Muon radiography and deformation analysis of the lava dome formed by the 1944 eruption of Usu, Hokkaido —Contact between high-energy physics and volcano physics—

Lava domes are one of the conspicuous topographic features on volcanoes. The subsurface structure of the lava dome is important to discuss its formation mechanism. In the 1944 eruption of Volcano Usu, Hokkaido, a new lava dome was formed at its eastern foot. After the completion of the lava dome, various geophysical methods were applied to the dome to study its subsurface structure, but resulted in a rather ambiguous conclusion. Recently, from the results of the levelings, which were repeated during the eruption, “pseudo growth curves” of the lava dome were obtained. The curves suggest that the lava dome has a bulbous shape. In the present work, muon radiography, which previously proved effective in imaging the internal structure of Volcano Asama, has been applied to the Usu lava dome. The muon radiography measures the distribution of the “density length” of volcanic bodies when detectors are arranged properly. The result obtained is consistent with the model deduced from the pseudo growth curves. The measurement appears to afford useful method to clarify the subsurface structure of volcanoes and its temporal changes, and in its turn to discuss volcanic processes. This is a point of contact between high-energy physics and volcano physics

Non-integrability of Self-dual Yang-Mills-Higgs System

We examine integrability of self-dual Yang-Mills system in the Higgs phase, with taking simpler cases of vortices and domain walls. We show that the vortex equations and the domain-wall equations do not have Painleve property. This fact suggests that these equations are not integrable.Comment: 15 pages, no figures, v2: references added, v3: typos corrected, the final version to appear in NP

Solitons in the Higgs phase -- the moduli matrix approach --

We review our recent work on solitons in the Higgs phase. We use U(N_C) gauge theory with N_F Higgs scalar fields in the fundamental representation, which can be extended to possess eight supercharges. We propose the moduli matrix as a fundamental tool to exhaust all BPS solutions, and to characterize all possible moduli parameters. Moduli spaces of domain walls (kinks) and vortices, which are the only elementary solitons in the Higgs phase, are found in terms of the moduli matrix. Stable monopoles and instantons can exist in the Higgs phase if they are attached by vortices to form composite solitons. The moduli spaces of these composite solitons are also worked out in terms of the moduli matrix. Webs of walls can also be formed with characteristic difference between Abelian and non-Abelian gauge theories. We characterize the total moduli space of these elementary as well as composite solitons. Effective Lagrangians are constructed on walls and vortices in a compact form. We also present several new results on interactions of various solitons, such as monopoles, vortices, and walls. Review parts contain our works on domain walls (hep-th/0404198, hep-th/0405194, hep-th/0412024, hep-th/0503033, hep-th/0505136), vortices (hep-th/0511088, hep-th/0601181), domain wall webs (hep-th/0506135, hep-th/0508241, hep-th/0509127), monopole-vortex-wall systems (hep-th/0405129, hep-th/0501207), instanton-vortex systems (hep-th/0412048), effective Lagrangian on walls and vortices (hep-th/0602289), classification of BPS equations (hep-th/0506257), and Skyrmions (hep-th/0508130).Comment: 89 pages, 33 figures, invited review article to Journal of Physics A: Mathematical and General, v3: typos corrected, references added, the published versio

Defective Erythrocyte Pyruvate Kinase with Impaired Kinetics and Reduced Optimal Activity

A unique mutant form of erythrocyte pyruvate kinase has been found associated with chronic haemolytic anaemia in a child who is apparently doubly heterozygous for the mutant isoenzyme and for pyruvate kinase deficiency of the classical quantitative type. Clinical and laboratory findings conformed closely to those typically observed in homozygous pyruvate kinase deficiency anaemia. Assayed in fresh haemolysates, the isoenzyme exhibited reduced optimal activity ( c 45% of normal) and an increased Michaelis constant for phosphoenolpyruvate (four to five times greater than normal). The kinetic anomaly was only partially corrected by activation with fructose-1,6-disphosphate. Despite some common characteristics, this isoenzyme appears distinct from others reported in the literature and lends support to the polymorphous nature of heritable baemolytic anaemias secondary to defective pyruvate kinase.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73844/1/j.1365-2141.1972.tb05713.x.pd

