The role of soil in vegetated gravelly river braid plains: more than just a passive response?

This paper reviews the role of alluvial soils in vegetated gravelly river braid plains. When considering decadal time scales of river evolution, we argue that it becomes vital to consider soil development as an emergent property of the developing ecosystem. Soil processes have been relatively overlooked in accounts of the interactions between braided river processes and vegetation, although soils have been observed on vegetated fluvial landforms. We hypothesise that soil development plays a major role in the transition (speed and pathway) from a fresh sediment deposit to a vegetated soil-covered landform. Disturbance (erosion and/or deposition), vertical sediment structure (process history), vegetation succession, biological activity and water table fluctuation are seen as the main controls on early alluvial soil evolution. Erosion and deposition processes may not only act as soil disturbing agents, but also as suppliers of ecosystem resources, because of their role in delivering and changing access (e.g. through avulsion) to fluxes of water, fine sediments and organic matter. In turn, the associated initial ecosystem may influence further fluvial landform development, such as through the trapping of fine-grained sediments (e.g. sand) by the engineering action of vegetation and the deposit stabilisation by the developing above and belowground biomass. This may create a strong feedback between geomorphological processes, vegetation succession and soil evolution which we summarise in a conceptual model. We illustrate this model by an example from the Allondon River (CH) and identify the research questions that follow.

ATP release due to Thy-1-integrin binding induces P2X7-mediated calcium entry required for focal adhesion formation.

Thy-1, an abundant mammalian glycoprotein, interacts with αvβ3 integrin and syndecan-4 in astrocytes and thus triggers signaling events that involve RhoA and its effector p160ROCK, thereby increasing astrocyte adhesion to the extracellular matrix. The signaling cascade includes calcium-dependent activation of protein kinase Cα upstream of Rho; however, what causes the intracellular calcium transients required to promote adhesion remains unclear. Purinergic P2X7 receptors are important for astrocyte function and form large non-selective cation pores upon binding to their ligand, ATP. Thus, we evaluated whether the intracellular calcium required for Thy-1-induced cell adhesion stems from influx mediated by ATP-activated P2X7 receptors. Results show that adhesion induced by the fusion protein Thy-1-Fc was preceded by both ATP release and sustained intracellular calcium elevation. Elimination of extracellular ATP with Apyrase, chelation of extracellular calcium with EGTA, or inhibition of P2X7 with oxidized ATP, all individually blocked intracellular calcium increase and Thy-1-stimulated adhesion. Moreover, Thy-1 mutated in the integrin-binding site did not trigger ATP release, and silencing of P2X7 with specific siRNA blocked Thy-1-induced adhesion. This study is the first to demonstrate a functional link between αvβ3 integrin and P2X7 receptors, and to reveal an important, hitherto unanticipated, role for P2X7 in calcium-dependent signaling required for Thy-1-stimulated astrocyte adhesion.

Regulation of catecholamine release and tyrosine hydroxylase in human adrenal chromaffin cells by interleukin-1beta: role of neuropeptide Y and nitric oxide.

Adrenal chromaffin cells synthesize and secrete catecholamines and neuropeptides that may regulate hormonal and paracrine signaling in stress and also during inflammation. The aim of our work was to study the role of the cytokine interleukin-1beta (IL-1beta) on catecholamine release and synthesis from primary cell cultures of human adrenal chromaffin cells. The effect of IL-1beta on neuropeptide Y (NPY) release and the intracellular pathways involved in catecholamine release evoked by IL-1beta and NPY were also investigated. We observed that IL-1beta increases the release of NPY, norepinephrine (NE), and epinephrine (EP) from human chromaffin cells. Moreover, the immunoneutralization of released NPY inhibits catecholamine release evoked by IL-1beta. Moreover, IL-1beta regulates catecholamine synthesis as the inhibition of tyrosine hydroxylase decreases IL-1beta-evoked catecholamine release and the cytokine induces tyrosine hydroxylase Ser40 phosphorylation. Moreover, IL-1beta induces catecholamine release by a mitogen-activated protein kinase (MAPK)-dependent mechanism, and by nitric oxide synthase activation. Furthermore, MAPK, protein kinase C (PKC), protein kinase A (PKA), and nitric oxide (NO) production are involved in catecholamine release evoked by NPY. Using human chromaffin cells, our data suggest that IL-1beta, NPY, and nitric oxide (NO) may contribute to a regulatory loop between the immune and the adrenal systems, and this is relevant in pathological conditions such as infection, trauma, stress, or in hypertension.

