In this study, structural characterization, electrical properties and energy storage performance of plasticized polymer electrolytes based on polyvinyl alcohol/methylcellulose/ammonium thiocyanate (PVA/MC-NH4SCN) were carried out. An X-ray diffraction (XRD) study displayed that the plasticized electrolyte system with the uppermost value of direct current (DC) ionic conductivity was the most amorphous system. The electrolyte in the present work realized an ionic conductivity of 2.903 × 10-3 Scm-1 at room temperature. The main charge carrier in the electrolyte was found to be the ions with the ionic transference number (tion) of 0.912, compared to only 0.088 for the electronic transference number (telec). The electrochemical stability potential window of the electrolyte is 2.1 V. The specific capacitance was found to reduce from 102.88 F/g to 28.58 F/g as the scan rate increased in cyclic voltammetry (CV) analysis. The fabricated electrochemical double layer capacitor (EDLC) was stable up to 200 cycles with high efficiency. The specific capacitance obtained for the EDLC by using charge-discharge analysis was 132.7 F/g at the first cycle, which is slightly higher compared to the CV plot. The equivalent series resistance (ESR) increased from 58 to 171 Ω throughout the cycles, which indicates a good electrolyte/electrode contact. Ions in the electrolyte were considered to have almost the same amount of energy during the conduction process as the energy density is approximately at 14.0 Wh/kg throughout the 200 cycles. The power density is stabilized at the range of 1444.3 to 467.6 W/kg as the EDLC completed the cycles.

Three types of Zinc oxide (ZnO) nanostructures viz. ZnO nanocrystals (ZnONCs), ZnO nanoparticles (ZnONPs) and ZnO nanobelts (ZnONBs) were synthesized and characterized by UV-Vis, FTIR and SEM. A comparison of signal amplification by these ZnO nanostructures as judged by cyclic voltammetry (CV), electrochemical impedance spectroscopy (EIS) and Linear Sweep Voltammetry (LSV) revealed that ZnONCs are better sensing interface for electrochemical detection. When these ZnO nanostructure were compared electrochemically for sensing Vitamin C, ZnONC\'s sensor outperformed the ZnONP and ZnONB sensor and previously reported sensors. The ZnONCs/MB/FTO electrode showed a wide linear sensing range (0.001μM to 4000μM), low detection limit (0.0001μM), a small response time (5s) and a storage stability of 6months. To the best of our knowledge, this elevated sensitivity and remarkable stability for electrochemical Vitamin C detection using ZnONC\'s have not been reported so far.

Cetyl trimethyl ammonium bromide (CTAB) binds calf thymus (ct-) DNA like anionic biopolymers electrostatically and established equilibrium both in the ground as well as in excited state in aqueous medium at pH 7. Anionic sodium dodecyl sulfate (SDS) does not show even hydrophobic interaction with ct-DNA at low concentration. On contrary, SDS can establish well defined equilibrium with DNA bound CTAB in ground state where the same CTAB-DNA isosbestic point reappears. First report of internal charge transfer (ICT) based binding of CTAB with ct-DNA as well as ICT based interaction of anionic SDS with DNA bound CTAB that shows dynamic quenching contribution also. The reappearance of anodic peak and slight increase in cathodic peak current with increasing concentration (at lower range) of anionic SDS, possibly reflect the release of CTAB from DNA bound CTAB by SDS.

