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Introduction. We evaluated the effects of foot reflexology on bodily vital signs. Methods. Randomized controlled trials (RCTs) evaluating the effects of foot reflexology on vital signs were collected for a meta-analysis. Statistical analysis was conducted using RevMan5.4 software and pooled estimates of the effects were reported as mean differences (MDs) with 95% confidence intervals (CIs). Results. Thirteen studies, including 819 patients, met our inclusion criteria. Our results showed that systolic blood pressure (SBP) (MD = -4.62, 95% CI: -5.58 to -3.66; P < 0.00001 ), diastolic blood pressure (DBP) (MD = -3.32, 95% CI: -4.48 to -2.17; P < 0.00001 ), heart rate (HR) (MD = -4.76, 95% CI: -6.49 to -3.04; P < 0.00001 ), respiratory rate (RR) (MD = -0.77, 95% CI: -1.50 to -0.48; P < 0.00001 ), and pulse oxygen saturation (SpO2) (MD = 0.95, 95% CI: 0.39 to 1.52; P = 0.0009 ) showed statistical significance in the foot reflexology group. Conclusions. Short-term followup results showed that foot reflexology exerted positive effects on vital signs, reduced BP, HR, and RR and increased SpO2.

Myocardial fibrosis is a pathological process characterized by excessive accumulation of extracellular matrix in myocardial interstitial spaces. Myocardial fibrosis is a fundamental process in ventricular remodeling and a primary contributor to the progression of heart failure. Liquiritigenin (LQ) is a flavanone compound with anti-oxidative, anti-carcinogenic, anti-inflammatory and estrogenic properties. The present study aimed to investigate the regulatory potential of LQ treatment in a mouse model of isoprenaline (ISO)-induced cardiac fibrosis and in cultured H9C2 cardiomyocytes stimulated with angiotensin II (Ang II). The treatment of ISO-induced mice with LQ significantly decreased the levels of cardiac injury-related proteins in the serum and ECM accumulation in mouse heart tissues. LQ treatment also effectively alleviated cardiac dysfunction in ISO-treated mice. Further analyses revealed that LQ inhibited ISO-induced collagen formation and activation of the transforming growth factor-β1 (TGF-β1)/Smad2 and protein kinase B (AKT)/extracellular signal-regulated kinase (ERK) signaling pathways. As a major pathological event in myocardial fibrosis, the apoptosis of cardiomyocytes has been considered a key mechanism contributing to impaired left ventricle performance. The pretreatment of rat cardiomyocytes with LQ significantly reduced the apoptosis of H9C2 cells, and inhibited Ang II-induced activation of the TGF-β1/Smad2 and AKT/ERK pathways. In conclusion, the present study revealed that LQ ameliorated ISO-induced myocardial fibrosis in mice and inhibited the apoptosis of cardiomyocytes in vitro by inhibiting the TGF-β1/Smad2 and AKT/ERK signaling pathways. These results suggested the anti-fibrotic and cardioprotective potential of LQ in fibrosis, thus supporting the use of LQ for the management of cardiomyocyte injury and myocardial fibrosis in patients with cardiac diseases.

In this work, sulfonated poly(ether ether ketone) (SPEEK) nanocomposite membranes were prepared with high loading of phosphotungstic acid (HPW) immobilized by polydopamine coated halloysite nanotubes (DHNTs). XPS and FTIR analysis revealed the formation of acid-base interactions between HPW and DHNTs in the nanocomposite membranes, indicating the successful immobilization of HPW on the surface of high aspect-ratio DHNTs, which helped shorten the distance of proton hopping and create more continuous proton transport pathways along the high aspect-ratio nanotubes. The activation energy for the proton transfer in the nanocomposite membranes was greatly reduced and membrane proton conductivity was significantly enhanced. Compared with the SPEEK control membrane, the nanocomposite membrane with 42.9 wt% HPW loading achieved 114% increase in proton conductivity, up from 0.048 S cm−1 to 0.117 S cm−1, and the membrane water uptake remained almost the same. Under the long term water immersion test, the SPEEK/DHNTs/HPW nanocomposite membrane exhibited much slower decrease in proton conductivity than the SPEEK/HPW membrane without DHNTs, indicating the strong HPW-binding effect from DHNTs on slowing down the leakage of HPW.

