88 research outputs found

    Effect of atherothrombotic aorta on outcomes of total aortic arch replacement

    Get PDF
    ObjectiveThe effect of an atherothrombotic aorta on the short- and long-term outcomes of total aortic arch replacement, including postoperative neurologic deficits, remains unknown. We evaluated this relationship and also elucidated the synergistic effect of multiple other risk factors, in addition to an atherothrombotic aorta, on the neurologic outcome.MethodsA group of 179 consecutive patients undergoing total aortic arch replacement were studied. An atherothrombotic aorta was present in 34 patients (19%), more than moderate leukoaraiosis in 71 (39.7%), and significant extracranial carotid artery stenosis in 27 (15.1%). In-hospital deaths occurred in 2 patients, 1 (2.9%) of 34 patients with and 1 (0.7%) of 145 patients without an atherothrombotic aorta (P = .26). Permanent neurologic deficits occurred in 4 (2.2%) and transient neurologic deficits in 17 (9.5%) patients. Multivariate analysis demonstrated that the risk factors for transient neurologic deficits were an atherothrombotic aorta (odds ratio, 4.4), extracranial carotid artery stenosis (odds ratio, 5.5), moderate/severe leukoaraiosis (odds ratio, 3.6), and cardiopulmonary bypass time (odds ratio, 1.02). To calculate the probability of transient neurologic deficits, the following equation was derived: probability of transient neurologic deficits = {1 + exp [7.276 − 1.489 (atherothrombotic aorta) − 1.285 (leukoaraiosis) − 1.701 (extracranial carotid artery stenosis) − 0.017 (cardiopulmonary bypass time)]}−1. An exponential increase occurred in the probability of transient neurologic deficits with presence of an atherothrombotic aorta and other risk factors in relation to the cardiopulmonary bypass time. Survival at 3 years after surgery was significantly reduced in patients with vs without an atherothrombotic aorta (75.0% ± 8.8% vs 89.2% ± 3.1%, P = .01).ConclusionsPatients with an atherothrombotic aorta and associated preoperative comorbidities might be predisposed to adverse short- and long-term outcomes, including transient neurologic deficits

    Early patency rate and fate of reattached intercostal arteries after repair of thoracoabdominal aortic aneurysms

    Get PDF
    ObjectivesThe present study analyzes the early patency of intercostal artery reconstruction, using graft interposition and aortic patch anastomosis, and determines the fate of reattached intercostal arteries after repair of thoracoabdominal aortic aneurysms.MethodsWe selected 115 patients (mean age, 63 ± 15 years; range, 19-83 years; male, n = 83) treated by thoracoabdominal aortic aneurysm repair with 1 or more reconstructed intercostal arteries at the Kobe University Graduate School of Medicine between October 1999 and December 2012. The intercostal arteries were reconstructed using graft interposition (n = 66), aortic patch anastomosis (n = 42), or both (n = 7).ResultsThe hospital mortality rate was 7.8% (n = 9). Eleven patients (9.6%) developed spinal cord ischemic injury (permanent, n = 6, transient, n = 5). The average number of reconstructed intercostal arteries per patient was 3.0 ± 1.5 (1-7), and 345 intercostal arteries were reattached. The overall patency rate was 74.2% (256/345) and that of aortic patch anastomosis was significantly better than that of graft interposition (90.8% [109/120] vs 65.3% [147/225], P < .01), but significantly worse for patients with than without spinal cord ischemic injury (51.9% [14/27] vs 76.1% [242/318], P = .01). There was no patch aneurysm in graft interposition during a mean of 49 ± 38 (range, 2-147) postoperative months, but aortic patch anastomosis including 4 intercostal arteries became dilated in 2 patients.ConclusionsAortic patch anastomosis might offer better patency rates and prevent spinal cord ischemic injury compared with graft interposition. Although aneurysmal changes in intercostal artery reconstructions are rare, large blocks of aortic wall reconstruction should be closely monitored

