The efficacy of baroreflex activation therapy for heart failure: A meta-analysis of randomized controlled trials.

INTRODUCTION: The efficacy of baroreflex activation therapy for heart failure is elusive. This meta-analysis aims to evaluate the impact of baroreflex activation therapy on treatment efficacy of heart failure. METHODS: Several databases including PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases have been searched, and we include randomized controlled trials (RCTs) regarding the efficacy of baroreflex activation therapy for patients with heart failure. RESULTS: This meta-analysis includes 4 RCTs. Baroreflex activation therapy shows significantly positive impact on the quality of life score (standard mean difference SMD = -4.61; 95% confidence interval CI = -6.24 to -2.98; P < .00001), 6-minute hall walk (6MHW) distance (SMD = 2.83; 95% CI = 1.44- 4.22; P < .0001), New York Heart Association (NYHA) Class (SMD = -3.23; 95% CI = -4.76 to -1.69; P < .0001), N-terminal pro-brain natriuretic peptide (NT-proBNP) (SMD = -1.24; 95% CI = -1.58 to -0.89; P < .00001) and the duration of hospitalization (SMD = -1.65; 95% CI = -2.90 to -0.39; P = .01) compared with control group for heart failure, but has no obvious effect on left ventricular ejection fraction (LVEF) (SMD = 1.43; 95% CI = -0.15-3.01; P = .08), or the number of hospitalization per year (SMD = -1.17; 95% CI = -2.56-0.22; P = .10). CONCLUSIONS: Baroreflex activation therapy can improve the treatment efficacy for heart failure.

LVRT capability enhancement of DFIG based wind turbine with coordination control of dynamic voltage restorer and inductive fault current limiter.

According to the coordination control of a dynamic voltage restorer (DVR) and an inductive fault current limiter (FCL), this paper proposes an efficient low-voltage ride-through (LVRT) scheme for a doubly fed induction generator (DFIG) based wind turbine. The DVR is located to the DFIG's stator circuit for stabilizing the terminal voltage and decreasing the generator current. The inductive FCL is connected to the DFIG's rotor circuit for suppressing the rotor overcurrent and protecting the converter. Theoretical discussions on structure, principle and scale criterion of the combined DVR-FCL are conducted, and simulation analyses of the proposed approach to handle symmetrical and asymmetrical faults are done in MATLAB/Simulink. In this study, the dynamic characteristics of the DFIG during the faults are analyzed from multiple aspects, and a detailed comparison of the proposed approach and the single action of DVR or FCL is carried out. From the simulation results, the effectiveness and superiority of the proposed approach are well demonstrated.

Gold nanoparticles based molecular beacons for in vitro and in vivo detection of the matriptase expression on tumor.

Matriptase, a type II transmembrane serine protease, is responsible for the early stage proliferation of a wide range of human cancers. It is highly expressed on the surface of tumor cells, allowing the protease to serve as a biomarker of cancer detection. Hence, in this study, we designed two molecular beacons consisting of a fluorescent dye-peptide conjugate attached to gold nanoparticles (Au NPs) for in vitro and in vivo detection of the matriptase expression on tumor cells. The peptide substrate (GRQSRAGC) for matriptase served as the linker between dye (donor) and Au NP (acceptor). In this configuration, the dye fluorescence was quenched by Au NP under physiological conditions and recovered after selective cleavage of the GRQSRAGC by matriptase. To maximize spectral overlap between dye fluorescence and Au NP absorption and optimize the quenching efficiency mediated by fluorescence resonance energy transfer (FRET), the visible dye (fluorescein) and near-infrared (NIR) dye peptide conjugates were each attached to spherical and rod-shaped Au NP for in vitro and in vivo detection, respectively. Both in vitro cell and in vivo animal studies indicate that these two molecular beacons are sensitive and specific for the detection of matriptase expression in the tumor, thereby paving the way to image the activities of this diagnostic protease in living organisms.

Genistein protection against acetaminophen-induced liver injury via its potential impact on the activation of UDP-glucuronosyltransferase and antioxidant enzymes.

The purpose of this study was to investigate genistein's influence on the relationship between the activation of uridine diphosphate glucuronosyltransferase (UGTs) and the protection against acetaminophen-induced liver toxicity. Animal experimental results revealed that genistein (50, 100 or 200mg/BWkg) significantly ameliorated the biomarkers alanine aminotransferase, alanine aminotransferase, lactate dehydrogenase and malondialdehyde, as indicators of acute liver damage caused by APAP (200mg/BWkg). The level of GSH declined sharply after treatment with APAP within 1h in both the liver and blood with and without genistein. However, after 16h, the levels approached or returned to the original level. Genistein may accelerate and promote APAP glucuronidation as the results showed that APAP-glucuronide increased by 18.44%, 46.79%, and 66.49% for 4h of treatment with genistein dosages of 50, 100 or 200mg/BWkg, respectively, compared with the APAP-only treatment. The activation of UGTs and glutathione peroxidase and the inhibition of CYP2E1 by genistein were observed, and UGTs mRNA expression level with genistein was measured. These findings suggest that genistein can prevent and protect against APAP-induced liver toxicity due to the inhibition of APAP biotransformation and the resistance to oxidative stress via the modulation of the activities of metabolism and the antioxidant enzyme.