874 research outputs found

    Swelling of cell walls in mature sweet cherry fruit : factors and mechanisms

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    Main conclusion: Swelling of sweet cherry cell walls is a physical process counterbalanced by turgor. Cell turgor prevents swelling in intact cells, whereas loss of turgor allows cell walls to swell. Abstract: Swelling of epidermal cell walls precedes skin failure in sweet cherry (Prunus avium) cracking. Swollen cell walls lead to diminished cell:cell adhesions. We identify the mechanism of cell wall swelling. Swelling was quantified microscopically on epidermal sections following freeze/thaw treatment or by determining swelling pressure or swelling capacity of cell wall extracts. Releasing turgor by a freeze/thaw treatment increased cell wall thickness 1.6-fold within 2 h. Pressurizing cell wall extracts at > 12 kPa prevented swelling in water, while releasing the pressure increased swelling. The effect was fully reversible. Across cultivars, cell wall thickness before and after turgor release in two subsequent seasons was significantly correlated (before release of turgor: r = 0.71**, n = 14; after release of turgor: r = 0.73**, n = 14) as was the swelling of cell walls upon turgor release (r = 0.71**, n = 14). Close relationships were also identified for cell wall thickness of fruit of the same cultivars grown in the greenhouse and the field (before release of turgor: r = 0.60, n = 10; after release of turgor: r = 0.78**, n = 10). Release of turgor by heating, plasmolysis, incubation in solvents or surfactants resulted in similar swelling (range 2.0–3.1 ”m). Cell wall swelling increased from 1.4 to 3.0 ”m as pH increased from pH 2.0 to 5.0 but remained nearly constant between pH 5.0 and 8.0. Increasing ethanol concentration decreased swelling. Swelling of sweet cherry cell walls is a physical process counterbalanced by turgor. © 2020, The Author(s)

    Calcium decreases cell wall swelling in sweet cherry fruit

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    Swelling of epidermal cell walls decreases cell-to-cell adhesion and increases cracking susceptibility in sweet cherry. Ca is suggested to decrease cracking susceptibility by crosslinking of cell wall components and, possibly, by decreasing swelling. The objective is to test this hypothesis. The effect of Ca on swelling of anticlinal epidermal cell walls was quantified microscopically in vivo using excised skin sections and in vitro using extracted cell walls. After removal of turgor, cell wall thickness increased. Incubation in CaCl2 decreased cell wall thickness up to 3 mM CaCl2. At higher concentrations thickness remained constant. Decreased cell wall swelling in vivo also occurred with other salts of divalent and trivalent cations, but not with those of monovalent cations. Decreased swelling was due to the Ca cation, the anions had no effect. Ca also decreased swelling of cell walls that were already swollen. CaCl2 also decreased swelling of extracted cell walls in vitro. There was no effect on swelling pressure. The effect on swelling increased as the CaCl2 concentration increased. Chlorides of divalent and trivalent cations, but not those of monovalent cations decreased swelling in vitro. The decrease in swelling among the divalent cations was linearly related to the radius of the cation. The results indicate that Ca decreases cracking susceptibility by decreasing swelling

    What Drives a Successful Adoption of E-Learning Modules for Sustainable Management? An Empirical Investigation of Influencing Factors and Challenges

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    In order to have corporations contributing to the environmental and social challenges of the coming years, employees have to develop competences for sustainable management. These competences are necessary to reduce environmental impacts of production or to increase efficiency in terms of energy consumption. In this context, E-Learning modules can offer learner-centered scenarios in which employees can simulate the consequences of their decisions and thereby develop competences for sustainable management. However, such modules focusing on sustainable management have not been used widely. Therefore, the aim of this paper is to investigate the determinants of a successful adoption and the challenges facing this adoption process of E-Learning modules for sustainable management. To achieve this aim, we conducted a literature review and a qualitative interview study. Thereby, we identified eleven general and eight specific influencing factors as well as twelve related challenges that affect the adoption of E-Learning modules for sustainable management

