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Abstract A broadband dual‐polarised antenna with L‐shaped strips for long‐term evolution (LTE)/5th generation mobile networks (5G) is proposed in this article. Based on the principle of multi‐mode resonance, wide bandwidth is achieved with L‐shaped strips and H‐shaped strips. The metal strips and dipoles are printed on the same substrate, which also contributes to antenna miniaturisation. The short pins are designed for impedance matching and improving isolation. The metal reflector is designed to control beamwidth and increase gain. A prototype was fabricated using an easy Printed Circuit Board technique to verify the proposed design. Low‐profile of 0.2λ0 (λ0 is the free‐space wavelength at the centre frequency) is achieved. The measured results show that the relative bandwidth is 74% (2.3–5.0 GHz) at Voltage Standing Wave Ratio

Objectives: Cardiovascular diseases are one of the primary causes of death. Cardiomyocyte loss is a significant feature of cardiac injury. Ferroptosis is iron-dependent cell death, which occurs due to excess iron and reactive oxygen species (ROS) accumulation causing lipid peroxidation, and subsequent cell death. Ferroptosis has been confirmed to mediate ischemia/reperfusion-induced cardiomyopathy and chemotherapy-induced cardiotoxicity. Berberine (BBR) has been proven to protect the heart from cardiomyopathies, including cardiac hypertrophy, heart failure, myocardial infarction, and arrhythmias. It protects cardiomyocytes from apoptosis and autophagy. However, the relation between BBR and ferroptosis is still unknown. This study aimed to confirm if BBR reduces cardiac cell loss via inhibiting ferroptosis. Materials and Methods: We used erastin and Ras-selective lethal small molecule 3 (RSL3) to establish a ferroptosis model in an H9c2 cardiomyoblast cell line and rat neonatal cardiomyocytes to prove that BBR has a protective effect on cardiac cells via inhibiting ferroptosis. Results: In H9c2 cardiomyoblasts, the results showed that BBR reduced erastin and RSL3-induced cell viability loss. Moreover, BBR decreased ROS accumulation and lipid peroxidation in cells induced with ferroptosis. Furthermore, quantitative polymerase chain reaction results showed that Ptgs2 mRNA was reduced in BBR-treated cells. In rat neonatal cardiomyocytes, BBR reduced RSL3-induced loss of cell viability. Conclusion: These results indicated that BBR inhibited ferroptosis via reducing ROS generation and reducing lipid peroxidation in erastin and RSL3-treated cardiac cells.

Adipogenic differentiation from stem cells has become a research target due to the increasing interest in obesity. It has been indicated that adipocytes can secrete palmitic acid methyl ester (PAME), which is able to regulate stem cell proliferation. However, the effects of PAME on adipogenic differentiation in stem cell remain unclear. Here, we present that the adipogenic differentiation medium supplemented with PAME induced the differentiation of rat adipose tissue-derived mesenchymal stem cells (rAD-MSCs) into adipocyte. rAD-MSCs were treated with PAME for 12 days and then subjected to various analyses. The results from the present study show that PAME significantly increased the levels of adipogenic differentiation markers, PPARγ and Gpd1, and enhanced adipogenic differentiation in rAD-MSCs. Furthermore, the level of GPR40/120 protein increased during induction of adipocyte differentiation in rAD-MSCs. Cotreatment with PAME and a GPR40/120 antagonist together inhibited the PAME-enhanced adipogenic differentiation. Moreover, PAME significantly increased phosphorylation of extracellular signal-regulated kinases (ERK), but not AKT and mTOR. Cotreatment with PAME and a GPR40/120 antagonist together inhibited the PAME-enhanced ERK phosphorylation and adipogenic differentiation. PAME also increased the intracellular Ca2+ levels. Cotreatment with PAME and a Ca2+ chelator or a phospholipase C (PLC) inhibitor prevented the PAME-enhanced ERK phosphorylation and adipogenic differentiation. Our data suggest that PAME activated the GPR40/120/PLC-mediated pathway, which in turn increased the intracellular Ca2+ levels, thereby activating the ERK, and eventually enhanced adipogenic differentiation in rAD-MSCs. The findings from the present study might help get insight into the physiological roles and molecular mechanism of PAME in regulating stem cell differentiation.