Molecular determinants of vesicular storage and release of the gliotransmitter D-serine from cortical astrocytes

Neuron-astrocyte reciprocal communication at synapses has emerged as a novel signalling pathway in brain function. Astrocytes sense the level of synaptic activity and, in turn, influence its efficacy through the regulated release of 'gliotransmitters' such as glutamate, ATP or D-serine. A calcium-dependent exocytosis is proposed to drive the release of gliotransmitters but its existence is still debated. Over the last years, we have been studying the molecular determinants governing D-serine release from glia using different approaches. Using a novel bioassay for D-serine, we have been able to show that D-serine release occurs mainly through a calcium- and SNARE proteindependent mechanism just supporting the idea that this amino acid is released by exocytosis from glia. We next have pursued our exploration by confocal imaging and tracking of the exocytotic routes for Dserine- mediated gliotransmission and have shown that D-serine releasable pools are confined to synaptobrevin2/cellubrevin-bearing vesicles. To shed light onto the mechanisms controlling the storage and the release of gliotransmitters and namely D-serine, we have developed a new method for the immunoisolation of synaptobrevin 2- positive vesicles from rat cortical astrocytes in culture while preserving their content in gliotransmitters. The purified organelles are clear round shape vesicles of excellent purity with homogeneous size (40 nm) as judged by electron microscopy. Immunoblotting analysis revealed that isolated vesicles contain most of the major proteins already described for neuron-derived vesicles like synaptic vesicle protein 2 (SV2) and the proton pump H?-ATPase. In addition, we have analyzed the content for various amino acids of these vesicles by means of chiral capillary electrophoresis coupled to laser-induced fluorescence detection. The purified vesicles contain large amount of D-serine. We also detect peaks corresponding to unidentified compounds that may correspond to others amino acids. Postembedding immunogold labelling of the rat neocortex further revealed the expression of D-serine in astrocytes processes contacting excitatory synapses. Finally, we have examined the uptake properties for Dserine and glutamate inside the isolated glial vesicles. Our results provide significant support for the existence of an uptake system for D-serine in secretory glial vesicles and for the storage of chemical substances like D-serine and glutamate. 11th International Congress on Amino Acids, Peptides and Proteins 763 123

Low density polyethylene (LDPE) passive samplers for the investigation of polychlorinated biphenyl (PCB) point sources in rivers

This study aims to provide a passive sampling approach which can be routinely used to investigate polychlorinated biphenyl (PCB) sources in rivers. The approach consists of deploying low density polyethylene (LDPE) strips downstream and upstream of potential PCB sources as well as in their water discharges. Concentrations of indicator PCBs (iPCBs) absorbed in samplers (Cs) from upstream and downstream sites are compared with each other to reveal increases of PCB levels. Cs measured in water discharges are used to determine if released amounts of PCBs are compatible with increases revealed in the river. As water velocity can greatly vary along a river stretch and influences the uptake at each site in a different way, differences in velocity have to be taken into account to correctly interpret Cs. LDPE strips were exposed to velocities between 1.6 and 37 cm s−1 using a channel system built in the field. Relationships between velocity and Cs were established for each iPCB to determine the expected change in Cs due to velocity variations. For PCBs 28 and 52, this change does not exceed a factor 2 for velocity variations in the range from 1.6 to 100 cm s−1 (extrapolated data above 37 cm s−1). For PCBs 101, 138, 153 and 180, this change only exceeds a factor 2 in the case of large velocity variations. The approach was applied in the Swiss river Venoge to first conduct a primary investigation of potential PCB sources and then conduct thorough investigations of two suspected sources.

Calcium-sensing receptors modulate renin release in vivo and in vitro in the rat.

