Anestesia peribulbar com ropivacaína como alternativa ao bloqueio neuromuscular para facectomia em cães

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Influência do butorfanol sobre os períodos de latência e de ação da ropivacaína pela via peridural na ovariossalpingo-histerectomia em cadelas

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Leishmune (R) vaccine blocks the transmission of canine visceral leishmaniasis - Absence of Leishmania parasites in blood, skin and lymph nodes of vaccinated exposed dogs

Leishmune (R) vaccine is the first licensed vaccine against canine visceral leishmaniasis. It contains the Fucose-Mannose-ligand (FML) antigen of Leishmania donovani. The potential Leishmune (R) vaccine effect on the interruption of the transmission of the disease, was assayed by monitoring, in untreated (n = 40) and vaccinated dogs (n = 32) of a Brazilian epidemic area: the kala-azar clinical signs, the FML-seropositivity and the Leishmania parasite evidence by immunohistochemistry of skin and PCR for Leishmanial DNA of lymph node and blood samples. on month I I after vaccination, untreated controls showed: 25% of symptomatic cases, 50% of FML-seropositivity, 56.7% of lymph node PCR, 15.7% of blood PCR and 25% of immunohistochemical positive reactions. The Leishmune (R)-vaccinated dogs showed 100% of seropositivity to FML and a complete absence of clinical signs and of parasites (0%) in skin, lymph node and blood PCR samples (P < 0.01). The positivity in FML-ELISA in untreated dogs significantly correlates with the PCR in lymph node samples (p < 0.001) and with the increase in number of symptoms (p = 0.006) being strong markers of infectiousness. The absence of symptoms and of evidence of Leishmania DNA and parasites in Leishmune (R)-vaccinated animals indicates the non-infectious condition of the Leishmune (R)-vaccinated dogs. (c) 2005 Elsevier Ltd. All rights reserved.

Actinobacillus actinomycetemcomitans lipopolysaccharide induces interleukin-6 expression through multiple mitogen-activated protein kinase pathways in periodontal ligament fibroblasts

Actinobacillus actinomycetemcomitans plays a major role in the pathogenesis of aggressive periodontitis. Lipopolysaccharide (LPS) derived from A. actinomycetemcomitans is a key factor in inflammatory cytokine generation within periodontal tissues. In this study, we identify major mitogen-activated protein kinase (MAPK) signaling pathways induced by A. actinomycetemcomitans LPS, Escherichia coli LPS and interleukin-1 beta (IL-1 beta) in a murine periodontal ligament (mPDL) fibroblast cell line. Immunoblot analysis was used to assess the phosphorylated forms of p38, extracellular-regulated kinase (ERK) and c-jun N-terminal kinase (JNK) MAPK following stimulation with A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta. IL-6 mRNA induction was detected via reverse transcription-polymerase chain reaction, while protein levels were quantified via enzyme-linked immunosorbent assays (ELISA). We utilized biochemical inhibitors of p38, ERK and JNK MAPK to identify the MAPK signaling pathways needed for IL-6 expression. Additional use of stable mPDL cell lines containing dominant negative mutant constructs of MAPK kinase-3 and -6 (MKK-3/6) and p38 null mutant mouse embryonic fibroblast (MEF) cells were used to substantiate the biochemical inhibitor data. Blocking p38 MAPK with SB203580 reduced the induction of IL-6 mRNA by A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta by > 70%, > 95% and similar to 60%, respectively. IL-6 ELISA indicated that blocking p38 MAPK reduced the IL-6 protein levels induced by A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta by similar to 60%, similar to 50% and similar to 70%, respectively. All MAPK inhibitors significantly reduced the IL-6 protein levels induced by A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta whereas only p38 inhibitors consistently reduced the A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta induction of IL-6 mRNA steady-state levels. The contribution of p38 MAPK LPS-induced IL-6 expression was confirmed using MKK-3/6 dominant negative stable mPDL cell lines. Wild-type and p38 alpha(-/-) MEF cells provided additional evidence to support the role of p38 alpha MAPK in A. actinomycetemcomitans LPS-stimulated IL-6. Our results indicate that induction of IL-6 by E. coli LPS, IL-1 beta and A. actinomycetemcomitans LPS requires signaling through MKK-3-p38 alpha ERK, JNK and p38 MAPK in mPDL cells.