Old age has been proven to be related to progressed arterial or aortic stiffness. Aortic stiffness is an independent predictor of all-cause and cardiovascular disease mortalities in patients who have undergone coronary artery bypass grafting (CABG) surgery. Higher serum concentrations of adipocyte fatty-acid-binding protein (A-FABP) could be considered a predictor of aortic stiffness in patients with hypertension or diabetes mellitus. This study aims to investigate the relationships between A-FABP and aortic stiffness in patients who have received CABG. A total of 84 CABG patients were enrolled in our study from September 2018 to May 2019. Serum A-FABP levels were determined using a commercial enzyme immunoassay. Carotid–femoral pulse wave velocity (cfPWV) > 10 m/s was defined as aortic stiffness. Of the 84 CABG patients, 28 (33.3%) with aortic stiffness had a higher average age; exhibited higher rates of diabetes; and had higher serum creatinine, C-reactive protein, and A-FABP levels compared to controls. Multivariable logistic regression revealed that serum A-FABP levels (odds ratio (OR) = 1.068, 95% confidence interval (CI) 1.017–1.121, p = 0.008) and age (OR = 1.204, 95% CI 1.067–1.359, p = 0.003) were independent predictors of aortic stiffness. Multivariable stepwise linear regression revealed significant positive correlations of age and A-FABP levels with cfPWV values. Serum A-FABP level is positively correlated with cfPWV values, and a high serum A-FABP level is associated with aortic stiffness in patients who have undergone CABG.

Abstract In this study, we synthesized a periodic polystyrene nanosphere (PS NS) array using the dip-drop method with post-deposition etching to improve the light extraction efficiency (LEE) of InGaN/GaN light-emitting diodes (LEDs). The dip-drop method has advantages such as simple procedure, inexpensive equipment, room temperature deposition, and easy implementation in LEDs. The arrangement of PS NSs on an indium-tin-oxide (ITO)-coated glass substrate depends on the average dip-drop speed and the concentration of the PS NS suspension. The periodic PS NS array can modulate the in-plane wave vector of emission light from a semiconductor to free space and thus increase the escape probability. The calculated and experimental results indicated that the light output intensity of the InGaN/GaN LEDs can be improved by using the periodic PS NS array as a window layer; this array comprises PS NSs with a diameter of 100 nm separated with periods of 100 and 100 nm in the x and y directions. Because of the improved LEE, the InGaN/GaN LEDs with the optimal PS NS array window layers exhibited a 38% increase in light output intensity compared with the conventional InGaN/GaN LEDs under 20-mA driving current.

Background/Aims: Intermittent hypoxia (IH) has been shown to exert preconditioning-like cardioprotective effects. It also has been reported that IH preserves intracellular pH (pHi) during ischemia and protects cardiomyocytes against ischemic reperfusion injury. However, the exact mechanism is still unclear. Methods: In this study, we used proton indicator BCECF-AM to analyze the rate of pHi recovery from acidosis in the IH model of rat neonatal cardiomyocytes. Neonatal cardiomyocytes were first treated with repetitive hypoxia-normoxia cycles for 1-4 days. Cells were then acid loaded with NH4Cl, and the rate of pHi recovery from acidosis was measured. Results: We found that the pHi recovery rate from acidosis was much slower in the IH group than in the room air (RA) group. When we treated cardiomyocytes with Na+-H+ exchange (NHE) inhibitors (Amiloride and HOE642) or Na+-free Tyrode solution during the recovery, there was no difference between RA and IH groups. We also found intracellular Na+ concentration ([Na+]i) significantly increased after IH exposure for 4 days. However, the phenomenon could be abolished by pretreatment with ROS inhibitors (SOD and phenanathroline), intracellular calcium chelator or Na+-Ca2+ exchange (NCX) inhibitor. Furthermore, the pHi recovery rate from acidosis became faster in the IH group than in the RA group when inhibition of NCX activity. Conclusions: These results suggest that IH would induce the elevation of ROS production. ROS then activates Ca2+-efflux mode of NCX and results in intracellular Na+ accumulation. The rise of [Na+]i further inhibits the activity of NHE-mediated acid extrusion and retards the rate of pHi recovery from acidosis during IH.

