Excitation mechanisms and effects of dopant concentration in Gd2O2S : Tb3+ phosphor

Gadolinium oxysulfide powders doped with different Tb3+ concentrations were prepared from sulfur vaporization on rare earths' basic carbonate precursors. Single-phase Gd2O2S samples were obtained, with Tb3+ doping up to 9 at%. The study of the excitation mechanisms revealed that the Tb3+ emission might occur after the direct Tb3+ excitation either by energy transfer from Gd3+ or from the phosphor host. The characteristic terbium emission lines were observed, resulting from the radiative decay from D-5(3) or D-5(4), to F-7(j) levels. The cross-relaxation phenomenon was observed and its effects on the materials emission color were discussed based on the CIE diagram. By using time-resolved spectroscopy, D-5(3) -> F-7(J) and D-5(4) -> F-7(J) transitions were separated. (c) 2007 Elsevier B.V. All rights reserved.

Reproductive mechanisms in a Nasutitermes species (Isoptera: Termitidae)

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Time dependence and energy-transfer mechanisms in Tm3+Ho3+ and Tm3+-Ho3+ co-doped alkali niobium tellurite glasses sensitized by Yb3+

Glass samples with the composition (mol%) 80TeO(2)-10Nb(2)O(5)-5K(2)O-5Li(2)O, stable against crystallization, were prepared containing Yb3+, Tm3+ and Ho3+. The energy transfer and energy back transfer mechanisms in samples containing 5% Yb3+-5% Tm3+ and 5% Yb3+-5% Tm3+-0.5% Ho3+ were estimated by measuring the absorption and fluorescence spectra together with the time dependence of the Yb3+ F-2(5/2) excited state. A good fit for the luminescence time evolution was obtained with the Yokota-Tanimoto's diffusion-limited model. The up-conversion fluorescence was also studied in 5% Yb-5% Tm. 5% Yb-0.5% Ho and 5% Yb-5% Tm-0.5% Ho tellurite glasses under laser excitation at 975 nm. Strong emission was observed from (1)G(4) and F-3(2) Tm3+ energy levels in all samples. The S-5(2) Ho3+ emission was observed only in Yb3+Ho3+ samples being completely quenched in Yb3+/Tm3+/Tm3+ samples. (C) 2001 Elsevier B.V. B.V. All rights reserved.

Serotonergic mechanisms of the lateral parabrachial nucleus in renal and hormonal responses to isotonic blood volume expansion

This study investigated the involvement of serotonergic mechanisms of the lateral parabrachial nucleus (LPBN) in the control of sodium (Na+) excretion, potassium (K+) excretion, and urinary volume in unanesthetized rats subjected to acute isotonic blood volume expansion (0.15 M NaCl, 2 ml/100 g of body wt over 1 min) or control rats. Plasma oxytocin (OT), vasopressin (VP), and atrial natriuretic peptide (ANP) levels were also determined in the same protocol. Male Wistar rats with stainless steel cannulas implanted bilaterally into the LPBN were used. In rats treated with vehicle in the LPBN, blood volume expansion increased urinary volume, Na+ and K+ excretion, and also plasma ANP and OT. Bilateral injections of serotonergic receptor antagonist methysergide (1 or 4 mu g/200 eta 1) into the LPBN reduced the effects of blood volume expansion on increased Na+ and K+ excretion and urinary volume, while LPBN injections of serotonergic 5-HT2a/HT2c receptor agonist, 2.5-dimetoxi-4-iodoamphetamine hydrobromide (DOI;1 or 5 mu g/200 eta 1) enhanced the effects of blood volume expansion on Na+ and K+ excretion and urinary volume. Methysergide (4 mu g) into the LPBN decreased the effects of blood volume expansion on plasma ANP and OT, while DOI (5 mu g) increased them. The present results suggest the involvement of LPBN serotonergic mechanisms in the regulation of urinary sodium, potassium and water excretion, and hormonal responses to acute isotonic blood volume expansion.

