Abstract. Water stress is a defining characteristic of Mediterranean ecosystems, and is likely to become more severe in the coming decades. Simulation models are key tools for making predictions, but our current understanding of how soil moisture controls ecosystem functioning is not sufficient to adequately constrain parameterisations.Canopy-scale flux data from four forest ecosystems with Mediterranean-type climates were used in order to analyse the physiological controls on carbon and water flues through the year. Significant non-stomatal limitations on photosynthesis were detected, along with lesser changes in the conductance-assimilation relationship. New model parameterisations were derived and implemented in two contrasting modelling approaches.The effectiveness of two models, one a dynamic global vegetation model ("ORCHIDEE"), and the other a forest growth model particularly developed for Mediterranean simulations ("GOTILWA+"), was assessed and modelled canopy responses to seasonal changes in soil moisture were analysed in comparison with in situ flux measurements.In contrast to commonly held assumptions, we find that changing the ratio of conductance to assimilation under natural, seasonally-developing, soil moisture stress is not sufficient to reproduce forest canopy CO 2 and water fluxes. However, accurate predictions of both CO 2 and water fluxes under all soil moisture levels encountered in the field are obtained if photosynthetic capacity is assumed to vary with soil moisCorrespondence to: T. Keenan (t.keenan@creaf.uab.es) ture. This new parameterisation has important consequences for simulated responses of carbon and water fluxes to seasonal soil moisture stress, and should greatly improve our ability to anticipate future impacts of climate changes on the functioning of ecosystems in Mediterranean-type climates.

The histopathological hallmarks of Alzheimer disease are the self-aggregation of the amyloid ␤ peptide (A␤) in extracellular amyloid fibrils and the formation of intraneuronal Tau filaments, but a convincing mechanism connecting both processes has yet to be provided. Here we show that the endogenous polysaccharide chondroitin sulfate B (CSB) promotes the formation of fibrillar structures of the 42-residue fragment, A␤ 1-42 . Atomic force microscopy visualization, thioflavin T fluorescence, CD measurements, and cell viability assays indicate that CSB-induced fibrils are highly stable entities with abundant ␤-sheet structure that have little toxicity for neuroblastoma cells. We propose a wedged cylinder model for A␤ 1-42 fibrils that is consistent with the majority of available data, it is an energetically favorable assembly that minimizes the exposure of hydrophobic areas, and it explains why fibrils do not grow in thickness. Fluorescence measurements of the effect of different A␤ 1-42 species on Ca 2؉ homeostasis show that weakly structured nodular fibrils, but not CSB-induced smooth fibrils, trigger a rise in cytosolic Ca 2؉ that depends on the presence of both extracellular and intracellular stocks. In vitro assays indicate that such transient, local Ca 2؉ increases can have a direct effect in promoting the formation of Tau filaments similar to those isolated from Alzheimer disease brains. Pathogenesis in Alzheimer disease (AD)3 is linked to the accumulation of the highly amyloidogenic self-associating amyloid ␤ peptide (A␤). The amyloid cascade hypothesis postulates that AD pathology is initiated by an extracellular accumulation of A␤ that in turn triggers a transmembrane signal having as ultimate effect the formation of neurofibrillary tangles by the microtubule-associated protein Tau (1-3), followed by collapse of the microtubular cytoskeleton. Some of the mechanisms that have been proposed to explain how extracellular A␤ exerts its cytotoxic effects include the promotion of oxidative stress (4

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Abstract. Water stress is a defining characteristic of Mediterranean ecosystems, and is likely to become more severe in the coming decades. However, our current understanding of how soil moisture controls ecosystem functioning is not sufficient to adequately constrain model parameterisations. Canopy-scale flux data from four forest ecosystems with Mediterranean-type climates were analysed in order to determine the physiological controls on carbon and water flues through the year. Stomatal and non-stomatal limitations on photosynthesis were separated, and new parameterisations were derived and implemented in two independent modelling approaches. The effectiveness of the two approaches to ecosystem process-based modelling, one a dynamic global vegetation model (ORCHIDEE), and the other a forest growth model (GOTILWA+), was assessed and modelled canopy responses to seasonal changes in soil moisture were analysed with respect to in situ flux measurements. In contrast to commonly held assumptions, we find that stomatal control does not dominate photosynthesis under natural seasonally-developing soil moisture stress. However, applying a soil moisture dependency to photosynthetic capacity results in accurate prediction of both carbon and water fluxes under all soil moisture levels encountered in the field. The new parameterisation has important consequences for simulated responses of carbon and water fluxes to seasonal soil moisture stress, and will greatly improve our ability to anticipate future impacts of climate changes on the functioning of Mediterranean ecosystems.

Chylomicron and very low density lipoprotein (VLDL)1 remnants can be taken up via the endocytic ␣ 2 -macroglobulin receptor/LDL receptor-related protein (␣ 2 MR/LRP) either mediated by apolipoprotein E, or by lipoprotein lipase (LpL) or hepatic lipase associated with the lipoproteins (1-4). Recent results provide evidence that the uptake via ␣ 2 MR/LRP occurs in vivo, since remnant lipoproteins accumulate in mice that express reduced amounts of ␣ 2 MR/LRP and also lack functional LDL receptors (5). It has been suggested that the LpL-mediated pathway may be particularly important in the vascular wall, since ␣ 2 MR/LRP is abundant in macrophages and smooth muscle cells of atherosclerotic lesions and since LpL is secreted by macrophages in the lesions (6). In addition, it was recently shown that, whereas normal macrophages incubated with VLDL accumulate massive amounts of lipids, this does not occur in LpL-deficient macrophages (7). LpL binds to cell surface heparan sulfate proteoglycans (HSPG) as reflected in its strong affinity for binding to heparin. This property is physiologically important for the docking on endothelial cells exposing the lipase to circulating lipoproteins. LpL also binds to HSPG of other cell types as recently shown directly by immunofluorescence studies (8), and studies in Chinese hamster ovary cells have shown that uptake and degradation of LpL can be mediated by HSPG (9). In addition, the docking of LpL on HSPG of cells rich in ␣ 2 MR/LRP is important for uptake of LpL and for LpL-mediated uptake of lipoproteins via this receptor (4, 10, 11).LpL is a member of the mammalian lipase family also comprising the homologous hepatic and pancreatic lipases. The crystallographic structure of pancreatic lipase (12) shows that it consists of two folding domains, a larger N-terminal and a smaller C-terminal domain. Based upon the similarities in sequence it is thought that the domain organization is similar for LpL, and a three-dimensional model was recently proposed (13). LpL circulates both as a 96-kDa homodimer, which is the normally secreted and catalytically active form, and as a catalytically inactive monomer (14 -16). Although not known, it is likely that the LpL dimer is arranged head-to-tail in a way that allows enough space for conformational changes following substrate binding (13). The dimeric structure of LpL causes an increase in the affinity for heparin, presumably because sites in both monomers can participate in binding of one heparin molecule (13), and helps efficient ␣ 2 MR/LRP-mediated lipoprotein uptake, possibly because only the dimer can bind to a lipoprotein particle and to the receptor at the same time (10,17).The N-terminal folding domain of human LpL, comprising