450 resultados para Tryptophan


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

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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

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

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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tabula tabular tachyauxesis tachyblastic tachygen tachygenesis tachytelic tactic tactile tactoreceptors taenia taeniate taenidium taenioglossate tagma tagmata tagmosis tail tailfan Takakura's talon talus tandem tangent tangoreceptor tanylobous tapetal tapetum tapinoma-odor Tardigrada tardigrades tarsal tarsation tarsite tarsomere tarsungulus tarsus taste tautonomy tautonym taxa taxes taxis taxis taxodont taxometrics taxon taxonomic taxonomist taxonomy tectiform tectostracum tectum teeth teges tegillum tegmen tegmentum tegula tegular tegulum tegumen tegument tegumentary tela telaform telamon telegonic teleiochrysalis telenchium teleoconch teleodont teleology teleotrocha telepod telescope telescopic teletrophic telioderma teliophan telmophage telocentric telodendria telofemur telogonic telolecithal telomitic telophase telophragma telopod telopodite telorhabdions telosonic telostome telosynapsis telosyndesis telotarsus telotaxis telotroch telson template temporal tenacipeds tenaculum tenent teneral tensor tentacle tentacular tentaculocyst tentaculozooid tentilla tentorial tentorium tenuous teratocyte teratogen teratogenesis teratogyne teratology terebella terebra terebrant terebrate teres terete terga tergal tergite tergolateral tergopleural tergopore tergum tergum termen terminal terminalia termitarium termitophile terranes terrestrial terricolous territory tertiary tertibrach tertibrachial tessellate test testaceology testaceous test-cross testes testis testisac testudinate tetanus tetany tetractinal tetractine tetrad tetradelphic tetramerous tetramorphic tetraploid tetrapod tetrapterous tetrasomic tetrathyridial tetrathyridium tetraxon tetraxonid thalassophilous thallus thamnophilous thanatocoenosis thanatosis theca thecae thecal thecate thelycum thelygenesis thelygenous thelyotokous thelyotoky theory thermocline thermophile thermophobe thermoreceptor thermotaxis thickness thigmotactic thigmotaxis thigmotropism third-form thoraces thoracic thoracomere thoracopod(ite) thorax thoraxes thread thylacium thylacogen thyridial thyridium thyroid thysanuriform tibia tibial tibiotarsal tibiotarsus Tiedemann's tiled timbal tinctorial tine tissue tissue titilla titillae titillator tocopherol tocospermal tocospermia tocostome tokostome tomentose tomentum Tomosvary tone tonic tonofibrillae tonus topochemical topogamodeme topomorph topomorphic toponym topotype tori torma tormogen tornote tornus torose torpid torqueate torsion tortuose torulose torus totipotent totomount toxa toxicognath toxicology toxin toxinosis toxoglossate toxoid trabecula trabeculate trabeculated trachea tracheae tracheal tracheate tracheoblast tracheolar tracheoles trachychromatic tract Tragardh's tragus transad transcoxa transcurrent transect transection transformation transient transitional translocation translucent transmission transposed transscutal transstadial transtilla transverse trapeziform trapezium trapezoid trema tremata Trematoda trenchant trepan triact triactinal triad triaene triage triangle triangular triangulate triaulic triaxial triaxon tribe tribocytic trichite trichobothrium trichobranchia trichobranchiate trichocerous trichodes trichodeum trichodragmata trichogen trichoid trichomes trichophore trichopore trichosors trichostichal trichotomous trichroism tricolumella tricomes tricostate tricrepid tricuspid tricuspidate tridactyl trident tridentate trifid trifurcate triglycerides trignathan trigonal trigoneutism trilabiate trilateral trilobate trilocular trimorphic trimorphism Trinominal triordinal tripartite tripectinate triplet triploblastic triploid triquetral triquetrous triradiate triradiates tritocerebral tritocerebrum tritocerebrum tritonymph tritosternum triturate triungulin triungulinid trivial trivium trivoltine trixenic troch trochal trochalopodous trochantellus trochanter trochanteral trochantin trochi trochiform trochlea trocholophous trochophore trochosphere trochus troglobiont troglodytic troglophile trogloxene tropeic trophal trophallactic trophallaxis trophamnion trophi trophic trophidium trophobiont trophobiont trophobiosis trophobiotic trophocytes trophodisc trophogeny trophoporic trophorhinium trophosome trophotaxis trophothylax trophozooid trophus tropis tropism tropotaxis trumpet truncate truncation trunk trypsin tryptic tryptophan tryptophane T-tubule tube tube-feet tubercle tubercula tuberculate tuberculose tuberiferous tubicolous tubifacient tubule tubulus tubus tuft Tullgren tumefaction tumescence tumid tumulus tunic tunica tunicary tunicate turbinate turgid turreted turriculate tychoparthenogenesis tylasters tylenchoid tyli tyloid tyloides tylosis tylostyle tylote tylus tymbal tympanal tympanal tympanic tympanum Tyndall type typhlosole typologist typolysis typostasis