OBJECTIVE: This study sought to evaluate the clinical relevance of potential clopidogrel drug-drug interactions.
BACKGROUND: Some studies have demonstrated that statins and calcium-channel blockers (CCBs) may attenuate the pharmacodynamic effects of clopidogrel.
METHODS: The TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis in Myocardial Infarction 38) enrolled 13,608 patients with an acute coronary syndrome (ACS) and planned percutaneous coronary intervention (PCI), and randomized them to clopidogrel or prasugrel. Use of a statin or CCB was left to the discretion of the treating physician. A multivariable Cox model with propensity score was employed to evaluate the association between statin or CCB use and clinical outcomes.
RESULTS: Of the 6,795 subjects assigned to clopidogrel, 4,794 (70.6%) were on a CYP3A4-metabolized statin, and 966 (14.2%) were on a CCB at randomization. The risk of cardiovascular (CV) death, myocardial infarction (MI), or stroke was similar regardless of baseline use of statins (adjusted hazard ratio [HR]: 1.02, 95% confidence interval [CI]: 0.85 to 1.22) or CCBs (adjusted HR: 1.16; 95% CI: 0.94 to 1.43) in clopidogrel-treated patients. Further, the combined use of a CCB and atorvastatin 80 mg daily (adjusted HR: 0.82; 95% CI: 0.37 to 1.84), or a CCB, statin, and proton pump inhibitor (adjusted HR: 1.04; 95% CI: 0.70 to 1.54) were not associated with an increased risk of CV death, MI, or stroke. The use of statins or CCBs did not modify the relative efficacy of prasugrel versus clopidogrel for the primary endpoint (p for interaction = 0.43, 0.55, respectively).
CONCLUSIONS: In patients with ACS undergoing PCI, the use of statins or CCBs was not associated with an increased risk of CV events in clopidogrel-treated patients. Consistent results were observed when the drugs were administered alone, together, or in combination with proton pump inhibitors.

Progesterone (PROG) is promising as an important protective agent against various injuries to the nervous system. The present study was designed to investigate whether starting PROG administration, when symptomatology is already established, would alleviate the expression of nociceptive behaviors (mechanical allodynia and thermal hyperalgesia) and electrophysiological changes in a chronic constriction injury (CCI) model of neuropathic pain in rats. Male rats were given PROG (1.5, 3, 6 and 12 mg/kg, i.p.) 12 days after CCI induction, and dosing continued daily until day 26. Behavioral tests were done immediately before surgery (day 0) and on days 12, 26, 28, and 35 post-CCI, and were followed by electrophysiological measurements in the last day. PROG at doses of 6 or 12 mg/kg reduced both the thermal hyperalgesia and mechanical allodynia induced by CCI. Electrophysiological data indicated that CCI-induced animals had a remarkable decrement of both compound muscle and nerve action potential amplitudes recorded in the gastrocnemius muscle and sural nerve, respectively. CCI also caused a significant reduction in motor and sensory conduction velocities measured in the sural and tibial nerves, respectively. PROG at doses of 6 or 12 mg/kg induced a significant recovery of all electrophysiological changes. Our data indicated that starting PROG therapy when symptomatology is already established, and continuing it for a sufficient period of time, may have a therapeutic effect. This suggests that PROG may offer new strategies for the treatment of neuropathic pain.

OBJECTIVE: This study sought to define the ability of AMG 145, a monoclonal antibody directed against proprotein convertase subtilisin kexin type 9 (PCSK9), to enable subjects at high risk for major adverse cardiovascular events to achieve National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATP III) parameters for low-density lipoprotein cholesterol (LDL-C) and other lipid goals.
BACKGROUND: Many patients at high risk for adverse cardiovascular events are unable to achieve the NCEP-ATP III LDL-C goal of <70 mg/dl, even with high-potency statin therapy.
METHODS: In 282 subjects from the LAPLACE-TIMI 57 (LDL-C Assessment with PCSK9 monoclonaL Antibody Inhibition Combined With Statin thErapy-Thrombolysis In Myocardial Infarction 57) trial at high risk according to NCEP-ATP III criteria, we compared the proportion of subjects achieving the NCEP-ATP III recommended LDL-C goal of <70 mg/dl across treatment arms. Other outcomes included the triple goals of LDL-C <70 mg/dl, non-high-density lipoprotein cholesterol (HDL-C) <100 mg/dl, and apolipoprotein B (ApoB) <80 mg/dl.
RESULTS: During the dosing interval, more than 90% of subjects in both of the top dose groups every 2 weeks and every 4 weeks attained this lipid target over the dosing interval, with similar success rates for the triple lipid goal.
CONCLUSIONS: PCSK9 inhibition with AMG 145 enables high-risk patients to achieve established lipid goals. If this therapy demonstrates efficacy for reducing cardiovascular events with a favorable safety profile in ongoing phase 3 trials, we believe it will have major public health implications.

