A Much Faster Algorithm for Finding a Maximum Clique

We present improvements to a branch-and-bound maximumclique-finding algorithm MCS (WALCOM 2010, LNCS 5942, pp. 191–203) that was shown to be fast. First, we employ an efficient approximation algorithm for finding a maximum clique. Second, we make use of appropriate sorting of vertices only near the root of the search tree. Third, we employ a lightened approximate coloring mainly near the leaves of the search tree. A new algorithm obtained from MCS with the above improvements is named MCT. It is shown that MCT is much faster than MCS by extensive computational experiments. In particular, MCT is shown to be faster than MCS for gen400 p0.9 75 and gen400 p0.9 65 by over 328,000 and 77,000 times, respectively

The Benefits of Urban Agglomeration: Is Tokyo a Unique Case? (Japanese)

The greater the density of working population in the vicinity of an office building, the greater the potential number of face-to-face contacts per day, and the greater the productivity of office operations. Such is the benefit of urban agglomeration. The productivity of offices located in central Tokyo is far greater than the productivity of those located in other Japanese cities. Is this high productivity essentially attributable to the greater agglomeration in Tokyo? Or is a totally different production function occurring due to the uniqueness of goods and services produced there, or because Tokyo is Japan's capital? This paper analyzes these issues. Office rents are relatively high in areas with a high degree of agglomeration. Taking advantage of this correlation, a production function for office operations within a single city has been estimated. In this paper, the same measurement method is applied to a number of cities. Based on the micro-data on seven major government-decreed cities, the paper shows that output-input relationships occur in all but one city, Sapporo. This can basically be explained by a single production function. In other words, it demonstrates that even if a dummy variable corresponding to the respective cities is added to the production function, it does not produce a statistically significant effect. This analysis has found that the productivity difference between Tokyo and other cities stems fundamentally from the difference in the economy of scale, and is neither attributable to the uniqueness of goods and services produced in Tokyo, nor to its being the national capital.

Nrf2 deficiency does not affect denervation‐induced alterations in mitochondrial fission and fusion proteins in skeletal muscle

Oxidative stress-induced mitochondrial dysfunction is associated with age-related and disuse-induced skeletal muscle atrophy. However, the role ofnuclear factor erythroid 2-related factor 2 (Nrf2) during muscle fiber atrophyremains to be elucidated. In this study, we examined whether deficiency ofNrf2, a master regulator of antioxidant transcription, promotes denervation-induced mitochondrial fragmentation and muscle atrophy. We found that theexpression of Nrf2 and its target antioxidant genes was upregulated at 2 weeksafter denervation in wild-type (WT) mice. The response of these antioxidantgenes was attenuated in Nrf2 knockout (KO) mice. Nrf2 KO mice exhibitedelevated levels of 4-hydroxynonenal in the skeletal muscle, whereas the proteinlevels of the mitochondrial oxidative phosphorylation complex IV wasdeclined in the denervated muscle of these mice. Increased in mitochondrialfission regulatory proteins and decreased fusion proteins in response to dener-vation were observed in both WT and KO mice; however, no difference wasobserved between the two groups. These findings suggest that Nrf2 deficiencyaggravates denervation-induced oxidative stress, but does not affect the alter-ations in mitochondrial morphology proteins and the loss of skeletal musclemass

Single C−F Bond Activation of the CF3 Group with a Lewis Acid: CF3‐Cyclopropanes as Versatile 4,4‐Difluorohomoallylating Agents

The selective activation of one C−F bond (single activation) of the CF3 group on cyclopropanes was achieved for the first time. When (trifluoromethyl)cyclopropanes were treated with arenes, allylsilanes, silyl enol ethers, or hydrosilanes in the presence of Me2AlCl, fluoride elimination and the subsequent ring opening proceeded to afford 4,4‐difluorohomoallylated products. In the absence of external nucleophiles, an alkyl group of AlR3 was effectively introduced to provide the corresponding 1,1‐difluoroalkenes

Genetic Interactions in Zebrafish Midline Development

AbstractMutational analyses have shown that the genesno tail(ntl, Brachyuryhomolog),floating head(flh,aNothomeobox gene), andcyclops(cyc) play direct and essential roles in the development of midline structures in the zebrafish. In bothntlandflhmutants a notochord does not develop, and incycmutants the floor plate is nearly entirely missing. We made double mutants to learn how these genes might interact. Midline development is disrupted to a greater extent incyc;flhdouble mutants than in eithercycorflhsingle mutants; their effects appear additive. Both the notochord and floor plate are completely lacking, and other phenotypic disturbances suggest that midline signaling functions are severely reduced. On the other hand, trunk midline defects inflh;ntldouble mutants are not additive, but are most often similar to those inntlsingle mutants. This finding reveals that loss ofntlfunction can suppress phenotypic defects due to mutation atflh,and we interpret it to mean that the wild-type allele ofntl(ntl+) functions upstream toflhin a regulatory hierarchy. Loss of function ofntlalso strongly suppresses the floor plate deficiency incycmutants, for we found trunk floor plate to be present incyc;ntldouble mutants. From these findings we propose thatntl+plays an early role in cell fate choice at the dorsal midline, mediated by the Ntl protein acting to antagonize floor plate development as well as to promote notochord development

Effects of Nrf2 deficiency on mitochondrial oxidative stress in aged skeletal muscle

Oxidative stress and mitochondrial dysfunction are associated with the aging process. However, the role of nuclear factor erythroid 2 ‐related factor 2 (Nrf2) in skeletal muscle during aging remains to be clarified. In the current study, we assessed whether the lack of Nrf2, which is known as a master regulator of redox homeostasis, promotes age‐related mitochondrial dysfunction and muscle atrophy in skeletal muscle. Here, we demonstrated that mitochondrial 4‐hydroxynonenal and protein carbonyls, markers of oxidative stress, were robustly elevated in aged Nrf2 knockout (KO) mice because of the decreased expression of Nrf2‐target antioxidant genes. Mitochondrial respiration declined with aging; however, there was no difference between Nrf2 KO and age‐matched WT mice. Similarly, cytochrome c oxidase activity was lower in aged WT and Nrf2 KO mice compared with young WT mice. The expression of Mfn1 and Mfn2 mRNA was lower in aged Nrf2 KO muscle. Mitochondrial reactive oxygen species production per oxygen consumed was elevated in aged Nrf2 KO mice. There was no effect of Nrf2 KO on muscle mass normalized to body weight. These results suggest that Nrf2 deficiency exacerbates age‐related mitochondrial oxidative stress but does not affect the decline of respiratory function in skeletal muscle

Lactate administration increases mRNA expression of PGC-1α and UCP3 in mouse skeletal muscle

To examine the potential role of lactate as a signaling molecule in skeletal muscle, we performed global gene expression analysis of the mouse gastrocnemius muscle, 3 h after lactate administration using the Affymetrix GeneChip system. Among the top 15 genes with the largest fold change, increased expression of Ppargc1a, Pdk4, and Ucp3 was confirmed using real-time quantitative PCR. Our findings suggest that lactate serves as a signal for upregulating genes related to mitochondrial function.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author