Nitrogen diffusion in Zinc Oxide

Nitrogen migration in ZnO was investigated by nitrogen isotope diffusion. The samples were deposited using plasma assisted pulsed laser deposition. Nitrogen concentration depth profiles were obtained from secondary ion mass spectrometry measurements, and in gas effusion measurements, the molecular nitrogen flux was measured as a function of the heating rate. Measurements performed on sample stacks that were doped with isotopically enriched 15N and 14N in the top and bottom half of the samples, respectively, clearly demonstrate that nitrogen diffusion is governed by atomic diffusion and molecules are formed primarily at the sample surface. At high nitrogen concentrations, the diffusion coefficient, D, is thermally activated, while for low concentration diffusion, D is independent of temperature. The data can be described by a model, where N diffusion occurs between minimum energy positions by surmounting the barrier between sites at a saddle point. Separated in energy from the transport sites are deep levels with a concentration of amp; 8776;1018 amp; 8201;cm amp; 8722;3. For high concentration diffusion, the N chemical potential, amp; 956;N, resides at amp; 8776;1.36 amp; 8201;eV below the migration saddle point. For low concentration diffusion, amp; 956;N shifts deeper in energy with a rate of amp; 8776;2.8 amp; 8201;meV K as the temperature increases. From N effusion data, the nitrogen density of states is derived. For high N concentration diffusion, two peaks are observed at ES amp; 956;N amp; 8201; amp; 8201; amp; 8722;0.93 and amp; 8722;1.26 amp; 8201;eV, while for low N concentration diffusion, a prominent peak at ES amp; 956;N amp; 8201; amp; 8201; amp; 8722;1.63 amp; 8201;eV occurs. Applying density functional theory calculations, different microscopic diffusion mechanisms are evaluated, and the corresponding transition states are derive

Ferromagnetism and Electronic Structure of (Ga,Mn)As:Bi and (Ga,Mn)As Epitaxial Layers

The photoreflectance (PR) spectroscopy was applied to study the band-structure in GaAs:Bi, (Ga,Mn)As and (Ga,Mn)As:Bi layers with the 4% of Mn and 1 % of Bi content and, as a reference, undoped GaAs layer. All films were grown by low temperature (LT) MBE on semi-insulating (001) GaAs substrates. Photoreflec-tance studies were supported by Raman spectroscopy and high resolution X-ray diffractometry (XRD) measurements. Magnetic properties of the films were characterized with a superconducting quantum in-terference device (SQUID) magnetometer. Our findings were interpreted in terms of the model, which as-sumes that the mobile holes residing in the valence band of GaAs and the Fermi level position determined by the concentration of valence-band holes. When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/3533

Embracing the polypill as a cardiovascular therapeutic: is this the best strategy?

INTRODUCTION: Cardiovascular disease (CVD) is an important cause of mortality and morbidity worldwide. CVD morbidity and mortality are associated with significant financial costs related to hospitalization, medication, and lost productivity. The concept of the 'polypill' for the reduction of cardiovascular risk was proposed in 2000. A polypill is a fixed combination of drugs in a single tablet or capsule. The initial polypill consisted of three different classes of antihypertensive drugs (each at half dose), in addition to aspirin, a statin, and folic acid. The challenge today is to produce polypills containing drugs with established efficacy and complementary actions. Areas covered: The authors provide their expert perspectives on the polypill and consider the randomized clinical trials that have evaluated the safety, efficacy, adherence, and cost-effectiveness of polypills. Expert opinion: The polypill makes prescribing easier by reducing the need for complex treatment algorithms and dose titration. It also appears to be cost-effective. However, there are several issues that need to be addressed before the polypill can be used routinely. A single polypill formulation may not be suitable for all patients. It may be necessary to develop several types of polypill to meet the needs of different patient groups

Efficacy of Statin Therapy in Pulmonary Arterial Hypertension : a Systematic Review and Meta-Analysis

