Security Event-Trigger-Based Distributed Energy Management Of Cyber-Physical Isolated Power System With Considering Nonsmooth Effects.

Due to cyber-physical fusion and nonsmooth characteristics of energy management, this article proposes a security event-trigger-based distributed approach to address these issues with developed smoothing technique. To tackle with nonconvex and nondifferentiable issue, a randomized gradient-free-based successive convex approximation is developed to smooth economic objective function. Due to resilience ability against security issue, a security event-triggered mechanism-based distributed energy management is proposed to optimize social welfare, which coordinately controls both power generators and load demand. The security event-triggered mechanism is designed to reduce power system security risks, and relieve communication burden caused by smoothing calculation, the convergence of proposed distributed algorithm is also properly proved. According to those obtained results on both IEEE 9-bus and IEEE 39-bus systems, it reveals that the proposed approach can achieve good convergence performance and have less security risks than other alternatives, which also proves that the proposed approach can be a viable and promising way for tackling with energy management issue of cyber-physical isolated power system.

Association of serum adropin with the presence of atrial fibrillation and atrial remodeling.

OBJECTIVE: Adropin, a newly identified regulatory protein encoded by Enho gene, suppressed tumor necrosis factor α-induced THP1 monocyte adhesion to human umbilical vein endothelial cells. In addition, inflammation is demonstrated to be involved in the mechanism of atrial fibrillation (AF). Atrial remodeling is correlated with the persistence and progression of AF. Adropin is hypothesized to correlated with AF and atrial remodeling. This study aims to determine the correlation of serum adropin and the presence of AF and remodeling. METHODS: This study consisted of 344 AF patients and 210 healthy controls. AF patients were then divided into three subgroups of paroxysmal AF, persistent AF, and permanent AF. Serum adropin concentrations were examined using enzyme-linked immunosorbent assay method. Left atrial diameter (LAD) was measured to evaluate atrial remodeling. RESULTS: Decreased serum adropin concentrations were found in AF patients compared with healthy controls. Logistic regression analysis confirmed that serum adropin was inversely associated with the presence of AF (OR 0.218, 95% CI 0.15-0.316; P < 0.001). Permanent AF patients had significantly reduced serum adropin concentrations compared with persistent and paroxysmal AF patients. There were decreased serum adropin concentrations in persistent AF group than those in paroxysmal AF group. Simple linear regression analyses showed that serum adropin in AF patients were negatively correlated with BMI, SBP, and LAD. Multiple stepwise regression analysis showed that LAD remained to be inversely associated with serum adropin (ß = 0.2, P = 0.010). CONCLUSION: Serum adropin concentrations are inversely correlated with the presence of AF and atrial remodeling.

Efficacy and safety of Zhibitai in combination with atorvastatin for lipid lowering in patients with coronary heart disease.

BACKGROUND: Zhibitai, a natural lipid-lowering Chinese medicine, is well tolerated in patients and has low incidence of adverse events. In this study, we evaluated the efficacy, safety, and side effects of Zhibitai in combination with low dose Atorvastatin compared to high dose Atorvastatin in patients with coronary heart disease or at high risk of coronary heart disease. METHODS: This was a randomized, double-blind, multi-center clinical trial on 720 patients with coronary heart disease or at high risk of coronary heart disease. The patients were randomly assigned to a Zhibitai-Atorvastatin group (480 mg Zhibitai twice daily plus 10 mg atorvastatin once daily) or Monotherapy group (40 mg Atorvastatin once daily). Blood samples were obtained at baseline, week 4, and week 8 after a minimum 8-hour fast. Efficacy was evaluated in terms of the changes in the following parameters: lipoprotein profiles [total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C)]. Safety was assessed throughout the study by clinical laboratory tests including liver function [alanine transaminase, aspartate transaminase] and renal function [blood urea nitrogen], and creatine kinase; physical examination; and adverse events monitoring. RESULTS: TC, TG, LDL-C levels were significantly decreased andHDL-C levels were significantly increased at week 4 and week 8 (all P < 0.05) in both groups but had no significant differences between the two groups (P > 0.05). In subgroup analyses, Zhibitai-Atorvastatin Group produced significantly greater reduction in TG compared with Monotherapy Group at week 8 in patients with TG > 203.72mg/dL (P < 0.01). Among patients with LDL-C levels > 131.48 mg/dL, Zhibitai-Atorvastatin Group produced a greater reduction of LDL-C levels compared with the Monotherapy Group at week 4 (P < 0.05). The incidence of liver dysfunction, headache, or gastrointestinal intolerance was significantly lower in the Zhibitai-Atorvastatin Group compared with Monotherapy Group during the 8-week study peroid (P < 0.001). There were no significant differences in renal function, myopathy, and other adverse events between the groups. CONCLUSION: Overall the two groups have similar lipid regulation efficacy. Zhibitai plus low dose Atorvastatin is more efficacious in lowering TG in patients with TG > 203.72 mg/dL at week 8. There are fewer side effects in Zhibitai plus low dose Atorvastatin group. Long term follow up is required to evaluate cardiovascular outcomes.

