RESUMO
The input of new nitrogen into the euphotic zone constrains the export of organic carbon to the deep ocean and thereby the biologically mediated long-term CO2 exchange between the ocean and atmosphere. In low-latitude open-ocean regions, turbulence-driven nitrate diffusion from the ocean's interior and biological fixation of atmospheric N2 are the main sources of new nitrogen for phytoplankton productivity. With measurements across the tropical and subtropical Atlantic, Pacific and Indian oceans, we show that nitrate diffusion (171±190 µmol m(-2) d(-1)) dominates over N2 fixation (9.0±9.4 µmol m(-2) d(-1)) at the time of sampling. Nitrate diffusion mediated by salt fingers is responsible for ca. 20% of the new nitrogen supply in several provinces of the Atlantic and Indian Oceans. Our results indicate that salt finger diffusion should be considered in present and future ocean nitrogen budgets, as it could supply globally 0.23-1.00 Tmol N yr(-1) to the euphotic zone.
Assuntos
Atmosfera/química , Dióxido de Carbono/metabolismo , Nitratos/metabolismo , Fixação de Nitrogênio , Nitrogênio/metabolismo , Fitoplâncton/metabolismo , Água do Mar/química , Dióxido de Carbono/química , Cianobactérias/metabolismo , Difusão , Nitratos/química , Nitrogênio/química , Oceanos e Mares , Oscillatoria/metabolismo , Salinidade , Cloreto de Sódio , TemperaturaRESUMO
Neurotransmission unavoidably increases mitochondrial reactive oxygen species. However, the intrinsic antioxidant defense of neurons is weak and hence the mechanism whereby these cells are physiologically protected against oxidative damage is unknown. Here we found that the antioxidant defense of neurons is repressed owing to the continuous protein destabilization of the master antioxidant transcriptional activator, nuclear factor-erythroid 2-related factor-2 (Nrf2). By contrast, Nrf2 is highly stable in neighbor astrocytes explaining their robust antioxidant defense and resistance against oxidative stress. We also show that subtle and persistent stimulation of N-methyl-d-aspartate receptors (NMDAR) in astrocytes, through a mechanism not requiring extracellular Ca²âº influx, upregulates a signal transduction pathway involving phospholipase C-mediated endoplasmic reticulum release of Ca²âº and protein kinase Cδ activation. Active protein kinase Cδ promotes, by phosphorylation, the stabilization of p35, a cyclin-dependent kinase-5 (Cdk5) cofactor. Active p35/Cdk5 complex in the cytosol phosphorylates Nrf2 at Thr(395), Ser(433) and Thr(439) that is sufficient to promote Nrf2 translocation to the nucleus and induce the expression of antioxidant genes. Furthermore, this Cdk5-Nrf2 transduction pathway boosts glutathione metabolism in astrocytes efficiently protecting closely spaced neurons against oxidative damage. Thus, intercellular communication through NMDAR couples neurotransmission with neuronal survival.
Assuntos
Astrócitos/metabolismo , Quinase 5 Dependente de Ciclina/metabolismo , Fator 2 Relacionado a NF-E2/metabolismo , Receptores de N-Metil-D-Aspartato/metabolismo , Animais , Astrócitos/efeitos dos fármacos , Western Blotting , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/genética , Células Cultivadas , Quinase 5 Dependente de Ciclina/genética , Citometria de Fluxo , Células HEK293 , Humanos , Peróxido de Hidrogênio/metabolismo , Imunoprecipitação , Lipídeos/farmacologia , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Fator 2 Relacionado a NF-E2/genética , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Ratos , Ratos Wistar , Receptores de N-Metil-D-Aspartato/genética , Transdução de SinaisRESUMO
Risk factors for Pseudomonas aeruginosa (PA) isolation in patients hospitalised for chronic obstructive pulmonary disease (COPD) exacerbation remain controversial. The aim of our study was to determine the incidence and risk factors for PA isolation in sputum at hospital admission in a prospective cohort of patients with acute exacerbation of COPD. We prospectively studied all patients with COPD exacerbation admitted to our hospital between June 2003 and September 2004. Suspected predictors of PA isolation were studied. Spirometry tests and 6-min walking tests were performed 1 month after the patients were discharged. High-resolution computed tomography (HRCT) was performed in a randomised manner in one out of every two patients to quantify the presence and extent of bronchiectasis. Patients were followed up during the following year for hospital re-admissions. A total of 188 patients were included, of whom 31 (16.5%) had PA in sputum at initial admission. The BODE (body mass index, airflow obstruction, dyspnoea, exercise capacity) index (OR 2.18, CI 95% 1.26-3.78; p = 0.005), admissions in the previous year (OR 1.65, CI 95% 1.13-2.43; p = 0.005), systemic steroid treatment (OR 14.7, CI 95% 2.28-94.8; p = 0.01), and previous isolation of PA (OR 23.1, CI 95% 5.7-94.3; p<0.001) were associated with PA isolation. No relationship was seen between bronchiectasis in HRCT and antibiotic use in the previous 3 months. PA in sputum at hospital admission is more frequent in patients with poorer scoring on the BODE index, previous hospital admissions, oral corticosteroids and prior isolation of PA.