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Un-doped VO2, tungsten (W)-doped VO2, and W/Zn co-doped VO2 thin films were successfully prepared by two DC magnetron sources and co-sputtered at a substrate temperature of 425°C onto soda lime glass substrates. The aim was to find whether co-doping of VO2 films with W and Zn could decrease the transition temperature and increase both luminous transmittance and solar transmittance modulation (ΔTsol) of VO2 -based thin films. The thin films were characterized by x-ray diffraction, atomic force microscopy, Rutherford backscattering spectroscopy, the two-point probe technique, Hall effect measurement system, and a PerkinElmer Lambda 1050+ UV/VIS/NIR) spectrometer. This work revealed that a controlled amount of Zn in the W-doped VO2 films showed solar transmittance modulation of 4%. It further improves the luminous transmittance to ~ 46%, lowering the phase transition temperature to below 27°C, compared to un-doped VO2 and W-doped VO2 thin films at 64.8°C and 44°C, respectively. These results show that the combined effect of W and Zn doping on VO2 films has the potential to make the films useful for smart window applications. [ABSTRACT FROM AUTHOR]

The effect of thermal annealing on epitaxial GeSn (6.5% Sn) strained layers grown on Ge-buffered Si(100) wafers has been investigated using Rutherford backscattering spectrometry and X-ray diffraction to unambiguously determine the Sn substitutional content as well as the elastic strain in the layers. Vacuum annealing at temperatures below 400 °C for 20 min has no noticeable effect on the strain in the epitaxial layers. Once the temperature was raised above 400 °C, however, relaxation of the layer sets in and the GeSn layer has essentially completely relaxed following a 20 min anneal at 650 °C. Using Rutherford backscattering and channelling spectrometry to provide compositional information as a function of depth enables one to monitor the effect of the thermal anneal on the Sn distribution throughout the layer, and also to directly extract their substitutional fraction (i.e., their solubility in the lattice). The results obtained show that when the relaxation initially sets in both the Ge and the Sn remain firmly bound in substitutional lattice sites and it is only around 600 °C, and after substantial relaxation has taken place, that Sn is finally expelled from lattice sites and diffuses to the surface of the sample. [ABSTRACT FROM AUTHOR]

This study investigated the essential element (P, Cl, K, Ca, Mn,Fe,Cu and Zn) concentrations of some local and imported rice commonly consumed in Nigeria. This is done in order to select the rice with high nutrient to combat malnutrition, especially in children. Proton-induced X-ray emission (PIXE) techniques available at iThemba Labs Someset West, South Africa was used for the analysis. The elemental concentration obtained for Ofada are 8805.5±221, 276.5±32, 3704.5±39, 212±8, 110.5±8, 125.5±7, 14.5±1 and 44.5±4 ppm, while for the imported rice we got 2862.5±150, 399±22, 1433±28, 4.15±2, 8.4±0.8, 4.75±1 and 9.5±2 ppm for P, Cl, K, Ca, Mn, Fe, Cu and Zn respectively. Phosporus (P) has the highest elemental concentration in all samples. Ofada, one of the local rice was found to have the highest elemental concentration while pure imported rice had the lowest concentrations of the elements. The study suggests that consumption of locally-cultivated (Ofada) rice should be encouraged in order to reduce malnutrition in children in Nigeria. [ABSTRACT FROM AUTHOR]

Noble gas ion sputtering combined with Auger electron spectroscopy (AES) analysis has been applied extensively for elemental composition depth profiling of the target materials. Such depth profiles have been used widely not only for elemental composition analysis but also for extracting the sputtering yields of the target materials. Despite a large number of publications on sputtering yields there are only a small number of reports (in literature) on the measured sputtering yields of indium compounds. Indium is used to dope semiconductors for electronic devices (transistor) and thin film solar cells. In order to obtain accurate depth information (for indium thin films) with Ar+ ion profiling, it is essential to have reliable sputtering yields for the In metal. In this study, the argon ion sputtering yields of indium films are reported for a range of low ion beam energies (0.5-4.0 keV). The indium films (106 nm) were deposited on SiO2 substrates under vacuum by electron beam evaporation. The films were subjected to Ar+ ion sputtering combined with AES analysis to obtain the depth profiles, which were used to extract the sputtering yield values. The obtained sputtering yield values are in the range of 2 to 6 atoms/ions for Ar+ ion beam energies in the range of 0.5-4.0 keV, respectively. The Monte Carlo simulation code, Stopping and Range of Ions in Materials (SRIM) were used to simulate the Ar+ ion bombardment of the indium film and to obtain the surface sputtering yields and influences the structures as deposited and the corresponding activities induced. These were also calculated using a semi-empirical formula developed for such predictions. The sputtering yields obtained from SRIM and the semi-empirical formula are in agreement with the experimental values. [ABSTRACT FROM AUTHOR]