OBJECTIVE: Cardiac cachexia (CC) is associated with changes in body composition. Lipolysis and increased energy expenditure caused by A- and B natriuretic peptides (NPs) have been suggested to play a role in CC. We tested the hypothesis that neurohormones and adipokines are associated with body composition in CC and that a progressive loss of fat free mass (FFM) and fat mass (FM) takes place.
METHODS: Body composition with regard to FFM, FM, and body fat distribution was assessed by dual energy X-ray absorptiometry (DXA) in 19 non-diabetic patients with chronic heart failure (CHF) and CC and 38 controls (non-cachectic CHF and individuals with prior myocardial infarction-both n = 19) who were followed for 12 months. Biomarkers of neurohormonal stimulation, inflammation, and endothelial dysfunction were measured.
RESULTS: N-terminal proBNP (NT-proBNP), midregional proANP (MR-proANP), and total adiponectin were elevated in CHF (p<0.001) and correlated inversely to BMI and FM. An inverse correlation was observed between pro-adrenomedullin (MR-proADM) and FFM. During follow up body weight was unaltered in all groups even though FM increased by 1.35 kg (p<0.05) and FFM decreased by 0.5 kg (p<0.05) in CC patients. The latter correlated inversely to baseline NT-proBNP, MR-proANP, and MR-proADM (p<0.05). No correlation to changes in FM was found.
CONCLUSIONS: FM was associated with plasma NPs and total adiponectin at baseline; whereas changes in FM and FFM did not correlate to changes in NPs or adiponectin during follow up. Prospectively, FFM decreased but FM increased, despite stable body weight in CC.

BACKGROUND: Minimally invasive esophagectomy (MIE) has been advantageous for lowering pulmonary complications compared with open approaches.(1) However, pulmonary complications remain the most common morbidity after surgical resection of esophageal cancer.(2,3) The aim of this prospective, randomized, controlled, clinical trial was designed to see whether low tidal volume (VT) could further minimize pulmonary complications after MIE.
METHODS: Between June 2011 and July 2012, a total of 101 patients who underwent MIE received left-lung ventilation during thoracoscopic esophagectomy. All patients received left-lung ventilation during thoracoscopic esophagectomy. Patients were randomly assigned to a low VT (5 mL/kg + 5 cm H2O positive end-expiratory pressure) preserved ventilation (PV) group (n = 53) and a conventional VT (8 mL/kg) controlled ventilation (CV) group (n = 48) in the thoracic stage. Alveolar lavage fluid was harvested from the ventilated lung at intubation and at 18 hours after surgery for analysis of interleukin (IL)-1ß, IL-6, and IL-8 levels. Clinical characteristics, including patient demographics, operation features, and changes in oxygenation index, were recorded and analyzed. Pulmonary complications were identified and statistically compared between the 2 groups.
RESULTS: The clinical characteristics and operation features were comparable between the 2 groups. IL-1ß, IL-6, and IL-8 expressions in preoperative alveolar lavage fluid were similar between the 2 groups. Significantly lower IL expressions were observed in the PV group than those in the CV group at 18 hours after MIE (IL-1ß, 25.42 ± 31.01 vs 94.96 ± 118.24 pg/mL; IL-6, 30.86 ± 75.78 vs 92.99 ± 72.90 pg/mL; IL-8, 258.75 ± 188.24 vs 403.95 ± 151.44 pg/mL; all P < .05). The 18-hour postoperative oxygenation index was lower in the CV group than that in the PV group (292.85 ± 28.74 vs 326.35 ± 34.43; P = .046). Pulmonary complications were observed in 18 cases of our series, occurring more frequently on the ventilation side (right, 6 cases; and left, 12 cases). All patients were cured by conservative therapy without severe sequelae. The occurrence of pulmonary complications in the PV group was lower than that in the CV group (9.43% vs 27.08%; P = .021).
CONCLUSIONS: Lung injury due to intraoperative single-lung ventilation may contribute to pulmonary complications after MIE. Low VT ventilation could decrease ventilation-associated lung inflammation, thus minimizing pulmonary complications after MIE. Further studies, based on a larger volume of populations, are required to confirm these findings.

