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In this Letter, the new classes of non-paraxial autofocusing beams are introduced for the first time, to the best of our knowledge. We investigate both numerically and experimentally non-paraxial circular Mathieu and Weber autofocusing beams based on the solutions of the Helmholtz equation in elliptical and parabolic coordinates, respectively. The results show that such beams can significantly shorten the focus distance, and eliminate the intense oscillation effectively after the focusing point. The focal length and the peak intensity can be controlled by tunable parameters. In addition, we further experimentally realize their application of such beams in optical trapping.

Exopolysaccharide (EPS) isolated from Lactobacillus helveticus SNA12 were purified, and one fraction (SNA12-EPS) was obtained. The structure of SNA12-EPS was proposed using Fourier-transform infrared spectroscopy, gas chromatography-mass spectrometry, and nuclear magnetic resonance. Results showed that SNA12-EPS was rich in galactose and glucose with the molar ratios of 2.1:1.0, and SNA12-EPS possessed the repeat units of →3)-β-D-Glcp-(1→3)-β-D-Glcp-(1→4)-β-D-Galp-(1→ with an average molecular weight of 3.81 × 10

Cereal grains and oils contain various functional ingredients, such as amino acids, peptides, polyphenols, dietary fiber, linoleic acid, and natural pigments. Their biological activities are of great significance. Benefiting from its robust genetic function and simple cultivation, Caenorhabditis elegans, as one of the most important model organisms has been widely used to screen antiaging substances and investigate the underlying molecular mechanisms. In this paper, the recent advances in the use of C. elegans in antiaging research into active substances from cereals and oils will be assessed, and their potential signal transduction mechanisms will be systematically reviewed. This research aims to provide a theoretical reference for the use of active substances from cereals and oils to prevent and delay aging and aging-associated diseases.

Objective: Spatial and temporal ventilation distributions in patients with acute respiratory failure during high flow nasal cannula (HFNC) therapy were previously studied with electrical impedance tomography (EIT). The aim of the study was to explore the possibility of predicting HFNC failure based on various EIT-derived parameters.Methods: High flow nasal cannula failure was defined reintubation within 48 h after HFNC. EIT was performed with the patients spontaneously breathing in the supine position at the start of HFNC. EIT-based indices (comprising the global inhomogeneity index, center of ventilation, ventilation delay, rapid shallow breathing index, minute volume, and inspiration to expiration time) were explored and evaluated at three time points (prior to HFNC, T1; 30 min after HFNC started, T2; and 1 h after, T3).Results: A total of 46 subjects were included in the final analysis. Eleven subjects had failed HFNC. The time to failure was 27.8 ± 12.4 h. The ROX index (defined as SpO2/FiO2/respiratory rate) for HFNC success patients was 8.3 ± 2.7 and for HFNC failure patients, 6.2 ± 1.8 (p = 0.23). None of the investigated EIT-based parameters showed significant differences between subjects with HFNC failure and success. Further subgroup analysis indicated that a significant difference in ventilation inhomogeneity was found between ARDS and non-ARDS [0.54 (0.37) vs. 0.46 (0.28) as evaluated with GI, p < 0.01]. Ventilation homogeneity significantly improved in ARDS after 60-min HFNC treatment [0.59 (0.20) vs 0.57 (0.19), T1 vs. T3, p < 0.05].Conclusion: Spatial and temporal ventilation distributions were slightly but insignificantly different between the HFNC success and failure groups. HFNC failure could not be predicted by changes in EIT temporal and spatial indexes of ventilation distribution within the first hour. Further studies are required to predict the outcomes of HFNC.

Magnetic resonance spectroscopy (MRS) is a unique non-invasive method for detecting cardiac metabolic changes. However, MRS in cardiac diagnosis is limited due to insensitivity and low efficiency. Taurine (Tau) is the most abundant free amino acid in the myocardium. We hypothesized that Tau levels may indicate myocardial ischemia and early infarction. Sprague-Dawley rats were divided into seven groups according to different time points during the course of myocardial ischemia, which was induced by left anterior descending coronary artery ligation. Infarcted myocardial tissue was obtained for high-resolution magic angle spinning (1)H nuclear magnetic resonance (NMR) analysis. Results were validated via high-performance liquid chromatography. The Tau levels in the ischemic myocardial tissue were reduced significantly within 5 min compared with those in the control group (relative ratio from 20.27±6.48 to 8.81±0.04, P0.05) and were maintained for 6 h post-ischemia. Tau levels declined more markedly (56.5%) than creatine levels (48.5%) at 5 min after ligation. This suggests that Tau may have potential as an indicator in the early detection of myocardial ischemia by (1)H MRS.

