979 resultados para 1,10-fenantrolina-5,6-diona


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O objetivo deste estudo foi determinar a influência da idade cronológica e da maturação biológica sobre o consumo máximo de oxigênio (VO2max) e a velocidade de corrida correspondente ao VO2max em crianças e adolescentes brasileiros, do sexo masculino, com idade entre 10 e 15 anos, não praticantes de atividade física sistemática. Participaram do estudo 40 voluntários, divididos em dois grupos, segundo a idade cronológica (GC1 - n = 20; 11,4 ± 0,6 anos; 38,8 ± 8,6kg; 143,6 ± 8,2cm e GC2 - n = 20; 14,1 ± 0,6 anos; 55,9 ± 14,2kg; 163,3 ± 10,2cm) e maturação biológica (GB1 - n = 20; estágios 1, 2 e 3; e GB2 - n = 20; estágios 4 e 5). O VO2max foi mensurado em um teste progressivo e intermitente de corrida em esteira rolante, com estágios de três minutos e pausa de 20 segundos, incrementos de 1km/h a começar com 9km/h, até a exaustão voluntária. A velocidade correspondente ao VO2max (vVO2max) foi considerada como a menor velocidade em que se observou o maior valor de VO2. A máxima velocidade aeróbia (Va max) foi calculada pela fórmula proposta por di Prampero (1986). Houve diferença significante para os valores de VO2max(l/min), Va max(km/h)e vVO2max(km/h) entre os grupos GC1 e GC2 (1,84 ± 0,41 / 2,81 ± 0,61; 11,8 ± 1,2 / 12,6 ± 1,2; 12,1 ± 1,2 / 12,9 ± 1,1, respectivamente), GB1 e GB2 (1,80 ± 0,37 / 2,87 ± 0,56; 12,1 ± 1,2 / 12,9 ± 1,1; 11,8 ± 1,2 / 12,5 ± 1,1, respectivamente), mas não para os valores de VO2max em ml.kg-1.min-1 para todos os grupos (GC1 e GC2: 47,9 ± 6,8 / 50,4 ± 5,5; GB1 e GB2: 47,9 ± 6,8 / 50,3 ± 5,5, respectivamente). Com base nos resultados obtidos, pode-se concluir que o VO2max (l/min), aVa max e a vVO2max têm seus valores aumentados como um provável efeito do crescimento e desenvolvimento, podendo, ainda, expressar melhora da economia de movimento, mesmo em indivíduos não praticantes de atividade física sistemática.

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A hipovolemia é caracterizada por uma perda de fluido corpóreo, cursando com inadequado fluxo circulatório e consequentemente lesão tecidual. Neste trabalho, objetivou-se comparar a expansão volêmica resultante da administração de solução salina hipertônica (NaCl 7,5%), isolada ou em associação com hidroxietilamido 130/0,4 (HES 130/0,4), em gatas com hipovolemia induzida, sob anestesia geral inalatória com isofluorano. Foram utilizadas 12 gatas, sem raça definida, adultas, com massa corporal média de 3,07±0,56kg. Os animais foram anestesiados com isofluorano e, após a preparação cirúrgica, foram mantidos em 1CAM sob ventilação controlada. Após a estabilização do plano anestésico, foram avaliados os parâmetros basais. em ato contínuo, iniciou-se a fase de hipovolemia, por meio da retirada de 30ml kg-1 de sangue da artéria femoral. Após 60 minutos da estabilização do quadro de hipovolemia, foi realizada nova mensuração dos dados, alocando-se os animais aleatoriamente em dois grupos: GSH (grupo solução hipertônica, n=6), que receberam, na fase de expansão volêmica, NaCl 7,5% isolada, na dose de 4ml kg-1, e GSHC (grupo salina hipertônica associado ao coloide, n=6), que receberam NaCl 7,5%, na mesma dose citada, em associação com HES 130/0,4, na dose de 30ml kg-1. Após realização do tratamento, foram avaliados novamente os efeitos cardiovasculares e hemogasométricos por 120 minutos. As pressões arteriais média (PAM), sistólica (PAS) e diastólica (PAD) foram maiores logo após a expansão volêmica (T0) para o GSH. de T45 até T120, as PAM, PAS e PAD foram maiores para o GSHC, em comparação com o GSH. A pressão venosa central foi maior no GSHC até T60. Não foram observadas diferenças entre grupos para frequência cardíaca e respiratória, íons sódio e potássio, déficit de base, bicarbonato, saturação de oxigênio na hemoglobina, glicose, PaCO2, PaO2 e pH. Conclui-se que a administração de NaCl 7,5% isoladamente aumenta rapidamente a PAM, PAS e PAD em gatos com hipovolemia induzida, mantendo esse efeito por apenas 30 minutos, enquanto que a administração de hidroxietilamido 130/0,4 associado à NaCl 7,5% promove reestabelecimento mais tardio (após 30 minutos), porém mais duradouro (até 120 minutos) da PAM, PAS e PAD em gatas com hipovolemia induzida. A administração de HES 130/0,4 associada à NaCl 7,5% promove aumento acentuado da PVC por até 60 minutos após a administração.