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We examined the interaction of the cationic antimicrobial peptide (AMP) tritrpticin (VRRFPWWWPFLRR, TRP3) with Langmuir monolayers of zwitterionic (dipalmitoyl phosphatidylcholine, DPPC, and dipalmitoyl phosphatidylethanolamine, DPPE) and negatively charged phospholipids (dipalmitoyl phosphatidic acid, DPPA, and dipalmitoyl phosphatidylglycerol, DPPG). Both surface pressure and surface potential isotherms became more expanded upon addition of TRP3 (DPPE similar to DPPC << DPPA < DPPG). The stronger interaction with negatively charged phospholipids agrees with data for vesicles and planar lipid bilayers, and with AMPs greater activity against bacterial membranes versus mammalian cell membranes. Considerable expansion of negatively charged monolayers occurred at 10 and 30 mol% TRP3, especially at low surface pressure. Moreover, a difference was observed between PA and PG, demonstrating that the interaction, besides being modulated by electrostatic interactions, displays specificity with regard to headgroup, being more pronounced in the case of PG, present in large quantities in bacterial membranes. In previous studies, it was proposed that the peptide acts by a toroidal pore-like mechanism [1,2]. Considering the evidence from the literature that PG shows a propensity to form a positive curvature as do toroidal pores, the observation of TRP3's preference for the PG headgroup and the dramatic increase in area promoted by this interaction represent further support for the toroidal pore mechanism of action proposed for TRP3. (C) 2012 Elsevier B.V. All rights reserved.

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OBJETIVO: Comparar os achados histopatológicos e de apoptose em pulmões de ratos preservados em soluções low-potassium dextran (LPD, baixo potássio dextrana), histidine-tryptophan-ketoglutarate (HTK, histidina-triptofano-cetoglutarato) ou salina normal (SN) em 6 h e 12 h de isquemia pela utilização de um modelo experimental de perfusão pulmonar ex vivo. MÉTODOS: Sessenta ratos Wistar foram anestesiados, randomizados e submetidos à perfusão anterógrada pela artéria pulmonar com uma das soluções preservadoras. Após a extração, os blocos cardiopulmonares foram preservados por 6 ou 12 h a 4ºC, sendo então reperfundidos com sangue homólogo em um sistema de perfusão ex vivo durante 60 min. Ao final da reperfusão, fragmentos do lobo médio foram extraídos e processados para histopatologia, sendo avaliados os seguintes parâmetros: congestão, edema alveolar, hemorragia alveolar, hemorragia, infiltrado inflamatório e infiltrado intersticial. O grau de apoptose foi avaliado pelo método TdT-mediated dUTP nick end labeling. RESULTADOS: A histopatologia demonstrou que todos os pulmões preservados com SN apresentaram edema alveolar após 12 h de isquemia. Não houve diferenças em relação ao grau de apoptose nos grupos estudados. CONCLUSÕES: No presente estudo, os achados histopatológicos e de apoptose foram semelhantes com o uso das soluções LPD e HTK, enquanto a presença de edema foi significativamente maior com o uso de SN.

