RESUMO
Deoxygenation is a major threat to the coastal ocean health as it impacts marine life and key biogeochemical cycles. Understanding its drivers is crucial in the thriving and highly exploited Peru upwelling system, where naturally low-oxygenated subsurface waters form the so-called oxygen minimum zone (OMZ), and a slight vertical shift in its upper limit may have a huge impact. Here we investigate the long-term deoxygenation trends in the upper part of the nearshore OMZ off Peru over the period 1970-2008. We use a unique set of dissolved oxygen in situ observations and several high-resolution regional dynamical-biogeochemical coupled model simulations. Both observation and model present a nearshore deoxygenation above 150 m depth, with a maximum trend of - 10 µmol kg-1 decade1, and a shoaling of the oxycline depth (- 6.4 m decade-1). Model sensitivity analysis shows that the modeled oxycline depth presents a non-significant (+ 0.9 m decade-1) trend when remote forcing is suppressed, while a significant oxycline shoaling (- 3 m decade-1) is obtained when the wind variability is suppressed. This indicates that the nearshore deoxygenation can be attributed to the slowdown of the near-equatorial eastward currents, which transport oxygen-rich waters towards the Peruvian shores. The large uncertainties in the estimation of this ventilation flux and the consequences for more recent and future deoxygenation trends are discussed.
RESUMO
Corticocortical disconnection in Alzheimer's disease occurs by the progressive impairment and eventual loss of a small subset of pyramidal neurons in layers III and V of association areas of the neocortex. These neurons exhibit large somatic size, extensive dendritic arborization and high levels of nonphosphorylated neurofilaments of medium and high molecular weight that can be identified using a monoclonal SMI-32 antibody. It is thought that the accumulation of amyloid Abeta and neurofibrillary tangles may provoke metabolic disturbances that result in the loss of these SMI-32 immunoreactive neurons. The recent detection of increased levels of caspase-3 cleaved fodrin in frontal, temporal and parietal association areas in Alzheimer's disease brains suggests that programmed cell death may contribute to the destruction of SMI-32 positive neurons. In the present study, we utilized an antibody that selectively recognizes the 120 kDa breakdown product of alphaIIspectrin (fodrin) generated by caspase-3 to determine whether this protease is activated in vulnerable pyramidal neurons located in layers III and V of Alzheimer's disease brains. Neurons immunoreactive for caspase-3 cleaved alphaIIspectrin were located predominantly in layers III and V of the inferior frontal and superior temporal cortices of patients with Alzheimer's disease but not age-matched controls. Pyramidal neurons immunoreactive for caspase-3 cleaved alphaIIspectrin invariably displayed SMI-32 immunoreactivity suggesting that caspase-3 activation is a pathological event that may be responsible for the loss of a subset of pyramidal neurons that comprise corticocortical projections.