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We show that the photonic crystal (PhC) made of dielectric cuboids with their centers forming a honeycomb lattice is characterized by a ℤ 2 ${\mathbb{ℤ}}_{2}$ topological index when the longer sides of six cuboids point towards the center of hexagonal unit cell. While the C 6v symmetry regarding the center of unit cell is preserved, the C 3 symmetry regarding honeycomb sites is broken, which opens a bandgap in the Dirac dispersion of honeycomb structure and induces a band inversion between p modes and d modes. Rotating cuboids around their individual centers closes the bandgap and reopens a trivial bandgap. We discuss that this feature can be exploited for realizing a reconfigurable topological waveguide.

Topological insulators are materials that behave as insulators in the bulk and as conductors at the edge or surface due to the particular configuration of their bulk band dispersion. However, up to date possible practical applications of this band topology on materials' bulk properties have remained abstract. Here, we propose and experimentally demonstrate a topological bulk laser. We pattern semiconductor nanodisk arrays to form a photonic crystal cavity showing topological band inversion between its interior and cladding area. In-plane light waves are reflected at topological edges forming an effective cavity feedback for lasing. This band-inversion-induced reflection mechanism induces single-mode lasing with directional vertical emission. Our topological bulk laser works at room temperature and reaches the practical requirements in terms of cavity size, threshold, linewidth, side-mode suppression ratio and directionality for most practical applications according to Institute of Electrical and Electronics Engineers and other industry standards. We believe this bulk topological effect will have applications in near-field spectroscopy, solid-state lighting, free-space optical sensing and communication.

Pulmonary artery adventitial fibroblasts, the most abundant cellular constituent of adventitia, are often the first to be activated and reprogrammed to then influence the tone and structure of the vessel wall in pulmonary arterial hypertension (PAH). Our previous study found that interruption of CD40 ligand (CD40L)-CD40 signaling improves the efficacy of transplanted endothelial progenitor cells in monocrotaline induced-PAH. However, whether CD40L-CD40 signaling is involved in the activation of adventitial fibroblasts in PAH and whether Drosophila behavior human splicing (DBHS) protein family members have any roles during adventitial fibroblasts activation are completely unclear. Here, we show that soluble CD40L (sCD40L) stimulation progressively increases pro-inflammatory activity, proliferation, and migration of pulmonary adventitial fibroblasts. Besides, sCD40L stimulation decreases splicing factor proline- and glutamine-rich protein (SFPQ) protein (one member of DBHS protein family) expression, while SFPQ overexpression suppresses sCD40L stimulation-induced proliferation and migration of pulmonary adventitial fibroblasts by repressing CD40 transcription. Moreover, ChIP assays found that sCD40L stimulation promotes histone H3 tri-methylation at lysine 4 (H3K4me3), H3K36me3, and H3K27 acetylation (H3K27ac) modifications on CD40 promoter region in pulmonary adventitial fibroblasts, while SFPQ overexpression decreases H3K36me3 modification and increases H3K36ac on CD40 promoter region by interacting with histone deacetylase-1 (HDAC1) to inhibit CD40 transcription. This in-depth study shows that CD40L-CD40 signaling promotes activation of pulmonary adventitial fibroblasts by increasing proliferation, migration, and pro-inflammatory activity of adventitial fibroblasts, and SFPQ could inhibit CD40 transcription though switching H3K36me3 to H3K36ac modifications on its promoter by interacting with HDAC1. This study, first, uncovers the roles of SFPQ on CD40L-CD40 signaling-mediated activation of pulmonary adventitial fibroblasts.

Background To estimate the public health risk related to cooked meat in bulk products contaminated with Listeria monocytogenes, a generic Bayesian network (BN) risk-assessment model was developed to simulate influencing factors and processes of products from the industry level to the consumer level. To quantify the model, parameter values of prior distributions were acquired from the literature, websites, and expert opinions. Using the Markov chain Monte Carlo (MCMC) simulation approach, posterior probability distributions were calculated according to the incorporated evidence, which allowed us to predict various risks affected by processing variability from production to consumption. Results The average risks of listeriosis from consuming cooked meat in bulk products are 8.40 × 10-7 , 2.58 × 10-8 , 8.24 × 10-7 , and 1.05 × 10-6 per meal for children, young people, elderly people, and pregnant women, respectively. The estimated mean number of listeriosis cases is 5 per 100 000 people per year in China. Conclusion Although only a conceptual BN model is given, it manifests the principles and characteristics of mathematical methods. The BN model can also provide significant benefits for quantitative risk assessment by incorporating all available data and by updating beliefs. © 2018 Society of Chemical Industry.

We report on a topological bulk laser based on band-inversion-induced reflection constructed by trivial and topological photonic crystal arrays. It provides a novel lasing mode selection mechanism and renders high-performance laser devices. © 2020 The Author(s)

Background/Aims: Tanshinone IIA (Tan IIA) is effective in the treatment of inflammation and atherosclerosis. The adhesion of inflammatory cells to vascular endothelium plays important role in atherogenic processes. This study examined the effects of Tan IIA on expression of adhesion molecules in tumor necrosis factor-α (TNF-α)-induced endothelial progenitor cells (EPCs). Methods: EPCs were pretreated with Tan IIA and stimulated with TNF-α. Mononuclear cell (MNC) adhesion assay was performed to assess the effects of Tan IIA on TNF-α-induced MNC adhesion. Expression of vascular cell adhesion molecule-1 (VCAM-1)/intracellular adhesion molecule-1 (ICAM-1) and activation of Nuclear factor κB (NF-κB) signaling pathway were measured. Results: The results showed that the adhesion of MNCs to TNF-α-induced EPCs and expression of VCAM-1/ICAM-1 in EPCs were promoted by TNF-α, which were reduced by Tan IIA. TNF-α increased the amount of phosphorylation of NF-κB, IκB-α and IKKα/β in cytosolic fractions and NF-κB p65 in nucleus, while Tan IIA reduced its amount. Conclusion: This study demonstrated a novel mechanism for the anti-inflammatory/anti-atherosclerotic activity of Tan IIA, which may involve down-regulation of VCAM-1 and ICAM-1 through partial blockage of TNF-α-induced NF-κB activation and IκB-α phosphorylation by the inhibition of IKKα/β pathway in EPCs.

