1,721,006 research outputs found

    The spliceosomal intron of rolA gene of Agrobacterium rhizogenes is a prokaryotic promoter.

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    Agrobacterium rhizogenes transfers DNA (T-DNA)from its Ri plasmid to plant cells. All T-DNA genesare expressed in plant cells. The rolA gene is the onlyT-DNA gene that contains an intron in the untranslatedleader region of its mRNA. This paper showsthat (i) the rolA gene is also transcribed in bacteria;(ii) the 85 bp corresponding to the spliceosomalintron drives prokaryotic gene expression in agrobacteria,in free-living rhizobia and in bacteroidswithin root nodules; and (iii) promoter activity isabolished by the deletion of 63 bp from its 50 end andis reduced by mutations changing its sequence nearthe putative 210 region. The expression pattern of achimeric reporter gene shows that, in free-livingbacteria, gene expression takes place during theexponential phase of growth and increases at theonset of the stationary phase. Within root nodules,reporter gene expression occurs in the invasion,nitrogen fixing and senescent zones

    Effect of high-intensity-interval-training (HIT) on maximal aerobic power and ventilatory threshold in older adults

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    We tested if 8 weeks of HIT can induce a significant increase of V’O2max and of the V’O2 corresponding to gas exchange threshold (GET) and to respiratory compensation point (RCP) in older men. To this aim, we measured in 12 healthy male volunteers (68.7±3.9 yy; 79.0±10.8 kg, 171.4±5.4 cm) V’O2max, GET and RCP before (PRE) and after (POST) 8 weeks of HIT performed 3 times a week cycling 7 times for 2 minutes, interspersed with 2 minutes of recovery, at about 85-90 % of V’O2max. GET was measured during an incremental test up to the limit of individual tolerance. V’O2max was measured during a subsequent constant–workload test performed at 105 % the maximal work-rate achieved on the ramp test. Absolute and relative V’O2max significantly increased by 5.4 % (PRE: 2.34±0.32 l/min; POST: 2.48±0.29 l/min, p < 0.05, effect size (ES) = 0.7) and 11.7 % (PRE: 28.8±5.66 ml/min kg; POST: 32.6±5.66 ml/min kg, p < 0.05, ES = 0.8), respectively. V’O2 at GET and RCP increased by 7.2% (PRE: 17.0±2.86 ml/min kg; POST: 18.3±3.81 ml/min kg, p < 0.05, ES = 0.7) and 15.4 % (PRE: 22.8±3.75 ml/min kg; POST: 27.0±5.30 ml/min kg, p < 0.05, ES = 1.3), respectively. Moreover, RCP increased from 76.5 % of V’O2max to 82.9 % of V’O2max (p <0.05, ES = 0.7). It is concluded that 8 weeks of HIT are able to induce significant increases of V’O2max and of exercise resistance in older adults

    Determination of maximal lactate steady state in healthy adults: Can NIRS help?

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    PURPOSE: We tested the hypothesis that the maximal lactate steady state (MLSS) can be accurately determined in healthy subjects based on measures of deoxygenated hemoglobin (deoxyHb), index of oxygen extraction measured non-invasively by near-infrared spectroscopy (NIRS). METHODS: 32 healthy men (average age 48±17 yrs, range 23-74 yrs) performed an incremental cycling test to exhaustion and square wave tests for MLSS determination. Cardiorespiratory variables were measured bbb and deoxyHb was monitored non-invasively on the right vastus lateralis with a quantitative NIRS device. The individual values of V O2 and heart rate (HR) corresponding to the MLSS were calculated and compared to the NIRS-derived MLSS (NIRSMLSS) that was, in turn, determined by double linear function fitting of deoxyHb during the incremental exercise. RESULTS: V O2 and HR at MLSS were 2.25±0.54 L•min-1 (76±9 % V O2max) and 133±14 b•min-1 (81±7 %HRmax) respectively. Muscle O2 extraction increased as a function of exercise intensity up to a deflection point, NIRSMLSS, at which V O2 and HR were 2.23±0.59 L•min-1 (76±9 % V O2max) and 136±17 b•min-1 (82±8 %HRmax) respectively. For both V O2 and HR, the difference of NIRSMLSS from MLSS values was not significant and the measures were highly correlated (r2=0.81 and r2=0.76). The Bland Altman analysis confirmed a not significant bias for V O2 and HR (-0.015 L•min-1 and 3 b•min-1, respectively) and a small imprecision of 0.26 L•min-1 and 8 b•min-1. CONCLUSIONS: A plateau in muscle O2 extraction was demonstrated in coincidence with MLSS during an incremental cycling exercise, confirming the hypothesis that this functional parameter can be accurately estimated with a quantitative NIRS device. The main advantages of NIRSMLSS over lactate-based techniques are the non-invasiveness and the time/cost efficiency

    Skeletal muscle mass is controlled by the MRF4-MEF2 axis.