    Hydropower Operation in a Changing Market Environment – A Swiss Case Study

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    Hydropower (HP) is expected to play an important role in the European energy transition by providing back-up and storage capacity as well as flexibility for intermittent renewable energies. However, due to low electricity market prices the profitability of HP decreased in recent years. In this paper, we analyze historic revenue potentials and future market prospects for HP taking into account different development paths. Using a short-term HP operation model to capture market opportunities as well as technical and natural constraints of HP plants, we model three representative Swiss HP plants. The results indicate that in the last years, balancing markets could have provided significant additional revenues for HP plants. However, accounting for uncertainties and market characteristics, the potential of balancing markets is reduced but cross-market optimization is still beneficial. Looking into the future, market price prospects for the coming decade are low to modest. Global fuel markets and the European Union Emissions Trading System (ETS) will be the main drivers for decisions for Swiss HP. The revenue potential from balancing markets will be reduced significantly in the future if all Swiss HP operators aim for balancing. While optimized operation across markets helps Swiss HP to increase its revenues, it is limited in scale

    Decreased deposition and increased swelling of cell walls contribute to increased cracking susceptibility of developing sweet cherry fruit

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    Main conclusion: During fruit development, cell wall deposition rate decreases and cell wall swelling increases. The cell wall swelling pressure is very low relative to the fruit’s highly negative osmotic potential. Abstract: Rain cracking of sweet cherry fruit is preceded by the swelling of the cell walls. Cell wall swelling decreases both the cell: cell adhesion and the cell wall fracture force. Rain cracking susceptibility increases during fruit development. The objectives were to relate developmental changes in cell wall swelling to compositional changes taking place in the cell wall. During fruit development, total mass of cell wall, of pectins and of hemicelluloses increases, but total mass of cellulose remains constant. The mass of these cell wall fractions increases at a lower rate than the fruit fresh mass—particularly during stage II and early stage III. During stage III, on a whole-fruit basis, the HCl-soluble pectin fraction, followed by the water-soluble pectin fraction, the NaOH-soluble pectin fraction and the oxalate-soluble pectin fraction all increase. At maturity, just the HCl-soluble pectin decreases. Cell wall swelling increases during stages I and II of fruit development, with little change thereafter. This was indexed by light microscopy of skin sections following turgor release, and by determinations of the swelling capacity, water holding capacity and water retention capacity. The increase in cell wall swelling during development was due primarily to increases in NaOH-soluble pectins. The in vitro swelling of cell wall extracts depends on the applied pressure. The swelling pressure of the alcohol-insoluble residue is low throughout development and surprisingly similar across different cell wall fractions. Thus, swelling pressure does not contribute significantly to fruit water potential. © 2020, The Author(s)

    Crack initiation and propagation in sweet cherry skin: A simple chain reaction causes the crack to ‘run’

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    Rain cracking severely affects the commercial production of many fleshy-fruit species, including of sweet cherries. The objectives were to investigate how the gaping macroscopic cracks (macrocracks) of a rain-cracked fruit can develop from microscopic cracks in the cuticle (microcracks). Incubating fruit in deionized water is well known to cause significant macrocracking. We found that after a lag phase of 2 h, the numbers and lengths of macrocracks increased. Macrocrack number approached an asymptote at 12 h, whereas macrocrack length continued to increase. The rate of macrocrack propagation (extension at the crack tip) was initially 10.8 mm h-1 but then decreased to a near-constant 0.5 mm h-1. Light microscopy revealed three characteristic zones along a developing macrocrack. In zone I (ahead of the crack), the cuticle was intact, the epidermal cells were unbroken and their cell walls were thin. In zone II, the cuticle was fractured, the first epidermal cells died and their cell walls began to thicken (swell). In zone III, most epidermal cells had died, their cell walls were swollen and cell:cell separation began along the middle lamellae. The thickness of the anticlinal epidermal cell walls and the percentage of intact living cells along a crack were closely and negatively related. Cracks were stained by calcofluor white, but there was no binding of monoclonal antibodies (mAbs) specific for hemicelluloses (LM11, LM21, LM25). Strong binding was obtained with the anti-homogalacturonan mAb (LM19), indicating the presence of unesterified homogalacturonans on the crack surface. We conclude that macrocrack propagation is related to cell death and to cell wall swelling. Cell wall swelling weakens the cell:cell adhesion between neighbouring epidermal cells, which separate along their middle lamellae. The skin macrocrack propagates like a ‘run’ in a fine, knitted fabric