Myocardial ischemia/reperfusion (I/R) injury has been associated with ferroptosis, which is characterized by an iron-dependent accumulation of lipid peroxide to lethal levels. Gossypol acetic acid (GAA), a natural product taken from the seeds of cotton plants, prevents oxidative stress. However, the effects of GAA on myocardial I/R-induced ferroptosis remain unclear. This study investigated the ability of GAA to attenuate I/R-induced ferroptosis in cardiomyocytes along with the underlying mechanisms in a well-established rat model of myocardial I/R and isolated neonatal rat cardiomyocytes. H9c2 cells and cardiomyocytes were treated with the ferroptosis inducers erastin, RSL3, and Fe-SP. GAA could protect H9c2 cells against ferroptotic cell death caused by these ferroptosis inducers by decreasing the production of malondialdehyde and reactive oxygen species, chelating iron content, and downregulating mRNA levels of Ptgs2. GAA could prevent oxygen-glucose deprivation/reperfusion-induced cell death and lipid peroxidation in the cardiomyocytes. Moreover, GAA significantly attenuated myocardial infarct size, reduced lipid peroxidation, decreased the mRNA levels of the ferroptosis markers Ptgs2 and Acsl4, decreased the protein levels of ACSL4 and NRF2, and increased the protein levels of GPX4 in I/R-induced ex vivo rat hearts. Thus, GAA may play a cytoprotectant role in ferroptosis-induced cardiomyocyte death and myocardial I/R-induced ferroptotic cell death.

Intermittent hypoxia (IH), characterized as cyclic episodes of short-period hypoxia followed by normoxia, occurs in many physiological and pathophysiological conditions such as pregnancy, athlete, obstructive sleep apnea, and asthma. Hypoxia can induce autophagy, which is activated in response to protein aggregates, in the proteotoxic forms of cardiac diseases. Previous studies suggested that autophagy can protect cells by avoiding accumulation of misfolded proteins, which can be generated in response to ischemia/reperfusion (I/R) injury. The objective of the present study was to determine whether IH-induced autophagy can attenuate endoplasmic reticulum (ER) stress and cell death. In this study, H9c2 cell line, rat primary cultured cardiomyocytes, and C57BL/6 male mice underwent IH with an oscillating O2 concentration between 4 and 20% every 30 min for 1–4 days in an incubator. The levels of LC3, an autophagy indicator protein and CHOP and GRP78 (ER stress-related proteins) were measured by Western blotting analyses. Our data demonstrated that the autophagy-related proteins were upregulated in days 1–3, while the ER stress-related proteins were downregulated on the second day after IH. Treatment with H2O2 (100 μM) for 24 h caused ER stress and increased the level of ER stress-related proteins, and these effects were abolished by pre-treatment with IH condition. In response to the autophagy inhibitor, the level of ER stress-related proteins was upregulated again. Taken together, our data suggested that IH could increase myocardial autophagy as an adaptive response to prevent the ER stress and apoptosis.

The bitcoin lightning network (BLN), a so-called ‘second layer’ payment protocol, was launched in 2018 to scale up the number of transactions between bitcoin owners. In this paper, we analyse the structure of the BLN over a period of 18 months, ranging from 12th January 2018 to 17th July 2019, at the end of which the network has reached 8.216 users, 122.517 active channels and 2.732,5 transacted bitcoins. Here, we consider three representations of the BLN: the daily snapshot one, the weekly snapshot one and the daily-block snapshot one. By studying the topological properties of the binary and weighted versions of the three representations above, we find that the total volume of transacted bitcoins approximately grows as the square of the network size; however, despite the huge activity characterising the BLN, the bitcoins distribution is very unequal: the average Gini coefficient of the node strengths (computed across the entire history of the Bitcoin Lightning Network) is, in fact, ≃0.88 causing the 10% (50%) of the nodes to hold the 80% (99%) of the bitcoins at stake in the BLN (on average, across the entire period). This concentration brings up the question of which minimalist network model allows us to explain the network topological structure. Like for other economic systems, we hypothesise that local properties of nodes, like the degree, ultimately determine part of its characteristics. Therefore, we have tested the goodness of the undirected binary configuration model (UBCM) in reproducing the structural features of the BLN: the UBCM recovers the disassortative and the hierarchical character of the BLN but underestimates the centrality of nodes; this suggests that the BLN is becoming an increasingly centralised network, more and more compatible with a core-periphery structure. Further inspection of the resilience of the BLN shows that removing hubs leads to the collapse of the network into many components, an evidence suggesting that this network may be a target for the so-called split attacks .

