An Improved Fixed-Parameter Algorithm for One-Page Crossing Minimization

Book embedding is one of the most well-known graph drawing models and is extensively studied in the literature. The special case where the number of pages is one is of particular interest: an embedding in this case has a natural circular representation useful for visualization and graphs that can be embedded in one page without crossings form an important graph class, namely that of outerplanar graphs. In this paper, we consider the problem of minimizing the number of crossings in a one-page book embedding, which we call one-page crossing minimization. Here, we are given a graph G with n vertices together with a non-negative integer k and are asked whether G can be embedded into a single page with at most k crossings. Bannister and Eppstein (GD 2014) showed that this problem is fixed-parameter tractable. Their algorithm is derived through the application of Courcelle\u27s theorem (on graph properties definable in the monadic second-order logic of graphs) and runs in f(L)n time, where L = 2^{O(k^2)} is the length of the formula defining the property that the one-page crossing number is at most k and f is a computable function without any known upper bound expressible as an elementary function. We give an explicit dynamic programming algorithm with a drastically improved running time of 2^{O(k log k)}n

Development of Autonomous Demand Area Power System",

ABSTRACT In 6.6kV power distribution system of Japan, the introduction of many distributed power generations (DGs

Effects of Insulin and Glucagon on Energy and Carbohydrate Metabolism of Rat Hepatocytes in Primary Culture

We studied the effects of insulin and glucagon on energy and carbohydrate metabolism of rat hepatocytes in primary culture. The aim of this study is to elucidate the mechanism of the synergistic action of insulin and glucagon and to evaluate the combined effects of these hormones on liver injury. Insulin increased the level of adenosine triphosphate in hepatocytes in the presence of glucagon. Insulin increased the activities of glucokinase (EC 2.7.1.1), phosphofructokinase (EC 2.7.1.11), pyruvate kinase (EC 2.7.1.40) type L and glucose 6-phosphate dehydrogenase (EC 1.1.1.49). Glucagon had no antagonistic effect on these increases. Glucagon increased the activity of glucose 6-phosphate (EC 3.1.3.9) (G6Pase) in the presence or absence of insulin, while insulin had no effects on the levels of G6Pase and fructose 1,6-bisphosphatase (EC 3.1.3.11) in the presence or absence of glucagon. Metabolite analysis of cultured hepatocytes indicated that insulin and glucagon have antagonistic effects on the glycolytic activity of hepatocytes. These combined effects of insulin and glucagon may partially explain the preventive effects of these hormones on liver injury.</p

The yeast Arf-GAP Glo3p is required for the endocytic recycling of cell surface proteins

Small GTP-binding proteins of the Ras superfamily play diverse roles in intracellular trafficking. Among them, the Rab, Arf, and Rho families function in successive steps of vesicle transport, in forming vesicles from donor membranes, directing vesicle trafficking toward target membranes and docking vesicles onto target membranes. These proteins act as molecular switches that are controlled by a cycle of GTP binding and hydrolysis regulated by guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). In this study we explored the role of GAPs in the regulation of the endocytic pathway using fluorescently labeled yeast mating pheromone α-factor. Among 25 non-essential GAP mutants, we found that deletion of the GLO3 gene, encoding Arf-GAP protein, caused defective internalization of fluorescently labeled α-factor. Quantitative analysis revealed that glo3Δ cells show defective α-factor binding to the cell surface. Interestingly, Ste2p, the α-factor receptor, was mis-localized from the plasma membrane to the vacuole in glo3Δ cells. Domain deletion mutants of Glo3p revealed that a GAP-independent function, as well as the GAP activity, of Glo3p is important for both α-factor binding and Ste2p localization at the cell surface. Additionally, we found that deletion of the GLO3 gene affects the size and number of Arf1p-residing Golgi compartments and causes a defect in transport from the TGN to the plasma membrane. Furthermore, we demonstrated that glo3Δ cells were defective in the late endosome-to-TGN transport pathway, but not in the early endosome-to-TGN transport pathway. These findings suggest novel roles for Arf-GAP Glo3p in endocytic recycling of cell surface proteins

Quantum-grade nanodiamonds for ultrabright spin detection in live cells

Optically accessible spin-active nanomaterials are promising as quantum nanosensors for probing biological samples. However, achieving bioimaging-level brightness and high-quality spin properties for these materials is challenging and hinders their application in quantum biosensing. Here, we demonstrate ultrabright fluorescent nanodiamonds (NDs) containing 0.6-1.3-ppm nitrogen-vacancy (NV) centers by spin-environment engineering via enriching spin-less 12C-carbon isotopes and reducing substitutional nitrogen spin impurities. The NDs, readily introduced into cultured cells, exhibited substantially narrow optically detected magnetic resonance (ODMR) spectra, requiring 16-times less microwave excitation power to give an ODMR depth comparable to that of conventional type-Ib NDs. They show average spin-relaxation times of T1 = 0.68 ms and T_2 = 1.6 us (1.6 ms and 2.7 us maximum) that were 5- and 11-fold longer than those of type-Ib, respectively. The bulk-like NV spin properties and bright fluorescence demonstrated in this study significantly improve the sensitivity of ND-based quantum sensors for biological applications

Focus-formation of replication protein A, activation of checkpoint system and DNA repair synthesis induced by DNA double-strand breaks in Xenopus egg extract

金沢大学大学院自然科学研究科 信頼性システム工学The response to DNA damage was analyzed using a cell-free system consisting of Xenopus egg extract and demembranated sperm nuclei. In the absence of DNA-damaging agents, detergent-resistant accumulation of replication protein A appeared in nuclei after a 30 minute incubation, and a considerable portion of the replication protein A signals disappeared during a further 30 minute incubation. Similar replication protein A accumulation was observed in the nuclei after a 30 minute incubation in the extract containing camptothecin, whereas a further 30 minute incubation generated discrete replication protein A foci. The addition of camptothecin also induced formation of γ-H2AX foci, which have been previously shown to localize at sites of DSBs. Analysis of the time course of DNA replication and results obtained using geminin, an inhibitor of licensing for DNA replication, suggest that the discrete replication protein A foci formed in response to camptothecin-induced DNA damage occur in a DNA-replication- dependent manner. When the nuclei were incubated in the extract containing EcoRI, discrete replication protein A foci were observed at 30 minutes as well as at 60 and 90 minutes after incubation, and the focus-formation of replication protein A was not sensitive to geminin. DNA replication was almost completely inhibited in the presence of EcoRI and the inhibition was sensitive to caffeine, an inhibitor of ataxia telangiectasia mutated protein (ATM) and ATM- and Rad3-related protein (ATR). However, the focus-formation of replication protein A in the presence of EcoRI was not influenced by caffeine treatment. EcoRI-induced incorporation of biotin-dUTP into chromatin was observed following geminin-mediated inhibition of DNA replication, suggesting that the incorporation was the result of DNA repair. The biotin-dUTP signal co-localized with replication protein A foci and was not significantly suppressed or stimulated by the addition of caffeine