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Intrinsic kinetics of continuous growth and ethanol production of a flocculating fusant yeast strain SPSC01.

The intrinsic kinetics of continuous yeast cell growth and ethanol production for a self-flocculating fusant yeast strain SPSC01 was investigated by means of mechanically dispersing the flocs and correspondingly established floc size distribution on-line monitoring technique using the focused beam reflectance measurement system, through which the floc intra-particle mass transfer limitation was effectively eliminated, but its ethanol formation metabolism was not affected. Modified kinetic models were developed, which can be used to predict the continuous kinetic behaviors of SPSC01, especially when low dilution rates are applied and limiting substrate concentrations are undetectable and almost all kinetic models developed previously are failed in predicting corresponding kinetic behaviors. Both substrate and product inhibitions reported for freely suspended yeast cell ethanol production were also observed for SPSC01 when high gravity media were fed and relatively high levels of residual sugar and ethanol presented. Model parameters were evaluated through numerical calculation method and validated by experimental data mu = 0.584C(s)/0.155 + C(s) + C(2)(s)/160.7(1 -P/125)(3.68) + 0.004 for growth, nu = 1.998C(s)/0.427 + C(s) + C(2)(s)/366.7(1- P/125)(1.72) + 0.060 for ethanol production These intrinsic kinetic models can be further used to develop the observed kinetic models that quantitatively correlate the impact of the self-flocculating yeast cell size distributions on their apparent rates for yeast cell growth, substrate uptake and ethanol production and optimize the ethanol production process.

Algorithms↗

New methodology to determine the rate-limiting adsorption kinetics mechanism from experimental dynamic surface tension data.

We present a new methodology to determine the rate-limiting adsorption kinetics mechanism (diffusion-controlled vs mixed diffusion-barrier controlled), including deducing the kinetics parameters (the diffusion coefficient, D, and the energy-barrier parameter, beta), from the experimental short-time dynamic surface tension (DST) data. The new methodology has the following advantages over the existing procedure used to analyze the experimental DST data: (a) it does not require using a model for the equilibrium adsorption isotherm, and (b) it only requires using the experimental short-time DST data measured at two initial surfactant bulk solution concentrations. We apply the new methodology to analyze the experimental short-time DST data of the following alkyl poly(ethylene oxide), CiEj, nonionic surfactants: C12E4, C12E6, C12E8, and C10E8 measured using the pendant-bubble apparatus. We find that for C12E4 and C12E6, the effect of the energy barrier on the overall rate of surfactant adsorption can be neglected for surfactant bulk solution concentrations below their respective critical micelle concentrations (CMCs), and therefore, that the rate-limiting adsorption kinetics mechanism for C12E4 and C12E6 is diffusion-controlled at any of their premicellar surfactant bulk solution concentrations. On the other hand, for C12E8 and C10E8, we find that their respective CMC values are large enough to observe a significant effect of the energy barrier on the overall rate of surfactant adsorption. In other words, for C12E8 and C10E8, the rate-limiting adsorption kinetics mechanism shifts from diffusion-controlled to mixed diffusion-barrier controlled as their premicellar surfactant bulk solution concentrations increase. We test the new methodology by predicting the short-time DST profiles at other initial surfactant bulk solution concentrations, and then comparing the predicted DST profiles with those measured experimentally. Very good agreement is obtained for the four CiEj nonionic surfactants considered. We also compare the results of implementing the new methodology with those of implementing the existing procedure, and conclude that using a model for the equilibrium adsorption isotherm can lead not only to different values of D and beta, but it can also lead to a completely different determination of the rate-limiting adsorption kinetics mechanism. Since the new methodology proposed here does not require using a model for the equilibrium adsorption isotherm, we conclude that it should provide a more reliable determination of the rate-limiting adsorption kinetics mechanism, including the deduced kinetics parameters, D and beta.

Journal Article↗

Pharmacokinetic parameters of genotoxic activity inferred from the comparison of the kinetics of MN-PCE induced by chemical agents and ionizing radiation.