In this article, we used a two-step chemical vapor deposition (CVD) method to synthesize methylammonium lead-tin triiodide perovskite films, MAPb 1-x Sn x I 3 , with x varying from 0 to 1. We successfully controlled the concentration of Sn in the perovskite films and used Rutherford backscattering spectroscopy (RBS) to quantify the composition of the precursor films for conversion into perovskite films. According to the RBS results, increasing the SnCl 2 source amount in the reaction chamber translate into an increase in Sn concentration in the films. The crystal structure and the optical properties of perovskite films were examined by X-ray diffraction (XRD) and UV-Vis spectrometry. All the perovskite films depicted similar XRD patterns corresponding to a tetragonal structure with I4cm space group despite the precursor films having different crystal structures. The increasing concentration of Sn in the perovskite films linearly decreased the unit volume from about 988.4 Å 3 for MAPbI 3 to about 983.3 Å 3 for MAPb 0 . 39 Sn 0 . 61 I 3 , which consequently influenced the optical properties of the films manifested by the decrease in energy bandgap (E g ) and an increase in the disorder in the band gap. The SEM micrographs depicted improvements in the grain size (0.3-1 µm) and surface coverage of the perovskite films compared with the precursor films.

Cowpea is a nutritionally important drought-resistant legume in sub-Saharan Africa. It is, however, underutilised, in part due to the hard-to-cook (HTC) defect caused by adverse storage conditions resulting in seeds not softening during cooking. This study introduced a novel evaluation of the potential role that minerals play in the development of the HTC defect. The mineral distribution in the cotyledons of normal and HTC cowpeas were analysed by Proton Induced X-ray Emission (PIXE) spectrometry. The phytate, tannin and total phenolic contents were analysed together with in vitro mineral bioaccessibility. In HTC cowpeas, Ca and Mg were more concentrated in the cell wall-middle lamella area of the parenchyma cells. This, together with the reduction in phytate content, confirmed the 'phytase-phytate-mineral' hypothesis as a mechanism for development of the HTC defect. Despite the phytate reduction in stored cowpeas, the HTC defect decreased the bioaccessibility of Ca, Fe and Zn in cowpeas., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Specific binding of [3H]-N-alpha-methylhistamine to homogenates from cerebral cortex tissue was analyzed in aged Wistar Kyoto (WKY) and Spontaneously Hypertensive rats (SHR). Scatchard plot analysis of [3H]-N-alpha-methylhistamine binding of the H3 receptor in the cerebral cortex from aged (6, 9, 12, and 16 week) SHR animals indicated that Bmax increased, respectively, 38.05 +/- 1.58, 59.63 +/- 2.48, 79.17 +/- 5.02, and 84.41 +/- 3.72 fmol/mg of protein. Binding studies using tissue from WKY rats indicated that maximal binding (Bmax) of the ligand to the receptor was not significantly altered. The analyses also yielded Kd values of 5, 7.2, 6.3 and 3.8 nM in SHR tissue respectively. Primers based on the sequence of the third intracellular loop of the H3 receptor were amplified at 35 cycles yielding several amplicons. These amplicons expressed sizes 875, 485, and 280 bp in 6 and 9 week cortical tissue from WKY animals where as in cortical tissue from 6 and 9 week SHR animals only two amplicons were expressed, 485 and 280 bp, respectively. Differences in gene expression for 12 and 16 week WKY and SHR rats were also compared using identical primers. Five amplicons were expressed in cortical tissue from 12 and 16 week WKY rats with 1000, 900, 821, 485, and 430 bp where as in 12 and 16 week SHR animals only one amplicon was expressed at 485 bp. The present results imply (1) that H3 receptor density in cortical tissue of SHR animals increases with age where as the number of the expressed amplicons of the detected H3 receptor decreases; and (2) even though a decrease in number of expressed amplicons of the H3 receptor were observed, an increase in expression of the larger amplicon (~500 bp) is evident.