Objective. Oxidative damage is a pathological factor that causes cardiovascular damage in the clinic and is increasingly serious. This study focused on the effect of fasudil on H2O2-induced oxidative damage in cardiomyocytes. Materials and Methods. H9C2 cardiomyocytes were cultured in vitro and divided into three groups: control group (Con group), H2O2 treatment (H2O2 group), and fasudil and H2O2 cotreatment (H2O2+fasudil group). The content levels of LDH and MDA in the supernatant were detected, and the morphology of H9C2 cardiomyocytes was observed by light microscopy. 8-OHdG staining was observed by a fluorescence inversion microscope. Cell Counting Kit (CCK-8), western blotting, real-time polymerase chain reaction (RT-PCR), and enzyme-linked immunosorbent assay (ELISA) were used to investigate the effect of fasudil on the Rho/ROCK signaling pathway. Results. Our results showed that after H2O2 treatment, the H9C2 cardiomyocytes were irregular in shape and elliptical. But the morphology of the H2O2+fasudil group was similar to that of the Con group. The green fluorescence of the H2O2 group was significantly enhancer than that of the Con group, while the green fluorescence of the H2O2+fasudil group was weaker than those of the H2O2 group. By detecting the supernatant, it was found that the contents of LDH were significantly increased, and the contents of SOD and CAT in the H2O2 group were significantly decreased. And the expression of antioxidant indicators in the H2O2 group was significantly decreased by western blotting. The results of RT-PCR showed that SOD1 and SOD2 mRNA in the H2O2 group was significantly reduced, and the contents of GPX1 and GPX3 in the H2O2 group were significantly decreased by enzyme-linked immunosorbent assay (ELISA). The expression of ROCK1, ROCK2, and downstream phosphorylation of myosin phosphatase target subunit-1 (p-MYPT-1) was significantly increased in the H2O2 group, while fasudil inhibited the increase of ROCK1, ROCK2, and p-MYPT-1. Conclusions. Fasudil can inhibit the Rho/ROCK signaling pathway induced by H2O2 and reduce oxidative stress response, inhibit apoptosis, and improve antioxidant enzyme activity in H9C2 cardiomyocytes thereby delaying cell senescence.

To better understand the effect of rectorite and carbon black (CB) on the aging performance of styrene-butadiene rubber (SBR), SBR/CB, SBR/CB/rectorite and SBR/rectorite nanocomposites with the same total filler loading were prepared. The microstructure of the three SBR nanocomposites was characterized by XRD, TEM and SEM. After thermal aging, oxygen-containing molecules were found to be formed in the SBR nanocomposites, as verified by FTIR analysis. The SBR/rectorite nanocomposite showed the highest aging coefficient and the lowest change rate of tensile strength and stress at 100% strain among the three SBR nanocomposites, indicating that the introduction of nano-dispersed rectorite layers can enhance the thermal aging resistance of the nanocomposites. For the SBR/CB/rectorite nanocomposite, the addition of CB helped to improve the interfacial compatibility between the filler and matrix, resulting in the best crack resistance as the aged SBR/CB/rectorite nanocomposite always demonstrated the least cracks on the surface during either stretching or bending experiments.

Acute coronary syndrome (ACS) is a dangerous and urgent clinical pattern of coronary artery disease. Aspirin and adenosine diphosphate P2Y12 receptor antagonists are the standard dual anti-platelet therapy for patients with ACS. Ticagrelor is a new oral antagonist of the adenosine diphosphate P2Y12 receptor. Randomized controlled trials (RCTs) have evaluated the efficacy and safety of ticagrelor compared to clopidogrel or prasugrel in patients with ACS, obtaining conflicting results. Thus, we conducted a meta-analysis of these RCTs to determine the efficacy and safety of ticagrelor in patients with ACS. Results of the meta-analysis indicate that ticagrelor decreased the risk of major adverse cardiovascular events (MACE) and all-cause death, but increased the risk of bleeding events. In Asiatic patients, analysis indicates that ticagrelor did not decrease the risk of MACE and all-cause death, while increasing the risk of bleeding events. Together, this meta-analysis suggests that ticagrelor was more effective, but less safe than clopidogrel and prasugrel in patients with ACS. Subgroup analysis indicates that ticagrelor was not more effective, although less safe than clopidogrel in Asiatic patients, thus more evidence is needed to further evaluate the efficacy and safety of ticagrelor in Asiatic patients.

