Active cycle of breathing technique may reduce pulmonary complications after esophagectomy: A randomized clinical trial.

BACKGROUND: The purpose of the study was to determine whether the active cycle of breathing technique (ACBT) has an impact on postoperative pulmonary complication (PPC) after esophagectomy. METHODS: In this prospective randomized trial, patients who were candidates for esophagectomy were randomized into groups, wherein they received either ACBT (n = 146) or conventional chest physiotherapy (control group, n = 145) on postoperative days (POD) 1-3. The primary outcome was PPC. The secondary outcomes included the incidence of anastomotic leakage (AL), efficacy of airway clearance, and postoperative hospital length of stay (LOS). RESULTS: After esophagectomy, the PPC rate was significantly lower in the ACBT group (15.2%) than in the control group (31.0%) (p = 0.001). The incidences of AL were 5.5% and 12.4% in the ACBT and control groups, respectively (p = 0.042). Mean hospital LOS was 12.3 days for the ACBT group and 16.8 days for the control group (p = 0.008). ACBT significantly increased the mean sputum wet weight (g) on POD 1-3 when compared with conventional therapy (POD 1 9.08 vs. 6.47, POD 2 16.86 vs. 10.92, POD 3 24.65 vs. 13.52, all p < 0.001). Multivariable analysis revealed that ACBT decreased the rates of PPC (odds ratio [OR] 0.403, p = 0.003), AL (OR 0.379，p = 0.038)，arrhythmia (OR 0.397, p = 0.028), and bronchoscopy aspiration (OR 0.362, p = 0.016). CONCLUSION: ACBT is an effective airway clearance technique that significantly reduces the incidence of PPC after esophagectomy. ACBT could also significantly reduce both AL and LOS.

Reactive oxygen species burst induced by aluminum stress triggers mitochondria-dependent programmed cell death in peanut root tip cells.

Recent studies had certified that aluminum (Al) induced ROS production and programmed cell death (PCD) in higher plants. The relationship between ROS production and PCD occurrence under Al stress is uncovered. The results showed that root elongation inhibition and PCD occurrence was induced by 100 µM AlCl3. Al stress induced ROS burst, up-regulated Rboh and COX gene expression, increased mitochondrial permeability transition pore (MPTP) opening, decreased inner mitochondrial membrane potential (ΔΨm), released cytochrome c from mitochondria to cytoplasm, activated caspase 3-like protease activity. Exogenous H2O2 aggravated the changes caused by Al and accelerated PCD occurrence, but ROS scavenger CAT and AsA reversed the changes caused by Al and inhibited PCD production. A potential cascade of cellular events during Al induced PCD via mitochondria dependent pathway and the mechanism of ROS on regulating PCD induced by Al is proposed.

Mitochondrial alterations during Al-induced PCD in peanut root tips.

Previous study found there was a negative relationship between Al-induced PCD and Al-resistance in peanut. The present research was undertaken to verify whether mitochondria play a significant role in PCD induced by Al in peanut. The roots of Al-tolerant plants were found to exhibit more intensive root growth, while accumulating less Al³âº than Al-sensitive plants under Al treatment. The different enhancement of ROS production was observed in the mitochondria isolated from two peanut cultivars. The concentration of mitochondrial MDA in root tips increased after Al treatment, which was higher in Zhonghua 2 than in 99-1507. With the increase of Al concentration, mitochondrial Ca²âº concentration decreased, and Ca²âº concentration of Zhonghua 2 decreased faster than that of 99-1507. The opening of mitochondrial permeability transition pore was more extensively in mitochondria isolated from Zhonghua 2 than from 99-1507. The collapse of inner mitochondrial membrane potential (ΔΨm) was also observed with a release of Cytochrome c (Cyt c) from mitochondria, it was more obvious in Zhonghua 2 than in 99-1507 with Al concentration increasing. The results showed that mitochondrial membrane structure and function were damaged seriously in Al-induced PCD, the increase of mitochondrial antioxidant system activity decreased cellular damages under Al stress. To sum up, compared with Al-sensitive peanut cultivar, Al-tolerant peanut cultivar has less Al³âº absorption, mitochondrial ROS and membrane lipid peroxidation level, higher control of MPT opening, ΔΨm maintaining, Cty c release from mitochondria and mitochondrial respiratory functions so that it is not easy to produce PCD under Al stress.

Aluminum induces rapidly mitochondria-dependent programmed cell death in Al-sensitive peanut root tips.

BACKGROUND: Although many studies suggested that aluminum (Al) induced programmed cell death (PCD) in plants, the mechanism of Al-induced PCD and its effects in Al tolerance is limited. This study was to investigate the mechanism and type of Al induced PCD and the relationship between PCD and Al tolerance. RESULTS: In this study, two genotypes of peanut 99-1507 (Al tolerant) and ZH2 (Al sensitive) were used to investigate Al-induced PCD. Peanut root growth inhibition induced by AlCl3 was concentration and time-dependent in two peanut varieties. AlCl3 at 100 µM could induce rapidly peanut root tip PCD involved in DNA cleavage, typical apoptotic chromatin condensation staining with DAPI, apoptosis related gene Hrs203j expression and cytochrome C (Cyt c) release from mitochondria to cytosol. Caspase3-like protease was activated by Al; it was higher in ZH2 than in 99-1507. Al increased the opening of mitochondrial permeability transition pore (MPTP), decreased inner membrane potential (ΔΨm) of mitochondria. Compared with the control, Al stress increased O2•- and H2O2 production in mitochondria. Reactive oxygen species (ROS) burst was produced at Al treatment for 4 h. CONCLUSIONS: Al-induced PCD is earlier and faster in Al-sensitive peanut cultivar than in Al-tolerant cultivar. There is a negative relationship between PCD and Al resistance. Mitochondria- dependence PCD was induced by Al and ROS was involved in this process. The mechanism can be explained by the model of acceleration of senescence under Al stress.

Aluminum-induced programmed cell death promoted by AhSAG, a senescence-associated gene in Arachis hypoganea L.

Programmed cell death (PCD) is a foundational cellular process in plant development and elimination of damaged cells under environmental stresses. In this study, Al induced PCD in two peanut (Arachis hypoganea L.) cultivars Zhonghua 2 (Al-sensitive) and 99-1507 (Al-tolerant) using DNA ladder, TUNEL detection and electron microscopy. The concentration of Al-induced PCD was lower in Zhonghua 2 than in 99-1507. AhSAG, a senescence-associated gene was isolated from cDNA library of Al-stressed peanut with PCD. Open reading frame (ORF) of AhSAG was 474bp, encoding a SAG protein composed of 157 amino acids. Compared to the control and the antisense transgenic tobacco plants, the fast development and blossom of the sense transgenic plants happened to promote senescence. The ability of Al tolerance in sense transgenic tobacco was lower than in antisense transgenic tobacco according to root elongation and Al content analysis. The expression of AhSAG-GFP was higher in sense transgenic tobacco than in antisense transgenic tobacco. Altogether, these results indicated that there was a negative relationship between Al-induced PCD and Al-resistance in peanut, and the AhSAG could induce or promote the occurrence of PCD in plants.