Accumulating evidence has demonstrated that endothelial progenitor cells (EPCs) could facilitate the reendothelialization of injured arteries by replacing the dysfunctional endothelial cells, thereby suppressing the formation of neointima. Meanwhile, other findings suggest that EPCs may be involved in the pathogenesis of age-related vascular remodeling. This review is presented to summarize the characteristics of EPCs and age-related vascular remodeling. In addition, the role of EPCs in age-related vascular remodeling and possible solutions for improving the therapeutic effects of EPCs in the treatment of age-related diseases are discussed.

The continuous cropping of peanuts is a primary cause of yield and quality loss. Solutions to this problem should be therefore developed to ensure the sustainability of peanut production.In this study, colonization by the endophytic fungus Phomopsis liquidambari was detected, which led to significantly improved rhizosphere soil microenvironment, enhanced N, P and K assimilation and suppressed incidence of peanut disease. Statistical analysis demonstrated that the yield enhancement was significantly correlated with improvement of the rhizosphere soil microenvironment and the peanut's physiological status by P. liquidambari colonization. In addition, P. liquidambari colonization also significantly improved peanut quality.Our results indicate that the practical application of the endophytic fungus P. liquidambari has a strong potential to alleviate the obstacles associated with continuous peanut cropping under field conditions. © 2018 Society of Chemical Industry.

Tanshinone IIA (Tan IIA) is a Traditional Chinese Medicine commonly used in Asian and Western countries for the prevention and treatment of cardiovascular disorders, such as atherosclerosis. Endothelial dysfunction and associated inflammatory processes have a critical role in the development of atherosclerosis. Endothelial progenitor cells (EPCs) have been demonstrated to be involved in certain aspects of the endothelial repair process. The present study aimed to investigate the putative protective effects of Tan IIA on EPCs injured by tumor necrosis factor-α (TNF-α). The potential effects of Tan IIA on TNF-α-stimulated EPC proliferation, migration, adhesion, in vitro tube formation ability and paracrine activity were investigated in the current study. The results indicated that TNF-α impaired EPC proliferation, migration, adhesion capacity and vasculogenesis ability in vitro as well as promoted EPC secretion of inflammatory cytokines, including monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6) and soluble CD40 ligand (sCD40L). However, Tan IIA was able to reverse these effects. In conclusion, these findings demonstrated that Tan IIA may have the potential to protect EPCs against damage induced by TNF-α. Therefore, these results may provide evidence for the pharmacological basis of Tan IIA and its potential use in the prevention and treatment of early atherosclerosis associated with EPC and endothelial damage.

Background/Aims: Transplantation of endothelial progenitor cells (EPCs) plays a therapeutic role in pulmonary arterial hypertension (PAH). Meanwhile, recruitment of progenitors has potential inflammatory effects and exaggerates vascular injury. CD40 pathway is identified as a major player in vascular inflammatory events. In this study, we investigated the role of CD40 pathway in regulating early outgrowth EPC functions, and searched for improvements in PAH cell therapy. Methods: EPCs were isolated from rat bone marrow and cultured for 7 days. After treatment with soluble CD40 ligand (sCD40L) for 24 hours, EPC migration, adhesion, proliferation, paracrine and vasculogenesis functions were tested. Rat PAH model was founded by subcutaneous injection of monocrotaline (MCT). Control EPCs or lentivirus vectors (Lv)-shRNA-CD40 EPCs were infused via tail vein at day 7, 14, and 21 after MCT injection. Therapeutic effects were evaluated at day 28. Results: sCD40L dose-dependently impaired EPC migration, adhesion, proliferation, and vasculogenesis functions. However, paracrine effects of soluble intercellular adhesion molecule-1, vascular endothelial growth factor and interleukin-6 were dose-dependently improved by sCD40L. Control EPC-derived conditioned medium protected endothelial cell in vitro vasculogenesis, while sCD40L-pretreated ones showed detrimental effects. After MCT injection, sCD40L levels in rat serum increased gradually. Other than in vitro results, benefits of both two EPC treatments were obvious, even taken at day 21. Benefits of control EPCs wore off over time, but those of Lv-shRNA-CD40 EPCs were more effective and enduring, as characterized by both ameliorated rat hemodynamic and reversed vascular remodeling. Furthermore, Lv-shRNA-CD40 EPCs integrated into endothelium better, rather than into adventitia and media. Conclusion: sCD40L impaired protective effects of EPCs. Traditional EPC treatments were limited in PAH, while interruption of CD40 pathway of transplanted cells could apparently improve the therapeutic efficacy.