Some kinetic parameters of clastogenic activity of cyclophosphamide were inferred by means of the comparison of its kinetics of micronucleated polychromatic erythrocytes (MN-PCE) formation with the kinetics induced by radiation. The same reasoning was also applied to the kinetics obtained by treatment with mitomycin C (MMC), arabinocyl cytosine (Ara-C) and 6-mercaptopurine (6-MOP), based on previously reported data from the literature. The results indicate that the latency period (LP) and half-lives (HL) vary from one mutagen to another. For MMC, they are very similar to radiation indicating a rapid distribution and reaction. CP presents very long LP and HL which agree with the requirement of mutagen activation. Ara-C showed a very short LP which suggests a rapid activation and fast induction of damage in DNA. 6-MOP presented a very long LP which agreed with the requirement of its incorporation into DNA to cause micronucleus (MN). From the data obtained in the present work, it can be concluded that the comparison of the kinetics of MN-PCE formation induced by chemical agents with that obtained by the exposure to an acute dose of radiation permits one to estimate some parameters of the kinetics of clastogenic activity of chemical agents, like the LP and the HL. This seems to be valid for agents that act through the induction of DNA lesions; in the case of agents whose clastogenic activity is through other mechanisms, such as the inhibition or alteration of the process of duplication of the DNA, the kinetic parameters are not equivalent to the LP and HL; however, they could provide information on their possible mechanism of action.

Animals↗

Electrical properties and defect chemistry of TiO2 single crystal. IV. Prolonged oxidation kinetics and chemical diffusion.

Measurements of both electrical conductivity and thermoelectric power were used to monitor the equilibration kinetics of undoped single-crystal TiO(2) during prolonged oxidation at 1123 and 1323 K and p(O(2)) = 75 kPa. Two kinetics regimes were revealed: kinetics regime I (rapid kinetics), which is rate-controlled by the transport of oxygen vacancies, and kinetics regime II (slow kinetics), which is rate-controlled by the transport of titanium vacancies. The incorporation of titanium vacancies allows undoped p-type TiO(2) to be processed in a controlled manner. The kinetics data were used to determine the chemical diffusion coefficient (D(chem)) associated with the transport of titanium vacancies, which is equal to D(chem) = 8.9 x 10(-14) m(2) s(-1) and D(chem) = 9.3 x 10(-15) m(2) s(-1) at 1323 and 1123 K, respectively.

Journal Article↗

A collision theory-based derivation of semiempirical equations for modeling dispersive kinetics and their application to a mixed-phase crystal decomposition.

In recent works, the author has shown the utility of new, semiempirical kinetic model equations for treating dispersive chemical processes ranging from slow (minute/hour time scale) solid-state phase transformations to ultrafast (femtosecond) reactions in the gas phase. These two fundamental models (one for homogeneous/deceleratory sigmoidal conversion kinetics and the other for heterogeneous/acceleratory sigmoidal kinetics; isothermal conditions), based on the assumption of a "Maxwell-Boltzmann-like" distribution of molecular activation energies, provide a novel, quantum-based interpretation of the kinetics. As an extension to previous work, it is shown here that the derivation of these dispersive kinetic equations is supported by classical collision theory (i.e., for gas-phase applications). Furthermore, the successful application of the approach to the kinetic modeling of the solid-state decomposition of a binary system, CO2.C2H2, is demonstrated. Finally, the models derived appear to explain some of the (solid-state) kinetic data collected using isoconversional techniques such as those often reported in the thermal analysis literature.

Journal Article↗

Kinetics and mechanism of the reactions of [FeCl4]- with PhS- or PhSH in MeCN, and the role of cations containing N-H groups.

The kinetics of the reactions between [FeCl4]- and an excess of PhS- have been studied using stopped-flow spectophotometry. The associated absorbance-time curves can be fitted to two exponentials, and these first and second phases correspond to the formation of [FeCl3(SPh)]- and [FeCl2(SPh)2]-, respectively. It seems likely that the steps involving formation of [FeCl(SPh)3]- and [Fe(SPh)4]- are associated with much smaller changes in absorbance and so are not detected. The kinetics of the first phase exhibit a non-linear dependence on the concentration of PhS- indicating an associative mechanism in which PhS- rapidly binds to [FeCl4]- to form [FeCl4(SPh)]2- prior to rate-limiting dissociation of chloride and formation of [FeCl3(SPh)]-. The kinetics indicate that at high concentrations of PhS-, the five-coordinate intermediate attains stoichiometric concentrations. This is confirmed by the spectroscopic changes. The second phase shows analogous kinetics. The kinetics of the reactions between [FeCl4]- and an excess of PhSH have also been studied. For the first phase the reaction occurs at a rate independent of the concentration of PhSH, consistent with an associative mechanism in which the solvent (MeCN) is the nucleophile to form [FeCl3(NCMe)]. Subsequent rapid replacement of the coordinated solvent by PhSH yields [FeCl3(SHPh)]. The kinetics of the second phase of the reaction with PhSH exhibits a non-linear dependence on the concentration of PhSH, analogous to the kinetics observed with PhS- and consistent with an associative mechanism. The cations [NHEt3]+, [NH2Et2]+ and [lutH]+ (lut = 2,6-dimethylpyridine) form ion pairs with [FeCl4]- which undergo substitution more rapidly than free [FeCl4]-.

