Nonlinear edge enhancement imaging based on Laguerre-Gaussian superimposed vortex filters.

Nonlinear reconstruction, which is based on the principle of cross correlation, is a commonly employed reconstruction technique in incoherent correlated digital holography systems. However, the modulation of phase masks in these systems is suppressed during the reconstruction process, resulting in an inability to express the characteristics of the phase masks. Consequently, achieving edge enhancement within these systems is constrained. We propose a nonlinear reconstruction method utilizing Laguerre-Gaussian superimposed vortex filters, which modulates the spectrum of the target during the reconstruction process. Experimental results demonstrate that this method performs well in reconstructing image edges for various phase-masked incoherent imaging systems and effectively suppresses noise. Additionally, this method enables directional edge enhancement.

Hsa_circ_0007478 aggravates NLRP3 inflammasome activation and lipid metabolism imbalance in ox-LDL-stimulated macrophage via miR-765/EFNA3 axis.

Coronary heart disease can be effectively prevented by alleviating atherosclerotic plaque progression. Ox-LDL-induced inflammatory response in macrophages is a critical factor in the pathophysiology of atherosclerosis. It is well known that circular RNAs (circRNAs) are associated with the progression of several human diseases, such as coronary artery diseases, by sponging microRNAs (miRNAs), but the function and hidden mechanisms of circRNAs in macrophage inflammation and lipid metabolism remain unclear. In our study, we established an ox-LDL-stimulated macrophage model and used microarray to detect circRNA expression in macrophages. The results revealed distinct profiles of circRNA expression across the ox-LDL-stimulated macrophage group and the control group. Among them, hsa_circ_0007478 was upregulated in ox-LDL-stimulated macrophages, accompanied by reduced miR-765 and increased EFNA3 expression. Activation of NLRP3 inflammasome and IL-1ß in macrophages was decreased following silencing of hsa_circ_0007478 or transfection of miR-765 mimics. In addition, we demonstrated that as a direct target gene of miR-765, the expression of EFNA3 regulated NLRP3 inflammasome and IL-1ß levels in macrophages. Besides, hsa_circ_0007478 promoted EFNA3 expression by acting as a miR-765 sponge. We further showed that hsa_circ_0007478/miR-765/EFNA3 axis could also be involved in the inhibition of the lipid metabolism and foam cells formation in ox-LDL-macrophages. Taken together, these findings suggest that Hsa_circ_0007478 may be a potential molecular target against the inflammatory response and foam cells during atherosclerosis.

Efficient reclamation phosphate by alginate-g-BMOF using poly(N-isopropyl acrylamide-co-acrylamide) as coating for temperature-responsive slow-release P-fertilizer.

Poly(N-isopropyl acrylamide) and its derived copolymer, as a temperature-responsive material, are widely used in the field of anticancer drug carrier. And it also plays an important role as carrier in slow-release fertilizer in recent years. In this paper, a smart poly(N-isopropyl acrylamide-co-acrylamide)-coated Alg-BMOF (PABMOF) was fabricated in ionic liquids microemulsion ([Bmim]PF6/TX-100/water) as nano-reactor. The structure and morphology of PABMOF were characterized by FT-IR, XRD, XPS, SEM, TG and BET. The resultant PABMOF was used as a adsorbent for H2PO4- adsorption. The adsorption kinetics, isotherms and mechanism of H2PO4- onto the resultant PABMOF were studied. The adsorption kinetic data was well suitable for pseudo-second-order kinetic model, and adsorption isotherm results demonstrated that the equilibrium data was fitted for Freundlich model. The water-holding and water-retention capacity of soil with TRSRFs addition of 2 wt% were74.3% and 52.13% at 30th day, respectively. Moreover, the release behavior of TRSRFs in water show that the cumulative release rate (Cr%) were 81.4% at 45 °C and 97.6% at 25 °C within 172 h, which displayed the excellent temperature-responsive property. The effect of TRSRFs on the growth of Chinese cabbage was investigated, which was indexed with the germination rate, plant height and root length of the crop.

Preparation of Fe-filled MOF-Al-based hydrogel for efficient reclaim of phosphate from wastewater and reusing as a slow-release fertilizer.