A preliminary trial indicated that the replanting obstacle of watermelon could be mitigated by the addition of the endophytic fungus Ceratobasidium stevensii B6 to the soil. The mechanism by which this treatment reduced the obstacles to continuous cropping was not clear, although the phenolic acids secreted by watermelon are a known problem. Consequently, we investigated the degradation of phenolic acids by C. stevensii, using 4-hydroxybenzoic acid (4-HBA) as a model. When the concentration of 4-HBA rose to 500 mg/L, it completely inhibited the germination of watermelon seeds. We therefore investigated the optimal conditions for 4-HBA degradation. When active C. stevensii broth was inoculated into degradation culture broth at a density of 5% (v/v), the 4-HBA concentration decreased to a level below the level of detection after 6 days. C. stevensii could also degrade 4-HBA when it was used as a sole carbon source. Glucose, sucrose, starch, and fructose stimulated the degradation of 4-HBA. High concentrations of glucose enhanced 4-HBA degradation. The optimal conditions for the degradation of 4-HBA by C. stevensii were 28°C, initial pH 5.5, and a shaking speed of 150 rpm. The addition of 500 mg/kg of 4-HBA to dried soil lasted for 2 months, followed by addition of C. stevensii which reduced the concentration of 4-HBA in soil below the level of detection after 7 days. Watermelon seedlings cultured in treated soil had a significantly increased number of stems and greater leaf length compared to controls. Therefore, C. stevensii has great potential in effectively lessening the obstacles to watermelon continuous cropping caused by 4-HBA accumulation. Key words: Ceratobasidum stevensii, 4-hydroxybenzoic acid, watermelon, continuous cropping obstacles, degradation.

Background aims Tissue inhibitor of metalloproteinases-1 (TIMP-1) plays an important role in the development of pulmonary arterial hypertension. However, the molecular regulatory mechanisms of TIMP-1 in the pulmonary arteries are not fully understood, especially in human pulmonary arterial smooth muscle cells (HPASMCs). We investigated the signaling pathway involved in the regulation of TIMP-1 in HPASMCs induced by transforming growth factor (TGF)-β1. Methods Cultured HPASMCs were incubated with different concentrations of TGF-β1 (0–40 ng/mL) for 24 h or with 10 ng/mL TGF-β1 for different times (1–48 h). Results Western blot, real-time polymerase chain reaction and enzyme-linked immunosorbent assay analyses showed that TGF-β1 enhanced the expression and secretion of TIMP-1 in a time-dependent and dose-dependent fashion. TGF-β1 could phosphorylate two of the three mitogen-activated protein kinases—extracellular signal-regulated kinase 1/2 (ERK1/2) and p38, but not c-Jun NH2-terminal kinase. Of these kinases, only the inhibition of ERK1/2 by U0126, which was a specific inhibitor of mitogen-activated protein kinase/ERK1/2, effectively blocked the TGF-β1-induced expression of TIMP-1. Mithramycin, an inhibitor of Sp1 transcription factor, also significantly inhibited the expression of TIMP-1. Additionally, electrophoretic mobility shift assay showed that TGF-β1 could up-regulate the DNA-binding activity of Sp1 and that U0126 and mithramycin could effectively inhibit these events. Conclusions TGF-β1 could stimulate the expression and secretion of TIMP-1 in HPASMCs in a time-dependent and dose-dependent fashion, and ERK1/2 and Sp1 signaling pathways might be involved in these activities.

A growing body of evidence in animal models and clinical studies supports the concept that endothelial progenitor cell (EPC)-mediated therapy ameliorates pulmonary arterial hypertension (PAH) and thus may represent a novel approach to treat it. Conversely, several experimental findings suggest that EPCs may be involved in PAH pathogenesis and disease progression. These discrepant results confuse the application of EPC transplantation as an effective treatment strategy for PAH. To improve the study of EPC transplantation in PAH therapy, it is high time that we resolve this dilemma. In this review, we examine the pathobiological changes of PAH, the characteristics of EPCs, and the underlying mechanisms of EPC effects on PAH.

Pulmonary arterial hypertension (PAH) is a fatal disease characterized by a progressive increase in pulmonary vascular resistance and vascular remodeling leading to right heart failure and early death. The pathology of PAH is associated with endothelium dysfunction and vascular remodeling in pulmonary arteries. In diseased pulmonary arteries, the balance between matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) is broken down. In this process, TIMP are up-regulated, which inhibits MMP, promotes extracellular matrix (ECM) deposition and finally leads to vascular remodeling. So, what would happen to PAH if the expression of TIMP was down-regulated in diseased pulmonary vessels? We hypothesize that the attenuation of TIMP at the advanced stage of PAH might reverse severe PAH, via ameliorating vascular remodeling and endothelium repair.

Background aims Cell labeling with superparamagnetic iron oxide (SPIO) nanoparticles enables non-invasive tracking of transplanted cells. The aim of this study was to investigate whether SPIO nanoparticles have an effect on endothelial progenitor cell (EPC) functional activity and the feasibility of a protocol for labeling swine- and rat-origin EPC using SPIO nanoparticles at an optimized low dosage. Methods EPC were isolated from the peripheral blood of swine and bone marrow of rat and characterized. After ex vivo cultivation, EPC were labeled with SPIO nanoparticles (to make a series of final concentrations, 50, 100, 200 and 400μg/mL) or vehicle control. We also investigated the long-term effects of 200μg/mL SPIO nanoparticles on EPC (4, 8, 12 and 16 days after labeling). The labeling efficiency was tested through Prussian blue (PB) staining and the intracellular iron uptake was also measured quantitatively and confirmed. EPC proliferation and migration were determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and transwell chamber assay, respectively. An EPC adhesion assay was performed by replating the cells on fibronectin-coated dishes and then counting the adherent cells. EPC apoptosis was evaluated using an Annexin V–FITC apoptosis kit. Results SPIO nanoparticles impaired EPC migration and promoted EPC adhesion. EPC proliferation and apoptosis were not affected. SPIO nanoparticles could label EPC efficiently at 200μg/mL overnight without significantly affecting EPC functional activity. Conclusions SPIO nanoparticles impaired the EPC migration ability and promoted the EPC adhesion capacity. EPC could be labeled efficiently at an appropriate concentration (200μg/mL) without significantly affecting their functional activity.