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The two-dimensional hybrid organic-inorganic materials Zn-2-Cr and Zn-2-Al-LDHs (Layered Double Hydroxides) containing 4-(1H-pyrrol-1yl)benzoate anions as the interlayer anions were synthesized by the co-precipitation method at constant pH followed by subsequent hydrothermal treatment for 72 h. The materials were characterized by PXRD, C-13 CP-MAS NMR, ESR, TGA, and TEM. The basal spacing found by the X-ray diffraction technique is coincident with the formation of bilayers of the intercalated anions. Solid-state C-13 NMR and ESR data strongly suggest the partial in situ polymerization of the 4-(1H-pyrrol-1yl)benzoate anions during coprecipitation. (c) 2006 Elsevier Ltd. All rights reserved.

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We report the synthesis and characterization of organic-inorganic hybrid materials: Zn-2-Al-LDHs (layered double hydroxides) containing 3-(1H-pyrrol-1-yl)-propanoate and 7-(1H-pyrrol-l-yl)-heptanoate as the interlayer anions. The LDHs were synthesized by the co-precipitation method at constant pH followed by hydrothermal treatment for 72 h. The materials were characterized by PXRD, C-13 CP-MAS NMR, TGA, and ESR. The basal spacing found by PXRD technique is coincident with the formation of bilayers of the intercalated anions. The solid state C-13 NMR showed that the interlayered anions remain identical after intercalation. ESR data suggest that the monomers connect each other in a limited number of guests when a thermal treatment is applied. The inorganic LDH sheets delay the temperature of degradation of the monomers. (c) 2006 Elsevier Ltd. All rights reserved.

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The rat tail artery has been used for the study of vasoconstriction mediated by alpha(1A)-adrenoceptors (ARs). However, rings from proximal segments of the tail artery (within the initial 4 cm, PRTA) were at least 3- fold more sensitive to methoxamine and phenylephrine (n = 6 - 12; p < 0.05) than rings from distal parts (between the sixth and 10th cm, DRTA). Interestingly, the imidazolines N-[ 5-( 4,5- dihydro- 1H- imidazol-2-yl)-2-hydroxy-5,6,7,8- tetrahydronaphthalen- 1- yl] methanesulfonamide hydrobromide (A-61603) and oxymetazoline, which activate selectively alpha(1A)- ARs, were equipotent in PRTA and DRTA (n = 4 - 12), whereas buspirone, which activates selectively alpha(1D)-AR, was approximate to 70-fold more potent in PRTA than in DRTA (n = 8; p < 0.05). The selective alpha(1D)-AR antagonist 8-[2-[4-(methoxyphenyl)-1-piperazinyl] ethyl]-8-azaspiro[4.5] decane-7,9-dione dihydrochloride (BMY- 7378) was approximate to 70- fold more potent against the contractions induced by phenylephrine in PRTA (pK(B) of approximate to 8.45; n = 6) than in DRTA (pK B of approximate to 6.58; n = 6), although the antagonism was complex in PRTA. 5-Methylurapidil, a selective alpha(1A)-antagonist, was equipotent in PRTA and DRTA (pK(B) of approximate to 8.4), but the Schild slope in DRTA was 0.73 +/- 0.05 ( n = 5). The noncompetitive alpha(1B)-antagonist conotoxin rho-TIA reduced the maximal contraction induced by phenylephrine in DRTA, but not in PRTA. These results indicate a predominant role for alpha(1A)-ARs in the contractions of both PRTA and DRTA but with significant coparticipations of alpha(1D)-ARs in PRTA and alpha(1B)-ARs in DRTA. Semiquantitative reverse transcription-polymerase chain reaction revealed that mRNA encoding alpha(1A)- and alpha(1B)-ARs are similarly distributed in PRTA and DRTA, whereas mRNA for alpha(1D)-ARs is twice more abundant in PRTA. Therefore, alpha(1)-ARs subtypes are differentially distributed along the tail artery. It is important to consider the segment from which the tissue preparation is taken to avoid misinterpretations on receptor mechanisms and drug selectivities. antagonism was complex in PRTA. 5- Methylurapidil, a selective alpha(1A)-antagonist, was equipotent in PRTA and DRTA (pK(B) of approximate to 8.4), but the Schild slope in DRTA was 0.73 +/- 0.05 ( n = 5). The noncompetitive alpha(1B)-antagonist conotoxin rho-TIA reduced the maximal contraction induced by phenylephrine in DRTA, but not in PRTA. These results indicate a predominant role for alpha(1A)-ARs in the contractions of both PRTA and DRTA but with significant coparticipations of alpha(1D)-ARs in PRTA and alpha(1B)-ARs in DRTA. Semiquantitative reverse transcription-polymerase chain reaction revealed that mRNA encoding alpha(1A)- and alpha(1B)- ARs are similarly distributed in PRTA and DRTA, whereas mRNA for alpha(1D)-ARs is twice more abundant in PRTA. Therefore, alpha(1)-ARs subtypes are differentially distributed along the tail artery. It is important to consider the segment from which the tissue preparation is taken to avoid misinterpretations on receptor mechanisms and drug selectivities.

