Luminescent and thermo-optical properties of Nd(3+)-doped yttrium aluminoborate laser glasses

In this work we performed a thorough spectroscopic and thermo-optical investigation of yttrium aluminoborate glasses doped with neodymium ions. A set of samples, prepared by the conventional melt-quenching technique and with Nd(2)O(3) concentrations varying from 0.1 to 0.75 mol %, were characterized by ground state absorption, photoluminescence, excited state lifetime measurements, and thermal lens technique. For the neodymium emission at 1064 nm ((4)F(3/2) -> (4)I(11/2) transition), no significant luminescence concentration quenching was observed and the experimental lifetime values ranged around 70 mu s. The obtained values of thermal conductivity and diffusivity of approximately 10.3 x 10(-3) W / cm K and 4.0 x 10(-3) cm(2) / s, respectively, are comparable to those of commercial laser glasses. Moreover, the fluorescence quantum efficiency of the glasses, calculated using the Judd-Ofelt formalism and luminescence decay, lies in the range from 0.28 to 0.32, larger than the typical values obtained for Nd(3+) doped YAl(3)(BO(3))(4) crystals. (c) 2009 American Institute of Physics. [DOI: 10.1063/1.3176503]

Energy transfer upconversion determination by thermal-lens and Z-scan techniques in Nd(3+)-doped laser materials

The Z-scan and thermal-lens techniques have been used to obtain the energy transfer upconversion parameter in Nd(3+)-doped materials. A comparison between these methods is done, showing that they are independent and provide similar results. Moreover, the advantages and applicability of each one are also discussed. The results point to these approaches as valuable alternative methods because of their sensitivity, which allows measurements to be performed in a pump-power regime without causing damage to the investigated material. (C) 2009 Optical Society of America

Nonlinear refraction and absorption through phase transition in a Nd:SBN laser crystal

Time-resolved Z-scan measurements were performed in a Nd(3+)-doped Sr(0.61)Ba(0.39)Nb(2)O(6) laser crystal through ferroelectric phase transition. Both the differences in electronic polarizability (Delta alpha(p)) and cross section (Delta sigma) of the neodymium ions have been found to be strongly modified in the surroundings of the transition temperature. This observed unusual behavior is concluded to be caused by the remarkable influence that the structural changes associated to the ferro-to-paraelectric phase transition has on the 4f -> 5d transition probabilities. The maximum polarizability change value Delta alpha(p)=1.2x10(-25) cm(3) obtained at room temperature is the largest ever measured for a Nd(3+)-doped transparent material.

Induced Modules for Affine Lie Algebras

We study induced modules of nonzero central charge with arbitrary multiplicities over affine Lie algebras. For a given pseudo parabolic subalgebra P of an affine Lie algebra G, our main result establishes the equivalence between a certain category of P-induced G-modules and the category of weight P-modules with injective action of the central element of G. In particular, the induction functor preserves irreducible modules. If P is a parabolic subalgebra with a finite-dimensional Levi factor then it defines a unique pseudo parabolic subalgebra P(ps), P subset of P(ps). The structure of P-induced modules in this case is fully determined by the structure of P(ps)-induced modules. These results generalize similar reductions in particular cases previously considered by V. Futorny, S. Konig, V. Mazorchuk [Forum Math. 13 (2001), 641-661], B. Cox [Pacific J. Math. 165 (1994), 269-294] and I. Dimitrov, V. Futorny, I. Penkov [Comm. Math. Phys. 250 (2004), 47-63].