Bone marrow-derived mesenchymal cells (BM-MSCs) are able to differentiate into adipocytes, which can secrete adipokines to affect BM-MSC proliferation and differentiation. Recent evidences indicated that adipocytes can secrete fatty acid metabolites, such as palmitic acid methyl ester (PAME), which is able to cause vasorelaxation and exerts anti-inflammatory effects. However, effects of PAME on BM-MSC proliferation remain unclear. The aim of this study was to investigate the effect of PAME on human BM-MSC (hBM-MSC) proliferation and its underlying molecular mechanisms. hBM-MSCs were treated with PAME for 48 h and then subjected to various analyses. The results from the present study show that PAME significantly reduced the levels of G2/M phase regulatory proteins, cyclin-dependent kinase 1 (Cdk1), and cyclin B1 and inhibited proliferation in hBM-MSCs. Moreover, the level of Mdm2 protein decreased, while the levels of p21 and p53 protein increased in the PAME-treated hBM-MSCs. However, PAME treatment did not significantly affect apoptosis/necrosis, ROS generation, and the level of Cdc25C protein. PAME also induced intracellular acidosis and increased intracellular Ca2+ levels. Cotreatment with PAME and Na+/H+ exchanger inhibitors together further reduced the intracellular pH but did not affect the PAME-induced decreases of cell proliferation and increases of the cell population at the G2/M phase. Cotreatment with PAME and a calcium chelator together inhibited the PAME-increased intracellular Ca2+ levels but did not affect the PAME-induced cell proliferation inhibition and G2/M cell cycle arrest. Moreover, the half-life of p53 protein was prolonged in the PAME-treated hBM-MSCs. Taken together, these results suggest that PAME induced p53 stabilization, which in turn increased the levels of p53/p21 proteins and decreased the levels of Cdk1/cyclin B1 proteins, thereby preventing the activation of Cdk1, and eventually caused cell cycle arrest at the G2/M phase. The findings from the present study might help get insight into the physiological roles of PAME in regulating hBM-MSC proliferation.

The Bitcoin lightning network (BLN), a so-called ‘second layer’ payment protocol, was launched in 2018 to scale up the number of transactions between Bitcoin owners. In this paper, we analyse the structure of the BLN over a period of 18 months, ranging from 12th January 2018 to 17th July 2019, at the end of which the network has reached 8.216 users, 122.517 active channels and 2.732,5 transacted Bitcoins. Here, we consider three representations of the BLN: the daily snapshot one, the weekly snapshot one and the daily-block snapshot one. By studying the topological properties of the binary and weighted versions of the three representations above, we find that the total volume of transacted Bitcoins approximately grows as the square of the network size; however, despite the huge activity characterising the BLN, the Bitcoins distribution is very unequal: the average Gini coefficient of the node strengths (computed across the entire history of the Bitcoin lightning network) is, in fact, ≃0.88 causing the 10% (50%) of the nodes to hold the 80% (99%) of the Bitcoins at stake in the BLN (on average, across the entire period). This concentration brings up the question of which minimalist network model allows us to explain the network topological structure. Like for other economic systems, we hypothesise that local properties of nodes, like the degree, ultimately determine part of its characteristics. Therefore, we have tested the goodness of the undirected binary configuration model (UBCM) in reproducing the structural features of the BLN: the UBCM recovers the disassortative and the hierarchical character of the BLN but underestimates the centrality of nodes; this suggests that the BLN is becoming an increasingly centralised network, more and more compatible with a core-periphery structure. Further inspection of the resilience of the BLN shows that removing hubs leads to the collapse of the network into many components, an evidence suggesting that this network may be a target for the so-called split attacks .

