A influência do volume na performance dos fundos de investimento em ações no Brasil

Tendo como base a literatura internacional sobre fundos mútuos, o presente estudo busca encontrar algumas características que influenciam a performance dos fundos de investimentos em ações no Brasil de janeiro de 1999 até abril de 2005. O objetivo principal do trabalho é perceber se os fundos de investimento em ações têm retorno decrescente de escala. Ao mesmo tempo, sabe-se que a persistência de uma boa rentabilidade depende do grau de profissionalismo dos gestores e também de uma boa relação entre o gestor responsável e o investidor e, um contrato ótimo entre ambos. Observou-se que o volume não tem influência negativa no retorno do fundo, pelo contrário, quanto maior o fundo melhor é a rentabilidade do mesmo. Os resultados também apresentaram que os fundos que cobram taxa de performance têm um desempenho melhor do que os que não cobram. Foi identificado também que os fundos que utilizam a marca d água como incentivo de remuneração aos gestores têm rentabilidade um pouco maior do que os fundos que pagam taxa de performance, mas não utilizam a marca d água no regulamento. Chegou-se a conclusão que há uma relação direta entre incentivo e desempenho. Os resultados aqui encontrados buscam facilitar o conhecimento e a tomada de decisão de pesquisadores, investidores, empresas gestoras, Corretoras e Distribuidoras, fundos de pensão e dos demais interessados na indústria de fundos de investimento em ações no Brasil.

Role of catecholaminergic neurones of the caudal ventrolateral medulla in cardiovascular responses induced by acute changes in circulating volume in rats

Several findings suggest that catecholaminergic neurones in the caudal ventrolateral medulla (CVLM) contribute to body fluid homeostasis and cardiovascular regulation. The present study sought to determine the effects of lesions of these neurones on the cardiovascular responses induced by changes in circulating volume. All experiments were performed in male Wistar rats (320-360 g). Medullary catecholaminergic neurones were lesioned by microinjection of anti-dopamine beta-hydroxylase-saporin (6.3 ng in 60 nl; SAP rats, n = 14) into the CVLM, whereas sham rats received microinjections of free saporin (1.3 ng in 60 nl, n = 15). Two weeks later, rats were anaesthetized (urethane, 1.2 g kg(-1), I.V..), instrumented for measurement of mean arterial pressure (MAP), renal blood flow (RBF) and renal vascular conductance (RVC), and infused with hypertonic saline (HS; 3 M NaCl, 0.18 ml (100 g body weight)(-1), I.V.) or an isotonic solution (volume expansion, VE; 4% Ficoll, 1% of body weight, I.V.). In sham rats, HS induced sustained increases in RBF and RVC (155 +/- 7 and 145 +/- 6% of baseline, at 20 min after HS). In SAP rats, RBF responses to HS were blunted (125 +/- 6%) and RVC increases were abolished (108 +/- 5%) 20 min after HS. Isotonic solution increased RBF and RVC in sham rats (149 +/- 10 and 145 +/- 12% of baseline, respectively, at 20 min). These responses were reduced in SAP rats (131 +/- 6 and 126 +/- 5%, respectively, at 20 min). Pressor responses to HS were larger in SAP rats than in sham rats (17 +/- 5 versus 9 +/- 2 mmHg, at 20 min), whereas during VE these responses were similar in both groups (6 +/- 3 versus 4 +/- 6 mmHg, at 20 min). Immunohistochemical analysis indicates that microinjections of anti-D beta H-saporin produced extensive destruction within the A1/C1 cell groups in the CVLM. These results suggest that catecholaminergic neurones mediate the cardiovascular responses to VE or increases in plasma sodium levels.

