排序方式: 共有12条查询结果,搜索用时 31 毫秒
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Kseniya Khamina Andreas B. Diendorfer Susanna Skalicky Moritz Weigl Marianne Pultar Teresa L. Krammer Catharine Aquino Fournier Amy L. Schofield Carolin Otto Aaron Thomas Smith Nina Buchtele Christian Schoergenhofer Bernd Jilma Bernhard J. H. Frank Jochen G. Hofstaetter Regina Grillari Johannes Grillari Klemens Ruprecht Christopher E. Goldring Hubert Rehrauer Warren E. Glaab Matthias Hackl 《International journal of molecular sciences》2022,23(3)
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The promise of a broadband fibre communications network has attracted the interest of CATV and Telco concerns. Various networks and topologies have been discussed. Cost is a drawback in some of the proposed networks, particularly those networks which require switching. This paper discusses a low cost broadcast tree and branch network which uses optical amplifiers to extend the network penetration. Recent work in the development of optical amplifiers suggests that the Erbium fibre amplifier may be compatible with VSB-AM. The characteristics of such an amplifier will be discussed. This scenario allows an orderly transition from the present-day AM backbone system to the tree and branch fibre architecture. Once the broadband fibre plant is in place new services can be implemented that exploit the broadband nature of fibre. 相似文献
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A Umar M Koi JI Risinger WE Glaab KR Tindall RD Kolodner CR Boland JC Barrett TA Kunkel 《Canadian Metallurgical Quarterly》1997,57(18):3949-3955
The human DNA mismatch repair genes hMSH2 and hMSH6 encode the proteins that, together, bind to mismatches to initiate repair of replication errors. Human tumor cells containing mutations in these genes have strongly elevated mutation rates in selectable genes and at microsatellite loci, although mutations in these genes cause somewhat different mutator phenotypes. These cells are also resistant to killing by certain drugs and are defective in mismatch repair. Because the elevated mutation rates in these cells may lead to mutations in additional genes that are causally related to the other defects, here we attempt to establish a cause-effect relationship between the hMSH2 and hMSH6 gene mutations and the observed phenotypes. The endometrial tumor cell line HEC59 contains mutations in both alleles of hMSH2. The colon tumor cell line HCT15 contains mutations in hMSH6 and also has a sequence change in a conserved region of the coding sequence for DNA polymerase delta, a replicative DNA polymerase. We introduced human chromosome 2 containing the wild-type hMSH2 and hMSH6 genes into HEC59 and HCT15 cells. Introduction of chromosome 2 to HEC59 cells restored microsatellite stability, sensitivity to N-methyl-N'-nitro-N-nitrosoguanidine treatment, and mismatch repair activity. Transfer of chromosome 2 to HCT15 cells also reduced the mutation rate at the HPRT locus and restored sensitivity to N-methyl-N'-nitro-N-nitrosoguanidine treatment and mismatch repair activity. The results demonstrate that the observed defects are causally related to mutations in genes on chromosome 2, probably hMSH2 or hMSH6, but are not related to sequence changes in other genes, including the gene encoding DNA polymerase delta. 相似文献
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WE Glaab JI Risinger A Umar TA Kunkel JC Barrett KR Tindall 《Canadian Metallurgical Quarterly》1998,273(41):26662-26669
The role of specific mismatch repair (MMR) gene products was examined by observing several phenotypic end points in two MMR-deficient human endometrial carcinoma cell lines that were originally isolated from the same tumor. The first cell line, HEC-1-A, contains a nonsense mutation in the hPMS2 gene, which results in premature termination and a truncated hPMS2 protein. In addition, HEC-1-A cells carry a splice mutation in the hMSH6 gene and lack wild-type hMSH6 protein. The second cell line, HEC-1-B, possesses the same defective hMSH6 locus. However, HEC-1-B cells are heterozygous at the hPMS2 locus; that is, along with carrying the same nonsense mutation in hPMS2 as in HEC-1-A, HEC-1-B cells also contain a wild-type hPMS2 gene. Initial recognition of mismatches in DNA requires either the hMSH2/hMSH6 or hMSH2/hMSH3 heterodimer, with hPMS2 functioning