What we believe to be a new technique, based on a modified Gerchberg-Saxton algorithm (MGSA) and a phase modulation scheme in the Fresnel-transform domain, is proposed to reduce cross talks existing in multiple-image encryption and multiplexing. First, each plain image is encoded and multiplexed into a phase function by using the MGSA and a different wavelength/position parameter. Then all the created phase functions are phase modulated to result in different shift amounts of the reconstruction images before being combined together into a single phase-only function. Simulation results show that the cross talks between multiplexed images have been significantly reduced, compared with prior methods [Opt. Lett.30, 1306 (2005); J. Opt. A8, 391 (2006)], thus presenting high promise in increasing the multiplexing capacity and encrypting grayscale and color images.

Recent studies demonstrate that cyclooxygenase-2 (COX-2) expression is frequently associated with lymph node metastasis. However, the mechanism by which COX-2 increases the invasion of cancer cells to lymph node is unclear. CCR7 is a chemokine receptor that plays important roles in the mediation of

Background-Catheter ablation of atrial fibrillation (AF) became an effective therapy for patients with drug-refractory AF, and the indications have broadened to include nonparoxysmal AF patients. However, data about the long-term effectiveness of ablation in patients with nonparoxysmal AF are lacking. The aim of the present study was to investigate the long-term outcomes of catheter ablation in patients with nonparoxysmal AF. Methods and Results-A total of 88 nonparoxysmal AF patients who received a stepwise catheter ablation (isolation of the pulmonary veins plus substrate modification) from 2006 to 2008 were enrolled. Freedom of recurrence was defined as the absence of atrial arrhythmias without using any antiarrhythmic agents after the catheter ablation. There were 63 patients (71.6%) with recurrences (47 patients with AF and 16 patients with atrial flutter/atrial tachycardia) after the initial procedure during a median follow-up period of 36.8 months. A CHADS 2 score of ≥3 and the left atrial (LA) diameter were significant predictors of recurrences in the multivariable analysis. Of the patients with CHADS 2 scores of ≥3 and an LA dimension ≥44 mm, all had recurrences within 1 year after the initial procedure. The overall recurrence-free rate could increase to 47.7% after the second procedure and 51.1% after the third procedure. Conclusions-The long-term recurrence-free rate of ablation in nonparoxysmal AF was only 28.4% after a single procedure, and multiple procedures were necessary to raise the recurrence-free rate. The CHADS 2 score and LA dimension may help us to identify patients who will have recurrences after catheter ablations of nonparoxysmal AF.(Circ Arrhythm Electrophysiol. 2012;5:514-520.)

Matrix metalloproteinase (MMP) inhibitory proteins may negatively regulate MMP activity to suppress tumor metastasis. In this study, we demonstrate that the HER-2/neu oncogene inhibits the expression of the MMP inhibitor RECK to promote cell invasion. RECK was inhibited via transcriptional repression in B104-1-1 cells, which express constitutively active HER-2/neu. Overexpression of HER-2/neu in NIH/3T3 or HaCaT cells also suppressed RECK expression. Deletion and mutation assays showed that HER-2/neu repressed RECK via the Sp1-binding site localized in the ؊82/؊71 region from the translational start site. DNA affinity precipitation and chromatin immunoprecipitation assays indicated that binding of Sp1 and Sp3 to this consensus site was increased in B104-1-1 cells. We also found that HER-2/neu inhibited RECK via the ERK signaling pathway. Sp1 proteins phosphorylated at Thr 453 and Thr 739 by ERK bound preferentially to the RECK promoter, and this binding was reversed by HER-2/neu and ERK inhibitors. Furthermore, our data indicate that HER-2/neu obviously increased HDAC1 binding to the Sp1-binding site localized in the ؊82/؊71 region of the RECK promoter. The histone deacetylase inhibitor trichostatin A reversed HER-2/neu-induced inhibition of RECK. HER-2/neu activation was associated with increased MMP-9 secretion and activation. Re-expression of RECK in HER-2/neu-overexpressing cells inhibited MMP-9 secretion and cell invasion. Taken together, our results suggest that HER-2/neu induces the binding of Sp proteins and HDAC1 to the RECK promoter to inhibit RECK expression and to promote cell invasion. Restoration of RECK provides a novel strategy for the inhibition of HER-2/neu-induced metastasis.The HER-2/neu oncogene (also known as erbB2) encodes a transmembrane glycoprotein that belongs to the human epidermal growth factor receptor family (1, 2). Structural analysis of HER-2/neu and the epidermal growth factor receptor revealed significant sequence homology and identical gross structural organization between these two proteins (3-5). Amplification and overexpression of HER-2/neu have been found in breast, ovarian, lung, gastric, and cervical carcinomas (6 -10). Up-regulation of this oncogene is frequently linked with increased metastasis and poor prognosis. The mechanism underlying HER-2/neuinduced metastasis is a field of intensive study, and several candidates involved in this process have been identified recently. The first candidate is the vascular endothelial growth factor. HER-2/neu may stimulate vascular endothelial growth factor expression, and neutralizing antibody against HER-2/neu suppresses vascular endothelial growth factor production and metastasis of cancer cells (11,12). The second is the urokinase-type plasminogen activator. Induction of the urokinase-type plasminogen activator by HER-2/neu has been shown to be correlated with increased metastasis (13). The third is cyclooxygenase-2. Cyclooxygenase-2 plays a critical role in tumor metastasis and may be a potential target for chemoprevention (14)...