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    Purpose of reviewThe review is focused on the unexpected role of myogenic regulatory factor 4 (MRF4) in controlling muscle mass by repressing myocyte enhancer binding factor 2 (MEF2) activity in adult skeletal muscle, and on the emerging role of MEF2 in skeletal muscle growth.Recent findingsThe MRF4s of the MyoD family (MyoD, MYF5, MRF4, myogenin) and the MEF2 factors are known to play a major role in embryonic myogenesis. However, their function in adult muscle tissue is not known. A recent study shows that MRF4 loss in adult skeletal muscle causes muscle hypertrophy and prevents denervation atrophy. This effect is mediated by MEF2 factors that promote muscle growth, with MRF4 acting as a repressor of MEF2 activity. The role of MEF2 in skeletal muscle growth is supported by the finding that muscle regeneration is impaired by muscle-specific triple knockout of Mef2a, c, and d genes.SummaryThe finding that the MRF4-MEF2 axis controls muscle growth opens a new perspective for preventing muscle wasting. A unique feature of this pathway is that MRF4 is exclusively expressed in skeletal muscle, thus reducing the risk that interventions aimed at down-regulating MRF4 or interfering with the interaction between MRF4 and MEF2 may have off-target effects in other tissues

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    Effects of ultramarathon running on mitochondrial function of platelets and oxidative stress parameters: a pilot study

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    Only a few studies have evaluated changes in mitochondrial function and oxidative stress associated with ultramarathon running. Invasive biopsies are needed to assess mitochondrial function of skeletal muscle, which may not be well tolerated by some individuals. Platelets (PLTs) as a metabolically highly active and homogenous cell population were suggested as a potentially valuable surrogate to investigate mitochondrial function. Thus, this study was aimed to evaluate mitochondrial function of PLTs and its association with individual race performance and markers of oxidative stress, muscle damage and renal dysfunction. Race performance and mitochondrial function (high-resolution respirometry, HRR) of PLTs using different substrates inducing ROUTINE, LEAK, N-pathway control state (Complex I linked oxidative phosphorylation; CI, OXPHOS), NS-pathway control state (CI + II linked OXPHOS and electron transfer pathway; ET), S-pathway control state (CII linked ET) as well as parameters of oxidative stress and antioxidant capacity, and markers of muscle and renal injury were assessed in eight male ultramarathon runners (26-45 years) before, immediately after and 24 h after an ultramarathon race (PRE, POST, and REC). Ultramarathon running induced an increase in LEAK O-2 flux of PLT mitochondria and slight, largely non-significant changes in the oxidant/antioxidant balance. Levels of creatine kinase (CK), lactate dehydrogenase (LDH), blood urea nitrogen, and creatinine were all significantly elevated POST and remained high in REC. There were inverse correlations between race time and N-linked substrate state PRE-POST, and changes in CK and LDH levels were significantly related to PLT mitochondrial LEAK and N-linked respiration PRE. Although race-related changes in respirometry parameters of PLT mitochondria were rather small, a somewhat more pronounced increase in the relative N-linked respiration in faster runners might suggest PLT CI as indicator of physical fitness. The higher PLT LEAK PRE and diminished increase of CK during the race may represent a prophylactic preconditioning and the slight but non-significant elevation of the antioxidant potential post-race as a protective consequence of the race-related oxidative stress and potential threat to the kidney. Our findings point toward an interrelationship between mitochondrial function of PLTs, individual fitness levels and extreme physical and metal stresses, which stimulates further research

    Effect of hiking training at high-altitude on V'O2 and Q' kinetics in healthy sedentary women