    Influence of Temperature on the Flower Bud Formation in Freesia

    Get PDF
    フリージアの開花誘導や,促成栽培の際よくみられる高温障害による異常花の発生に対する温度の影響を明らかにするため実験を行なった. 結果を要約すると次のとおりであった. 1.‘ラインベルトゴールデンイエロー’の球茎を25℃の湿潤状態で発芽時まで貯蔵した. この発芽した植物体を15℃に0,1,3,5,7週間おいたのち再び25℃条件で栽培を続けた. これらのうち花芽分化をしたのは3週間以上処理した区であり,開花に至ったのは5週間以上処理した区であった. しかし,花茎も正常に伸長したのは7週間処理区だけであった. 2.8℃で40日間冷蔵した球茎を15℃の湿潤状態に0,2,4,6,8,10,12,14日間おいて発芽処理をした. これらの異なった発芽ステージにある植物体を30℃に1週間おいて高温処理したのち温室で栽培を続けた. 結果として開花時に高温障害による異常花序(花下がり)が発生した. 異常花序の発生頻度は遅く処理した区で高く,第1小花と第2小花の間隔は早期に処理した区において大きかった. 3.高温の影響を受けた若い花序を検鏡すると,第1小花は正常に発達中であるにもかかわらず,花茎の伸長が強く抑圧されたり,あるいは上位にある小花の原基が側枝に転換している状態が観察された

    Modest antiviral activity of Toll-like receptor 3 (TLR3) against

    Get PDF
    Human respiratory syncytial virus (RSV) is the leading cause of acute lower respiratory infections in infants and Toll-like receptors (TLRs) are the first line of host defense against such infections. In this study, we aimed to elucidate the antiviral effect of TLR3 against RSV infection. The human TLR3 gene was either transiently or stably overexpressed in A549 cells and they were infected with the Long strain of RSV. In both cases, RSV production determined by plaque assay was modestly but significantly decreased in the TLR3-overexpressed cells compared with control cells. Less interferon (IFN)-β, measured by ELISA, was produced in the supernatant of the TLR3- overexpressed cells. Neutralization of IFN-β in the supernatant of the TLR3-overexpressed cells failed to increase RSV production to the same level as controls. These results indicate that TLR3 has modest anti-RSV activity and IFN-β seems not to be a significant mediator of this activity

    Infrequent RAS mutation is not associated with specific histological phenotype in gliomas

    Get PDF
    BACKGROUND: Mutations in driver genes such as IDH and BRAF have been identified in gliomas. Meanwhile, dysregulations in the p53, RB1, and MAPK and/or PI3K pathways are involved in the molecular pathogenesis of glioblastoma. RAS family genes activate MAPK through activation of RAF and PI3K to promote cell proliferation. RAS mutations are a well-known driver of mutation in many types of cancers, but knowledge of their significance for glioma is insufficient. The purpose of this study was to reveal the frequency and the clinical phenotype of RAS mutant in gliomas. METHODS: This study analysed RAS mutations and their clinical significance in 242 gliomas that were stored as unfixed or cryopreserved specimens removed at Kyoto University and Osaka National Hospital between May 2006 and October 2017. The hot spots mutation of IDH1/2, H3F3A, HIST1H3B, and TERT promoter and exon 2 and exon 3 of KRAS, HRAS, and NRAS were analysed with Sanger sequencing method, and 1p/19q codeletion was analysed with multiplex ligation-dependent probe amplification. DNA methylation array was performed in some RAS mutant tumours to improve accuracy of diagnosis. RESULTS: RAS mutations were identified in four gliomas with three KRAS mutations and one NRAS mutation in one anaplastic oligodendroglioma, two anaplastic astrocytomas (IDH wild-type in each), and one ganglioglioma. RAS-mutant gliomas were identified with various types of glioma histology. CONCLUSION: RAS mutation appears infrequent, and it is not associated with any specific histological phenotype of glioma

    Current Performance and On-Going Improvements of the 8.2 m Subaru Telescope

    Full text link
    An overview of the current status of the 8.2 m Subaru Telescope constructed and operated at Mauna Kea, Hawaii, by the National Astronomical Observatory of Japan is presented. The basic design concept and the verified performance of the telescope system are described. Also given are the status of the instrument package offered to the astronomical community, the status of operation, and some of the future plans. The status of the telescope reported in a number of SPIE papers as of the summer of 2002 are incorporated with some updates included as of 2004 February. However, readers are encouraged to check the most updated status of the telescope through the home page, http://subarutelescope.org/index.html, and/or the direct contact with the observatory staff.Comment: 18 pages (17 pages in published version), 29 figures (GIF format), This is the version before the galley proo
    corecore