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The advanced glycation end products (AGEs) are associated with increased cardiac endothelial injury. However, no causative link has been established between increased AGEs and enhanced endothelial injury after ischemia/reperfusion. More importantly, the molecular mechanisms by which AGEs may increase endothelial injury remain unknown. Adult rat cardiac microvascular endothelial cells (CMECs) were isolated and incubated with AGE-modified bovine serum albumin (BSA) or BSA. After AGE-BSA or BSA preculture, CMECs were subjected to simulated ischemia (SI)/reperfusion (R). AGE-BSA increased SI/R injury as evidenced by enhanced lactate dehydrogenase release and caspase-3 activity. Moreover, AGE-BSA significantly increased SI/R-induced oxidative/nitrative stress in CMECs (as measured by increased inducible nitric oxide synthase expression, total nitric oxide production, superoxide generation, and peroxynitrite formation) and increased SI/R-induced nitrative inactivation of thioredoxin-1 (Trx-1), an essential cytoprotective molecule. Supplementation of EUK134 (peroxynitrite decomposition catalyst), human Trx-1, or soluble receptor of advanced end product (sRAGE) (a RAGE decoy) in AGE-BSA precultured cells attenuated SI/R-induced oxidative/nitrative stress, reduced SI/R-induced Trx-1 nitration, preserved Trx-1 activity, and reduced SI/R injury. Our results demonstrated that AGEs may increase SI/R-induced endothelial injury by increasing oxidative/nitrative injury and subsequent nitrative inactivation of Trx-1. Interventions blocking RAGE signaling or restoring Trx activity may be novel therapies to mitigate endothelial ischemia/reperfusion injury in the diabetic population.

As zoom motion is common in video applications, a linear motion model is derived to describe zoom motion based on the analyses of camera imaging principles. Based on the motion model, a motion vector predictor for videos involving zoom motion is proposed. A rate distortion (RD) criterion is used to choose the optimal motion vector predictor between the one utilized in H.264/AVC and the one derived from the linear motion model. Experimental results demonstrate that by implementing the proposed method into Key Technology Area test platform version 2.2r1(KTA2.2r1), the maximum and average bit rate savings can be achieved as high as 7.66% and 4.90% respectively, while maintaining the same quality of reconstructed videos.

Background Up-regulation of angiotensin II (AngII) occurs in cardiac diseases, such as congestive heart failure, cardiac hypertrophy, myocardial ischemia and atrial fibrillation, which represent major health problems. Evidence from in vivo studies suggests that the level of Apolipoprotein-J (ApoJ) is also elevated but plays a protective role in cardiovascular disease. This study aimed to evaluate the protective effects of ApoJ against cytotoxicity of AngII in neonatal rat ventricular cells (NRVCs). Methods and results In culture, NRVCs were damaged by exposure to AngII, and ApoJ overexpression using an adenovirus vector significantly reduced the AngII-induced cell injury. ApoJ also prevented AngII from augmenting Nox2/gp91phox expression. The reactive oxygen species (ROS) scavenger, Mn(III)TBAP, showed similar results of attenuating AngII-induced cell damage. Furthermore, ApoJ overexpression increased phosphorylation of Akt, and the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 diminished the antioxidant effects of ApoJ, and prevented the protective effect of ApoJ against the cytotoxicity of AngII. Moreover, upregulation of nuclear factor κB (NF-κB) p65 expression and phosphorylation of p38 mitogen-activated protein kinase (MAPK) mediated by AngII in cultured NRVCs were significantly inhibited by overexpression of ApoJ. The p38 MAPK inhibitor SB203580 and the NF-κB inhibitor PDTC protected NRVCs from injury caused by AngII. Conclusions ApoJ serves as a cytoprotective protein in NRVCs against cytotoxicity of AngII through the PI3K-Akt-ROS and MAPK/ NF-κB pathways.

design because of the large scale of data, and the high power consumption especially for wireless terminals. An adaptive and random access-obeyed reference pictures memory compression (RPMC) scheme based on as small granularity as 2x2 blocks for 2-bit truncation is proposed in this paper to solve the problems. The impact of granularity in RPMC to memory access bandwidth during motion estimation and/or motion compensation is analyzed firstly. Then an adaptive RPMC scheme based on 2x2 block size is proposed, based on min-max scalar quantization (MMSQ). Finally, the results based on HM are provided which show that compared with the common used 4x4 block-based methods, little performance loss is introduced. At the same time, based on the adaptively merge scheme, the average memory access bandwidth is saved than the 4x4 block based method by up to 17%.