OBJECTIVES: Calcium-sensing receptors (CaSRs) have been localized in the juxtaglomerular apparatus where they may contribute to the regulation of renin release. In the present study, we investigated the in-vitro and in-vivo effects of the calcimimetic R-568 on renin release. METHODS: In vitro, the effect of calcimimetics on renin release was assessed by incubating freshly isolated rat juxtaglomerular cells with or without R-568 (1 and 10 mumol/l) in serum-free medium in the presence or absence of forskolin or CaCl2. In vivo, we measured the impact of R-568 (20 ng/min intravenously) on the acute changes in plasma renin activity (PRA) induced by either a 90 min infusion of the angiotensin-converting enzyme inhibitor captopril, or the beta-receptor agonist isoproterenol, or of a vehicle in or after a furosemide challenge in conscious Wistar rats. RESULTS: In vitro, R-568 dose-dependently blunted renin release, but also reduced the increase in renin due to forskolin (P < 0.01). Both isoproterenol and enalapril increased in vivo PRA to 3.1 +/- 0.3 and 3.7 +/- 0.5 ng Ang I/ml per h, respectively (P < 0.01), compared with vehicle (1.5 +/- 0.2 ng Ang I/ml per h). R-568 significantly reduced PRA to 2.1 +/- 0.1 ng/ml per h in isoproterenol-treated rats and to 1.6 +/- 0.2 ng/ml per h in enalapril-treated rats (P < 0.05). In low-salt treated animals, acute infusion of furosemide increased PRA from 8.7 +/- 3.2 to 18.6 +/- 2.3, whereas R-568 partially blunted this rise to 11.2 +/- 1.5 (P = 0.02). In vivo, R-568 significantly lowered serum calcium and PTH1-84, but the drug-induced changes in PRA were independent of the changes in calcium and parathyroid hormone. CONCLUSION: After the recent discovery of CaSRs in juxtaglomerular cells of mice, our results confirm the presence of such receptors in rats and demonstrate that these receptors modulate renin release both in vitro and in vivo. This suggests that CaSRs play a role as a regulatory pathway of renin release.

Passive knee-extension test to measure hamstring tightness: influence of gravity correction

CONTEXT: A passive knee-extension test has been shown to be a reliable method of assessing hamstring tightness, but this method does not take into account the potential effect of gravity on the tested leg. OBJECTIVE: To compare an original passive knee-extension test with 2 adapted methods including gravity's effect on the lower leg. DESIGN: Repeated measures. SETTING: Laboratory. PARTICIPANTS: 20 young track and field athletes (16.6 ± 1.6 y, 177.6 ± 9.2 cm, 75.9 ± 24.8 kg). INTERVENTION: Each subject was tested in a randomized order with 3 different methods: In the original one (M1), passive knee angle was measured with a standard force of 68.7 N (7 kg) applied proximal to the lateral malleolus. The second (M2) and third (M3) methods took into account the relative lower-leg weight (measured respectively by handheld dynamometer and anthropometrical table) to individualize the force applied to assess passive knee angle. MAIN OUTCOME MEASURES: Passive knee angles measured with video-analysis software. RESULTS: No difference in mean individualized applied force was found between M2 and M3, so the authors assessed passive knee angle only with M2. The mean knee angle was different between M1 and M2 (68.8 ± 12.4 vs 73.1 ± 10.6, P < .001). Knee angles in M1 and M2 were correlated (r = .93, P < .001). CONCLUSIONS: Differences in knee angle were found between the original passive knee-extension test and a method with gravity correction. M2 is an improved version of the original method (M1) since it minimizes the effect of gravity. Therefore, we recommend using it rather than M1.

Role of Na+-K+-ATPase in insulin-induced lactate release by skeletal muscle.

Hyperinsulinemia increases lactate release by various organs and tissues. Whereas it has been shown that aerobic glycolysis is linked to Na+-K+-ATPase activity, we hypothesized that stimulation by insulin of skeletal muscle Na+-K+-ATPase is responsible for increased muscle lactate production. To test this hypothesis, we assessed muscle lactate release in healthy volunteers from the [13C]lactate concentration in the effluent dialysates of microdialysis probes inserted into the tibialis anterior muscles on both sides and infused with solutions containing 5 mmol/l [U-13C]glucose. On one side, the microdialysis probe was intermittently infused with the same solution additioned with 2.10(-5) M ouabain. In the basal state, [13C]lactate concentration in the dialysate was not affected by ouabain. During a euglycemic-hyperinsulinemic clamp, [13C]lactate concentration increased by 135% in the dialysate without ouabain, and this stimulation was nearly entirely reversed by ouabain (56% inhibition compared with values in the dialysate collected from the contralateral probe). These data indicate that insulin stimulates muscle lactate release by activating Na+-K+-ATPase in healthy humans.