Journal Article↗

Urea kinetics during sustained low-efficiency dialysis in critically ill patients requiring renal replacement therapy.

Continuous renal replacement therapies have practical and theoretical advantages compared with conventional intermittent hemodialysis in hemodynamically unstable or severely catabolic patients with acute renal failure (ARF). Sustained low-efficiency dialysis (SLED) is a hybrid modality introduced July 1998 at the University of Arkansas for Medical Sciences that involves the application of a conventional hemodialysis machine with reduced dialysate and blood flow rates for 12-hour nocturnal treatments. Nine critically ill patients with ARF were studied during a single SLED treatment to determine delivered dialysis dose and the most appropriate model for the description of urea kinetics during treatment. Five patients were men, mean Acute Physiology and Chronic Health Evaluation (APACHE) II score was 28.9 and mean weight was 92.5 kg. Kt/V was determined by the reference method of direct dialysate quantification (DDQ) combined with an equilibrated postdialysis plasma water urea nitrogen (PUN) concentration and four other methods that were either blood or dialysate based, single or double pool, or model independent (whole-body kinetic method). Solute removal indices (SRIs) were determined from net urea removal and urea distribution volume supplied from DDQ (reference method) and by mass balance using variables supplied from blood-based formal variable-volume single-pool (VVSP) urea kinetic modeling. Equivalent renal urea clearances (EKRs) were calculated from urea generation rates and time-averaged concentrations for PUN based on weekly mass balance with kinetic variables supplied by either DDQ (reference method) or formal blood-based VVSP modeling. Mean Kt/V determined by the reference method was 1.40 and not significantly different when determined by formal VVSP modeling, DDQ using an immediate postdialysis PUN, or the whole-body kinetic method. Correction of single-pool Kt/V by a Daugirdas rate equation did not yield plausible results. Mean SRI and EKR by the reference methods were 0.61 and 24.8 mL/min, respectively, and not significantly different when determined by blood-based methods. A single-pool urea kinetic model adequately described intradialytic PUN profiles, indicating that SLED was associated with minimal urea disequilibrium. This was supported by the parity between hemodialyzer and whole-body urea clearances, and the mean postdialytic urea rebound of 4.1% (P = 0.13 versus zero). Additional prospective studies are needed in this setting to define the optimal method for dialysis quantification, targets for azotemic control, and optimal modality of renal replacement therapy. In conclusion, SLED delivers a high dose of dialysis with minimal associated urea disequilibrium and can be quantified by Kt/V, SRI, and EKR from blood-based methods using single-pool urea kinetic models.

Acute Kidney Injury↗

Autocatalytic oscillations in the early phase of the photoreduced methyl viologen-initiated fast kinetic reaction of hydrogenase.

The kinetic characteristics of the hydrogen uptake reaction of hydrogenase, obtained by conventional activity measurements, led to the proposal of an autocatalytic reaction step in the hydrogenase cycle or during the activation process. The autocatalytic behavior of an enzyme reaction may result in oscillating concentrations of enzyme intermediates and/or products contributing to the autocatalytic step. This behavior has been investigated in the early phase of the hydrogenase-methyl viologen reaction. To measure fast hydrogenase kinetics, flash-reduced methyl viologen has been used as a light-induced trigger in transient kinetic phenomena associated with intermolecular electron transfer to hydrogenase. Here we report fast kinetic measurements of the hydrogenase-methyl viologen reaction by use of the excimer laser flash-reduced redox dye. The results are evaluated on the assumption of an autocatalytic reaction in the hydrogenase kinetic cycle. The kinetic constants of the autocatalytic reaction, i.e. the methyl viologen binding to and release from hydrogenase, were determined, and limits of the kinetic constants relating to the intramolecular (intraenzyme) reactions were set.

