Circulating tumor necrosis factor-α, interleukin-1ß, and interleukin-17A estimates increased major adverse cardiac event risk in acute myocardial infarction patients.

BACKGROUND: Inflammatory cytokines are implicated in the development of atherosclerosis and cardiomyocyte injury during acute myocardial infarction (AMI). This study aimed to investigate the correlation of eight common inflammatory cytokines with major adverse cardiac event (MACE) risk and further establish a prognostic model in AMI patients. METHODS: Serum samples of 210 AMI patients and 20 angina pectoris patients were, respectively, collected at admission, to detect tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1ß, IL-6, IL-8, IL-10, IL-17A, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule 1 (ICAM-1) via enzyme-linked immunosorbent assay. RESULTS: TNF-α, IL-6, IL-8, IL-17A, VCAM-1, and ICAM-1 were elevated (all p < 0.050); IL-10 (p = 0.009) was declined; IL-1ß (p = 0.086) was not varied in AMI patients compared with angina pectoris patients. TNF-α (p = 0.008), IL-17A (p = 0.003), and VCAM-1 (p = 0.014) were elevated in patients with MACE occurrence compared to patients without MACE occurrence; meanwhile, they possessed a relatively good value for identifying MACE risk via receiver-operating characteristic (ROC) analysis. Subsequent multivariate logistic regression analysis revealed that the independent risk factors for MACE contained TNF-α (odds ratio (OR) = 1.038, p < 0.001), IL-1ß (OR = 1.705, p = 0.044), IL-17A (OR = 1.021, p = 0.009), history of diabetes mellitus (OR = 4.188, p = 0.013), history of coronary heart disease (OR = 3.287, p = 0.042), and symptom-to-balloon time (OR = 1.064, p = 0.030), whose combination disclosed a satisfying prognostic value for MACE risk (area under the curve: 0.877, 95% CI: 0.817-0.936). CONCLUSION: Elevated levels of serum TNF-α, IL-1ß, and IL-17A independently correlated with MACE risk in AMI patients, which perhaps provide novel auxiliary for AMI prognostic prediction.

MicroRNA­203a­3p improves bleomycin and pingyangmycin sensitivity by inactivating the PI3K/AKT pathway in hemangioma.

MicroRNAs (miRs) have been found to play a fundamental role in the pathology and progression of hemangioma. Of note, miR-203a-3p prevents hemangioma progression via inactivation of the PI3K/AKT pathway. Bleomycin and pingyangmycin are drugs used in sclerotherapy, but certain hemangioma patients experience drug resistance, leading to poor clinical outcomes. The present study aimed to explore the impact of miR-203a-3p on bleomycin and pingyangmycin sensitivity in hemangioma, as well as the involvement of the PI3K/AKT pathway. miR-203a-3p or negative control mimics were transfected into human hemangioma endothelial cells, which were treated with 0-20 µM bleomycin or pingyangmycin. Subsequently, 740 Y-P, a PI3K/AKT pathway agonist, was added. Cell viability, rate of apoptosis and the expression levels of proteins involved in the PI3K/AKT pathway, including phosphorylated (p)-PI3K, PI3K, p-AKT and AKT, were detected. miR-203a-3p overexpression significantly decreased the half-maximal inhibitory concentration (IC50) values of bleomycin (5.84±0.87 vs. 14.23±2.17 µM; P<0.01) and pingyangmycin (5.13±0.55 vs. 12.04±1.86 µM; P<0.01), compared with untreated cells. In addition, under bleomycin or pingyangmycin treatment, miR-203a-3p overexpression significantly reduced the proportion of EdU positive cells (both P<0.05) and B-cell leukemia/lymphoma-2 (BCL2) protein expression levels (both P<0.05), whilst increasing cell apoptosis rate (both P<0.05) and cleaved caspase 3 protein expression levels (both P<0.05) compared with untreated controls. Furthermore, miR-203a-3p overexpression significantly inhibited the phosphorylation of PI3K and AKT (both P<0.05), an effect that was significantly diminished by 740 Y-P treatment (both P<0.01). In addition, 740 Y-P significantly increased IC50 values of bleomycin (P<0.01) and pingyangmycin (P<0.001) and also significantly increased the proportion of EdU-positive cells and BCL2 protein expression levels, while decreasing the apoptosis rate and cleaved caspase 3 protein expression levels in cells treated with bleomycin or pingyangmycin (all P<0.05). Of note, 740 Y-P weakened the effect of miR-203a-3p overexpression on the aforementioned cellular characteristics. The present study demonstrated that miR-203a-3p improved the sensitivity of cells to bleomycin and pingyangmycin treatment by inhibiting PI3K/AKT signaling in hemangioma.