The receptor for advanced glycation end products (RAGE) and thioredoxin (Trx) play opposing roles in diabetic myocardial ischemia-reperfusion (MI/R) injury. We recently demonstrated nitrative modification of Trx leads to its inactivation and loss of cardioprotection. The present study is to determine the relationship between augmented RAGE expression and diminished Trx activity pertaining to exacerbated MI/R injury in the diabetic heart. The diabetic state was induced in mice by multiple intraperitoneal low-dose streptozotocin injections. RAGE small-interfering RNA (siRNA) or soluble RAGE (sRAGE, a RAGE decoy) was via intramyocardial and intraperitoneal injection before MI/R, respectively. Mice were subjected to 30 min of myocardial infarction followed by 3 or 24 h of reperfusion. At 10 min before reperfusion, diabetic mice were randomized to receive EUK134 (peroxynitrite scavenger), recombinant hTrx-1, nitrated Trx-1, apocynin (a NADPH oxidase inhibitor), or 1400W [an inducible nitric oxide synthase (iNOS) inhibitor] administration. The diabetic heart manifested increased RAGE expression and Nε-(carboxymethyl)lysine (CML, major advanced glycation end product subtype) content, reduced Trx-1 activity, and increased Trx nitration after MI/R. RAGE siRNA or administration of sRAGE in diabetic mice decreased MI/R-induced iNOS and gp91phox expression, reduced Trx nitration, preserved Trx activity, and decreased infarct size. Apocynin or 1400W significantly decreased nitrotyrosine production and restored Trx activity. Conversely, administration of either EUK134 or reduced hTrx, but not nitrated hTrx, attenuated MI/R-induced superoxide production, RAGE expression, and CML content and decreased cardiomyocyte apoptosis in diabetic mice. Collectively, we demonstrate that RAGE modulates the MI/R injury in a Trx nitrative inactivation fashion. Conversely, nitrative modification of Trx blocked its inhibitory effect upon RAGE expression in the diabetic heart. This is the first direct evidence demonstrating the alternative cross talk between RAGE overexpression and nitrative Trx inactivation, suggesting that interventions interfering with their interaction may be novel means of mitigating diabetic MI/R injury.

Type 1 diabetes (T1DM) portends poor prognosis concerning ischemic heart disease. Adiponectin (APN), an adipocytokine possessing insulin sensitizing and metabolic regulatory effects, has been recognized as a potent cardioprotective molecule. However, the relationship between APN and T1DM remains controversial and the role of cardiac-derived APN in T1DM is unclear. This study is aimed to investigate the dynamic change of both plasma and cardiac-derived APN expressions in T1DM, and the particular role of cardiac-derived APN in T1DM against myocardial ischemia/reperfusion (MI/R) injury. T1DM was established via intraperitoneal injection of streptozocin and followed by twice-daily subcutaneous injection of insulin or vehicle for 14 days. Non-diabetic mice of wild type and APN knockout were subjected to insulin or vehicle injection. MI/R was induced in Langendorff-perfused hearts. Compared to non-diabetic mice, plasma APN levels of diabetic mice significantly increased at 7 days, and slightly decreased at 14 days, while cardiac-derived APN levels gradually decreased over time. The MI/R injury measured as infarct size and cardiomyocyte apoptosis nearly doubled in diabetic mice. 14 days of insulin treatment increased both plasma and cardiac-derived APN levels in diabetic mice and attenuated myocardial injury via increasing AMPK phosphorylation in T1DM, which was partly reversed by Compound C (an AMPK inhibitor). Moreover, APN deficiency aggravated MI/R injury and partly abolished the protective effect of insulin treatment against MI/R injury, which was associated with decreased AMPK phosphorylation. The results suggest that cardiac-derived APN stimulated by long-term insulin treatment in T1DM exerts cardioprotection against MI/R injury via myocardial AMPK activation.