    The repeated bout effect of traditional resistance exercises on running performance across three bouts

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    Purpose This study investigated the repeated bout effect of three typical lower-body resistance training (RT) sessions on maximal and sub-maximal effort running performance. Methods Twelve resistance-untrained men (age 24±4 years; height 1.81±0.10 m; body mass 79.3±10.9 kg; VO2peak 48.2±6.5 mL∙kg-1∙min-1; six-repetition maximum squat 71.7±12.2kg) undertook three bouts of RT sessions at six-repetition maximum. Counter-movement-jump (CMJ), lower-body ROM, muscle soreness and creatine kinase (CK) were examined prior to (T0), immediately-post (T1), 24 (T24) and 48 (T48) h post each RT bout. Sub-maximal (i.e. below anaerobic threshold [AT]) and maximal (i.e. above AT) running performance were also conducted at T24 and T48. Results Most indirect muscle damage markers (i.e., CMJ, ROM and muscle soreness) and sub-maximal running performance were significantly improved (P 0.05). Conclusions The initial bout induced the greatest change in CK, however at least two bouts were required to produce protective effects on other indirect muscle damage markers and sub-maximal running performance measures. This suggests that sub-maximal running sessions should be avoided for at least 48 hours post RT until the third bout, although a greater recovery period may be required for maximal running sessions

    PL-018 Effects and safety of exercise combined with medication and diet in treatment of diabetes and comorbidity

