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Transversely localized resonance of antisymmetric-bound surface plasmons (ab-SP) at ultrathin metal stripes in a subwavelength array suppresses optical transmission in a broadband. Here, asymmetric binary arrays of ultrathin metal stripes are proposed to introduce a narrow transmission peak in the stop-band (i.e., plasmon-induced transparency), based on destructive interference of antisymmetrically excited ab-SP resonance modes at the neighboring binary metal stripes. The phenomenon is numerically demonstrated and explained with a mesoscopic model, in which mesoscopic interaction processes are abstracted as different transmission channels to cooperatively result in the narrow peak in a broad transmission valley. In spite of the ultrathin feature of the structure for convenience in fabrication, its excellent performance facilitates potential applications.

Background/aims: Plasma norepinephrine (NE) and brain natriuretic peptide (BNP, termed BNP-45 in rats) are considered as essential neurohormones indicating heart failure progression. The purposes of this study were to examine the effects of ivabradine (IBD) on cardiac function and plasma NE and BNP-45 after chronic ischemic heart failure (CHF) in non-diabetic rats and diabetic rats. We further determined if sympathetic NE uptake-1 (a major pathway to metabolize NE) mechanism is responsible for the role played by IBD., Methods: We ligated rat's coronary artery to induce CHF; and injected streptozotocin (STZ) to induce diabetic hyperglycemia. Echocardiography was employed to determine cardiac function. We used ELISA to examine plasma NE and BNP-45; and Western Blot analysis to examine the protein levels of NE uptake-1 in sympathetic nerves., Results: CHF increased the levels of NE and BNP-45 in non-STZ rats and STZ rats. Systemic injection of IBD significantly attenuated the augmented NE and BNP-45 and impaired left ventricular function induced by CHF in those rats. This effect appeared to be less in STZ rats. A liner relation was observed between the NE/BNP-45 levels and left ventricular function after administration of IBD. Also, IBD was observed to have a recovery effect on the downregulated NE uptake-1 evoked by CHF, but to a smaller degree in STZ rats., Conclusion: Our data revealed specific signaling mechanisms by which IBD improves the cardiac function as IBD alleviates impaired NE uptake-1and thereby decreases heightened NE and BNP-45 induced by CHF. Our data also demonstrated that the effects of IBD are weakened after diabetic hyperglycemia likely due to worsen NE uptake-1 pathway. Thus, targeting sympathetic NE uptake-1 signaling molecules has clinical implications for treatment and management of CHF in diabetes. Our data were also to shed light on strategies for application of this drug because NE and BNP play an important role in regulation of progression and prognosis of CHF, and in particular, because IBD affects NE uptake-1 pathway in hyperglycemic animals to a less degree., (© 2016 The Author(s) Published by S. Karger AG, Basel.)

We propose a scheme using cooperative interaction of antiphase resonance modes to enhance optical trapping in plasmonic nanostructures. This is implemented with a subwavelength array of asymmetric binary nanogrooves (e.g. different depths) in metal. When damping and inter-coupling of antiphase fields in the nanogrooves are mediated satisfying a critical condition, light can be cooperatively trapped in the nanogrooves, demonstrating perfect absorption at nearly the intrinsic resonance frequency of the deeper nanogrooves. A harmonic oscillator model is developed to interpret the cooperative interaction processes. The phenomenon has been also implemented in asymmetric ternary nanogroove arrays. In terms of compositions and intra-coupling mechanisms, the asymmetric binary/ternary plasmonic nanostructure arrays are crystalline molecular-metamaterials, analogous to electronic crystals composed of covalence-bond molecules.