Eddy Formation in the Tropical Atlantic Induced by Abrupt Changes in the Meridional Overturning Circulation

The variability of the meridional overturning circulation (MOC) in the upper tropical Atlantic basin is investigated using a reduced-gravity model in a simplified domain. Four sets of idealized numerical experiments are performed: (i) switch-on of the MOC until a fixed value when a constant northward flow is applied along the western boundary; (ii) MOC with a variable flow; (iii) MOC in a quasi-steady flow; and (iv) shutdown of the MOC in the Northern Hemisphere. Results from experiments (i) show that eddies are generated at the equatorial region by shear instability and detached northward; eddies are responsible for an enhancement of the mean flow and the variability of the MOC. Results from experiments (ii) show a transitional behavior of the MOC related to the eddy generation in interannual-decadal time scales as the Reynolds number varies due to the variations in the MOC. In experiments (iii), a critical Reynolds number Re(c) around 30 is found, above which eddies are generated. Experiments (iv) demonstrate that even after the collapse of MOC in the Northern Hemisphere, eddies can still be generated and carry energy across the equator into the Northern Hemisphere; these eddies act to attenuate the impact of the MOC shutdown on short time scales. The results described here may be particularly pertinent to ocean general circulation models in which the Reynolds number lies close to the bifurcation point separating the laminar and turbulent regimes.

Giant Vesicles under Oxidative Stress Induced by a Membrane-Anchored Photosensitizer

We have synthesized the amphiphile photosensitizer PE-porph consisting of a porphyrin bound to a lipid head-group. We studied by optical microscopy the response to light irradiation of giant unilamellar vesicles of mixtures of unsaturated phosphatidylcholine lipids and PE-porph. In this configuration, singlet oxygen is produced at the bilayer surface by the anchored porphyrin. Under irradiation, the PE-porph decorated giant unilamellar vesicles exhibit a rapid increase in surface area with concomitant morphological changes. We quantify the surface area increase of the bilayers as a function of time and photosensitizer molar fraction. We attribute this expansion to hydroperoxide formation by the reaction of the singlet oxygen with the unsaturated bonds. Considering data from numeric simulations of relative area increase per phospholipid oxidized (15%), we measure the efficiency of the oxidative reactions. We conclude that for every 270 singlet oxygen molecules produced by the layer of anchored porphyrins, one eventually reacts to generate a hydroperoxide species. Remarkably, the integrity of the membrane is preserved in the full experimental range explored here, up to a hydroperoxide content of 60%, inducing an 8% relative area expansion.

Knoop Microhardness and FT-Raman Spectroscopic Evaluation of a Resin-Based Dental Material Light-Cured by an Argon Ion Laser and Halogen Lamp: An in Vitro Study

Objective: The purpose of this study was to evaluate in vitro the Knoop microhardness (Knoop hardness number [KHN]) and the degree of conversion using FT-Raman spectroscopy of a light-cured microhybrid resin composite (Z350-3M-ESPE) Vita shade A3 photopolymerized with a halogen lamp or an argon ion laser. Background Data: Optimal polymerization of resin-based dental materials is important for longevity of restorations in dentistry. Materials and Methods: Thirty specimens were prepared and inserted into a disc-shaped polytetrafluoroethylene mold that was 2.0 mm thick and 3 mm in diameter. The specimens were divided into three groups (n = 10 each). Group 1 (G1) was light-cured for 20 sec with an Optilux 501 halogen light with an intensity of 1000 mW/cm(2). Group 2 (G2) was photopolymerized with an argon laser with a power of 150 mW for 10 sec, and group 3 (G3) was photopolymerized with an argon laser at 200 mW of power for 10 sec. All specimens were stored in distilled water for 24 h at 37 degrees C and kept in lightproof containers. For the KHN test five indentations were made and a depth of 100 mu m was maintained in each specimen. One hundred and fifty readings were obtained using a 25-g load for 45 sec. The degree of conversion values were measured by Raman spectroscopy. KHN and degree of conversion values were obtained on opposite sides of the irradiated surface. KHN and degree of conversion data were analyzed by one-way ANOVA and Tukey tests with statistical significance set at p < 0.05. Results: The results of KHN testing were G1 = 37.428 +/- 4.765; G2 = 23.588 +/- 6.269; and G3 = 21.652 +/- 4.393. The calculated degrees of conversion (DC%) were G1 = 48.57 +/- 2.11; G2 = 43.71 +/- 3.93; and G3 = 44.19 +/- 2.71. Conclusions: Polymerization with the halogen lamp ( G1) attained higher microhardness values than polymerization with the argon laser at power levels of 150 and 200 mW; there was no difference in hardness between the two argon laser groups. The results showed no statistically significant different degrees of conversion for the polymerization of composite samples with the two light sources tested.

