A promising RVO4:Eu3+,Li+@SiO2 (R = Gd,Y and Gd/Y) red‐emitting phosphor with improved luminescence (cd/m2) and colour purity for optical display applications

Red emission intensity was optimized in three stages, by investigating the effects of: (i) host composition (Gd, Y and Gd/Y), (ii) codoping Li⁺ as a sensitizer and, finally, (iii) with a SiO₂ shell coating as a protecting layer. Lanthanide vanadate powder phosphors were synthesized using a modified colloidal precipitation technique. The effects of SiO₂ coating on phosphor particles were characterized using scanning electron microscopy (SEM)‐EDAX, transmission electron microscopy (TEM), Fourier transform infrared (FTIR) and photoluminescence (PL) measurements. An improvement in the PL intensity on Li codoping was due to improved crystallinity, which led to higher oscillating strengths for the optical transitions, and also a lowering of the inversion symmetry of Eu³⁺ ions. Red emission intensity due to ⁵D₀ → ⁵D₂ transition of the phosphor Y_0.94VO₄:Eu³⁺_0.05,Li⁺_0.01 was enhanced by 22.28% compared with Y_0.95VO₄:Eu³⁺_0.05, and was further improved by 58.73% with SiO₂ coating. The luminescence intensity (I) and colour coordinates (x, y) of the optimized phosphor Y_0.94VO₄:Eu³⁺_0.05,Li⁺_0.01@SiO₂, where I = 13.07 cd/m² and (x = 0.6721, y = 0.3240), were compared with values for a commercial red phosphor (Y₂O₂S:Eu³⁺), where I = 27 cd/m² and (x = 0.6522, y = 0.3437). The measured colour coordinates are superior to those of the commercial red phosphor, and moreover, match well with standard NTSC values (x = 0.67, y = 0.33). Copyright © 2015 John Wiley & Sons, Ltd.     

Seasonal incidence of aphid,Amphorophora ampullata Bukton (Homoptera: Aphididae) on fern,Hypolepis polypodioides (Blume) Hook (Hypolepidaceae) from Western Himalaya

Seasonal incidence of aphid, Amphorophora ampullata on Hypolepis polypodioides was recorded throughout the year from November 2012 to November 2013 at weekly interval. Peak incidence of aphid was recorded during third week of November 2012 (25.94 ± 2.39 aphids/pinna), later the aphid population gradually decreased from December 2012 onwards and reached below threshold level during the last week of January (0.1 ± 0 aphids/pinna). The aphid population starts building up again from first week of February 2013 (1.6 ± 0.13 aphids/pinna) and attained its peak in the last week of August (32.17 ± 1.22 aphids/pinna) then decreased gradually in the first week of September (20.82 ± 4.70 aphids/pinna). Aphid densities again increased gradually from second week of September (21.62 ± 3.02 aphids/pinna) to November 2013 and reached maximum aphid densities during November (56.55 ± 4.34 aphids/pinna). Among weather parameters, aphid population showed significant positive correlation with relative humidity during morning hours.     

Calcitroic acid, end product of renal metabolism of 1,25-dihydroxyvitamin D3 through C-24 oxidation pathway

About a decade ago calcitroic acid was isolated as a major side chain cleaved water-soluble metabolite of 1,25-dihydroxyvitamin D3 [Esvelt, R. P., Schnoes, H. K., & Decula, H. F. (1979) Biochemistry 18, 3977]. Presently, calcitroic acid is being considered as the major excretory form of 1,25-dihydroxyvitamin D3. However, the exact site or sites of calcitroic acid production and the possible side chain modified intermediary metabolites that may be formed during the conversion of 1,25-dihydroxyvitamin D3 into calcitroic acid are not fully understood. In the mean time there have been many advances in our understanding of the side-chain metabolism of 1,25-dihydroxyvitamin D3. It is now well established that both the kidney and the intestine metabolize 1,25-dihydroxyvitamin D3 through the C-24 oxidation pathway according to the following steps: 1,25-dihydroxyvitamin D3----1,24,25-trihydroxyvitamin D3----1,25-dihydroxy-24-oxovitamin D3-----1,23,25-trihydroxy-24-oxovitamin D3. Recently, we identified 1,23-dihydroxy-24,25,26,27-tetranorvitamin D3 (C-23 alcohol) as a major side chain cleaved lipid-soluble metabolite of 1,25-dihydroxyvitamin D3 and further extended the aforementioned C-24 oxidation pathway in the kidney by demonstrating 1,23,25-trihydroxy-24-oxovitamin D3 as the precursor of C-23 alcohol [Reddy, G. S., Tserng, K. Y., Thomas, B. R., Dayal, R., & Norman, A. W. (1987) Biochemistry 26, 324]. In this present study, we investigated the metabolic fate of 1,25-dihydroxyvitamin D3 (3 X 10(-10) M) in the perfused rat kidney and identified calcitroic acid as the major water-soluble metabolite of 1,25-dihydroxyvitamin D3.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in myocardial contractile protein ATPases in chronically adrenalectomized rats with and without glucocorticoid replacement

