Decomposition of meron configuration of SU(2) gauge field

For the meron configuration of the SU(2) gauge field in the four dimensional Minkowskii spacetime, the decomposition into an isovector field \bn, isoscalar fields $\rho$ and $\sigma$, and a U(1) gauge field $C_{\mu}$ is attained by solving the consistency condition for \bn. The resulting \bn turns out to possess two singular points, behave like a monopole-antimonopole pair and reduce to the conventional hedgehog in a special case. The $C_{\mu}$ field also possesses singular points, while $\rho$ and $\sigma$ are regular everywhere.Comment: 18 pages, 5 figures, Sec.4 rewritten. 5 refs. adde

Anti-tumour compounds illudin S and Irofulven induce DNA lesions ignored by global repair and exclusively processed by transcription- and replication-coupled repair pathways.

Illudin S is a natural sesquiterpene drug with strong anti-tumour activity. Inside cells, unstable active metabolites of illudin cause the formation of as yet poorly characterised DNA lesions. In order to identify factors involved in their repair, we have performed a detailed genetic survey of repair-defective mutants for responses to the drug. We show that 90% of illudin's lethal effects in human fibroblasts can be prevented by an active nucleotide excision repair (NER) system. Core NER enzymes XPA, XPF, XPG, and TFIIH are essential for recovery. However, the presence of global NER initiators XPC, HR23A/HR23B and XPE is not required, whereas survival, repair and recovery from transcription inhibition critically depend on CSA, CSB and UVS, the factors specific for transcription-coupled NER. Base excision repair and non-homologous end-joining of DNA breaks do not play a major role in the processing of illudin lesions. However, active RAD18 is required for optimal cell survival, indicating that the lesions also block replication forks, eliciting post-replication-repair-like responses. However, the translesion-polymerase DNA pol eta is not involved. We conclude that illudin-induced lesions are exceptional in that they appear to be ignored by all of the known global repair systems, and can only be repaired when trapped in stalled replication or transcription complexes. We show that the semisynthetic illudin derivative hydroxymethylacylfulvene (HMAF, Irofulven), currently under clinical trial for anti-tumour therapy, acts via the same mechanism

Measurement of the Xi-p Scattering Cross Sections at Low Energy

In this paper we report cross-section measurements for $\Xi^-p$ elastic and inelastic scatterings at low energy using a scintillating fiber active target. Upper limit on the total cross-section for the elastic scattering was found to be 24 mb at 90% confidence level, and the total cross section for the $\Xi^-p\to\Lambda\Lambda$ reaction was found to be $4.3^{+6.3}_{-2.7}$ mb. We compare the results with currently competing theoretical estimates.Comment: 9 page

Search for Lepton-Flavor-Violating and Lepton-Number-Violating tau to lhh' Decay Modes

We search for lepton-flavor-violating and lepton-number-violating tau decays into a lepton (l = electron or muon) and two charged mesons (h, h' = pion or Kaon) using 854 fb^{-1} of data collected with the Belle detector at the KEKB asymmetric-energy e^+e^- collider. We obtain 90% confidence level upper limits on the tau to lhh' branching fractions in the range (2.0-8.4)*10^{-8}. These results improve upon our previously published upper limits by factors of about 1.8 on average.Comment: 14 pages, 5 figures, submitted to Phys. Lett.

Functional relationships of FANCC to homologous recombination, translesion synthesis and BLM.

Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair

Cascade hypernuclei in the (K-,K+) reaction on 12C

Cascade hypernuclei have been studied in the (K-,K+) reaction on a scintillating fiber target. The experimental result is compared with a theoretical calculation in order to extract information concerning the Ξ- nucleus potential