[Mitral valve replacement after previous coronary artery bypass grafting with functioning left internal thoracic artery graft: effectiveness of the method using a direct vision retrosternal approach; report of a case].

Performing a redo-sternotomy when a mammary artery graft is patent can be rather difficult. We previously reported a redo-sternotomy technique involving direct visualization with a retrosternal dissection (DR) method using a Kent's retractor. The DR method in detail is as follows: 1) A midline skin incision is extended to the abdomen about 5 cm. 2) The bilateral costal arches are divided from the rectal muscle. 3). A pair of retractors is placed under the costal arch. 4) A stainless steel wire is applied to the previous sternal wire at the center of the sternum. 5) The retractor and sternal wire are lifted up using the Kent's retractor to widen the retrosternal space. 6) The sternum and sub-sternal tissue are carefully divided using an electronic scalpel or metal retractor with an entirely sternal length. 7) Routine sternotomy is performed using a Stryker. Herein, we report a patient who had undergone cardiac surgery, coronary artery bypass grafting (CABG), using a left internal mammary artery and mitral annuloplasty 2 years previously, and then developed mitral regurgitation caused by infectious endocarditis. He successfully underwent redo-sternotomy and mitral valve replacement using the DR method. In a patient with a patent internal mammary artery, the DR method greatly reduces the risk of graft injury.

[Usefulness of the axillary artery perfusion in open heart surgery in a patient with severe ascending aortic calcification].

Because of high-aging Japanese society, high-risk patients with multiple co-morbidities have been increasing in regular open-heart surgery. Especially, extensive aortic atherosclerosis with severe calcification that involves the ascending aorta can complicate the choice of sites of cannulations and aortic cross-clamping for cardiopulmonary bypass. To date, the standard peripheral arterial cannulation site in such cases has been the common femoral artery;however, this approach carries the risk of atheroembolism due to retrograde aortic perfusion, or it is undesirable in case of severe iliofemoral disease. Recently, it has been reported that arterial perfusion through the axillary artery provides sufficient antegrade aortic flow associated with fewer atheroembolic complications. In this paper, we report 3 successful cases of valvular surgeries in which axillary artery cannulation was used to avoid complications of brain. In cases of extensive aortic atherosclerosis with severe calcification, arterial perfusion through the axillary artery is a safe and effective method to provide sufficient arterial inflow during cardiopulmonary bypass, and is an excellent alternative to femoral artery cannulation.

The ATR-Chk1 pathway plays a role in the generation of centrosome aberrations induced by Rad51C dysfunction.

Rad51C is a central component of two complexes formed by five Rad51 paralogs in vertebrates. These complexes are involved in repairing DNA double-strand breaks through homologous recombination. Despite accumulating evidence suggesting that the paralogs may prevent aneuploidy by controlling centrosome integrity, Rad51C's role in maintaining chromosome stability remains unclear. Here we demonstrate that Rad51C deficiency leads to both centrosome aberrations in an ATR-Chk1-dependent manner and increased aneuploidy in human cells. While it was reported that Rad51C deficiency did not cause centrosome aberrations in interphase in hamster cells, such aberrations were observed in interphase in HCT116 cells with Rad51C dysfunction. Caffeine treatment and down-regulation of ATR, but not that of ATM, reduced the frequency of centrosome aberrations in the mutant cells. Silencing of Rad51C by RNA interference in HT1080 cells resulted in similar aberrations. Treatment with a Chk1 inhibitor and silencing of Chk1 also reduced the frequency in HCT116 mutants. Accumulation of Chk1 at the centrosome and nuclear foci of gamma H2AX were increased in the mutants. Moreover, the mutant cells had a higher frequency of aneuploidy. These findings indicate that the ATR-Chk1 pathway plays a role in increased centrosome aberrations induced by Rad51C dysfunction.

Haploinsufficiency of RAD51B causes centrosome fragmentation and aneuploidy in human cells.

The Rad51-like proteins, Rad51B, Rad51C, Rad51D, XRCC2, and XRCC3, have been shown to form two distinct complexes and seem to assist Rad51 in the early stages of homologous recombination. Although these proteins share sequence similarity with Rad51, they do not show functional redundancy. Among them, Rad51B is unique in that the gene maps to the human chromosome 14q23-24, the region frequently involved in balanced chromosome translocations in benign tumors particularly in uterine leiomyomas. Despite accumulating descriptive evidence of altered Rad51B function in these tumors, the biological significance of this aberration is still unknown. To assess the significance of reduced Rad51B function, we deleted the gene in the human colon cancer cell line HCT116 by gene targeting. Here, we show that haploinsufficiency of RAD51B causes mild hypersensitivity to DNA-damaging agents, a mild reduction in sister chromatid exchange, impaired Rad51 focus formation, and an increase in chromosome aberrations. Remarkably, haploinsufficiency of RAD51B leads to centrosome fragmentation and aneuploidy. In addition, an approximately 50% reduction in RAD51B mRNA levels by RNA interference also leads to centrosome fragmentation in the human fibrosarcoma cell line HT1080. These findings suggest that the proper biallelic expression of RAD51B is required for the maintenance of chromosome integrity in human cells.