A TR beta-selective agonist confers resistance to diet-induced obesity

Thyroid hormone receptor beta (TR beta also listed as THRB oil the MGI Database)-selective agonists activate brown adipose tissue (BAT) thermogenesis, while only minimally affecting cardiac activity or lean body mass. Here, we tested the hypothesis that daily administration of the TR beta agonist GC-24 prevents the metabolic alterations associated with a hypercaloric diet. Rats were placed on a high-fat diet and after a month exhibited increased body weight (BW) and adiposity, fasting hyperglycemia and glucose intolerance, increased plasma levels of triglycerides, cholesterol, nonesterified Fatty acids and interleukin-6. While GC-24 administration to these animals did not affect food ingestion or modified the progression of BW gain, it did increase energy, g the increase in adiposity Without expenditure, eliminating causing cardiac hypertrophy Fasting hyperglycemia remained unchanged, but treatment with GC-24 improved glucose I tolerance by increasing insulin Sensitivity and also normalized plasma triglyceride levels. plasma cholesterol levels were only Partially normalized and liver cholesterol content remained high in the GC-24-treated animals. Gene expression in liver, skeletal muscle, and white adipose tissue was only minimally affected by treatment with GC-24, with the main target being BAT In conclusion, during high-fat feeding treatment with the TR beta-selective agonist, GC-24 only partially improves metabolic control probably as a result Of accelerating the resting metabolic rate. Journal of Endocrinology (2009) 203, 291-299

Cuff-induced vascular intima thickening is influenced by titration of the Ace gene in mice

Lacchini S, Heimann AS, Evangelista FS, Cardoso L, Silva GJ, Krieger JE. Cuff-induced vascular intima thickening is influenced by titration of the Ace gene in mice. Physiol Genomics 37: 225-230, 2009. First published March 3, 2009; doi:10.1152/physiolgenomics.90288.2008.-We tested the hypothesis that small changes in angiotensin I-converting enzyme (ACE) expression can alter the vascular response to injury. Male mice containing one, two, three, and four copies of the Ace gene with no detectable vascular abnormality or changes in blood pressure were submitted to cuff-induced femoral artery injury. Femoral thickening was higher in 3- and 4-copy mice (42.4 +/- 4.3% and 45.7 +/- 6.5%, respectively) compared with 1- and 2-copy mice (8.3 +/- 1.3% and 8.5 +/- 0.9%, respectively). Femoral ACE levels from control and injured vessels were assessed in 1- and 3-copy Ace mice, which represent the extremes of the observed response. ACE vascular activity was higher in 3- vs. 1-copy Ace mice (2.4-fold, P < 0.05) in the control uninjured vessel. Upon injury, ACE activity significantly increased in both groups [2.41-fold and 2.14-fold (P < 0.05) for 1- and 3-copy groups, respectively] but reached higher levels in 3- vs. 1-copy Ace mice (P < 0.05). Pharmacological interventions were then used as a counterproof and to indirectly assess the role of angiotensin II (ANG II) on this response. Interestingly, ACE inhibition (enalapril) and ANG II AT(1) receptor blocker (losartan) reduced intima thickening in 3-copy mice to 1-copy mouse values (P < 0.05) while ANG II treatment significantly increased intima thickening in 1-copy mice to 3-copy mouse levels (P < 0.05). Together, these data indicate that small physiologically relevant changes in ACE, not associated with basal vascular abnormalities or blood pressure levels, do influence the magnitude of cuff-induced neointima thickening in mice.