Catalysis↗

Kinetic therapy improves oxygenation in critically ill pediatric patients.

OBJECTIVE: To compare changes in oxygenation after manual turning and percussion (standard therapy) and after automated rotation and percussion (kinetic therapy). DESIGN: Randomized crossover trial. SETTING: General and cardiac pediatric intensive care units. PATIENTS: Intubated and mechanically ventilated pediatric patients who had an arterial catheter and no contraindications to using a PediDyne bed. INTERVENTIONS: Patients were placed on a PediDyne bed (Kinetic Concepts) and received 18 hrs blocks of standard and kinetic therapy in an order determined by randomization. MEASUREMENTS AND MAIN RESULTS: Arterial blood gases were measured every 2 hrs during each phase of therapy. Oxygenation index and arterial-alveolar oxygen tension difference [P(A-a)O(2)] were calculated. Indexes calculated at baseline and after each 18-hr phase of therapy were analyzed. Fifty patients were enrolled. Data from 15 patients were either not collected or not used due to reasons that included violation of protocol and inability to tolerate the therapies in the study. Indexes of oxygenation were not normally distributed and were compared using Wilcoxon signed rank testing. Both therapies led to improvements in oxygenation, but only those from kinetic therapy achieved statistical significance. In patients receiving kinetic therapy first, median oxygenation index decreased from 7.4 to 6.19 (p = .015). The median P(A-a)O(2) decreased from 165.2 to 126.4 (p = .023). There were continued improvements in oxygenation after the subsequent period of standard therapy, with the median oxygenation index decreasing to 5.52 and median P(A-a)O(2) decreasing to 116.0, but these changes were not significant (p = .365 and .121, respectively). When standard therapy was first, the median oxygenation index decreased from 8.83 to 8.71 and the median P(a-a)o(2) decreased from 195.4 to 186.6. Neither change was significant. Median oxygenation index after the subsequent period of kinetic therapy was significantly lower (7.91, p = .044) and median P(A-a)O(2) trended lower (143.4, p = .077). CONCLUSIONS: Kinetic therapy is more efficient than standard therapy at improving oxygenation and produces improvements in oxygenation that are more persistent.

Analysis of Variance↗

Kinetic roughening model with opposite Kardar-Parisi-Zhang nonlinearities.

We introduce a model that simulates a kinetic roughening process with two kinds of particle: one follows ballistic deposition (BD) kinetics and the other restricted solid-on-solid Kim-Kosterlitz (KK) kinetics. Both of these kinetics are in the universality class of the nonlinear Kardar-Parisi-Zhang equation, but the BD kinetics has a positive nonlinear constant while the KK kinetics has a negative one. In our model, called the BD-KK model, we assign the probabilities p and (1-p) to the KK and BD kinetics, respectively. For a specific value of p, the system behaves as a quasilinear model and the up-down symmetry is restored. We show that nonlinearities of odd order are relevant in this low nonlinear limit.

Journal Article↗

Detailed kinetic analysis of Shay chloroleukaemia cell population propagated in permanent suspension culture in vitro.

Detailed kinetic analysis of a growing cell population is difficult, even when assay conditions are nearly ideal. Therefore, it is usually essential to perform several types of experiments and analyse all the results in terms of a mathematical model, the use of which is not limited a priori by a specified application. In the present study we investigated cell population kinetics using rat chloroleukaemia cells propagated in suspension culture in vitro. The parameters were measured: doubling time of the population, fraction of labelled mitoses, changes in labelling index with time after pulse labelling, continuous labelling and stathmokinetic index. Analysis of the results was based on a computer program CECAM, which is a stochastic model capable of simulating essentially all types of kinetic experiments based on presently known assay techniques. The results showed that precise and reliable information on cell population kinetics could not be obtained from the analysis of any single type of experimental data. In particular, the technique of labelled mitoses underestimated the duration of the G1 phase, owing to subtle label-induced changes in population behaviour. These changes could not have been detected with any certainty without rigorous quantitative comparisons with other types of experimental data. As a whole, however, results obtained by the different techniques were in agreement and the kinetic behaviour of chloroleukaemia cells in vitro could be established in detail. In certain circumstances even minute changes in the kinetic parameters of the cells can modify population behaviour drastically. To study these cases adequately the experiments must be designed with utmost care, preferably with the aid of preceding simulations. This is because demonstration of small primary changes in population kinetics may be beyond the limit of detection of any single assay method.