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A wealth of evidence indicates that the dorsal raphe nucleus (DR) is not a homogenous structure, but an aggregate of distinctive populations of neurons that may differ anatomically, neurochemically and functionally. Other findings suggest that serotonergic neurons within the mid-caudal and caudal part of the DR are involved in anxiety processing while those within the lateral wings (IwDR) and ventrolateral periaqueductal gray (vIPAG) are responsive to panic-evoking stimuli/situations. However, no study to date has directly compared the activity of 5-HT and non-5HT neurons within different subnuclei of the DR following the expression of anxiety- and panic-related defensive responses. In the present investigation, the number of doubly immunostained cells for Fos protein and tryptophan hydroxylase, a marker of serotonergic neurons, was assessed within the rat DR, median raphe nucleus (MRN) and PAG following inhibitory avoidance and escape performance in the elevated T-maze, behaviors associated with anxiety and panic, respectively. Inhibitory avoidance, but not escape, significantly increased the number of Fos-expressing serotonergic neurons within the mid-caudal part of the dorsal subnucleus, caudal and interfascicular subnuclei of the DR and in the MRN. Escape, on the other hand, caused a marked increase in the activity of non-5HT cells within the IwDR, vIPAG, dorsolateral and dorsomedial columns of the PAG. These results strongly corroborate the view that different subsets of neurons in the DR are activated by anxiety- and panic-relevant stimuli/situations, with important implications for the understanding of the pathophysiology of generalized anxiety and panic disorders. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.

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The association between major depressive disorder (MDD) and cardiovascular disease (CVD) is among the best described medical comorbidities. The presence of MDD increases the risk of cardiac admissions and mortality and increases healthcare costs in patients with CVD, and similarly, CVD affects the course and outcome of MDD. The potential shared biological mechanisms involved in these comorbid conditions are not well known. However, the enzyme monoamine oxidase-A (MAO-A), which has a key role in the degradation of catecholamines, has been associated with the pathophysiology and therapeutics of both MDD and CVD. Increased MAO-A activity results in the dysregulation of downstream targets of this enzyme and thus affects the pathophysiology of the two diseases. These deleterious effects include altered noradrenaline turnover, with a direct elevation in oxidative stress parameters, as well as increased platelet activity and cytokine levels. These effects were shown to be reversed by MAO inhibitors. Here, a model describing a key role for the MAO-A in comorbid MDD and CVD is proposed, with focus on the shared pathophysiological mechanisms and the potential therapeutic relevance of agents targeting this enzyme.

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Herein, we demonstrate the physical and chemical characterizations of the supramolecular complex formed between beta-cyclodextrin (beta CD) and bradykinin potentiating nonapeptide (BPP9a), an endogenous toxin found in Bothrops jararaca. Circular dichroism results indicate a conformational change in the BPP9a secondary structure upon its complexation with beta CD. Nuclear magnetic resonance results, mainly from NOESY experiments, and theoretical calculations showed a favorable interaction between the tryptophan residue of BPP9a and the beta CD cavity. Thermodynamic inclusion parameters were investigated by isothermal titration calorimetry, demonstrating that beta CD/BPP9a complex formation is an exothermic process that results in a reduction in entropy. Additionally, in vitro degradation study of BPP9a against trypsin (37 degrees C, pH 7.2) showed higher stability of peptide in presence of beta CD. This beta CD/BPP9a complex, which presents new chemical properties arising from the peptide inclusion process, may be useful as an antihypertensive drug in oral pharmaceutical formulations. (C) 2011 Elsevier B.V. All rights reserved.

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Glucokinase (GCK) catalyzes the rate-limiting step of glucose catabolism in the pancreas, where it functions as the body's principal glucose sensor. GCK dysfunction leads to several potentially fatal diseases including maturity-onset diabetes of the young type II (MODY-II) and persistent hypoglycemic hyperinsulinemia of infancy (PHHI). GCK maintains glucose homeostasis by displaying a sigmoidal kinetic response to increasing blood glucose levels. This positive cooperativity is unique because the enzyme functions exclusively as a monomer and possesses only a single glucose binding site. Despite nearly a half century of research, the mechanistic basis for GCK's homotropic allostery remains unresolved. Here we explain GCK cooperativity in terms of large-scale, glucose-mediated disorder-order transitions using 17 isotopically labeled isoleucine methyl groups and three tryptophan side chains as sensitive nuclear magnetic resonance (NMR) probes. We find that the small domain of unliganded GCK is intrinsically disordered and samples a broad conformational ensemble. We also demonstrate that small-molecule diabetes therapeutic agents and hyperinsulinemia-associated GCK mutations share a strikingly similar activation mechanism, characterized by a population shift toward a more narrow, well-ordered ensemble resembling the glucose-bound conformation. Our results support a model in which GCK generates its cooperative kinetic response at low glucose concentrations by using a millisecond disorder-order cycle of the small domain as a "time-delay loop," which is bypassed at high glucose concentrations, providing a unique mechanism to allosterically regulate the activity of human GCK under physiological conditions.