Previous studies have underlined the importance of endothelial dysfunction and microvascular occlusion in the pathogenesis of pulmonary artery hypertension (PAH). Since the endothelial progenitor cells (EPCs) are involved in maintaining endothelial homeostasis, we observed the change of peripheral EPCs in canines before and after PAH onset. PAH was induced by intra-pulmonary artery injection of dehydromonocrotaline (DHMC) in nine beagles. Before and 48 h and 6 weeks after DHMC injection, 40 ml peripheral blood was obtained from the femoral vein. Circulating EPCs were identified as CD133 + KDR + cells and numerated by fluorescence-activated cell sorter; the EPCs functional capacity was determined by in vitro tubule-forming assay. The senescence of EPCs was determined by beta-galactosidase staining. At each time point, 2 ml blood from femoral artery was obtained for arterial oxygen pressure (PaO(2)). Forty-eight hours after DHMC injection, treated beagles suffered from hypoxemia; however, both the number and the tubule-forming capacity of EPCs were transiently raised. Six weeks later, PAH was confirmed by obviously high mean pulmonary arterial pressure (20.2 +/- 1.64 vs. 11.3 +/- 2.0 mmHg, p0.05) and low PaO(2) (69.30 +/- 9.15 vs. 95.94 +/- 1.43 mmHg, p0.01) in beagles after DHMC treatment, and their EPCs exhibited a predominant decrease in either the number (206.1 +/- 26.8 vs. 632.8 +/- 42.8 cells/ml blood, p0.01) or the tubule-forming capacity (21.1 +/- 2.8 vs. 11.2 +/- 2.8 tubules/x200 field, p0.01). Additionally, senescence-associated beta-galactosidase-positive EPCs were significantly increased. Our data suggested that, after the acute stage of DHMC injury to pulmonary vessels, the EPCs from PAH beagles suffered from exhaustion and senescence.

Endothelial apoptosis underlies the pathophysiology of pulmonary arterial hypertension (PAH). Some factors/cytokines released by endothelial progenitor cells (EPC) have been revealed as potent inhibitors of apoptosis. The aim of this study was to investigate the effects of EPC on pulmonary microvascular endothelial cell (PMVEC) survival with the PAH condition.PMVEC apoptosis was induced by high shear stress (HSS) with serum starvation or pro-inflammatory factors in an artificial capillary system. EPC were delivered into monocrotaline-induced PAH nude rats.PMVEC apoptosis under HSS and serum starvation conditions was significantly inhibited by EPC conditioned medium (CM). It was attenuated by vascular endothelial growth factor (VEGF)-A or -B blocking. EPC CM promoted PMVEC proliferation, which was weakened by VEGF-A or interleukin (IL)-8 blocking. The EPC CM caused less apoptosis of PMVEC induced by HSS plus pro-inflammatory factors. The anti-apoptotic effect of EPC CM was attenuated by blockade of either vascular endothelial growth factor receptor (VEGFR)-1 or -2. However, the pro-proliferating effect appeared to be weakened only by VEGFR-2 blocking. Both Erk1/2 and Akt phosphorylation were enhanced by EPC CM. VEGFR-2 blockage led to significant inhibition of Erk1/2 and Akt activation; VEGFR-1 blockage only of Erk1/2 activation. Human-origin VEGF co-localized with incorporated EPC in small pulmonary arterioles, and EPC transplantation resulted in down-regulation of caspase-3 expression.The VEGF-A/B-VEGFR-1/2-Erk1/2 signal pathway took major responsibility for the anti-apoptotic effects of EPC on PMVEC, and VEGF-A-VEGFR-2-Akt for pro-proliferating effects. Growth factors, secreted in a paracrine manner by transplanted EPC, inhibited cell apoptosis in PAH lung.

Resveratrol (3,5,4'-trihydroxystilbene) is a naturally occurring compound shown to decrease the incidence of thromboembolic disease. Although considerable data are available as to the inhibitory effect of resveratrol on the platelet aggregation and thrombopoiesis in human, its underlying mechanism, at the cellular level, has not been rigorously studied. In this experiment, we studied the effect of resveratrol and 1-[6-[[17-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione, a phospholipase C inhibitor (U-73122) on the thromboxane A2 receptor agonist (9,11-dideoxy-11 alpha,9 alpha-epoxymethanoprostaglandin F(2 alpha), U46619)-induced platelet aggregation, platelet P-selectin expression, and the activity of phospho-phospholipase C beta 3 (P-PLC beta 3) and total-phospholipase C beta 3 (T-PLC beta 3), which play key roles in the signal transduction system of platelet in human. It was found that resveratrol blocked platelet aggregation and platelet P-selectin expression induced by U46619 in a concentration-dependent manner. U-73122 and resveratrol had additive effect in inhibiting platelet aggregation and platelet P-selectin expression. Resveratrol (final concentration was 50 microM) could reduce the ratio of P-PLC beta 3 to T-PLC beta 3. Taken together, these results show that resveratrol suppresses U46619-induced platelet aggregation and P-selectin expression partly through the decrease of the activity of phospholipase C beta of platelets.