The relationship between cardiac oxidative stress, inflammatory cytokine response, cardiac pump function, and prognosis post-myocardial infarction.

This study delves into the potential connections between cardiac oxidative stress, inflammatory cytokine response, cardiac pump function, and prognosis in individuals following myocardial infarction. A total of 276 patients were categorized into two groups: the control group (n = 130) and the observation group (n = 146), based on the drug intervention strategies. The control group received standard drug treatment, while the observation group received early drug intervention targeting antioxidant and anti-inflammatory treatment in addition to standard treatment. Serum levels of inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and interleukin-9 (IL-6), were assessed using enzyme-linked immuno sorbent assay (ELISA) kits. The Forkhead Box Protein A2 (FOX2) reagent was used to determine the overall oxidation level. Left Ventricular End-Diastolic Diameter (LVEDD), Left Ventricular Ejection Fraction (LVEF), and End-Systolic Diameter (ESD) were measured using Doppler ultrasound. The observation group exhibited significantly reduced serum levels of TNF-α, IL-1ß, and IL-6 compared to the control group (P < 0.05). Moreover, the observation group exerted lower total oxidation levels, OSI, EDD, and ESD compared to the control group (P < 0.05), while the LVEF and TAS levels in the observation group were higher than those in the control group (P < 0.05). Remarkably, the observation group experienced a significant reduction in the incidences of reinfarction, heart failure, arrhythmia, and abnormal valve function compared to the control group (P < 0.05). Decreased cardiac pump function and a more unfavorable prognosis were associated with elevated levels of cardiac oxidative stress and inflammatory factors (P < 0.05). Timely intervention with appropriate medications have a crucial effect in decreasing inflammatory marker levels, mitigating oxidative pressure, and enhancing cardiac pumping capacity and overall prognosis.

MicroRNA­203a­3p suppresses endothelial cell proliferation and invasion, and promotes apoptosis in hemangioma by inactivating the VEGF­mediated PI3K/AKT pathway.

Our previous study demonstrated that microRNA-203a-3p (miR-203a-3p) was involved in the regulation of long non-coding RNA MEG8-mediated the progression of hemangioma, which is a benign tumor characterized by endothelial hyperplasia in the blood vessels and primarily occurring in infants and females. Therefore, the present study aimed to further investigate the effects of miR-203a-3p on endothelial cell proliferation, invasion and apoptosis, as well as its underlying mechanism in hemangioma. Human hemangioma endothelial cells (HemECs) were first transfected with either miR-203a-3p mimics or a miR-203a-3p inhibitor. Subsequently, vascular endothelial growth factor A (VEGFA) was overexpressed in these cells. Cell proliferation (by Cell Counting Kit-8 assay), apoptosis (by TUNEL assay), invasion (by Transwell assay) and PI3K/AKT signaling (by western blot) were assessed following transfection of these cells. Notably, transfection with miR-203a-3p mimics caused a reduction in cell proliferation, invasion and in the phosphorylation levels of PI3K and AKT, and promoted cell apoptosis in HemECs. By contrast, transfection with the miR-203a-3p inhibitor exerted the opposite effects compared with those of the miR-203a-3p mimics. miR-203a-3p was revealed to directly suppress VEGFA expression in HemECs. VEGFA overexpression alone increased cell proliferation and invasion, but decreased apoptosis. Furthermore, VEGFA co-transfection reversed the effects mediated by miR-203a-3p mimics transfection in HemECs. Mechanistically, miR-203a-3p was demonstrated to inactivate the PI3K/AKT pathway, whereas VEGFA overexpression produced the opposite effect. VEGFA co-transfection also attenuated the miR-203a-3p mimics-induced inactivation of PI3K/AKT signaling in HemECs. In conclusion, these data suggested that miR-203a-3p may inhibit endothelial cell proliferation and invasion, and promote apoptosis by inactivating VEGFA and PI3K/AKT signaling in hemangioma. These findings also implicated miR-203 as a possible treatment option for this disease.

Knockdown of lncRNA MEG8 inhibits cell proliferation and invasion, but promotes cell apoptosis in hemangioma, via miR­203­induced mediation of the Notch signaling pathway.