Objective: To analyze the prognostic value of serum albumin for in-hospital mortality in patients with heart failure., Methods: A total of 2 430 consecutive heart failure patients aged at (68±14) years were enrolled in the study. Patients were divided into 2 groups according to serum albumin concentration on admission: the normoalbuminemia group (≥35 g/L) and the hypoalbuminemia group (<35 g/L). Propensity score matching was conducted to reduce confounding bias between the groups. Cox proportional-hazards regression models were used to evaluate the prognostic value of serum albumin for in-hospital mortality in patients with heart failure before and after matching., Results: Compared with those in the normoalbuminemia group, subjects in the hypoalbuminemia group were older, and had higher NYHA functional status and higher in-hospital mortality. More patients were diagnosed with dilated cardiomyopathy and valvular heart disease, and fewer were with hypertension in the hypoalbuminemia group than those patients in the normoalbuminemia group. Moreover, patients in this group presented with faster heart rate and lower systolic blood pressure than those in the normoalbuminemia group. They had higher levels of direct bilirubin, alkaline phosphatase, glutamyltranspetidase, creatinine, uric acid, urea, and B-type natriuretic peptide (BNP) and lower levels of hemoglobin, total cholesterol (TC), and serum sodium compared with subjects in the normoalbuminemia group. Left ventricular ejection fractions (LVEF) of patients were lower in the hypoalbuminemia group than those of patients in the normoalbuminemia group. More patients were of long-duration and treated with spirolactone. With protensity score matching, 631 pairs of patients were successfully matched. Before matching, the in-hospital mortality in normoalbuminemia group was 1.2% and that in hypoalbuminemia group was 5.7%. The multivariate Cox regression analysis indicated that the risk for in-hospital death in patients with heart failure was 12.0% greater for each 1 g/L decrement in albumin level after adjusted for all clinical factors (HR 1.120, 95% CI 1.057-1.186; P<0.001). The same held after matching. The in-hospital mortality in normoalbuminemia group was 2.9%, and that in hypoalbuminemia group was 5.7%. The multivariate Cox regression analysis showed that the risk for in-hospital death in patients with heart failure was 11.0% greater for each 1 g/L decrement in albumin level after adjusted for all clinical factors (HR 1.110, 95% CI 1.043-1.181; P=0.001)., Conclusions: Serum albuminis is an independent risk factor for in-hospital mortality in patients with heart failure. Treatment of hypoalbuminemia may lower the in-hospital mortality in patients with heart failure.

Essential hypertension is a complex disease affected by genetic and environmental factors and serves as a major risk factor for cardiovascular diseases. Serum lysophosphatidic acid correlates with an elevated blood pressure in rats, and lysophosphatidic acid interacts with 6 subtypes of receptors. In this study, we assessed the genetic association of lysophosphatidic acid receptors with essential hypertension by genotyping 28 single-nucleotide polymorphisms from genes encoding for lysophosphatidic acid receptors, LPAR1, LPAR2, LPAR3, LPAR4, LPAR5, and LPAR6 and their flanking sequences, in 3 Han Chinese cohorts consisting of 2630 patients and 3171 controls in total. We identified a single-nucleotide polymorphism, rs531003 in the 3'-flanking genomic region of LPAR1, associated with hypertension (the Bonferroni corrected P=1.09×10(-5), odds ratio [95% confidence interval]=1.23 [1.13-1.33]). The risk allele C of rs531003 is associated with the increased expression of LPAR1 and the susceptibility of hypertension, particularly in those with a shortage of sleep (P=4.73×10(-5), odds ratio [95% confidence interval]=1.75 [1.34-2.28]). We further demonstrated that blood pressure elevation caused by sleep deprivation and phenylephrine-induced vasoconstriction was both diminished in LPAR1-deficient mice. Together, we show that LPAR1 is a novel susceptibility gene for human essential hypertension and that stress, such as shortage of sleep, increases the susceptibility of patients with risk allele to essential hypertension., (© 2015 American Heart Association, Inc.)

Background: Ginsenoside Rd (GSRd), one of the most abundant ingredients of Panax ginseng, protects the heart via multiple mechanisms including the inhibition of Ca(2+) influx. We intended to explore the effects of GSRd on L-type Ca(2+) current (I Ca,L) and define the mechanism of the suppression of I Ca,L by GSRd., Methods: Perforated-patch recording and whole-cell voltage clamp techniques were applied in isolated rat ventricular myocytes., Results: (1) GSRd reduced I Ca,L peak amplitude in a concentration-dependent manner [half-maximal inhibitory concentration (IC50) = 32.4 ± 7.1 μmol/L] and up-shifted the current-voltage (I-V) curve. (2) GSRd (30 μmol/L) significantly changed the steady-state activation curve of I Ca,L (V 0.5: -19.12 ± 0.68 vs. -16.26 ± 0.38 mV; n = 5, p < 0.05) and slowed down the recovery of I Ca,L from inactivation [the time content (ζ) from 91 ms to 136 ms, n = 5, p < 0.01]. (3) A more significant inhibitive effect of GSRd (100 μmol/L) was identified in perforated-patch recording when compared with whole-cell recording [65.7 ± 3.2% (n = 10) vs. 31.4 ± 5.2% (n = 5), p < 0.01]. (4) Pertussis toxin (G i protein inhibitor) completely abolished the I Ca,L inhibition induced by GSRd. There was a significant difference in inhibition potency between the two cyclic adenosine monophosphate elevating agents (isoprenaline and forskolin) prestimulation [55 ± 7.8% (n = 5) vs. 17.2 ± 3.5% (n = 5), p < 0.01]. (5) 1H-[1,2,4]Oxadiazolo[4,3-a]-quinoxalin-1-one (a guanylate cyclase inhibitor) and N-acetyl-l-cysteine (a nitric oxide scavenger) partly recovered the I Ca,L inhibition induced by GSRd. (6) Phorbol-12-myristate-13-acetate (a protein kinase C activator) and GF109203X (a protein kinase C inhibitor) did not contribute to the inhibition of GSRd., Conclusion: These findings suggest that GSRd could inhibit I Ca,L through pertussis toxin-sensitive G protein (Gi) and a nitric oxide-cyclic guanosine monophosphate-dependent mechanism.

