Optimal Distributed Covering Algorithms

We present a time-optimal deterministic distributed algorithm for approximating a minimum weight vertex cover in hypergraphs of rank f. This problem is equivalent to the Minimum Weight Set Cover problem in which the frequency of every element is bounded by f. The approximation factor of our algorithm is (f+epsilon). Let Delta denote the maximum degree in the hypergraph. Our algorithm runs in the congest model and requires O(log{Delta} / log log Delta) rounds, for constants epsilon in (0,1] and f in N^+. This is the first distributed algorithm for this problem whose running time does not depend on the vertex weights nor the number of vertices. Thus adding another member to the exclusive family of provably optimal distributed algorithms. For constant values of f and epsilon, our algorithm improves over the (f+epsilon)-approximation algorithm of [Fabian Kuhn et al., 2006] whose running time is O(log Delta + log W), where W is the ratio between the largest and smallest vertex weights in the graph. Our algorithm also achieves an f-approximation for the problem in O(f log n) rounds, improving over the classical result of [Samir Khuller et al., 1994] that achieves a running time of O(f log^2 n). Finally, for weighted vertex cover (f=2) our algorithm achieves a deterministic running time of O(log n), matching the randomized previously best result of [Koufogiannakis and Young, 2011]. We also show that integer covering-programs can be reduced to the Minimum Weight Set Cover problem in the distributed setting. This allows us to achieve an (f+epsilon)-approximate integral solution in O((1+f/log n)* ((log Delta)/(log log Delta) + (f * log M)^{1.01}* log epsilon^{-1}* (log Delta)^{0.01})) rounds, where f bounds the number of variables in a constraint, Delta bounds the number of constraints a variable appears in, and M=max {1, ceil[1/a_{min}]}, where a_{min} is the smallest normalized constraint coefficient. This improves over the results of [Fabian Kuhn et al., 2006] for the integral case, which combined with rounding achieves the same guarantees in O(epsilon^{-4}* f^4 * log f * log(M * Delta)) rounds

Chronic smoke exposure is associated with autophagy in murine Peyer's patches

INTRODUCTION: Cigarette smoke causes oxidative stress, leading to smoke-induced autophagy in several organs. Autophagy is a homeostatic process regulating the turnover of proteins and cytoplasmatic organelles. However, recently it has also been associated with many autoimmune and inflammatory disorders, among which Crohn’s disease. The purpose of the present study was to investigate whether cigarette smoke exposure is associated with increased autophagy in Peyer’s patches and its epithelium. AIMS & METHODS: C57BL/6 mice were exposed to cigarette smoke or air. After 24 weeks, the animals were sacrificied and Peyer’s patches were collected. m RNA expression of autophagy-related genes was determined by RT-PCR. Transmission electron microscopy (TEM) was used to evaluate the presence of autophagic vesicles in the follicleassociated epithelium of Peyer’s patches. RESULTS: Expression of Beclin-1, a protein involved in the nucleation of autophagosomes, and of Atg5 and Atg7, which both play a role in the autophagosome vesicle elongation and completion, increased after chronic smoke exposure. Furthermore, electron microscopy of the follicle-associated epithelium demonstrated that the mean area of autophagic vesicles per epithelial cell increased considerably from 1.1 μm2 ± 0.4 μm2 in the air group to 2.4 μm2 ± 0.4 μm2 in the smoke group (p < 0.05). Epithelial cells had a significantly higher number of autophagic vesicles after smoke exposure (1.1 ± 0.1 after smoke exposure versus 0.5 ± 0.1 vesicles per cell after air exposure, p < 0.05), but the size of the vesicles did not differ between both groups. CONCLUSION: Here we provide the first evidence that chronic exposure to cigarette smoke is associated with autophagy in murine Peyer’s patches, and more in particular in the follicle-associated epithelium covering Peyer’s patches. Our findings can help to understand the role of smoking in the pathogenesis of inflammatory bowel disease, such as Crohn’s disease

The Role of Dendritic Cells in the Pathogenesis of COPD: Liaison Officers in the Front Line

Dendritic cells are professional antigen presenting cells linking innate and adaptive immune responses. Different dendritic cell subsets were identified in human lung, each with their own functional characteristics. As innate and adaptive immune responses are activated in Chronic Obstructive Pulmonary Disease (COPD), dendritic cells could play a role in the pathogenesis of this disease. Indeed, cigarette smoke appears to modulate dendritic cell function in vitro and alters dendritic cell numbers and function in cigarette smoke exposed mice. The number of pulmonary dendritic cells differs between COPD patients, smokers and non-smokers. Moreover, the number of Langerhans-type dendritic cells increases with the severity of the disease. In this review we will discuss the scientific evidence regarding the role of dendritic cells in COPD and we will put forward the concept of modulation of dendritic cell differentiation and function as a crucial step in the pathogenesis of COPD

Cigarette smoking alters intestinal barrier function and Peyer's Patch composition

