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Background and Objectives: This study aims to illustrate the mechanisms underlying the therapeutic effect of Icariin after myocardial infarction (MI). Materials and Methods: Based on the network pharmacology strategy, we predict the therapeutic targets of Icariin against MI and investigate the pharmacological molecular mechanisms. A topological network was created. Biological process and Kyoto Encyclopedia of Genes and Genomes pathway enrichment were also performed. We also conducted the molecular docking analysis to stimulate the component–target interaction further and validate the direct bind effect. Results: Network pharmacology analysis identified 61 candidate genes related to the therapeutic effect of Icariin against MI. EGFR, AKT1, TP53, JUN, ESR1, PTGS2, TNF, RELA, HSP90AA1, and BCL2L1 were identified as hub genes. The biological processes of the candidate targets were significantly involved in the reactive oxygen species metabolic process, response to hypoxia, response to decreased oxygen levels, response to oxidative stress, regulation of reactive oxygen species metabolic process, and so forth. Overall, biological process enrichment analysis indicated that the protective effect of Icariin against MI might be associated with oxidative stress. Moreover, the pathway analysis showed that the candidate targets were closely associated with lipid and atherosclerosis, AGE-RAGE signaling pathway in diabetic complications, HIF-1 signaling pathway, etc. We identified the conformation with the lowest affinity score as the docking conformation. The simulated molecular docking was displayed to illustrate the topical details of the binding sites between Icariin and TNF protein. Conclusions: This study provides an overview of the mechanisms underlying the protective effect of Icariin against MI.

Several studies are conducted to understand the reducing reaction of the [Fe.sub.3][O.sub.4] nanowires in various nanoscopic reactors of amorphous C:H nanotubes (a-CNTs), which are then used to analyze the chemical reaction mechanism in such reactors. The results show that the carbon in the a-CNT shell exhibit better reducing properties than hydrogen, which is not the case with a macroscopic system.

Reduction features of NO over a potassium-doped C12A7-[O.sup.-] catalyst were studied. The C12A7-[O.sup.-]/K catalyst shows good NO storage/reduction abilities with a good sulfur tolerance and the NO conversion and [N.sub.2] selectivity on the C12A7-[O.sup.-]/K catalyst depends on the sample temperature, percentage of potassium, the reduction agent and the composition in the mixture gases.

[Bi.sub.4-x][Eu.sub.x][Ti.sub.3][O.sub.12] (BEuT) ferroelectric thin films are prepared on SrTi[O.sub.3] (STO) substrates with different orientations by using chemical solution deposition and the effects of Eu ion concentration crystallographic orientation on the photoluminescent property are examined. The orientation dependent photoluminescence is attributed to low light scattering of well-aligned grains with c-axis oriented growth.

PEP 1-Cu/Zn superoxide dismutase (PEP-1-SOD1) fusion protein preconditioning has been reported to protect the myocardium from ischemia/reperfusion (I/R)-induced injury by decreasing the infarct size, reducing levels of cardiomyocyte apoptosis and reducing the release of myocardial-specific biomarkers. The aim of the present study was to examine the effects of PEP-1-SOD1 pretreatment on I/R-induced ventricular arrhythmias in Langendorff-perfused rat hearts. The isolated rat hearts were pretreated with PEP-1-SOD1 prior to I/R, and the I/R-induced hemodynamic parameters, infarct size and ventricular arrhythmias were then assessed. Compared with the unprotected hearts, PEP-1-SOD1 preconditioning significantly improved the hemodynamic parameters, decreased the cardiac lactate dehydrogenase and creatine kinase-MB (CK-MB) levels, reduced the infarct size and attenuated the ventricular arrhythmia. Further investigation showed that PEP-1-SOD1 preconditioning reduced both the incidence and duration of ventricular tachycardia/ventricular fibrillation. In addition, the intracellular reactive oxygen species (ROS) levels were decreased. The results of the present study suggest that PEP-1-SOD1 preconditioning can protect the heart against I/R injury and attenuate I/R-induced arrhythmia by downregulating the generation of ROS. [ABSTRACT FROM AUTHOR]