Diurnal variation in the release of alpha-MSH from rat hypothalamus and pituitary

Release of alpha-MSH from rat hypothalamic slices was characterized with respect to ionic requirements and possible diurnal variations using a sensitive radioimmunoassay. Addition of 47 mM KCl to the superfusion medium resulted in a twofold increase in alpha-MSH functions as a neurotransmitter or neuromodulator in the hypothalamus. Both spontaneous and potassium-induced alpha-MSH release compared to spontaneous release. Removal of calcium from the superfusion medium abolished the potassium-evoked release of alpha-MSH. This supports the concept that alpha-MSH release were related to diurnal variation. Marked release from the slices was observed at 10.10 h, corresponding to a peak in the alpha-MSH concentration in the hypothalamus [18] and to a lower levels of alpha-MSH in the blood. Contrarily, no significant release from the hypothalamus was obtained at 17.00 h when hypothalamic alpha-MSH content was low, but blood levels exhibited a peak. These findings suggest that there are differences in the regulation of the alpha-MSH from the pituitary and that in the hypothalamus.

Influence of the timing of low-dose aspirin on tolerability of prolonged-release nicotinic acid in patients at elevated cardiovascular risk

OBJECTIVES: To investigate the effect of low-dose aspirin administered in the morning or evening on the rate of discontinuation of prolonged-release nicotinic acid (Niaspan) due to flushing in patients at elevated cardiovascular risk. RESEARCH DESIGN AND METHODS: This was an observational, non-interventional study in patients at elevated cardiovascular risk due to cardiovascular disease or type 2 diabetes. Patients received prolonged-release nicotinic acid and aspirin under the usual care of their physician for 15 weeks. MAIN OUTCOME MEASURES: The main outcome measure was the rate of treatment discontinuation for flushing. Other adverse drug reactions (ADRs) were also recorded. Lipid parameters were also measured. RESULTS: The patient population included 539 subjects (70% male); 36% had type 2 diabetes, 80% had prior cardiovascular disease, and 37% had a family history of cardiovascular disease. The rate of treatment discontinuation due to flushing did not differ (p = 0.3375) between the morning aspirin group (10.6%) and the evening aspirin group (13.8%). The overall incidence of flushing was 57%. Most flushes were of mild or moderate severity and decreases occurred over time in both frequency and intensity. ADRs unrelated to flushing occurred in 6.6% of the morning aspirin group and 7.4% of the evening aspirin group. HDL-cholesterol increased by +21.3% in the overall population, together with moderate improvements in other lipid parameters. CONCLUSIONS: Flushing was the most common ADR with prolonged-release nicotinic acid treatment, as expected. The timing of aspirin administration did not influence the rate of treatment discontinuations for flushing. Marked increases in HDL-cholesterol were observed.

Peroxynitrite enhances the myocardial expression of HMGB1 during MIR and triggers the HMGB1 release in cardiomyocytes and in non cardiomyocytes

Temps de parole: 30 minutes

A mutation in the gene encoding the vaccinia virus 37,000-M(r) protein confers resistance to an inhibitor of virus envelopment and release.

Plaque formation in vaccinia virus is inhibited by the compound N1-isonicotinoyl-N2-3-methyl-4-chlorobenzoylhydrazine (IMCBH). We have isolated a mutant virus that forms wild-type plaques in the presence of the drug. Comparison of wild-type and mutant virus showed that both viruses produced similar amounts of infectious intracellular naked virus in the presence of the drug. In contrast to the mutant, no extracellular enveloped virus was obtained from IMCBH-treated cells infected with wild-type virus. Marker rescue experiments were used to map the mutation conferring IMCBH resistance to the mutant virus. The map position coincided with that of the gene encoding the viral envelope antigen of M(r) 37,000. Sequence analysis of both wild-type and mutant genes showed a single nucleotide change (G to T) in the mutant gene. In the deduced amino acid sequence, the mutation changes the codon for an acidic Asp residue in the wild-type gene to one for a polar noncharged Tyr residue in the mutant.