Fault Estimation Observer Design for Discrete-Time Takagi-Sugeno Fuzzy Systems Based on Homogenous Polynomially Parameter-Dependent Lyapunov Functions.

This paper investigates the problem of robust fault estimation (FE) observer design for discrete-time Takagi-Sugeno fuzzy systems via homogenous polynomially parameter-dependent Lyapunov functions. First, a novel framework of the fuzzy FE observer is established with the help of a maximum-minimum-priority-based switching mechanism. Then, for every activated switching case, a targeted result is achieved by the aid of exploring an important property of improved homogenous polynomials. Since the helpful information of the underlying system can be duly updated and effectively utilized at every sampled point, the conservatism of previous results is availably reduced. Furthermore, the proposed result is further improved by eliminating those redundant terms of the introduced matrix-valued variables. Simulation results based on a discrete-time nonlinear truck-trailer model are provided to show the advantages of the theoretic result that is developed in this paper.

Control Synthesis of Discrete-Time T-S Fuzzy Systems via a Multi-Instant Homogenous Polynomial Approach.

This paper deals with the problem of control synthesis of discrete-time Takagi-Sugeno fuzzy systems by employing a novel multiinstant homogenous polynomial approach. A new multiinstant fuzzy control scheme and a new class of fuzzy Lyapunov functions, which are homogenous polynomially parameter-dependent on both the current-time normalized fuzzy weighting functions and the past-time normalized fuzzy weighting functions, are proposed for implementing the object of relaxed control synthesis. Then, relaxed stabilization conditions are derived with less conservatism than existing ones. Furthermore, the relaxation quality of obtained stabilization conditions is further ameliorated by developing an efficient slack variable approach, which presents a multipolynomial dependence on the normalized fuzzy weighting functions at the current and past instants of time. Two simulation examples are given to demonstrate the effectiveness and benefits of the results developed in this paper.

Effects of angiotensin-(1-7) on the proliferation and collagen synthesis of arginine vasopressin-stimulated rat cardiac fibroblasts: role of mas receptor-calcineurin-NF-κB signaling pathway.

: Interstitial fibrosis is a common pathological change in various heart diseases, especially cardiac hypertrophy. Arginine vasopressin (AVP), one of the hallmarks of heart failure, exhibits a profibrotic effect by promoting the proliferation and differentiation of cardiac fibroblasts (CFs). In contrast, angiotensin-(1-7) [Ang-(1-7)] was reported to be beneficial for cardiac remodeling by its antifibrotic effect. To evaluate the effect of Ang-(1-7) on AVP-stimulated CFs and the subsequent signaling molecules involved, CFs isolated from neonatal rat hearts were incubated with AVP and treated with or without Ang-(1-7). Cell proliferation, cell cycle, collagen production, and related cellular signaling molecules were then assessed. The results showed that Ang-(1-7) dose-dependently inhibited cell proliferation and collagen production in AVP-stimulated CFs. In addition, Ang-(1-7) also significantly suppressed calcineurin activity in a dose-dependent manner in AVP-stimulated CFs, which was associated with reduced collagen production. Accordingly, the nuclear translocation and transcriptional activity of nuclear factor-kappa B (NF-κB), downstream signal of calcineurin, were also notably restrained by Ang-(1-7) in AVP-stimulated CFs. Furthermore, the inhibitory effect of Ang-(1-7) on AVP-activated calcineurin-NF-κB signaling was completely reversed by the Mas receptor antagonist A-799. These findings suggest that Ang-(1-7) exerts an antifibrotic effect by inhibiting AVP-stimulated CF proliferation and collagen synthesis by inactivating Mas receptor-calcineurin-NF-κB signaling pathway.