Rhubarb, used as a traditional Chinese medicine for centuries, offers therapeutic potential for cardiovascular and other diseases. Emodin, extracted from the root extract of rhubarb has sparked increasing interest for therapeutic application. The main objective was to study the effect of emodin on cultured vascular smooth muscle cells (VSMCs) proliferation induced by angiotensin II (Ang II) and the expression of proto-oncogene c-myc. VSMCs were cultured by the explant method, then incubated for 24, 48 and 72 h with emodin (10–80 µm) and Ang II, or were left untreated (control). Cell proliferation was measured by MTT assay and immunohistochemical staining for proliferating cell nuclear antigen (PCNA), respectively. The expression of c-myc was measured by immunohistochemical staining and image analysis technique. Ang II increased the cell proliferation compared with the control group (p < 0.01). The expression of PCNA and c-myc was increased compared with the control group (p < 0.01). After pretreatment with emodin, the above indexes were obviously reduced compared with the Ang II group (p < 0.01). These findings suggested that emodin inhibited VSMCs proliferation induced by Ang II. Inhibition of the expression of c-myc might be correlated with the inhibitory effects. Copyright © 2007 John Wiley & Sons, Ltd.

Objective. Molecular mechanisms of nephrosclerosis caused by hypertension are not well known. Understanding changes in renal protein expression in hypertension may provide further information on how hypertension caused renal injury. Methods and Results. In the present study, we showed the protein expression profiles of the kidney in spontaneously hypertensive rats and Wistar-Kyoto rats using two-dimensional gel electrophoresis (2-DE). Differentially expressed protein spots were excised, underwent in-gel tryptic digestion, and were analyzed by MALDI-TOF MS. Eleven spots were identified. Of these identified spots, four spots were newly appeared, five spots up-regulated, and two spots down-regulated. The identified spots were mainly involved in energy metabolism, lipid transferring between membranes, and cell proliferation. Conclusions. The expression of many proteins have changed significantly in the kidney of spontaneously hypertensive rat. NADP + -dependent isocitrate dehydrogenase may be a candidate for further investigation of pathophysiological mechanisms of renal injury in hypertension.

Aim This study was to investigate the effect of serum from rats treated orally with GUD on vascular smooth muscle cells (VSMCs) proliferation in vitro. Methods Cell proliferation was measured by Methyl thiazolyl tetrazolium (MTT) assay. Expression of proliferating cell nuclear antigen (PCNA) and proto-oncogene c-myc were measured by immunochemical staining and image analysis. Griess reagent were used to detect nitric oxide (NO) level. Endothelin-1 (ET-1) level was measured by radioimmunoassay. Results GUD serum (2.5%-10%) inhibited VSMCs proliferation in a dose and time-dependent manner. GUD serum inhibited the expression of PCNA and c-myc. Moreover, GUD serum increased nitric oxide (NO), and decreased Endothelin-1 (ET-1) level in culture medium. Conclusion GUD serum exhibited directly inhibitory effect in VSMCs proliferation. Inhibiting the expression of PCNA and c-myc, increasing NO level and decreasing ET-1 level might be associated with the antiproliferative effect.

Magnetic abrasive finishing (MAF) is a kind of method for polishing the surfaces and the edges. The investigation for the technique of MAF and the development of the ferromagnetic poles lay a theoretical foundation for developing a new method for finishing the curved surfaces automatically under the numerical control. In the paper, the performance parameters of the developed magneto poles, which are used for finishing the plane surfaces and the curved ones, have been tested. The curvature of the finished surface, the sloping angle of the machined surface and the rotation speed of the poles, which affect the surface roughness, are studied theoretically. What mentioned above supply references to the practical uses of the MAF, especially in the mould manufacturing.

Objectives The goal of this study was to investigate the feasibility, safety, and initial clinical outcome of intravenous infusion of autologous endothelial progenitor cells (EPCs) in patients with idiopathic pulmonary arterial hypertension (IPAH). Background Experimental data suggest that transplantation of EPCs attenuates monocrotaline-induced pulmonary hypertension in rats and dogs. In addition, clinical studies suggest that autologous progenitor cell transplantation is feasible and safe in patients with ischemic diseases. Methods We conducted a prospective, randomized trial comparing the effects of EPC transplantation plus conventional therapy with those of conventional therapy alone in patients with IPAH. The primary end point was change in the 6-min walk distance using a standardized protocol. The secondary end points were changes in hemodynamic variables as assessed by right heart catheterization. Results After 12 weeks of follow-up, the mean distance walked in 6 min increased by 48.2 m in the cell infusion group (from 263 ± 42 m to 312 ± 34 m), and an increase of 5.7 m occurred in the conventional therapy group (from 264 ± 42 m to 270 ± 44 m). The mean difference between the 2 groups was 42.5 m (95% confidence interval 28.7 to 56.3 m, p Conclusions This preliminary study showed that intravenous infusion of autologous EPCs seemed to be feasible and safe, and might have beneficial effects on exercise capacity and pulmonary hemodynamics in patients with IPAH. (Safety and Efficacy Study of Transplantation of EPCs to Treat Idiopathic Pulmonary Arterial Hypertension; http://www.clinicaltrials.gov/ct/show/NCT00257413?order=1; NCT00257413).

Idiopathic pulmonary arterial hypertension (IPAH) is a rare disease of unknown etiology. The exact pathogenesis of pulmonary arterial hypertension is still not well known. In the past decades, many protein molecules have been found to be involved in the development of IPAH. With proteomic techniques, profiling of human plasma proteome becomes more feasible in searching for disease-related markers. In present study, we showed the protein expression profiles of the serum of IPAH and healthy controls after depleting a few high-abundant proteins in serum. Thirteen spots had changed significantly in IPAH compared with healthy controls and were identified by LC-MS/MS. Alpha-1-antitrypsin and vitronectin were down-regulated in IPAH and may be valuable candidates for further explorations of their roles in the development of IPAH.