The NO reduction features over a noble-metal-free NOxstorage/reduction catalyst (Ca24Al28O644•4O-/K, defined as C12A7−O-/K), including the NO conversion, the N2selectivity, and sulfur tolerance, were investigated with hydrogen and C3H6as the reducing agents in a fixed-bed continuous flow reactor. The NO conversion and the N2selectivity on the C12A7−O-/K catalyst mainly depends on the sample temperature, the percentage of potassium, the reducing agents, and the composition of the mixture of gases. The C12A7−O-/10%K catalyst possessed the highest selective reduction ability (to N2) among the catalysts C12A7−O-/x%K. Over 50% of NO can be reduced to N2with H2as the reduction agent at 550−700 °C. The C12A7−O-/K catalyst also shows higher NOxstorage capacity (183.9 mol/g at about 550 °C) as well as sulfur tolerance for both the NOxstorage and the reduction processes. The catalyst characteristics and the intermediate species formed in the NO storage and reduction processes were investigated by the X-ray diffraction, X-ray photoelectron spectroscopy, Fourier transform infrared spectroscopy, and time-of-flight mass spectrometry. The mechanism of NOxreduction was addressed according to the above investigations. [ABSTRACT FROM AUTHOR]

Background H-type hypertension seriously affects people's health and quality of life. Currently, the clinical treatment of hypertension mainly selects drugs based on the experience, and the antihypertensive effect is not ideal. It is urgent to explore the pharmacogenetic polymorphisms of antihypertensive drugs and provide individualized medication guidance for hypertensive patients. Objective To investigate pharmacogenetic polymorphisms and the intervention effects of folic acid combined with vitamin D in patients with H-type hypertension in Jinan community, and provide reference for the implementation of integrated precision medicine for hypertension. Methods From June 2020 to June 2022, 200 hypertensive patients with poorly controlled blood pressure in 20 community health service centers of Huaiyin District, Jinan City, Shandong Province were randomly selected as the research objects. Before treatment, the gene polymorphisms of five commonly used individualized antihypertensive drugs, including diuretics, β-blockers, angiotensin-converting enzyme inhibitors (ACEI) , calcium channel inhibitors (CCB) , angiotensin-Ⅱ receptor antagonists (ARB) , were detected. Patients were randomly divided into the gene-directed treatment group (genome group) and gene-directed synergistic folic acid and vitamin D treatment group (gene-directed group) , with 100 cases in each group. The genome group adjusted the drug according to the characteristics of the detected hypertension gene loci; the gene-directed group received folic acid and vitamin D in addition to the genomic therapy regimen. Sitting systolic and diastolic blood pressures in the morning without antihypertensive drugs were collected from patients at the initial intervention (M0) , 3 months of intervention (M3) , and 6 months of intervention (M6) . Case status, adverse reactions and stroke were recorded, gene sequencing was performed, and serum homocysteine (Hcy) concentration was detected. Pearson correlation analysis or Spearman's rank correlation analysis were used to explore the correlation between sex, age, systolic blood pressure, diastolic blood pressure and Hcy. Results Gender (rs=-0.463) , systolic blood pressure (r=0.181) and diastolic blood pressure (r=0.188) were correlated with Hcy level (PC) , CYP2D6 (c.100C>T) were associated with polymorphism loci of drug metabolism enzyme genes, respectively. ADRB1, ACEI (I/D) , AGTR1 and NPPA were associated with the polymorphic loci of drug target sensitivity genes. Genome A6986G:CYP3A5*1/*1 (AA) , ACEI (I/D) :D/D, C.100 C>T:CYP2D6*1/*1 (CC) patients at M3 and M6 had lower diastolic blood pressure than M0, A6986G:CYP3A5a1/a3 (AG) , ADRB1 C.1165 G>C:GG, c.1075A>C:CYP2C9*1/*3 (AC) , c.1075A>c:CYP2C9*3/*3 (CC) patients at M6 had lower systolic and diastolic blood pressure than M0, A6986G:CYP3A5*3/*3 (GG) , ADRB1 C.1165 G>C:CC, ACEI (I/D) :I/I, c.1075A>C:CYP2C9*1/*1 (AA) , AGTR1 C.1166A>c:AA, NPPA T2238C:TT, c.100 C>T:CYP2D6*10/*10 (TT) patients at M3 and M6 had lower systolic and diastolic blood pressure than M0, ADRB1 C.1165 G>C:GC, ACEI (I/D) :I/D, c.100 C>T:CYP2D6*1/*10 (CT) patients at M6 had lower systolic blood pressure than M0, and lower diastolic blood pressure than M0, the difference was statistically significant (P