Involvement of L-type calcium channel and SERCA2a in myocardial dysfunction induced by obesity

Obesity has been shown to impair myocardial performance. Nevertheless, the mechanisms underlying the participation of calcium (Ca(2+)) handling on cardiac dysfunction in obesity models remain unknown. L-type Ca(2+) channels and sarcoplasmic reticulum (SR) Ca(2+)-ATPase (SERCA2a), may contribute to the cardiac dysfunction induced by obesity. The purpose of this study was to investigate whether myocardial dysfunction in obese rats is related to decreased activity and/or expression of L-type Ca(2+) channels and SERCA2a. Male 30-day-old Wistar rats were fed standard (C) and alternately four palatable high-fat diets (Ob) for 15 weeks. Obesity was determined by adiposity index and comorbidities were evaluated. Myocardial function was evaluated in isolated left ventricle papillary muscles under basal conditions and after inotropic and lusitropic maneuvers. L-type Ca(2+) channels and SERCA2a activity were determined using specific blockers, while changes in the amount of channels were evaluated by Western blot analysis. Phospholamban (PLB) protein expression and the SERCA2a/PLB ratio were also determined. Compared with C rats, the Ob rats had increased body fat, adiposity index and several comorbidities. The Ob muscles developed similar baseline data, but myocardial responsiveness to post-rest contraction stimulus and increased extracellular Ca(2+) was compromised. The diltiazem promoted higher inhibition on developed tension in obese rats. In addition, there were no changes in the L-type Ca(2+) channel protein content and SERCA2a behavior (activity and expression). In conclusion, the myocardial dysfunction caused by obesity is related to L-type Ca(2+) channel activity impairment without significant changes in SERCA2a expression and function as well as L-type Ca(2+) protein levels. J. Cell. Physiol. 226: 2934-2942, 2011. (C) 2011 Wiley-Liss, Inc.

Cardiac and peripheral adjustments induced by early exercise training intervention were associated with autonomic improvement in infarcted rats: role in functional capacity and mortality

Aims To test the effects of early exercise training (ET) on left ventricular (LV) and autonomic functions, haemodynamics, tissues blood flows (BFs), maximal oxygen consumption (VO(2) max), and mortality after myocardial infarction (MI) in rats. Methods and results Male Wistar rats were divided into: control (C), sedentary-infarcted (SI), and trained-infarcted (TI). One week after MI, TI group underwent an ET protocol (90 days, 50-70% VO2 max). Left ventricular function was evaluated noninvasively and invasively. Baroreflex sensitivity, heart rate variability, and pulse interval were measured. Cardiac output (CO) and regional BFs were determined using coloured microspheres. Infarcted area was reduced in TI (19 +/- 6%) compared with SI (34 +/- 5%) after ET. Exercise training improved the LV and autonomic functions, the CO and regional BF changes induced by MI, as well as increased SERCA2 expression and mRNA vascular endothelial growth factor levels. These changes brought about by ET resulted in mortality rate reduction in the TI (13%) group compared with the SI (54%) group. Conclusion Early aerobic ET reduced cardiac and peripheral dysfunctions and preserved cardiovascular autonomic control after MI in trained rats. Consequently, these ET-induced changes resulted in improved functional capacity and survival after MI.

Angiotensin receptor blockade improves the net balance of cardiac Ca(2+) handling-related proteins in sympathetic hyperactivity-induced heart failure