Background/Aims: Intermittent hypoxia (IH) may exert pre-conditioning-like cardioprotective effects and alter Ca2+ regulation; however, the exact mechanism of these effects remains unclear. Thus, we examined Ca2+-handling mechanisms induced by IH in rat neonatal cardiomyocytes. Methods: Cardiomyocytes were exposed to repetitive hypoxia-re-oxygenation cycles for 1-4 days. Mitochondrial reactive oxygen species (ROS) generation was determined by flow cytometry, and intracellular Ca2+ concentrations were measured using a live-cell fluorescence imaging system. Protein kinase C (PKC) isoforms and Ca2+-handling proteins were analysed using immunofluorescence and western blotting. Results: After IH exposure for 4 days, the rate of Ca2+ extrusion from the cytosol to the extracellular milieu during 40-mM KCl-induced Ca2+ mobilization increased significantly, whereas ROS levels increased mildly. IH activated PKC isoforms, which translocated to the membrane from the cytosol, and Na+/Ca2+ exchanger-1, leading to enhanced Ca2+ efflux capacity. Simultaneously, IH increased sarcoplasmic reticulum (SR) Ca2+-ATPase and ryanodine receptor 2 (RyR-2) activities and RyR-2 expression, resulting in improved Ca2+ uptake and release capacity of SR in cardiomyocytes. Conclusions: IH-induced mild elevations in ROS generation can enhance Ca2+ efflux from the cytosol to the extracellular milieu and Ca2+-mediated SR regulation in cardiomyocytes, resulting in enhanced Ca2+-handling ability.

AIM: To observe the efficiency of phacoemulsification with intraocular lens implantation in the treatment of cataract and glaucoma. METHODS:Totally 60 patients(70 eyes)with cataract and glaucoma were included between March 2010 and March 2012 in our hospital. The phacoemulsification with intraocular lens implantation was performed. The observation of surgical efficiency, including the patient's IOP, anterior chamber depth, vision and complications, were compared before and after surgery. RESULTS:Compared with preoperation, the patients' vision and anterior chamber depth were increased and the IOP was reduced significantly(PCONCLUSION: Phacoemulsification with IOL implantation is a safe and effective treatment for cataract and glaucoma.

Nestedness refers to the structural property of complex networks that the neighborhood of a given node is a subset of the neighborhoods of better-connected nodes. Following the seminal work by Patterson and Atmar (1986), ecologists have been long interested in revealing the configuration of maximal nestedness of spatial and interaction matrices of ecological communities. In ecology, the BINMATNEST genetic algorithm can be considered as the state-of-the-art approach for this task. On the other hand, the fitness-complexity ranking algorithm has been recently introduced in the economic complexity literature with the original goal to rank countries and products in World Trade export networks. Here, by bringing together quantitative methods from ecology and economic complexity, we show that the fitness-complexity algorithm is highly effective in the nestedness maximization task. More specifically, it generates matrices that are more nested than the optimal ones by BINMATNEST for 61.27% of the analyzed mutualistic networks. Our findings on ecological and World Trade data suggest that beyond its applications in economic complexity, the fitness-complexity algorithm has the potential to become a standard tool in nestedness analysis.

A neutropenic patient with an acute abdomen could confuse the medical doctor in the decision making of whether or not a surgical intervention is essential to resolve the medical problem. Here, we report a 62-yearold female with acute monoblastic leukemia that was complicated by neutropenic fever and abdominal pain on the 13th day after receiving the first chemotherapy consisting of 1-beta-D-arabinofuranosylcytosine and idarubicin. Abdominal computed tomography revealed colitis involving the entire ascending colon. Neutropenic enterocolitis with Enterobacter cloacae septicemia was the final diagnosis. She received conservative management with close observation and recovered eventually. We discuss the etiologies of acute abdomen in patients receiving chemotherapy and their differential diagnosis.

