Made available in DSpace on 2016-04-28T20:17:25Z (GMT). No. of bitstreams: 1 2007-Geisi Ferreira Marine.pdf: 800208 bytes, checksum: b24185c0919f8244f06ce7f08948693e (MD5) Previous issue date: 2007-06-22 / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior / The okadaic acid phycotoxin AO is produced by a group of micro seaweed known as Dinoflagellated. The mussels when feeding themselves from this micro seaweed accumulate in their hepatopancreas, this toxin, trigging in the human being the Syndrome or Diarrhetic Shellfish Poisoning (DSP). The symptoms appear at around 30 minutes after the consumption of the contaminated clam; the symptoms vary among abdominal nauseas, pains, vomits and diarrhea. When the toxin ingestion happens in amounts lower than 48 μg.g-1, the above described symptoms do not develop, however, its continued consumption favors the appearing of tumors in the gastrointestinal tract due to the high carcinogenic power of AO. This study intended to detect and quantify the diarrheic toxin AO in Perna perna mussels collected between the months of May and December of the 2006 and verification of the potentially toxic micro seaweed presence, in the seasons Spring/Summer (from September until December of 2006). Since May until december of 2006, mussels (Perna perna) were collected and analyzed regarding to the presence of the Phycotoxin Ao .In order to collect the micro seaweed were used a plankton net (20μm of mesh) and Bomb Rule 2000. The identification of the dinoflagellates ones was carried through in inverted biological microscope. The detection of AO in the mussels was carried through by High Efficiency of Liquid Chromatography with Fluorimetric Detection (HPLC-FC). The chromatographic results had indicated the presence of AO toxin in all the gotten mussel samples from May until October of 2006 in low concentrations. In the analyses of phytoplankton, the diatoms were the most representative group compared with the Dinoflagellated. The species Prorocentrum micans and P. gracile examined were not pointed as toxin producers until the moment. Among the Dino-flagellated potentially toxic were found the species : Dinophysis acuminata, D. tripos, D. rotundata and D. fortii. The results indicate the necessity of elaboration and effective application of a hygienic-sanitary controlling program of the clams as well as monitoring the environment, aiming above everything the public health Safety. / A ficotoxina ?cido ocadaico (AO) ? produzida por um grupo de microalgas conhecidas como dinoflagelados. Os mexilh?es ao se alimentarem destas microalgas acumulam em seu hepatop?ncreas, esta toxina, desencadeando no ser humano a S?ndrome ou Envenenamento Diarr?ico por Moluscos - EDM. Os sintomas se apresentam em torno de 30 minutos ap?s o consumo do molusco contaminado; variando entre n?useas, dores abdominais, v?mitos e diarr?ia. Quando a ingest?o da toxina acontece em quantidades inferiores a 48 μg.g-1, os sintomas acima descritos n?o se desenvolvem, por?m, seu consumo continuado favorece o surgimento de tumores no trato gastrointestinal devido ao poder carcinog?nico do AO. Este estudo pretendeu detectar e quantificar a toxina diarr?ica AO em mexilh?es Perna perna coletados entre os meses de maio e dezembro de 2006, e a verifica??o da presen?a de microalgas potencialmente t?xicas, nas esta??es primavera/ver?o (setembro a dezembro de 2006). De maio a dezembro de 2006, mexilh?es (Perna perna) foram coletados e analisados quanto ? presen?a da ficotoxina AO. As microalgas foram coletadas entre setembro e dezembro de 2006, com aux?lio de uma rede de pl?ncton (de 20μm de malha) e Bomba Rule 2000. A identifica??o dos dinoflagelados foi realizada em microsc?pio biol?gico invertido. A detec??o do AO nos mexilh?es foi realizada por Cromatografia L?quida de Alta Efici?ncia com Detec??o Fluorim?trica (CLAE-DF). Os resultados cromatogr?ficos indicaram a presen?a da toxina AO em todas as amostras obtidas de mexilh?es, de maio a outubro de 2006, em baixas concentra??es. Nas an?lises do fitopl?ncton, as diatom?ceas foram o grupo mais representativo comparado aos dinoflagelados. As esp?cies Prorocentrum micans e P. gracile observadas n?o foram apontadas como produtoras de toxinas at? o momento. Dentre os dinoflagelados potencialmente t?xicos foram encontradas as esp?cies: Dinophysis acuminata, D. tripos, D. rotundata e D. fortii. Os resultados indicam a necessidade da elabora??o e aplica??o efetiva de um programa de controle higi?nico-sanit?rio dos moluscos assim como monitoramento do ambiente, objetivando acima de tudo a seguran?a ? sa?de p?blica.

Hyperphosphorylated tau plays an important role in the formation of neurofibrillary tangles in brains of patients with Alzheimer's disease (AD) and related tauopathies and is a crucial factor in the pathogenesis of these disorders. Though diverse kinases have been implicated in tau phosphorylation, protein phosphatase 2A (PP2A) seems to be the major tau phosphatase. Using murine primary neurons from wild-type and human tau transgenic mice, we show that the antidiabetic drug metformin induces PP2A activity and reduces tau phosphorylation at PP2A-dependent epitopes in vitro and in vivo. This tau dephosphorylating potency can be blocked entirely by the PP2A inhibitors okadaic acid and fostriecin, confirming that PP2A is an important mediator of the observed effects. Surprisingly, metformin effects on PP2A activity and tau phosphorylation seem to be independent of AMPK activation, because in our experiments (i) metformin induces PP2A activity before and at lower levels than AMPK activity and (ii) the AMPK activator AICAR does not influence the phosphorylation of tau at the sites analyzed. Affinity chromatography and immunoprecipitation experiments together with PP2A activity assays indicate that metformin interferes with the association of the catalytic subunit of PP2A (PP2Ac) to the so-called MID1-alpha4 protein complex, which regulates the degradation of PP2Ac and thereby influences PP2A activity. In summary, our data suggest a potential beneficial role of biguanides such as metformin in the prophylaxis and/or therapy of AD.