In this study, a novel Fe-filled MOF-Al-based hydrogel (SA@Fe@MOF-Al) was prepared and characterized by X-ray diffraction, scanning electron microscopy, thermogravimetric analysis. The SA@Fe@MOF-Al hydrogel bead was used as an adsorbent to adsorb H2PO4- from wastewater. The effects on adsorption were investigated, including pH and coexist ion. The adsorption reached equilibrium within 30 min. The maximum H2PO4- adsorption capacity of SA@Fe@MOF-Al was 103.09 mg g-1 at 298K with pH 7.0. Meanwhile, thermodynamic results confirmed that adsorption is exothermic and spontaneous. The adsorption kinetics displayed that SA@Fe@MOF-Al adsorption process was suitable to the pseudo-first-order and Langmuir model. Moreover, the feasibility of reusing the P-laden carrier material as a slow-release fertilizer was determined. The study results indicated that the product demonstrated excellent slow-release and water-retention properties. Thus, it has potential applications in improving soil moisture content and reducing soil moisture evaporation rate.

Suppression of Netrin-1 attenuates angiotension II-induced cardiac remodeling through the PKC/MAPK signaling pathway.

BACKGROUND: Myocardial remodeling caused by angiotensin II (Ang II) is essential for the pathological process of heart failure. Netrin-1, which is an axonal guidance cue, has been shown to be involved in the inflammatory response, tumorigenesis, and angiogenesis in non-neuronal tissues. However, the role of Netrin-1 in cardiac remodeling has not been fully elucidated. METHODS: The rat cardiomyocyte cell line H9c2 and primary neonatal rat cardiomyocytes were treated with Ang II. Cells were transfected with siRNA to silence Netrin-1 expression. Real-time polymerase chain reaction and Western blot analysis were used to detect the markers for fibrosis, apoptosis, and hypertrophy in cardiomyocytes. An Annexin V-EGFP/PI cell apoptosis detection kit was used to measure the level of apoptosis caused by angiotensin II. RESULTS: We found that Netrin-1 expression was upregulated in the H9c2 cells and the neonatal rat cardiomyocytes stimulated by Ang II. The increased Netrin-1 expression was decreased by valsartan to block AT1R. Importantly, the application of Netrin-1 siRNA significantly alleviated the degrees of myocardial hypertrophy, fibrosis (reflected by Myhc, collagen I, and TGF-ß) and apoptosis (reflected by the level of Caspase 3, Bax, and Bcl-2) induced by Ang II. In addition, the silencing of Netrin-1 substantially decreased the phosphorylation of PKCα, JNK, and P38. We treated H9c2 cells with LY317615, SP600125, and SB203580, inhibitors of PKCα, JNK, and P38, respectively, thereby resulting in a substantial decrease in hypertrophy, fibrosis, and apoptosis. CONCLUSIONS: Ang II produces cardiac hypertrophy, fibrosis, and apoptosis through the upregulation of Netrin-1 and the activation of the AT1R/PKCα/MAPK (JNK, P38) pathway. Suppression of Netrin-1 can relieve Ang II-induced cardiac remodeling via inhibition of the PKCα/MAPK (JNK and P38) signaling pathway. Thus, Netrin-1 may be a novel therapeutic target for Ang II-mediated cardiac remodeling.

Schizandrin B attenuates angiotensin II induced endothelial to mesenchymal transition in vascular endothelium by suppressing NF-κB activation.

BACKGROUND: Angiotensin II (Ang II)-induced chronic inflammation and oxidative stress often leads to irreversible vascular injury, in which the endothelial to mesenchymal transition (EndMT) in the endothelial layers are involved. Schisandrin B (Sch B), a natural product isolated from traditional Schisandra chinensis, has been reported to exert vascular protective properties with unclear mechanism. HYPOTHESIS/PURPOSE: This study investigated the protective effects and mechanism of Sch B against Ang II-induced vascular injury. METHODS: C57BL/6 mice were subcutaneous injected of Ang II for 4 weeks to induce irreversible vascular injury. In vitro, Ang II-induced HUVECs injury was used to study the underlying mechanism. The markers of EndMT, inflammation and oxidative stress were studied both in vitro and in vivo. RESULTS: Pre-administration of Sch B effectively attenuated phenotypes of vascular EndMT and fibrosis in Ang II-treated animals, accompanied with decreased inflammatory cytokine and ROS. The in vitro data from HUVECs suggest that Sch B directly targets NF-κB activation to suppress Ang II-induced EndMT and vascular injury. The activation of EndMT in the presence of Ang II is regulated by the NF-κB, a common player in inflammation and oxidative stress. Ang II-induced inflammation and oxidative stress also contributed to vascular EndMT development and Sch B inhibited inflammation/ROS-mediated EndMT by suppressing NF-κB. CONCLUSION: EndMT contributes to vascular injury in Ang II-treated mice, and it can be prevented via suppressing NF-κB activation by Sch B treatment. These results also imply that NF-κB might be a promising target to attenuate vascular remodeling induced by inflammation and oxidative stress through an EndMT mechanism.