Animals↗

[Ultrastructure and cytochemistry of the pellicle and apical complexes of the kinete of Babesia bigemina and Babesia ovis in the hemolymph and oavry of the tick].

The term kinete is used in this paper for the cigar-shaped, motile development stages (VERMICULE") OF Babesia occurring intra- and extracellularly in hemolymph and overy (including oocytes) of vectors, hard ticks (Ixodoidea). The structure of, and cytochemical activities of hydrolases (acid phosphatase, nonspecific esterase) in the pellicle and the apical complex was studied at the fine-structural level in kinetes of Babesia bigemina Smith & Kilborne, in hemolympho of female Boophilus microplus Canestrini. The cytochemistry of acid hydrolases was studied also in kinetes of Babesia ovis (Babès) Starcovici, in hemolymph and ovary of Rhipicephalus bursa Canestrini & Fanzago. The pellicle of the B. bigemina kinetes is composted of 3 membranes (pellicular complex): an outer membrane, approximately 8 nm thick (the plasmalemma) and 2 innder ones, each approximately nm thick, lying closely together. The outer membrane appears to be covered by a structureless coat, 3 nm thick. The space between the inner double membrane and the plasmalemma is 7.5 nm. The whole pellicular complex is 30 nm in diameter. The 2 inner pellicular membranes appear to be derived from the endoplasmic reticulum (ER) for the following reasons: (a) a layer of hydrolase-active material is enclosed by these membranes; (b) in the spheroid parasite stages which transform from kinetes inside hemocytes, the inner double membrane is apparently replaced by an ER cisterna; (c) the thickness of each of the inner pellicular membranes is approximately the same as that of the ER membrane. There are circular openings in the pellicular double membrane with average diameters of 100 nm; despite some similarity to micropores, they have a specific structure. The term Intrapellikularfenster (IPF) (intrapellicular windows) or pseudomicropores is proposed for these pellicular differentiations. The margin of an IPF is formed by the 2 inner membranes folding into each other; cytoplasmic, electron-dense material is accumulated alongside this edge. Unlike that of micropores, the plasmalemma of the IPF is not invaginated. The IPF appears as a single, dark ring in tangential sections. At times, rhoptry-like bodies are associated with the openings. The function of the IPF is not known. An intrapellicular opening similar to the IPF, although wider, is present at the apex of the parasite. Its margin coincides with the inners edge of the apical ring. Typical subpellicular microtubuli were not observed in the Babesia kinetes. The apical complex of the B. bigemina kinetes consists of an Apikalschirm (apical umbrella), a crown of microtubuli beneath it, and rhoptries: micronemes are also present in large numbers. The Apikalschirm is located beneath the pellicle of the apical pole of the parasite. It is a wheel-like structure composed of spokes radiating from a wide, hub=like central ring (apical ring). It should be stressed that the apical ring is not identical with the polar ring described as an integral part of the pellicular complex in other Apicomplexa...

Acid Phosphatase↗

Muscle capillary blood flow kinetics estimated from pulmonary O2 uptake and near-infrared spectroscopy.

The near-infrared spectroscopy (NIRS) signal (deoxyhemoglobin concentration; [HHb]) reflects the dynamic balance between muscle capillary blood flow (Q(cap)) and muscle O(2) uptake (Vo(2)(m)) in the microcirculation. The purposes of the present study were to estimate the time course of Q(cap) from the kinetics of the primary component of pulmonary O(2) uptake (Vo(2)(p)) and [HHb] throughout exercise, and compare the Q(cap) kinetics with the Vo(2)(p) kinetics. Nine subjects performed moderate- (M; below lactate threshold) and heavy-intensity (H, above lactate threshold) constant-work-rate tests. Vo(2)(p) (l/min) was measured breath by breath, and [HHb] (muM) was measured by NIRS during the tests. The time course of Q(cap) was estimated from the rearrangement of the Fick equation [Q(cap) = Vo(2)(m)/(a-v)O(2), where (a-v)O(2) is arteriovenous O(2) difference] using Vo(2)(p) (primary component) and [HHb] as proxies of Vo(2)(m) and (a-v)O(2), respectively. The kinetics of [HHb] [time constant (tau) + time delay [HHb]; M = 17.8 +/- 2.3 s and H = 13.7 +/- 1.4 s] were significantly (P < 0.001) faster than the kinetics of Vo(2) [tau of primary component (tau(P)); M = 25.5 +/- 8.8 s and H = 25.6 +/- 7.2 s] and Q(cap) [mean response time (MRT); M = 25.4 +/- 9.1 s and H = 25.7 +/- 7.7 s]. However, there was no significant difference between MRT of Q(cap) and tau(P)-Vo(2) for both intensities (P = 0.99), and these parameters were significantly correlated (M and H; r = 0.99; P < 0.001). In conclusion, we have proposed a new method to noninvasively approximate Q(cap) kinetics in humans during exercise. The resulting overall Q(cap) kinetics appeared to be tightly coupled to the temporal profile of Vo(2)(m).

