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Nuclear magnetic resonance spectroscopy was employed to monitor the change in chemical structures, olefin units (cis, trans and vinyl) and hydroxyl value on stabilized Hydroxyl‐terminated polybutadiene (HTPB) under accelerated ageing condition. Thermal ageing of HTPB was carried out at 65 °C for 10‐weeks and periodically withdrawn sample for NMR analysis. 1H and 13C NMR spectroscopy provided detailed structural information for all HTPB samples, including the quantification of olefin units and the determination of hydroxyl value. The analysis revealed a decrease in signal intensity, particularly for the olefin near or at the molecular end, suggesting that they were oxidized before those in the middle position within the chain. The quantitative assessment of olefin units indicates a slight decrease of 2 % in 1,2‐vinyl unit after 10‐weeks of ageing. The NMR spectra did not show any detectable signals corresponding to epoxides, peroxides or alcohols in any HTPB samples. However, a slight increase in the OH value was observed after 8 and 10 weeks of ageing, suggesting the possible incorporation of new hydroxyl groups due to thermal‐oxidation. The antioxidants used to stabilize HTPB exhibited limited effectiveness in preventing degradation reactions, even after 4 weeks of ageing at 65 °C. [ABSTRACT FROM AUTHOR]

Flexibility is a key advantage of organic solar cells (OSCs), and the power conversion efficiencies (PCEs) of flexible OSCs (FOSCs) are primarily constrained by flexible transparent electrodes (FTEs). While much attention has been devoted to the study of conductive layers on FTEs, the importance of flexible substrates in influencing the properties of FTEs and the performance of FOSCs is often overlooked. In this study, an FTE is developed using an eco‐friendly ethyl cellulose (EC) substrate and silver nanowires (AgNWs) as the conductive electrode. The FTE exhibits a high transmittance of up to 88% at 550 nm and a low sheet resistance of 17.65 Ω/□. Consequently, FOSCs based on the EC/PI FTEs achieve a remarkable PCE of 18.05%, comparable to that on the rigid ITO substrate. The flexible devices also demonstrate excellent bending and peeling durability even under extreme bending conditions. [ABSTRACT FROM AUTHOR]

As the key component of transceiver, power amplifier (PA) plays an extremely important role in wireless communication system. In order to accurately characterize the performance variation of PA at any temperature, the temperature behavior of a gallium arsenide (GaAs) pseudomorphic high electron mobility transistor (pHEMT) high gain monolithic microwave integrated circuit (MMIC) PA is modeled in this paper. In this modeling, the resilient back propagation neural network (BPNN) is utilized to do the temperature behavior modeling for this PA. The investigation shows that the minimum mean square error (MSE) of the prediction results is 4.9607 × 10−4, which implies that it is feasible to use this modeling method to characterize the temperature behavior of PA. This modeling not only theoretically overcomes the problem of slow convergence speed of BPNN, but also solves the limitation of experimental devices and time setting. It will provide a more convenient guidance for test engineers. [ABSTRACT FROM AUTHOR]

Exploitation of key protected wild plant resources makes great sense, but their limited populations become the major barrier. A particular strategy for breaking this barrier was inspired by the exploration of a resource‐saving fungal endophyte Penicillium sp. DG23, which inhabits the key protected wild plant Schisandra macrocarpa. Chemical studies on the cultures of this strain afforded eight novel indole diterpenoids, schipenindolenes A−H (1–8), belonging to six diverse skeleton types. Importantly, semisyntheses suggested some key nonenzymatic reactions constructing these molecules and provided targeted compounds, in particular schipenindolene A (Spid A, 1) with low natural abundance. Remarkably, Spid A was the most potent HMG‐CoA reductase (HMGCR) degrader among the indole diterpenoid family. It degraded statin‐induced accumulation of HMGCR protein, decreased cholesterol levels and acted synergistically with statin to further lower cholesterol. Mechanistically, transcriptomic and proteomic profiling suggested that Spid A potentially activated the endoplasmic reticulum‐associated degradation (ERAD) pathway to enhance the degradation of HMGCR, while simultaneously inhibiting the statin‐activated expression of many key enzymes in the cholesterol and fatty acid synthesis pathways, thereby strengthening the efficacy of statins and potentially reducing the side effects of statins. Collectively, this study suggests the potential of Spid A for treating cardiovascular disease. [ABSTRACT FROM AUTHOR]

The problem of event‐triggered finite‐time trajectory tracking control of perturbed Euler–Lagrange systems with nonlinear dynamics and disturbances is addressed in this article. Extreme learning machine (ELM) framework is employed to formulate unknown nonlinearities, and adaptive technique is adopted to adjust output weights of the ELM networks and remedy the negative impacts of disturbances, nonlinearities, and residual errors. Then to ensure the system follows the desired position trajectory within a finite‐time, an adaptive ELM‐based sliding mode control strategy is developed. Moreover, event‐triggered control technique is proposed to regulate control outputs on the basis of the developed control strategy for reducing actuator actions and saving communication resources. Lyapunov stability theorem is utilized to confirm bounded trajectory tracking results and finite‐time convergence of the Euler–Lagrange system. Finally, the effectiveness of the developed adaptive ELM‐based event‐triggered sliding‐mode control strategies is substantiated by simulations in a robotic manipulator system. [ABSTRACT FROM AUTHOR]

Currently, machine‐learning algorithms have been considered the most promising approach to reach a clinical diagnosis at the individual level. This study aimed to investigate whether the whole‐brain resting‐state functional connectivity (RSFC) metrics combined with machine‐learning algorithms could be used to identify essential tremor (ET) patients from healthy controls (HCs) and further revealed ET‐related brain network pathogenesis to establish the potential diagnostic biomarkers. The RSFC metrics obtained from 127 ET patients and 120 HCs were used as input features, then the Mann–Whitney U test and the least absolute shrinkage and selection operator (LASSO) methods were applied to reduce feature dimensionality. Four machine‐learning algorithms were adopted to identify ET from HCs. The accuracy, sensitivity, specificity and the area under the curve (AUC) were used to evaluate the classification performances. The support vector machine, gradient boosting decision tree, random forest and Gaussian naïve Bayes algorithms could achieve good classification performances with accuracy at 82.8%, 79.4%, 78.9% and 72.4%, respectively. The most discriminative features were primarily located in the cerebello‐thalamo‐motor and non‐motor circuits. Correlation analysis showed that two RSFC features were positively correlated with tremor frequency and four RSFC features were negatively correlated with tremor severity. The present study demonstrated that combining the RSFC matrices with multiple machine‐learning algorithms could not only achieve high classification accuracy for discriminating ET patients from HCs but also help us to reveal the potential brain network pathogenesis in ET. [ABSTRACT FROM AUTHOR]