Participation of alpha-1 and alpha-2 adrenoceptors of the lateral hypothalamic area in water intake, and renal sodium, potassium and urinary Volume excretion induced by central administration of angiotensin II

The circumventricular structures and the lateral hypothalamus (LH) have been shown to be important for the central action of angiotensin II (ANGII) on water and electrolyte regulation. Several anatomical findings have demonstrated neural connection between circumventricular structures and the LH, the present experiments were conducted to investigate the role of the alpha-adrenergic antagonists and agonistic injected into the LH on the water intake, sodium and potassium excretion elicited by injections of ANGII into the lateral ventricle (LV), the water intake was measured every 30 min over a period of 120 min. The sodium, potassium and urinary volume were measured over a period of 120 min in water-loaded rats. The injection of ANGII into the LV increased the water intake, which was reduced by previous injection of clonidine (an alpha-2-adrenergic agonist) into the LH. The injection of yohimbine (an alpha-2-adrenergic antagonist) and prazosin (an alpha-l-adrenergic antagonist) into the LH, which was done before injecting ANGII into the LV, also reduced the water intake induced by ANGII. The injection of ANGII into the LV reduced the sodium, potassium and urinary volume. Previous treatment with clonidine attenuated the action of ANGII in reducing the sodium, potassium and urinary volume, whereas previous treatment with yohimbine attenuated the effects of ANGII but with less intensity than that caused by clonidine. Previous treatment with prazosin increased the inhibitory effects of ANGII in those parameters. The injection of yohimbine and prazosin, which was done before the injection of clonidine, attenuated the effect of clonidine on the ANGII mechanism. The results of this study led us to postulate that when alpha-2-adrenergic receptors are blocked, the clonidine may act on the imidazoline receptors to produce its effects on the ANGII mechanism. We may also conclude that the LH is involved with circumventricular structures, which present excitatory and inhibitory mechanisms. Such mechanisms are responsible for regulating the renal excretion of sodium, potassium and water, (C) 2000 Elsevier B.V.

Central nitrergic system regulation of neuroendocrine secretion, fluid intake and blood pressure induced by angiotensin-II

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

Regulation of ventilation in the caiman (Caiman latirostris): effects of inspired CO2 on pulmonary and upper airway chemoreceptors

In order to study the relative roles of receptors in the upper airways, lungs and systemic circulation in modulating the ventilatory response of caiman (Caiman latirostris) to inhaled CO2, gas mixtures of varying concentrations of CO2 Were administered to animals breathing through an intact respiratory system, via a tracheal cannula by-passing the upper airways (before and after vagotomy), or via a cannula delivering gas to the upper airways alone. While increasing levels of hypercarbia led to a progressive increase in tidal volume in animals with intact respiratory systems (Series 1), breathing frequency did not change until the CO2 level reached 7%, at which time it decreased. Despite this, at the higher levels of hypercarbia, the net effect was a large and progressive increase in total ventilation. There were no associated changes in heart rate or arterial blood pressure. on return to air, there was an immediate change in breathing pattern; breathing frequency increased above air-breathing values, roughly to the same maximum level regardless of the level of CO2 the animal had been previously breathing, and tidal volume returned rapidly toward resting (baseline) values. Total ventilation slowly returned to air breathing values. Administration of CO2 via different routes indicated that inhaled CO2 acted at both upper airway and pulmonary CO2-sensitive receptors to modify breathing pattern without inhibiting breathing overall. Our data suggest that in caiman, high levels of inspired CO2 promote slow, deep breathing. This will decrease deadspace ventilation and may reduce stratification in the saccular portions of the lung.

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.

A randomized clinical trial of high volume peritoneal dialysis versus extended daily hemodialysis for acute kidney injury patients

Background: Acute kidney injury (AKI) requiring dialysis in critically ill patients is associated with an in-hospital mortality rate of 50-80 %. Extended daily hemodialysis (EHD) and high volume peritoneal dialysis (HVPD) have emerged as alternative modalities. Methods: A double-center, randomized, controlled trial was conducted comparing EHD versus HVPD for the treatment for AKI in the intensive care unit (ICU). Four hundred and seven patients were randomized and 143 patients were analyzed. Principal outcome measure was hospital mortality, and secondary end points were recovery of renal function and metabolic and fluid control. Results: There was no difference between the two groups in relation to median ICU stay [11 (5.7-20) vs. 9 (5.7-19)], recovery of kidney function (26.9 vs. 29.6 %, p = 0.11), need for chronic dialysis (9.7 vs. 6.5 %, p = 0.23), and hospital mortality (63.4 vs. 63.9 %, p = 0.94). The groups were different in metabolic and fluid control. Blood urea nitrogen (BUN), creatinine, and bicarbonate levels were stabilized faster in EHD group than in HVPD group. Delivered Kt/V and ultrafiltration were higher in EHD group. Despite randomization, there were significant differences between the groups in some covariates, including age, pre-dialysis BUN, and creatinine levels, biased in favor of the EHD. Using logistic regression to adjust for the imbalances in group assignment, the odds of death associated with HVPD was 1.4 (95 % CI 0.7-2.4, p = 0.19). A detailed investigation of the randomization process failed to explain the marked differences in patient assignment. Conclusions: Despite faster metabolic control and higher dialysis dose and ultrafiltration with EHD, this study provides no evidence of a survival benefit of EHD compared with HVPD. The limitations of this study were that the results were not presented according to the intention to treat and it did not control other supportive management strategies as nutrition support and timing of dialysis initiation that might influence outcomes in AKI. © 2012 Springer Science+Business Media Dordrecht.

