How soil characteristics and water quality influence the biogeochemical response to flooding in riverine wetlands

Although phosphate concentrations have been reduced, the rivers Meuse and Rhine are still polluted with sulphate, which most probably affects vegetation development in newly created riverine wetlands. The influence of flooding with river water rich in sulphate was tested on three soil types from floodplains of the river Meuse using flow-through and batch experiments. Soils were selected for contrasting concentrations of iron and organic matter and originated from a floating fen (iron-poor, organic), an alder carr (iron-rich, organic) and a clay pit (iron-rich, low in organic matter). Flooding induced mobilisation of phosphate. Sulphate only enhanced this effect in the alder carr soil, where sulphide and phosphate competed for binding to iron. Only in the floating fen soil did the addition of sulphate result in the formation of free sulphide, which reduced the growth of Glyceria maxima, serving as a phytometer. In addition, the floating soil started to sink, due to falling methane concentrations. In the different soil types methane production was hampered by the presence of more favourable electron acceptors such as sulphate in the water and Fe(III) in the soil. It was concluded that the effects of inundation with sulphate-polluted water strongly depend on the soil type: under iron-poor circumstances, free sulphide may accumulate, leading to phytotoxicity, while in soils rich in iron, sulphide toxicity is prevented, but phosphate availability may be increased. In addition, shortage of easily degradable organic matter can limit the formation of potential toxicants such as ammonium, iron and sulphide. Results are discussed in terms of their implications for nature management.     

Hypothermia induction and recovery in free-ranging rats

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To avoid anesthesia confounders, free-ranging rats were exposed (4 h) to cool water (CW; 10 °C; 5 cm), warm water (WW; 35 °C; 5 cm) or temperate air (TA; 25 °C) to induce hypothermia, or control for water or novel environment stress, respectively.     

Model-projected mechanistic bases for sex differences in growth hormone regulation in humans

Models of physiological systems facilitate rational experimental design, inference, and prediction. A recent construct of regulated growth hormone (GH) secretion interlinks the actions of GH-releasing hormone (GHRH), somatostatin (SRIF), and GH secretagogues (GHS) with GH feedback in the rat (Farhy LS, Veldhuis JD. Am J Physiol Regul Integr Comp Physiol 288: R1649-R1663, 2005). In contrast, no comparable formalism exists to explicate GH dynamics in any other species. The present analyses explore whether a unifying model structure can represent species- and sex-defined distinctions in the human and rodent. The consensus principle that GHRH and GHS synergize in vivo but not in vitro was explicable by assuming that GHS 1) evokes GHRH release from the brain, 2) opposes inhibition by SRIF both in the hypothalamus and on the pituitary gland, and 3) stimulates pituitary GH release directly and additively with GHRH. The gender-selective principle that GH pulses are larger and more irregular in women than men was conferrable by way of 4) higher GHRH potency and 5) greater GHS efficacy. The overall construct predicts GHRH/GHS synergy in the human only in the presence of SRIF when the brain-pituitary nexus is intact, larger and more irregular GH pulses in women, and observed gender differences in feedback by GH and the single and paired actions of GHRH, GHS, and SRIF. The proposed model platform should enhance the framing and interpretation of novel clinical hypotheses and create a basis for interspecies generalization of GH-axis regulation.     

The FXIIIVal34Leu, common and risk factors of venous thrombosis in early middle-age Costa Rican patients

In this study, eight common polymorphisms associated with venous thrombosis (VT) and thrombophilia factors were analyzed in a Costa Rican case-control study. With the use of polymerase chain reaction (PCR) methods the polymorphisms were detected in 120 patients and 133 controls (mean age <40 years old). It was concluded that a high level of fibrinogen, antiphospholipid antibodies, family history, and the genotype 34LeuLeu of FXIII OR 0.42 (0.20-0.89) showed a significant effect on the risk of VT.Associations between the risk of VT and genetic polymorphisms have been established. Some of these polymorphisms are highly prevalent in Caucasians, but there is a significant geographic variation in their prevalence among different populations. The results of this study support the protective effect of FXIII Val34Leu polymorphism in VT. These findings are consistent with previous reports that included other populations.     

