263 research outputs found

    Compared Productivity of Local Ecotypes and Selected Cultivars of Perennial Ryegrass (Lolium Perenne) in High Belgium

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    The objective of the trials was to compare the productivity of local ecotypes of perennial ryegrass (Lolium perenne) issued from old permanent pastures of High Belgium to that of adapted cultivars. During 3 consecutive years 2 local ecotypes were compared, in pure seedling at 2 different levels of nitrogenous manure, to 2 cultivars frequently used in seed mixtures for pastures. Results obtained using a cutting cycle wich simulated grazing did not reveal significant differences in terms of forage production or feeding value. These results explain the weak increase in forage production recorded in pastures renovated by reseeding as compared to non-renovated pastures under the same environmental conditions

    Monitoring of Intake and Energetic Efficiency of the Grass in a Pasture Rotationally Grazed by Bulls using NIRS Applied to the Faeces

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    The objective of this approach was to characterise variations that one can observe in the course of a pasture season using near infrared spectrometry (NIRS) applied to the analysis of the grass and faeces collected during the season. Available grass and faeces of Belgian Blue White young bulls have been collected 3 times a week since the beginning of May until mid-October. The samples have been predicted in NIRS technique according to a calibration previously developed on the faeces of sheep fed ad libitum in cage with green grass. The NIRS provides a useful tool to provide a relative description and a monitoring of the evolution of the quality and of the daily intake of grass, that could provide useful information to adapt the supplementation according to the changing quality of the grass

    A new fasciocutaneous flap model identifies a critical role for endothelial Notch signaling in wound healing and flap survival.

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    Flap surgery is a common treatment for severe wounds and a major determinant of surgical outcome. Flap survival and healing depends on adaptation of the local flap vasculature. Using a novel and defined model of fasciocutaneous flap surgery, we demonstrate that the Notch ligand Delta-like 1 (Dll1), expressed in vascular endothelial cells, regulates flap arteriogenesis, inflammation and flap survival. Utilizing the stereotyped anatomy of dorsal skin arteries, ligation of the major vascular pedicle induced strong collateral vessel development by end-to-end anastomosis in wildtype mice, which supported flap perfusion recovery over time. In mice with heterozygous deletion of Dll1, collateral vessel formation was strongly impaired, resulting in aberrant vascularization and subsequent necrosis of the tissue. Furthermore, Dll1 deficient mice showed severe inflammation in the flap dominated by monocytes and macrophages. This process is controlled by endothelial Dll1 in vivo, since the results were recapitulated in mice with endothelial-specific deletion of Dll1. Thus, our model provides a platform to study vascular adaptation to flap surgery and molecular and cellular regulators influencing flap healing and survival

    Blood flow controls bone vascular function and osteogenesis

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    While blood vessels play important roles in bone homeostasis and repair, fundamental aspects of vascular function in the skeletal system remain poorly understood. Here we show that the long bone vasculature generates a peculiar flow pattern, which is important for proper angiogenesis. Intravital imaging reveals that vessel growth in murine long bone involves the extension and anastomotic fusion of endothelial buds. Impaired blood flow leads to defective angiogenesis and osteogenesis, and downregulation of Notch signalling in endothelial cells. In aged mice, skeletal blood flow and endothelial Notch activity are also reduced leading to decreased angiogenesis and osteogenesis, which is reverted by genetic reactivation of Notch. Blood flow and angiogenesis in aged mice are also enhanced on administration of bisphosphonate, a class of drugs frequently used for the treatment of osteoporosis. We propose that blood flow and endothelial Notch signalling are key factors controlling ageing processes in the skeletal system

    CSF-1 and Notch signaling cooperate in macrophage instruction and tissue repair during peripheral limb ischemia

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    Ischemia causes an inflammatory response featuring monocyte-derived macrophages (MF) involved in angiogenesis and tissue repair. Angiogenesis and ischemic macrophage differentiation are regulated by Notch signaling via Notch ligand Delta-like 1 (Dll1). Colony stimulating factor 1 (CSF-1) is an essential MF lineage factor, but its role in ischemic macrophage development and the interaction with Notch signaling is so far unclear. Using a mouse model of hind limb ischemia with CSF-1 inhibitor studies and Dll1 heterozygous mice we show that CSF-1 is induced in the ischemic niche by a subpopulation of stromal cells expressing podoplanin, which was paralleled by the development of ischemic macrophages. Inhibition of CSF-1 signaling with small molecules or blocking antibodies impaired macrophage differentiation but prolonged the inflammatory response, resulting in impaired perfusion recovery and tissue regeneration. Yet, despite high levels of CSF-1, macrophage maturation and perfusion recovery were impaired in mice with Dll1 haploinsufficiency, while inflammation was exaggerated. In vitro, CSF-1 was not sufficient to induce full MF differentiation from donor monocytes in the absence of recombinant DLL1, while the presence of DLL1 in a dose-dependent manner stimulated MF differentiation in combination with CSF-1. Thus, CSF-1 is an ischemic niche factor that cooperates with Notch signaling in a non-redundant fashion to instruct macrophage cell fate and maturation, which is required for ischemic perfusion recovery and tissue repair

    "A Decentralized Operations Concept for the European Payloads on the International Space Station"

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    The European Module Columbus of the International Space Station (ISS) is planned to be launched 2004. For its exploitation phase as well as for the early utilisation of the Space Station starting from 2003 onwards the operations procedures are now being defined in detail and the implementation of specific infrastructure has started. A decentralised operations concept will allow the investigators to perform their experiments using the telescience technique of remote experiment operations whenever feasible. User Support and Operation Centres (USOCs) will act as Facility Responsible Centres (FRC) performing the operations for multi user experiment facilities. The Columbus Control Centre (COL-CC) will perform the Columbus system operations, co-ordinate the European payload operations and provide the European Communications network. This paper gives an overview on the operations concepts and the tasks and set up of the involved sites

    Critical role of endothelial Notch1 signaling in postnatal angiogenesis

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    Notch receptors are important mediators of cell fate during embryogenesis, but their role in adult physiology, particularly in postnatal angiogenesis, remains unknown. Of the Notch receptors, only Notch1 and Notch4 are expressed in vascular endothelial cells. Here we show that blood flow recovery and postnatal neovascularization in response to hindlimb ischemia in haploinsufficient global or endothelial-specific Notch1(+/-) mice, but not Notch4(-/-) mice, were impaired compared with wild-type mice. The expression of vascular endothelial growth factor (VEGF) in response to ischemia was comparable between wild-type and Notch mutant mice, suggesting that Notch1 is downstream of VEGF signaling. Treatment of endothelial cells with VEGF increases presenilin proteolytic processing, gamma-secretase activity, Notch1 cleavage, and Hes-1 (hairy enhancer of split homolog-1) expression, all of which were blocked by treating endothelial cells with inhibitors of phosphatidylinositol 3-kinase/protein kinase Akt or infecting endothelial cells with a dominant-negative Akt mutant. Indeed, inhibition of gamma-secretase activity leads to decreased angiogenesis and inhibits VEGF-induced endothelial cell proliferation, migration, and survival. Overexpression of the active Notch1 intercellular domain rescued the inhibitory effects of gamma-secretase inhibitors on VEGF-induced angiogenesis. These findings indicate that the phosphatidylinositol 3-kinase/Akt pathway mediates gamma-secretase and Notch1 activation by VEGF and that Notch1 is critical for VEGF-induced postnatal angiogenesis. These results suggest that Notch1 may be a novel therapeutic target for improving angiogenic response and blood flow recovery in ischemic limbs
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