121 research outputs found

    Use of a Hanging-weight System for Isolated Renal Artery Occlusion

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    In hospitalized patients, over 50% of cases of acute kidney injury (AKI) are caused by renal ischemia 1-3. A recent study of hospitalized patients revealed that only a mild increase in serum creatinine levels (0.3 to 0.4 mg/dl) is associated with a 70% greater risk of death than in persons without any increase 1. Along these lines, surgical procedures requiring cross-clamping of the aorta and renal vessels are associated with a renal failure rates of up to 30% 4. Similarly, AKI after cardiac surgery occurs in over 10% of patients under normal circumstances and is associated with dramatic increases in mortality. AKI are also common complications after liver transplantation. At least 8-17% of patients end up requiring renal replacement therapy 5. Moreover, delayed graft function due to tubule cell injury during kidney transplantation is frequently related to ischemia-associated AKI 6. Moreover, AKI occurs in approximately 20% of patients suffering from sepsis 6.The occurrence of AKI is associated with dramatic increases of morbidity and mortality 1. Therapeutic approaches are very limited and the majority of interventional trials in AKI have failed in humans. Therefore, additional therapeutic modalities to prevent renal injury from ischemia are urgently needed 3, 7-9

    Parkin loss of function contributes to RTP801 elevation and neurodegeneration in Parkinson"s disease

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    Mutations in the PARK2 gene are associated with an autosomal recessive form of juvenile parkinsonism (AR-JP). These mutations affect parkin solubility and impair its E3 ligase activity, leading to a toxic accumulation of proteins within susceptible neurons that results in a slow but progressive neuronal degeneration and cell death. Here, we report that RTP801/REDD1, a pro-apoptotic negative regulator of survival kinases mTOR and Akt, is one of such parkin substrates. We observed that parkin knockdown elevated RTP801 in sympathetic neurons and neuronal PC12 cells, whereas ectopic parkin enhanced RTP801 poly-ubiquitination and proteasomal degradation. In parkin knockout mouse brains and in human fibroblasts from AR-JP patients with parkin mutations, RTP801 levels were elevated. Moreover, in human postmortem PD brains with mutated parkin, nigral neurons were highly positive for RTP801. Further consistent with the idea that RTP801 is a substrate for parkin, the two endogenous proteins interacted in reciprocal co-immunoprecipitates of cell lysates. A potential physiological role for parkin-mediated RTP801 degradation is indicated by observations that parkin protects neuronal cells from death caused by RTP801 overexpression by mediating its degradation, whereas parkin knockdown exacerbates such death. Similarly, parkin knockdown enhanced RTP801 induction in neuronal cells exposed to the Parkinson's disease mimetic 6-hydroxydopamine and increased sensitivity to this toxin. This response to parkin loss of function appeared to be mediated by RTP801 as it was abolished by RTP801 knockdown. Taken together these results indicate that RTP801 is a novel parkin substrate that may contribute to neurodegeneration caused by loss of parkin expression or activity

    Transition from Democracy - Loss of Quality, Hybridisation and Breakdown of Democracy

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    Permeation, regulation and control of expression of TRP channels by trace metal ions

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    Modellregionen in der Biotechnologie. Modellregion Rheinland: Entwicklung von Methoden zur Nutzung genomischer Informationen fuer die Pharmaforschung Erfolgskontrollbericht und Abschlussbericht

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    SIGLEAvailable from TIB Hannover: F03B179 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekBundesministerium fuer Bildung und Forschung, Berlin (Germany)DEGerman

    Biopolymers for biosensors : polypeptide nanotubes for optical biosensing

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    In this work, N-carboxy anhydride (NCA) monomer molecules were condensed on the pore walls of an initiator-coated nanoporous alumina template, leading to polypeptide (poly(gamma-benzyl-L-glutamate), PBLG) film formation. Three different ways were followed for peptide nanotube formation: NCA polymerization in solution, in melt and polymerization from surface-nitiated vapor deposition. While the NCA monomer was polymerized within the pores, the wall thickness of the resulting polypeptide was tuned by changing the polymerization time. This polypeptide-coated alumina membrane will be used as planar optical waveguide to monitor both the changes in the refractive index and fluorescent signals of the composite membrane through specific binding of a bioanalyte. We monitored for the first time the in-situ formation of an initiator layer (3-Aminopropyltriethoxysilane, APTE) inside the pores of an alumina membrane via optical waveguide spectroscopy. Attachment of initiator molecule effectively changed the dielectric constants of the interfaces, resulting in detectable shifts of the waveguide modes. We have previously demonstrated that unmodified nanoporous alumina waveguide sensor having a 10 times higher sensitivity than surface plasmon spectroscopy (SPR). The sensitivity may be further increased if the pores are coated with PBLG polypeptides, which has many functional sites on each polypeptide chain

    La motivation du chirurgien-dentiste (approche psychologique et sociologique)

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    L'interrogation sur la motivation du chirurgien-dentiste, en tant qu'acteur de santé publique et garant de son propre équilibre physique et psychique, est posée. Dans une première partie, le concept de motivation professionnelle est abordé sous diverses approches : physiologique, psychologique ou sociologique. Puis dans une deuxième partie, les nombreux et potentiels facteurs de motivation concernant la profession de chirurgien-dentiste sont décrits. La troisième partie est consacrée aux risques de la " démotivation ". Des propositions pour éviter ou surmonter cette situation sont présentées. Enfin, la quatrième partie illustre les propos précédents par une enquête de motivation sur une promotion de jeunes praticiens.TOULOUSE3-BU Santé-Centrale (315552105) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF
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