Participação do grupamento catecolaminérgico A2 do núcleo do trato solitário comissural nos ajustes cardiovasculares e do equilíbrio hidroeletrolitíco induzidos por alterações da osmolaridade ou volume plasmático

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Efeitos da expansão de volume extracelular sobre o conteúdo de catecolaminas e a ativação neuronal de estruturas do hipotálamo e do tronco cerebral de ratos

A regulação fina do volume e osmolaridade dos líquidos corporais é fundamental para a sobrevivência. Qualquer variação na composição do meio interno ativa mecanismos comportamentais, neurais e hormonais compensatórios que controlam a ingestão e excreção de água e eletrólitos a fim de manter a homeostase hidroeletrolítica. Alterações na faixa de 1-2% na osmolaridade sanguínea estimulam a liberação de arginina vasopressina (AVP) que resulta em antidiurese além de ocitocina (OT) e peptídeo natriurético atrial (ANP) que promovem a natriurese. Trabalhos realizados em nosso laboratório utilizando o modelo experimental de expansão do volume extracelular (EVEC) mostraram ativação de neurônios magnocelulares ocitocinérgicos localizados no núcleo paraventricular (PVN) e núcleo supra-óptico (SON) responsáveis pela secreção de OT e AVP, igualmente alteradas em resposta a este estímulo. A participação do sistema nervoso simpático nestas condições tem sido levantada. Projeções medulares e tronco-encefálicas (simpáticas) para o hipotálamo poderiam atuar de forma seletiva inibindo sinalizações para a ingestão e estimulando sinalizações para excreção de água e eletrólitos. O papel de vias noradrenérgicas tronco-encefálicas nesta regulação ainda precisa ser mais bem estabelecido. Assim sendo, objetivamos neste estudo esclarecer o papel do sistema nervoso simpático (via noradrenérgicas) na regulação das alterações induzidas pelo modelo de EVEC, analisando por cromatografia líquida de alta eficácia o conteúdo de noradrenalina (NA), adrenalina (AD) e serotonina (5-HT) em estruturas do tronco cerebral como núcleo do trato solitário (NTS), bulbo rostro-ventro lateral (RVLM), locus coeruleus (LC) e núcleo dorsal da rafe (NDR) e estruturas hipotalâmicas como SON e PVN. Procuramos ainda, através de estudos imunocitoquímicos determinar alterações no padrão de ativação neuronal pela análise de Fos-TH ou Fos-5HT nas estruturas acima mencionadas em condições experimentais nas quais são induzidas alterações do volume do líquido extracelular.

Variação da distribuição do diâmetro eritrocitário e do volume corpuscular médio em cães anêmicos

The anisocytosis is a hematologic finding that is routinely evaluated from the mean corpuscular volume (MCV) and erythrocyte morphology in assessment of blood smears. The present study tested the hypothesis that the coefficient of variation of the red cell distribution width (RDW-CV - Red Cell Distribution Width) is a more sensitive parameter in the evaluation of hematologic anisocytosis, considering different levels of anemia in dogs and reticulocytosis. Blood counts of 102 anemic dogs and 353 control dogs made by automated hematology counter. The anemic animals were grouped according to the degree of anemia (mild, moderate and severe) and also as medullary response by manual reticulocyte count (none, weak, moderate and strong). The RDW-CV was different to the animal groups with moderate and severe anemia, which were higher, compared to the control group and mild anemia. The highest average value of RDW-CV (14.45%) occurred in patients with severe anemia. In the control group had higher MCV value that anemic animals , this may be due to a mixed population of erythrocytes in that group of animals. However, there wasn’t difference in MCV between different degrees of anemia and reticulocytosis. Therefore, the RDW is a more sensitive indicator anisocytosis than VCM and its value is directly proportional to the degree of anemia and reticulocytosis; when combined, the sensitivity for detection of anisocytosis in anemic dogs is greater. The use of reference values established by the clinical laboratory itself is mighty important.