Radiotherapy (RT) is a major modality of hepatoma treatment. However, liver tumors often acquire radioresistance, which contributes to RT failure. The exact mechanisms of the radioresistance in hepatoma cells are largely unknown. Glutathione S-transferase M3 (GSTM3) is a phase II transferase, however, recent studies have suggested that GSTM3 is a potential tumor suppressor. The purpose of the present study was to investigate the role of GSTM3 in reversing radioresistance, and to explore the molecular mechanism of this in the human radiation-resistant PRF/PLC/5R hepatocellular carcinoma (HCC) cell line. The radioresistant PLC/PRF/5R cells were used as cell model, and were derived from PLC/PRF/5 parental cells using fractionated irradiation. The radiosensitivity of the cells was tested by clonogenic assay and flow cytometry analyses. The expression of B-cell chronic lymphocytic leukemia/lymphoma 2 (Bcl-2), Bax, p21, p27 and p53 was analyzed by quantitative polymerase chain reaction and immunoblotting with or without radiation. The results showed that the expression levels of GSTM3 were significantly lower in the PLC/PRF/5R cells than in the PLC/PRF/5 parental cells. GSTM3 overexpression sensitized the PLC/PRF/5R cells to radiation mainly though induction of apoptosis. According to the evidence from Annexin-V/PI staining, it markedly increased the percentage of apoptotic PRF/PLC/5R cells. The clonogenic assay indicated that GSTM3 significantly decreased the RT survival fraction in PRF/PLC/5R cells. Furthermore, GSTM3 increased the expression of cell cycle- and apoptosis-related genes (Bcl-2, Bax, p21, p27 and p53) in PRF/PLC/5R cells with irradiation. These findings suggest that GSTM3 plays an pivotal role in reversing the radioresistance of HCC and may be a potential target for sensitizing HCC cells to RT. The underlying mechanisms may be linked to the cell cycle arrest and apoptosis facilitation.

Background: Left atrial flutter (left AFL) is common in patients who undergo atrial fibrillation ablation and cardiac surgery; however, few reports describe left AFL in detail in a seemingly normally structured heart, and the mechanisms of the occurrence of such arrhythmia are still not clear. We describe left AFL in patients without prior cardiac surgery or catheter ablation and discuss the electrophysiological characteristics that may explain the preferential generation and perpetuation of such tachycardia., Methods and Results: Eleven patients with left AFL, who had no history of cardiac surgery or interventions, underwent electrophysiological studies and 3-dimensional electroanatomic mapping studies. Echocardiography revealed a relatively mild dilation of the left atrium, mild to moderate mitral regurgitation, and a normal left ventricular ejection fraction. The electroanatomic mapping during tachycardia showed a "reentrant" activation pattern in all patients. The mean tachycardia cycle length was 266 ± 17 ms. A single-loop reentrant circuit was identified in 7 patients. A counterclockwise left atrial flutter evolved around the mitral valve annulus in 6 patients. The tachycardia rotated around the left atrial anterior wall in 1 patient. Four patients exhibited a double-loop reentrant circuit with a "figure of 8" pattern reentry. Double potentials as the critical isthmus of the circuit were identified in the left atrial anterior wall near the mitral annulus which displayed a low-voltage area matched with the left atrium-aorta contiguity. The conduction velocity was significantly slower in the double-potential recording area than in the lateral mitral annulus (0.36 ± 0.03 m/s vs 0.74 ± 0.12 m/s; P<0.05). Successful ablation around the double-potential recording site caused an interruption of the tachycardia, and remained free of recurrence during a 12-month follow-up in all patients., Conclusion: Left AFL in patients without a history of surgery or ablation is rarely observed in clinical practice. The successful site of ablation was within the anterior wall near the mitral annulus showing the double potentials as the critical part of the reentrant circuit. This suggests that perhaps a double potential-targeted ablation may be effective for these patients., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