MKK3/6-p38 MAPK signaling is required for IL-1 beta and TNF-alpha-induced RANKL expression in bone marrow stromal cells

Coupled bone turnover is directed by the expression of receptor-activated NF-kappa B ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG). Proinflammatory cytokines, such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) induce RANKL expression in bone marrow stromal cells. Here, we report that IL-1 beta and TNF-alpha-induced RANKL requires p38 mitogen-activating protein kinase (MAPK) pathway activation for maximal expression. Real-time PCR was used to assess the p38 contribution toward IL-1 beta and TNF-alpha-induced RANKL mRNA expression. Steady-state RANKL RNA levels were increased approximately 17-fold by IL-1 beta treatment and subsequently reduced similar to 70%-90% when p38 MAPK was inhibited with SB203580. RANKL mRNA stability data indicated that p38 MAPK did not alter the rate of mRNA decay in IL-1 beta-induced cells. Using a RANKL-luciferase cell line receptor containing a 120-kB segment of the 5' flanking region of the RANKL gene, reporter expression was stimulated 4-5-fold by IL-1 beta or TNF-alpha treatment. IL-1 beta-induced RANKL reporter expression was completely blocked with specific p38 inhibitors as well as dominant negative mutant constructs of MAPK kinase-3 and -6. In addition, blocking p38 signaling in bone marrow stromal cells partially inhibited IL-1 beta and TNF-alpha-induced osteoclastogenesis in vitro. Results from these studies indicate that p38 MAPK is a major signaling pathway involved in IL-1 beta and TNF-alpha-induced RANKL expression in bone marrow stromal cells.

Multistratum response surface designs

Response surface designs are usually described as if the treatments have been completely randomized to the experimental units. However, in practice there is often a structure to the units, implying the need for blocking. If, in addition, some factors are more difficult to vary between units than others, a multistratum structure arises naturally. We present a general strategy for constructing response surface designs in multistratum unit structures. Designs are constructed stratum by stratum, starting in the highest stratum. In each stratum a prespecified treatment set for the factors applied in that stratum is arranged to be nearly orthogonal to the units in the higher strata, allowing-for all the effects that have to be estimated. Three examples are given to show the applicability of the method and are also used to check the relationship of the final design to the choice of treatment set. Finally, some practical considerations in randomization are discussed.

An algorithm for arranging response surface designs in small blocks

We consider the problem of blocking response surface designs when the block sizes are prespecified to control variation efficiently and the treatment set is chosen independently of the block structure. We show how the loss of information due to blocking is related to scores defined by Mead and present an interchange algorithm based on scores to improve a given blocked design. Examples illustrating the performance of the algorithm are given and some comparisons with other designs are made. (C) 2000 Elsevier B.V. B.V. All rights reserved.

Variance dispersion graphs for comparing blocked response surface designs

In this paper, we extend the use of the variance dispersion graph (VDG) to experiments in which the response surface (RS) design must be blocked. Through several examples we evaluate the prediction performances of RS designs in non-orthogonal block designs compared with the equivalent unblocked designs and orthogonally blocked designs. These examples illustrate that good prediction performance of designs in small blocks can be expected in practice. Most importantly, we show that the allocation of the treatment set to blocks can seriously affect the prediction properties of designs; thus, much care is needed in performing this allocation.

Some practical advice on polynomial regression analysis from blocked response surface designs

It is often necessary to run response surface designs in blocks. In this paper the analysis of data from such experiments, using polynomial regression models, is discussed. The definition and estimation of pure error in blocked designs are considered. It is recommended that pure error is estimated by assuming additive block and treatment effects, as this is more consistent with designs without blocking. The recovery of inter-block information using REML analysis is discussed, although it is shown that it has very little impact if thc design is nearly orthogonally blocked. Finally prediction from blocked designs is considered and it is shown that prediction of many quantities of interest is much simpler than prediction of the response itself.

Neutralization of snake venom phospholipase A(2) toxins by aqueous extract of Casearia sylvestris (Flacourtiaceae) in mouse neuromuscular preparation

Aqueous extract of Casearia sylvestris (Flacourtiaceae) has been shown to inhibit enzymatic and biological properties of some Bothrops and Crotalus venoms and their purified phospholipase A(2) (PLA(2)) toxins. In this work we evaluated the influence of C sylvestris aqueous extract upon neuromuscular blocking and muscle damaging activities of some PLA(2)S (crotoxin from C. durissus terrificus, bothropstoxin-I from B.jararacussu, piratoxin-I from B. pirajai and myotoxin-II from B. moojeni) in mouse phrenic-diaphragm preparations. Crotoxin (0.5 mu M) and all other PLA2 toxins (1.0 mu M) induced irreversible and time-dependent blockade of twitches. Except for crotoxin, all PLA2 toxins induced significant muscle damage indices, assessed by microscopic analysis. Preincubation of bothropstoxin-I, piratoxin-I or myotoxin-II with C. sylvestris extract (1:5 (w/w), 30 min, 37 degrees C significantly prevented the neuromuscular blockade of preparations exposed to the mixtures for 90 min; the extent of protection ranged from 93% to 97%. The vegetal extract also neutralized the muscle damage (protection of 80-95%). Higher concentration of the C. sylvestris extract (1: 10, w/w) was necessary to neutralize by 90% the neuromuscular blockade induced by crotoxin. These findings expanded the spectrum of C. sylvestris antivenom activities, evidencing that it may be a good source of potentially useful PLA2 inhibitors. (c) 2007 Elsevier B.V.. All rights reserved.