Central serotonergic and adrenergic/imidazoline inhibitory mechanisms on sodium and water intake

Recent studies have shown the existence of two important inhibitory mechanisms for the control of NaCl and water intake: one mechanism involves serotonin in the lateral parabrachial nucleus (LPBN) and the other depends on alpha(2)-adrenergic/imidazoline receptors probably in the forebrain areas. In the present study we investigated if alpha(2)-adrenergic/imidazoline and serotonergic inhibitory mechanisms interact to control NaCl and water intake. Male Holtzman rats with cannulas implanted simultaneously into the lateral ventricle (LV) and bilaterally into the LPBN were used. The ingestion of 0.3 M NaCl and water was induced by treatment with the diuretic furosemide (10 mg/kg of body weight)+the angiotensin converting enzyme inhibitor captopril (5 mg/kg) injected subcutaneously 1 h before the access of rats to water and 0.3 M NaCl. Intracerebroventricular (i.c.v.) injection of the alpha(1)-adrenergic/imidazoline agonist clonidine (20 nmol/l RI) almost abolished water (1.6 +/- 1.2, vs. vehicle: 7.5 +/- 2.2 ml/2 h) and 0.3 M NaCl intake (0.5 +/- 0.3, vs. vehicle: 2.2 0.8 ml/2 h). Similar effects were produced by bilateral injections of the 5HT(2a/2b) serotonergic agonist 2,5-dimetoxy-4-iodoamphetamine (DOI, 5 mug/0.2 mul each site) into the LPBN on water (3.6 +/- 0.9 ml/2 h) and 0.3 M NaCl intake (0.4 +/- 0.2 m1/2 h). Injection of the (alpha(2)-adrenergic/imidazoline antagonist idazoxan (320 nmol) i.c.v. completely blocked the effects of clonidine on water (8.4 +/- 1.5 ml/2 h) and NaCl intake (4.0 +/- 1.2 ml/2 h), but did not change the effects of LPBN injections of DOI on water (4.2 +/- 1.0 ml/2 h) and NaCl intake (0.7 +/- 0.2 ml/2 h). Bilateral injections of methysergide (4 mug/0.2 mul each site) into the LPBN increased 0.3 M NaCl intake (6.4 +/- 1.9 ml/2 h), not water intake. The inhibitory effect of i.c.v. clonidine on water and 0.3 M NaCl was still present after injections of methysergide into the LPBN (1.5 +/- 0.8 and 1.7 +/- 1.4 ml/2 h, respectively). The results show that the inhibitory effects of the activation of a,-adrenergic/imidazoline receptors in the forebrain are still present after blockade of the LPBN serotonergic mechanisms and vice versa for the activation of serotonergic mechanisms of the LPBN. Therefore, each system may act independently to inhibit NaCl and water intake. (C) 2002 Elsevier B.V. B.V. All rights reserved.

POSSIBLE MECHANISMS FOR REDUCTION OF CIRCULATING CONCENTRATIONS OF PROGESTERONE BY INTERFERON-ALPHA IN COWS - EFFECTS ON HYPERTHERMIA, LUTEAL CELLS, METABOLISM OF PROGESTERONE AND SECRETION OF LH

Experiments were performed to determine the mechanism by which recombinant bovine interferon-alpha(I)1 (rbIFN-alpha) causes an acute reduction in plasma concentrations of progesterone. In experiment 1, administration of a prostaglandin synthesis inhibitor blocked rbIFN-alpha-induced hyperthermia but did not prevent the decline in plasma concentrations of progesterone. The decline in progesterone concentrations caused by rbIFN-alpha was, therefore, not a direct consequence of the associated hyperthermia or of pathways mediated through prostaglandin synthesis. It is also unlikely that rbIFN-alpha acts to increase the clearance of progesterone since injection of rbIFN-alpha did not decrease plasma concentrations of progesterone in ovariectomized cows given an intravaginal implant of progesterone (experiment 2). In experiment 3, rbIFN-alpha did not affect basal and LH-induced release of progesterone from cultured luteal slices, indicating that rbIFN-alpha is unlikely to affect luteal function directly. Injection of rbIFN-alpha did, however, cause a decrease in plasma concentrations of LH in ovariectomized cows (experiment 4) that coincided temporally with the decrease in progesterone concentrations seen in cows having a functional corpus luteum. The present results strongly suggest that rbIFN-alpha acts to reduce secretion of progesterone by interfering with pituitary support for luteal synthesis of progesterone. The finding that rbIFN-alpha can inhibit LH secretion implies that interferon-alpha molecules should be considered among the cytokines that can regulate hypothalamic or pituitary function.