ß3-Adrenoreceptor stimulation protects against myocardial infarction injury via eNOS and nNOS activation.

ß3-adrenergic receptor (AR) and the downstream signaling, nitric oxide synthase (NOS) isoforms, have been emerged as novel modulators of heart function and even potential therapeutic targets for cardiovascular diseases. However, it is not known whether ß3-AR plays cardioprotective effects against myocardial infarction (MI) injury. Therefore, the present study was designed to determine the effects of ß3-AR on MI injury and to elucidate the underlying mechanism. MI model was constructed by left anterior descending (LAD) artery ligation. Animals were administrated with ß3-AR agonist BRL37344 (BRL) or ß3-AR inhibitor SR59230A (SR) respectively at 0.1 mg/kg/hour one day after MI operation. The scar area, cardiac function and the apoptosis of myocardial were assessed by Masson's trichrome stain, echocardiography and TUNEL assay respectively. Western blot analysis was performed to elucidate the expressions of target proteins. ß3-AR activation with BRL administration significantly attenuated fibrosis and decreased scar area after MI. Moreover, BRL also preserved heart function, and reduced the apoptosis of cardiomyocyte induced by MI. Furthermore, BRL treatment altered the phosphorylation status of endothelial NOS (eNOS) and increased the expression of neuronal NOS (nNOS). These results suggested that ß3-AR stimulation has a substantial effect on recovery of heart function. In addition, the activations of both eNOS and nNOS may be associated with the cardiac protective effects of ß3-AR.

Validation of the Andon KD-5917 automatic upper arm blood pressure monitor, for clinic use and self-measurement, according to the European Society of Hypertension International Protocol revision 2010.

OBJECTIVE: To validate the Andon KD-5917 automatic upper arm blood pressure monitor according to the European Society of Hypertension International Protocol revision 2010. MATERIALS AND METHODS: Sequential same-left-arm measurements of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were obtained in 33 participants using the mercury sphygmomanometer and the test device. According to the validation protocol, 99 pairs of test device and reference blood pressure measurements (three pairs for each of the 33 participants) were obtained in the study. RESULTS: The device produced 73, 98, and 99 measurements within 5, 10, and 15 mmHg for SBP and 86, 98, and 99 for DBP, respectively. The mean ± SD device-observer difference was 3.07 ± 3.68 mmHg for SBP and -0.89 ± 3.72 mmHg for DBP. The number of patients with two or three of the device-observer difference within 5 mmHg was 26 for SBP and 29 for DBP, and no patient had a device-observer difference within 5 mmHg. CONCLUSION: The Andon KD-5917 automatic upper arm blood pressure monitor can be recommended for clinical use and self-measurement in an adult population on the basis of the European Society of Hypertension International Protocol revision 2010.

Cardioprotective and antioxidant activities of a polysaccharide from the root bark of Aralia elata (Miq.) Seem.

A water-soluble polysaccharide (AEP-w1) was isolated from the root bark of Aralia elata and its molecular weight was about 4.5×10(4)Da. Monosaccharide component analysis indicated that AEP-w1 appeared to be arabinogalactan, consisting of arabinose, galactose and trace glucose with molar ratios of 6.3:3.5:0.2. The antioxidant and cardioprotective potential of AEP-w1 were evaluated in vitro for the first time. AEP-w1 showed potent superoxide and hydroxyl radical scavenging activities and reducing power in vitro. Treatment with H2O2 resulted in the death of H9c2 cells, whereas pretreatment with 50-400µg/ml AEP-w1 for 24h prior to H2O2 exposure significantly increased cell viability. Furthermore, AEP-w1 evidently suppressed cardiomyocyte apoptosis, the mitochondrial membrane potential change and cytochrome c release in H2O2-treated H9c2 cells. In addition, intracellular reduced glutathione (GSH) reduction caused by H2O2 in H9c2 cells was also restored by AEP-w1 pretreatment. Taken together, these date provided the first evidence that the cardioprotective effects of AEP-w1 in H9c2 cells were at least in part associated with its antioxidant activity and inhibition effect on mitochondrial dysfunction.