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    Aim: Previous studies have shown faster pulmonary oxygen uptake (V’O2) kinetics in men after moderate intensity exercise performed either in normoxia [2] or in hypobaric hypoxia [1]. We tested the hypothesis that 2 weeks of trekking performed at sea level and at high-altitude can induce a significant acceleration of the V'O2 and cardiac output (Q’) kinetics in adult women as compared to a similar training performed at the sea level (normoxia). Methods: 7 moderately active women (25±7 yy; 68±11 kg, 165±8 cm) were recruited by the Department of Basic and Applied Medical Sciences of the University ‘G.d’Annunzio’-Chieti-Pescara. A sea level (SL) the training program consisted in trekking on irregular and undulating terrain for 2weeks (3 to 6h every day) with absolute altitudes ranging from 160m to 800 asl (SL). The same training program was repeated after 5 months at high altitude (HA) (>5000m) (Ama Dablam, Nepal) with the same absolute variations of altitude. Before and immediately after trekking, breath-by-breath V’O2 and beat-by-beat Q’ were measured. These were evaluated during: i) an incremental ramp cycling test up to exhaustion, to calculate V’O2max, and; ii) three consecutive square wave tests (separated by 6 min of recovery) performed at approximately 50 % of V’O2max. V’O2 and Q’ values of each test were 1-s normalized, aligned and ensemble-averaged. Then, a bi-exponential models was iteratively fitted to the data in order to describe V’O2 and Q’ kinetics during square-wav exercise transitions. Friedman’s test was applied to evaluate the differences of the selected parameter in the various conditions. Results: Absolute and relative V’O2max (PRE-SL 32,90±6,27ml/kg/min; POST-SL 33,45±4,64ml/kg/min; PRE-HA 33,43±4,10ml/kg/min; POST-HA 35,26±4,53ml/kg/min) and Q’max (PRE-SL 13,1±2,2l; POST-SL 13,3±1,9l; PRE-HA 12,8±1,5l; POST-HA 13,3±1,8) values did not increase as a result of training at SL and HA. τ2of V’O2 kinetics (PRE-SL 25,43±5,29s; POST-SL 17,76±4,58s; PRE-HA 17,78±3,60s; POST-HA 13,84±4,70s) were significantly smaller after each training (P < 0.05). τ2 of Q’ kinetics (PRE-SL 23,97±6,47s; POST-SL 18,99±3,66s; PRE-HA 22,97±12,74s; POST-HA 18,82±7,67s) were unaffected by training. Conclusion: 2 weeks of trekking, at SL and at HA do not modify V’O2max and Q’max, confirming that this sort of moderate intensity exercise, either in normoxia or hypobaric hypoxia, does not affect the responses to maximal exercise [2]. At the contrary [3], this kind of training is able to elicit a substantial acceleration of V’O2 kinetics

    Effects of high-intensity-interval-training (HIT) on cardiovascular fitness and cardiometabolic risk in the elderly.

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    HIT has been shown improve cardiovascular fitness and seems to induce beneficial modifications of some cardiometabolic risk factors in healthy subjects or patients. Less is known about the efficacy of HIT applied to healthy older adults. PURPOSE This proof-of-concept study tested the hypothesis that 8 weeks of HIT can induce significant improvements of cardiovascular fitness, exercise capacity and of selected cardiometabolic risk factors in healthy older adults. METHODS In 12 healthy male volunteers (68.7 ± 3.9 yy; 79.0 ± 10.8 kg; 171.4 ± 5.4 cm) who participated in the study, we measured V’O2max, gas exchange threshold (GET ) and respiratory compensation point (RCP), resting mean, systolic and diastolic blood pressures (MBP, SDP, DBP), fasting blood glucose concentration (GLU), total cholesterol/HDL ratio (TC/HDL), % Body fat (BF) and waist circumference (WC) before (PRE) and after (POST) an 8-week training program HIT consisting in 7 bouts of 2-min near-maximal cycling (i.e. 85-90 %V’O2max) interspersed with 2 minutes of recovery performed 3 times a week. RESULTS Absolute and relative V’O2max significantly increased by 5.4 % (P < 0.05; effect size, ES = 0.7) and 11.7 % (P < 0.05, ES = 0.8), respectively. V’O2 at GET and RCP increased by 7.2 % (P < 0.05, ES = 0.7) and 15.4 % (ES = 1.3), respectively. MBP, SDP and DBP decreased by 7 % (ES = 0.8), 9 % (P < 0.05, ES = 0.9) and 4 % (ns), respectively. GLU was diminished by 7 % (ES = 0.5) and TC/HDL decreased by 5 % (P < 0.05, ES = 0.2). BF and WC decreased by 4 % (ES = 0.2) and 1.4 % (P < 0.05, ES = 0.14), respectively. CONCLUSION 8 weeks of HIT promote significant changes of maximal aerobic power and exercise resistance in healthy male elderly subjects. In addition, they induce significant improvements of some selected cardiometabolic risk factors. Supported by ESA Contract Nr 400010258

    Ras is involved in nerve-activity-dependent regulation of muscle genes

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    Gene expression in skeletal muscle is regulated by the firing pattern of motor neurons, but the signalling systems involved in excitation-transcription coupling are unknown. Here, using in vivo transfection in regenerating muscle, we show that constitutively active Ras and a Ras mutant that selectively activates the MAPK(ERK) pathway are able to mimic the effects of slow motor neurons on expression of myosin genes. Conversely, the effect of slow motor neurons is inhibited by a dominant-negative Ras mutant. MAPK(ERK) activity is increased by innervation and by low-frequency electrical stimulation. These results indicate that Ras-MAPK signalling is involved in promoting nerve-activity-dependent differentiation of slow muscle fibres in vivo
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