12 research outputs found

    Nederlandse tarwe heeft nog een toekomst

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    Supplementing exposure to hypoxia with a copper depleted diet does not exacerbate right ventricular remodeling in mice

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    BACKGROUND: Pulmonary hypertension and subsequent right ventricular (RV) failure are associated with high morbidity and mortality. Prognosis is determined by occurrence of RV failure. Currently, adequate treatment for RV failure is lacking. Further research into the molecular basis for the development of RV failure as well as the development of better murine models of RV failure are therefore imperative. We hypothesize that adding a low-copper diet to chronic hypoxia in mice reinforces their individual effect and that the combination of mild pulmonary vascular remodeling and capillary rarefaction, induces RV failure. METHODS: Six week old mice were subjected to normoxia (N; 21% O2) or hypoxia (H; 10% O2) during a period of 8 weeks and received either a normal diet (Cu+) or a copper depleted diet (Cu-). Cardiac function was assessed by echocardiography and MRI analysis. RESULTS AND CONCLUSION: Here, we characterized a mouse model of chronic hypoxia combined with a copper depleted diet and demonstrate that eight weeks of chronic hypoxia (10%) is sufficient to induce RV hypertrophy and subsequent RV failure. Addition of a low copper diet to hypoxia did not have any further deleterious effects on right ventricular remodeling

    Radiation-induced Activation of Nuclear Factor-κB Involves Selective Degradation of Plasma Membrane-associated IκBα

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    In contrast to nuclear factor-κB (NF-κB) activation by tumor necrosis factor-α (TNF-α), the specific processes involved in the activation of this transcription factor by ionizing radiation (IR) have not been completely defined. According to the classical paradigm, a critical event in NF-κB activation is the degradation of IκBα. Data presented herein show that, in contrast to treatment with TNF-α, IR-induced NF-κB activation was not accompanied by degradation of IκBα in the U251 glioblastoma cell line as determined in whole cell lysates. However, treatment with the proteosome inhibitor MG-132 inhibited NF-κB activation induced by IR, suggesting that IκBα degradation was a critical event in this process. To reconcile these results, U251 cell lysates were separated into soluble and insoluble fractions and IκBα levels evaluated. Although IκBα was found in both subcellular fractions, treatment with IR resulted in the degradation of IκBα only in the insoluble fraction. Further subcellular fractionation suggested that the IR-sensitive, insoluble pool of IκBα was associated with the plasma membrane. These data suggest that the subcellular location of IκBα is a critical determinant in IR-induced NF-κB activation
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