Smokers have a two-fold increased risk to develop Crohn’s disease (CD). However, little is known about the mechanisms through which smoking affects CD pathogenesis. Interestingly, the Peyer’s patches in the terminal ileum are the sites where the first CD lesions develop. To investigate whether smoke exposure causes alterations in Peyer’s patches, we studied C57BL/6 mice after exposure to air or cigarette smoke for 24 weeks. First, barrier function of the follicle-associated epithelium overlying Peyer’s patches was evaluated. We demonstrate that chronic smoke exposure is associated with increased apoptosis in the follicle-associated epithelium. Furthermore, immune cell numbers and differentiation along with chemokine expression were determined in the ileal Peyer’s patches. We observed significant increases in total dendritic cells (DC), CD4+ T-cells (including regulatory T-cells) and CD8+ T-cells after smoke exposure compared with air-exposed animals. The CD11b+ DC subset almost doubled. Interestingly, these changes were accompanied by an up-regulated mRNA expression of the chemokines CCL9 and CCL20, which are known to attract CD11b+ DC towards the subepithelial dome of Peyer’s patches. Our results demonstrate that cigarette smoke exposure induces apoptosis in follicle-associated epithelium and is associated with immune cell accumulation in Peyer’s patches, changes which can predispose to the development of CD

Landmarks or panoramas: what do navigating ants attend to for guidance?

<p>Abstract</p> <p>Background</p> <p>Insects are known to rely on terrestrial landmarks for navigation. Landmarks are used to chart a route or pinpoint a goal. The distant panorama, however, is often thought not to guide navigation directly during a familiar journey, but to act as a contextual cue that primes the correct memory of the landmarks.</p> <p>Results</p> <p>We provided <it>Melophorus bagoti </it>ants with a huge artificial landmark located right near the nest entrance to find out whether navigating ants focus on such a prominent visual landmark for homing guidance. When the landmark was displaced by small or large distances, ant routes were affected differently. Certain behaviours appeared inconsistent with the hypothesis that guidance was based on the landmark only. Instead, comparisons of panoramic images recorded on the field, encompassing both landmark and distal panorama, could explain most aspects of the ant behaviours.</p> <p>Conclusion</p> <p>Ants navigating along a familiar route do not focus on obvious landmarks or filter out distal panoramic cues, but appear to be guided by cues covering a large area of their panoramic visual field, including both landmarks and distal panorama. Using panoramic views seems an appropriate strategy to cope with the complexity of natural scenes and the poor resolution of insects' eyes. The ability to isolate landmarks from the rest of a scene may be beyond the capacity of animals that do not possess a dedicated object-perception visual stream like primates.</p

Inhaled corticosteroids and COVID-19 reply

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Cigarette smoke induces apoptosis in the follicle-associated epithelium of murine Peyer's patches

Background: Recently, cigarette smoking has been associated with the development of several auto-immune diseases, including rheumatoid arthritis and inflammatory bowel disease (IBD). The cellular and molecular mechanisms through which cigarette smoking predisposes to IBD are unknown. Cigarette smoke-induced apoptosis is described in several in vivo and in vitro experiments, and might play a role in the pathogenesis of several smoke-associated diseases. The aim of this study was to quantify apoptosis in normal murine Follicle-Associated Epithelium (FAE) and compare this to apoptosis in FAE of smoking mice. Methods: 8 C57BL/6 male mice were exposed to cigarette smoke for 24 weeks (chronic exposure); a control group of 8 mice was exposed to air during the same period. After 24 weeks the mice were sacrificed and Peyer’s patches of each mouse were dissected for histology. Immunohistochemistry for caspase-3 was performed on paraffin-embedded tissue sections of 11 Peyer’s patches of smoking animals and 11 Peyer’s patches of controls. To compare apoptotic activities between smokers and controls, the apoptotic index (percentage of apoptotic cells per 100 cells) in the FAE was calculated. An unpaired student T-test was applied. Results: A statistically significant increase in apoptosis of FAE cells was observed in smoking mice compared to air-exposed mice (P=0.002). In the FAE of smoking animals, the mean apoptotic index was 1.82 with a range of 1.11 to 3.00, whereas the mean apoptotic index in non-smoking animals was 0.92 (range 0.24 -2.06). Most apoptotic cells in both groups were seen at the apex of the FAE. Conclusion: We quantified rates of apoptosis in the FAE of murine Peyer’s patches. Furthermore we compared apoptosis in the FAE of smoking mice versus non-smoking siblings and observed an increased apoptotic index in the FAE of smoking animals. Our results demonstrate that cigarette smoke induces a significant increase of apoptosis in the FAE of murine Peyer’s patches and may point to a role for smoking in the pathogenesis of intestinal inflammation. Further investigation needs to clarify whether this increase in apoptosis influences normal function of the FAE

Role of the nitric oxide-soluble guanylyl cyclase pathway in obstructive airway diseases

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