Sleep apnea syndrome, characterized by intermittent hypoxia (IH), is linked with increased oxidative stress. This study investigates the mechanisms underlying IH and the effects of IH-induced oxidative stress on cerebellar astrocytes. Rat primary cerebellar astrocytes were kept in an incubator with an oscillating O2 concentration between 20% and 5% every 30 min for 1-4 days. Although the cell loss increased with the duration, the IH incubation didn't induce apoptosis or necrosis, but rather a G0/G1 cell cycle arrest of cerebellar astrocytes was noted. ROS accumulation was associated with cell loss during IH. PARP activation, resulting in p21 activation and cyclin D1 degradation was associated with cell cycle G0/G1 arrest of IH-treated cerebellar astrocytes. Our results suggest that IH induces cell loss by enhancing oxidative stress, PARP activation and cell cycle G0/G1 arrest in rat primary cerebellar astrocytes.

The aim of the present study was to construct angiopoietin-2 (Ang2)-small interfering (si)RNA chitosan magnetic nanoparticles and to observe the interference effects of the nanoparticles on the expression of the Ang2 gene in human malignant melanoma cells. Ang2-siRNA chitosan magnetic nanoparticles were constructed and transfected into human malignant melanoma cells in vitro. Red fluorescent protein expression was observed, and the transfection efficiency was analyzed. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to assess the inhibition efficiency of Ang2 gene expression. Ang2-siRNA chitosan magnetic nanoparticles were successfully constructed, and at a mass ratio of plasmid to magnetic chitosan nanoparticles of 1:100, the transfection efficiency into human malignant melanoma cells was the highest of the ratios assessed, reaching 61.17%. RT-qPCR analysis showed that the magnetic chitosan nanoparticles effectively inhibited Ang2 gene expression in cells, and the inhibition efficiency reached 59.56% (P<0.05). Ang2-siRNA chitosan magnetic nanoparticles were successfully constructed. The in vitro studies showed that the nanoparticles inhibited Ang2 gene expression in human malignant melanoma tumor cells, which laid the foundation and provided experimental evidence for additional future in vivo studies of intervention targeting malignant melanoma tumor growth in nude mice. [ABSTRACT FROM AUTHOR]

Background Intermittent hypoxia (IH) plays a critical role in sleep breathing disorder-associated hippocampus impairments, including neurocognitive deficits, irreversible memory and learning impairments. IH-induced neuronal injury in the hippocampus may result from reduced precursor cell proliferation and the relative numbers of postmitotic differentiated neurons. However, the mechanisms underlying IH-induced reactive oxygen species (ROS) generation effects on cell proliferation and neuronal differentiation remain largely unknown. Results ROS generation significantly increased after 1-4 days of IH without increased pheochromocytoma-12 (PC12) cell death, which resulted in increased protein phosphatase 2A (PP2A) mRNA and protein levels. After 3-4 days of IH, extracellular signal-regulated kinases 1/2 (ERK1/2) protein phosphorylation decreased, which could be reversed by superoxide dismutase (SOD), 1,10-phenanthroline (Phe), the PP2A phosphorylation inhibitors, okadaic acid (OKA) and cantharidin, and the ERK phosphorylation activator nicotine (p < 0.05). In particular, the significantly reduced cell proliferation and increased proportions of cells in the G0/G1 phase after 1-4 days of IH (p < 0.05), which resulted in decreased numbers of PC12 cells, could be reversed by treatment with SOD, Phe, PP2A inhibitors and an ERK activator. In addition, the numbers of nerve growth factor (NGF)- induced PC12 cells with neurite outgrowths after 3-4 days of IH were less than those after 4 days of RA, which was also reversed by SOD, Phe, PP2A inhibitors and an ERK activator. Conclusions Our results suggest that IH-induced ROS generation increases PP2A activation and subsequently downregulates ERK1/2 activation, which results in inhibition of PC12 cell proliferation through G0/G1 phase arrest and NGF-induced neuronal differentiation. [ABSTRACT FROM AUTHOR]