Objective— Comparative studies are lacking that show the effects of different microenvironments on the activity of engrafted stem cells after myocardial infarction (MI). Here, we analyzed the temporal and spatial variations of angiogenesis, collateralization, and the expression of Akt-related signals after MI to test whether the effects of endothelial progenitor cells (EPCs) were different. Methods and Results— After the induction of MI, pigs were selected that did not develop a collateral coronary circulation (R0) or developed a significant collateral coronary circulation (R2). Both sets were allocated randomly to 4 groups: phosphate-buffered saline (intramyocardial injection of phosphate-buffered saline), EPC transplantation, LY294002 (intramyocardial injection of an Akt inhibitor), and EPCs plus LY294002. Infarcted porcine hearts at different time points and under different collateralized conditions exhibited a variety of vascular microenvironments. At 14 days post-MI, angiogenesis and the expression of Akt-mediated angiogenic cytokines predominated in R2 porcine hearts. When grafted into this microenvironment, EPCs induced the greatest effects in impeding the development of heart failure, preserving left ventricular function and dimensions, and inhibiting infarct expansion. LY294002 significantly reduced these effects. Conclusion— These findings suggest that the microenvironment that coexists with collateralization and Akt-mediated angiogenesis appears to be more beneficial to cardiac repair induced by EPC therapy than other niches after MI.

Aims Recombinant human neuregulin-1 (rhNRG-1) improves cardiac function in experimental heart failure models, but the underlying mechanism remains largely unknown. In this study, we evaluated whether rhNRG-1 could improve cardiac function via the cardiac myosin light chain kinase/myosin light chain 2 ventricular (cMLCK/MLC-2v) pathway in rats with myocardial infarction (MI). Methods and results Rats with MI were intravenously infused with rhNRG-1 (5 µg/kg/h) for 7 days through osmotic pumps. The mechanism of action of rhNRG-1 was investigated by assaying the non-infarcted myocardium with gene chips. The cMLCK expression, phosphorylated MLC-2v and cardiac function were significantly up-regulated, as assessed by real-time PCR, Western blot and echocardiography, in those animals treated with rhNRG-1. Moreover, the restoration of rhNRG-1-induced sarcomeric organization in serum-free cultured neonatal rat cardiomyocytes with rhNRG-1 was inhibited by cMLCK RNA interference or ML-7, an inhibitor of MLCKs. Adenovirus containing the rat cMLCK coding region was injected into non-infarcted myocardium, and cardiac function was monitored using echocardiography and a haemodynamic machine. The d P /d t and fractional shortening decreasing significantly after MI, and improved by 15.7 and 32.1%, respectively, following local cMLCK application (all P < 0.05). Conclusion Our results suggest that cMLCK is a downstream effector of rhNRG-1 involved in rhNRG-1-induced cardiac function improvement, and that myocardial cMLCK up-regulation can improve cardiac function in rats with MI.

The aim of the study was to evaluate the association between beta-fibrinogen gene -455G/A polymorphism and the plasma fibrinogen level in Chinese patients with different subtypes of coronary heart disease (CHD).We investigated beta-fibrinogen gene -455G/A polymorphism and plasma fibrinogen level in non-CHD control subjects (n = 466) and CHD patients (n = 1,019) including patients with stable angina pectoris (SAP) (n = 674), and acute coronary syndrome (ACS) (n = 345). Increased plasma fibrinogen levels were observed in the CHD groups compared with the control subjects (ACS: 380.92 +/- 92.35 mg/dl, SAP: 352.49 +/- 94.89 mg/dl, control: 311.72 +/- 87.09* mg/dl, *P0.001 vs. ACS and SAP). Individuals with the -455A/A genotype were associated with the highest plasma fibrinogen in the control subjects (P0.001) and patients with SAP (P0.001) but not in patients with ACS (P0.05). Allele frequency and genotype distribution were similar among the three groups (P = 0.314).This study demonstrated that elevated plasma fibrinogen level is related to increased CHD risk. The presence of -455A allele is significantly associated with higher fibrinogen in non-CHD control subjects and SAP patients but not in ACS patients while -455G/A polymorphism is not a risk factor for CHD in the Chinese population.

