In Vitro Antiophidian Properties of Dipteryx alata Vogel Bark Extracts

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Extracts from Dipteryx alata bark obtained with different solvents (hexane, dichloromethane, ethyl acetate and methanol) were mixed in vitro with Bothrops jararacussu (Bjssu, 40 mu g/mL) and Crotalus durissus terrificus (Cdt, 15 mu g/mL) snake venoms, and applied to a mouse phrenic nerve-diaphragm preparation to evaluate the possible neutralization of venom effects. Cdt venom neurotoxic effect was not inhibited by any of the extracts, while the neurotoxic and myotoxic actions of Bjssu venom were decreased by the methanolic extract. This inhibition appears to be augmented by tannins. Dichloromethane bark extract inhibited similar to 40% of Bjssu venom effects and delayed blockade induced by Cdt. The methodology used to determine which extract was active allows inferring that: (i) phenolic acids and flavonoids contained in the methanolic extract plus tannins were responsible mostly for neutralization of Bjssu effects; (ii) terpenoids from the dichloromethane extract may participate in the anti-Cdt and anti-Bjssu venom effects; (iii) a given extract could not inhibit venoms from different species even if those belong to the same family, so it is improper to generalize a certain plant as antiophidian; (iv) different polarity extracts do not present the same inhibitory capability, thus demonstrating the need for characterizing both venom pharmacology and the phytochemistry of medicinal plant compounds.15959565970Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)PROBIC/UNISOConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)FAPESP [Proc. FAPESP 04/09705-8, 07/53883-6]FAPESP [07/51414-9, 08/05459-3]CNPq [Proc. 302206/2008-6

Phenobarbital Pharmacological Findings on the Nerve-Muscle Basis

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Phenobarbital and carbamazepine are antiepileptic drugs that act at the nervous central system by different mechanisms of action. In this work we investigated the pharmacological effects of these drugs on mouse phrenic nerve-diaphragm preparations through the myographic technique. Carbamazepine (0.105, 1.05, 2.1 and 4.2 mM, n = 8, 6, 6 and 6, respectively), induced a dose-dependent neuromuscular blockade, under indirect or direct muscle stimulation and the neurotransmission was reestablished after washing. Conversely, phenobarbital caused an unexpected facilitatory effect, under several formulations, such as the acid-extracted commercial tablets (1.05, 2.1 and 4.2 mM, n = 7, 6 and 7, respectively), commercial phenobarbital solution (4.2 mM, n = 7) or its correspondent pure active ingredient (4.2 and 2.1 mM, n = 6 each). Only at a higher concentration the acid-extracted phenobarbital performed a neuromuscular blockade (8.4 mM, n = 10). The different responses between carbamazepine (paralysis) and phenobarbital (facilitatory effect) evidentiated a new effect for phenobarbital until now concealed at the neuromuscular junction and may involve the glutamatergic regulation, since its role as an acethyl-choline co-transmitter in motoneurons was already established.282211218Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)PROBIC/UNISOFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)FAPESP [04/09705-8