Adult↗

Processing of kinetically defined boundaries in areas V1 and V2 of the macaque monkey.

We recorded responses in 107 cells in the primary visual area V1 and 113 cells in the extrastriate visual area V2 while presenting a kinetically defined edge or a luminance contrast edge. Cells meeting statistical criteria for responsiveness and orientation selectivity were classified as selective for the orientation of the kinetic edge if the preferred orientation for a kinetic boundary stimulus remained essentially the same even when the directions of the two motion components defining that boundary were changed by 90 degrees. In area V2, 13 of the 113 cells met all three requirements, whereas in V1, only 4 cells met the criteria of 107 that were tested, and even these demonstrated relatively weak selectivity. Correlation analysis showed that V1 and V2 populations differed greatly (P < 1.0 x 10(-6), Student's t-test) in their selectively for specific orientations of kinetic edge stimuli. Neurons in V2 that were selective for the orientation of a kinetic boundary were further distinguished from their counterparts in V1 in displaying a strong, sharply tuned response to a luminance edge of the same orientation. We concluded that selectivity for the orientation of kinetically defined boundaries first emerges in area V2 rather than in primary visual cortex. An analysis of response onset latencies in V2 revealed that cells selective for the orientation of the motion-defined boundary responded about 40 ms more slowly, on average, to the kinetic edge stimulus than to a luminance edge. In nonselective cells, that is, those presumably responding only to the local motion in the stimulus, this difference was only about 20 ms. Response latencies for the luminance edge were indistinguishable in KE-selective and -nonselective neurons. We infer that while responses to luminance edges or local motion are indigenous to V2, KE-selective responses may involve feedback entering the ventral stream at a point downstream with respect to V2.

Analysis of Variance↗

Cellular Senescence: Ex Vivo p53-Dependent Asymmetric Cell Kinetics.

Although senescence is a defining property of euploid mammalian cells, its physiologic basis remains obscure. Previously, cell kinetics properties of normal tissue cells have not been considered in models for senescence. We now provide evidence that senescence is in fact the natural consequence of normal in vivo somatic stem cell kinetics extended in culture. This concept of senescence is based on our discovery that cells engineered to conditionally express the well-recognized tumor suppressor protein and senescence factor, p53, exhibit asymmetric cell kinetics. In vivo, asymmetric cell kinetics are essential for maintenance of somatic stem cells; ex vivo, the same cell kinetics yield senescence as a simple kinetic endpoint. This new "asymmetric cell kinetics model" for senescence suggests novel strategies for the isolation and propagation of somatic tissue stem cells in culture.

Journal Article↗

Oxygen uptake kinetics of older humans are slowed with age but are unaffected by hyperoxia.