A variety of adult stem cells have been used to transplant into the infarcted (MI) heart, however, comparative studies are lacking to show more suitable source of cells for transplantation. We have identified a single non-hematopoietic mesenchymal stem cell subpopulation (snMSCs) isolated from human bone marrow and clonally purified, that over 99% of them expressed MSC marker proteins and cardiomyocyte marker proteins when induction in vitro. We also compared the effects of the snMSCs with unpurified MSC (uMSCs), mononuclear cells (BMMNCs), or peripheral blood mononuclear cells (PBMNCs) on myocardial repair after induction of MI in rats. Ninety days later, we observed a better cardiac function assessed by ejection fraction, fraction of shortening and lung wet/dry weight ratios, less remodeling of left ventricle (LV), lower collagen density in the LV, and more vessels in the ischemic wall in the snMSCs transplantation group than in other cell-transplanted groups. Furthermore, the transplanted cells expressing cardiomyocyte specific proteins or vascular endothelial cell marker proteins were more in the snMSCs group than in other ones. We conclude that transplantation with single clonally purified MSCs seems to be more beneficial to the cardiac repair than with other stem cells after MI.

Background Increasing evidence suggests a critical role for mitochondrial aldehyde dehydrogenase 2 ( ALDH 2) in protection against cardiac injuries; however, the downstream cytosolic actions of this enzyme are largely undefined. Methods and Results Proteomic analysis identified a significant downregulation of mitochondrial ALDH 2 in the heart of a rat heart failure model after myocardial infarction. The mechanistic insights underlying ALDH 2 action were elucidated using murine models overexpressing ALDH 2 or its mutant or with the ablation of the ALDH 2 gene ( ALDH 2 knockout) and neonatal cardiomyocytes undergoing altered expression and activity of ALDH 2. Left ventricle dilation and dysfunction and cardiomyocyte death after myocardial infarction were exacerbated in ALDH 2 ‐knockout or ALDH 2 mutant‐overexpressing mice but were significantly attenuated in ALDH 2‐overexpressing mice. Using an anoxia model of cardiomyocytes with deficiency in ALDH 2 activities, we observed prominent cardiomyocyte apoptosis and increased accumulation of the reactive aldehyde 4‐hydroxy‐2‐nonenal (4‐ HNE ). We subsequently examined the impacts of mitochondrial ALDH 2 and 4‐ HNE on the relevant cytosolic protective pathways. Our data documented 4‐ HNE ‐stimulated p53 upregulation via the phosphorylation of JNK , accompanying increased cardiomyocyte apoptosis that was attenuated by inhibition of p53. Importantly, elevation of 4‐ HNE also triggered a reduction of the cytosolic HSP 70, further corroborating cytosolic action of the 4‐ HNE instigated by downregulation of mitochondrial ALDH 2. Conclusions Downregulation of ALDH 2 in the mitochondria induced an elevation of 4‐ HNE , leading to cardiomyocyte apoptosis by subsequent inhibition of HSP 70, phosphorylation of JNK , and activation of p53. This chain of molecular events took place in both the mitochondria and the cytosol, contributing to the mechanism underlying heart failure.

TongXinLuo (TXL) is a traditional Chinese herbal medicine with multiple vasoprotective activities. Dendritic cells (DCs) play an active role in the immunological processes related to atherosclerosis. The purpose of this study was to determine the effect and possible mechanisms of TXL on oxidized low-density lipoprotein (OX-LDL)-induced maturation and immune function of DCs. Human monocyte-derived DCs were incubated with TXL or ciglitazone and were subsequently stimulated with OX-LDL to induce maturation. Similar to ciglitazone, a peroxisome proliferator-activated receptor (PPAR) gamma agonist, TXL could significantly reduce the maturation-associated markers induced by OX-LDL, such as CD40, CD86, CD1a, and human leukocyte antigen-DR; improved the endocytotic function; and decreased secretions of cytokine interleukin-12 and tumor necrosis factor alpha. These inhibitory effects of TXL could be partly reversed by silencing the expression of PPAR gamma in DCs. In conclusion, TXL could inhibit OX-LDL-induced maturation of DCs through activating PPAR gamma pathway.

