908 research outputs found

    The parameterized hardness of the k-center problem in transportation networks

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    In this paper we study the hardness of the k-Center problem on inputs that model transportation networks. For the problem, an edge-weighted graph G=(V,E) and an integer k are given and a center set C subseteq V needs to be chosen such that |C|<= k. The aim is to minimize the maximum distance of any vertex in the graph to the closest center. This problem arises in many applications of logistics, and thus it is natural to consider inputs that model transportation networks. Such inputs are often assumed to be planar graphs, low doubling metrics, or bounded highway dimension graphs. For each of these models, parameterized approximation algorithms have been shown to exist. We complement these results by proving that the k-Center problem is W[1]-hard on planar graphs of constant doubling dimension, where the parameter is the combination of the number of centers k, the highway dimension h, and even the treewidth t. Moreover, under the Exponential Time Hypothesis there is no f(k,t,h)* n^{o(t+sqrt{k+h})} time algorithm for any computable function f. Thus it is unlikely that the optimum solution to k-Center can be found efficiently, even when assuming that the input graph abides to all of the above models for transportation networks at once! Additionally we give a simple parameterized (1+{epsilon})-approximation algorithm for inputs of doubling dimension d with runtime (k^k/{epsilon}^{O(kd)})* n^{O(1)}. This generalizes a previous result, which considered inputs in D-dimensional L_q metrics

    Work-related correlates of occupational sitting in a diverse sample of employees in Midwest metropolitan cities

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    The worksite serves as an ideal setting to reduce sedentary time. Yet little research has focused on occupational sitting, and few have considered factors beyond the personal or socio-demographic level. The current study i) examined variation in occupational sitting across different occupations, ii) explored whether worksite level factors (e.g., employer size, worksite supports and policies) may be associated with occupational sitting. Between 2012 and 2013, participants residing in four Missouri metropolitan areas were interviewed via telephone and provided information on socio-demographic characteristics, schedule flexibility, occupation, work related factors, and worksite supports and policies. Occupational sitting was self-reported (daily minutes spent sitting at work), and dichotomized. Occupation-stratified analyses were conducted to identify correlates of occupational sitting using multiple logistic regressions. A total of 1668 participants provided completed data. Those employed in business and office/administrative support spent more daily occupational sitting time (median 330 min) compared to service and blue collar employees (median 30 min). Few worksite supports and policies were sitting specific, yet factors such as having a full-time job, larger employer size, schedule flexibility, and stair prompt signage were associated with occupational sitting. For example, larger employer size was associated with higher occupational sitting in health care, education/professional, and service occupations. Work-related factors, worksite supports and policies are associated with occupational sitting. The pattern of association varies among different occupation groups. This exploratory work adds to the body of research on worksite level correlates of occupational sitting. This may provide information on priority venues for targeting highly sedentary occupation groups

    Token Jumping in minor-closed classes

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    Given two kk-independent sets II and JJ of a graph GG, one can ask if it is possible to transform the one into the other in such a way that, at any step, we replace one vertex of the current independent set by another while keeping the property of being independent. Deciding this problem, known as the Token Jumping (TJ) reconfiguration problem, is PSPACE-complete even on planar graphs. Ito et al. proved in 2014 that the problem is FPT parameterized by kk if the input graph is K3,K_{3,\ell}-free. We prove that the result of Ito et al. can be extended to any K,K_{\ell,\ell}-free graphs. In other words, if GG is a K,K_{\ell,\ell}-free graph, then it is possible to decide in FPT-time if II can be transformed into JJ. As a by product, the TJ-reconfiguration problem is FPT in many well-known classes of graphs such as any minor-free class

    Peroxisome Proliferator-Activated Receptor alpha (PPAR alpha) down-regulation in cystic fibrosis lymphocytes