As a member of the long non­coding (lnc)RNA family, lncRNA maternally expressed 8, small nucleolar RNA host gene (MEG8), has been reported to serve an oncogenic role in several types of malignancies, including hepatocellular carcinoma, non­small cell lung cancer and pancreatic cancer. The current study aimed to investigate the effect of the knockdown of MEG8 on human hemangioma endothelial cell (HemEC) proliferation, apoptosis and invasion, in addition to determining the underlying molecular mechanism. The knockdown of lncRNA MEG8 was achieved by transfecting lncRNA MEG8 small interfering (si)RNA into HemECs, while the combined knockdown of lncRNA MEG8 knockdown and microRNA (miR)­203 was established by co­transfecting lncRNA MEG8 siRNA and a miR­203 inhibitor into HemECs. The cell proliferation, apoptosis and invasion and the expression levels of miR­34a, miR­200b, miR­200b and Notch signaling pathway­related factors were detected via CCK­8 Kit, flow cytometry, Transwell, reverse transcription­quantitative PCR and western blot assay, respectively. The knockdown of lncRNA MEG8 significantly inhibited proliferation (P<0.05) and invasion (P<0.05), but promoted apoptosis (P<0.01) in HemECs. Furthermore, lncRNA MEG8 knockdown upregulated miR­203 (P<0.01) expression, but did not alter miR­34a or miR­200b expression (both P>0.05). Subsequent experiments revealed that miR­203 silencing exerted no significant effect on the expression levels of lncRNA MEG8 (P>0.05) in HemECs. In addition, miR­203 silencing increased cell proliferation (P<0.05) and invasion (P<0.01), but suppressed apoptosis (P<0.05). miR­203 silencing also reversed the effect of lncRNA MEG8 knockdown on the proliferation (P<0.05), apoptosis (P<0.001) and invasion (P<0.01) of HemECs. Moreover, lncRNA MEG8 knockdown downregulated jagged canonical notch ligand 1 (JAG1; P<0.05) and Notch1 (P<0.05) expression levels, while miR­203 silencing upregulated JAG1 (P<0.01) and Notch1 (P<0.01) expression levels and reversed the effects of lncRNA MEG8 knockdown on JAG1 (P<0.01) and Notch1 (P<0.01) expression in HemECs. In conclusion, the findings of the present study suggested that lncRNA MEG8 knockdown may inhibit cell proliferation and invasion, but promote cell apoptosis in hemangioma via miR­203­induced mediation of the Notch signaling pathway.

A superhydrophobic coating harvesting mechanical robustness, passive anti-icing and active de-icing performances.

HYPOTHESIS: Ice accretion is a challenging issue for various residential activities and industrial facilities. However, most of the current anti/de-icing coatings fail to maintain their properties when subject to frequent mechanical wear, and their limited functionality (either anti-icing or de-icing individually) cannot meet the requirement of all-weather utilization. EXPERIMENTS: Herein, a multifunctional superhydrophobic coating is prepared by compositing ferroferric oxide nanoparticles (Fe3O4 NPs) with fluorinated epoxy resin via an inverse infiltration process. The surface composition, morphology and wettability are systematically characterized using Fourier-transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM) coupled with energy dispersive X-ray spectroscopy (EDX), laser scanning microscopy and contact angle tensiometer. The anti-icing and de-icing performances are evaluated by investigating the freezing delay and photothermal effect, respectively. FINDINGS: This coating shows outstanding water repellency (water contact angle up to 161.0°, sliding angle down to 1.4°) and can maintain superhydrophobicity within 400 cycles of tape peeling, 260 cycles of sandpaper abrasion or 25 cycles of sand impact. Besides, because the hydrophobic nano/micro hierarchical structures tremendously retard the heat transfer, the freezing process of water droplet on this coating can be apparently delayed by up to 35 min as compared to the uncoated substrate. Moreover, owing to the photothermal effect of the Fe3O4 NPs, the coating's surface temperature can be rapidly increased above 0 °C under infrared irradiation, which facilitates the ice melting on cold surfaces. Our work offers a versatile approach to address the icing problems in diverse weather conditions, which exhibits great prospects in various engineering applications.

Different-Shaped Ultrafine MoNbTaW HEA Powders Prepared via Mechanical Alloying.

Different-shaped ultrafine MoNbTaW high-entropy alloy powders were firstly prepared by a convenient mechanical alloying method. The phase composition and microstructure of the powders were characterized. The powders are ultrafine with nano-sized grains and a good homogeneous microstructure. All the powders have a single body-centered cubic solid solution phase and form the high-entropy alloy during mechanical alloying. These powders with different shapes are quite attractive for developing high-performance MoNbTaW high-entropy alloy bulk and coatings combined with a following sintering, spraying, or additive manufacturing technique.