Pacing parameters and success rates of permanent His-bundle pacing in patients with narrow QRS: a single-centre experience.

AIMS: High and unstable capture thresholds affect the success rate of permanent His-bundle pacing (HBP). We aimed to introduce the modified techniques during different periods and the corresponding success rate of HBP implantation. METHODS AND RESULTS: Patients from a single centre who had intrinsic QRS < 120 ms and HBP attempts were included in the study. The success rate and pacing parameters were described for three periods based on procedural modifications, i.e. Stage 1 using the conventional HBP procedure (August 2012 to May 2013), Stage 2 with addition of the dual-lead method (June 2013 to October 2014), and Stage 3 with the further addition of stability assessment during fixation (November 2014 to October 2016). The patients with successful permanent HBP were followed. A total of 310 patients were included with the average age of 70.3 ± 10.7 years. The success rate of acute HBP was 84.85%, 98.3%, and 99.20% during Stages 1-3, respectively (P < 0.001). The permanent HBP implantation rates increased from 77.3% during Stage 1 to 85.7% during Stage 2 and 89.6% during Stage 3 (P = 0.07). The acute His-bundle capture threshold reduced from 1.30 ± 0.7 V/0.5 ms during Stage 1 to 1.11 ± 0.6 V/0.5 ms during Stage 2 and further to 0.85 ± 0.51 V/0.5 ms during Stage 3 (P < 0.001). At the 12-month follow-up, the mean change in the HBP threshold decreased from 0.60 ± 0.59 V/0.5 ms during Stage 1 to 0.33 ± 0.39 V/0.5 ms during Stage 3 (P = 0.002). CONCLUSION: The HBP implantation success rate, pacing threshold, and its stability during follow-up were improved by using the dual-lead method and stability assessment techniques.

P2X7 receptor regulates EMMPRIN and MMP­9 expression through AMPK/MAPK signaling in PMA­induced macrophages.

The rupture of atherosclerotic plaques may result in the formation of thrombi, which may induce subsequent cardiac events such as acute myocardial infarction. Overproduction of matrix metalloproteinases (MMPs) and extracellular matrix metalloproteinase inducers (EMMPRINs) by monocytes and macrophages may lead to rupture of atherosclerotic plaques as a result of the degradation of the extracellular matrix. The purinergic 2X7 receptor (P2X7R) is expressed in macrophages that are assembled in atherosclerotic lesions of human carotid arteries. P2X7R may serve a crucial role in the development of atherosclerosis; therefore, the present study aimed to determine whether P2X7R regulated the expression of EMMPRIN and MMP­9 in phorbol 12­myristate 13­acetate (PMA)­induced macrophages. In addition, the potential molecular mechanisms involved in this process were investigated. THP­1 human monocytic cells were pretreated with A­438079 (a specific inhibitor of P2X7R) for 1 h and subsequently incubated with or without PMA for 48 h. Exposure to A­438079 significantly decreased the expression of MMP­9 and EMMPRIN in the PMA­induced macrophages and attenuated the activation (phosphorylation) of mitogen­activated protein kinase (MAPK) signaling, including c­Jun N­terminal kinase, p38 and extracellular signal­regulated kinase. The present study also demonstrated that 5'­AMP­activated protein kinase (AMPK) was activated by PMA exposure during differentiation from monocytes to macrophages. This activation was reversed by A­438079 treatment through the inhibition of P2X7R expression. These results suggested that the inhibition of P2X7R may be able to suppress the AMPK/MAPK signaling pathway and consequently downregulate both EMMPRIN and MMP­9 expression in PMA­induced macrophages.