Aims: Sodium‐glucose cotransporter 2 inhibitors (SGLT2is) have made considerable progress in the field of heart failure, but their application in arrhythmia remains to be in‐depth. Right heart disease (RHD) often leads to right heart dysfunction and is associated with atrial fibrillation (AF). Here, we explored the possible electrophysiologic effect of dapagliflozin (a type of SGLT2is) in the development of AF in rats with RHD. Methods and results: Rats in the experimental group were intraperitoneally injected with a single dose of 60 mg/kg monocrotaline (MCT group, n = 32) on the first day of the experiment, whereas rats in the control group were injected with vehicle (CTL group, n = 32). Rats in the treatment subgroup were treated with dapagliflozin solution orally (MCT + DAPA and CTL + DAPA groups) for a total of 4 weeks, whereas rats in the rest of subgroups were given sterile drinking water. After 4 weeks, echocardiography demonstrated that MCT group rats developed obvious pulmonary arterial hypertension and right heart dysfunction. In addition, there were also obvious inflammatory infiltration, fibrosis, and muscularization in right atrial and pulmonary arteries. The P‐wave duration (17.00 ± 0.53 ms, vs. 14.43 ± 0.57 ms in CTL; 14.00 ± 0.65 ms in CTL + DAPA; 14.57 ± 0.65 ms in MCT + DAPA; P < 0.05), RR interval (171.60 ± 1.48 ms, vs. 163.10 ± 1.10 ms in CTL; 163.30 ± 1.19 ms in CTL + DAPA; 163.10 ± 1.50 ms in MCT + DAPA; P < 0.05), Tpeak‐Tend interval (65.93 ± 2.55 ms, vs. 49.55 ± 1.71 ms in CTL; 48.27 ± 3.08 ms in CTL + DAPA; P < 0.05), and corrected QT interval (200.90 ± 2.40 ms, vs. 160.00 ± 0.82 ms in CTL; 160.40 ± 1.36 ms in CTL + DAPA; 176.6 ± 1.57 ms in MCT + DAPA; P < 0.01) were significantly prolonged in the MCT group after 4 weeks, whereas P‐wave amplitude (0.07 ± 0.0011 mV, vs. 0.14 ± 0.0009 mV in CTL; 0.14 ± 0.0011 mV in CTL + DAPA; 0.08 ± 0.0047 mV in MCT + DAPA; P < 0.05) and T‐wave amplitude (0.04 ± 0.002 mV, vs. 0.13 ± 0.003 mV in CTL; 0.13 ± 0.003 mV in CTL + DAPA; P < 0.01) were decreased, and atrial 90% action potential duration (47.50 ± 0.93 ms, vs. 59.13 ± 2.1 ms in CTL; 59.75 ± 1.13 ms in CTL + DAPA; 60.63 ± 1.07 ms in MCT + DAPA; P < 0.01) and effective refractory periods (41.14 ± 0.88 ms, vs. 62.86 ± 0.99 ms in CTL; 63.14 ± 0.67 ms in CTL + DAPA; 54.86 ± 0.70 ms in MCT + DAPA; P < 0.01) were shortened. Importantly, the inducibility rate (80%, vs. 0% in CTL; 10% in CTL + DAPA; 40% in MCT + DAPA; P < 0.05) and duration of AF (30.85 ± 22.90 s, vs. 0 ± 0 s in CTL; 0.24 ± 0.76 s in CTL + DAPA; 5.08 ± 7.92 s in MCT + DAPA; P < 0.05) were significantly increased, whereas the expression levels of cardiac ion channels and calcium‐handling proteins such as potassium/calcium channels and calmodulin were decreased. Mechanistically, 'NACHT, LRR, and PYD domain‐containing protein 3' inflammasome‐related pathway was significantly activated in the MCT group. Nevertheless, in the MCT + DAPA group, the above abnormalities were significantly improved. Conclusions: Dapagliflozin reduces pulmonary vascular damage and right heart dysfunction, as well as the susceptibility to AF in RHD rats. [ABSTRACT FROM AUTHOR]

This article is concerned with the fixed‐time path‐following control problem of a perturbed cart‐pendulum robot with linear quadratic (LQ) performance optimization. In order to ensure the displacements of cart and pendulum of the robot following the desired paths within fixed‐time, adaptive anti‐perturbation sliding mode control schemes with a novel fixed‐time sliding mode surface are developed to withstand the adverse influence of perturbations. Furthermore, an adaptive radial basis function neural network (RBFNN)‐based sliding mode control algorithm is employed to approximate the continuous perturbations, so that the path‐following LQ control problem can be further dealt with. The fixed‐time stability and path‐following results of the cart‐pendulum robotic system are achieved by Lyapunov stability theory. A simulation example for a heavy material handling agricultural robot is proposed to verify the effectiveness of the developed method. [ABSTRACT FROM AUTHOR]

SUMMARY: Modification of the O‐acetylation level of xyloglucan (XyG) appears to affect aluminum (Al) sensitivity in Arabidopsis by modulating its binding capacity to Al. However, the transcriptional regulation of this process remains largely unknown. In our previous studies, we found that the expression of TRICHOME BIREFRINGENCE‐LIKE27 (TBL27), which is responsible for the O‐acetylation of XyG, was downregulated under Al stress. In the present study, we showed that the expression of an R2R3‐type transcription factor‐encoding gene, MYB103, was also inhibited by Al exposure and exhibited a co‐expression pattern with TBL27 in roots and siliques, suggesting a potential link between MYB103 and TBL27. The loss of function of MYB103 resulted in increased Al sensitivity, as indicated by more inhibited root growth and elevated root Al content compared with the wild type. Moreover, we also detected increased Al accumulation in the root cell wall and the hemicellulose fraction, which was attributed to the changes in the O‐acetylation level of XyG rather than the XyG content itself. In addition, further analysis revealed that MYB103 positively activated TBL27 expression by directly binding to the TBL27 promoter region, and TBL27 overexpression in the myb103 mutant rescued the Al‐sensitive phenotype of the mutant to the wild‐type level. Taken together, we conclude that MYB103 acts upstream of TBL27 to positively regulate Al resistance by modulating the O‐acetylation of the cell wall XyG. Significance Statement: In this study, a member of the MYB family that is involved in the regulation of aluminum (Al) sensitivity in Arabidopsis, MYB103, was identified. Further analysis indicated that MYB103 acts upstream of TRICHOME BIREFRINGENCE‐LIKE27 in regulating Al sensitivity by modulating the O‐acetylation level of the cell wall xyloglucan. [ABSTRACT FROM AUTHOR]