Compared to simulcast, the utilization of inter-view prediction at key pictures can dramatically improve the compression efficiency of multiview video coding (MVC). The reconstructed key picture in previous adjacent view is used as the inter-view reference picture of the key picture in the current coding view. The efficiency of inter-view prediction may deteriorate due to the existence of mismatch between views. An efficient prediction structure for key pictures is proposed by introducing multiple reference pictures prediction scheme. Experimental results show that average gains of 0.219dB can be achieved for key pictures compared to the reference prediction structure of MVC.

Recent clinical observations have indicated that nonlethal mechanical trauma significantly increases myocardial infarction risk even in the presence of completely normal coronary arteries. We investigated the molecular mechanisms responsible for exacerbation of ischemic myocardial injury after nonlethal mechanical trauma with a special focus on the role of tumor necrosis factor α and its potential downstream effector adiponectin, a novel adipokine with anti-inflammatory and cardioprotective properties.Laboratory study.University research unit.Male adult adiponectin knockout mice and wild-type mice.The animals were subjected to nonlethal mechanical trauma using the Noble-Collip drum (40 rpm ± 5 mins) followed by myocardial ischemia/reperfusion injury 7 days posttrauma. We also investigated the effects of neutralizing tumor necrosis factor α with etanercept and exogenous adiponectin supplementation on ischemic myocardial injury after trauma.Trauma significantly sensitized myocardium to ischemia/reperfusion injury as evidenced by increased apoptosis, enlarged infarct size, and decreased cardiac function. Plasma adiponectin concentrations were reduced after traumatic injury (the nadir occurring 3 days posttrauma), an effect abrogated by etanercept-mediated tumor necrosis factor α blockade. The downregulation of adiponectin was accompanied by increased myocardial superoxide and nitric oxide generation and peroxynitrite formation. Both etanercept and exogenous adiponectin supplementation (on day 3 posttrauma or 10 mins before reperfusion on day 7 posttrauma) markedly inhibited oxidative/nitrative stress and ischemia/reperfusion injury in posttraumatic ischemic/reperfused hearts of wild-type mice, whereas only adiponectin supplementation (but not tumor necrosis factor α inhibition) substantially attenuated posttraumatic ischemia/reperfusion injury in adiponectin knockout mice.Tumor necrosis factor α-induced downregulation of adiponectin and the resultant enhanced oxidative/nitrative stress are involved in exacerbated posttraumatic ischemic myocardial injury. Therapeutic approaches blocking tumor necrosis factor α production or restoring adiponectin might have prophylactic value against secondary myocardial ischemic injury after a primary nonlethal mechanical trauma.

Reliable video transmission over mobile wireless channels faces many challenges due to the time-varying multi-path fading. In this paper, a novel 3-D interleaving method, called Spatial Frequency Temporal Interleaving (SFTI), is proposed for video transmission over OFDM systems in this kind of channels. SFTI means the video data will be interleaved both at bit level in spatial domain, which can disperse the error bits to make the channel coding more effective, and slice level in Frequency and temporal domain, which can alleviate the impact of burst bit errors by limiting the bit errors in some area of the picture, thus the error concealment is facilitated. Simulation results show that the proposed method can improve the quality of the reconstructed video.

The motion information of the macroblock signaled as the spatial DIRECT mode can be derived from the neighboring blocks. The closest reference picture in the reference picture list used by the neighboring blocks is selected as the reference picture of the macroblock. Both temporal and interview reference pictures are put into the reference picture list in order to improve the coding efficiency in MVC. A flexible reference picture selection method taking the diversity of reference picture list into account is proposed in this paper. The experimental results show that the proposed method can improve coding efficiency especially when the interview reference pictures are put ahead of the temporal reference pictures.

