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Recovery Kinetics (recovery + kinetics)
Selected AbstractsDerivation of Recovery Kinetics From Stress Relaxation Tests,ADVANCED ENGINEERING MATERIALS, Issue 3 2010Sheila Bhaumik The recovery behavior of a commercial aluminum alloy 3103 was investigated by the means of two alternative experimental methods: stress relaxation (SR) and double tension tests (DT). In case of SR, the stress,time evolution after deformation was recorded, and for DT the yield stress after several recovery times were measured. The DT tests were further sub-divided into tests with and without external load during recovery. The results revealed that the recovery kinetics is clearly accelerated by the external stress during the SR. However, the difference between the DT and SR stresses is much larger. It is caused by continued dislocation glide after the deformation, which causes continued plastic elongation of the specimens. This is demonstrated quantitatively by appropriate evaluation models for both experiments. In contrast to DT, the SR evaluation accounts for the elastic SR due to plastic elongation, but the recovery parameters are the same ones as for DT. This makes it possible to replace DT by SR experiments, which are materially less laborious. [source] Nitric oxide bioavailability modulates the dynamics of microvascular oxygen exchange during recovery from contractionsACTA PHYSIOLOGICA, Issue 2 2010D. M. Hirai Abstract Aim:, Lowered microvascular PO2 (PO2mv) during the exercise off-transient likely impairs muscle metabolic recovery and limits the capacity to perform repetitive tasks. The current investigation explored the impact of altered nitric oxide (NO) bioavailability on PO2mv during recovery from contractions in healthy skeletal muscle. We hypothesized that increased NO bioavailability (sodium nitroprusside: SNP) would enhance PO2mv and speed its recovery kinetics while decreased NO bioavailability (l -nitro arginine methyl ester: l -NAME) would reduce PO2mv and slow its recovery kinetics. Methods:,PO2mv was measured by phosphorescence quenching during transitions (rest,1 Hz twitch-contractions for 3 min,recovery) in the spinotrapezius muscle of Sprague,Dawley rats under SNP (300 ,m), Krebs-Henseleit (Control) and l -NAME (1.5 mm) superfusion conditions. Results:, Relative to recovery in Control, SNP resulted in greater overall microvascular oxygenation as assessed by the area under the PO2mv curve (PO2 AREA; Control: 3471 ± 292 mmHg s; SNP: 4307 ± 282 mmHg s; P < 0.05) and faster off-kinetics as evidenced by the mean response time (MRToff; Control: 60.2 ± 6.9 s; SNP: 34.8 ± 5.7 s; P < 0.05), whereas l -NAME produced lower PO2 AREA (2339 ± 444 mmHg s; P < 0.05) and slower MRToff (86.6 ± 14.5 s; P < 0.05). Conclusion:, NO bioavailability plays a key role in determining the matching of O2 delivery-to-O2 uptake and thus the upstream O2 pressure driving capillary-myocyte O2 flux (i.e. PO2mv) following cessation of contractions in healthy skeletal muscle. Additionally, these data support a mechanistic link between reduced NO bioavailability and prolonged muscle metabolic recovery commonly observed in ageing and diseased populations. [source] Derivation of Recovery Kinetics From Stress Relaxation Tests,ADVANCED ENGINEERING MATERIALS, Issue 3 2010Sheila Bhaumik The recovery behavior of a commercial aluminum alloy 3103 was investigated by the means of two alternative experimental methods: stress relaxation (SR) and double tension tests (DT). In case of SR, the stress,time evolution after deformation was recorded, and for DT the yield stress after several recovery times were measured. The DT tests were further sub-divided into tests with and without external load during recovery. The results revealed that the recovery kinetics is clearly accelerated by the external stress during the SR. However, the difference between the DT and SR stresses is much larger. It is caused by continued dislocation glide after the deformation, which causes continued plastic elongation of the specimens. This is demonstrated quantitatively by appropriate evaluation models for both experiments. In contrast to DT, the SR evaluation accounts for the elastic SR due to plastic elongation, but the recovery parameters are the same ones as for DT. This makes it possible to replace DT by SR experiments, which are materially less laborious. [source] Reduction in the Sodium Currents in Isolated Ventricular Myocytes of Guinea Pigs Treated by Chronic L-Thyroxin MedicationJOURNAL OF CARDIAC SURGERY, Issue 6 2002Yu-Ping Ma Objective: Cardiac remodeling induced by chronic medication of L-thyroxin is manifested by a much more severe cardiac arrhythmias on the occlusion/reperfusion of the coronary artery in rats. A pattern of changes in ion currents in a diseased heart (L-thyroxin induced cardiac remodeling) is possibly provided as a basis of promoting malignant cardiac arrhythmias. An enhanced delayed outward rectifier potassium currents the rapid (IKr) and slow (IKS) component was found in the remodeled heart by L-thyroxin chronic medication. It is interested to investigate the changes in the