Our previous work demonstrated that the amount of residual solvent (RS) content plays an important role in determining the structure and properties of sulfonated poly(ether ether ketone) (SPEEK) membranes cast from dimethylacetamide (DMAc). In this work, another three most commonly used solvents during the preparation of proton exchange membranes (PEMs), including dimethylformamide (DMF), dimethylsulfoxide (DMSO) and N-methyl-2-pyrrolidone (NMP), were employed to prepare SPEEK membranes of different degrees of sulfonation (DSs) with controlled amount of RS content. It was found that the effect of RS content on membrane water uptake is quite universal, as the treated SPEEK membranes of the same DS always showed the same water uptake with the same amount of RS content, regardless of solvent types. Larger RS content always corresponded to the higher water uptake. For SPEEK membranes with relatively high DS, proton conductivity remained almost the same for the treated membranes cast by different solvents when the RS content is the same. While at low DS, the solvent type came into play and also affected the membrane structure and properties: the SPEEK membrane cast by DMSO always exhibited higher proton conductivity than those cast by other solvents with the same RS content. Such phenomena were related to the characteristic structure difference including the size of hydrophilic domains, crystalline structure and polymer chain mobility, which was caused by the different degree of solvent-polymer interaction.

Hydroxysafflor Yellow A (HSYA) may reduce ischemia/reperfusion (I/R) injury. However, the underlying molecular mechanisms remain unclear. The present study explored the effect and the mechanisms of HSYA on myocardial injury in vivo and in vitro. Myocardial infarct size was assessed by Evans blue/2,3,5-triphenyltetrazoliumchloride staining. Levels of cardiac troponin I (cTnI), interleukin-6 (IL-6), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) were measured using commercial kits. Alteration of mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) generation was determined by fluorescent signals. Apoptosis was detected by terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labeling staining, flow cytometry assay and caspase-3 activity. Expression levels of the apoptosis-associated proteins were detected by reverse transcription quantitative polymerase chain reaction and western blot analysis. In vivo, animals treated with HSYA presented less severe myocardial injury and decreased janus kinase 2 (JAK2)/signal transducer and activator of transcription 1 (STAT1) activity, improved antioxidant capacity and decreased apoptosis. In vitro, compared with the hypoxia (H)/reoxygenation (R) + HSYA group, AG490 and S1491 treatment decreased the releases of cTnI, IL-6 and LDH and enhanced the resistance to oxidative stress by maintaining MMP and decreasing ROS generation. In addition, AG490 and S1491 were also identified to alleviate the H/R-induced apoptosis by inhibiting caspase 3 activity and modulating the expression levels of cleaved caspase-3, tumor necrosis factor receptor superfamily member 6 (Fas), Fas ligand, B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein. These data suggested that inactivation of the JAK2/STAT1 pathway strengthened the HSYA-induced protective effect in H/R-induced myocardial injury. In conclusion, the treatment of HSYA was effective in decreasing IR-induced myocardial injury, and this may be largely dependent on the JAK2/STAT1 pathway. Therefore, the present study provided a potential strategy to prevent myocardial I/R injury.

To achieve high proton conductivity, the nanocomposite proton exchange membranes (PEMs) require a good dispersion of inorganic nano-fillers that bear proton transport facilitating functional groups. In this work, we demonstrate that a facile approach based on dopamine-initiated atom transfer radical polymerization (ATRP) can be employed to prepare sulfonated halloysite nanotubes (SHNTs). Polystyrene sulfonic acid (PSSA) was successfully grafted on both inner and outer surfaces of nanotubes, which was confirmed by the transmission electron microscopy analysis. The kinetics of PSSA grafting reaction reflected the living nature of ATRP process. The presence of sulfonic acid groups on the surface of SHNTs significantly improved the compatibility and interfacial adhesion between the nano-fillers and sulfonated poly(ether ether ketone) (SPEEK) matrix, resulting in the uniform and void-free morphology of the nanocomposite membranes. Adding SHNTs into SPEEK matrix also enhanced the phase separation which enabled to form larger hydrophilic domains and improved the proton transport. In addition, the grafted PSSA also provided additional pathways for proton conduction both inside the lumens and along the outer surfaces of nanotubes. Therefore, the enhancement in proton conductivity and the reduction in the activation energy for proton transport were achieved for the SPEEK/SHNT nanocomposite membranes. Compared to that of SPEEK control membrane, the proton conductivity of SPEEK/SHNT membrane with 15 wt% SHNTs was 54% higher at fully hydrated state and more than 2 orders of magnitude higher at 47% and 59% relative humidity (RH).