2-Aminophenoxazine-3-one and 2-amino-4,4α-dihydro-4α,7-dimethyl-3H-phenoxazine-3-one cause cellular apoptosis by reducing higher intracellular pH in cancer cells

We examined intracellular pH (pHi) of ten cancer cell lines derived from different organs and two normal cell lines including human embryonic lung fibroblast cells (HEL) and human umbilical vein endothelial cells (HUVEC) in vitro, and found that pHi of most of these cancer cells was evidently higher (pH 7.5 to 7.7) than that of normal cells (7.32 and 7.44 for HEL and HUVEC, respectively) and that of primary leukemic cells and erythrocytes hitherto reported (≤7.2). Higher pHi in these cancer cells could be related to the Warburg effect in cancer cells with enhanced glycolytic metabolism. Since reversal of the Warburg effect may perturb intracellular homeostasis in cancer cells, we looked for compounds that cause extensive reduction of pHi, a major regulator of the glycolytic pathway and its associated metabolic pathway. We found that phenoxazine compounds, 2-aminophenoxazine-3-one (Phx-3) and 2-amino-4,4α-dihydro-4α,7-dimethyl-3H-phenoxazine-3-one (Phx-1) caused a rapid and drastic dose-dependent decrease of pHi in ten different cancer cells within 30 min, though the extent of the decrease of pHi was significantly larger for Phx-3 (ΔpHi = 0.6 pH units or more for 100 µM Phx-3) than for Phx-1 (ΔpHi = 0.1 pH units or more for 100 µM Phx-1). This rapid and drastic decrease of pHi in a variety of cancer cells caused by Phx-3 and Phx-1 possibly perturbed their intracellular homeostasis, and extensively affected the subsequent cell death, because these phenoxazines exerted dose-dependent proapoptotic and cytotoxic effects on these cells during 72 h incubation, confirming a causal relationship between ΔpHi and cytotoxic effects due to Phx-3 and Phx-1. Phx-3 and Phx-1 also reduced pHi of normal cells including HEL and HUVEC, although they exerted less proapoptotic and cytotoxic effects on these cells than on cancer cells. Drugs such as Phx-3 and Phx-1 that reduce pHi and thereby induce cellular apoptosis might serve as benevolent anticancer drugs

Reduction of Hydrophilic Ubiquinones by the Flavin in Mitochondrial NADH:Ubiquinone Oxidoreductase (Complex I) and Production of Reactive Oxygen Species†

ABSTRACT: NADH:ubiquinone oxidoreductase (complex I) from bovine heart mitochondria is a complicated, energy-transducing, membrane-bound enzyme that contains 45 different subunits, a non-covalently bound flavin mononucleotide, and eight iron-sulfur clusters. The mechanisms of NADH oxidation and intramolecular electron transfer by complex I are gradually being defined, but the mechanism linking ubiquinone reduction to proton translocation remains unknown. Studies of ubiquinone reduction by isolated complex I are problematic because the extremely hydrophobic natural substrate, ubiquinone-10, must be substituted with a relatively hydrophilic analogue (such as ubiquinone-1). Hydrophilic ubiquinones are reduced by an additional, non-energy-transducing pathway (which is insensitive to inhibitors such as rotenone and piericidin A). Here, we show that inhibitor-insensitive ubiquinone reduction occurs by a ping-pong type mechanism, catalyzed by the flavin mononucleotide cofactor in the active site for NADH oxidation. Moreover, semiquinones produced at the flavin site initiate redox cycling reactions with molecular oxygen, producing superoxide radicals and hydrogen peroxide. The ubiquinone reactant is regenerated, so the NADH:Q reaction becomes superstoichiometric. Idebenone, an artificial ubiquinone showing promise in the treatment of Friedreich’s Ataxia, reacts at the flavin site. The factors which determine the balance of reactivity between the two sites of ubiquinone reduction (the energy-transducing site and the flavi