Primary pulmonary hypertension (PPH) is a fatal cardiovascular disease characterized by increased pulmonary vascular resistance and progressive right heart failure. It is associated with a very high morbidity and mortality rate. The therapeutic effects of current pharmacological management of PPH are limited. Recent studies have demonstrated that endothelial dysfunction and cell loss play a critical role in the pathogenesis of PPH. Emerging evidence also shows that circulating endothelial progenitor cells instigate new vessel formation via vasculogenesis and revascularization, and provide ongoing endothelial repair by homing to site of endothelial damage. We hypothesized that autologous endothelial progenitor cells transplantation may be a feasible adjunctive therapeutic option for PPH.

String cosmological models with bulk viscosity are investigated in Kantowski-Sachs space-time. To obtain a determinate solution, it is assumed that the coefficient of bulk viscosity is a power function of the scalar of expansion ζ = kθm and the scalar of expansion is proportional to the shear scalar θ ∝ σ, which leads to a relation between metric potentials R = AS n . The physical and geometrical aspects of the model are also discussed. It is shown that the bulk viscosity has significant influence on the evolution of the universe. There is a ‘big bang’ start in the model when m ≤ 1 but there is no ‘big bang’ start when m > 1.

Recently, some studies have shown that nicotine increased neovascularization, which involves endothelial progenitor cells (EPCs). The effects of nicotine on EPCs are still unclear at present. Therefore, the authors investigated whether nicotine had influences on EPC number and activity. The EPCs were stimulated with nicotine (to make a series of final concentrations: 10(-12) mol/L, 10(-10) mol/L, 10(-8) mol/L, 10(-6) mol/L, 10(-4) mol/L) or vehicle control for the respective time points(12, 18, 24, 32, and 48 hours). The EPCs were characterized as adherent cells double positive for DiLDL uptake and lectin binding by direct fluorescent staining under a laser-scanning confocal microscope. They were further documented by demonstrating the expression of KDR, VEGFR-2, and AC133 with flow cytometry. The EPC proliferation, migration, and in vitro vasculogenesis activity were assayed with the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay; the modified Boyden chamber assay; and the in vitro vasculogenesis kit, respectively. The EPC adhesion assay was performed by replating those on fibronectin-coated dishes and then counting the adherent cells. As a result, nicotine dose dependently increased the EPC number and the proliferative, migratory, adhesive, and in vitro vasculogenesis capacity at nicotine concentrations of 10(-12) to 10(-8) mol/L. The peak effects on EPCs were observed at concentrations of nicotine 10(-8) mol/L, similar to those in the blood of smokers. In addition, nicotine (10(-8) mol/L) time dependently increased the EPC number and activity. However, cytotoxicity was seen at higher nicotine concentrations (> 10(-6) mol/L). In conclusion, nicotine had complex effects on EPCs: nicotine might induce the augmentation of EPCs with enhanced functional activity at relatively low concentrations. However, cytotoxicity was seen at higher nicotine concentrations.

Some locally rotationally symmetric (LRS) Bianchi type I cosmological models for a cloud string with bulk viscosity and magnetic field are presented. Where an equation of state ρ = kλ and a relation between metric potential R = ASn are considered. The solution describes a shearing and nonrotating model with a big bang start. In the absence of magnetic field it reduces to a string model with bulk viscosity, where the relation between the coefficient of bulk viscosity and energy density is ζ ∝ ρ1/2. After choosing k = \(k = \frac{{1 + n}}{{1 - n}}\), it further reduces to a string model without viscosity and magnetic field.

Endothelial dysfunction is thought to play a crucial role in the pathogenesis of atherosclerosis induced by ox-LDL. Recently, a variety of evidence suggested that endothelial progenitor cells (EPCs) participated in neovascularization and reendothelialization. However, effects of ox-LDL on EPCs number and activity are ill understood.Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. After 7 days culture, attached cells were stimulated with ox-LDL (to make a series of final concentrations: 25 microg/mL, 50 microg/mL, 100 microg/mL, 200 microg/mL), native LDL (100 microg/mL) or vehicle control for the respective time points (6 h, 12 h, 24 h and 48 h). EPCs were characterized as adherent cells double positive for DiLDL-uptake and lectin binding by direct fluorescent staining under a laser scanning confocal microscope. EPCs were further documented by demonstrating the expression of KDR, VEGFR-2 and AC133 with flow cytometry. Proliferation, migration and in vitro vasculogenesis activity of EPCs were assayed by MTT assay, modified Boyden chamber assay and in vitro vasculogenesis kit, respectively. EPCs adhesion assay was performed by replating those on fibronectin-coated dishes, and then counting adherent cells.Incubation of isolated human EPCs with ox-LDL decreased the number of EPCs in concentration-dependent manner, maximum at 200 microg/mL (approximately 70% reduction, P0.001). In time-course experiments performed with an ox-LDL concentration of 100 microg/mL, decrease of EPCs number became apparent at 12 hours and reached the maximum at 24 hours (approximately 50% reduction, P0.01). In addition, ox-LDL dose and time dependently impaired EPC proliferative, migratory, adhesive and in vitro vasculogenesis capacity.The results of the present study defined a novel mechanism of action of ox-LDL: the reduction of EPCs with decreased functional activity.

A 55-year-old man was admitted to our hospital because of chest distress, associated with activity. Two-dimensional echocardiography (2DE) demonstrated a suspected trabeculation versus false tendon of the left ventricular apex cordis but not meeting the diagnostic criteria of noncompaction of the ventricular myocardium (NVM). Threedimensional echocardiography (3DE) revealed more prominent trabeculations and deeper intertrabecular recesses of the left ventricular apex, which were consistent with the diagnostic criteria of NVM. In contrast to 2DE, 3DE provides wide, pyramid-shaped datasets that encompass the entire left ventricle. (Neth Heart J 2009;17:208-10.).