Studies were conducted to examine the effects of chronic adrenalectomy (Adx) and adrenalectomy plus glucocorticoid replacement therapy on rat cardiac contractile protein ATPase activities. The Ca2+-dependent Mg-ATPase activity of myofibrils isolated from rat ventricles 3 weeks postadrenalectomy (Adx) was significantly decreased at all pCa2+ concentrations (P less than 0.01), compared to sham-operated (SO) rats. Similarly, Ca2+-, K+-EDTA, and actin-activated myosin ATPase activities of Adx rat hearts were markedly decreased below that of SO rats (P less than 0.01). Dexamethasone administration to Adx rats prevented the decrease of Ca2+- and K+-ATPase activities of myosin, but not of myofibrillar Ca2+-dependent Mg-ATPase or actin-activated myosin Mg-ATPase activities. These studies suggest that glucocorticoid insufficiency induced by adrenalectomy results in altered myocardial contractile protein ATPase activity which may underlie impaired cardiac performance.     

Early treatment with deferoxamine limits myocardial ischemic/reperfusion injury

Oxygen-derived free radicals (the superoxide anion O2- and hydroxyl radical.OH) have been implicated in myocardial injury associated with coronary artery occlusion followed by reperfusion. Transition metals (such as iron or copper) are needed to catalyze the formation of the .OH radical and subsequent .OH-mediated lipid peroxidation, yet the role of these transition metals in the pathogenesis of myocyte necrosis remains undefined. To address this issue, 21 dogs underwent 2 h of coronary artery occlusion and 4 h of reperfusion. Each animal was randomly assigned into 1 of 3 treatment groups: 7 received the iron chelator deferoxamine beginning 30 min preocclusion, 7 received deferoxamine beginning 5 min prior to reperfusion, while 7 dogs served as saline controls. Deferoxamine effectively chelated free iron in both treatment groups (total urine iron content averaged 42 +/- 16, 662 +/- 177 and 803 +/- 2.5 micrograms in control, pretreated, and deferoxamine at reperfusion groups respectively; p less than 0.05), but had no significant effect on in vivo area at risk (AR), hemodynamic parameters, collateral blood flow during occlusion, or myocardial blood flow following reperfusion. Area of necrosis (AN) in dogs pretreated with deferoxamine (34.6 +/- 3.7% of the AR; p less than 0.05) was significantly smaller than that observed in the saline control group (55.4 +/- 4.7% of the AR). Deferoxamine administered at the time of reperfusion, however, had no significant effect on infarct size (AN/AR = 54.3 +/- 8.7%, p = NS vs. controls). Thus, early treatment with the iron chelator deferoxamine acutely reduced the extent of myocyte necrosis produced by 2 h of transient coronary artery occlusion in the canine model.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of prolactin on DNA methylation in the liver and kidney of rat

Prolactin is an important growth modulatory hormone in fetal and adult tissues. It stimulates DNA synthesis and enzymatic markers of the G1 phase of cell cycle in rat liver and other tissues. In this study the effects of prolactin on 5-methyl cytosine content in liver and kidney of rats was studied using HPLC. Prolactin treatment caused hypomethylation of DNA in the liver and kidney of immature rats at 48 h after treatment and the effect remained even at 72 h. Prolactin also caused hypomethylation of DNA in the kidney and liver of adult rats at 48 h after treatment. These results indicate that prolactin probably regulates DNA methylation in the liver and kidney of immature and adult rats.