36 research outputs found

    Complexity and Inapproximability Results for Parallel Task Scheduling and Strip Packing

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    We study the Parallel Task Scheduling problem PmsizejCmaxPm|size_j|C_{\max} with a constant number of machines. This problem is known to be strongly NP-complete for each m5m \geq 5, while it is solvable in pseudo-polynomial time for each m3m \leq 3. We give a positive answer to the long-standing open question whether this problem is strongly NPNP-complete for m=4m=4. As a second result, we improve the lower bound of 1211\frac{12}{11} for approximating pseudo-polynomial Strip Packing to 54\frac{5}{4}. Since the best known approximation algorithm for this problem has a ratio of 43+ε\frac{4}{3} + \varepsilon, this result narrows the gap between approximation ratio and inapproximability result by a significant step. Both results are proven by a reduction from the strongly NPNP-complete problem 3-Partition

    Central pathways causing fatigue in neuro-inflammatory and autoimmune illnesses

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    Therapeutic antibodies elicited by immunization against TNF-alpha.

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    Tumor necrosis factor-alpha (TNF-alpha) is critically involved in the pathogenesis of several chronic inflammatory diseases. Monoclonal antibodies against TNF-alpha are currently used for the treatment of rheumatoid arthritis and Crohn's disease. This report describes a simple and effective method for active immunization against self TNF-alpha. This vaccination approach leads to a T-cell-dependent polyclonal and sustainable anti-TNF-alpha autoantibody response that declines upon discontinuation of booster injections. The autoantibodies are elicited by injecting modified recombinant TNF-alpha molecules containing foreign immunodominant T-helper epitopes. In mice immunized with such molecules, the symptoms of experimental cachexia and type II collagen-induced arthritis are ameliorated. These results suggest that vaccination against TNF-alpha may be a useful approach for the treatment of rheumatoid arthritis and other chronic inflammatory diseases

    Therapeutic antibodies elicited by immunization against TNF-alpha.

    No full text
    Tumor necrosis factor-alpha (TNF-alpha) is critically involved in the pathogenesis of several chronic inflammatory diseases. Monoclonal antibodies against TNF-alpha are currently used for the treatment of rheumatoid arthritis and Crohn's disease. This report describes a simple and effective method for active immunization against self TNF-alpha. This vaccination approach leads to a T-cell-dependent polyclonal and sustainable anti-TNF-alpha autoantibody response that declines upon discontinuation of booster injections. The autoantibodies are elicited by injecting modified recombinant TNF-alpha molecules containing foreign immunodominant T-helper epitopes. In mice immunized with such molecules, the symptoms of experimental cachexia and type II collagen-induced arthritis are ameliorated. These results suggest that vaccination against TNF-alpha may be a useful approach for the treatment of rheumatoid arthritis and other chronic inflammatory diseases
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