Obesity, which has unknown pathogenesis, can increase the frequency and seriousness of acute myocardial infarction (AMI). This study evaluated effect of Huayu Qutan Recipe (HQR) pretreatment on myocardial apoptosis induced by AMI by regulating mitochondrial function via PI3K/Akt/Bad pathway in rats with obesity. For in vivo experiments, 60 male rats were randomly divided into 6 groups: sham group, AMI group, AMI (obese) group, 4.5, 9.0 and 18.0 g/kg/d HQR groups. The models fed on HQR with different concentrations for 2 weeks before AMI. For in vitro experiments, the cardiomyocytes line (H9c2) was used. Cells were pretreated with palmitic acid (PA) for 24 h, then to build hypoxia model followed by HQR-containing serum for 24 h. Related indicators were also detected. In vivo, HQR can lessen pathohistological damage and apoptosis after AMI. In addition, HQR improves blood fat levels, cardiac function, inflammatory factor, the balance of oxidation and antioxidation, as well as lessen infarction in rats with obesity after AMI. Meanwhile, HQR can diminish myocardial cell death by improving mitochondrial function via PI3K/Akt/Bad pathway activation. In vitro, HQR inhibited H9c2 cells apoptosis, improved mitochondrial function and activated the PI3K/Akt/Bad pathway, but effects can be peripeteiad by LY294002. Myocardial mitochondrial dysfunction occurs following AMI and can lead to myocardial apoptosis, which can be aggravated by obesity. HQR can relieve myocardial apoptosis by improving mitochondrial function via the PI3K/Akt/Bad pathway in rats with obesity. [ABSTRACT FROM AUTHOR]

Fibrosis is a pathological process characterized by abnormal activation of fibroblasts with increased synthesis of extracellular matrix components, including collagens. It may lead to loss of proper tissue architecture and organ function in clinical diseases such as systemic sclerosis and liver fibrosis. Excess accumulation of collagens is considered the primary indicator of fibrosis. Notch signaling has been reported to be involved in the fibrosis of many different organs, including the liver. Our previous study showed that the uterine‐specific over‐activation of canonical Notch1 signaling in the mouse uterus (Pgrcre/+Rosa26N1ICD/+, OEx) results in complete infertility as a consequence of multiple developmental and physiological defects, together with increased collagen accumulation evidenced by Masson's staining. In this study, we further detected expressions of all 44 collagen genes in these Notch1 gain‐of‐function transgenic mice and found that 18 collagens have been largely affected. In another aspect, using an intrauterine adhesion model (IUA), we mimicked fibrosis in the mouse uterine. The results suggested that Notch receptors were upregulated only 3 days after induction, and most of the fibril‐forming collagen began to upregulate 6 days after the surgery. Furthermore, when induced IUA in the N1ICD‐OEx mice, the expression of collagens and fibrosis levels were significantly enhanced. At last, as a Notch signaling inhibitor, the γ‐secretase inhibitor N‐[N‐(3,5‐difl uorophenacetyl)‐L‐alanyl]‐S‐phenylglycine t‐butyl ester (DAPT) pretreatment could alleviate the expression of collagens and the symptoms of fibrosis. These results demonstrate that Notch signaling may play a role in upregulating collagens expression in endometrial fibrosis and might be a potential target of fibrosis therapy in the endometrium. [ABSTRACT FROM AUTHOR]

Introduction: Septic cardiomyopathy is a common complication of sepsis with high morbidity and mortality, but lacks specific therapy. This study aimed to reveal the role of circTLK1 and its potential mechanisms in septic cardiomyopathy. Materials and Methods: The in vitro and in vivo models of septic cardiomyopathy were established. Cell viability and apoptosis were detected by CCK8, TUNEL and flow cytometry, respectively. LDH, CK, SOD, MDA, ATP, 8‐OHdG, NAD+/NADH ratio, ROS level, mitochondrial membrane potential and cytochrome C distribution were evaluated using commercial kits. qRT‐PCR and western blotting were performed to detect RNA and protein levels. Mitochondrial DNA (mtDNA) copy number and transcription were assessed by quantitative PCR. Dual‐luciferase assay, RNA immunoprecipitation and co‐immunoprecipitation were performed to verify the interaction between circTLK1/PARP1 and miR‐17‐5p. Results: CircTLK1, PARP1 and HMGB1 were up‐regulated in the in vitro and in vivo models of septic cardiomyopathy. CircTLK1 inhibition restrained LPS‐induced up‐regulation of PARP1 and HMGB1. Moreover, circTLK1 knockdown repressed sepsis‐induced mtDNA oxidative damage, mitochondrial dysfunction and consequent cardiomyocyte apoptosis by inhibiting PARP1/HMGB1 axis in vitro and in vivo. In addition, circTLK1 enhanced PARP1 expression via sponging miR‐17‐5p. Inhibition of miR‐17‐5p abolished the protective effects of circTLK1 silencing on oxidative mtDNA damage and cardiomyocyte apoptosis. Conclusion: CircTLK1 sponged miR‐17‐5p to aggravate mtDNA oxidative damage, mitochondrial dysfunction and cardiomyocyte apoptosis via activating PARP1/HMGB1 axis during sepsis, indicating that circTLK1 may be a putative therapeutic target for septic cardiomyopathy. [ABSTRACT FROM AUTHOR]

Summary: In this article, the robust adaptive output tracking control problem is addressed for a class of nonlinear systems with nonlinear dynamics and unknown system parameters. The nonlinear dynamics including internal parameter uncertainties and external disturbances are formulated as time‐varying state/input‐dependent perturbations. Radial‐basis function neural networks (RBFNNs) are developed to approximate the perturbations. A robust adaptive RBFNN‐based output feedback control strategy against the perturbations is developed by using backstepping technique with immeasurable states and without knowing any system parameter. Based on Lyapunov stability theorem, the asymptotic output tracking results of the closed‐loop nonlinear system are obtained in the presence of perturbations, immeasurable states, and unknown system parameters. The efficacy of the proposed adaptive RBFNN‐based output feedback control strategy is validated by simulation in a DC–DC buck converter system. [ABSTRACT FROM AUTHOR]