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    Objective The role of exercise in the prevention and treatment of chronic diseases is widely accepted and regular physical exercise may play an irreplaceable role beyond traditional medicine and drug treatments. However,  current guidelines do not provide details on the characteristics of exercise programs which are aimed to be carried out concomitantly to drug treatments. Moroever, the safety of combined exercise and drug treatments has rarely been considered. The future of exercise is medicine research will likely need to focus on questions such as how to build customized exercise programs for different patients in the context of individual physiological responses to exercise? When combining drug and concomitant exercise treatment, what is the optimal exercise prescription in terms of timing, intensity and duration? Does exercise only have an additive effect or may exercise actually reverse or even cancel out some of the expected effects induced by the drug treatment?  What is the role of diet in exercise interventions? Does a given exercise program affect the lipid and glucose metabolism to the same extent? In this report, we will present different randomized clinical trials conducted in our research group to tackle some of the abovementioned questions. This particularly includes patients with comorbidity conditions (prediabetes and non-alcohol fatty liver disease,NAFLD), as well as patients with type 2 diabetes (T2D). Methods Two different randomized trials are included, both of which were conducted in China (ChiCTR-IOR-16008469 and ISRCTN 42622771). The ChiCTR-IOR-16008469 study was a randomized crossover trial. The aim of this study was to assess whether the duration between metformin administration and high-intensity cycling (HIIT) affects the glucose metabolism. T2D patients performed a single session of  HIIT (~25 minutes) at 30 (EX30), 60 (EX60), and 90 (EX90) minutes following breakfast and metformin administration in a randomized order. Subjects’ diurnal glucose metabolism was assessed between 8:00 a.m. and 4:00 p.m. (Metf) of each exercise day as well as on a control day. Furthermore, insulin was assessed both before and immediately after each exercise bout. The ISRCTN42622771 trial was a four arm randomized trial. Six-hundred and three patients from seven clinics were recruited, out of which 115 individuals aged 50-65-year fulfilled the inclusion criteria (impaired fasting glucose (IFG) or impaired glucose tolerance (IGT) and NAFLD) and were randomly assigned (1:1:1:1) to either of the four groups: aerobic exercise (AEx, n = 29), diet intervention (Diet, n = 28), aerobic exercise plus diet intervention (AED = 29), or no intervention (NI = 29). The study spanned over anaverage period of 8.6 months (7-11 months). Progressive supervised aerobic exercise training (60-75% intensity) was carried out 2-3 times/week in 30-60 min/sessions, and the diet intervention consisted of a lunch with 38% carbohydrate and diet fibre of 12g per day, while the remaining meals were freely chosen but with supervised nutrition intakes. The hepatic fat content (HFC) assessed by 1H MRS, glycated haemoglobin (HbA1c) and insulin sensitivity were assessed by conventional methods. Results In study 1, we found that in diabetes patient glucose levels significantly decreased in all exercise settings, irrespective of the timing.  However, whenHIIT was performed at 30 minutes post-metformin administration, the peak glucose was lowered, thereby further stabilizing the postprandial glucose fluctuation. The risk for hypoglycemia at different times to exercise after metformin administration was highest in EX90 (22.2%) compared to EX30 (3.7%) and EX60 (7.4%). While the lactate level was 19% higher in EX60 and 8% higher in EX90 compared to EX30. Compared with Metformin, the decrease in insulin was larger in EX30 and EX60 (both p < 0 001). These results indicate that timing of exercise is an important factor to consider when prescribing exercise as adjuvant to metformin therapy for T2DM patients. In study 2, we showed that in patients with morbidity (prediabetes with NAFLD), HFC was significantly reduced in the AEx (–24.4%), diet (–23.2%), and AED (–47.9%) groups, as opposed to the 20.9% increase in the NI group (p=0.006, p=0.002, and P<0.0001, respectively).Importantly, HFC decreased to normal levels (<5.6%) in ten (44%) out of 23 participants in the exercise plus diet group and nine (41%) out of 22 participants in the diet group, while the in the exercise group it decreased only in three (14%) out of 29  participants. Further, all intervention groups showed improvements ininsulin sensitivity (AEx 33%, p=0.023, Diet 37%, p=0.012, and AED 34%, p=0.029) but only the AED group significantly decreased HbA1c (-4.4%, p=0.01) compared with the NI group (1.9% and -0.6%). However, after controlling for the change of body weight as well as for the duration of the intervention and baseline values, the significant differences in HbA1cand insulin sensitivity between the groups disappeared. Furthermore, based on HbA1c IFG or IGT, no significant remission and progression from prediabetes to diabetes were observed between the intervention and NI. Conclusions The results derived from these two trials imply that: 1) the combined effects of exercise and metformin therapy on T2D should take into account that both exercise and metformin are likely to affect the lactic metabolism because T2D is considered as a redox disease. For the acute effect of exercise combined with metformin therapy, exercising at 30 minutes post-metformin administration appeared to be optimal for reducing glucose fluctuation. To avoid the risk for hypoglycemia and lactases with the combined treatment, selecting optimal timing may be the first and easiest step towards personalized exercise medicine. Thus, when exercise is recommended to diabetic patients, the timing of exercise may be an important consideration so that the therapeutic effects of metformin are not compromised. However, further studies are warranted to elucidate the long-term effects of combining metformin and exercise on glycemic control and lactic metabolism as well as the underlying mechanisms. 2) Aerobic exercise training combined with a fibre-enriched diet can aid reduce HFC more effectively than either exercise or increased fibre intake alone in pre-diabetic patients with NAFLD. However, the effect on glycaemic control and insulin sensitivity is not substantial. Therefore, it remains to be addressed why the same intervention protocol did not show the similar effect on the HFC and glycaemic control/insulin sensitivity in the same subjects. When these questions being uncovered, the combined intervention could be considered as an integral part of lifestyle interventions for patients with a cordiality condition for an increased risk of developing T2D
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