sodium currents in the L-thyroxin remodeled guinea pig ventricle. Method: The remodeling model in guinea pig was developed by L-thyroxin 4 mg po for 10 days. On d 11, the heart was removed and perfused to isolate ventricular myocytes with medium of Ca2+ free medium containing collagen. The whole cell holding technique was applied. Results: The INa density in the L-thyroxin caused hypertrophied myocytes was reduced significantly at holding potential ,30 mV, ,53.20 +/,10.78pA/pF against ,73.78+/,14.66pA/pF in the normal. (n = 45, p < 0.001). No difference in the steady-state inactivation and recovery kinetics between the remodeled and the normal was found. The recovery constant 37.54+/,3.63 ms in the remodeled vs 36.57+/,2.81 ms in the normal (n = 18, p > 0.05). The accelerated deactivation time constant 3.67+/,0.14 of the remodeled (n = 39) against the normal 4.14+/,0.15 ms (n = 43) (p < 0.05). Conclusion: There is a reduced INa in the L-thyroxin remodeled ventricular myocytes and the deactivation of the current is accelerated. A changed depolarization of the affected myocardium is likely involved in the mechanism of arrhythmogenesis of the remodeled ventricle. [source] PHOTOINHIBITION IN RED ALGAL SPECIES WITH DIFFERENT CAROTENOID PROFILES,JOURNAL OF PHYCOLOGY, Issue 6 2008Nadine Schubert Members of the Rhodophyta present different carotenoid profiles. In a majority of the species, lutein constitutes >50% of the total carotenoid content, while in other species, it is replaced by zeaxanthin or antheraxanthin. Given that carotenoids have specific roles in photoprotection, different carotenoid profiles of red algae species could be related to their capacity to cope with photoinhibitory stress. Therefore, in the present work, the sensitivity to light stress of red algal species with different carotenoid profiles was investigated. Photoinhibition of photosynthesis induced by high-light stress and the subsequent recovery in dim-light conditions was measured using maximal PSII quantum efficiency (Fv/Fm). The degree of decrease and recovery of Fv/Fm and their respective kinetics were related to the carotenoid profile of the species. Although no relationship between sensitivity to high-light stress and the carotenoid profile was observed, there were clear carotenoid profile-related differences in the decrease and recovery kinetics. In species with zeaxanthin or antheraxanthin as the major carotenoid, Fv/Fm reduction and recovery was principally associated with slowly activated and relaxed processes. In contrast, in species with lutein as the major carotenoid, rapidly activated processes appear to play a major role in the down-regulation of photosynthesis during light-stress conditions. In these species, the repair of D1 is also important during light-stress conditions. This finding could imply differential expression of mechanisms involved in photoprotection in red algae that seems to be related to the carotenoid profile of the species. [source] Subunit-specific desensitization of heteromeric kainate receptorsTHE JOURNAL OF PHYSIOLOGY, Issue 4 2010David D. Mott Kainate receptor subunits can form functional channels as homomers of GluK1, GluK2 or GluK3, or as heteromeric combinations with each other or incorporating GluK4 or GluK5 subunits. However, GluK4 and GluK5 cannot form functional channels by themselves. Incorporation of GluK4 or GluK5 into a heteromeric complex increases glutamate apparent affinity and also enables receptor activation by the agonist AMPA. Utilizing two-electrode voltage clamp of Xenopus oocytes injected with cRNA encoding kainate receptor subunits, we have observed that heteromeric channels composed of GluK2/GluK4 and GluK2/GluK5 have steady state concentration,response curves that were bell-shaped in response to either glutamate or AMPA. By contrast, homomeric GluK2 channels exhibited a monophasic steady state concentration,response curve that simply plateaued at high glutamate concentrations. By fitting several specific Markov models to GluK2/GluK4 heteromeric and GluK2 homomeric concentration,response data, we have determined that: (a) two strikingly different agonist binding affinities exist; (b) the high-affinity binding site leads to channel opening; and (c) the low-affinity agonist binding site leads to strong desensitization after agonist binding. Model parameters also approximate the onset and recovery kinetics of desensitization observed for macroscopic currents measured from HEK-293 cells expressing GluK2 and GluK4 subunits. The GluK2(E738D) mutation lowers the steady state apparent affinity for glutamate by 9000-fold in comparison to GluK2 homomeric wildtype receptors. When this mutant subunit was expressed with GluK4, the rising phase of the glutamate steady state concentration,response curve overlapped with the wildtype curve, whereas the declining phase was right-shifted toward lower affinity. Taken together, these data are consistent with a scheme whereby high-affinity agonist binding to a non-desensitizing GluK4 subunit opens the heteromeric channel, whereas low-affinity agonist binding to GluK2 desensitizes the whole channel complex. [source] | ||||||||||