Norcantharidin (NCTD), the demethylated analog of cantharidin isolated from Mylabris, is known to inhibit renal fibrosis. However, the underlying mechanism is largely unknown. The present study investigates whether NCTD exerts this effect through regulation of the protein phosphatase 2A catalytic subunit (PP2Ac)‒Smad3 pathway. HK‐2 human renal proximal tubule cells exposed to transforming growth factor (TGF)‐β1 were used as an in vitro model of renal fibrosis. The levels of total Smad3, C‐terminal‐phosphorylated Smad3 (p‐Smad3), PP2Ac, and fibronectin (Fn) were evaluated by Western blotting. A PP2Ac overexpression plasmid and the PP2Ac inhibitor okadaic acid (OA) were used for functional analyses. The subcellular localization of Smad3 was visualized by immunofluorescence labeling. The results showed that PP2Ac overexpression increased Smad3 phosphorylation and nuclear translocation in HK‐2 cells, while pharmacologic inhibition of PP2Ac with OA had the opposite effect. NCTD suppressed Fn and p‐Smad3 expression and TGF‐β1‐induced nuclear entry of Smad3, but these effects were abrogated by inhibition of PP2Ac. Thus, the anti‐renal interstitial fibrosis effect of NCTD is exerted through inhibition of PP2Ac‐mediated C‐terminal phosphorylation of Smad3. These findings highlight the therapeutic potential of NCTD for the treatment of renal interstitial fibrosis. [ABSTRACT FROM AUTHOR]

This study deals with the fault-tolerant control problem for a class of two independent wheeled mobile robot systems with actuator faults and unknown robot parameters. Partial loss of control effectiveness and bias-actuator faults are addressed without knowing eventually faulty information of actuators. Adaptive schemes are developed to estimate unknown faulty parameters of actuator faults and unknown robot parameters of viscous friction factor and driving gain. Then, the backstepping control technique is utilised to construct the state feed-back control strategy based on the adaptive estimations. By using the Lyapunov stability theory, it is shown that the forward speed and azimuthal angle of wheeled mobile robots can track the given trajectory asymptotically in the case of actuator faults and unknown parameters. The effectiveness of the proposed designs is illustrated via a mobile robot system. [ABSTRACT FROM AUTHOR]

This study deals with the fault‐tolerant control problem for a class of two independent wheeled mobile robot systems with actuator faults and unknown robot parameters. Partial loss of control effectiveness and bias‐actuator faults are addressed without knowing eventually faulty information of actuators. Adaptive schemes are developed to estimate unknown faulty parameters of actuator faults and unknown robot parameters of viscous friction factor and driving gain. Then, the backstepping control technique is utilised to construct the state feed‐back control strategy based on the adaptive estimations. By using the Lyapunov stability theory, it is shown that the forward speed and azimuthal angle of wheeled mobile robots can track the given trajectory asymptotically in the case of actuator faults and unknown parameters. The effectiveness of the proposed designs is illustrated via a mobile robot system. [ABSTRACT FROM AUTHOR]

Summary: In this paper, the problem of fault‐tolerant insensitive control is addressed for a class of linear time‐invariant continuous‐time systems against bounded time‐varying actuator faults and controller gain variations. Adaptive mechanisms are developed to adjust controller gains in order to compensate for the detrimental effects of partial loss of control effectiveness and bias‐actuator faults. Variations of controller gains arise from time‐varying and bounded perturbations that are supposed to always exist in adaptive mechanisms. Based on the disturbed outputs of adaptive mechanisms, three different adaptive control strategies are constructed to achieve bounded stability results of the closed‐loop adaptive fault‐tolerant control systems in the presence of actuator faults and controller gain variations. Furthermore, comparisons of convergence boundaries of states and limits of control inputs among adaptive strategies are developed in this paper. The efficiency of the proposed adaptive control strategies and their comparisons are demonstrated by a rocket fairing structural‐acoustic model. [ABSTRACT FROM AUTHOR]

Elevated kynurenine (Kyn) production from tryptophan (Trp) metabolism is a biomarker of immune dysregulation in depression, but its mechanistic contributions to the behavioral symptoms are poorly defined. In this study, Kyn was shown to be a metabolic regulator of proinflammatory monocytes that orchestrated peripheral immune activation and neuroinflammation in depressive mice. Kyn-induced depressive behavior was paralleled by brain infiltration of proinflammatory monocytes and astrocytic activation. Kyn enhanced chemokine (C-C motif) ligand-2-mediated chemotaxis of monocytes and their proinflammatory capability on cocultured astrocytes in vitro, which involved the activation of aryl hydrocarbon receptor (AhR) signaling. Kyn augmented, whereas pharmacological AhR blockade rescued, systemic inflammation-induced monocyte trafficking, neuroimmune disturbance, and depressive-like behavior in mice. The behavior-exacerbating effects of the Kyn-AhR axis were dampened with prior depletion of functional monocytes in the periphery. The findings in our study extend understanding of an immunologic effect of Kyn that links Trp metabolism and inflammatory signaling in depression pathology, with potential therapeutic implications for depressive disorders. [ABSTRACT FROM AUTHOR]

SUMMARY Joint service involving several clouds is an emerging form of cloud computing. In hybrid clouds, the schedulers within 1 cloud must not only self-adapt to the job arrival processes and the workload but also mutually adapt to the scheduling polices of other schedulers. However, as a combinatorial optimization problem, scheduling is challenged by the adaptation to those dynamics and uncertain behaviors of the peers. This article studies the collaboration among benevolent clouds that are cooperative in nature and willing to accept jobs from other clouds. We take advantage of machine learning and propose a distributed scheduling mechanism to learn the knowledge of job model, resource performance, and others' policies. Without explicit modeling and prediction, machine learning guides scheduling decisions based on experiences. To examine the performance of our approach, we conducted simulation using the SP2 job workload log of the San Diego Supercomputer Center under a test bed based on agent-based systems-SWARM. The results validate that our approach has much shorter mean response time than 5 typical dynamic scheduling algorithms-opportunistic load balancing, minimum execution time, minimum completion time, switching algorithm, and k-percent best. A better collaboration in hybrid cloud is achieved by full adaptation. [ABSTRACT FROM AUTHOR]

