[Efficacy of patient skin dose reduction by a compensating filter through of irradiation field overlaps on the area during percutaneous coronary intervention].

Our study was involved with entrance surface dose reduction and irradiation field by the filter use of PCI, and insertion in place of an effective compensating filter to maximize entrance surface dose reduction, which we verified. The radiation dosimetry put a 6cc ion chamber on the back side of the thorax phantom, and changed the filter of the four corners (a: upper left, b: upper right, c: lower right, d: lower left) of the monitor confirmed with fluoroscopy [(0) no filter, (1) one filter, (2) two filters]. The angle of C arm was assumed to be eight directions and 0 degrees adopted by this hospital. It was compared with a corrective rate of which one was no filter. Next, the presence of filter and irradiation field overlaps on the area in monitor in the angle of C arm was verified by this hospital's classic example. As for corrective rate, (1) becomes 0.41 and (2) become 0.25 at fluoroscopy, (1) becomes 0.26 and (2) become 0.16 at exposure. Irradiation field overlaps on the area (+) compensating filter (-) was many with d of RAO/CAU, a of RAO and c of CAU at left CAG, c of LAO at right CAG, b of LAO/CRA (left CAG), b of CRA (right CAG) and a and d of RAO (right CAG) at both CAG. Irradiation field overlaps on the area (+) compensating filter (+) was many with b of CRA at left CAG, a of LAO/CRA at right CAG, b of CRA (left CAG) and b of RAO (right CAG) at both CAG. When the compensating filter is used the entrance surface dose reduction effect was great. If automatic exposure control protects the part of irradiation field overlaps on the area in the range without operating excessively, the radiological risk can be reduced, and it is conceivable as useful clinical setting.

Genetic evidence for single-strand lesions initiating Nbs1-dependent homologous recombination in diversification of Ig v in chicken B lymphocytes.

Homologous recombination (HR) is initiated by DNA double-strand breaks (DSB). However, it remains unclear whether single-strand lesions also initiate HR in genomic DNA. Chicken B lymphocytes diversify their Immunoglobulin (Ig) V genes through HR (Ig gene conversion) and non-templated hypermutation. Both types of Ig V diversification are initiated by AID-dependent abasic-site formation. Abasic sites stall replication, resulting in the formation of single-stranded gaps. These gaps can be filled by error-prone DNA polymerases, resulting in hypermutation. However, it is unclear whether these single-strand gaps can also initiate Ig gene conversion without being first converted to DSBs. The Mre11-Rad50-Nbs1 (MRN) complex, which produces 3' single-strand overhangs, promotes the initiation of DSB-induced HR in yeast. We show that a DT40 line expressing only a truncated form of Nbs1 (Nbs1(p70)) exhibits defective HR-dependent DSB repair, and a significant reduction in the rate--though not the fidelity--of Ig gene conversion. Interestingly, this defective gene conversion was restored to wild type levels by overproduction of Escherichia coli SbcB, a 3' to 5' single-strand-specific exonuclease, without affecting DSB repair. Conversely, overexpression of chicken Exo1 increased the efficiency of DSB-induced gene-targeting more than 10-fold, with no effect on Ig gene conversion. These results suggest that Ig gene conversion may be initiated by single-strand gaps rather than by DSBs, and, like SbcB, the MRN complex in DT40 may convert AID-induced lesions into single-strand gaps suitable for triggering HR. In summary, Ig gene conversion and hypermutation may share a common substrate-single-stranded gaps. Genetic analysis of the two types of Ig V diversification in DT40 provides a unique opportunity to gain insight into the molecular mechanisms underlying the filling of gaps that arise as a consequence of replication blocks at abasic sites, by HR and error-prone polymerases.

The 9-1-1 DNA clamp is required for immunoglobulin gene conversion.

Chicken DT40 cells deficient in the 9-1-1 checkpoint clamp exhibit hypersensitivity to a variety of DNA-damaging agents. Although recent work suggests that, in addition to its role in checkpoint activation, this complex may play a role in homologous recombination and translesion synthesis, the cause of this hypersensitivity has not been studied thoroughly. The immunoglobulin locus of DT40 cells allows monitoring of homologous recombination and translesion synthesis initiated by activation-induced deaminase (AID)-dependent abasic sites. We show that both the RAD9(-/-) and RAD17(-/-) mutants exhibit substantially reduced immunoglobulin gene conversion. However, the level of nontemplated immunoglobulin point mutation increased in these mutants, a finding that is reminiscent of the phenotype resulting from the loss of RAD51 paralogs or Brca2. This suggests that the 9-1-1 complex does not play a central role in translesion synthesis in this context. Despite reduced immunoglobulin gene conversion, the RAD9(-/-) and RAD17(-/-) cells do not exhibit a prominent defect in double-strand break-induced gene conversion or a sensitivity to camptothecin. This suggests that the roles of Rad9 and Rad17 may be confined to a subset of homologous recombination reactions initiated by replication-stalling lesions rather than those associated with double-strand break repair.