PRESSER MECHANISMS IN ADRIAMYCIN-INDUCED NEPHROPATHY WITH HYPERTENSION IN RATS

We explored the role of angiotensin II and vasopressin in the maintenance of blood pressure during the nephrotic syndrome of adriamycin-induced nephropathy in rats. All 91 rats treated with adriamycin developed chronic renal failure with nephrotic syndrome, which was more pronounced in the normotensive rats than the 35% who became hypertensive. Angiotensin II blockade with DuP 753 produced a significantly greater hypotensive response in both the adriamycin-hypertensive (-16+/-3 mmHg) and adriamycin-normotensive (-14+/-5 mmHg) groups than the saline-treated controls (-5+/-1 mm Hg, P<.05). Vasopressin blockade with either a V1V2 inhibitor or a selective V-1 inhibitor produced a hypotensive response in adriamycin-hypertensive rats only (by -16+/-4 and -17+/-2 mm Hg, respectively, P<.01), although the nonselective vasopressin inhibitor produced similar fluid loss and body weight reduction in all three groups. The data suggest that in adriamycin-induced nephropathy with nephrotic syndrome, angiotensin II contributes to blood pressure maintenance in both hypertensive and normotensive animals, whereas the presser action of vasopressin contributes to elevated blood pressure in hypertensive animals only.

Lateral parabrachial nucleus and serotonergic mechanisms in the control of salt appetite in rats

This study investigated the effects of bilateral injections of serotonergic receptor agonist and antagonist into the lateral parabrachial nucleus (LPBN) on the ingestion of water and 0.3 M NaCl induced by intracerebroventricular angiotensin II (ANG II) or by combined subcutaneous injections of the diuretic furosemide (Furo) and the angiotensin-converting enzyme inhibitor captopril (Cap). Rats had stainless steel cannulas implanted bilaterally into the LPBN and into the left lateral ventricle. Bilateral LPBN pretreatment with the serotonergic 5-HT1/5-HT2 receptor antagonist methysergide (4 mu g/200 nl each site) increased 0.3 M NaCl and water intakes induced by intracerebroventricular ANG II (50 ng/mu l) and 0.3 M NaCl intake induced by subcutaneous Furo + Cap. Pretreatment with bilateral LPBN injections of a serotonergic 5-HT2A/2C receptor agonist DOI (5 mu g/200 nl) significantly reduced 0.3 M NaCl intake induced by subcutaneous Furo + Cap. Pretreatment with methysergide or DOI into the LPBN produced no significant changes in the water intake induced by subcutaneous Furo + Cap. These results suggest that serotonergic mechanisms associated with the LPBN may have inhibitory roles in water and sodium ingestion in rats.

Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite

Central cholinergic mechanisms are suggested to participate in osmoreceptor-induced water intake. Therefore, central injections of the cholinergic agonist carbachol usually produce water intake (i.e., thirst) and are ineffective in inducing the intake of hypertonic saline solutions (i.e., the operational definition of sodium appetite). Recent studies have indicated that bilateral injections of the serotonin receptor antagonist methysergide into the lateral parabrachial nucleus (LPBN) markedly increases salt intake in models involving the activation of the renin-angiotensin system or mineralocorticoid hormones. The present studies investigated whether sodium appetite could be induced by central cholinergic activation with carbachol (an experimental condition where only water is typically ingested) after the blockade of LPBN serotonergic mechanisms with methysergide treatment in rats. When administered intracerebroventricularly in combination with injections of vehicle into both LPBN, carbachol (4 nmol) caused water drinking but insignificant intake of hypertonic saline. In contrast, after bilateral LPBN injections of methysergide (4 mug), intracerebroventricular carbachol induced the intake of 0.3 M NaCl. Water intake stimulated by intracerebroventricular carbachol was not changed by LPBN methysergide injections. The results indicate that central cholinergic activation can induce marked intake of hypertonic NaCl if the inhibitory serotonergic mechanisms of the LPBN are attenuated.

Energy-transfer mechanisms and emission quantum yields in Eu3+-based siloxane-poly(oxyethylene) nanohybrids

We report the energy-transfer mechanisms and emission quantum yield measurements of sol-gel-derived Eu3+-based nanohybrids. The matrix of these materials, classified as diureasils and termed U(2000) and U(600), includes urea cross-links between a siliceous backbone and polyether-based segments of two molecular weights, 2000 and 600, respectively. These materials are full-color emitters in which the Eu3+ (5)Do --> F-7(0-4) lines merge with the broad green-blue emission of the nanoscopic matrix's backbone. The excitation spectra show the presence of a large broad band (similar to 27000-29000 cm(-1)) undoubtedly assigned to a ligand-to-metal charge-transfer state. Emission quantum yields range from 2% to 13.0% depending on the polymer molecular weight and Eu3+ concentration. Energy transfer between the hybrid hosts and the cations arises from two different and independent processes: the charge-transfer band and energy transfer from the hybrid's emitting centers. The activation of the latter mechanisms induces a decrease in the emission quantum yields (relative to undoped nanohybrids) and permits a fine-tuning of the emission chromaticity across the Comission Internacionalle d'Eclairage diagram, e.g., (x, y) color coordinates from (0.21, 0.24) to (0.39, 0.36). Moreover, that activation depends noticeably on the ion local coordination. For the diureasils with longer polymer chains, energy transfer occurs as the Eu3+ coordination involves the carbonyl-type oxygen atoms of the urea bridges, which are located near the hybrid's host emitting centers. on the contrary, in the U(600)-based diureasils, the Eu3+ ions are coordinated to the polymer chains, and therefore, the distance between the hybrid's emitting centers and the metal ions is large enough to allow efficient energy-transfer mechanisms.