Aldehyde dehydrogenase 2 (ALDH2), a mitochondrial-specific enzyme, has been proved to be involved in oxidative stress-induced cell apoptosis, while little is known in cardiomyocytes. This study was aimed at investigating the role of ALDH2 in antimycin A-induced cardiomyocytes apoptosis by suppressing ALDH2 activity with a specific ALDH2 inhibitor Daidzin. Antimycin A (40μg/ml) was used to induce neonatal cardiomyocytes apoptosis. Daidzin (60μM) effectively inhibited ALDH2 activity by 50% without own effect on cell apoptosis, and significantly enhanced antimycin A-induced cardiomyocytes apoptosis from 33.5±4.4 to 56.5±6.4% (Hochest method, p0.05), and from 57.9±1.9 to 74.0±11.9% (FACS, p0.05). Phosphorylation of activated MAPK signaling pathway, including extracellular signal-regulated kinase (ERK1/2), c-Jun NH2-terminal kinase (JNK) and p38 was also increased in antimycin A and daidzin treated cardiomyocytes compared to the cells treated with antimycin A alone. These findings indicated that modifying mitochondrial ALDH2 activity/expression might be a potential therapeutic option on reducing oxidative insults induced cardiomyocytes apoptosis.

BACKGROUND: Until now there were no clinical studies or systematic reviews to investigate the impact of timing on efficacy and safety of intracoronary bone marrow stem cell (BMSC) transfer in patients with acute myocardial infarction (AMI). HYPOTHESIS: Timing of BMSC administration might play an important role in the therapeutic response in AMI patients. METHODS: A systematic literature search of PubMed, MEDLINE, and Cochrane Evidence‐Based Medicine (EBM) databases was made on randomized controlled trials with at least 3‐month follow‐up data for patients with AMI undergoing emergent percutaneous coronary intervention (PCI) and receiving intracoronary BMSC transfer thereafter. RESULTS: A total of 7 trials with 660 patients were available for analysis. Compared to baseline level, BMSC transfer at 4 to 7 days post‐AMI significantly improved left ventricular ejection fraction (LVEF; 4.63% increase, 95% confidence interval [CI]: 1.00%‐8.26%, P = 0.01), reduced left ventricular (LV) end‐systolic dimensions (95% CI: − 0.53 − 0.02, P = 0.03), decreased the incidences of revascularization (odds ratio [OR]: 0.60, 95% CI: 0.37–0.97, P = 0.04), decreased the cumulative clinical events of death or recurrent myocardial infarction (OR: 0.32, 95% CI: 0.11–0.95, P = 0.04), and decreased culprit artery restenosis or ventricular arrhythmia (OR: 0.59, 95% CI: 0.36–0.96, P = 0.03) however these improvements did not reach statistical significance in emergent transfer trials (within 24 hour post‐AMI). Compared with emergent transfer, intracoronary BMSC therapy at 4 to 7 days also significantly reduced the incidence of revascularization (P for interaction = 0.02). CONCLUSIONS: BMSC transfer at 4 to 7 days post‐AMI was superior to that within 24 hours in improving LVEF, decreasing LV end‐systolic dimensions, and reducing the incidence of revascularization. Copyright © 2009 Wiley Periodicals, Inc.

Percutaneous coronary intervention is the main therapy for revascularization of occluded coronary arteries. However, a progressive artery restenosis caused by abnormal proliferation and migration of vascular smooth muscle cells (VSMC) hinders the effective treatment. In this study, we examined the effect of emodin, a natural anthraquinoid compound, on cultured VSMC. Lower doses of emodin suppressed cell proliferation and induced unscheduled DNA synthesis. Higher doses of emodin increased lumpy chromatin condensation and lysosomes in VSMC, suggesting the occurrence of apoptosis and autophagy. Emodin increased production of reactive oxygen species (ROS), which was abolished by an NADPH oxidase inhibitor diphenylene iodonium (DPI). DPI could also decrease the number of apoptosis induced by emodin, suggesting the involvement of ROS in emodin-induced apoptosis. Emodin upregulated the protein levels of p53 in a dose-dependent manner. Laser confocal microscope showed most of emodin scattering in the cytoplasms and a little within the nuclei. These findings collectively indicated that emodin induces both growth arrest and death of human VSMCs in 2 independent manners, implying it as a promising therapy for preventing restenosis.