To analyse the alterations of protein expression in the kidney of spontaneously hypertensive rat with losartan.The proteins of the kidney were isolated by two-dimensional gel electrophoresis. The protein spots with significant changes were selected for further identification by LC-MS/MS.The number of average protein spots of two groups was 570 +/- 48 and 686 +/- 30 respectively. Compared with the SHR, 13 spots had changed significantly after treated with losartan. There were 5 protein spots detected only in SHR group, while 4 up-regulated and 4 down-regulated protein spots were detected in SHR-L group. These differentially expressed proteins were detected by mass spectrometry. 7 spots were identified. There were Heat shock protein (Hsp), Tubulin alpha-1 chain, Transthyretin precursor, Liver regeneration-related protein LRRG03, Ezrin-radixin-moesin binding phosphoprotein 50, Phosphoglycerate kinase 1 and Anionic trypsin I precursor.The different protein spots expression may play important roles in Losartan's effective protection to hypertension rats renal tissue.

With the development of immunology, the role of immune inflammation in idiopathic pulmonary arterial hypertension (IPAH) has attracted interest. Recently, it was discovered that dendritic cells, which are key players in immune inflammation, are implicated in the pathogenesis of IPAH. To elucidate the role of dendritic cells in human IPAH, we compared the changes in the number and immunological function of monocyte-derived dendritic cells (MoDCs) from the peripheral blood of patients with IPAH and healthy controls. The numbers of MoDC subsets (including plasmacytoid dendritic cells (pDCs) and myeloid dendritic cells (mDCs)) in circulating peripheral blood mononuclear cells (PBMCs) was analyzed by flow cytometry, and the concentrations of interleukin (IL)-12, IL-10, and tumor necrosis factor-alpha were measured by enzyme-linked immunosorbent serologic assay kits. The morphology, phenotypic expression, and the ability to stimulate T cell proliferation of MoDCs, cultured from PBMCs in vitro with granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-4, was analyzed by microscopy, flow cytometry, and MTT assay. The results of the study are as follows: (1) The number of circulating mDCs was lower in IPAH patients than in controls (0.07 ± 0.01% to 0.14 ± 0.02%; p

A 24-year-old woman admitted with mild chest distress associated with activity without chest complaint for twenty days. Two orifices were visible at the level of the mitral valve with a transthoracic short-axis view of the two-dimensional and three-dimensional echocardiography. The left ventricle was mildly dilatated and the left ventricular wall was thickened, especially at the apex and anterolateral wall, and appeared sponge-like. There were numerous, excessively prominent trabeculations associated with intertrabecular recesses. Although the coexistence of NVM and DOMV could be a coincidence, we believe that both defects were probably caused by a developmental arrest of the left ventricular myocardium in the present case.

To determine the quantitive and functional changes of circulating endothelial progenitor cells (EPCs) in dogs with dehydromonocrotaline-induced pulmonary artery hypertension (PAH).Dehydromonocrotaline was injected into the canine right ventricle to induce pulmonary hypertension. Circulating EPCs were enumerated as AC+(113), KDR+ cells by fluorescence-activated cell sorter using counting beads, and the number and activity of EPCs after in vitro expansion were determined by acLDL uptake/lectin staining assay and in vitro tubule forming assay.Nine of the 10 beagles survived after dehydromonocrotaline injection. Six weeks later, mean pulmonary artery pressure increased from (11.3 +/- 2.0) mm Hg (1 mm Hg = 0.133 kPa) to (20.2 +/- 1.6) mm Hg (t =10.307, P0.01), and the AC+(133) and KDR+ cells decreased from (632.8 +/- 42.8) cells/ml to (206.1 +/- 26.8) cells/ml (t = 25.361, P0.01). UEA- I and DiLDL positive cells deceased from (41 +/- 6) EPCs/ x 200 field to (22 +/- 6) EPCs/ x 200 field (t = 6.510, P0.01). In addition, in vasculogenesis assay, PAH EPCs formed less quantitative (11.2 +/- 2.8 vs 21.1 +/- 2.8 tubules/ x 200 field, respectively, t = 7. 583, P0. 01) and less qualitive tubules than baseline EPCs.The number and vessel forming ability of EPCs are impaired in this canine model of dehydromonocrotaline-induced pulmonary hypertension.

To observe the effect and mechanism of resveratrol on cardiac fibroblast (cFs) proliferation induced by angiotensin II (Ang II).The in vitro cFs proliferation model was established by stimulating cultured cFs of new born rats with Ang II by differential attachment method. Cell proliferation was measured by MTT assay, and the effect of resveratrol, L-NAME and ODQ on cell proliferation were observed respectively. Besides, the hypertrophic response of cFs was estimated by measuring expressions of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) mRNA, with the levels of ANP and BNP in culture medium determined by radioimmunoassay and ELISA respectively; and their mRNA expressions determined by reverse transcription polymerase chain reaction (RT-PCR). Level of nitric oxide (NO) in the culture medium was measured by Griess reagent; nitric oxide synthase (NOS) level by chemical colorimetric method; and cGMP by radioimmunoassay.Resveratrol at the dose of 25-100 micromol/L inhibited cFs proliferation in a time and dose dependent manner, which could be partially blocked by pretreatment with L-NAME or ODQ. NO and cGMP levels increased, ANP, BNP levels and their mRNA expression lowered after resveratrol treatment.Resveratrol in a definite concentration range could inhibit cFs proliferation and hypertrophic response induced by Ang II, up-regulating the signal pathway of NO and cGMP might be one of the acting paths of the inhibitory effects.

