Stable determination of sound-hard polyhedral scatterers by a minimal number of scattering measurements

The aim of the paper is to establish optimal stability estimates for the determination of sound-hard polyhedral scatterers by a minimal number of far-field measurements. This work is a significant and highly nontrivial extension of the stability estimates for the determination of sound-soft polyhedral scatterers by far-field measurements, proved by one of the authors, to the much more challenging sound-hard case. The admissible polyhedral scatterers satisfy minimal apriori assumptions of Lipschitz type and may include at the same time solid obstacles and screen-type components. In this case we obtain a stability estimate with N far-field measurements, N being the space dimension. Important features of such an estimate are that we have an explicit dependence on the parameter h representing the minimal size of the cells forming the boundaries of the admissible polyhedral scatterers, and that the modulus of continuity, provided the error is small enough with respect to h, does not depend on h. If we restrict to N=2,3 and to polyhedral obstacles, that is to polyhedra, then we obtain stability estimates with fewer measurements, namely first with N-1 measurements and then with a single measurement. In this case the dependence on h is not explicit anymore and the modulus of continuity depends on h as well

Cell cycle- and DNA repair pathway-specific effects of apoptosis on tumor suppression

The DNA damage response comprises DNA repair, cell-cycle checkpoint control, and DNA damage-induced apoptosis that collectively promote genomic integrity and suppress tumorigenesis. Previously, we have shown that the Chk2 kinase functions independently of the Mre11 complex (Mre11, Rad50, and Nbs1) and ATM in apoptosis and suppresses tumorigenesis resulting from hypomorphic alleles of Mre11 or Nbs1. Based on this work, we have proposed that Chk2 limits the oncogenic potential of replication-associated DNA damage. Here we further address the role of Chk2 and damage-induced apoptosis in suppressing the oncogenic potential of chromosome breaks. We show that loss of Chk2 or a mutation in p53 (R172P), which selectively impairs its function in apoptosis, rescued the lethality of mice lacking Lig4, a ligase required for nonhomologous end-joining (NHEJ) repair of DNA double-strand breaks in G0/G1. In contrast to Lig4(−/−)p53(−/−) mice, Lig4(−/−)Chk2(−/−) and Lig4(−/−)p53(R172P/R172P) mice were not prone to organ-specific, rapid tumorigenesis. Although the severe NHEJ deficiency of Lig4(−/−) was a less potent initiator of tumorigenesis in the p53(R172P/R172P) and Chk2(−/−) backgrounds, where p53 cell-cycle functions are largely intact, even mild defects in the intra-S and G2/M checkpoints caused by mutations in Nbs1 are sufficient to influence malignancy in p53(R172P/R172P) mice. We conclude that the oncogenic potential of double-strand breaks resulting from NHEJ deficiency is highly restricted by nonapoptotic functions of p53, such as the G1/S checkpoint or senescence, suggesting that the particular facets of the DNA damage response required for tumor suppression are dictated by the proliferative status of the tumor-initiating cell

Modeling cancer genomic data in yeast reveals selection against ATM function during tumorigenesis

The DNA damage response (DDR) comprises multiple functions that collectively preserve genomic integrity and suppress tumorigenesis. The Mre11 complex and ATM govern a major axis of the DDR and several lines of evidence implicate that axis in tumor suppression. Components of the Mre11 complex are mutated in approximately five percent of human cancers. Inherited mutations of complex members cause severe chromosome instability syndromes, such as Nijmegen Breakage Syndrome, which is associated with strong predisposition to malignancy. And in mice, Mre11 complex mutations are markedly more susceptible to oncogene- induced carcinogenesis. The complex is integral to all modes of DNA double strand break (DSB) repair and is required for the activation of ATM to effect DNA damage signaling. To understand which functions of the Mre11 complex are important for tumor suppression, we undertook mining of cancer genomic data from the clinical sequencing program at Memorial Sloan Kettering Cancer Center, which includes the Mre11 complex among the 468 genes assessed. Twenty five mutations in MRE11 and RAD50 were modeled in S. cerevisiae and in vitro. The mutations were chosen based on recurrence and conservation between human and yeast. We found that a significant fraction of tumor-borne RAD50 and MRE11 mutations exhibited separation of function phenotypes wherein Tel1/ATM activation was severely impaired while DNA repair functions were mildly or not affected. At the molecular level, the gene products of RAD50 mutations exhibited defects in ATP binding and hydrolysis. The data reflect the importance of Rad50 ATPase activity for Tel1/ATM activation and suggest that inactivation of ATM signaling confers an advantage to burgeoning tumor cells