A quasi-transverse electric (TE) surface wave mode exists at a metal surface coated with an ultrathin high-index dielectric layer. As the coating is in dielectric stripe arrays, nearly perfect absorption of TE-polarized incidence light is observed in simulations, due to resonances of the quasi-surface waves at each segment of the dielectric-coated metal surfaces. In analysis, the Fabry-Perot-like nature of the resonances is clarified, and effects of symmetry on different behaviors of the odd- and even-order resonance modes are discussed. While the absorption peak is tunable, perfect absorption appears near cut-off wavelength of the surface mode.

Objective: To assess the feasibility and accuracy of CT coronary angiography (CTCA) combined with CT first-pass myocardial perfusion imaging (CT first-pass MPI) at rest for diagnosis of obstructive coronary artery disease (CAD)., Methods: Fifty-five patients, suspected or diagnosed as CAD, were performed with CTCA and CAG within 2 weeks. CT first-pass MPI detected myocardial ischemia through analyzing the raw date of CTCA., Results: Comparison with the results of CAG, the sensibility, specificity, positive predictive value (PPV), negative predictive value (NPV) and accuracy of CT first-pass MPI at rest for detecting obstructive CAD were 84.6%, 68.8%, 86.8%, 64.7% and 80.0%, respectively; and 92.3%, 93.8%, 97.3%, 83.3%, 92.7% for CTCA combined with CT first-pass MPI, respectively., Conclusion: CTCA combined with CT first-pass MPI at rest could detect obstructive CAD feasible and accurately.

Objective: To investigate the effects of arginine vasopressin (AVP) and its receptor antagonist conivaptan (CON) on the proliferation of cardiac fibroblasts (CFs) and the production of collagen I and III., Methods: CFs were isolated by collagenase II method and purified with differential attachment and detachment methods. The cell viability of CFs after AVP and/or CON administration was assessed by cell counting kit-8 (CCK-8). The expressions of COL1A1 and COL3A1 mRNA were detected by RT-PCR, and the protein levels of (collagen type 1, alpha 1, COL1A1) and COL3A1 were assessed by Western blotting., Results: At 24 h after intervention, 10(-7); mol/L AVP promoted the proliferation of CFs in comparison with that in control group (P<0.01), and 10(-7); mol/L CON inhibited the effect significantly (P<0.01). At 12 h after intervention, 10(-7); mol/L AVP significantly enhanced the expressions of COL1A1 and COL3A1 at both mRNA and protein levels, and 10(-7); mol/L CON inhibited the effect again., Conclusion: AVP promoted the proliferation of CFs and enhanced the COL1A1 and COL3A1 expressions at both mRNA and protein levels, while CON could restrain the AVP effects partially.

To identify the characterization of culprit lesions in acute coronary syndrome (ACS) compared with stable angina pectoris (SAP) by dual-source computed tomography (DSCT). 65 patients with ACS and 75 controls with SAP and a similar atherosclerotic risk profile were studied. Computed tomography (CT) coronary angiography was performed using a DSCT scanner before invasive catheterization. Using DSCT and quantitative coronary angiography (QCA), lesion characteristics [luminal cross-section area (L-CSA), vascular cross-section area (V-CSA), plaque area and degree of stenosis) were detected. Plaque types, mean and minimum CT density (Hounsfield Unit; HU), remodeling index, and presence of "spotty" calcifications were analyzed using DSCT. A good correlation was observed between DSCT and QCA for all lesion characteristics (P < 0.05). Culprit lesions in ACS had much larger V-CSA (20.5 ± 6.0 vs. 14.8 ± 4.8 mm(2)), plaque area (15.3 ± 5.0 vs. 11.1 ± 3.3 mm(2)) and remodeling index (1.3 ± 0.2 vs. 1.0 ± 0.4) than stable lesions in SAP (P < 0.05). The prevalence of non-calcified/calcified/mixed plaque was 30/0/35 in ACS versus 25/15/35 stable lesions in SAP (P < 0.01). The proportion of "spotty" calcified plaques was 21.5 % in culprit lesions (14 of 65) versus 1.3 % in SAP (1 of 75). The mean/minimum HU of culprit lesions was 88.6 ± 43.2/154.2 ± 98.7 in ACS versus 45.9 ± 34.7/98.2 ± 76.8 in SAP (both P < 0.01). DSCT is a feasible means of detecting coronary stenosis with good accuracy compared with QCA. Culprit lesions in ACS display a greater proportion of non-calcified material with lower CT attenuation, "spotty" calcifications and higher remodeling index compared with SAP lesions.