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The influence of additions of 1.3, 2.5, 3.8, 5.1, and 6.3 at.% Ag on the aging behavior of the Cu-10.4at.%Al alloy was studied using microhardness measurements, scanning electron microscopy (SEM) and energy dispersive X-ray (EDX) analysis. The results indicated that with silver additions it is possible to obtain a response to age hardening, and that for large aging times there is a decrease in the alloy hardness, with a process that leads to Ag and Al segregation. © 1998 Elsevier Science S.A.

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We determined the effects of AT 1 and AT 2 (selective no peptides antagonists angiotensin receptors), arginine vasopressin V 1 receptor antagonist as well as L-arginine, a nitric oxide donor and N W-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, injected into supraoptic nucleus (SON) on water and sodium intake induced by the injection of angiotensin II (ANGII). Male Holtzman rats weighing 200-250 g with canulae implanted into the SON were used. The drugs were injected in 0.5 μL over 30-60 sec. The water intake after injection of saline SAL+SAL 0.15 M NaCl was 0.40±0.1 mL 2 h -1; SAL+ANGII increase water intake. Losartan decreased the water intake induced by ANGII. PD123319 injected prior to produce no change in water intake induced by ANGII. AVPA prior to ANGII reduced the water intake with a less intensity than losartan. L-arginine prior to ANGII decreases the water intake at a same intensity than losartan. L-NAME prior to ANGII potentiated the dipsogenic effect of ANGII. Losartan injected simultaneously with L-arginine prior to ANGII blocked the dipsogenic effect of ANGII. These results confirm the importance of SON in the control of water intake and strongly suggest that AT 1, V 1 receptors interact with nitrergic pathways within the SON influencing the dipsogenic effect of ANGII.

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An involvement of the transient receptor potential vanilloid (TRPV) 1 channel in the regulation of body temperature (T b) has not been established decisively. To provide decisive evidence for such an involvement and determine its mechanisms were the aims of the present study. We synthesized a new TRPV1 antagonist, AMG0347 [(E)-N-(7-hydroxy-5,6,7,8-tetrahydronaphthalen-1- yl)-3-(2-(piperidin-1-yl)-6-(trifluoromethyl)pyridin-3-yl)acrylamide], and characterized it in vitro. We then found that this drug is the most potent TRPV1 antagonist known to increase T b of rats and mice and showed (by using knock-out mice) that the entire hyperthermic effect of AMG0347 is TRPV1 dependent. AMG0347-induced hyperthermia was brought about by one or both of the two major autonomic cold-defense effector mechanisms (tail-skin vasoconstriction and/or thermogenesis), but it did not involve warmth-seeking behavior. The magnitude of the hyperthermic response depended on neither T b nor tail-skin temperature at the time of AMG0347 administration, thus indicating that AMG0347-induced hyperthermia results from blockade of tonic TRPV1 activation by nonthermal factors. AMG0347 was no more effective in causing hyperthermia when administered into the brain (intracerebroventricularly) or spinal cord (intrathecally) than when given systemically (intravenously), which indicates a peripheral site of action. We then established that localized intra-abdominal desensitization of TRPV1 channels with intraperitoneal resiniferatoxin blocks the T b response to systemic AMG0347; the extent of desensitization was determined by using a comprehensive battery of functional tests. We conclude that tonic activation of TRPV1 channels in the abdominal viscera by yet unidentified nonthermal factors inhibits skin vasoconstriction and thermogenesis, thus having a suppressive effect on T b. Copyright © 2007 Society for Neuroscience.