Cross-sectional studies have compared the oxygen uptake (VO2) kinetics during the on-transient of moderate intensity exercise in older and younger adults. The slower values in the older adults may have been due to an age-related reduction in the capacity for O2 transport or alternatively a reduced intramuscular oxidative capacity. We studied: (1) the effects of ageing on VO2 kinetics in older adults on two occasions 9 years apart, and (2) the effect of hyperoxia on VO2 kinetics at the second test time. After a 9 year period, follow-up testing was undertaken on seven older adults (78 +/- 5 years, mean +/- S.D.). They each performed six repeats of 6 min bouts of constant-load cycle exercise from loadless cycling to 80% of their ventilatory threshold. They breathed one of two gas mixtures (euoxia: inspired O2 fraction, FI,O2, 0.21; hyperoxia: FI,O2, 0.70) on different trials determined on a random basis. Breath-by-breath VO2 data were time aligned and ensemble averaged. VO2 kinetics, modelled with a single exponential from phase 2 onset (+20 s) to steady state and described by the exponential time constant (tau) were compared with data collected from the same adults 9 years earlier. One-way repeated measures analysis of variance revealed that tau was slowed significantly with age (from 30 +/- 8 to 46 +/- 10 s), but was unaffected by hyperoxia (43 +/- 15 s). We concluded that: (1) in older adults studied longitudinally over a 9 year period, the on-transient VO2 kinetics are slowed, in agreement with, but to a greater extent, than from cross-sectional data; and (2) the phase 2 time constant (tau) for these older adults was not accelerated by hyperoxic breathing. Thus the expected hyperoxia-induced increase in the capacity for O2 transport was not associated with faster on-transient VO2 kinetics suggesting either that O2 transport may not limit VO2 kinetics during the 8th decade, or that O2 transport was not improved with hyperoxia.

Aged↗

[Nadir PSA and kinetics of PSA decline between the 3rd and 6th month after external beam radiotherapy for T1 T2 Nx M0 localized prostate cancer: value of the prediction of the risk of biological progression].

INTRODUCTION: This study analyses the results of external beam radiotherapy in stage T1 T2 Nx M0 prostate cancer, with reference to the nadir PSA and the kinetics of PSA decline. MATERIAL AND METHODS: 65 patients with T1 T2 Nx M0 localized prostate cancer were treated by external beam radiotherapy (conventional or conformal) between 1990 and 1999. Two populations of 22 and 25 patients were distinguished according to the nadir PSA: population A with a nadir < or = 0.5 ng/ml or not yet reached, but with PSA < or = 0.5 ng/ml and population B with a nadir > 0.5 ng/ml. The various clinical and laboratory parameters and the kinetics of PSA decline (calculation based on the course of PSA between the first 3 and 6 months after irradiation) were compared by statistical tests (Chi-square, Student t test). According to the ASTRO criteria, the results in terms of absence of biochemical progression were evaluated by non-parametric Kaplan-Meier estimate. RESULTS: No biochemical progression was observed in population A with a mean follow-up of 29.5 months. The absence of biochemical progression in population B at 42 months was 52.77%. The baseline PSA (p = 0.009), the dose delivered (p = 0.027), and the kinetics of PSA decline (p = 0.0069) were identified as predictive factors. The patient with a zero kinetic developed biochemical progression, while 91.3% of patients with a kinetic < 0.35 ng/ml/month remained free of biochemical progression. A group of patients (median nadir: 0.8 ng/ml, baseline PSA < 10 ng/ml and kinetic < 0.35 ng/ml/month) was distinguished by its good prognosis. CONCLUSION: In stage T1-T2 prostate cancer, the value of the nadir PSA is an essential prognostic factor. The kinetics of PSA decline appear to have an early predictive role.

Aged↗

A review of urea and creatinine kinetics in predicting CAPD outcome.

The adequacy of the peritoneal dialysis prescription is of great concern. Although the use of urea kinetics has become the standard in hemodialysis, its usefulness in peritoneal dialysis is unclear. It has been suggested that creatinine clearance may correlate with clinical outcome in CAPD but, as with urea kinetics, its predictive value is not established. The efficacy number (EN), which only requires a four hour exchange, was introduced as a simpler approach to creatinine kinetics. These three kinetic models were correlated to clinical outcome in 18 stable CAPD patients over a 12 month study period. The patients were divided into three groups: good (G), intermediate (I), and poor (P) based on uremic symptoms, mortality, hospital days, biochemical indices and the need for transfer to hemodialysis. Both forms of creatinine kinetics (weekly creatinine clearance, EN) were able to differentiate between the G, I, and P outcome groups (P < 0.05). The weekly uea Kt/V was able to differentiate between the G and P groups (P < 0.05) but not between the I and the other two outcome groups. Both urea and creatinine kinetics predict clinical outcome in CAPD. However, creatinine kinetics may be a more sensitive predictor. The efficacy number was just as sensitive as creatinine clearance in predicting clinical outcome yet simpler to gather the data for its calculation.

Creatinine↗