A água: distribuição, regulamentação e uso na agricultura, com enfase ao arroz irrigado.

bitstream/item/45267/1/documento-250.pd

Excitation of the 3.071mm Hyperfine Line in Li-Like 57-Fe in Astrophysical Plasmas

As noted first by Sunyaev & Churazov (1984), the 3.071 mm hyperfine line from $^{57}Fe^{+23}$ might be observable in astrophysical plasmas. We assess the atomic processes which might contribute to the excitation of this line. We determine the intensity of the hyperfine line from an isothermal, coronal plasma in collisional ionization equilibrium and for a coronal plasma cooling isobarically due to its own radiation. Comparisons of the hyperfine line to other lines emitted by the same ion, Fe$^{+23}$, are shown to be useful for deriving the isotopic fraction of $^{57}$Fe. We calculate the ratios of the hyperfine line to the 2s--2p EUV lines at 192 \AA and 255 \AA, and the 2s--3p X-ray doublet at 10.6 \AA.Comment: 28 pages text+figures, Accepted to ApJ in Jan 98, also at http://www.astro.virginia.edu/~nld2n/research.htm

The Rad50 coiled-coil domain is indispensable for Mre11 complex functions

The Mre11 complex (Mre11, Rad50 and Xrs2 in Saccharomyces cerevisiae) influences diverse functions in the DNA damage response. The complex comprises the globular DNA-binding domain and the Rad50 hook domain, which are linked by a long and extended Rad50 coiled-coil domain. In this study, we constructed rad50 alleles encoding truncations of the coiled-coil domain to determine which Mre11 complex functions required the full length of the coils. These mutations abolished telomere maintenance and meiotic double-strand break (DSB) formation, and severely impaired homologous recombination, indicating a requirement for long-range action. Nonhomologous end joining, which is probably mediated by the globular domain of the Mre11 complex, was also severely impaired by alteration of the coiled-coil and hook domains, providing the first evidence of their influence on this process. These data show that functions of Mre11 complex are integrated by the coiled coils of Rad50.Swiss National Science Foundation and Eugen and Elisabeth Schellenberg Foundation GM56888, PBZH33-112756, PA0033-117484Ministerio de Ciencia e Innovación BFU2006-05260, 2010 CSD2007-01

Interdependence of the Rad50 hook and globular domain functions

Rad50 contains a conserved Zn2+ coordination domain (the Rad50 hook) that functions as a homodimerization interface. Hook ablation phenocopies Rad50 deficiency in all respects. Here we focused on rad50 mutations flanking the Zn2+-coordinating hook cysteines. These mutants impaired hook-mediated dimerization, but recombination between sister chromatids was largely unaffected. This may reflect that cohesin-mediated sister chromatid interactions are sufficient for double strand break repair. However, Mre11 complex functions specified by the globular domain, including Tel1 (ATM) activation, nonhomologous end-joining, and DNA double strand break end resection were affected, suggesting that dimerization exerts a broad influence on Mre11 complex function. These phenotypes were suppressed by mutations within the coiled coil and globular ATPase domain, suggesting a model in which conformational changes in the hook and globular domains are transmitted via the extended coils of Rad50. We propose that transmission of spatial information in this manner underlies the regulation of Mre11 complex functions

String interactions and discrete symmetries of the pp-wave background

Free string theory on the plane-wave background displays a discrete Z2 symmetry exchanging the two transverse SO(4) rotation groups. This symmetry should be respected also at the interacting level. We show that the zero mode structure proposed in hep-th/0208148 can be completed to a full kinematical vertex, contrary to claims appeared in the previous literature. We also comment on the relation with recent works on the string-bit formalism and on the comparison with the field theory side of the correspondence.Comment: Proceeding of the 35th Symposium Ahrenshoop Aug 2002 and the Leuven RTN-workshop Sept 200

The 3-string vertex and the AdS/CFT duality in the PP-wave limit

We pursue the study of string interactions in the PP-wave background and show that the proposal of hep-th/0211188 can be extended to a full supersymmetric vertex. Then we compute some string amplitudes in both the bosonic and fermionic sector, finding agreement with the field theory results at leading order in lambda'.Comment: Latex, 25 pages. Comments added and typos correcte