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Inactivation Curve (inactivation + curve)
Selected AbstractsA model of non-isothermal degradation of nutrients, pigments and enzymesJOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 3 2004Maria G Corradini Abstract Published isothermal degradation curves for chlorophyll A and thiamine in the range 100,150 °C and the inactivation curves of polyphenol oxidase (PPO) in the range 50,80 °C could be described by the model C(t)/C0 = exp[,b(T)tn] where C(t) and C0 are the momentary and initial concentrations, respectively, b(T) a temperature dependent ,rate parameter' and n, a constant. This suggested that the temporal degradation/inactivation events of all three had a Weibull distribution with a practically constant shape factor. The temperature dependence of the ,rate parameter' could be described by the log logistic model, b(T) = loge[1 + exp[k(T , Tc)], where Tc is a marker of the temperature level where the degradation/inactivation occurs at a significant rate and k the steepness of the b(T) increase once this temperature range has been exceeded. These two models were combined to produce a non-isothermal degradation/inactivation model, similar to one recently developed for microbial inactivation. It is based on the assumption that the local slope of the non-isothermal decay curve, ie the momentary decay rate, is the slope of the isothermal curve at the momentary temperature at a time that corresponds to the momentary concentration of the still intact or active molecules. This model, in the form of a differential equation, was solved numerically to produce degradation/inactivation curves under temperature profiles that included heating and cooling and oscillating temperatures. Such simulations can be used to assess the impact of planned commercial heat processes on the stability of compounds of nutritional and quality concerns and the efficacy of methods to inactivate enzymes. Simulated decay curves on which a random noise was superimposed were used to demonstrate that the degradation/inactivation parameters, k and Tc, can be calculated directly from non-isothermal decay curves, provided that the validity of the Weibullian and log logistic models and the constancy of the shape factor n could be assumed. Copyright © 2004 Society of Chemical Industry [source] Inhibitory Effect of Lamotrigine on A-type Potassium Current in Hippocampal Neuron,Derived H19-7 CellsEPILEPSIA, Issue 7 2004Chin-Wei Huang Summary:,Purpose: We investigated the effects of lamotrigine (LTG) on the rapidly inactivating A-type K+ current (IA) in embryonal hippocampal neurons. Methods: The whole-cell configuration of the patch-clamp technique was applied to investigate the ion currents in cultured hippocampal neuron,derived H19-7 cells in the presence of LTG. Effects of various related compounds on IA in H19-7 cells were compared. Results: LTG (30 ,M,3 mM) caused a reversible reduction in the amplitude of IA. The median inhibitory concentration (IC50) value required for the inhibition of IA by LTG was 160 ,M. 4-Aminopyridine (1 mM), quinidine (30 ,M), and capsaicin (30 ,M) were effective in suppressing the amplitude of IA, whereas tetraethylammonium chloride (1 mM) and gabapentin (100 ,M) had no effect on it. The time course for the inactivation of IA was changed to the biexponential process during cell exposure to LTG (100 ,M). LTG (300 ,M) could shift the steady-state inactivation of IA to a more negative membrane potential by approximately ,10 mV, although it had no effect on the slope of the inactivation curve. Moreover, LTG (100 ,M) produced a significant prolongation in the recovery of IA inactivation. Therefore in addition to the inhibition of voltage-dependent Na+ channels, LTG could interact with the A-type K+ channels to suppress the amplitude of IA. The blockade of IA by LTG does not simply reduce current magnitude, but alters current kinetics, suggesting a state-dependent blockade. LTG might have a higher affinity to the inactivated state than to the resting state of the IA channel. Conclusions: This study suggests that in hippocampal neurons, during exposure to LTG, the LTG-mediated inhibition of these K+ channels could be one of the ionic mechanisms underlying the increased neuronal excitability. [source] Solar disinfection of poliovirus and Acanthamoeba polyphaga cysts in water , a laboratory study using simulated sunlightLETTERS IN APPLIED MICROBIOLOGY, Issue 2 2006W. Heaselgrave Abstract Aims:, To determine the efficacy of solar disinfection (SODIS) in disinfecting water contaminated with poliovirus and Acanthamoeba polyphaga cysts. Methods and Results:, Organisms were subjected to a simulated global solar irradiance of 850 Wm,2 in water temperatures between 25 and 55°C. SODIS at 25°C totally inactivated poliovirus after 6-h exposure (reduction of 4·4 log units). No SODIS-induced reduction in A. polyphaga cyst viability was observed for sample temperatures below 45°C. Total cyst inactivation was only observed after 6-h SODIS exposure at 50°C (3·6 log unit reduction) and after 4 h at 55°C (3·3 log unit reduction). Conclusions:, SODIS is an effective means of disinfecting water contaminated with poliovirus and A. polyphaga cysts, provided water temperatures of 50,55°C are attained in the latter case. Significance and Impact of the Study:, This research presents the first SODIS inactivation curve for poliovirus and provides further evidence that batch SODIS provides effective protection against waterborne protozoan cysts. [source] The actions of azelnidipine, a dihydropyridine-derivative Ca antagonist, on voltage-dependent Ba2+ currents in guinea-pig vascular smooth muscleBRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2006H-L Zhu Background and purpose: Although azelnidipine is used clinically to treat hypertension its effects on its target cells, Ca2+ channels, in smooth muscle have not been elucidated. Therefore, its effects on spontaneous contractions and voltage-dependent L-type Ca2+ channels were investigated in guinea-pig portal vein. Experimental approach: The inhibitory potency of azelnidipine on spontaneous contractions in guinea-pig portal vein was compared with those of other dihydropyridine (DHP)-derived Ca antagonists (amlodipine and nifedipine) by