Involvement of reactive oxygen species and JNK in increased expression of MCP-1 and infiltration of inflammatory cells in pressure-overloaded rat hearts.

Increasing evidence has shown that inflammation is involved in pressure overload-induced cardiac remodeling. Monocyte chemoattractant protein-1 (MCP-1) plays a pivotal role in the inflammatory process. However, the mechanisms underlying the upregulation of MCP-1 expression remain poorly understood. In the present study, we examined the hypothesis that an increased production of reactive oxygen species (ROS) mediates the upregulation of MCP-1. In a pressure-overloaded rat heart model with abdominal aortic coarctation (AC), superoxide dismutase-inhibitable cytochrome C reduction assay showed that ROS generation in the myocardium increased significantly at 1 week by 61% (n=8, P<0.01), peaked at 2 weeks and maintained these high levels for 4 weeks. The elevation of ROS was paralleled by the increased expression of MCP-1 and left ventricular remodeling (cardiac hypertrophy, perivascular and interstitial fibrosis). The oral administration of the antioxidant, N-acetylcysteine (NAC, 0.2 g/kg/day), for 2 or 4 weeks, significantly attenuated ROS production by 69 and 68%, respectively (n=8, P<0.01), as well as left ventricular remodeling. NAC treatment for 2 weeks also significantly reduced the MCP-1 mRNA and protein levels by 52 and 60%, respectively (n=4-8, both P<0.01), but had no effect on blood pressure. In the rats with AC at 2 weeks, when MCP-1 expression and inflammation changes were overt, immunoblotting with phospho-specific antibodies revealed that extracellular regulated kinase (ERK) and c-jun NH2-terminal kinase (JNK), but not p38 mitogen-activated protein kinase, were activated. NAC administration attenuated JNK activation, but had no effect on ERK. Our results suggest that increased ROS production may play an important role in the increased expression of MCP-1 in pressure overload-induced cardiac remodeling. JNK is likely involved in the signaling pathway.

Serum omentin-1 levels are inversely associated with the presence and severity of coronary artery disease in patients with metabolic syndrome.

CONTEXT: Omentin-1, an adipokine secreted from visceral adipose tissue, has been reported to be associated with coronary artery disease (CAD) and metabolic disorders. OBJECTIVE: To clarify the relationship between serum omentin-1 levels and the presence and severity of CAD in patients with metabolic syndrome (MetS). METHODS: We measured serum omentin-1 levels in 175 consecutive patients with MetS and in 46 controls. RESULTS: Serum omentin-1 levels are inversely associated with the presence and angiographic severity of CAD in MetS patients. CONCLUSIONS: Serum omentin-1 might be a potential biomarker to predict the development and progression of CAD in MetS patients.

[The relationship between reactive oxygen species-dependent activation of p38 MAPK and the expression of tumor necrosis factor-α in cultured cardiomyocytes].

AIM: To investigate the role of p38 mitogen-activated protein kinase(MAPK) in lipopolysaccharide (LPS)-induced tumor necrosis factor-α (TNF-α) expression in neonatal rat cardiomyocytes and to determine the relationship between reactive oxygen species (ROS) and p38 MAPK activation. METHODS: Cardiomyocytes were isolated from neonatal Sprague-Dawley rats and cultured by differential adhesion. Expression of TNF-α was determined in culture medium by ELISA. Activation of p38 MAPK was determined by Western blot analysis with phospho-specific antibody. ROS generation in cardiomyocytes was determined by peroxide specific probe 2', 7'-dichlorofluorescin diacetate (DCF-DA). RESULTS: In cardiomyocytes stimulated with LPS, the content of TNF-α in culture medium correlated with the activity of p38 MAPK in a time-dependent manner. The activation of p38 was observed after stimulation of 1 mg/L LPS for 1 h. TNF-α accumulated significantly in culture medium at 3 h after stimulation of LPS (P<0.05), which was remarkably attenuated by pretreatment with p38 MAPK specific inhibitor SB203580 (P<0.01). Furthermore, the production of ROS in cardiomyocytes stimulated with LPS was also increased at 1 h after stimulation of LPS, consistent with p38 MAPK activity. Pretreatment with antioxidants such as N-acetylcysteine and diphenyleneiodonium significantly inhibited the activation of p38 MAPK compared with LPS control (P<0.05). There was no significance in the activity of p38 MAPK among antioxidants pretreatment and non-LPS control groups. CONCLUSION: The activation of p38 MAPK plays an important role in TNF-α expression in LPS-stimulated cardiomyocytes and the increase of ROS production is prerequisite for the activation of p38 MAPK.