Inhibition of LncRNA-HRIM Increases Cell Viability by Regulating Autophagy Levels During Hypoxia/Reoxygenation in Myocytes.

Backgrund/Aims: Ischemia reperfusion (I/R) promotes the severity of cardiomyocyte injury. Long noncoding RNAs (LncRNAs) are key regulators in cardiovascular diseases. However, the association between LncRNAs and myocardial I/R injury has not been thoroughly characterized to date. We attempted to clarify the potential biological role of a LncRNA (E230034O05Rik), which we named hypoxia/reoxygenation (H/R) injury-related factor in myocytes (HRIM), by investigating the differential expression of LncRNAs between groups of myocytes exposed to either a normal level of oxygen or to H/R. METHODS: Microarray analysis was used to determine analyze the global differential expression of LncRNAs in H9c2 myocytes exposed either to a normal level of oxygen or to H/R. Target LncRNA levels were further verified in vitro and ex vivo by real-time polymerase chain reaction (qPCR). Cell viability was analyzed using the Cell Counting Kit-8 assay. Autophagy levels were confirmed by Western blotting, transmission electron microscopy, and autophagic double-labeled (mRFP-GFP-LC3) adenovirus analyses. RESULTS: Gene expression profiling revealed that 797 LncRNAs and 1898 mRNAs were differentially expressed in the H/R group compared with the normal oxygen group. Among these LncRNAs and mRNAs, 6 upregulated LncRNAs and 2 downregulated LncRNAs in the H/R group were selected and further validated by qPCR in vitro and ex vivo. Additionally, LncRNA-HRIM was inhibited by specific siRNAs in H9c2 myocytes exposed to H/R. The inhibition of LncRNA-HRIM by siRNA prevented cell death by suppressing excessive autophagic activity in myocytes, This finding suggests a detrimental role of LncRNA-HRIM in the regulation of I/R injury. CONCLUSIONS: LncRNAs are involved in H/R injury of H9c2 myocytes. Inhibition of LncRNA-HRIM increased cell viability by reducing autophagy in myocytes during H/R.

Acute circulatory failure-chronic liver failure-sequential organ failure assessment score: a novel scoring model for mortality risk prediction in critically ill cirrhotic patients with acute circulatory failure.

BACKGROUND AND AIM: Acute circulatory failure (ACF) is associated with high mortality rates in critically ill cirrhotic patients. Only a few accurate scoring models exist specific to critically ill cirrhotic patients with acute circulatory failure (CICCF) for mortality risk assessment. The aim was to develop and evaluate a novel model specific to CICCF. PATIENTS AND METHODS: This study collected and analyzed the data on CICCF from the Multiparameter Intelligent Monitoring in Intensive Care-III database. The acute circulatory failure-chronic liver failure-sequential organ failure assessment (ACF-CLIF-SOFA) score was derived by Cox's proportional hazards regression. Performance analysis of ACF-CLIF-SOFA against CLIF-SOFA and model for end-stage liver disease systems was completed using area under the receiver operating characteristic curve. RESULTS: ACF-CLIF-SOFA identified six independent factors: mean arterial pressure [hazard ratio (HR)=0.984, 95% confidence interval (CI): 0.978-0.990, P<0.001], vasopressin (HR=1.548, 95% CI: 1.273-1.883, P<0.001), temperature (HR=0.764, 95% CI: 0.694-0.840, P<0.001), bilirubin (HR=1.031, 95% CI: 1.022-1.041, P<0.001), lactate (HR=1.113, 95% CI: 1.084-1.142, P<0.001), and urine output (HR=0.854, 95% CI: 0.767-0.951, P=0.004). ACF-CLIF-SOFA showed a better predictive performance than CLIF-SOFA and model for end-stage liver disease in terms of predicting mortality (0.769 vs. 0.729 vs. 0.713 at 30 days, 0.757 vs. 0.707 vs. 0.698 at 90 days, 0.733 vs. 0.685 vs. 0.691 at 1 year, respectively, all P<0.05). CONCLUSION: ACF-CLIF-SOFA, as the first model specific to CICCF, enables a more accurate prediction at 30-day, 90-day, and 1-year follow-up periods than other existing scoring systems.