Aims: The clinical benefits of angiotensin II type 1 (AT1) receptor blockers (ARB) in heart failure (HF) include cardiac anti-remodeling and improved ventricular function. However, the cellular mechanisms underlying the benefits of ARB on ventricular function need to be better clarified. In the present manuscript, we evaluated the effects of AT1 receptor blockade on the net balance of Ca(2+) handling proteins in hearts of mice lacking alpha(2A) and alpha(2C) adrenoceptors (alpha(2A)/alpha(2C)ARKO), which develop sympathetic hyperactivity (SH) induced-HF. Main methods: A cohort of male wild-type (WT) and congenic alpha(2A)/alpha(2C)ARKO mice in a C57BL6/J genetic background (5-7 mo of age) was randomly assigned to receive either placebo or ARB (Losartan, 10 mg/kg for 8wks). Ventricular function (VF) was assessed by echocardiography, and cardiac myocyte width and ventricular fibrosis by a computer-assisted morphometric system. Sarcoplasmic reticulum Ca(2+) ATPase (SERCA2), phospholamban (PLN), phospho-Ser(16)-PLN, phospho-Thr(17)-PLN, phosphatase 1 (PP1), Na(+)-Ca(2+) exchanger (NCX), Ca(2+)/calmodulin-dependent protein kinase 11 (CaMKII) and phospho-Thr(286)-CaMKII were analyzed by Western blot. Key findings: alpha(2A)/alpha(2C)ARKO mice displayed ventricular dysfunction, cardiomyocyte hypertrophy and cardiac fibrosis paralleled by decreased SERCA2 and increased phospho-Thr(17)-PLN, CaMKII, phospho-Thr(286)-CaMKII and NCX levels. ARB induced anti-cardiac remodeling effect and improved VF in alpha(2A)/alpha(2C)ARKO associated with increased SERCA2 and phospho-Ser(16)-PLN levels, and SERCA2:NCX ratio. Additionally, ARB decreased phospho-Thr(17)-PLN levels as well as reestablished NCX, CaMKII and phospho-Thr(286)-CaMKII toward WT levels. Significance: Altogether, these data provide new insights on intracellular Ca(2+) regulatory mechanisms underlying improved ventricular function by ARB therapy in HF. (c) 2011 Elsevier Inc. All rights reserved.

Heat and exercise acclimation increases intracellular levels of Hsp72 and inhibits exercise-induced increase in intracellular and plasma Hsp72 in humans

In order to verify the effects of heat and exercise acclimation (HA) on resting and exercise-induced expression of plasma and leukocyte heat shock protein 72 (Hsp72) in humans, nine healthy young male volunteers (25.0 +/- 0.7 years; 80.5 +/- 2.0 kg; 180 +/- 2 cm, mean +/- SE) exercised for 60 min in a hot, dry environment (40 +/- 0A degrees C and 45 A +/- 0% relative humidity) for 11 days. The protocol consisted of running on a treadmill using a controlled hyperthermia technique in which the work rate was adjusted to elevate the rectal temperature by 1A degrees C in 30 min and maintain it elevated for another 30 min. Before and after the HA, the volunteers performed a heat stress test (HST) at 50% of their individual maximal power output for 90 min in the same environment. Blood was drawn before (REST), immediately after (POST) and 1 h after (1 h POST) HST, and plasma and leukocytes were separated and stored. Subjects showed expected adaptations to HA: reduced exercise rectal and mean skin temperatures and heart rate, and augmented sweat rate and exercise tolerance. In HST1, plasma Hsp72 increased from REST to POST and then returned to resting values 1 h POST (REST: 1.11 A +/- 0.07, POST: 1.48 A +/- 0.10, 1 h POST: 1.22 A +/- 0.11 ng mL(-1); p < 0.05). In HST2, there was no change in plasma Hsp72 (REST: 0.94 A +/- 0.08, POST: 1.20 A +/- 0.15, 1 h POST: 1.17 A +/- 0.16 ng mL(-1); p > 0.05). HA increased resting levels of intracellular Hsp72 (HST1: 1 A +/- 0.02 and HST2: 4.2 A +/- 1.2 density units, p < 0.05). Exercise-induced increased intracellular Hsp72 expression was observed on HST1 (HST1: REST, 1 A +/- 0.02 vs. POST, 2.9 A +/- 0.9 density units, mean +/- SE, p < 0.05) but was inhibited on HST2 (HST2: REST, 4.2 +/- 1.2 vs. POST, 4.4 +/- 1.1 density units, p > 0.05). Regression analysis showed that the lower the pre-exercise expression of intracellular Hsp72, the higher the exercise-induced increase (R = -0.85, p < 0.05). In conclusion, HA increased resting leukocyte Hsp72 levels and inhibited exercise-induced expression. This intracellular adaptation probably induces thermotolerance. In addition, the non-increase in plasma Hsp72 after HA may be related to lower stress at the cellular level in the acclimated individuals.