Effects of indoramin in rat vas deferens and aorta: concomitant alpha(1)-adrenoceptor and neuronal uptake blockade

1 the actions of the alpha(1)-adrenoceptor antagonist indoramin have been examined against the contractions induced by noradrenaline in the rat vas deferens and aorta taking into account a putative neuronal uptake blocking activity of this antagonist which could. result in self-cancelling actions.2 Indoramin behaved as a simple competitive antagonist of the contractions induced by noradrenaline in the vas deferens and aorta yielding pA(2) values of 7.38 +/- 0.05 (slope = 0.98 +/- 0.03) and 6.78 +/- 0.14 (slope = 1.08 +/- 0.06), respectively.3 When the experiments were repeated in the presence of cocaine (6 mu M) the potency (pA(2)) of indoramin in antagonizing the contractions of the vas deferens to noradrenaline was increased to 8.72 +/- 0.07 (slope = 1.10 +/- 0.05) while its potency remained unchanged in the aorta (pA(2) = 6.69 +/- 0.12; slope = 1.04 +/- 0.05).4 In denervated vas deferens, indoramin antagonized the contractions to noradrenaline with a potency similar to that found in the presence of cocaine (8.79 +/- 0.07; slope = 1.09 +/- 0.06).5 It is suggested that indoramin blocks alpha(1)-adrenoceptors and neuronal uptake in rat vas deferens resulting in Schild plots with slopes not different from unity even in the absence of selective inhibition of neuronal uptake. As a major consequence of this double mechanism of action, the pA(2) values for this antagonist are underestimated when calculated in situations where the neuronal uptake is active, yielding spurious pK(B) values.

Nuclear incoherent photoproduction of pi(0) and eta from 4 to 12 GeV

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

Genetic diversity in Egeria densa and E. najas in Jupia Reservoir, Brazil

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

Survey for Foot-and-mouth Disease in the Endangered Marsh Deer (Blastocerus dichotomus) from Marshlands of the Parana River Basin, Brazil

Habitat fragmentation and diseases have resulted in a decline of the marsh deer (Blastocerus (dichotomus) throughout its South American range. Our objectives were to determine whether marsh deer intended for translocation from a region of the Rio Parana Basin had been infected previously by foot-and-mouth disease virus (FMDV) and whether they were carrying virus We captured marsh deer from June to October 1998 and collected blood from 108 animals and esophageal-pharyngeal fluid from 53 Serum was tested for antibodies against three FMDV serotypes (O, A, and C) by liquid-phase-blocking sandwich enzyme-linked immunosorbent assay (ELISA) Esophageal-pharyngeal fluid was tested for FMDV RNA by reverse transcription polymerase chain reaction (RT-PCR) and inoculation into three successive baby hamster kidney (BHK-21) cell subcultures, followed by RT-PCR of cultures We detected low log(10) titers (range 1 0-1 5) to FM DV subtype A(24) Cruzeiro in 19 of 108 sampled marsh deer, but failed to isolate FMDV or detect FMDV RNA in any samples we conclude that marsh deer from our study site were unlikely to carry FMDV, however, as a preventive measure, the 19 animals with titers for FMDV were not sent to FMDV-free Brazilian states

SOLID STATE ELECTROCHEMICAL BEHAVIOR of USNIC ACID AT A GLASSY CARBON ELECTRODE

The electrochemical redox behavior of usnic acid, mainly known for its antibiotic activity, has been investigated using cyclic, differential pulse and square wave voltammetry in aqueous electrolyte. These studies were carried out by solid state voltammetry with the solid mechanically attached on the surface of a glassy carbon electrode and at different pH values. Usnic acid did not present any reduction reaction. The pH-dependent electrochemical oxidation occurs in three steps, one electron and one proton irreversible processes, assigned to each of the hydroxyl groups in the molecule. Adsorption of the non-electroactive oxidation product was also observed, blocking the electrode surface. An oxidation mechanism was proposed and electroanalytical methodology was developed to determine usnic acid.