Histamine (HA) is one of many neurotransmitters that have been implicated in cardiovascular functioning. Alterations in vascular smooth muscle due to the effects of histamine have been suggested. We investigated the modulatory effect of HA on mitogen activated protein kinase (MAPK) expression, specifically extracellular regulating kinase (ERK) 1 & 2 in vascular smooth muscle cells (VSMCs) from both spontaneously hypertensive (SHR) and control Wistar Kyoto (WKY) rats. Cross-talking between calcium (Ca2+) and HA during HA-induced modulatory effect on MAPK expression in SHR VSMCs was also investigated. A stimulatory increase in expression of ERK 1 & 2 was observed to be dose and time dependent with maximum expression occurring within 5 min in both SHR and WKY VSMCs. The stimulatory increase in expression is persistent for 60 min in SHR VSMCs, whereas, in WKY cells the stimulatory effect persists for only 20 min. Mepyramine, the H1 receptor antagonist, reduced the HA-induced increase in ERK 1 & 2 significantly in SHR VSMCs. A reduction in the HA stimulated increase in ERK 1 & 2 expression was observed at 20 min of exposing cells to diltiazem, the calcium channel blocker, whereas, the calcium chelator, BAPTA effect on ERK 1 & 2 expression was observed within 5 min in SHR VSMCs. The data demonstrates that cross-talking occurs between HA stimulation and Ca2+ induction during HA-induced activation of ERK 1 & 2 in VSMCs of both cell types. Although both intracellular calcium ([Ca2+]i) and extracellular Ca2+ maybe involved in the activation of ERK 1 & 2 by HA, the dependence on [Ca2+]i is more dramatic than the dependence on extracellular Ca2+ in hypertensive cells, which may contribute to the role of HA as a risk factor of hypertension in VSMCs of the aorta.

Protein Kinase C (PKC) exists as one of twelve serine/threonine isoforms and has been found to mediate ethanol-induced activation of the Mitogen-Activated Protein Kinase (MAPK) pathway. The aim of this study was to determine the PKC isoform(s) that are mediators of ethanol-induced MAPK activity (ERK 1 and 2) and to verify the necessity of calcium in this activation process using cell culture in the presence and absence of ethanol, and other agents that modulate PKC expression. Western blotting analysis was used to assess the effect of ethanol on activating classical (alpha/ssII), novel (delta) and atypical (zeta/lambda) PKC isoforms in vascular smooth muscle cells (VSMCs). The results indicate that ethanol treated VSMCs express the classical PKC-alpha/ssII, novel PKC-delta, and atypical PKC-zeta/lambda isoforms. The expression of PKC-alpha/ssII was inhibited within the first two min of stimulation, followed by activation with maximum expression at 10 min. Similarly, PKC-delta and zeta expressions were suppressed during the first two min of ethanol stimulation with maximum increase in expressions at 10 min. The PKC inhibitor GF109203X and the calcium chelating agent BAPTA, enhanced ethanol-induced PKC expression, whereas, diltiazem reduced expression of PKC by 10% of control. On the other hand, BAPTA in the presence of GF10203X inhibited expression of ERK 1 & 2 downstream from the PKC pathway, whereas, BAPTA alone enhanced expression. These results demonstrate also that classical, novel, and atypical PKCs respond to ethanol during the initial phase of activation of ERK 1 & 2.