Long-Term Neurodevelopmental Outcome of Monochorionic and Matched Dichorionic Twins

Contains fulltext : 79941.pdf (publisher's version ) (Open Access)BACKGROUND: Monochorionic (MC) twins are at increased risk for perinatal mortality and serious morbidity due to the presence of placental vascular anastomoses. Cerebral injury can be secondary to haemodynamic and hematological disorders during pregnancy (especially twin-to-twin transfusion syndrome (TTTS) or intrauterine co-twin death) or from postnatal injury associated with prematurity and low birth weight, common complications in twin pregnancies. We investigated neurodevelopmental outcome in MC and dichorionic (DC) twins at the age of two years. METHODS: This was a prospective cohort study. Cerebral palsy (CP) was studied in 182 MC infants and 189 DC infants matched for weight and age at delivery, gender, ethnicity of the mother and study center. After losses to follow-up, 282 of the 366 infants without CP were available to be tested with the Griffiths Mental Developmental Scales at 22 months corrected age, all born between January 2005 and January 2006 in nine perinatal centers in The Netherlands. Due to phenotypic (un)alikeness in mono-or dizygosity, the principal investigator was not blinded to chorionic status; perinatal outcome, with exception of co-twin death, was not known to the examiner. FINDINGS: Four out of 182 MC infants had CP (2.2%) - two of the four CP-cases were due to complications specific to MC twin pregnancies (TTTS and co-twin death) and the other two cases of CP were the result of cystic PVL after preterm birth - compared to one sibling of a DC twin (0.5%; OR 4.2, 95% CI 0.5-38.2) of unknown origin. Follow-up rate of neurodevelopmental outcome by Griffith's test was 76%. The majority of 2-year-old twins had normal developmental status. There were no significant differences between MC and DC twins. One MC infant (0.7%) had a developmental delay compared to 6 DC infants (4.2%; OR 0.2, 95% 0.0-1.4). Birth weight discordancy did not influence long-term outcome, though the smaller twin had slightly lower developmental scores than its larger co-twin. CONCLUSIONS: There were no significant differences in occurrence of cerebral palsy as well as neurodevelopmental outcome between MC and DC twins. Outcome of MC twins seems favourable in the absence of TTTS or co-twin death

Intronic L1 Retrotransposons and Nested Genes Cause Transcriptional Interference by Inducing Intron Retention, Exonization and Cryptic Polyadenylation

Transcriptional interference has been recently recognized as an unexpectedly complex and mostly negative regulation of genes. Despite a relatively few studies that emerged in recent years, it has been demonstrated that a readthrough transcription derived from one gene can influence the transcription of another overlapping or nested gene. However, the molecular effects resulting from this interaction are largely unknown.Using in silico chromosome walking, we searched for prematurely terminated transcripts bearing signatures of intron retention or exonization of intronic sequence at their 3' ends upstream to human L1 retrotransposons, protein-coding and noncoding nested genes. We demonstrate that transcriptional interference induced by intronic L1s (or other repeated DNAs) and nested genes could be characterized by intron retention, forced exonization and cryptic polyadenylation. These molecular effects were revealed from the analysis of endogenous transcripts derived from different cell lines and tissues and confirmed by the expression of three minigenes in cell culture. While intron retention and exonization were comparably observed in introns upstream to L1s, forced exonization was preferentially detected in nested genes. Transcriptional interference induced by L1 or nested genes was dependent on the presence or absence of cryptic splice sites, affected the inclusion or exclusion of the upstream exon and the use of cryptic polyadenylation signals.Our results suggest that transcriptional interference induced by intronic L1s and nested genes could influence the transcription of the large number of genes in normal as well as in tumor tissues. Therefore, this type of interference could have a major impact on the regulation of the host gene expression