Aerobic exercise training improves skeletal muscle function and Ca(2+) handling-related protein expression in sympathetic hyperactivity-induced heart failure

Bueno CR Jr, Ferreira JC, Pereira MG, Bacurau AV, Brum PC. Aerobic exercise training improves skeletal muscle function and Ca(2+) handling-related protein expression in sympathetic hyperactivity-induced heart failure. J Appl Physiol 109: 702-709, 2010. First published July 1, 2010; doi: 10.1152/japplphysiol.00281.2010.-The cellular mechanisms of positive effects associated with aerobic exercise training on overall intrinsic skeletal muscle changes in heart failure (HF) remain unclear. We investigated potential Ca(2+) abnormalities in skeletal muscles comprising different fiber compositions and investigated whether aerobic exercise training would improve muscle function in a genetic model of sympathetic hyperactivity-induced HF. A cohort of male 5-mo-old wild-type (WT) and congenic alpha(2A)/alpha(2C) adrenoceptor knockout (ARKO) mice in a C57BL/6J genetic background were randomly assigned into untrained and trained groups. Exercise training consisted of a 8-wk running session of 60 min, 5 days/wk (from 5 to 7 mo of age). After completion of the exercise training protocol, exercise tolerance was determined by graded treadmill exercise test, muscle function test by Rotarod, ambulation and resistance to inclination tests, cardiac function by echocardiography, and Ca(2+) handling-related protein expression by Western blot. alpha(2A)/alpha(2C)ARKO mice displayed decreased ventricular function, exercise intolerance, and muscle weakness paralleled by decreased expression of sarcoplasmic Ca(2+) release-related proteins [alpha(1)-, alpha(2)-, and beta(1)-subunits of dihydropyridine receptor (DHPR) and ryanodine receptor (RyR)] and Ca(2+) reuptake-related proteins [sarco(endo) plasmic reticulum Ca(2+)-ATPase (SERCA) 1/2 and Na(+)/Ca(2+) exchanger (NCX)] in soleus and plantaris. Aerobic exercise training significantly improved exercise tolerance and muscle function and reestablished the expression of proteins involved in sarcoplasmic Ca(2+) handling toward WT levels. We provide evidence that Ca(2+) handling-related protein expression is decreased in this HF model and that exercise training improves skeletal muscle function associated with changes in the net balance of skeletal muscle Ca(2+) handling proteins.

Exercise training reduces cardiac angiotensin II levels and prevents cardiac dysfunction in a genetic model of sympathetic hyperactivity-induced heart failure in mice

The role of exercise training (ET) on cardiac renin-angiotensin system (RAS) was investigated in 3-5 month-old mice lacking alpha(2A-) and alpha(2C-)adrenoceptors (alpha(2A)/alpha(2C)ARKO) that present heart failure (HF) and wild type control (WT). ET consisted of 8-week running sessions of 60 min, 5 days/week. In addition, exercise tolerance, cardiac structural and function analysis were made. At 3 months, fractional shortening and exercise tolerance were similar between groups. At 5 months, alpha(2A)/alpha(2C)ARKO mice displayed ventricular dysfunction and fibrosis associated with increased cardiac angiotensin (Ang) II levels (2.9-fold) and increased local angiotensin-converting enzyme activity (ACE 18%). ET decreased alpha(2A)/alpha(2C)ARKO cardiac Ang II levels and ACE activity to age-matched untrained WT mice levels while increased ACE2 expression and prevented exercise intolerance and ventricular dysfunction with little impact on cardiac remodeling. Altogether, these data provide evidence that reduced cardiac RAS explains, at least in part, the beneficial effects of ET on cardiac function in a genetic model of HF.