Cadmium (Cd) is frequently used in various industrial applications and is a ubiquitous environmental toxicant, also present in tobacco smoke. An important route of exposure is the circulatory system whereas blood vessels are considered to be main stream organs of Cd toxicity. Our previous results indicate that cadmium chloride (CdCl2) affects mean arterial blood pressure in hypertensive rats. We hypothesized that Cd alters the intracellular calcium transient mechanism, by cadmium-induced stimulation of MAPKs (ERK 1 & 2) which is mediated partially through calcium-dependent PKC mechanism. To investigate this hypothesis, we exposed primary cultures of vascular smooth muscle cells (VSMCs) from wistar kyoto (WKY) and spontaneously hypertensive rats (SHR) to increased concentrations of CdCl2 on cell viability, expression of mitogen-activated protein kinases (MAPKs/ERK 1 & 2), and protein kinase C (PKC) which are activated by Cd in several cell types. The results from these studies indicate that CdCl2 decreased cell viability of both SHR and WKY VSMCs in a concentration dependent-manner. Viability of both cell types decreased 33+/-5.3 (SHR) and 39+/-2.3% (WKY) when exposed to 1 microM CdCl2, whereas, 8 and 16 microM reduced viability by 66+/-3.1 and 62+/-4.5% in SHR cells. CdCl2 increased ERK 1 & 2 in a biphasic manner with maximum increase occurring when cells are exposed to 1 and 4 muM in SHR VSMCs, whereas, a reduction in ERK 1 and 2 is observed when WKY cells are treated with 2 microM. The results also indicate that CdCl2 increased PKC a/Beta in both SHR and WKY VSMCs with a greater increase in expression in SHR VSMCs. In addition, the [Ca2+]i chelator, BAPTA, suppressed the CdCl2 effect, whereas, the PKC inhibitor, GF109203X, reduced the CdCl2 induced-effect on PKC expression. The present studies support the hypothesis that Cd can be a risk factor of hypertension through dysfunction of vascular smooth muscle cells under certain conditions.

The aim of this study was to determine the pathway(s) by which ethanol activates mitogen-activated protein kinase (MAPK) signaling and to determine the role of Ca2+ in the signaling process. MAPK signaling was determined by assessing MAPK activity, measuring phosphorylated extracellular signaling-regulated kinase (pp 44 ERK-1 and pp 42 ERK-2) expression and ERK activity by measuring ERK-2-dependent phosphorylation of a synthetic peptide as a MAPK substrate in rat vascular smooth muscle cells. Ethanol activated extracellular signal-regulated kinase expression (ERK 1 and 2) could be observed when vascular smooth muscle cells (VSMCs) were stimulated for 5 min or less, but was inhibited when cells are treated for 10 min or more with 1-16 mM of ethanol. Maximum ethanol-induced MAPK activity was observed within 5 min with 4 or 8 mM. Ethanol stimulated MAPK activity was blocked by the protein kinase C (PKC) inhibitor (GF109203X) and epidermal growth factor (EGF) receptor antagonist (PD153035) by 41 +/- 24 and 34 +/- 12.3%, respectively. The calcium channel blocker, diltiazem and the chelating agent, BAPTA, reduced the activation of MAPK activity by ethanol, significantly. The data demonstrate that ethanol-stimulated MAPK expression is mediated partially through both the EGF-receptor and PKC intermediates and that activation through the PKC intermediate is calcium-dependent.

The involvement of protein kinase C (PKC) in the regulation of [3H]choline cotransport was studied in Limulus brain hemi-slice preparations. The PKC activators, phorbol 12-myristate 13-acetate (PMA) or phorbol 12,13-dibutyrate (PDBu), significantly decreased [3H]choline cotransport. Conversely, the PKC inhibitors, staurosporine (STAURO) and polymyxin B (PMB), each increased [3H]choline cotransport. These PKC inhibitors prevented the phorbol ester-induced reduction of transport. Both the PMA induced decrease and the STAURO induced increase in [3H]choline cotransport were paralleled by respective and comparable changes in [3H]hemicholinium-3 (HC-3) specific binding. Pre-exposure of brain hemi-slices to elevated potassium chloride (120 mM KCl) resulted in a doubling of [3H]choline cotransport and [3H]HC-3 binding. The enhancement of [3H]choline cotransport by STAURO and antecedent 120 mM KCl treatment were additive. PMA did not significantly alter elevated potassium stimulated transport. Moreover, arachidonyltrifluoromethyl ketone (AACOCF3) and quinacrine (QUIN), both phospholipase A2 (PLA2) inhibitors, markedly decreased enhanced [3H]choline transport and [3H]HC-3 binding induced by antecedent exposure to depolarizing concentrations of potassium. These results suggest that PKC and PLA2 are involved in the regulation of [3H]choline cotransport but at different regulatory sites.