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    Background: PPARs exhibit anti-inflammatory capacities and are potential modulators of the inflammatory response. We hypothesized that their expression and/or function may be altered in cystic fibrosis (CF), a disorder characterized by an excessive host inflammatory response. Methods: PPARα, β and γ mRNA levels were measured in peripheral blood cells of CF patients and healthy subjects via RT-PCR. PPARα protein expression and subcellular localization was determined via western blot and immunofluorescence, respectively. The activity of PPARα was analyzed by gel shift assay. Results: In lymphocytes, the expression of PPARα mRNA, but not of PPARβ, was reduced (-37%; p < 0.002) in CF patients compared with healthy persons and was therefore further analyzed. A similar reduction of PPARα was observed at protein level (-26%; p < 0.05). The transcription factor was mainly expressed in the cytosol of lymphocytes, with low expression in the nucleus. Moreover, DNA binding activity of the transcription factor was 36% less in lymphocytes of patients (p < 0.01). For PPARα and PPARβ mRNA expression in monocytes and neutrophils, no significant differences were observed between CF patients and healthy persons. In all cells, PPARγ mRNA levels were below the detection limit. Conclusion: Lymphocytes are important regulators of the inflammatory response by releasing cytokines and antibodies. The diminished lymphocytic expression and activity of PPARα may therefore contribute to the inflammatory processes that are observed in CF

    Augmentation of osteochondral repair with hyperbaric oxygenation: a rabbit study

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    <p>Abstract</p> <p>Background</p> <p>Current treatments for osteochondral injuries often result in suboptimal healing. We hypothesized that the combination of hyperbaric oxygen (HBO) and fibrin would be superior to either method alone in treating full-thickness osteochondral defects.</p> <p>Methods</p> <p>Osteochondral repair was evaluated in 4 treatment groups (control, fibrin, HBO, and HBO+fibrin groups) at 2-12 weeks after surgical injury. Forty adult male New Zealand white rabbits underwent arthrotomy and osteochondral surgery on both knees. Two osteochondral defects were created in each femoral condyle, one in a weight-bearing area and the other in a non-weight-bearing area. An exogenous fibrin clot was placed in each defect in the right knee. Left knee defects were left empty. Half of the rabbits then underwent hyperbaric oxygen therapy. The defects in the 4 treatment groups were then examined histologically at 2, 4, 6, 8, and 12 weeks after surgery.</p> <p>Results</p> <p>The HBO+fibrin group showed more rapid and more uniform repair than the control and fibrin only groups, but was not significantly different from the group receiving HBO alone. In the 2 HBO groups, organized repair and good integration with adjacent cartilage were seen at 8 weeks; complete regeneration was observed at 12 weeks.</p> <p>Conclusions</p> <p>HBO significantly accelerated the repair of osteochondral defects in this rabbit model; however, the addition of fibrin produced no further improvement.</p

    Regulation of ErbB2 Receptor Status by the Proteasomal DUB POH1

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    Understanding the factors, which control ErbB2 and EGF receptor (EGFR) status in cells is likely to inform future therapeutic approaches directed at these potent oncogenes. ErbB2 is resistant to stimulus-induced degradation and high levels of over-expression can inhibit EGF receptor down-regulation. We now show that for HeLa cells expressing similar numbers of EGFR and ErbB2, EGFR down-regulation is efficient and insensitive to reduction of ErbB2 levels. Deubiquitinating enzymes (DUBs) may extend protein half-lives by rescuing ubiquitinated substrates from proteasomal degradation or from ubiquitin-dependent lysosomal sorting. Using a siRNA library directed at the full complement of human DUBs, we identified POH1 (also known as Rpn11 or PSMD14), a component of the proteasome lid, as a critical DUB controlling the apparent ErbB2 levels. Moreover, the effects on ErbB2 levels can be reproduced by administration of proteasomal inhibitors such as epoxomicin used at maximally tolerated doses. However, the extent of this apparent loss and specificity for ErbB2 versus EGFR could not be accounted for by changes in transcription or degradation rate. Further investigation revealed that cell surface ErbB2 levels are only mildly affected by POH1 knock-down and that the apparent loss can at least partially be explained by the accumulation of higher molecular weight ubiquitinated forms of ErbB2 that are detectable with an extracellular but not intracellular domain directed antibody. We propose that POH1 may deubiquitinate ErbB2 and that this activity is not necessarily coupled to proteasomal degradation
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