Integration of photolithographic simulation and a mask repair system into a single concurrent work cell

2005 ◽  
Author(s):  
Tod Robinson ◽  
Peter Brooker ◽  
Ron Bozak ◽  
David A. Lee
Keyword(s):  
Repair System ◽  
Work Cell

EFFECT OF ARYL HYDROCARBON RECEPTOR AGONISTS AND LIPOPOLYSACCHARIDE ON BENZO(A)PYRENE GENOTOXICITY MARKERS

2019 ◽  
pp. 19-25 ◽  
Author(s):  
V. N. Babakov ◽  
N. Yu. Rogovskaya ◽  
I. D. Kurdyukov ◽  
P. P. Beltyukov ◽  
S. A. Dulov ◽  
...  
Keyword(s):  
Dna Repair ◽  
Aryl Hydrocarbon Receptor ◽  
P53 Protein ◽  
Control Level ◽  
Repair System ◽  
Human Hepatoma Cells ◽  
Kinase Activation ◽  
Receptor Agonists ◽  
Checkpoint Kinases ◽  
Aryl Hydrocarbon

The effect of aryl hydrocarbon receptor agonists (FICZ and ITE), as well as lipopolysaccharide under the toxic action of benzo(a)pyrene in HepaRG human hepatoma cells was evaluated. Active forms of the key stress-activated kinase cascades and DNA repair system proteins were used as markers of the genotoxic action of benzo(a)pyrene. A mixture of lipopolysaccharide with benzo(a)pyrene increases benzo(a)pyrene cytotoxicity and reduces the activation of DNA repair system proteins below the control level. Aryl hydrocarbon receptor agonists (FICZ and ITE) exhibit a cytoprotective effect against benzo(a) pyrene, enhance Akt1 kinase activation, and downregulate activation of the p53 protein and Chk1 and Chk2 checkpoint kinases. Thus, FICZ and ITE reduce the genotoxicity of benzo(a)pyrene.

Functional Specifics of the MutL Protein of the DNA Mismatch Repair System in Different Organisms

2020 ◽  
Vol 46 (6) ◽  
pp. 875-890
Author(s):  
M. V. Monakhova ◽  
M. A. Milakina ◽  
R. M. Trikin ◽  
T. S. Oretskaya ◽  
E. A. Kubareva
Keyword(s):  
Mismatch Repair ◽  
Dna Mismatch Repair ◽  
Repair System ◽  
Dna Mismatch ◽  
Dna Mismatch Repair System ◽  
Mismatch Repair System

Design of Pipeline Composite Repairs: From Lab Scale Tests to FEA and Full Scale Testing

2014 ◽  
Author(s):  
Remy Her ◽  
Jacques Renard ◽  
Vincent Gaffard ◽  
Yves Favry ◽  
Paul Wiet
Keyword(s):  
Finite Element ◽  
Full Scale ◽  
Combined Loading ◽  
Material Strength ◽  
Repair System ◽  
Loading Conditions ◽  
Original Design ◽  
Composite Repair ◽  
Repair Systems ◽  
Composite Properties

Composite repair systems are used for many years to restore locally the pipe strength where it has been affected by damage such as wall thickness reduction due to corrosion, dent, lamination or cracks. Composite repair systems are commonly qualified, designed and installed according to ASME PCC2 code or ISO 24817 standard requirements. In both of these codes, the Maximum Allowable Working Pressure (MAWP) of the damaged section must be determined to design the composite repair. To do so, codes such as ASME B31G for example for corrosion, are used. The composite repair systems is designed to “bridge the gap” between the MAWP of the damaged pipe and the original design pressure. The main weakness of available approaches is their applicability to combined loading conditions and various types of defects. The objective of this work is to set-up a “universal” methodology to design the composite repair by finite element calculations with directly taking into consideration the loading conditions and the influence of the defect on pipe strength (whatever its geometry and type). First a program of mechanical tests is defined to allow determining all the composite properties necessary to run the finite elements calculations. It consists in compression and tensile tests in various directions to account for the composite anisotropy and of Arcan tests to determine steel to composite interface behaviors in tension and shear. In parallel, a full scale burst test is performed on a repaired pipe section where a local wall thinning is previously machined. For this test, the composite repair was designed according to ISO 24817. Then, a finite element model integrating damaged pipe and composite repair system is built. It allowed simulating the test, comparing the results with experiments and validating damage models implemented to capture the various possible types of failures. In addition, sensitivity analysis considering composite properties variations evidenced by experiments are run. The composite behavior considered in this study is not time dependent. No degradation of the composite material strength due to ageing is taking into account. The roadmap for the next steps of this work is to clearly identify the ageing mechanisms, to perform tests in relevant conditions and to introduce ageing effects in the design process (and in particular in the composite constitutive laws).