Background: Angiotensin receptor and neprilysin inhibition (ARNI) has been shown to reduce cardiovascular mortality by 20% as compared with enalapril in a randomized controlled trial. However, there is a paucity of real-world data on the effects of ARNI in heart failure patients with reduced ejection fraction (HFrEF), especially those with concurrent renal impairment or hypotension. Methods: Between 2016 and 2017, we recruited 466 HFrEF patients treated with sacubitril/valsartan (Group A) and 466 patients managed with standard HF treatment without ARNI (Group B) in a HF referral center. Baseline characteristics and clinical outcomes were collected between both groups. Results: Baseline characteristics were comparable between the two groups. During a follow-up period of 15 months, death from cardiovascular causes or first unplanned hospitalization for HF occurred in 100 patients in Group A (21.5%) and 144 in Group B (30.9%, hazard ratio 0.66; 95% CI 0.51-0.85; p = 0.001). The incidences of deaths from any causes, cardiovascular death, sudden death, and HF re-hospitalization were all significantly lower in Group A than Group B patients. Among patients with different chronic kidney disease stages and normotensive patients, treatment with sacubitril/valsartan showed more favorable outcomes than treatment with standard HF care without ARNI. However, in patients with baseline systolic blood pressure lower than 100 mmHg, there were no significant differences of outcomes in both groups. Among Group A patients, escalation of sacubitril/valsartan was associated with better outcomes. Conclusions: Our study demonstrated the effectiveness of sacubitril/valsartan on HFrEF patients in real world practice, including those with advanced renal impairment.

The CHADS(2) and CHA(2)DS(2)-VASc scores are useful predictors of adverse events after catheter ablation of AF.

RECK is a membrane-anchored glycoprotein that may negatively regulate matrix metalloproteinase activity to suppress tumor invasion and metastasis. Our previous study indicated that oncogenic RAS inhibited RECK expression via a histone deacetylation mechanism. In this study, we address whether DNA methyltransferases (DNMT) participate in the inhibition of RECK by RAS. Induction of Ha-RAS Val12 oncogene increased DNMT3b, but not DNMT1 and DNMT3a, expression in 2-12 cells. In addition, induction of DNMT3b by RAS was through the extracellular signal-regulated kinase signaling pathway. Oncogenic RAS increased the binding of DNMT3b to the promoter of RECK gene and this binding induced promoter methylation, which could be reversed by 5 ¶-azacytidine and DNMT3b small interfering RNA (siRNA). The MEK inhibitor U0126 also reversed RAS-induced DNMT3b binding and RECK promoter methylation. Treatment of 5 ¶-azacytidine and DNMT3b siRNA restored RECK expression in 2-12 cells and potently suppressed RAS-stimulated cell invasion. In addition, the inhibitory effect of 5 ¶-azacytidine on RAS-induced cell invasion was attenuated after knockdown of RECK by siRNA. Interestingly, human lung cancer cells harboring constitutively activated RAS exhibited lower RECK expression and higher promoter methylation of RECK gene. 5 ¶-Azacytidine and DNMT3b siRNA restored RECK expression in these cells and effectively suppressed invasiveness. Collectively, our results suggest that RAS oncogene induces RECK gene silencing through DNMT3b-mediated promoter methylation, and DNMT inhibitors may be useful for the treatment of RAS-induced metastasis. (Cancer Res 2006; 66(17): 8413-20)

Electrospray-assisted laser desorption/ionization (ELDI), an ionization method that combines laser desorption and electrospray ionization (ESI), can be used under ambient conditions to characterize organic compounds (including FD&C dyes, amines, extracts of a drug tablet) separated in the central track on a thin-layer chromatography (TLC) plate coated with either reversed-phase C18 particles or normal-phase silica gel. After drying, the TLC plate was placed on an acrylic sample holder set in front of the sampling skimmer of an ion trap mass analyzer. The chemicals at the center of the TLC plate were analyzed by pushing the sample holder into the path of a laser beam with a syringe pump. The molecules in the sample spot were desorbed by continuously irradiating the surface of the TLC plate with a pulsed nitrogen laser. Then, the desorbed sample molecules entered an ESI plume where they were ionized through the reactions with the charged species (including protons, hydronium ions and their cluster ions, solvent ions, and charged droplets) generated by electrospraying a methanol/water solution. MS/MS analyses were also performed to further characterize the analytes. The detection limit of TLC/ELDI/MS is approximately 10(-6) M. This was evaluated by using FD&C red dye as the standard. A linear relationship was found for the calibration curve with the concentration of FD&C red dye ranged from 10(-3) to 10(-6) M.