Phenobarbital Pharmacological Findings On The Nerve-muscle Basis

Phenobarbital and carbamazepine are antiepileptic drugs that act at the nervous central system by different mechanisms of action. In this work we investigated the pharmacological effects of these drugs on mouse phrenic nerve-diaphragm preparations through the myographic technique. Carbamazepine (0.105, 1.05, 2.1 and 4.2 mM, n = 8, 6, 6 and 6, respectively), induced a dose-dependent neuromuscular blockade, under indirect or direct muscle stimulation and the neurotransmission was reestablished after washing. Conversely, phenobarbital caused an unexpected facilitatory effect, under several formulations, such as the acid-extracted commercial tablets (1.05, 2.1 and 4.2 mM, n = 7, 6 and 7, respectively), commercial phenobarbital solution (4.2 mM, n = 7) or its correspondent pure active ingredient (4.2 and 2.1 mM, n = 6 each). Only at a higher concentration the acid-extracted phenobarbital performed a neuromuscular blockade (8.4 mM, n = 10). The different responses between carbamazepine (paralysis) and phenobarbital (facilitatory effect) evidentiated a new effect for phenobarbital until now concealed at the neuromuscular junction and may involve the glutamatergic regulation, since its role as an acetylcholine co-transmitter in motoneurons was already established.282211218Grozdanovic, Z., Baumgarten, H.G., (1999) Histol. Histopathol, 14, pp. 243-256Gorio, A., Hurlbut, W.P., Ceccarelli, B., (1978) J. Cell Biology, 78, pp. 716-733Nikolsky, E.E., Oranska, T.I., Vyskocil, F., (1996) Exp Physiol, 81, pp. 341-348Katz, B., Miledi, R., (1977) Proc. R. Soc. Lond. B. Biol. Sci, 196, pp. 59-72Vyskocil, F., Illés, P., (1978) Physiol. Bohemoslov, 27, pp. 449-455Vyas, S., Bradford, H.F., (1987) Neurosci. Lett, 82, pp. 58-64Waerhaug, O., Ottersen, O.P., (1993) Anat. Embryol. (Berl), 188, pp. 501-513Urazaev, A.Kh., N.V. Naumenko, G.I. Poletayev, E.E. Nikolsky & F. Vyskocil (1998) Mol. Chem. Neuropathol. 33: 163-74Grozdanovic, A., Gossrau, R., (1998) Cell Tissue Res, 291, pp. 57-63Urazaev, A., Naumenko, N., Malomough, A., Nikolsky, E., Vyskocil, F., (2000) Neurosci. Res, 37, pp. 255-263Malomouzh, A.I., Mukhtarov, M.R., Nikolsky, E.E., Vyskocil, F., (2007) J. Neurochem, 102, pp. 2110-2117Urazaev, A.K., Naumenko, N.V., Nikolsky, E.E., Vyskocil, F., (1999) Neurosci. Res, 33, pp. 81-86Malomouzh, A.I., Mukhtarov, M.R., Nikolsky, E.E., Vyskocil, F., Lieberman, E.M., Urazaev, A.K., (2003) J. Neurochem, 85, pp. 206-213Malomouzh, A.I., Nikolsky, E.E., Lieberman, E.M., Sherman, J.A., Lubischer, J.L., Grossfeld, R.M., Urazaev, A.K., (2005) J. Neurochem, 94, pp. 257-267Browser, M.S.H., (2008) Bethesda, , http://www.ncbi.nlm.nih.gov, MD, National Library of Medicine US, cited 2008 Jul 07, Phenobarbital and Carbamazepine. Available fromShorvon, S.D., Reynolds, E.H., (1982) J. Neurol. Neurosurg Psychiatry, 45, pp. 620-626Geraldini, C., Faedda, M.T., Sideri, G., (1984) Epilepsia, 25, pp. 502-505Bono, A., Beghi, E., Bogliun, G., Cavaletti, G., Curtó, N., Marzorati, L., Frattola, L., (1993) Epilepsia, 34, pp. 323-331Vázquez, A.J., Diamond, B.I., Sabelli, H.C., (1975) Epilepsia, 16, pp. 601-608Schwarz, J.R., (1979) Eur. J. Pharmacol, 56, pp. 51-60Jankovic, S.M., Jankovic, S.V., Kostic, J., Kostic, I., Jakovljevic, M., (2006) Eur. J. Clin. Pharmacol, 62, pp. 707-712Carenini, L., Bottacchi, E., Camerlingo, M., D'Alessandro, G., Mamoli, A., (1988) Epilepsia, 29, pp. 145-148Barcelos, de, C.C., (2007) Efeitos neuromusculares do atracúrio e do rocurônio em ratos pré tratados com carbamazepina e fenobarbital. Estudo in vitro e in vivo, , dissertation, Campinas SP, Universidade Estadual de CampinasBarcelos, de, C.C., Braga, A.F.A., Braga, F.S.S., Potério, G.B., Fernandes, S.C.A., Oshima-Franco, Y., Rodrigues-Simioni, L., (2008) Rev. Bras. 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Contribuições da Sociologia na América Latina à imaginação sociológica: análise, crítica e compromisso social Sociology's contribution in Latin America to sociological imagination: analysis, critique, and social commitment

O artigo aborda o papel desempenhado pela Sociologia na análise dos processos de transformação das sociedades latino-americanas, no acompanhamento do processo de construção do Estado e da Nação, na problematização das questões sociais na América Latina. São analisados seis períodos na Sociologia na América Latina e no Caribe: I) a herança intelectual da Sociologia ; II) a sociologia da cátedra; III) O período da "Sociologia Científica" e a configuração da "Sociologia Crítica"; IV) a crise institucional, a consolidação da "Sociologia Crítica" e a diversificação da sociologia; V) a sociologia do autoritarismo, da democracia e da exclusão; VI) a consolidação institucional e a mundialização da sociologia da América Latina (desde o ano de 2000), podendo-se afirmar que os traços distintivos do saber sociológico no continente foram: o internacionalismo, o hibridismo, a abordagem crítica dos processos e conflitos das sociedades latino-americanas e o compromisso social do sociólogo.<br>The article focuses on the role played by Sociology in the analysis of processes of change in Latin American societies, in the process of construction of Nation and State, in the debate of social issues in Latin America and the Caribbean. Six periods in Sociology in Latin America and the Caribbean are examined: I) sociology's intellectual legacy; II) sociology as a cathedra; III) the period of "Scientific Sociology"; IV) the institutional crisis, the consolidation of "Critical Sociology", and the diversifying of sociology; V) sociology of authoritarianism, democracy and exclusion; VI) institutional consolidation and globalization of Latin American sociology (since 2000). It may be said that the distinctive features of sociological knowledge in the continent were: internationalism, hybridism, the critical approach to processes and conflicts of Latin American societies, and the sociologist social commitment

Guidelines for the use and interpretation of assays for monitoring autophagy

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Guidelines for the use and interpretation of assays for monitoring autophagy

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field