASSO) regression and random forest (RF), and assessment of the confounders were applied to integrate a multi-class classification biomarker panel for HC, UA and AMI. Different metabolic landscapes were portrayed during the transition from HC to UA and then to AMI. Glycerophospholipid metabolism and arginine biosynthesis were predominant during the progression from HC to UA and then to AMI. The multiclass metabolic diagnostic model (MDM) dependent on ACS, including 2-ketobutyric acid, LysoPC(18:2(9Z,12Z)), argininosuccinic acid, and cyclic GMP, demarcated HC, UA, and AMI, providing a C-index of 0.84 (HC vs. UA), 0.98 (HC vs. AMI), and 0.89 (UA vs. AMI). The diagnostic value of MDM largely derives from the contribution of 2-ketobutyric acid, and LysoPC(18:2(9Z,12Z)) in serum. Higher 2-ketobutyric acid and cyclic GMP levels were positively correlated with ACS risk and atherosclerosis plaque burden, while LysoPC(18:2(9Z,12Z)) and argininosuccinic acid showed the reverse relationship. An independent multiclass biomarker panel for HC, UA, and AMI was constructed using the multinomial machine learning methods based on serum and urinary metabolite signatures

CA activated Nrf2/HO-1 signaling <i>in vivo</i>.

(A and B) The total protein levels of Nrf2 and HO-1 in different groups of cardiac tissues (n = 5) were assessed using western blot assay. (C and D) The nuclear protein levels of Nrf2 in different groups of cardiac tissues (n = 5) were assessed using western blot assay.</p

qRT-PCR primers were used in the study.

Although doxorubicin (DOX) is an efficient chemotherapeutic drug for human tumors, severe cardiotoxicity restricts its clinical use. Cinnamaldehyde (CA), a bioactive component isolated from Cinnamonum cassia, possesses potent anti-oxidative and anti-apoptotic potentials. The major aim of this study was to evaluate the protective role of CA against DOX-induced cardiotoxicity. To this end, cardiomyocyte injury models were developed using DOX-treated H9c2 cells and DOX-treated rats, respectively. Herein, we found that CA treatment increased cardiomyocyte viability and attenuated DOX-induced cardiomyocyte death in vitro. CA further protected rats against DOX-induced cardiotoxicity, as indicated by elevated creatine kinase (CK) and lactate dehydrogenase (LDH) levels, myocardium injury, and myocardial fibrosis. CA alleviated DOX-induced myocardial oxidative stress by regulating reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) levels. Mechanistically, CA markedly accelerated nuclear translocation of nuclear erythroid factor 2-related factor 2 (Nrf2) and increased heme oxygenase-1 (HO-1) expression. Consequently, CA decreased DOX-induced cardiomyocyte ferroptosis, while Erastin (a ferroptosis agonist) treatment destroyed the effect of CA on increasing cardiomyocyte viability. Taken together, the current results demonstrate that CA alleviates DOX-induced cardiotoxicity, providing a promising opportunity to increase the clinical application of DOX.</div

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Although doxorubicin (DOX) is an efficient chemotherapeutic drug for human tumors, severe cardiotoxicity restricts its clinical use. Cinnamaldehyde (CA), a bioactive component isolated from Cinnamonum cassia, possesses potent anti-oxidative and anti-apoptotic potentials. The major aim of this study was to evaluate the protective role of CA against DOX-induced cardiotoxicity. To this end, cardiomyocyte injury models were developed using DOX-treated H9c2 cells and DOX-treated rats, respectively. Herein, we found that CA treatment increased cardiomyocyte viability and attenuated DOX-induced cardiomyocyte death in vitro. CA further protected rats against DOX-induced cardiotoxicity, as indicated by elevated creatine kinase (CK) and lactate dehydrogenase (LDH) levels, myocardium injury, and myocardial fibrosis. CA alleviated DOX-induced myocardial oxidative stress by regulating reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) levels. Mechanistically, CA markedly accelerated nuclear translocation of nuclear erythroid factor 2-related factor 2 (Nrf2) and increased heme oxygenase-1 (HO-1) expression. Consequently, CA decreased DOX-induced cardiomyocyte ferroptosis, while Erastin (a ferroptosis agonist) treatment destroyed the effect of CA on increasing cardiomyocyte viability. Taken together, the current results demonstrate that CA alleviates DOX-induced cardiotoxicity, providing a promising opportunity to increase the clinical application of DOX.</div