Inappropriate platelet activation is the key point of thrombogenesis. The aim of the present study was to investigate the effects of resveratrol (RESV), a compound extracted from the Chinese medicinal herb Polygonum cuspidatum sieb et Zucc, on the platelet activation induced by adenosine diphosphate (ADP) and its possible mechanism. The percentage of platelet aggregation and surface P-selectin-positive platelets, and the activity of protein kinase C (PKC) of platelet were observed with platelet aggregometer, flow cytometry and phosphorimaging system, respectively. RESV at 25, 50 and 100 μM showed anti-platelet aggregation and inhibition of surface P-selectin-positive platelets in a concentration-dependent manner. RESV (50 μM) inhibited the activity of PKC in the membrane fraction of platelets and decreased the percentage of membrane associated PKC activity in total PKC activity. Moreover, DL-erythro-1,3-Dihydroxy-2-aminooctadecane, an elective protein kinase C inhibitor (PKCI), and RESV had additive effects of inhibiting the percentage of platelet aggregation and surface P-selectin-positive platelets. It is suggested that RESV may inhibit platelet aggregation, the percentage of surface P-selectin-positive platelets and subsequent thrombus formation. The mechanisms may be partly relative to the decrease of the activity of PKC of platelets.

To investigate the effects of emodin on the proliferation of cultured rat vascular smooth muscle cell (VSMC) induced by angiotensin II.VSMCs were cultured by explant method. Cell proliferation model was established by stimulation with Ang II. Cell proliferation was measured by MTT assay to observe the effects of emodin (10, 20, 40 and 80 micromol x L(-1)) and N(G)-nitro-L-arginine methyl ester (L-NAME, 100 micromol x L(-1)) on VSMC proliferation induced by Ang II. The expression of PCNA was measured by immunohistochemical staining. Nitric oxide (NO) level was measured by Griess reagent. Nitric oxide synthase (NOS) and inducible nitric oxide synthase (iNOS) levels were detected by chemical colorimetric method. mRNA expression of iNOS was measured by reverse transcription polymerase chain reaction (RT-PCR).Emodin at the doses range from 10 to 80 mol x L(-1) inhibited cell proliferation in a dose and time-dependent manner. The inhibitory effects were partly blocked by 100 mol x L(-1) of L-NAME. Emodin markedly decreased the expression of PCNA in VSMC, increased NO, NOS and iNOS levels, and increased iNOS mRNA expression in VSMC.Emodin could inhibite VSMCs proliferation induced by Ang II. Inhibiting the expression of PCNA, increasing the NO secretion and upregulating the iNOS gene expression might be associated with the inhibitory effects.

Endothelial progenitor cells (EPCs) play an important role in both reendothelialization and neovascularization. Ex vivo expansion of EPCs might be useful for potential clinical cell therapy of ischemic diseases. However, ex vivo cultivation of EPCs leads to rapid onset of EPCs senescence, thereby severely limiting the proliferative capacity and clonal expansion potential. Therefore, we investigated whether puerarin might be able to prevent senescence of EPCs. EPCs were isolated from peripheral blood and characterized. After ex vivo cultivation, EPCs became senescent as determined by acidic beta-galactosidase staining. Puerarin dose dependently prevented the onset of EPCs senescence in culture. Moreover, puerarin increased proliferation of EPCs as assessed by BrdU incorporation assay and colony-forming capacity. To get further insights into the underlying mechanisms of these effects induced by puerarin, we measured telomerase activity and determined the phosphorylation of serine/threonine protein kinase Akt by using western blot. Puerarin significantly increased telomerase activity and phosphorylation of Akt, a downstream effector of phosphoinositide 3-kinase (PI-3K). Moreover, pretreatment with PI-3K blockers, either wortmannin or LY294002, significantly attenuated the puerarin puerarin-induced telomerase activity. Taken together, the results of the present study indicated that puerarin delayed the onset of EPCs senescence, which may be related to the activation of telomerase through the PI-3K/Akt pathway. The inhibition of EPCs senescence by puerarin in vitro may improve the functional activity of EPCs in a way that is important for potential cell therapy.

To investigate the expression of angiotensin converting enzyme 2 (ACE2) and the changes treated with angiotensin converting enzyme inhibitor (ACEI), and its signal transduction pathway.Atrial tissues were obtained from 47 patients with RHD undergoing cardiac surgery. The mRNA of ACE2 and ACE were semi-qualified by RT-PCR and normalized to the gene beta-actin. Western blot analysis was employed to examine the expressions of ACE2, ACE, ERK1/2 and phosphorylated ERK (pERK1/2). The atrial tissue angiotensin II (Ang II) content was determined by radioimmunoassay detection.The expression of ACE2 was significantly decreased (P0.05), the expression of ACE and pERK1/2 were significantly increased (P0.05), and the level of atrial tissue Ang II was significantly increased in patients with chronic atrial fibrillation group (CAF) compared with sinus rhythm group (SR) (P0.05). Compared with CAF patients treated without ACEI, the expression of ACE2 significantly increased (P0.01), and the relative activity of ERK1/2 significantly decreased (P0.05), whereas the expression of ACE and the level of atrial tissue Ang II remained unchanged in CAF patients treated with ACEI.The study suggested that the dysequilibrium of ACE/ACE2 might play an important role in the process of atrial fibrillation, which may be related to the activation of ERK1/2 pathway. The clinical effect of long-term treatment of ACEI maybe associated with elevated ACE2 expression but not ACE expression.