Sintering mechanisms of ZrO2 center dot MgO with addition of TiO2 and CuO

Substitutions of Ti and Cu in ZrO2.MgO (Z), cause transformation from monoclinic (m) to cubic (c) and tetragonal (t). According to the vacancy model and solid Solution formation models, neither CuO nor TiO2 cause zirconia stabilization, which derives front other phenomena. Data analysis by TMA using the CRH (constant rate of heating) method shows a solid state reaction of ZrO2.MgO.TiO2 (Z.TiO2) demonstrating a dominant mechanism of volume diffusion (n = 1). However, the sintering of ZrO2.MgO.CuO (Z.CuO) shows a viscous flow mechanism (n = 0), a similar phenomena to that of by sintering of glass. Transformations, such as: CuO to Cu2O at 1000 degreesC, ZrO2 (m) to ZrO2 (t) at 1100 degreesC and Cu2O (s) to Cu2O (l) at 1230 degreesC cause successive rearrangements of microstructure inside of region I (sintering process) and lead to interpretation errors when the Bannister equation is used. (C) 2003 Elsevier Ltd and Techna Group S.r.l. All rights reserved.

GENETIC MECHANISMS FOR THE DEVELOPMENT OF REPRODUCTIVE-ORGANS OF APIS-MELLIFERA WORKERS AND DIPLOID DRONES - A COMPLEMENTARY HYPOTHESIS

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Mechanisms behind blue, green, and red photoluminescence emissions in CaWO4 and CaMoO4 powders

A combined experimental and theoretical study was conducted to analyze the photoluminescence (PL) properties of ordered and disordered CaWO4 (CW) and CaMoO4 (CM) powders. Two mechanisms were found to be responsible for photoluminescence emission in CW and CM powders. The first one, in the disordered powders, was caused by oxygen complex vacancies [MO3 center dot V-O(x)], [MO3 center dot V-O(center dot)] and [MO3 center dot V-O(center dot center dot)], where M=W or Mo, which leads to additional levels in the band gap. The second mechanism, in ordered powders, was caused by an intrinsic slight distortion of the [WO4] or [MoO4] tetrahedral in the short range. (c) 2007 American Institute of Physics.

Antitumor effects in vitro and in vivo and mechanisms of protection against melanoma B16F10-Nex2 cells by fastuosain, a cysteine proteinase from Bromelia fastuosa

In the present work, the antitumor effect of fastuosain, a cysteine proteinase from Bromelia fastuosa, was investigated. In the intravenous model of lung colonization in C57Bl/6 mice, fastuosain and bromelain injected intraperitoneally were protective, and very few nodules of B16F10-Nex2 melanoma cells were detected. Tumor cells treated with fastuosain showed reduced expression of CD44 and decreased invasion through Matrigel, lost their cytoplasmic extensions and substrate adherence, and became round and detached, forming strongly bound cell clusters in suspension. Peritoneal cells recruited and activated by fastuosain treatment ( mainly monocytic cells and lymphocytes) migrated to the lung, where pulmonary melanoma metastases grew. Adoptive transference of peritoneal cells recruited by fastuosain had no protective effect against lung metastases in recipient mice. Treatment of green fluorescent protein - chimeric animals with fastuosain did not change the number of cells that migrated to the lung, compared to PBS-injected control mice, but the number of positive major histocompatibility complex class II cells increased with fastuosain treatment. Murine antibodies against fastuosain, bromelain, and cathepsins B and L cross-reacted in ELISA and recognized surface and cytoplasmic components expressed on B16F10-Nex2 cells. Anti-fastuosain antibodies were cytotoxic/lytic to B16F10-Nex2 cells. Antitumor effects of fastuosain involve mainly the direct effect of the enzyme and elicitation of protective antibodies.