TGF-beta1 calcium signaling in osteoblasts

Transforming growth factor-beta1 (TGF-beta1) action is known to be initiated by its binding to multiple cell surface receptors containing serine/threonine kinase domains that act to stimulate a cascade of signaling events in a variety of cell types. We have previously shown that TGF-beta1 and BMP-2 treatment of primary human osteoblasts (HOBs) enhances cell-substrate adhesion. In this report, we demonstrate that TGF-beta1 elicits a rapid, transient, and oscillatory rise in the intracellular Ca(2+) concentration, [Ca(2+)](i), that is necessary for enhancement of cell adhesion in HOBs but does not alter the phosphorylation state of Smad proteins. This rise in [Ca(2+)](i) in HOB is not observed in the absence of extracellular calcium or when the cells are treated with the L-type Ca(2+) channel blocker, nifedipine, but is stimulated upon treatment with the L-type Ca(2+) channel agonist, Bay K 8644, or under high K(+) conditions. The rise in [Ca(2+)](i) is severely attenuated after treatment of the cells with thapsigargin, a selective endoplasmic reticulum Ca(2+) pump inhibitor. TGF-beta1 enhancement of HOB adhesion to tissue culture polystyrene is also inhibited in cells treated with nifedipine. These data suggest that intracellular Ca(2+) signaling is an important second messenger of the TGF-beta1 signal transduction pathway in osteoblast function.     

Site effects outweigh riparian influences on ground-dwelling beetles adjacent to first order streams in wet eucalypt forest

In wet eucalypt forest with a rainforest understorey the vegetation adjacent to first order streams does not form a distinct riparian strip. This study investigated the riparian response of terrestrial ground-dwelling beetles adjacent to four such streams in Tasmania, Australia. Beetle assemblages varied more between the four sites than they did with distance from stream within sites, where they exhibited a measurable but subtle riparian response. The extent of the riparian zone varied between the four study sites, with a 1–5 m riparian zone at three sites and a gradually changing community up to 50–100 m upslope at one site. There was a trend for greater between plot variability immediately adjacent to the streams, possibly because this is a more highly disturbed environment. None of the habitat variables measured were consistently associated with riparian or upslope assemblages of beetles, probably explaining the subtlety of the beetles’ riparian response. Forest conservation efforts for terrestrial species should not necessarily be focused on the riparian zone in preference to upslope areas.     

Discovery of N-phenyl nicotinamides as potent inhibitors of Kdr

Inhibition of tumor-induced angiogenesis is a promising strategy in anticancer research. Neovascularization is a process required for both tumor growth and metastasis. Enhanced understanding of the underlying molecular mechanisms has led to the discovery of a variety of pharmaceutically attractive targets. Decades of investigation suggest that vascular endothelial growth factor (VEGF) and its receptors, in particular VEGFR2 or kinase insert-domain-containing receptor (Kdr), play a critical role in the growth and survival of endothelial cells in newly forming vasculature. The clinical utility of inhibitors of this receptor tyrosine kinase is currently under intense investigation. Herein we report our efforts in this arena.     

Pseudoxanthoma elasticum: reduced gamma-glutamyl carboxylation of matrix gla protein in a mouse model (Abcc6-/-)

Pseudoxanthoma elasticum (PXE), a heritable multi-system disorder manifesting with ectopic mineralization of soft connective tissues, is caused by mutations in the ABCC6/MRP6 gene/protein system, but the mechanisms how the ABCC6 mutations lead to aberrant mineralization are currently unknown. In this study, we utilized a transgenic mouse model, Abcc6^−/−, to examine the mineralization processes. We focused on matrix gla protein (MGP) which has been shown to be critical, when activated by γ-carboxylation of glutamyl residues, for prevention of unwanted mineralization. The concentration of MGP in the serum of Abcc6^−/− mice was significantly reduced when compared to wild-type controls (p < 0.004). More importantly, MGP isolated from the liver of Abcc6^−/− mice was largely under-carboxylated and therefore possesses no activity. Finally, examination of the Abcc6^−/− mice revealed association of total and under-carboxylated forms of MGP with ectopic mineralization while the γ-carboxylated form was essentially absent. These results suggest that MGP in Abcc6^−/− mice is largely in inactive form and is unable to prevent the unwanted mineralization of connective tissues in PXE.