The pagenumber of k-trees is O(k)

AbstractA k-tree is a graph defined inductively in the following way: the complete graph Kk is a k-tree, and if G is a k-tree, then the graph resulting from adding a new vertex adjacent to k vertices inducing a Kk in G is also a k-tree. This paper examines the book-embedding problem for k-trees. A book embedding of a graph maps the vertices onto a line along the spine of the book and assigns the edges to pages of the book such that no two edges on the same page cross. The pagenumber of a graph is the minimum number of pages in a valid book embedding. In this paper, it is proven that the pagenumber of a k-tree is at most k+1. Furthermore, it is shown that there exist k-trees that require k pages. The upper bound leads to bounds on the pagenumber of a variety of classes of graphs for which no bounds were previously known

Complementarities in the diffusion of personal computers and the internet: Implications for the global digital divide

This paper studies the cross-country diffusion of personal computers (PCs) and the Internet, and examines how the diffusive interactions across these technologies affect the evolution of the global digital divide. We adopt a generalized diffusion model that incorporates the impact of one technology's installed base on the diffusion of the other technology. We estimate the model on data from 26 developing and developed countries between 1991 and 2005. We find that the codiffusion effects between PCs and the Internet are complementary in nature and the impact of PCs on Internet diffusion is substantially stronger in developing countries as compared to developed ones. Furthermore, our results suggest that these codiffusive effects are a significant driver of the narrowing of the digital divide. We also examine the policy implications of our results, especially with respect to how complementarities in the diffusion of PC and Internet technologies might be harnessed to further accelerate the narrowing of the global digital divide. © 2010 INFORMS

Graph Treewidth and Geometric Thickness Parameters

Consider a drawing of a graph $G$ in the plane such that crossing edges are coloured differently. The minimum number of colours, taken over all drawings of $G$, is the classical graph parameter "thickness". By restricting the edges to be straight, we obtain the "geometric thickness". By further restricting the vertices to be in convex position, we obtain the "book thickness". This paper studies the relationship between these parameters and treewidth. Our first main result states that for graphs of treewidth $k$, the maximum thickness and the maximum geometric thickness both equal $\lceil{k/2}\rceil$. This says that the lower bound for thickness can be matched by an upper bound, even in the more restrictive geometric setting. Our second main result states that for graphs of treewidth $k$, the maximum book thickness equals $k$ if $k \leq 2$ and equals $k+1$ if $k \geq 3$. This refutes a conjecture of Ganley and Heath [Discrete Appl. Math. 109(3):215-221, 2001]. Analogous results are proved for outerthickness, arboricity, and star-arboricity.Comment: A preliminary version of this paper appeared in the "Proceedings of the 13th International Symposium on Graph Drawing" (GD '05), Lecture Notes in Computer Science 3843:129-140, Springer, 2006. The full version was published in Discrete & Computational Geometry 37(4):641-670, 2007. That version contained a false conjecture, which is corrected on page 26 of this versio

Long Term Functional and Esthetic Outcomes After Fibula Free Flap Reconstruction of the Mandible

Objectives: To report functional and esthetic outcomes, after fibula free flap (FFF) reconstruction of the mandible for oral cancer, assessed by physicians, non-clinicians and patients. Materials and Methods: Twenty-five long term survivors from oral cancer after FFF reconstruction were recalled for head and neck examination by surgeons and patient reported outcomes, using EORTC, QLQ C-30, H&N-35 and FACE-Q questionnaires. Results: Physicians reported 64% restoration of functionality compared to normal. Patients reported high scores on QLQ-C30, but lower scores on H&N-35. Esthetic scores were reported higher by clinicians than non-clinicians. The decline in function and appearance was attributed to loss of lower dentition, trismus, mal occlusion, xerostomia and tissue atrophy. Conclusion: To minimize the decline in function and appearance, immediate dental implants in FFF, better reconstruction of the temporomandibular joint, newer methods of radiotherapy to minimize xerostomia and oral exercises to prevent trismus should be considered

GSK3-mediated raptor phosphorylation supports amino acid-dependent Q2 mTORC1-directed signalling

The mammalian or mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) is a ubiquitously expressed multimeric protein kinase complex that integrates nutrient and growth factor signals for the co-ordinated regulation of cellular metabolism and cell growth. Herein, we demonstrate that suppressing the cellular activity of glycogen synthase kinase-3 (GSK3), by use of pharmacological inhibitors or shRNA-mediated gene silencing, results in substantial reduction in amino acid (AA)-regulated mTORC1-directed signalling, as assessed by phosphorylation of multiple downstream mTORC1 targets. We show that GSK3 regulates mTORC1 activity through its ability to phosphorylate the mTOR-associated scaffold protein raptor (regulatory-associated protein of mTOR) on Ser(859). We further demonstrate that either GSK3 inhibition or expression of a S859A mutated raptor leads to reduced interaction between mTOR and raptor and under these circumstances, irrespective of AA availability, there is a consequential loss in phosphorylation of mTOR substrates, such as p70S6K1 (ribosomal S6 kinase 1) and uncoordinated-51-like kinase (ULK1), which results in increased autophagic flux and reduced cellular proliferation