The finite‐time robust fault‐tolerant control problem is addressed for a class of perturbed linear systems with actuator faults and input amplitude saturations. A compensation control strategy is proposed to eliminate the effects of actuator faults and non‐linear disturbance‐like inputs within a finite‐time, as well as to ensure the control inputs be limited within a desired constraint. Based on Lyapunov stability theory, it is shown that system states can converge to a small region in the cases of actuator faults and saturations by choosing suitable control parameters. Some relationships among convergence bounds, actuator faults and amplitude limits, as well as the control parameters are studied deeply and illustrated explicitly with formulas. Simulations of a linearised F‐18 longitudinal dynamical control model are given to verify the effectiveness of the proposed method. [ABSTRACT FROM AUTHOR]

ABSTRACT In this article, a compact multiband planar inverted-F antenna (PIFA) is proposed to cover three frequency bands for RFID operation: 920-925 MHz, 2.4-2.48 GHz, 5.815-5.875 GHz. The multiband PIFA has the advantage of compact size of 55 × 40 × 0.8 mm3. The antenna proposed herein was composed of a modified planar inverted-F with a loaded arm and a parasitic inverted-L. The lowest band is achieved by the modified planar inverted-F and the highest band is achieved by the parasitic inverted-L. With the loaded arm, the band from 2.4 GHz to 2.48 GHz is achieved. The current distribution and radiation patterns are studied in this article. The antenna was fabricated on the FR4 substrate, providing the return loss less than −10 dB over all bands of interest. © 2016 Wiley Periodicals, Inc. Microwave Opt Technol Lett 58:1934-1937, 2016 [ABSTRACT FROM AUTHOR]

ABSTRACT Rapid and adequate identification of anaerobic bacterial species still presents a challenge for most diagnostic laboratories, hindering the selection of appropriate therapy. In this study, the identification capacity of 16S rRNA sequence analysis, VITEK 2 (BioMérieux, Lyon, France) compact analysis and VITEK MS-mediated identification for anaerobic bacterial species was compared. Eighty-five anaerobic bacterial isolates from 11 provinces in China belonging to 14 genera were identified by these three methods. Differences in identification between these three methods were compared. Consistent identification results were obtained for 54 (54/85, 63.5%) isolates by all three methods, the most discordant results being concentrated in Clostridium XI ( n = 8) and Bacteroides fragilis ( n = 9) clusters. Using the VITEK MS system, 74 (74/90, 82.2%) isolates were identified as single species consistent with 16S rRNA sequence analysis, which was significantly better than the results obtained with VITEK 2 Compact ( P < 0.01). Misidentifications by the Vitek 2 Compact and Vitek MS systems were mainly observed in the Clostridium XI ( n = 8)and B. fragilis clusters ( n = 9). VITEK MS identified anaerobic bacteria even after they had been exposed to oxygen for a week. Identification by the Vitek MS system was more consistent with 16S rRNA sequence analysis than identification by Vitek 2 Compact. Continuous expansion of the VITEK MS database with rare described anaerobic species is warranted to improve both the efficiency and accuracy of VITEK MS identification in routine diagnostic microbiology. [ABSTRACT FROM AUTHOR]

The epidermal growth factor receptor (EGFR) is implicated in many types of cancer, including colorectal cancer (CRC), and has become one of the most common candidates for targeted therapy. Here, we found that Erbin, a member of the leucine-rich repeat and PDZ domain (LAP) family, plays a key role in EGFR signalling. Erbin inhibited EGFR ubiquitination and stabilized the EGFR protein by interacting with c-Cbl. Moreover, the PDZ domain of Erbin was critical for the interaction between Erbin and c-Cbl and EGFR ubiquitination. Interestingly, Erbin expression was elevated in tumour samples from CRC patients, increased in advanced clinical stage disease and correlated with EGFR expression. In vivo studies using mouse xenograft models of CRC showed that Erbin promotes tumour growth, and that the effects of Erbin on tumour growth are mainly related to the regulatory effects of Erbin on EGFR. The azoxymethane (AOM)-induced colon carcinogenesis model in ErbinΔC/ΔC mice, with the PDZ domain of Erbin deleted, demonstrated that the PDZ domain of Erbin and its regulation of EGFR signalling are necessary for the tumourigenesis and tumour growth of CRC. We found that Erbin promotes tumourigenesis and tumour growth in CRC by stabilizing EGFR. Our study sheds light on developing Erbin, especially its PDZ domain, as a potential target for CRC treatment. [ABSTRACT FROM AUTHOR]

ABSTRACT Dynamin 1 is a neuron-specific guanosine triphosphatase (GTPase) that is an essential component of membrane fission during synaptic vesicle recycling and endocytosis. This study evaluated the dynamin 1 expression pattern in the acute lithium-pilocarpine rat model and in patients with temporal lobe epilepsy (TLE) and investigated whether altering the dynamin 1 expression pattern affects epileptic seizures in vivo and in vitro. The immunofluorescence, western blot analysis, and reverse transcription-PCR results show that the dynamin 1 expression level increased significantly in experimental rats from day 1 to day 7 after the onset of seizures and was significantly higher in TLE patients. The behavioral study revealed that inhibiting dynamin 1 increased the latency time of the first seizure and decreased the frequency and severity of the seizures. In addition, electrophysiological recordings from brain slices showed that inhibiting dynamin 1 reduces the frequency of Mg-free induced seizure-like activity. The anticonvulsant effect of dynasore was more effective at 10 µM than at 1 µM or 160 µM. These results indicate that the altered level of dynamin 1 may contribute to the development of epileptic seizures and that the targeted regulation of dynamin 1 activity may control epileptic seizures. Synapse 69:67-77, 2015. © 2014 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Many studies have examined the association between the FABP2 (rs1799883) Ala54Thr gene polymorphism and type 2 diabetes mellitus risk (T2 DM) in various populations, but their results have been inconsistent. To assess this relationship more precisely, A Hu GE review and meta-analysis were performed. The PubMed and CNKI database was searched for case-control studies published up to April 2014. Data were extracted and pooled odds ratios ( OR) with 95% confidence intervals ( CI) were calculated. Ultimately, 13 studies, comprising 2020 T2 DM cases and 2910 controls were included. Overall, for the Thr carriers (Ala/Thr and Thr/Thr) versus the wild-type homozygotes (Ala/Ala), the pooled OR was 1.18 (95% CI = 1.04-1.34, P = 0.062 for heterogeneity), for Thr/Thr versus Ala/Ala the pooled OR was 1.17 (95% CI = 1.05-1.41 P = 0.087 for heterogeneity). In the stratified analysis by ethnicity, the significantly risks were found among Asians but not Caucasians. This meta-analysis suggests that the FABP2 (rs1799883) Ala54Thr polymorphisms are associated with increased susceptibility to T2 DM risk among Asians but not Caucasians. [ABSTRACT FROM AUTHOR]