In this paper, a moving objects extraction method based on true motion information is proposed. First of all, three dimensional recursive search algorithm (3DRS) combined with median filter is used instead of full search in searching for motion vectors (MVs) which reflect the true motion of objects in video sequences. After that a new parameter segmentation factor (SF) is constructed to describe motion feature of each block in a picture. Thus, moving objects extraction with the fuzzy C-means clustering algorithm (FCM) over SFs is implemented, during which gathering degree is used to distinguish the foreground which refers to the moving objects from the background. Experimental results show that this method is effective for still scenes or scenes with consistent global motion.

Orthogonal Frequency Division Multiplexing (OFDM) is a promising technique in broadband wireless communication systems. This paper presents a novel multi-reference scheme based on 3D interleaving for video coding and transmission over OFDM channel. Initially, a combining interleaving method in spatial, frequency and temporal domains, called SFTI, is proposed. With SFTI, different slices within one frame are transmitted in different sub-channels of OFDM, whose SNR can be estimated, and the transmission status of slices through these sub-channels are real-time feedback to the encoder. Based on the feedback information, a multi-reference scheme for video coding is proposed where the well-transmitted slices are selected as the reference picture of its consequent pictures in inter-frame coding to eliminate the impairment caused by error propagation in video transmission over wireless OFDM channels. Extensive experimental results have demonstrated the effectiveness of the proposed methods in error resilience.

This paper focuses on the issue of cross-layer control for H.264/AVC video transmission over OFDM. Jointly considering the error resilient (ER) tools provided by H.264/AVC and the characteristics of OFDM channels, a cross-layer scheme is proposed, in which a cross-layer allocator is used to allocate channel resources for different priority video data transmission, and feedback transmission status information to H.264/AVC encoder for error resilient encoding. By allocation, a 3-D interleaving is implemented to improve the reliance of the communication, and a cross-layer feedback is operated to inform the encoder for a more resilient coding processing to obtain optimal transmission quality. The experimental results indicate that the proposed scheme can dramatically improve the received video quality over wireless OFDM.

Objective Adiponectin, circulates as trimer, hexamer and high molecular weight form (HMW) in blood. Both adiponectin complexes concentration and their bioactivities are decreased in pathological state. Moreover, DsbA-L, a key regulator for adiponectin biosynthesis, is down-regulated in obese humans. However, the alterations of adiponectin multimers distribution, bioactivities and DsbA-L level in newly diagnosed Chinese type 2 diabetes (T2DM) patients are unknown. The objective of present study was to compare plasma adiponectin isoform status along with their bioactivities and DsbA-L concentration in T2DM with control subjects. Methods Plasma total adiponectin was measured by ELISA. Adiponectin multimers were analysed by western blot followed SDS-PAGE under nonheating nonreducing conditions. Plasma adiponectin multimers were isolated by chromotography techniques from plasma in ten T2DM and ten healthy control subjects respectively. Adiponectin bioactivity was detected by incubating HUVEC with isolated adiponectin isoforms and determining the phosphorylation level of AMPK and eNOS. DsbA-L protein expression level was determined by western blot. Results 189 T2DM (48.7±9.4 y) and 123 healthy people (42.8±8.0 y) were enrolled. In comparison with healthy control group, total adiponectin (p Conclusion This study directly demonstrated for the first time that human HMW adiponectin bioactivity was decreased in type 2 diabetes. We also provide a target for regulating HMW adiponectin concentration in diabetic patients.

Andersen-Tawil syndrome (ATS), also called Long QT syndrome 7, is a rare autosomal dominant genetic disorder characterized by a triad of episodic flaccid muscle weakness, ventricular arrhythmias and prolonged QT interval, and anomalies such as low-set ears, ocular hypertelorism, small mandible