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We present a study of eeγ and μμγ events using 1109 (1009) pb-1 of data in the electron (muon) channel, respectively. These data were collected with the DØ detector at the Fermilab Tevatron p over(p, ̄) collider at sqrt(s) = 1.96   TeV. Having observed 453 (515) candidates in the eeγ (μμγ) final state, we measure the Zγ production cross section for a photon with transverse energy ET > 7   GeV, separation between the photon and leptons Δ Rℓ γ > 0.7, and invariant mass of the di-lepton pair Mℓ ℓ > 30   GeV / c2, to be 4.96 ± 0.30 (stat . + syst .) ± 0.30 (lumi .)   pb, in agreement with the Standard Model prediction of 4.74 ± 0.22   pb. This is the most precise Zγ cross section measurement at a hadron collider. We set limits on anomalous trilinear Zγγ and ZZγ gauge boson couplings of - 0.085 < h30 γ < 0.084, - 0.0053 < h40 γ < 0.0054 and - 0.083 < h30 Z < 0.082, - 0.0053 < h40 Z < 0.0054 at the 95% C.L. for the form-factor scale Λ = 1.2   TeV.

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In the present study, we investigate whether mast cells and macrophages are involved in the control of IL-1β-induced neutrophil migration, as well as the participation of chemotactic mediators. IL-1β induced a dose-dependent neutrophil migration to the peritoneal cavity of rats which depends on LTB 4, PAF and cytokines, since the animal treatment with inhibitors of these mediators (MK 886, PCA 4248 and dexamethasone respectively) inhibited IL-1β-induced neutrophil migration. The neutrophil migration induced by IL-1β is dependent on mast cells and macrophages, since depletion of mast cells reduced the process whereas the increase of macrophage population enhanced the migration. Moreover, mast cells or macrophages stimulated with IL-1β released a neutrophil chemotactic factor, which mimicked the neutrophil migration induced by IL-1β. The chemotactic activity of the supernatant of IL-1β-stimulated macrophages is due to the presence of LTB4, since MK 886 inhibited its release. Moreover, the chemotactic activity of IL-1β-stimulated mast cells supernatant is due to the presence of IL-1β and TNF-α, since antibodies against these cytokines inhibited its activity. Furthermore, significant amounts of these cytokines were detected in the supernatant. In conclusion, our results suggest that neutrophil migration induced by IL-1β depends upon LTB4 released by macrophages and upon IL-1β and TNFα released by mast cells. © 2007 Springer Science+Business Media, LLC.

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Using data corresponding to an integrated luminosity of 1.3fb -1, we observe a narrow mass state decaying into Υ(1S)+γ, where the Υ(1S) meson is detected by its decay into a pair of oppositely charged muons, and the photon is identified through its conversion into an electron-positron pair. The significance of this observation is 5.6 standard deviations. The mass of the state is centered at 10.551±0.014(stat) ±0.017(syst)GeV/c2, which is consistent with that of the state recently observed by the ATLAS Collaboration. © 2012 American Physical Society.

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Despite the improvements in neoadjuvant chemotherapy, the outcome of patients with advanced bladder cancer has changed very little over the past 30 years. In the present study we tested and compared the in vitro antitumor activities of four different inhibitors of Polo-like kinase 1 (PLK1) (BI 2536, BI 6727, GW843682X, and GSK461364), against 3 bladder carcinoma cell lines RT4, 5637 and T24. The impact on radiosensitivity and drug interactions in simultaneous treatments with cisplatin, methotrexate, and doxorubicin were also investigated. Our results showed that PLK1 inhibition prevented cell proliferation and clonogenicity, causing significant inhibition of invasion of tumor cells, though modest differences were observed between drugs. Moreover, all PLK1 inhibitors induced G2/M arrest, with the subsequent induction of death in all 3 cell lines. Drug interactions studies showed auspicious results for all PLK1 inhibitors when combined with the commonly used cisplatin and methotrexate, though combinations with doxorubicin showed mostly antagonistic effects. Comparably, the four PLK1 inhibitors efficiently sensitized cells to ionizing radiation. Our findings demonstrate that irrespective of the inhibitor used, the pharmacological inhibition of PLK1 constrains bladder cancer growth and dissemination, providing new opportunities for future therapeutic intervention. However, further laboratorial and preclinical tests are still needed to corroborate the usefulness of using them in combination with other commonly used chemotherapeutic drugs. © 2013 Landes Bioscience.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)