During adaptation to environments, bacteria employ two-component signal transduction systems, which contain histidine kinases and response regulators, to sense and respond to exogenous and cellular stimuli in an accurate spatio-temporal manner. Although the protein phosphorylation process between histidine kinase and response regulator has been well documented, the molecular mechanism fine-tuning phosphorylation levels of response regulators is comparatively less studied. Here we combined genetic and biochemical approaches to reveal that a hybrid histidine kinase, SreS, is involved in the SreK- SreR phosphotransfer process to control salt stress response in the bacterium X anthomonas campestris. The N-terminal receiver domain of SreS acts as a phosphate sink by competing with the response regulator SreR to accept the phosphoryl group from the latter's cognate histidine kinase SreK. This regulatory process is critical for bacterial survival because the dephosphorylated SreR protein participates in activating one of the tandem promoters ( P2) at the 5′ end of the sreK - sreR - sreS - hppK operon, and then modulates a transcriptional surge of the stress-responsive gene hppK, which is required for folic acid synthesis. Therefore, our study dissects the biochemical process of a positive feedback loop in which a 'three-component' signalling system fine-tunes expression kinetics of downstream genes. [ABSTRACT FROM AUTHOR]

The synthesis and the solid state magnetic properties of (nitronyl nitroxide)-substituted trioxytriphenylamine radical cation tetrachlorogallate, NNTOT+⋅GaCl4 −, are reported. In the temperature region between 300 and 3 K, the magnetic behavior is characterized by the strong intramolecular ferromagnetic interaction ( J/ kB=+400 K) between the radical ( NN) and the radical cation ( TOT+) and the weak intermolecular antiferromagnetic interaction ( J/ kB=−1.9 K) between NNTOT+ ions. Below 3 K, a 3D-type long-range magnetic ordering into a weak ferromagnet was observed ( TN=2.65 K). The magnetic entropy ( Smag=8.97 J K−1 mol−1) obtained by the heat capacity measurement is in good agreement with the theoretical value of R ln3=9.13 J K−1 mol−1 based on the S=1 state. [ABSTRACT FROM AUTHOR]

Objective To evaluate the usefulness of needle biopsy in the diagnosis of early sacroiliitis to improve the diagnostic level and outcome of ankylosing spondylitis (AS). Methods One hundred nine patients in whom early AS was highly suspected, but in whom only sacroiliitis of grade I or lower on radiography/computed tomography (CT) was seen, were recruited for study. CT-guided needle biopsy of the sacroiliac joints was performed, and the patients were followed up for 5-10 years. Results Of the 109 patients, magnetic resonance imaging (MRI) was used to confirm the presence or absence of sacroiliitis in 77 patients. Of these, 23 patients were determined to have sacroiliitis on MRI, and 54 had no sacroiliitis on MRI. Needle biopsy was performed on all 109 patients. Features of inflammation were found in 85 patients, which included all 23 patients with MRI evidence of sacroiliitis and 38 of the 54 patients without MRI evidence of sacroiliitis. No features of inflammation were found on needle biopsy in 24 of the patients, including the remaining 16 patients who did not have sacroiliitis on MRI. The sensitivity and specificity of MRI for the early diagnosis of sacroiliitis in these patients were 37.7% and 100%, respectively. Thirty-four patients with pathologic evidence of sacroiliitis were followed up for 5-10 years. At the study end point, 16 of these 34 patients continued to show grade I or lower changes on CT, and 18 had changes of grade II or higher. These 18 patients included 7 of the 8 patients with evidence of sacroiliitis on MRI and 6 of the 20 patients confirmed not to have MRI evidence of sacroiliitis at baseline. Conclusion MRI, though of low sensitivity, is specific for the diagnosis of early sacroiliitis. Sacroiliitis can be detected earlier by needle biopsy than by MRI. [ABSTRACT FROM AUTHOR]

Down syndrome cell adhesion molecule (Dscam) is a neural adhesion molecule that plays an essential role in the establishment of neural circuits. Considerable evidence suggests that Dscam is required for axon guidance and dendritic arborization. Our aim was to investigate the expression of Dscam in the temporal lobes of patients with intractable epilepsy (IE) and of experimental animals. In this study, we used immunohistochemistry, immunofluorescence, and western blotting to examine Dscam expression in thirty-five surgical samples from brains of IE patients and 15 control brain samples. We also measured the levels of Dscam during the entire epileptic process in a rat model of temporal lobe epilepsy. Dscam expression in IE patients was significantly higher compared with that in the controls. In addition, Dscam was also highly expressed in the rat brain during the different phases of the epileptic process. It is the first time to find abnormal expression of Dscam in the brain tissues in patients with IE. And this finding provides an experimental evidence for the study of neuronal circuit remodeling and synaptic plasticity in IE, furthermore, our results also suggest that Dscam may be involved in the generation and the development of IE. Synapse, 2011. © 2011 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Gephyrin, which is a postsynaptic scaffolding protein participated in clustering GABAA receptors at inhibitory synapses, has been reported to be involved in temporal lobe epilepsy (TLE) recently. Here, we investigate gephyrin protein expression in the temporal lobe epileptic foci in epileptic patients and experimental animals in order to explore the probable relationship between gephyrin expression and TLE. Using immunohistochemistry, immunofluorescence, and western blot analysis, gephyrin expression was examined in 30 human temporal neocortex samples from patients who underwent surgery to treat drug-refractory TLE and 10 histological normal temporal neocortex from the controls. Meanwhile, we investigated the gephyrin expression in the hippocampus and adjacent neocortex from experimental rats on 24 h, 48 h, 1 week, 2 weeks, 1 month, and 2 months postseizure and from control rats. Gephyrin protein was mainly expressed in the membrane and cytoplasm of neurons in temporal lobe epileptic foci in humans and experimental rats. Gephyrin expression was significantly lower in the temporal neocortex of TLE patients compared to the controls. In experimental rats, the expression of gephyrin in temporal lobe was downregulated in epileptic groups compared to the control group. Gephyrin expression gradually decreased during the acute period and the latent period, but then began to increase below the levels seen in controls during the chronic phase. Our findings suggest that gephyrin may be involved in the development of TLE. Synapse, 2011. © 2011 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

The article studies the effects of interleukin-15 (IL-15), a master T cell growth factor whose role in bone remodeling is unknown, to IL-15 receptor-deficient mice. The IL-15 effects, including osteoclast development, T cell and dendritic cell activation and bone mass in intact and ovariectomized mice were studied. The study showed several converging mechanisms of osteoclastogenesis are inhibited in the absence of IL-15 signaling through T cells leading to a high bone mass phenotype. The IL-15 pathway is seen as a therapeutic approach to osteoporosis.