Since the evidence regarding statin therapy in PAH has not been conclusive, we assessed the impact of statin therapy in PAH through a systematic review and meta-analysis of available studies. We searched selected databases up to August 1, 2015 to identify the studies investigating the effect of statin administration on PAH. Meta-analysis was performed using either a fixed-effects or random-effect model according to I 2 statistic. Meta-analysis of 8 studies with 665 patients did not suggest any significant improvement in 6-min walking distance (6MWD) by statin therapy (weighed mean difference [WMD]:-6.08 m, 95% confidence interval [CI]:-25.66, 13.50, p = 0.543; Q = 8.41, I 2 = 28.64%). Likewise, none of the other indices including pulmonary arterial pressure (WMD:-0.97 mmHg, 95%CI:-4.39, 2.44, p = 0.577; Q = 14.64, I 2 = 79.51%), right atrial pressure (WMD: 1.01 mmHg, 95%CI:-0.93, 2.96, p = 0.307; Q = 44.88, I2 = 95.54%), cardiac index (WMD: 0.05 L/min/m2, 95%CI:-0.05, 0.15, p = 0.323; Q = 3.82, I 2 = 21.42%), and pulmonary vascular resistance (WMD:-1.42 dyn 17s/cm5, 95%CI:-72.11, 69.27, p = 0.969; Q = 0.69, I2 = 0%) was significantly altered by statin therapy. In conclusion, the results of the meta-analysis did not show a statistically significant effect of statin therapy in the improvement of 6MWD, pulmonary arterial pressure, right atrial pressure, cardiac index and pulmonary vascular resistance

Phosphorylation Regulates SIRT1 Function

BACKGROUND: SIR2 is an NAD(+)-dependent deacetylase [1]-[3] implicated in the regulation of lifespan in species as diverse as yeast [4], worms [5], and flies [6]. We previously reported that the level of SIRT1, the mammalian homologue of SIR2 [7], [8], is coupled to the level of mitotic activity in cells both in vitro and in vivo[9]. Cells from long-lived mice maintained SIRT1 levels of young mice in tissues that undergo continuous cell replacement by proliferating stem cells. Changes in SIRT1 protein level were not associated with changes in mRNA level, suggesting that SIRT1 could be regulated post-transcriptionally. However, other than a recent report on sumoylation [10] and identification of SIRT1 as a nuclear phospho-protein by mass spectrometry [11], post-translational modifications of this important protein have not been reported. METHODOLOGY/PRINCIPAL FINDINGS: We identified 13 residues in SIRT1 that are phosphorylated in vivo using mass spectrometry. Dephosphorylation by phosphatases in vitro resulted in decreased NAD(+)-dependent deacetylase activity. We identified cyclinB/Cdk1 as a cell cycle-dependent kinase that forms a complex with and phosphorylates SIRT1. Mutation of two residues phosphorylated by Cyclin B/Cdk1 (threonine 530 and serine 540) disturbs normal cell cycle progression and fails to rescue proliferation defects in SIRT1-deficient cells [12], [13]. CONCLUSIONS/SIGNIFICANCE: Pharmacological manipulation of SIRT1 activity is currently being tested as a means of extending lifespan in mammals. Treatment of obese mice with resveratrol, a pharmacological activator of SIRT1, modestly but significantly improved longevity and, perhaps more importantly, offered some protection against the development of type 2 diabetes mellitus and metabolic syndrome [14]-[16]. Understanding the endogenous mechanisms that regulate the level and activity of SIRT1, therefore, has obvious relevance to human health and disease. Our results identify phosphorylation by cell cycle dependent kinases as a major mechanism controlling the level and function of this sirtuin and complement recent reports of factors that inhibit [17], [18] and activate [19] SIRT1 by protein-protein interactions

The potential role of mitochondrial ATP synthase inhibitory factor 1 (IF1) in coronary heart disease: a literature review

Cardiovascular disease (CVD) is the leading cause of death worldwide, and so the search for innovative and accurate biomarkers for guiding prevention, diagnosis, and treatment is a valuable clinical and economic endeavor. Due to a recent findings that the serum concentration of mitochondrial ATP synthase inhibitory factor 1 (IF1) is an independent prognostic factor in patients with coronary heart disease (CHD), we reviewed the role of this protein in myocardial ischemic preconditioning, its correlation to plasma high density lipoprotein (HDL), the predictive potential in patients with CHD, and its interplay with angiogenesis. IF1 has been positively correlated with plasma HDL-cholesterol, and is independently negatively associated with all-cause and CV mortality in patients with CHD. However, this conclusion is prevalently based on limited data, and more research is needed to draw definitive conclusions. IF1 seems to play an additional role in increasing cell vulnerability in oncologic diseases but may also function as modest inhibitor of angiogenesis in physiological conditions. It has been also explored that IF1 may rather act as a modulator of other molecules more significantly involved in angiogenesis, especially apolipoprotein A1 on which the largest effect could be observed. In conclusion, more research is needed to characterize the role of IF1 in patients with CHD