Aims: We evaluated the association of ligand cyclophilin A (CypA) and receptor CD147 with hypoxia, angiogenesis, lymph node metastasis and prognosis of patients with tongue squamous cell carcinoma (TSCC)., Methods and Results: We studied the expression of CypA, CD147, hypoxia-inducible factor 1α (HIF-1α), vascular endothelial growth factor A and C (VEGF-A and VEGF-C) protein by immunohistochemistry in 80 specimens of TSCC. CypA, CD147, HIF-1α, VEGF-A and VEGF-C were overexpressed in TSCCs, and were significantly higher than those in normal oral mucosa tissues (P<0.01). Increased ligand CypA and receptor CD147 correlated significantly with expression of HIF-1α, VEGF-A and VEGF-C. A significant relationship between VEGF-A and VEGF-C was also detected (P<0.01). Patients with overexpression of CypA, CD147, HIF-1α and VEGF-C had significantly worse overall survival (P<0.05) using Kaplan-Meier analysis. Multivariate Cox regression analysis showed that HIF-1α, recurrence and distant metastasis were independent prognostic factors on overall survival in TSCC patients., Conclusions: The association of expression of ligand CypA and receptor CD147 with carcinogenesis, hypoxia, angiogenesis, metastasis and prognosis of TSCC suggests that ligand CypA and receptor CD147 may have prognostic value and could be regarded as potential therapeutic targets in TSCC., (© 2012 Blackwell Publishing Ltd.)

With-no-lysine (K) kinase-4 (WNK4) is a serine/threonine kinase that plays an essential role in the regulation of fluid and electrolyte homeostasis. The effects of glucocorticoids, key physiological regulators, on the WNK4 gene expression are still unknown. Here, we used dexamethasone (Dex) to treat the human embryo kidney 293 (HEK293) cells and found a decrease of human WNK4 (hWNK4) mRNA level by northern blot and real-time quantitative PCR. After an hWNK4 transcriptional initiation site was located by 5' rapid amplification of cDNA end assay, a series of 5'-deleted hWNK4 promoter-luciferase constructs were generated by PCR. Transfection of these constructs in COS-7 and HEK293 cells revealed that Dex inhibited the hWNK4 transcriptional activity in glucocorticoid receptor (GR)-dependent pattern. Two negative glucocorticoid response elements (nGREs) were identified at -285 and -337 of the hWNK4 gene promoter and the GR binding activity to them was increased by Dex as shown by electrophoretic mobility shift assay and chromatin immunoprecipitation. In summary, these data demonstrated that hWNK4 was a new glucocorticoid-regulated gene whose expression was inhibited through the interaction of GR with nGREs in the promoter region.

A three-joint robot is directly driven by ultrasonic motors with advantage of high torque at low speed. The speed of the ultrasonic motors is actually controlled by regulating their operating frequencies. The kinematic and kinetic analyses of the robot have been carried out using Adams. Due to the lack of accurate control model of ultrasonic motors and the time-varying motor parameters, a fuzzy auto-tuning proportional integral derivative (PID) controller for the robot is experimented, in which a simple method to tune parameters of the PID type fuzzy controller on-line is developed and a new position-speed feedback strategy is proposed and implemented. The effectiveness of the proposed control strategy and fuzzy logic controller is verified by experimental investigation.

Objective: To investigate the situation of reproductive health of perimenopausal and postmenopausal women in Chengdu and provide a basis for planning reproductive health care for these women., Methods: We conducted a population-based cross-sectional study in women who were over 45 years old in the central city and the nearby county of Chengdu., Results: The mean age of menopause was 48.1 years. There were sixty percent of women who had dysfunctional uterine bleeding before menopause. About half of the postmenopausal women had experienced perimenopausal symptoms. There were 460 women who ever used or currently use estrogen therapy. But only half of them visited doctors and sought medical therapy. And the main problems were hot flash, night sweats, dyssomnia, and urinary infection. Most of them took medicine for a short period (< 1 year)., Conclusion: We found that middle-aged and older women have many symptoms related to menopause. It is necessary for us to provide reproductive health care for them.