scholarly journals Poorly Repaired Mismatches in Heteroduplex DNA are Hyper-Recombinagenic in Saccharomyces cerevisiae

Genetics ◽  
1996 ◽  
Vol 142 (2) ◽  
pp. 407-416 ◽  
Author(s):  
P Manivasakam ◽  
Susan M Rosenberg ◽  
P J Hastings
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mismatch Repair ◽  
Genetic Markers ◽  
Meiotic Recombination ◽  
Repair System ◽  
Normal Allele ◽  
Heteroduplex Dna ◽  
Mismatch Repair System ◽  
Postmeiotic Segregation ◽  
System Operating

Abstract In yeast meiotic recombination, alleles used as genetic markers fall into two classes as regards their fate when incorporated into heteroduplex DNA. Normal alleles are those that form heteroduplexes that are nearly always recognized and corrected by the mismatch repair system operating in meiosis. High PMS (postmeiotic segregation) alleles form heteroduplexes that are inefficiently mismatch repaired. We report that placing any of several high PMS alleles very close to normal alleles causes hyperrecombination between these markers. We propose that this hyperrecombination is caused by the high PMS allele blocking a mismatch repair tract initiated from the normal allele, thus preventing corepair of the two alleles, which would prevent formation of recombinants. The results of three point crosses involving two PMS alleles and a normal allele suggest that high PMS alleles placed between two alleles that are normally corepaired block that corepair.

scholarly journals Idiopathic Infertility as a Feature of Genome Instability

Life ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 628
Author(s):  
Agrita Puzuka ◽  
Baiba Alksere ◽  
Linda Gailite ◽  
Juris Erenpreiss
Keyword(s):  
Life Expectancy ◽  
Male Infertility ◽  
Genome Instability ◽  
Repair System ◽  
Environmental Aspects ◽  
Strand Breaks ◽  
Testicular Dysfunction ◽  
Infertile Men ◽  
Dna Strand ◽  
Dynamic Mutations

Genome instability may play a role in severe cases of male infertility, with disrupted spermatogenesis being just one manifestation of decreased general health and increased morbidity. Here, we review the data on the association of male infertility with genetic, epigenetic, and environmental alterations, the causes and consequences, and the methods for assessment of genome instability. Male infertility research has provided evidence that spermatogenic defects are often not limited to testicular dysfunction. An increased incidence of urogenital disorders and several types of cancer, as well as overall reduced health (manifested by decreased life expectancy and increased morbidity) have been reported in infertile men. The pathophysiological link between decreased life expectancy and male infertility supports the notion of male infertility being a systemic rather than an isolated condition. It is driven by the accumulation of DNA strand breaks and premature cellular senescence. We have presented extensive data supporting the notion that genome instability can lead to severe male infertility termed “idiopathic oligo-astheno-teratozoospermia.” We have detailed that genome instability in men with oligo-astheno-teratozoospermia (OAT) might depend on several genetic and epigenetic factors such as chromosomal heterogeneity, aneuploidy, micronucleation, dynamic mutations, RT, PIWI/piRNA regulatory pathway, pathogenic allelic variants in repair system genes, DNA methylation, environmental aspects, and lifestyle factors.