Objective To review the effects of different immunosuppressive drugs on proliferation and function of regulatory T cells (Tregs). Methods We searched MEDLINE, Embase (from inception to September 2009), and the Cochrane Library (Issue 4, 2009) for clinical and basic research about the effects of various immunosuppressive drugs on Tregs. Data were extracted and methodological quality was assessed by two independent reviewers. Outcome measures for clinical research included blood Tregs levels, acute rejection episodes, and graft function. Outcomes for basic research included percentage of Tregs proliferation, function, Tregs phenotype, and evidence for possible mechanisms. We analyzed data qualitatively. Results Forty-two studies, including 19 clinical trials and 23 basic studies, were included. The immunosuppressive drugs studied were calcineurin inhibitors (CNIs), Rapa, anti-metabolism drugs, IL-2 receptor-blocking antibodies, T-cell depleting antibodies, and co-stimulation blockade antibodies. Most of the studies were on Rapa and CNIs. Eight basic studies on Rapa and CNIs showed that Rapa could promote the proliferation and function of Tregs, while CNIs could not. Five clinical trials involving a total of 158 patients showed that patients taking Rapa had higher blood concentration of Tregs than patients taking CNIs, but no difference was found in graft function (6-42 months follow-up). Conclusion There is substantial evidence that Rapa favors Tregs survival and function. However, the higher numbers of blood Tregs in patients treated with Rapa do not show any association with better graft function. Larger clinical studies with longer follow-up are needed to more thoroughly assess the efficacy of immunosuppressive drugs on Tregs, and reveal whether a relationship exists between Tregs and graft function. [ABSTRACT FROM AUTHOR]

A novel key-shaped CPW-fed monopole UWB antenna is proposed in this article. A high frequency structure simulator is used to analyze the proposed antenna in the design process. The proposed antenna has an extremely wide frequency band range, the impedance bandwidth of which is measured as 2.87–40 GHz (1:13.9) for return loss <−10 dB. Simulated and measured results are presented for the proposed antenna. © 2010 Wiley Periodicals, Inc. Microwave Opt Technol Lett 52:886–889, 2010; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/mop.25054 [ABSTRACT FROM AUTHOR]

Background Visfatin, a new adipocytokine, was reported to promote angiogenesis. Dimethylarginine dimethylaminohydrolase (DDAH), which could regulate vascular endothelial growth factor (VEGF) expression in endothelial cells, is thought as a novel modulator of angiogenesis. The aim of the study was to investigate the role of DDAH2 in visfatin-induced angiogenesis in human umbilical vein endothelial cells (HUVECs). Methods and Results Visfatin could concentration- and time-dependently enhance cell migration and tube formation reflecting angiogenic capability of HUVECs. Moreover, visfatin upregulated both mRNA and protein expressions of DDAH2 and VEGF. Angiogenic effects of visfatin were attenuated by DDAH2 small interfering RNA. Visfatin-induced protein kinase B (Akt) phosphorylation and phosphoinositide 3 kinase (PI3K) inhibitors could suppress visfatin-induced upregulation of DDAH2 and VEGF expressions. Conclusions Taken together, our results demonstrate that PI3K/Akt-mediated upregulation of DDAH2 expression plays a critical role in visfatin-promoted angiogenesis via regulating VEGF-dependent pathway. Copyright © 2009 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Peritendinous adhesions are an important complication of flexor tendon injury. Three hyaluronan (HA)-derived biomaterials were evaluated for the reduction of peritendinous adhesions following partial-thickness tendon injury in rabbits. Rabbits ( n = 24) were divided into three groups ( n = 8 per group), which were used for gross evaluation, histologic assessment, or biomechanical testing. The fourth and third toes from both hindpaws of each rabbit were randomly assigned to one of four treatments: (i) untreated control, (ii) Seprafilm®, (iii) Carbylan™-SX in situ crosslinked hydrogel, and (iv) preformed Carbylan™-SX film. Rabbits were sacrificed at 3 weeks postsurgery and evaluated anatomically, histologically, and mechanically. All materials used reduced adhesions relative to untreated controls for all three evaluations. Both the gross anatomic and histologic results revealed that Carbylan™-SX film was statistically superior to Seprafilm® and Carbylan™-SX gel in preventing tendon adhesion formation. In biomechanical tests, the Carbylan™-SX film-treated hindpaws required the least force to pull the tendon from the sheath. This force was statistically indistinguishable from that required to extrude an unoperated tendon ( n = 8). Carbylan™-SX gel was less effective than Carbylan™-SX film but superior to Seprafilm® for all evaluations. A crosslinked HA-derived film promoted healing of a flexor tendon injury without the formation of fibrosis at 3 weeks postoperatively. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:562-569, 2008 [ABSTRACT FROM AUTHOR]

We describe synthetic extracellular matrix (sECM) hydrogel films composed of co-crosslinked thiolated derivatives of chondroitin 6-sulfate (CS) and heparin (HP) for controlled-release delivery of basic fibroblast growth factor (bFGF) to full-thickness wounds in genetically diabetic ( db/db) mice. In this model for chronic wound repair, full-thickness wounds were treated with CS, CS-bFGF, or CS-HP-bFGF films. At 2 and 4 weeks postinjury, wound closure and formation of the new epidermis and dermis were determined. Both CS and CS-HP hydrogel films accelerated wound repair, even without bFGF. Addition of bFGF to CS films showed partial dose-dependent acceleration of wound repair. Importantly, addition of bFGF to co-crosslinked CS-HP sECM films showed a dramatic bFGF dose-dependent acceleration of wound healing, as well as improved dermis formation and vascularization. Compared with 27% wound closure in 2 weeks in the controls, 89% wound closure was observed for mice treated with the CS-HP-bFGF films. The synthetic CS-HP sECM films mimic the chemistry and biology of heparan sulfate proteoglycans, and may have clinical potential for topical delivery of growth factors to patients with compromised wound healing. [ABSTRACT FROM AUTHOR]

