BRASSICA NAPUSヒンシュ TOPAS ニ オケル レンゾクテキハイケイセイ オヨビ ニジハイ カラ ノ ショクブツタイサイセイケイ

Brassica napus品種`Topas\u27における連続的な二次胚形成及び植物体再生系の確立を試みた。熱ショックによって未熟種子胚より誘導した二次胚を,植物成長調節物質無添加のB5培地へ継代した。培養後70%の二次胚において,徒長した胚軸の表面に次代の二次胚が直接形成された。これら二次胚を同様に継代培養した結果,約70%の胚より新たな二次胚が形成され,次胚形成能が継代培養を通じて維持されていたことが示された。二次胚に10μMアブシジン酸(ABA)処理をした結果,胚は乾燥耐性を獲得し,60%の二次胚が乾燥後においても生育しその全てが正常に再生した。一方,ABA処理後,乾燥処理を行わなかった胚は胚軸が徒長する異常な生育を示し,ABA無処理胚は乾燥処理によって全て枯死した。A method for continuous secondary embryo formation and plant regeneration in Brassica napus cv. `Topas\u27 is described. Secondary embryos that emerged from immature zygotic embryos via heat shock were separated and subcultured onto B5 plant growth regulator-free medium. Most secondary embryos (i.e. 70%) produced secondary embryos in a subsequent generation directly on the surface of elongated hypocotyls. Similarly, about 70% of the secondary embryos formed newly produced secondary embryos in a subsequent generation after subculturing, and the embryogenic potential of these secondary embryos has been maintained by repetitive subculture. The application of 10μM abscisic acid (ABA) induced desiccation tolerance in secondary embryos. Consequently, 60% of the desiccated embryos grew, all of which regenerated into normal plants. On the other hand, ABA-treated secondary embryos without desiccation treatment grew abnormally having an elongated hypocotyl, and all secondary embryos not treated with ABA lost their viability after desiccation

Insufficient autophagy promotes bronchial epithelial cell senescence in chronic obstructive pulmonary disease.

Tobacco smoke-induced accelerated cell senescence has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cell senescence is accompanied by the accumulation of damaged cellular components suggesting that in COPD, inhibition of autophagy may contribute to cell senescence. Here we look at whether autophagy contributes to cigarette smoke extract (CSE) - induced cell senescence of primary human bronchial epithelial cells (HBEC), and further evaluate p62 and ubiquitinated protein levels in lung homogenates from COPD patients. We demonstrate that CSE transiently induces activation of autophagy in HBEC, followed by accelerated cell senescence and concomitant accumulation of p62 and ubiquitinated proteins. Autophagy inhibition further enhanced accumulations of p62 and ubiquitinated proteins, resulting in increased senescence and senescence-associated secretory phenotype (SASP) with interleukin (IL)-8 secretion. Conversely, autophagy activation by Torin1, a mammalian target of rapamycin (mTOR inhibitor), suppressed accumulations of p62 and ubiquitinated proteins and inhibits cell senescence. Despite increased baseline activity, autophagy induction in response to CSE was significantly decreased in HBEC from COPD patients. Increased accumulations of p62 and ubiquitinated proteins were detected in lung homogenates from COPD patients. Insufficient autophagic clearance of damaged proteins, including ubiquitinated proteins, is involved in accelerated cell senescence in COPD, suggesting a novel protective role for autophagy in the tobacco smoke-induced senescence-associated lung disease, COPD

Insufficient autophagy promotes bronchial epithelial cell senescence in chronic obstructive pulmonary disease

Tobacco smoke-induced accelerated cell senescence has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cell senescence is accompanied by the accumulation of damaged cellular components suggesting that in COPD, inhibition of autophagy may contribute to cell senescence. Here we look at whether autophagy contributes to cigarette smoke extract (CSE) - induced cell senescence of primary human bronchial epithelial cells (HBEC), and further evaluate p62 and ubiquitinated protein levels in lung homogenates from COPD patients. We demonstrate that CSE transiently induces activation of autophagy in HBEC, followed by accelerated cell senescence and concomitant accumulation of p62 and ubiquitinated proteins. Autophagy inhibition further enhanced accumulations of p62 and ubiquitinated proteins, resulting in increased senescence and senescence-associated secretory phenotype (SASP) with interleukin (IL)-8 secretion. Conversely, autophagy activation by Torin1, a mammalian target of rapamycin (mTOR inhibitor), suppressed accumulations of p62 and ubiquitinated proteins and inhibits cell senescence. Despite increased baseline activity, autophagy induction in response to CSE was significantly decreased in HBEC from COPD patients. Increased accumulations of p62 and ubiquitinated proteins were detected in lung homogenates from COPD patients. Insufficient autophagic clearance of damaged proteins, including ubiquitinated proteins, is involved in accelerated cell senescence in COPD, suggesting a novel protective role for autophagy in the tobacco smoke-induced senescence-associated lung disease, COPD

Risk factors of postoperative pulmonary complications in patients with asthma and COPD

Abstract Background Postoperative pulmonary complications (PPC) in patients with pulmonary diseases remain to be resolved clinical issue. However, most evidence regarding PPC has been established more than 10 years ago. Therefore, it is necessary to evaluate perioperative management using new inhalant drugs in patients with obstructive pulmonary diseases. Methods April 2014 through March 2015, 346 adult patients with pulmonary diseases (257 asthma, 89 chronic obstructive pulmonary disease (COPD)) underwent non-pulmonary surgery except cataract surgery in our university hospital. To analyze the risk factors for PPC, we retrospectively evaluated physiological backgrounds, surgical factors and perioperative specific treatment for asthma and COPD. Results Finally, 29 patients with pulmonary diseases (22 asthma, 7 COPD) had PPC. In patients with asthma, smoking index (≥ 20 pack-years), peripheral blood eosinophil count (≥ 200/mm3) and severity (Global INitiative for Asthma(GINA) STEP ≥ 3) were significantly associated with PPC in the multivariate logistic regression analysis [odds ratio (95% confidence interval) = 5.4(1.4–20.8), 0.31 (0.11–0.84) and 3.2 (1.04–9.9), respectively]. In patients with COPD, age, introducing treatment for COPD, upper abdominal surgery and operation time (≥ 5 h) were significantly associated with PPC [1.18 (1.00–1.40), 0.09 (0.01–0.81), 21.2 (1.3–349) and 9.5 (1.2–77.4), respectively]. Conclusions History of smoking or severe asthma is a risk factor of PPC in patients with asthma, and age, upper abdominal surgery, or long operation time is a risk factor of PPC in patients with COPD. Adequate inhaled corticosteroids treatment in patients with eosinophilic asthma and introducing treatment for COPD in patients with COPD could reduce PPCs