Pre Vertical Jump Performance to Regulate the Training Volume

The purpose of this study was to assess the effect of training load regulation, using the CMJ at the beginning of the session, on the total plyometric training load and the vertical jump performance. 44 males were divided into 4 groups: No Regulation Group (nRG), Regulation Group (RG), Yoked Group (YG) and Control Group (CG). The nRG received 6 weeks of plyometric training, with no adjustment in training load. The RG underwent the same training; however, the training load was adjusted according to the CMJ performance at the beginning of each session. The adjustment made in RG was replicated for the volunteers from the corresponding quartile in the YG, with no consideration given to the YG participant's condition at the beginning of its session. At the end of the training, the CMJ and SJ performance of all of the participants was reassessed. The total training load was significantly lower (p=0.036; ES=0.82) in the RG and the YG (1905 +/- 37 jumps) compared to the nRG (1926 +/- 0 jumps). The enhancement in vertical jump performance was significant for the groups that underwent the training (p<0.001). Vertical jump performance, performed at the beginning of the session, as a tool to regulate the training load resulted in a decrease of the total training load, without decreasing the long-term effects on vertical jump performance.

Deficiency in parvalbumin, but not in calbindin D-28k upregulates mitochondrial volume and decreases smooth endoplasmic reticulum surface selectively in a peripheral, subplasmalemmal region in the soma of Purkinje cells

The Ca(2+)-binding proteins parvalbumin (PV) and calbindin D-28k (CB) are key players in the intracellular Ca(2+)-buffering in specific cells including neurons and have profound effects on spatiotemporal aspects of Ca(2+) transients. The previously observed increase in mitochondrial volume density in fast-twitch muscle of PV-/- mice is viewed as a specific compensation mechanism to maintain Ca(2+) homeostasis. Since cerebellar Purkinje cells (PC) are characterized by high expression levels of the Ca(2+) buffers PV and CB, the question was raised, whether homeostatic mechanisms are induced in PC lacking these buffers. Mitochondrial volume density, i.e. relative mitochondrial mass was increased by 40% in the soma of PV-/- PC. Upregulation of mitochondrial volume density was not homogenous throughout the soma, but was selectively restricted to a peripheral region of 1.5 microm width underneath the plasma membrane. Accompanied was a decreased surface of subplasmalemmal smooth endoplasmic reticulum (sPL-sER) in a shell of 0.5 microm thickness underneath the plasma membrane. These alterations were specific for the absence of the "slow-onset" buffer PV, since in CB-/- mice neither changes in peripheral mitochondria nor in sPL-sER were observed. This implicates that the morphological alterations are aimed to specifically substitute the function of the slow buffer PV. We propose a novel concept that homeostatic mechanisms of components involved in Ca(2+) homeostasis do not always occur at the level of similar or closely related molecules. Rather the cell attempts to restore spatiotemporal aspects of Ca(2+) signals prevailing in the undisturbed (wildtype) situation by subtly fine tuning existing components involved in the regulation of Ca(2+) fluxes.

