Flexible Transparent Electrode Characteristics of Graphene Oxide/Cysteamine/AgNP/AgNW Structure.

Graphene oxide (GO)-cysteamine-Ag nanoparticles (GCA)-silver nanowire (AgNW) fabricated by depositing GCA over sprayed AgNWs on PET films were proposed for transparent and flexible electrodes, and their optical, electrical, and mechanical properties were analyzed by energy-dispersive X-ray spectroscopy, Fourier-transform infrared spectroscopy, Raman spectroscopy, atomic force microscopy, scanning electron microscopy, transmission electron microscopy, current-voltage measurements, and bending test. GCA-AgNW electrodes show optical transmittance of >80% at 550 nm and exhibit a high figure-of-merit value of up to 116.13 in the samples with sheet resistances of 20-40 Ω/◻. It was observed that the detrimental oxidation of bare AgNWs over time was considerably decreased, and the mechanical robustness was improved. To apply the layer as an actual electrode in working devices, a Pt/GO/poly(3,4-ethylenedioxythiophene) polystyrene sulfonate/GCA-AgNW/polyethylene terephthalate structure was fabricated, and resistive switching memory was demonstrated. On the basis of these results, we confirm that the proposed GCA-AgNW layer can be used as transparent and flexible electrode.

Trifolin induces apoptosis via extrinsic and intrinsic pathways in the NCI-H460 human non-small cell lung-cancer cell line.

BACKGROUND: Trifolin (kaempferol-3-O-galactoside), which is a galactose-conjugated flavonol, exhibits antifungal and anticancer effects. However, the mechanisms underlying its anticancer activities have not yet been examined. PURPOSE: In this study, the anticancer effects of trifolin were examined in human lung cancer cells. METHODS: Cytotoxicity was determined by evaluating cell viability. Apoptosis was analyzed through flow cytometry and western blotting analysis. Death receptors and inhibitors of apoptosis were evaluated through RT-PCR. RESULTS: Trifolin induced apoptosis in NCI-H460 human non-small cell lung cancer (NSCLC) cells by inhibiting the survival pathway and inducing the intrinsic and extrinsic apoptosis pathways. Trifolin decreased levels of Akt/p-Akt, whereas levels of expression of phosphatidylinositide 3-kinase (PI3K), cyclin D1, cyclin E, and cyclin A were not altered. Trifolin initiated cytochrome c release by inducing mitochondrial outer membrane permeabilization (MOMP). Trifolin increased Bcl-2-associated X protein (Bax) levels and decreased b-cell lymphoma 2 (Bcl-2) levels, while the levels of Bcl-xL were not altered. In addition, trifolin increased the levels of the death receptor involving the Fas/Fas ligand (FasL) and Fas-associated protein with the death domain (FADD), which consequently activated caspase-8, caspase-9, caspase-3, and the proteolytic cleavage of poly (ADP-ribose) polymerase (PARP). CONCLUSION: These results suggested that trifolin induced apoptosis via death receptor-dependent and mitochondria-dependent pathways and that trifolin can be used as a therapeutic agent in human lung cancer.

Adenosine Tc-99m tetrofosmin SPECT in differentiation of ischemic from nonischemic cardiomyopathy in patients with LV systolic dysfunction.