OBJECTIVE: This study sought to examine the relationship between baseline and on-study apolipoproteins (apo) A-1 and B and lipoprotein(a) [Lp(a)] levels and the development of subsequent cardiovascular (CV) events in the AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglyceride and Impact on Global Health Outcomes) trial.
BACKGROUND: Niacin has been reported to lower apoB and Lp(a) and to raise apoA-1.
METHODS: Individuals with CV disease and low baseline levels of high-density lipoprotein cholesterol were randomized to simvastatin plus placebo or simvastatin, plus extended-release niacin ([ERN], 1,500 to 2,000 mg/day), with ezetimibe added as needed, in both groups, to maintain an on-treatment low-density lipoprotein cholesterol in the range of 40 to 80 mg/dl. Hazard ratios (HRs) were used to evaluate the relationship between levels of apoA-1, apoB, and Lp(a), and CV events in each treatment group.
RESULTS: Baseline apoB and the apoB/apoA-I ratio were significantly predictive of CV events only for the placebo group (HR: 1.17 [p = 0.018] and HR: 1.19 [p = 0.016]). Baseline and on-study Lp(a) were predictive of CV events in both simvastatin plus placebo (baseline HR: 1.24 [p = 0.002] and on-study HR: 1.21 [p = 0.017]) and the simvastatin plus ERN group (baseline HR: 1.25 [p = 0.001] and on-study HR: 1.18 [p = 0.028]). The ERN modestly increased 1-year apoA-1 (7%), decreased apoB (13%), decreased the ApoB/ApoA-1 ratio (19%), and decreased Lp(a) 21%, but did not reduce CV events.
CONCLUSIONS: Lp(a) was associated with increased CV risk in both treatment groups indicating that it contributes to residual CV risk. However, there was no evidence that ERN reduced CV risk, despite favorable lipoprotein changes.

OBJECTIVE: This study sought to examine the relationship between niacin treatment, lipoproteins, and cardiovascular (CV) outcomes in this secondary analysis of the AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome With Low HDL/High Triglycerides and Impact on Global Health Outcomes) trial.
BACKGROUND: During a 3-year follow-up in 3,414 patients with established CV disease and low high-density lipoprotein cholesterol (HDL-C) levels, combined niacin + low-density lipoprotein cholesterol (LDL-C)-lowering therapy did not reduce CV events compared with LDL-C-lowering therapy alone.
METHODS: Subjects taking simvastatin and/or ezetimibe were randomized to receive extended-release (ER) niacin 1,500 to 2,000 mg or minimal immediate-release niacin (≤ 150 mg) as placebo at bedtime. LDL-C levels in both groups were maintained from 40 to 80 mg/dl. Hazard ratios were estimated by using Cox proportional hazards models for relationships between lipoproteins and the composite endpoint of CV death, myocardial infarction, acute coronary syndrome, ischemic stroke, or symptom-driven revascularization.
RESULTS: CV outcomes were not associated with ER niacin in any baseline lipoprotein tertile. In a subset of patients in both the highest triglyceride (≥ 198 mg/dl) and lowest HDL-C (<33 mg/dl) tertiles, ER niacin showed a trend toward benefit (hazard ratio: 0.74, p = 0.073). In-trial LDL-C levels, non-HDL-C levels, and the total cholesterol/HDL-C ratio were positively associated with CV events in the control group, but these relationships were absent in the ER niacin group.
CONCLUSIONS: Baseline lipoprotein tertiles did not predict differential benefit or harm with ER niacin added to LDL-C-lowering therapy, but a small dyslipidemic subgroup may benefit. ER niacin attenuated expected relationships of lipoprotein risk factors with CV events, raising the possibility that nonlipoprotein actions of niacin could affect risk. (Niacin Plus Statin to Prevent Vascular Events [AIM-HIGH]; NCT00120289).