DNA replication stress restricts ribosomal DNA copy number

Ribosomal RNAs (rRNAs) in budding yeast are encoded by ~100–200 repeats of a 9.1kb sequence arranged in tandem on chromosome XII, the ribosomal DNA (rDNA) locus. Copy number of rDNA repeat units in eukaryotic cells is maintained far in excess of the requirement for ribosome biogenesis. Despite the importance of the repeats for both ribosomal and non-ribosomal functions, it is currently not known how “normal” copy number is determined or maintained. To identify essential genes involved in the maintenance of rDNA copy number, we developed a droplet digital PCR based assay to measure rDNA copy number in yeast and used it to screen a yeast conditional temperature-sensitive mutant collection of essential genes. Our screen revealed that low rDNA copy number is associated with compromised DNA replication. Further, subculturing yeast under two separate conditions of DNA replication stress selected for a contraction of the rDNA array independent of the replication fork blocking protein, Fob1. Interestingly, cells with a contracted array grew better than their counterparts with normal copy number under conditions of DNA replication stress. Our data indicate that DNA replication stresses select for a smaller rDNA array. We speculate that this liberates scarce replication factors for use by the rest of the genome, which in turn helps cells complete DNA replication and continue to propagate. Interestingly, tumors from mini chromosome maintenance 2 (MCM2)-deficient mice also show a loss of rDNA repeats. Our data suggest that a reduction in rDNA copy number may indicate a history of DNA replication stress, and that rDNA array size could serve as a diagnostic marker for replication stress. Taken together, these data begin to suggest the selective pressures that combine to yield a “normal” rDNA copy number

LRRK2 is a negative regulator of <em>Mycobacterium tuberculosis</em> phagosome maturation in macrophages

\ua9 2018 EMBO. Mutations in the leucine-rich repeat kinase 2 (LRRK2) are associated with Parkinson\u27s disease, chronic inflammation and mycobacterial infections. Although there is evidence supporting the idea that LRRK2 has an immune function, the cellular function of this kinase is still largely unknown. By using genetic, pharmacological and proteomics approaches, we show that LRRK2 kinase activity negatively regulates phagosome maturation via the recruitment of the Class III phosphatidylinositol-3 kinase complex and Rubicon to the phagosome in macrophages. Moreover, inhibition of LRRK2 kinase activity in mouse and human macrophages enhanced Mycobacterium tuberculosis phagosome maturation and mycobacterial control independently of autophagy. In vivo, LRRK2 deficiency in mice resulted in a significant decrease in M. tuberculosis burdens early during the infection. Collectively, our findings provide a molecular mechanism explaining genetic evidence linking LRRK2 to mycobacterial diseases and establish an LRRK2-dependent cellular pathway that controls M. tuberculosis replication by regulating phagosome maturation

Impacts of climate change on plant diseases – opinions and trends

There has been a remarkable scientific output on the topic of how climate change is likely to affect plant diseases in the coming decades. This review addresses the need for review of this burgeoning literature by summarizing opinions of previous reviews and trends in recent studies on the impacts of climate change on plant health. Sudden Oak Death is used as an introductory case study: Californian forests could become even more susceptible to this emerging plant disease, if spring precipitations will be accompanied by warmer temperatures, although climate shifts may also affect the current synchronicity between host cambium activity and pathogen colonization rate. A summary of observed and predicted climate changes, as well as of direct effects of climate change on pathosystems, is provided. Prediction and management of climate change effects on plant health are complicated by indirect effects and the interactions with global change drivers. Uncertainty in models of plant disease development under climate change calls for a diversity of management strategies, from more participatory approaches to interdisciplinary science. Involvement of stakeholders and scientists from outside plant pathology shows the importance of trade-offs, for example in the land-sharing vs. sparing debate. Further research is needed on climate change and plant health in mountain, boreal, Mediterranean and tropical regions, with multiple climate change factors and scenarios (including our responses to it, e.g. the assisted migration of plants), in relation to endophytes, viruses and mycorrhiza, using long-term and large-scale datasets and considering various plant disease control methods

Gallium hydride vapor phase epitaxy of GaN nanowires

Straight GaN nanowires (NWs) with diameters of 50 nm, lengths up to 10 μm and a hexagonal wurtzite crystal structure have been grown at 900°C on 0.5 nm Au/Si(001) via the reaction of Ga with NH3 and N2:H2, where the H2 content was varied between 10 and 100%. The growth of high-quality GaN NWs depends critically on the thickness of Au and Ga vapor pressure while no deposition occurs on plain Si(001). Increasing the H2 content leads to an increase in the growth rate, a reduction in the areal density of the GaN NWs and a suppression of the underlying amorphous (α)-like GaN layer which occurs without H2. The increase in growth rate with H2 content is a direct consequence of the reaction of Ga with H2 which leads to the formation of Ga hydride that reacts efficiently with NH3 at the top of the GaN NWs. Moreover, the reduction in the areal density of the GaN NWs and suppression of the α-like GaN layer is attributed to the reaction of H2 with Ga in the immediate vicinity of the Au NPs. Finally, the incorporation of H2 leads to a significant improvement in the near band edge photoluminescence through a suppression of the non-radiative recombination via surface states which become passivated not only via H2, but also via a reduction of O2-related defects