[Effects of simvastatin on the left ventricular hypertrophy in spontaneously hypertensive rats and its relationship with the expression of protein kinase B].

OBJECTIVE: To investigate the effects of simvastatin on left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs) and its possible mechanism. METHODS: Sixteen male SHRs were randomly divided into 2 equal groups: treatment group and SHR control to be given simvastatin or glucose-normal saline by oral gavage for 10 weeks. Eight Wistar-Kyoto (WKY) rats were given normal saline as normal controls. Blood pressure was measured before the experiment and then once every week after the beginning of experiment. By the end of the experiment the rats were killed and their hearts were taken out to measure the left ventricle weight/body weight. RT-PCR was used to detect the mRNA expression of atrial natriuretic peptide (ANP) and of protein kinase B (PKB) in myocardium. Western blotting was used to examine the protein expression of PKB. RESULTS: (1) The systolic blood pressure of the SHR normal control and treatment groups were 221 mm Hg +/- 10 mm Hg and 217 mm Hg +/- 8 mm Hg respectively (P > 0.05) and the systolic pressure of the normal control group was 126 +/- 6 mm Hg, significantly lower than those of the 2 SHR groups (both P < 0.01). (2) The LVW/BW values of the SHR control group were 3.04 mg/g +/- 0.12 mg/g, 3.73 mg/g +/- 0.08 mg/g, and 4.10 mg/g +/- 0.13 mg/g in the normal control group, SHR treatment group and SHR control group respectively with significant difference between any 2 groups (all P < 0.01). (3) The mRNA expression levels of ANP were 0.44 +/- 0.33, 0.27 +/- 0.03, and 0.17 +/- 0.33 in the SHR control group, SHR treatment group, and normal control group respectively (P < 0.01 or P < 0.05). (4) The mRNA expression levels of PKB were 0.45 +/- 0.05, 0.32 +/- 0.03, and 0.19 +/- 0.02 in the SHR control group, SHR treatment group, and normal control group respectively (P < 0.01 or P < 0.05). CONCLUSION: Simvastatin reverses LVH and myocyte phenocyte transformation in the SHRs with the possible mechanism of decreasing the expression level of PKB.

[Arginine vasopressin-induced nitric oxide content changes in cultured cardiac fibroblasts and its relation to nuclear factor-kappaB].

To investigate the changes in the nitric oxide (NO) contents, nitric oxide synthase (NOS) activity and inducible nitric oxide (iNOS) mRNA expression in arginine vasopressin (AVP)-induced cardiac fibroblasts (CFs) in vitro and its relation to nuclear factor-kappaB (NF-kappaB), CFs were isolated by trypsin digestion method. Nitric acid reductase method, spectrophotometry, reverse transcription-polymerase chain reaction (RT-PCR), immunofluorescence-interactive laser cytometer techniques and Western blotting were used respectively to detect NO contents, NOS activity, iNOS mRNA expression and the activation of NF-kappaB in CFs. AVP increased NO contents, NOS activity and iNOS mRNA expressions in a concentration-dependent manner; NF-kappaB was activated and mobilized from cytoplasm to nucleus in AVP-induced CFs; PDTC, one of the inhibitors of NF-kappaB, could inhibit aforementioned increments. It is suggested that the increases in NO contents, elevation of NOS activity and increment of iNOS mRNA expression may be mediated through NF-kappaB activation pathway in cultured CFs induced by AVP, and that NF-kappaB is involved in the occurrence and development of myocardial fibrosis.