Myocardial infarction (MI) is life-threatening and is generally accompanied by myocardial hypertrophy. Notably, Hydroxysafflor yellow A (HSYA) can prevent tissue injuries. The objective of this study was to investigate the effect of HSYA on hypertrophy after MI. Hematoxylin and eosin (H&E) staining assays were performed to measure cell area. The protein synthesis rate was assessed using the 3H Leucine incorporation assay. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot analysis and the immunohistochemical assay were used to detect the expression of target genes. The activity of superoxide dismutase (SOD), malondialdehyde (MDA) and the reactive oxygen species (ROS) generation were examined using commercial kits. Decreased myocardial hypertrophy was observed in animals treated with HSYA. Furthermore, the expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) was higher in HSYA administration groups compared with that in the MI model group. In H9c2 cardiomyocytes, the pretreatment with HSYA increased the cell viability, however, it reduced protein synthesis rate, mitigated cell surface area and decreased the expression of Brain natriuretic factor (BNP) and β-myosin heavy chain (β-MHC). By contrast, the downregulation of Nrf2 deteriorated and reversed the effect of Ang II and HSYA. Furthermore, oxidative stress was alleviated by HSYA via inhibiting ROS generation, modulating the activities of SOD and MDA. In addition, the expression of NAD(P)H:quinone oxidoreductase 1 (NQO1) and heme oxygenase-1 (HO-1) were recovered by the pretreatment of HSYA that was combated by siNrf2. In conclusion, HSYA exerted anti-hypertrophic effects, which was pertinent with the activation of Nrf2/NQO-1/HO-1 signaling pathway. The findings of this study may inspire a novel strategy to combat MI.

Background Atrial fibrillation (AF) is a common complication after coronary artery bypass grafting (CABG). Several prospective randomized controlled trials (RCTs) have evaluated the effect of intact and removed anterior fat pads on the incidence of AF after CABG with conflicting results. We collected these RCTs and conducted a meta-analysis to determine whether anterior fat pad removal is effective in preventing the new onset of AF after CABG. Methods and Results Prospective RCTs were collected for analysis and the main outcomes include the occurrence of AF after CABG, total hospital stay, and major complications. Statistical analysis was conducted using RevMan 5.0.18 software (The Cochrane Collaboration), and pooled estimates of the effect were reported as risk ratios (RRs) or mean differences (MDs) with their 95% confidence intervals (CIs). The results of this meta-analysis indicate that anterior fat pad removal was not associated with a decreased risk of occurrence of AF after CABG (RR = 1.34, 95% CI: 0.88–2.03; P = 0.18), and it also did not increase the risk of major complications (RR = 1.05, 95% CI: 0.75–1.47; P = 0.79) or lengthen total hospital stay (MD = 0.06, 95% CI: −0.46 to 0.58; P = 0.83) compared with the control group. Conclusion Anterior fat pad removal did not decrease the risk of the occurrence of AF after CABG despite its safety and convenience, and it should not be used to prevent new-onset AF after CABG unless new evidence is provided.

Atrial fibrillation (AF) is a common complication after coronary artery bypass grafting (CABG). Several prospective randomized controlled trials (RCTs) have evaluated the effect of intact and removed anterior fat pads on the incidence of AF after CABG with conflicting results. We collected these RCTs and conducted a meta-analysis to determine whether anterior fat pad removal is effective in preventing the new onset of AF after CABG.Prospective RCTs were collected for analysis and the main outcomes include the occurrence of AF after CABG, total hospital stay, and major complications. Statistical analysis was conducted using RevMan 5.0.18 software (The Cochrane Collaboration), and pooled estimates of the effect were reported as risk ratios (RRs) or mean differences (MDs) with their 95% confidence intervals (CIs). The results of this meta-analysis indicate that anterior fat pad removal was not associated with a decreased risk of occurrence of AF after CABG (RR = 1.34, 95% CI: 0.88-2.03; P = 0.18), and it also did not increase the risk of major complications (RR = 1.05, 95% CI: 0.75-1.47; P = 0.79) or lengthen total hospital stay (MD = 0.06, 95% CI: -0.46 to 0.58; P = 0.83) compared with the control group.Anterior fat pad removal did not decrease the risk of the occurrence of AF after CABG despite its safety and convenience, and it should not be used to prevent new-onset AF after CABG unless new evidence is provided.