As a result, we do not observe an abrupt decease of the volume transport at a certain depth, but a gradual decrease instead (see Figures 7 and 8). The model results described above showed that the main transport of phosphorus into selleck kinase inhibitor the upper 10-m layer was from depths less than 30 m for the upwelling along both coasts, whereas for nitrogen transport it was from layers deeper than 40 m. This is explained by the difference of nutricline depths and shape: there is a remarkable increase in nitrate concentration starting from 40 m depth, whereas for phosphate

there is no such increase (Laanemets et al. 2004). Along the southern coast, where the depths are greater, nitrogen is more easily transported to the surface than off the northern coast, where the seabed is shallower and the amount of nitrogen in the offshore water

column is correspondingly lower. The total amounts of nutrients transported to the surface are larger during the upwelling along the southern coast. Laanemets et al. (2009) explained these larger amounts by the shorter distance that water particles carrying nutrients have to cover in order to reach the surface. Lips et al. (2009) showed that during the upwelling event along the southern coast, observed during the summer 2006 measuring campaign, 85% of the upwelled water was from the intermediate layer and the remaining 15% from the surface layer. The plots of the ratios of depth-accumulated amounts ATR inhibitor of nutrients transported to the upper 10-m layer in the Gulf from a depth range [75 m – given depth z] to the total amount of nutrients transported to the surface ( Figure 9) show that for the northern coast the main phosphorus transport is confined within Amobarbital the upper 40-m layer: 95% of nutrients are transported from there ( Figure 9a). During the upwelling along the southern coast 95% of

phosphorus was transported from the upper 55-m layer and 85% from the upper 40-m layer ( Figure 9c). On the other hand, the behaviour of nitrogen was different: 95% of the nitrogen found in the upper 10-m layer by day 6 came from depths shallower than 55 m off the northern ( Figure 9b) and 65 m off the southern coast ( Figure 9d). 40% of the surface layer nitrogen was from depths shallower than 33 m and 45 m for the northern and the southern coasts respectively. Simulations showed that off the southern coast the upwelled water was transported to the surface mostly from the intermediate layer, as suggested by Lips et al. (2009), whereas off the northern coast transport from the shallower layers has a larger impact. The intensity of nutrient transport from the middle layers was greater during the upwelling along the southern coast for the same wind forcing magnitude, because the water from the depths of 35–45 m reached the surface layer more quickly, at least in the course of one day (Figure 7, cf.

However, ERK 1/2 phosphorylation was shown to be involved in apoptotic morphological changes induced by heat stress at jejunal level ( Yu

et al., 2010). Similarly, a recent paper has indicated a correlation between decreased intestinal barrier function, decreased expression of tight junction proteins and the intestinal activation of MAPK ( Hu et al., 2012). So, the present results taken together with previous works allow to hypothesize that intestinal morphological alterations, such apical lyses of enterocytes and villi atrophy, were associated with changes in the tight junctions of the epithelium and the apoptosis induced by MAPK activation after exposure to DON. In conclusion, we demonstrated that, Selleckchem Alpelisib in in vivo and ex vivo models, the histological changes induced by DON are similar as well as the response observed for the expression of MAPK in both models. This strongly suggests that intestinal toxicity of DON involve MAPK activation. In addition, using histological and protein expression analysis, we confirmed that the explant model is a good alternative for the studies focused on gastrointestinal toxicity following exposure to low doses of toxins. This work was financially supported by the CAPES/COFECUB (593/08) international cooperation program, CNPq grant (474583/2010-4) and the French ANR Project DON & Co. “
“The Phoneutria nigriventer spider, popularly known as the wandering armed spider or banana spider accounts

for most notified cases of accidents in Brazil. The Selleck Gemcitabine majority of accidents only cause local edema and pain; less than 1% is considered severe ( Bucaretchi et al., 2000). Patients severely envenomed Fossariinae show tachycardia, hypertension, priapism, agitation, blurred vision, convulsion, and in some cases pulmonary edema and death. P. nigriventer venom (PNV) contains a notable amount of biologically active peptides, most of which are Na+, K+ and Ca2+ channel-acting neuropeptides which affect neurotransmitter release ( Fontana and Vital Brazil, 1985; Love and Cruz-Höfling, 1986; Gomez et al., 2002). In rats, the

venom induces excitatory effects such as intense salivation, lachrymation, piloerection, priapism, tonic convulsion and spastic and flaccid paralysis of the hindlimbs ( Diniz, 1963; Schenberg and Pereira Lima, 1971; Le Sueur et al., 2003; Rapôso et al., 2007; Mendonça et al., 2012). Transmission electron microscopy has shown that the venom can cause BBBb, evidenced by extravasation of extracellular tracer from brain microvessels and the presence of perivascular edema and edematous electron lucent endfeet of the perivascular astrocyte population ( Le Sueur et al., 2003, 2004; Rapôso et al., 2007). Swelling of astrocytic endfeet that follows BBB impairment may result from osmotic imbalance and accumulation of fluid into the brain provoking edema. The regulation of water permeability across the BBB is fundamental to maintain brain homeostasis.