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Entre março e julho/22, duas tecnologias complementares, EM® e Pulmão™, foram testadas para estudar a biorremediação na camada de lama da Lagoa de Piratininga, Niterói, RJ. Dados ortométricos, matéria orgânica, carbono orgânico, nitrogênio Kjeldahl total, fósforo e biopolímeros foram quantificados na superfície do sedimento. As concentrações crescentes de nitrogênio Kjeldahl indicaram aportes de esgoto doméstico ao sistema. O fósforo orgânico predominou sobre o total, pois foi consumido no processo de biorremediação. Ocorreram mudanças quali- quantitativas na composição da matéria orgânica lábil, com consumo de lipídio, molécula recalcitrante, e produção de proteínas e carboidratos. Os dados altimétricos indicaram maior tendência de consumo da lama na área que reuniu as tecnologias EM1®+Pulmão™, onde o aporte sedimentar foi praticamente anulado. Houve uma diminuição da espessura da lama, refletindo no aumento sutil de profundidade superficial da camada sedimentar. Estas modificações nas áreas experimentais indicam que o processo de restauração ambiental está ocorrendo.

Made available in DSpace on 2020-12-10T19:53:38Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-03-16 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Previous studies suggested the pharmacological potential of rat hemopressin (PVNFKFLSH) and its shorter synthetic peptide NFKF, to protect from pilocarpine-induced seizures in mice. Orally administered NFKF was shown to be hundred times more potent than cannabidiol in delaying the first seizure induced by pilocarpine in mice. Here, using an experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis we have shown that C57BL/6 J mice orally administrated with NFKF (500 mu g/kg) presented better EAE clinical scores and improved locomotor activity compared to saline administrated control mice. NFKF blocked the production of IL-1beta and IL-6, and has high scores binding cannabinoid type 2 receptors. Therefore, NFKF is an exciting new possibility to neurodegenerative diseases therapeutics. Proteimax Biotechnol, BR-05581001 Sao Paulo, Brazil Butantan Inst, Special Lab Pain & Signaling, BR-05503900 Sao Paulo, Brazil Univ Sao Paulo, Biomed Sci Inst, Dept Pharmacol, BR-05508900 Sao Paulo, Brazil Sao Paulo State Univ, Biosci Inst, BR-11330900 Sao Vicente, Brazil Remer Consultores Ltda, BR-01411001 Sao Paulo, SP, Brazil Sao Paulo State Univ, Biosci Inst, BR-11330900 Sao Vicente, Brazil FAPESP: 2016/04000-3 CNPq: 445363/2014-2 CNPq: 400944/2014-6

Intracellular peptides are produced by proteasomes following degradation of nuclear, cytosolic, and mitochondrial proteins, and can be further processed by additional peptidases generating a larger pool of peptides within cells. Thousands of intracellular peptides have been sequenced in plants, yeast, zebrafish, rodents, and in human cells and tissues. Relative levels of intracellular peptides undergo changes in human diseases and also when cells are stimulated, corroborating their biological function. However, only a few intracellular peptides have been pharmacologically characterized and their biological significance and mechanism of action remains elusive. Here, some historical and general aspects on intracellular peptides’ biology and pharmacology are presented. Hemopressin and Pep19 are examples of intracellular peptides pharmacologically characterized as inverse agonists to cannabinoid type 1 G-protein coupled receptors (CB1R), and hemopressin fragment NFKF is shown herein to attenuate the symptoms of pilocarpine-induced epileptic seizures. Intracellular peptides EL28 (derived from proteasome 26S protease regulatory subunit 4; Rpt2), PepH (derived from Histone H2B type 1-H), and Pep5 (derived from G1/S-specific cyclin D2) are examples of peptides that function intracellularly. Intracellular peptides are suggested as biological functional molecules, and are also promising prototypes for new drug development.