A 79 year-old woman was given a diagnosis of acute myocardial infarction and was immediately transferred to our hospital by a helicopter. Cardiologists successfully revascularized the occluded left anterior descending artery which was considered to be the care of this case. After that, they detected a large ventricular septal perforation by transthoracic echocardiography. We performed repair of the ventricular septal perforation 4 days later, with a modified infarct exclusion technique. Residual shunt flow was not seen by echocardiography after the operation. This patient recovered uneventfully and was discharged on postoperative day 55.

Objectives: Human T cell leukemia virus type-I (HTLV-I) is a causative agent of human T-cell leukemia and HTLV-I associated myelopathy (HAM/TSP). HTLV-I carriers are often infected vertically, especially via mother's milk. Since 1985, clinical measures have been adopted at a hospital in Okinawa to prevent vertical infections.
Methods: We examined HTLV-I antibodies in all of the women (total 11, 506) who gave birth after 24 gestational weeks at a hospital on the Okinawa main island from January 1985 to December 1999.
Results: The positive rate among all pregnant women was always higher than that among primipara alone. Both figures decreased over the period studied, but the primiparity rate (36-39%) did not change significantly. The percentage of HTLV-I positive primipara pregnant women among the HTLV-I positive total was close to the primiparity rate from 1985 to 1988, but it was considerably lower than the overall primiparity rate thereafter (22-26%).
Conclusions: Preventive measures against HTLV-I infection did not contribute to the decrease in HTLV-I positive mothers before 1999 because these measures were adopted from 1985, and so there must be other reasons for the decrease in HTLV-I positive rate. Further studies on social factors and by year of birth are needed to identify factors influencing HTLV-carrier ratios among pregnant women.

A 72-year-old woman underwent a double aortic valve replacement with the Freestyle aortic bioprosthesis and subcoronary implantation with the Mosaic mitral bioprosthesis because of rheumatic multivalvular heart disease in 2000. During her annual follow-up, her Sinotubular junction was observed to have gradually increased in diameter on echocardiography and computed tomography. Therefore, 9 years after surgery we performed a reoperation for severe aortic regurgitation. Intraoperatively, the stentless bioprosthesis was found to be structurally intact. We believe that the dilation of the Sinotubular junction associated with a stentless bioprosthesis in the subcoronary position have caused her severe aortic regurgitation.

A 78-year-old woman underwent mitral valve replacement (MVR) with bioprosthesis in 1984. By 1997 the valve had become dysfunctional and was replaced with a Mosaic valve. Dyspnea on exertion occurred in 2005 and a systolic murmur was detected at that time. Echocardiography revealed severe mitral regurgitation (MR). The mitral valve was replaced for the third time. The explanted valve showed commissural dehiscence at the stent position and calcified leaflets. The mitral valve of a 70-year-old man was replaced with a bioprosthesis in 1986, and again with a Mosaic valve in 1997 because the original bioprosthesis had become dysfunctional. Seven years later, a systolic murmur appeared and echocardiography revealed severe MR. The valve was replaced for the third time. A leaflet tear was found in the removed valve. The Mosaic valve is a third generation porcine bioprosthesis that reportedly has excellent long-term durability. However, in these cases, the Mosaic valves deteriorated prematurely, and no obvious causes of this early structural deterioration could be identified. Continued long-term follow up is necessary, and the possibility of premature deterioration should be considered when selecting bioprostheses.

Vasculo-Behçet disease (VBD) is a special type of Behçet disease (BD) involving some vascular disorders like aneurysmal formation, arterial occlusion, and venous thrombosis in various vessels. VBD has a poor prognosis due to aneurysmal rupture or recurrence of vascular disorders despite optimal treatment. However, definite diagnosis in BD is made on the basis of clinical features, and early diagnosis is difficult. We report 2 patients whose first clinical symptoms were femoral-pseudoaneurysms. They received a diagnosis of VBD after surgery. The first patient was a 69-year-old man, who underwent autologous-vein patch closure of a perforated region in the left femoral artery. One year later, he had a pseudoaneurysm of the right profunda femoris artery, which was ligated. The second patient was a 51-year-old man, who underwent the interposition of the saphenous vein for defective artery due to left superficial femoral-pseudoaneurysm.

We encountered a rare case of a 75-year-old woman who fell into right ventricular failure and shock with a comparatively rapid course due to a huge primary right atrial angiosarcoma occupying the right atrium. An emergency surgical excision of the tumor was performed and the right atrium was reconstructed with an EPTFE patch under cardiopulmonary bypass. On account of the positive margin, postoperative radiotherapy was added. There was no local recurrence, but adjuvant chemotherapy was performed for multiple lung and liver metastases 14 months after surgery. Primary cardiac angiosarcomas are extremely rare and have dismal prognoses. Although a complete surgical resection is the cornerstone of treatment, multidisciplinary therapy may improve patient outcomes.