Characterization of the regulation of renal Na+/H+ exchanger NHE3 by insulin

Insulin receptors are widely distributed in the kidney and affect multiple aspects of renal function. In the proximal tubule, insulin regulates volume and acid-base regulation through stimulation of the Na(+)/H(+) exchanger NHE3. This paper characterizes the signaling pathway by which insulin stimulates NHE3 in a cell culture model [opossum kidney (OK) cell]. Insulin has two distinct phases of action on NHE3. Chronic insulin (24 h) activates NHE3 through the classic phosphatidylinositol 3-kinase-serum- and glucocorticoid-dependent kinase 1 (PI3K-SGK1) pathway as insulin stimulates SGK1 phosphorylation and the insulin effect can be blocked by the PI3K inhibitor wortmannin or a dominant-negative SGK1. We showed that SGK1 transcript and protein are expressed in rat proximal tubule and OK cells. We previously showed that glucocorticoids augment the effect of insulin on NHE3 (Klisic J, Hu MC, Nief V, Reyes L, Fuster D, Moe OW, Ambuhl PM. Am J Physiol Renal Physiol 283: F532-F539, 2002). Part of this can be mediated via induction of SGK1 by glucocorticoids, and indeed the insulin effect on NHE3 can also be amplified by overexpression of SGK1. We next addressed the acute effect of insulin (1-2 h) on NHE3 by systematically examining the candidate signaling cascades and activation mechanisms of NHE3. We ruled out the PI3K-SGK1-Akt and TC10 pathways, increased surface NHE3, NHE3 phosphorylation, NHE3 association with calcineurin homologous protein 1 or megalin as mechanisms of acute activation of NHE3 by insulin. In summary, insulin stimulates NHE3 acutely via yet undefined pathways and mechanisms. The chronic effect of insulin is mediated by the classic PI3K-SGK1 route.

Cardiovascular regulation during administration of co-dergocrine to normal subjects

Whether and to what extent activation of peripheral presynaptic dopamine2-receptors may modulate the release of norepinephrine (NE) and so affect blood pressure (BP) in normal or hypertensive man is not clear. The hydrogenated ergotoxine derivative, co-dergocrine, given in effective antihypertensive rather than excessive experimental doses, has recently been shown to act predominantly as a peripheral dopamine2-receptor agonist in several species. Accordingly, BP regulation assessed has been in 8 normal men on placebo and after 3 weeks on codergocrine 4 mg/day. Co-dergocrine significantly reduced urinary NE excretion from 43 to 33 micrograms/24 h, supine and upright plasma NE 21 to 16 and 49 to 36 ng/dl, respectively, heart rate (-8 and -5%, respectively) and upright systolic BP, 115 to 102 mm Hg; upright diastolic BP also tended to be lower. A standard pressor dose of infused NE was lowered from 131 to 102 ng/kg/min, and the relationship between NE-induced changes in BP and concomitant NE infusion rate or plasma NE concentration was displaced to the left. Exchangeable sodium and plasma volume tended to be slightly decreased. Plasma and urinary electrolytes and epinephrine, plasma renin activity and aldosterone levels, pressor responsiveness to angiotensin II, the chronotropic responses to isoproterenol, and the NE-induced rise in BP, plasma clearance of NE, glomerular filtration rate and effective renal plasma flow were not consistently modified. The findings are consistent with effective peripheral dopamine2-receptor agonism by co-dergocrine in humans. Peripheral presynaptic dopaminergic activation may modulate sympathetic activity and BP in normal man.

Phosphoregulation of K(+)-Cl(-) cotransporter 4 during changes in intracellular Cl(-) and cell volume

It has long been stated that the K(+)-Cl(-) cotransporters (KCCs) are activated during cell swelling through dephosphorylation of their cytoplasmic domains by a protein phosphatase (PP) but that other enzymes are involved by targeting this PP or the KCCs directly. To date, however, the role of signaling intermediates in KCC regulation has been deduced from indirect evidence rather than in vitro phosphorylation studies, and examined after simulation of ion transport through cell swelling or N-ethylmaleimide treatment. In this study, the oocyte expression system was used to examine the effects of changes in cell volume (C(VOL)) and intracellular [Cl(-)] ([Cl(-)](i)) on the activity and phosphorylation levels (P(LEV)) of KCC4, and determine whether these effects are mediated by PP1 or phorbol myristate acetate (PMA)-sensitive effectors. We found that (1) low [Cl(-)](i) or low C(VOL) leads to decreased activity but increased P(LEV), (2) high C(VOL) leads to increased activity but no decrease in P(LEV) and (3) calyculin A (Cal A) or PMA treatment leads to decreased activity but no increase in P(LEV). Thus, we have shown for the first time that one of the KCCs can be regulated through direct phosphorylation, that changes in [Cl(-)](i) or C(VOL) modify the activity of signaling enzymes at carrier sites, and that the effectors directly involved do not include a Cal A-sensitive PP in contrast to the widely held view. J. Cell. Physiol. 219: 787-796, 2009. (c) 2009 Wiley-Liss, Inc.