scholarly journals Saturation of DNA Mismatch Repair and Error Catastrophe by a Base Analogue in Escherichia coli

Genetics ◽  
2002 ◽  
Vol 161 (4) ◽  
pp. 1363-1371
Author(s):  
Kazuo Negishi ◽  
David Loakes ◽  
Roel M Schaaper
Keyword(s):  
Escherichia Coli ◽  
Mismatch Repair ◽  
Dna Mismatch Repair ◽  
Repair System ◽  
Mutagenic Action ◽  
Wild Type ◽  
Dna Mismatch ◽  
Cell Counts ◽  
Error Catastrophe ◽  
Mismatch Repair System

Abstract Deoxyribosyl-dihydropyrimido[4,5-c][1,2]oxazin-7-one (dP) is a potent mutagenic deoxycytidine-derived base analogue capable of pairing with both A and G, thereby causing G · C → A · T and A · T → G · C transition mutations. We have found that the Escherichia coli DNA mismatch-repair system can protect cells against this mutagenic action. At a low dose, dP is much more mutagenic in mismatch-repair-defective mutH, mutL, and mutS strains than in a wild-type strain. At higher doses, the difference between the wild-type and the mutator strains becomes small, indicative of saturation of mismatch repair. Introduction of a plasmid containing the E. coli mutL+ gene significantly reduces dP-induced mutagenesis. Together, the results indicate that the mismatch-repair system can remove dP-induced replication errors, but that its capacity to remove dP-containing mismatches can readily be saturated. When cells are cultured at high dP concentration, mutant frequencies reach exceptionally high levels and viable cell counts are reduced. The observations are consistent with a hypothesis in which dP-induced cell killing and growth impairment result from excess mutations (error catastrophe), as previously observed spontaneously in proofreading-deficient mutD (dnaQ) strains.

scholarly journals Antagonism of Ultraviolet-Light Mutagenesis by the Methyl-Directed Mismatch-Repair System of Escherichia coli

Genetics ◽  
2000 ◽  
Vol 154 (2) ◽  
pp. 503-512 ◽  
Author(s):  
Hongbo Liu ◽  
Stephen R Hewitt ◽  
John B Hays
Keyword(s):  
Escherichia Coli ◽  
Mismatch Repair ◽  
Excision Repair ◽  
Spontaneous Mutation ◽  
Repair System ◽  
Uv Mutagenesis ◽  
Repair Protein ◽  
Mismatch Repair System

Abstract Previous studies have demonstrated that the Escherichia coli MutHLS mismatch-repair system can process UV-irradiated DNA in vivo and that the human MSH2·MSH6 mismatch-repair protein binds more strongly in vitro to photoproduct/base mismatches than to “matched” photoproducts in DNA. We tested the hypothesis that mismatch repair directed against incorrect bases opposite photoproducts might reduce UV mutagenesis, using two alleles at E. coli lacZ codon 461, which revert, respectively, via CCC → CTC and CTT → CTC transitions. F′ lacZ targets were mated from mut+ donors into mutH, mutL, or mutS recipients, once cells were at substantial densities, to minimize spontaneous mutation prior to irradiation. In umu+ mut+ recipients, a range of UV fluences induced lac+ revertant frequencies of 4–25 × 10−8; these frequencies were consistently 2-fold higher in mutH, mutL, or mutS recipients. Since this effect on mutation frequency was unaltered by an Mfd− defect, it appears not to involve transcription-coupled excision repair. In mut+ umuC122::Tn5 bacteria, UV mutagenesis (at 60 J/m2) was very low, but mutH or mutL or mutS mutations increased reversion of both lacZ alleles roughly 25-fold, to 5–10 × 10−8. Thus, at UV doses too low to induce SOS functions, such as Umu2′D, most incorrect bases opposite occasional photoproducts may be removed by mismatch repair, whereas in heavily irradiated (SOS-induced) cells, mismatch repair may only correct some photoproduct/base mismatches, so UV mutagenesis remains substantial.

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