Problem: To provide a less expensive and more convenient protocol for the treatment of tympanic membrane perforations (TMPs). Methods: Several materials were prepared and compared for TMP repair including Carbylan-SX, Gelatin-DTPH-PEGDA (GX), Carbylan-S/Gelatin-DTPH (Carbylan-GSX) (injectable and sponge), Gelfoam, Epifilm, and crosslinked thiolated chondroitin sulfate (CS-DTPH-PEGDA [CS-SX]). Hartley pigmented guinea pigs (Elm Hill) underwent bilateral myringotomy with 1 ear left as a control and the other treated with one of the previously mentioned materials. Results: Carbylan-GSX (injectable and sponge), Gelfoam with saline, and CS-SX had the shortest time for TMP closure. Epifilm, Carbylan, and gelatin preparations resulted in closure rates similar to controls. CS-SX showed a marked inflammatory reaction compared with controls and other materials based on neutrophil, lymphocyte, epitheloid counts, and degree of fibrosis. Conclusions: This study shows the validity of Carbylan-GSX compared with Gelfoam as a material to promote TMP closure in an acute TMP guinea pig model. [Copyright &y& Elsevier]

Injectable hydrogel and porous sponge formulations of Carbylan™-GSX, a crosslinked synthetic extracellular matrix (ECM), were used to deliver human demineralized bone matrix (DBM) in a rat femoral defect model. A cortical, full-thickness 5-mm defect was created in two femurs of each rat. Six rats were assigned to each of five experimental groups (thus, 12 defects per group). The defects were either untreated or filled with Carbylan™-GSX hydrogel or sponges with or without 20% (w/v) DBM. Radiographs were obtained on day 1 and at weeks 2, 4, 6, and 8 postsurgery of each femur. Animals were sacrificed at week 8 postsurgery and each femur was fixed, embedded, sectioned, and processed for Masson's Trichrome staining. The bone defects were measured from radiographs and the fraction of bone healing was calculated. The average fractions of bone healing for each group were statistically different among all groups, and all treatment groups were significantly better than the control group. The Carbylan™-GSX sponge with DBM was superior to the sponge without DBM and to the hydrogel with DBM. Histology showed that defects treated with the Carbylan™-GSX sponge plus DBM were completely filled with newly generated bone tissue with a thickness comparable to native bone. Carbylan™-GSX sponge was an optimal delivery vehicle for human DBM to accelerate bone healing. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:1454-1462, 2006 [ABSTRACT FROM AUTHOR]

Objective: This project studies the use of airway stents coated with a cross-linked derivative of hyaluronan (HA) in a rabbit airway model of subglottic stenosis (SGS). Study design and setting: An acute subglottic mucosal injury and airway stent placement design were used in a rabbit model. Thirty-six rabbits were randomized to 6 different study groups. Four groups had the subglottic mucosa denuded at the cricoid, and 2 groups received no injury. Airway stents coated with Carbylan-SX, a cross-linked derivative of HA, and controls were placed for 3 weeks. After sacrifice at 6 weeks, morphometric measurements of subglottic lumen were taken. Results: In posttraumatic models, no significant differences were seen in airway area measures between groups (P = 0.86). In non-injury groups, a significant difference between Carbylan-SX versus non–HA-derivative-coated stents was seen (P = 0.05). Conclusion: In this model of acute subglottic mucosal injury, the HA-derivative–coated stent did not improve healing. However, in the absence of mucosal injury, the Carbylan-SX film–coated stent yielded significantly larger airway areas compared with a noncoated stent. Significance: Stents or endotracheal tubes coated with a cross-linked derivative of HA may prevent stenosis in patients without airway injury but require long-term intubation or laryngotracheal stenting. [Copyright &y& Elsevier]

The mechanism of lovastatin-induced cell death was examined in three established human glioblastoma cell lines; U87, U251, and U138. Changes in potential modifiers of apoptosis, including Bcl-2 family proteins and MAP kinase targets after such lovastatin treatment, were evaluated. Lovastatin (5 μ m ) treatment causes extensive cell death in two of the cell lines, U87 and U251; but only minimal in a third, U138. Lovastatin-induced death occurs in correlation with significantly increased levels of the BH3-only protein, Bim. The up-regulation of Bim levels was directly associated with an increased incidence of apoptosis. Lovastatin treatment in U87 cells results in activation of targets of three major mitogen-activating protein kinase cascades including Erk1/2, JNK and p38. Changes in levels of Bim, as well as increase phosphorylation of Erk1/2, c-jun, and p38 are all prevented by co-incubation of lovastatin and the isoprenylation metabolite, geranylgeranyl pyrophosphate. Inhibition of the MAP kinase pathways failed to block the increased expression of Bim expression or cell death. Further elucidation of the mechanisms of lovastatin-induced up-regulation of Bim and apoptosis in glioblastoma cells are important in determining a potential role for lovastatin as a chemotherapy agent. [ABSTRACT FROM AUTHOR]

Hyaluronan (HA) hydrogels resist attachment and spreading of fibroblasts and most other mammalian cell types. A thiol-modified HA (3,3'-dithiobis(propanoic dihydrazide) [HA-DTPH]) was modified with peptides containing the Arg-Gly-Asp (RGD) sequence and then crosslinked with polyethylene glycol (PEG) diacrylate (PEGDA) to create a biomaterial that supported cell attachment, spreading, and proliferation. The hydrogels were evaluated in vitro and in vivo in three assay systems. First, the behavior of human and murine fibroblasts on the surface of the hydrogels was evaluated. The concentration and structure of the RGD peptides and the length of the PEG spacer influenced cell attachment and spreading. Second, murine fibroblasts were seeded into HA-DTPH solutions and encapsulated via in situ crosslinking with or without bound RGD peptides. Cells remained viable and proliferated within the hydrogel for 15 days in vitro. Although the RGD peptides significantly enhanced cell proliferation on the hydrogel surface, the cell proliferation inside the hydrogel in vitro was increased only modestly. Third, HA-DTPH/PEGDA/peptide hydrogels were evaluated as injectable tissue engineering materials in vivo. A suspension of murine fibroblasts in HA-DTPH was crosslinked using PEGDA plus PEGDA peptide, and the viscous, gelling mixture was injected subcutaneously into the flanks of nude mice; gels formed in vivo following injection. After 4 weeks, growth of new fibrous tissue had been accelerated by the sense RGD peptides. Thus, attachment, spreading, and proliferation of cells is dramatically enhanced on RGD-modified surfaces but only modestly accelerated in vivo tissue formation. © 2003 Wiley Periodicals, Inc. J Biomed Mater Res 68A: 365–375, 2004 [ABSTRACT FROM AUTHOR]