recording tension. Also its effects on voltage-dependent nifedipine-sensitive inward Ba2+ currents (IBa) in smooth muscle cells dispersed from guinea-pig portal vein were investigated by use of a conventional whole-cell patch-clamp technique. Key results: Spontaneous contractions in guinea-pig portal vein were reduced by all of the Ca antagonists (azelnidipine, Ki=153 nM; amlodipine, Ki=16 nM; nifedipine, Ki=7 nM). In the whole-cell experiments, azelnidipine inhibited the peak amplitude of IBa in a concentration- and voltage-dependent manner (-60 mV, Ki=282 nM; ,90 mV, Ki=2 ,M) and shifted the steady-state inactivation curve of IBa to the left at ,90 mV by 16 mV. The inhibitory effects of azelnidipine on IBa persisted after 7 min washout at ,60 mV. In contrast, IBa gradually recovered after being inhibited by amlodipine, but did not return to control levels. Both azelnidipine and amlodipine caused a resting block of IBa at -90 mV. Only nifedipine appeared to interact competitively with S(-)-Bay K 8644. Conclusions and implications: These results suggest that azelnidipine induces long-lasting vascular relaxation by inhibiting voltage-dependent L-type Ca2+ channels in vascular smooth muscle. British Journal of Pharmacology (2006) 149, 786,796. doi:10.1038/sj.bjp.0706919 [source] The functional properties of the human ether-à-go-go -like (HELK2) K+ channelEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2002Andrea Becchetti Abstract The voltage-dependent K+ channels belonging to the ether-à-go-go family (eag, erg, elk) are widely expressed in the mammalian CNS. Their neuronal function, however, is poorly understood. Among the elk clones, elk2 is the most abundantly expressed in the brain. We have characterized the human ELK2 channel (HELK2) expressed in mammalian cell lines. Moreover, we have detected helk2 mRNA and ELK2-like currents in freshly dissociated human astrocytoma cells. HELK2 was inhibited by Cs+ in a voltage-dependent way (Kd was 0.7 mm, at ,120 mV). It was not affected by Way 123398 (5 µm), dofetilide (10 µm), quinidine (10 µm), verapamil (20 µm), haloperidol (2 µm), astemizole (1 µm), terfenadine (1 µm) and hydroxyzine (30 µm), compounds known to inhibit the biophysically related HERG channel. The crossover of the activation and inactivation curves produced a steady state ,window' current with a peak around ,20 mV and considerably broader than it usually is in voltage-dependent channels, including HERG. Similar features were observed in the ELK2 clone from rat, in the same experimental conditions. Thus, ELK2 channels are active within a wide range of membrane potentials, both sub- and suprathreshold. Moreover, the kinetics of channel deactivation and removal of inactivation was about one order of magnitude quicker in HELK2, compared to HERG. Overall, these properties suggest that ELK2 channels are very effective at dampening the neuronal excitability, but less so at producing adaptation of action potential firing frequency. In addition, we suggest experimental ways to recognize HELK2 currents in vivo and raise the issue of the possible function of these channels in astrocytoma. [source] Thermal Inactivation Kinetics of Peroxidase and Lipoxygenase from Broccoli, Green Asparagus and CarrotsJOURNAL OF FOOD SCIENCE, Issue 1 2002E.F. Morales-Blancas ABSTRACT: Thewermal inactivation curves for peroxidase (POD) and lipoxygenase (LOX) in broccoli (florets), green asparagus (tip and stem), and carrots (cortex and core) extracts were determined in the range of 70 to 95 °C for 0 to 600 s. The capillary tube method was used to obtain quasi-isothermal conditions. The kinetics of both enzymes showed a biphasic first-order model, while at 70 °C, LOX in asparagus showed a monophasic first-order behavior. LOX activity was not detected for carrots. Kinetic parameters, k and Ea, were determined for heat-labile and heatresistant isoenzyme fractions. Additionally, initial and residual activities for both enzymes within tissue sections showed a different distribution and heat stability. [source] A model of non-isothermal degradation of nutrients, pigments and enzymesJOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 3 2004Maria G Corradini Abstract Published isothermal degradation curves for chlorophyll A and thiamine in the range 100,150 °C and the inactivation curves of polyphenol oxidase (PPO) in the range 50,80 °C could be described by the model C(t)/C0 = exp[,b(T)tn] where C(t) and C0 are the momentary and initial concentrations, respectively, b(T) a temperature dependent ,rate parameter' and n, a constant. This suggested that the temporal degradation/inactivation events of all three had a Weibull distribution with a practically constant shape factor. The temperature dependence of the ,rate parameter' could be described by the log logistic model, b(T) = loge[1 + exp[k(T , Tc)], where Tc is a marker of the temperature level where the degradation/inactivation occurs at a significant rate and k the steepness of the b(T) increase once this temperature range has been exceeded. These two models were combined to produce a non-isothermal degradation/inactivation model, similar to one recently developed for microbial inactivation. It is based on the assumption that the local slope of the non-isothermal decay curve, ie the momentary decay rate, is the slope of the isothermal curve at the momentary temperature at a time that corresponds to the momentary concentration of the still intact or active molecules. This model, in the form of a differential equation, was solved numerically to produce degradation/inactivation curves under temperature profiles that included heating and cooling and oscillating temperatures. Such simulations can be used to assess the impact of planned commercial heat processes on the stability of compounds of nutritional and quality concerns and the efficacy of methods to inactivate enzymes. Simulated decay curves on which a random noise was superimposed were used to demonstrate that the degradation/inactivation parameters, k and Tc, can be calculated directly from non-isothermal decay curves, provided that the validity of the Weibullian and log logistic models and the constancy of the shape factor n could be assumed. Copyright © 2004 Society of Chemical Industry [source] | ||||||||||||||||