downstream of damage recognition. Therefore, cells defective in hPMS2 should completely lack MMR (HEC-1-A), whereas cells mutant in hMSH6 only (HEC-1-B) can potentially repair damage via the hMSH2/hMSH3 heterodimer. The data presented here in HEC-1-B cells illustrate (i) the reduction of instability at microsatellite sequences, (ii) a significant decrease in frameshift mutation rate at HPRT, and (iii) the in vitro repair of looped substrates, relative to HEC-1-A cells, illustrating the repair of frameshift intermediates by hMSH2/hMSH3 heterodimer. Furthermore, the role of hMSH2/hMSH3 heterodimer in the repair of base:base mismatches is supported by observing the reduction in base substitution mutation rate at HPRT in HEC-1-B cells (hMSH6-defective but possessing wild-type hPMS2), as compared with HEC-1-A (hMSH6/hPMS2-defective) cells. These data support a critical role for hPMS2 in human MMR, while further defining the role of the hMSH2/hMSH3 heterodimer in maintaining genomic stability in the absence of a wild-type hMSH2/hMSH6 heterodimer. 相似文献
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WE Glaab JI Risinger A Umar JC Barrett TA Kunkel KR Tindall 《Canadian Metallurgical Quarterly》1998,398(1-2):197-207
Resistance to the cytotoxic effects of S(N)1 alkylating agents such as N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and N-methyl-N-nitrosourea (MNU) is well established in mismatch repair-defective cells, however, little is known about the cellular response to S(N)2 alkylating agents in these cells. Here we describe the cytotoxic response and the mutagenic response at the hypoxanthine-guanine phosphoribosyl transferase (HPRT) locus to the S(N)2 alkylating agent methyl methanesultfonate (MMS) in human cancer cell lines defective in mismatch repair (MMR). Our findings suggest that cytotoxicity to MMS is mediated through MMR, as indicated by an increased resistance to MMS in MMR-deficient cells. Cells in which specific MMR-gene defects were complemented by chromosome transfer were generally more sensitive to the cytotoxic effects of MMS. Additionally, the induced mutant frequency at HPRT following exposure to MMS is significantly increased in MMR-deficient lines. These findings suggest that resistance to S(N)2 alkylation damage is mediated by MMR genes, and that resistance to such damage in MMR-defective cells correlates with an increase in genomic mutations. The results are consistent with the hypothesis that abasic sites may be substrates for repair involving MMR-gene products in human cells. 相似文献
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Erik Öjefors Alvydas Lisauskas Diana Glaab Hartmut G. Roskos Ullrich R. Pfeiffer 《Journal of Infrared, Millimeter and Terahertz Waves》2009,30(12):1269-1280
Square-law power detection circuits with on-chip antennas and amplifiers are presented for the detection of 0.65-THz radiation
in a low-cost 0.25-μm CMOS technology. The circuit architecture combines metal-insulator-metal (MIM) coupling capacitors with NMOS transistors
to facilitate self-mixing in a resistive mixer. A low-frequency (quasi-static) and a high-frequency (non-quasi-static) analysis
of the broad-band circuit is presented. Current and voltage readout techniques of non-amplified detectors are compared, and
exhibit a measured responsivity of 5.3 mA/W and 150 V/W respectively. A monolithic integrated 3×5 pixel focal-plane array
has been used for single-pixel and multi-pixel imaging of concealed objects at 0.65 THz. 相似文献
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Galmarini S Bianconi R Klug W Mikkelsen T Addis R Andronopoulos S Astrup P Baklanov A Bartniki J Bartzis JC Bellasio R Bompay F Buckley R Bouzom M Champion H D'Amours R Davakis E Eleveld H Geertsema GT Glaab H Kollax M Ilvonen M Manning A Pechinger U Persson C Polreich E Potemski S Prodanova M Saltbones J Slaper H Sofiev MA Syrakov D Sørensen JH Van der Auwera L Valkama I Zelazny R 《Radiation protection dosimetry》2004,109(1-2):19-24
Is atmospheric dispersion forecasting an important asset of the early-phase nuclear emergency response management? Is there a 'perfect atmospheric dispersion model'? Is there a way to make the results of dispersion models more reliable and trustworthy? While seeking to answer these questions the multi-model ensemble dispersion forecast system ENSEMBLE will be presented. 相似文献