OBJECTIVESEpidemiological studies have suggested that exposure to environmental and occupational electromagnetic fields (EMFs) contribute to the induction of brain tumors, leukemia, and other neoplasms. The aim of this study was to investigate the genotoxic effects of exposure to 50-Hz EMFs. and of co-exposure to cisplatin, a mutagen and carcinogen, and 50-Hz EMFs, using an in vivo newborn rat astrocyte micronucleus assay.

METHODSThree day-old male Sprague-Dawley rats were co-exposed to 50-Hz EMFs and 1.25 or 2.5 mg/kg of cisplatin. Brain cells were dissociated into single cells and cultured for 96 hours, then stained with acridine orange and an antibody against glial fibrillary acidic protein. The frequency of micronucleated astrocytes was counted with a fluorescent microscope.

RESULTSThe frequency of micronuclei was not increased in rat astrocytes exposed to EMFs alone. However, the frequencies of micronuclei in co-exposure to 2.5 mg/kg cisplatin and EMFs (7.5- and 10-mT) were significantly increased, compared with those in exposure to 2.5 mg/kg cisplatin alone (sham-exposure, 0-mT EMFs) for 72 hours (p<0.01).

CONCLUSIONExposure to EMFs alone did not have a genotoxic effect but co-exposure to EMFs increased the genotoxic activity induced by cisplatin. Our findings suggest that EMFs enhance the genotoxic effects of cisplatin.

OBJECTIVESAn increase in incidence of the illegal use of tablets containing 3,4-methylenedioxymethamphetamine hydrochloride (MDMA) has recently become a widespread social problem. MDMA ingested orally reacts with nitrite in the stomach and is synthesized intoN-nitroso-3,4-methylenedioxymethamphetamine (N-MDMA). The aim of this study is to investigate the genotoxic effects of MDMA and N-MDMA on the basis of the results of an in vitro micronucleus (MN) test and an in vitro chromosomal aberration (CA) test using a Chinese hamster lung fibroblast cell line (CHL/IU).

METHODSTablets containing MDMA obtained from the Regional Bureau of the Ministry of Health, Labor and Welfare were purified, and N-MDMA was synthesized from MDMA in our laboratory. To evaluate the effects of MDMA and N-MDMA, the MN test established by our laboratory and the CA test in accordance with the guidelines for toxicity studies of drugs recommended by the Ministry of Health, Labor and Welfare were performed.

RESULTSIn the MN test, no increased frequency of MNs was not found for MDMA. On the other hand, an apparently increased frequency of MNs was observed for N-MDMA. In the CA test, no CA was found for MDMA, but CA was observed for N-MDMA apparently.

CONCLUSIONN-MDMA genotoxicity was observed in the MN and CA tests. However, no MDMA genotoxicity was observed.

OBJECTIVESIt is important to assess the risk of static magnetic fields (SMFs) on human health, because epidemiological studies have indicated that SMFs play a role in the development of diseases such as leukemia and brain tumor. In our environment, we have numerous chances to be exposed to not only SMFs but also many chemicals containing mutagens. The aim of this study is to investigate the effect of SMFs on the induction of micronuclei induced by some mutagens.

METHODSBALB/c mice were exposed to 4.7 tesla (T) SMF for 24 hr immediately after the injection of carboquone (alkylating agent), colcemid (spindle poison), mitomycin C (cross-linking agent), vincristine (spindle poison), sodium fluoride (a byproduct of aluminum plants under strong SMF) or 1-ethyl-1-nitrosourea (brain tumor-, gliomas- and thymic lymphoma-inducing chemical).

RESULTSThe frequency of micronuclei induced by six mutagens increased after co-exposure to SMF.

CONCLUSIONSAn additive/synergistic effect of SMF and chemicals was observed from the results of increased frequency of micronuclei induced by mutagens in mouse bone marrow erythrocytes.

OBJECTIVESKetamine hydrochloride (KT) is a secondary amine that has been safely used as an injectable anesthetic and analgesic to avoid the production of nitroso compounds in the stomach. However, ketamine in the tablet form has recently become an abused, recreational drug. The aim of this study was to investigate the genotoxic effects of N-nitrosoketamine (NKT) and KT on the basis of an in vitro micronucleus (MN) test using a Chinese hamster lung fibroblast cell line (CHL/IU).

METHODSNKT was synthesized from KT in our laboratory. In the MN tests, CHL/IU cells were continuously treated with either NKT or KT for 24, 48, or 72 hours without the S9 mix. The cells were also treated with NKT or KT with or without the S9 mix for 6 hours, followed by a recovery period of 18, 42, or 66 hours (short-term treatment). The results were considered to be statistically significant when the p-values of both Fisher's exact test and the trend test were less than 0.05.

RESULTSAfter the short-term treatment with either NKT or KT with and without the S9 mix, the frequency of micronuclei significantly increased. However, the frequency of micronuclei did not significantly increase after the continuous treatment with either NKT or KT. Both NKT and KT were determined to be genotoxic in the short-term treatment with or without the S9 mix, but they were determined to be nongenotoxic in continuous treatment.

CONCLUSIONOur findings suggest that NKT has a stronger genotoxic effect than KT.