BACKGROUND: The noninvasive differentiation of ischemic from nonischemic cardiomyopathy is clinically important. However, whether adenosine Tc-99m tetrofosmin SPECT can offer clear and accurate information was not known. The aim of this study is to investigate the usefulness of adenosine Tc-99m tetrofosmin SPECT in differentiation of ischemic from nonischemic etiology in patients with mild to severe LV systolic dysfunction and to compare the relationship between patients with mild LV systolic dysfunction and those with severe LV systolic dysfunction. METHODS: Seventy-five patients with chronic heart failure (LV ejection fraction 35%, group II (31 patients) had severe LV dysfunction, LVEF or=20%. Myocardial ischemia was defined by >or=70% stenosis in at least one vessel by coronary angiography. RESULTS: : In group I, 4 (30.8%) of 13 patients with small defects, 1 (25.0%) of 5 patients with a medium defect, and 22 (84.6%) of 26 patients with large defects demonstrated myocardial ischemia documented by coronary angiography. The relationship between the extent of the SPECT defect and myocardial ischemia was statistically significant in the group I population (P < 0.001). However, in group II, 1 (33.3%) of 3 patients with small defect, 3 (33.3%) of 9 patients with medium defects, and 7 (36.8%) of 19 patients with large defects demonstrated myocardial ischemia confirmed by coronary angiography. There was no statistical relationship between the extent of the SPECT defect and myocardial ischemia in group II. CONCLUSIONS: Adenosine Tc-99m tetrofosmin SPECT is a useful modality to differentiate ischemic from nonischemic etiology in patients with mild LV systolic dysfunction. However, other noninvasive approaches other this SPECT may be considered for confirming the etiology in patients with severe LV systolic dysfunction.

The association between current Helicobacter pylori infection and coronary artery disease.

BACKGROUND: The role of Helicobacter pylori (H. pylori) in the pathogenesis of coronary artery disease (CAD) is still controversial, and the relation between current H. pylori infection and CAD has not been fully examined. This study evaluated the relation between H. pylori infection as confirmed by gastroduodenoscopic biopsy and CAD. METHODS: We determined the presence of H. pylori infections, via gastroduodenoscopy, in 88 patients of the normal coronary angiographic group and also in 175 patients of the CAD group, and the latter patients had more than 50% coronary stenosis angiographically demonstrated. We excluded those patients with a history of previous H. pylori eradication and/or malignancy. A small piece of tissue from the antrum, which was obtained by gastroduodenoscopic biopsy, was stained by Warthin-starry silver stain. We defined a negative staining result that there was no stained tissue in the sample and the stained tissue was also positive for H. pylori infection. RESULTS: There was no significant difference, except for gender, age, smoking and high density lipoprotein cholesterol (HDL-c), of the demographic and laboratory characteristics between the groups. Twenty seven (30.7%) patients of the normal control group and 71 (40.6%) patients of the CAD group were positive of H. pylori infection, yet there was no statistical difference. We angiographically followed up the 80 patients of the CAD group who were treated by percutaneous coronary intervention (PCI) at 6 to 9 months after their primary intervention. Twenty two (37.9%) of the 58 patients of the H. pylori negative group and 10 (45.5%) of the 22 patients of the H. pylori positive group were treated with reintervention, but reintervention was also not significantly different between the group with H. pylori infection and the group without the infection. CONCLUSIONS: These data indicated that H. pylori infection had a modest influence on CAD and progressive atheroma, but the showed a tendency to increase. Further studies are needed to evaluate the relationship between H. pylori infection and CAD.

Digitized QT dispersion by the Valsalva maneuver in hypertensive patients.

BACKGROUND: Hypertension is an important risk factor for sudden cardiac death, of which the incidence increases with increases in blood pressure. Prolonged QT dispersion has been identified to indicate increased risk of life-threatening ventricular arrhythmia and sudden cardiac death. In this study, QT dispersion was investigated in hypertensive patients during the strain phase of the Valsalva maneuver. METHODS: The study population included 75 subjects: 25 with normal blood pressure (Control), 25 with stage I hypertension (Group A), and 25 with stage II hypertension (Group B). Electrocardiography for QT dispersion was recorded at 25 mm/sec paper speeds before and during the Valsalva maneuver. RESULTS: The patients in Group B were significantly older than the controls (p<0.05). Differences in sex, smoking, diabetes, angina, and hyperlipidemia were not statistically significant between the three groups. The basal QT dispersion was 25.3 +/- 18.3 ms in the controls, 39.0 +/- 17.8 ms in Group A, and 36.8 +/- 18.8 ms in Group B. The QT dispersion was significantly higher in group A patients than the controls (p<0.05). In Group B only, a significant increase in QT dispersion was observed during the Valsalva maneuver, compared to conditions prior to the Valsalva maneuver (p<0.05). CONCLUSION: The conditions that increase intrathoracic pressure may increase QT dispersion and severe hypertensive patients should avoid these conditions.